Pediatric Rehabilitation Principles and Practice 4th Edition

["Chapter 16 The Assessment of Human Gait, Motion, and Motor Function 473 Initial contact (Foot-strike) Tibia vertical Terminal Loading Opposite swing response Foot-off Mid- Swing Stance Mid- Heel-off swing period period stance (Body leads foot) Initial Terminal swing stance Feet adjacent Per- (Knee extends) swing Foot-off Opposite (Terminal contact) Initial contact Figure 16.12 Typical gait cycle wrapped around a unit circle and subdivided into eight gait phases that have functional signi\ufb01cance. The \ufb01rst phase is initial contact, and is equivalent to the temporal event by the same name. The phases are drawn in sequence and are equally spaced for clarity, but do not represent their usual duration. Refer to the text for a complete description of the phases and their functional signi\ufb01cance. event delineating the beginning and end of each phase. feet-adjacent, and tibia vertical. These terms have been Phases are shown equally spaced in this figure for clar- used by Whittle (5) and others (4,38) and are useful to ity; typically, each phase will not be of the same time delineate the phases in normal gait; however, there is not duration. Initial contact is considered a phase of gait yet a consensus among gait investigators if these are the since it marks an important transitional point between undisputed event markers. For example, Perry acknowl- swing limb advancement and the challenging task of edges that a rising heel usually marks the beginning of weight acceptance, although unlike the other phases, it terminal stance in normal subjects, but in patients with is a single instant in time. The other important transi- weak ankle plantar flexors, this heel-off may be delayed tional period (from stance to swing) occurs during final into pre-swing, which would technically eliminate the double support and is known as the phase of pre-swing. terminal stance phase. Dr. Perry prefers to identify the In terms of temporal events, final double support (and beginning of terminal stance as the point where the body therefore pre-swing) is considered part of stance period moves ahead of the limb and weight is transferred onto because this interval ends with foot-off. However, in the forefoot (39). Similarly, the event marking the tran- terms of gait phases, this interval also marks the first sition between initial swing and mid-swing has been phase of the swing limb advancement task, highlight- identified as the point where the feet are adjacent (5), ing the fact that from a functional standpoint, pre-swing when the swing limb is directly under the body (4,38), has more to do with preparing the limb for moving for- when swing limb acceleration changes to deceleration ward than supporting the body during stance (24). Also in normal gait (36), where the knee begins to extend notice that three new temporal events not associated and the foot clears the ground (39), and mid-swing (4). with foot\/floor contact have been introduced: heel-off, Fortunately, most investigators agree that the temporal","474 Pediatric Rehabilitation event marking the transition between mid-swing and events over the entire cycle, with one or more critical terminal swing is the point where the tibia is directly events in each of the 8 phases. Critical events occur at vertical. These slight differences in the definition of the the foot, ankle, knee, or hip, and are largely focused exact transition between phases are why some investi- on angular displacements in the sagittal plane. While gators report different phase durations for normal gait. there are other, more subtle motions occurring in all This shouldn\u2019t be a concern, however, because deter- three anatomical planes, these 13 critical events are mining the exact transition point between phases and considered the most essential to producing a normal comparing phase durations to normal are less impor- walking pattern, typically have the largest displace- tant than recognizing that there are distinct phases in ments, and are most easily observed from the walking gait that can be identified and that certain functional subject, with or without the help of recording instru- accomplishments must occur in each phase. ments. The significance of this approach is that once the critical events that are essential to producing a bipedal CRITICAL EVENTS LINK GAIT gait pattern are known, one can use the measures from IMPAIRMENTS TO POSSIBLE instrumented gait analysis to determine functional INTERVENTIONS reasons for why a particular critical event is absent, altered, or delayed. Interventions can then be focused With the gait cycle now subdivided both temporally on restoring critical events, leading to improved walk- and functionally into discrete phases, all that is left is ing performance. The critical events for each phase of to identify specific joint positions or motions in each gait are shown in Table 16.3, including their relationship phase that directly contribute to the accomplishment of to stance and swing periods and each gait task. Notice the three functional tasks of weight acceptance, single that critical events and temporal events are quite dif- limb support, and swing limb advancement. Dr. Perry ferent. As has been discussed throughout this chapter, and her colleagues at Rancho Los Amigos Medical temporal events are moments or instants in time used Center refer to these specific joint positions or motions to delineate periods in the gait cycle, and critical events as critical events (39). They have identified 13 critical are important functional components that can be used to identify gait impairments. 16.3 Relationship Between Periods, Tasks, Phases, Temporal Events, and Critical Events During the Gait Cycle STANCE PERIOD SWING PERIOD TASKS WEIGHT ACCEPTANCE SINGLE LIMB SUPPORT SWING LIMB ADVANCEMENT Phases Initial Loading Mid-stance Terminal Pre-swing Initial Mid-swing Terminal contact response (12%\u201330%) stance (50%\u201362%) swing (75%-87%) swing Temporal (0%) (0%\u201312%) (30%\u201350%) (62%\u201375%) (87%\u2013100%) events B: Opposite B: Opposite B: Foot-off B: Feet B: Tibia Initial B: Initial foot-off B: Heel-off initial E: Feet adjacent contact contact (body contact (knee vertical E: Heel-off leads adjacent extends) E: Initial E: Opposite (body leads foot) E: Foot-off (knee foot-off foot) extends) E: Tibia contact E: Opposite \u2022 Passive vertical Critical \u2022 Heel \u2022 Hip \u2022 Controlled initial knee \u2022 Max knee \u2022 Knee events first stability tibial contact flexion to flexion \u2022 Max hip extension initial advance- 40\u00b0 (>60\u00b0) flexion to neutral contact \u2022 Controlled ment \u2022 Controlled (25\u00b0) knee ankle DF \u2022 Rapid flexion with heel ankle PF \u2022 DF to for shock rise neutral absorption \u2022 Trailing \u2022 Controlled limb ankle PF posture B, beginning; DF, dorsiflexion; E, end; PF, plantarflexion.","Chapter 16 The Assessment of Human Gait, Motion, and Motor Function 475 Critical Events During demand (quadriceps avoidance gait). Again, these pat- terns are reflected in kinematic, kinetic, and dynamic the Weight Acceptance Task EMG measurements, within the context of meeting the needs of this critical event. Correctly controlled The two phases associated with weight acceptance, knee flexion during loading response is reflected in initial contact and loading response, coincide with the the slope and maximum knee flexion value during the period of initial double support, and include four critical first peak of the sagittal plane knee joint angular dis- events. The first critical event, a heel-first initial con- placement curve, in the magnitude of the knee exten- tact, must be present if forward momentum is to be pre- sor moment and power absorption curve, and the EMG served (24) and the energy from the falling body COM activity of different heads of the quadriceps. is to be redirected in the direction of progression (32). It is also necessary to prepare the new support limb The final critical event during loading response is for the demands of the next phase. The next three crit- controlled ankle plantar flexion. In this context, \u201ccon- ical events of hip stability, controlled knee flexion for trolled\u201d is referring to the ability of the ankle dorsi- shock absorption, and controlled ankle plantar flex- flexors to eccentrically contract and lower the initially ion, must occur during the loading response phase. neutral foot carefully to the ground to provide a more Hip stability requires dynamic joint stiffness in the stable base of support than can be provided by the sagittal and frontal planes at the hip to prevent unnec- calcaneus alone. This action is referred to as the heel essary forward pelvic tilt or increased pelvic obliquity, or first rocker (40), the first of three important mecha- respectively. This places a high demand on the torque nisms that occur at the foot and ankle and facilitate (moment) production ability of the hip extensors and progression of the entire stance limb (31). These three hip abductors of the forward load-bearing limb. This rockers are illustrated in Figure 16.13. If the pretibial demand is reflected in increased muscle activation muscles have sufficient strength to restrain the rate of (recorded using dynamic EMG) in the gluteus maxi- foot drop, the action of the first rocker pulls the tibia mus, gluteus medius, and hamstrings. If a patient has forward, which in turn is transferred to the femur by weak hip extensors and fails to compensate for this the active quadriceps that is attempting to restrain the weakness, there will be an increased anterior pelvic rate of knee flexion. This is how the energy of the tilt and\/or forward trunk lean directly associated with falling body COM is redirected to provide forward the inability of the hip extensors to meet the demand progression, an important energy-conserving mecha- of this critical event. Alternatively, if the subject is nism often lost when the heel rocker is absent. If the successfully compensating for the weakness, they will pretibial muscles did not have sufficient strength but exhibit a posterior trunk lean to position the whole the subject was able to achieve a heel-first initial con- body COM behind the hip joint center, thus reducing tact, a noticeable foot-slap would occur as the unsta- the torque production demand on the hip extensors. ble lever at the ankle allows the foot to plantar-flex Evidence of either strategy is reflected in recordings of uncontrollably. This is reflected in a steep descend- the hip sagittal plane angles (kinematics), the weight ing initial slope on the sagittal plane ankle kinematic line (ground reaction force vector), dynamic EMG of curve and absence of either a dorsiflexor moment or the hip extensors, or by calculating the hip extensor dorsiflexor power absorption on the corresponding moments and powers (kinetics). Similar strategies sagittal plane kinetic curve (22). Experienced clini- are used when there is weakness in the hip abduc- cians can also detect this event without all the mod- tors, leading to either uncompensated or compensated ern conveniences by simply listening for the sound of Trendelenburg\u2019s gait patterns in the frontal plane. All the foot-slap! The effects of uncontrolled ankle plantar can be related to the loss of the critical event of hip flexion at loading response are not as easy to detect stability during the loading response phase. when the subject fails to achieve a heel-first initial contact, as is the case with foot-flat, forefoot, or equi- Controlled knee flexion for shock absorption must nus initial contact. In this case, kinetic data are help- occur to prevent unnecessary knee flexion during ful, because as the point of foot\/floor load bearing loading response, which wastes energy and places a moves further in front of the ankle with progressively higher demand on the quadriceps. Similar to the hip, increasing plantar flexion at initial contact, there is a quadriceps weakness can also be either compensated proportional increase in the magnitude of the incor- or uncompensated. Uncompensated quadriceps weak- rect plantar flexor moment during loading response. ness will present as abnormal or increased knee joint This plantar flexor moment (via the triceps surae) has angular displacements in the sagittal plane (increased opposite the desired effect on the knee, as occurs with knee flexion) with possible collapse at the knee. eccentric contraction of the pretibial muscles when a Compensated patterns will display body postures that true heel rocker is present; the knee extends when shift the COM forward (forward trunk lean) so that it should be flexing (41). This reduces the effective- the ground reaction force vector is closer to or in front ness of knee shock absorption and may eliminate it of the knee joint, thereby reducing the quadriceps","476 Pediatric Rehabilitation Heel Rocker Ankle Rocker Forefoot Rocker Figure 16.13 The three rockers representing normal ankle function in gait: These are the heel or \ufb01rst rocker, the ankle or second rocker, and the forefoot or third rocker. The lighter gray skeleton represents the beginning of each rocker, and the arrows signify the movement that is associated with each. Refer to the text for a full description of these important critical events. completely, increasing bone-on-bone forces at the Critical Events During knee. The amount of shock-absorbing energy trans- ferred to the hip and ankle is reflected in the hip, the Single Limb Support Task knee, and ankle powers during this phase, and is use- ful for describing the potential degree of impairment As shown in Table 16.3, there are three critical associated with incorrect ankle function at loading events during the single limb support task. These response. Note that the magnitude of the EMG activity are controlled tibial advancement during mid-stance, of the pretibial and posterior compartment muscles by controlled ankle dorsiflexion with heel rise (heel-off) themselves do not explain the moments at the ankle, during terminal stance, and a trailing limb posture dur- since major force contributors arise from the inertial ing terminal stance (39). During the two phases of this and gravitational forces that occur during the first task (mid-stance and terminal stance), the responsi- rocker. The EMG activity does help sort out if the pat- bility of the stance limb is to simultaneously provide tern of motion is due to weakness (pretibial muscles support against gravity without losing balance and with first rocker present, triceps surae without it), contain the forward momentum built up by the con- neglect (often seen in traumatic brain injury [TBI]), or tralateral swinging limb. Both of these objectives can poor motor control (seen in cerebral palsy or cerebro- be accomplished by controlling tibial advancement in vascular accident [CVA]). This information can assist the first half of single support and controlling ankle in determining whether a solid, leaf-spring, hinged, dorsiflexion in the second half. This will lead to the or floor-reaction AFO, Botox injections into the calf trailing limb posture (body COM forward of the base musculature, or tendon lengthening or transfer sur- of support) necessary to permit a sufficient step length gery would be the most appropriate intervention to on the opposite side. If, at the end of loading response, use when the critical event of controlled ankle plantar the foot has achieved foot-flat, then during mid-stance, flexion is abnormal or absent. Table 16.4 summarizes the ankle becomes the axis of rotation for the body\u2019s many of the gait measurements that are useful for forward progression. This is referred to as the ankle identifying functional causes for absent or abnormal or second rocker, and this mechanism continues until critical events during the weight acceptance task, and maximum dorsiflexion is achieved in terminal stance while not exhaustive, can help organize the array of (Fig. 16.13). With the heel and forefoot firmly planted, measures available for assessing impairments during the tibia can rotate over the talus smoothly under the this task. selective control of the soleus, later assisted by both heads of the gastrocnemius, which simultaneously","16.4 Gait Measurements Useful for Identifying the Cause of an GAIT PHASE CRITICAL EVENT PHYSICAL EXAM TEMPOR AL \/DIST. K Initial contact (ABNORMAL OR MEASURES \u2022 ABSENT) Strength \u2022 Reduced swing \u2022 Loading Heel first initial \u2022 weak ankle DF \u2022 response period, or reduced contact: if absent, ROM single support time \u2022 also consider mid- on opposite side \u2022 swing and terminal \u2022 tight hamstrings or \u2022 Reduced step length \u2022 swing critical events triceps surae \u2022 \u2022 Prolonged initial Hip stability Neurologic triceps double support time \u2022 surae tone \u2022 Controlled knee \u2022 Prolonged initial flexion for shock Strength double support time \u2022 absorption \u2022 \u2022 weak hip \u2022 Prolonged initial \u2022 Controlled ankle extensors double support time plantarflexion (PF) \u2022 weak hip \u2022 Reduced time abductors to foot-flat, with possible foot-slap ROM \u2022 tight hip flexors, hip flexion contracture \u2022 femoral anteversion Strength \u2022 weak quadriceps ROM \u2022 tight hamstrings or knee flexion contracture Strength \u2022 weak ankle DF ROM \u2022 tight triceps surae or reduced DF \u2022 tight hamstrings or knee flexion contracture 477 DF, dorsiflexion; PF, plantarflexion; ROM, range of motion.","Absent or Abnormal Critical Event During the Weight Acceptance Task K INEMATICS KINETICS DYNAMIC EMG \u2022 Hip flexion > or < normal Refer to phases terminal \u2022 Excessive hip extensor or max of 30\u00b0 swing or loading response hamstring activity \u2022 Knee flexion >4\u00b0 \u2022 Reduced or absent ankle \u2022 Ankle not at neutral DF activity \u2022 Premature ankle PF activity \u2022 Hip flexion >30\u00b0 \u2022 Large hip extensor \u2022 Excessive hip flexor and \u2022 Increased pelvic tilt and\/or moment with possible hip adductor activity initial power absorption obliquity \u2022 Decreased hip extensor \u2022 Increased hip internal and abductor activity rotation \u2022 Pelvic retraction on side of weakness \u2022 Knee flexion < 4\u00b0 or > 20\u00b0 \u2022 Initial knee flexor moment \u2022 Excessive knee extensor \u2022 Abnormal knee flexion with no phase reversal activity (quad avoidance) wave \u2022 Increased co-contraction \u2022 Large knee extensor at the knee with prolonged \u2022 Tibia forward of vertical moment with excessive knee flexor activity with ankle in DF power absorption \u2022 Reduced or absent ankle \u2022 Abnormal 1st rocker (heel \u2022 Large PF moment with DF activity rocker) high power absorption \u2022 Premature ankle PF \u2022 Incorrect foot alignment activity with incorrect foot progression angle \u2022 Premature tibialis posterior activity","478 Pediatric Rehabilitation limits knee extension. The slow-twitch, fatigue- heel-off, spring-foot), the normal ankle and forefoot resistant muscle fibers of the soleus are usually well rocker mechanisms may not be effective, and the suited to the sustained eccentric contractions required three critical events of single limb support will not to control tibial advancement. Weakness in the tri- be achieved. In toe-toe gait (equinus) or jump knee ceps surae, however, results in the tibia advancing too gait (forefoot initial contact and excessive knee flexion quickly, which prematurely allows the tibia to move at loading response, followed by rapid knee extension past vertical and leads to sustained knee flexion dur- and ankle plantar flexion in mid stance), plantar flex- ing mid-stance, and premature or excessive dorsiflex- ors that are tight or have increased tone overly con- ion and lack of knee extension at terminal stance. In strain forward tibial advancement in mid-stance and this circumstance, a rigid AFO or, in extreme cases of dorsiflexion in terminal stance, leading to excess knee weakness, a floor-reaction AFO can effectively supple- extension and early heel-rise. While the mechanism ment the weak plantar flexors, restore a more normal is different from the case of weak plantar flexors, the plantar flexor moment, and control tibial advancement end result is the same; reduced effectiveness of second during mid-stance and dorsiflexion during terminal and third rockers and inability to achieve the three stance. Gage also suggests using a rear-entry, hinged, critical events. In these cases, Botox injections into the floor-reaction AFO in these circumstances (12), which triceps surae, tendoachilles lengthening, or intramus- permits ankle plantar flexion but resists dorsiflexion cular triceps surae lengthening (Strayer procedure) in mid-stance and terminal stance. can be effective in restoring second and third rockers, depending on severity. Ankle plantar flexion moments In normal adults and typically developing chil- and powers, and dynamic EMG recordings are quite dren, the forward progression of the body causes the useful in selecting which procedure is most appropri- origin of the ground reaction force vector (center of ate (22). Another example is crouch gait deformity, pressure or COP) to move forward to the metatarsal where hip and knee contractures combined with weak heads, causing the heel to rise at the beginning of ter- or overlengthened plantar flexors lead to early heel- minal stance. Now the axis of rotation for the body\u2019s rise and premature forward advancement of the tibia forward progression is the metatarsophalangeal (MTP) in mid-stance, and premature and excessive dorsiflex- joint, giving rise to the forefoot or third rocker (31) ion in terminal stance. In this case, the same impact (see Fig. 16.13). While the first two rockers were con- on the second and third rockers described previously straining forward progression using eccentric plantar for weak plantar flexors will often occur. Dr. Gage has flexor contractions, the forefoot rocker is an acceler- long been a proponent of performing single-event, ating rocker, as evidenced by the large ankle plantar multilevel (SEML) soft tissue and bony surgery for this flexor moment and transition from power absorp- deformity to restore the proper rocker mechanisms tion to power generation (36). With the help of strong and, with the proper orthotics, the plantar flexion\/ concentric contraction of the fast-twitch fibers of the knee extension couple that allows the patient to stand gastrocnemius, the ankle is stabilized and contin- more erect and walk more effectively (12). Other cen- ued dorsiflexion in terminal stance is halted. By the ters have taken a more conservative approach of staging end of terminal stance, the ankle is plantar flexing the procedures, which has the advantage of reducing in preparation for initial contact on the other side, the surgical impact at the time of the procedure, but which yields the trailing limb posture necessary for may cause muscle imbalances at other joints, leading maximum step length. When there is plantar flexor to additional surgeries down the road. In either case, weakness, the third rocker is ineffective, which fails or when nonsurgical interventions are warranted, the to control continued dorsiflexion, allows the knee to goal should be to restore the rocker mechanisms so prematurely drop into flexion, reduces trailing limb that the three critical events of single limb support can posture, and shortens the opposite side step length. All be realized. Table 16.5 summarizes many of the gait of these factors reduce overall walking performance. measurements that are useful in identifying causes for AFOs that store energy in the structure of the ortho- absent or abnormal critical events during the single sis as the ankle dorsiflexes (rigid, leaf-spring, floor- limb support task. reaction) can provide a plantar flexion assist as the foot is unweighted in early pre-swing, depending on Critical Events During the amount of stiffness and energy storage built into the Swing Limb Advancement Task the custom orthotic. This assist can return some of the reduced plantar flexor moment that would occur with- Swing limb advancement is the last task that must out orthotic use, and evidence of this can be found in be accomplished to complete the gait cycle, and, as the plantar flexor moment curve comparing orthotic shown in Table 16.3, this task contains four phases and barefoot conditions. and six critical events. There are two critical events in pre-swing: passive knee flexion to 40 degrees and If, at the beginning of mid-stance, the foot has either not achieved or is past foot-flat (equinus, early","16.5 Gait Measurements Useful for Identifying the Cause of an A GAIT PHASE CRITICAL EVENT PHYSICAL EXAM TEMPOR AL \/DIST. K Mid-stance (ABNORMAL OR MEASURES \u2022 ABSENT) Strength \u2022 \u2022 With equinus (early Controlled tibial \u2022 weak ankle PF heel-of f ) \u2022 advancement (advance too fast) \u2022 \u2022 excessive DF \u2022 Terminal stance Controlled ankle ROM without equinus dorsiflexion (DF) (delayed heel-off) \u2022 with heel-off \u2022 with equinus, \u2022 or excessive DF \u2022 Reduced single Trailing limb posture without equinus support time (advance too fast) \u2022 Reduced opposite \u2022 tight triceps surae step length or hamstrings (advance too slow) \u2022 With equinus (early heel-of f ) Neurologic \u2022 excessive DF \u2022 triceps surae tone without equinus Strength (delayed heel-off) \u2022 weak ankle PF (DF \u2022 Reduced single too fast) support time ROM \u2022 Reduced opposite step length \u2022 excessive DF or reduced PF (DF too \u2022 Reduced single fast) support time \u2022 tight or increased \u2022 Reduced opposite tone in ankle PF (slow step length DF, early heel-off) Strength \u2022 weak ankle PF \u2022 weak opposite hip abductor ROM \u2022 excessive DF or reduced PF \u2022 tight hamstrings or tight hip flexors 479 DF, dorsiflexion; PF, plantarflexion; ROM, range of motion","Absent or Abnormal Critical Event During the Single Limb Support Task K INEMATICS KINETICS DYNAMIC EMG \u2022 Tibia forward of vertical \u2022 Abnormal slope (too flat) \u2022 Prolonged ankle DF with ankle in excessive DF of the PF moment curve activity \u2022 Abnormal 2nd rocker (ankle \u2022 Reduced or absent PF rocker) activity \u2022 Prolonged hip and knee extensor activity \u2022 Abnormal 2nd rocker (ankle \u2022 Abnormal slope (too flat) of \u2022 Prolonged ankle DF rocker) the PF moment curve activity \u2022 Excessive DF \u2022 Reduced or absent PF \u2022 Reduced or absent PF, \u2022 Premature knee flexion power absorption inverter, and everter activity \u2022 Excessive hip flexion \u2022 Prolonged hip ext. moment \u2022 Any activity in the hip or \u2022 Excessive knee flexion or delayed\/absent hip knee flexors, and hip or flexor moment knee extensors (lack of passive stability) \u2022 Prolonged knee ext. moment or delayed\/absent knee flexor moment","480 Pediatric Rehabilitation rapid ankle plantar flexion. As previously discussed, In initial swing, the only critical event is to pre-swing is an important transitional phase that, achieve maximum knee flexion of at least 60 degrees. while still a component of stance period, is function- If 40 degrees of knee flexion has been achieved at the ally more associated with preparing the trailing limb end of pre-swing and the hip flexors and adductor lon- for the swing period to come. Achieving 40 degrees of gus stop firing before the end of initial swing, then in knee flexion before the foot leaves the ground is essen- the absence of inappropriate quadriceps or hamstring tial. This is because once the foot is airborne, the leg activity, sufficient knee flexion should occur naturally acts as a compound pendulum, so further knee flexion during this phase. The point of maximum knee flexion is completely dependent on concentric contraction of must occur before the end of initial swing (not during the hip flexors, including the adductor longus, and the mid-swing or terminal swing), since this is the point inertia of the lower leg and foot (36). At normal walk- where the swinging limb must be at its shortest func- ing speeds, knee flexion during pre-swing requires no tional length to successfully clear the ground. The active muscle contractions around the knee (passive). ankle dorsiflexors (pretibials) are firing concentrically It occurs by a complex mechanism that involves con- at this time to bring the foot from its point of maxi- tinuation of tibial advancement as the forefoot rocker mum plantar flexion at the end of pre-swing to at least continues from terminal stance; unloading of the limb neutral by the end of initial swing so that toe clearance as weight is transferred to the new stance limb; contin- can be assured in mid-swing. In this phase, kinemat- ued concentric contraction of the triceps surae, which ics can be used to quantify the progress of the swing- produces rapid plantar flexion that propels the knee ing limb, joint moments in the sagittal plane should be joint in front of the ground reaction force vector, and near zero, and dynamic EMG can be used to identify concentric contraction of the adductor longus to ini- inappropriate muscle firing. Of particular interest in tially accelerate the thigh forward (31). this phase is the activity of the rectus femoris. This biarticulate muscle initially is active in late pre-swing All of these actions push the ground reaction force to assist with accelerating the thigh forward. At the vector so far behind the knee that it collapses in the moment the foot leaves the ground, continued activity absence of an equalizing knee extension moment pro- of the rectus femoris may assist with hip flexion, but duced by the quadriceps that normally are silent dur- may have the negative consequence of providing open- ing pre-swing. So weakness in the plantarflexors, hip chain knee extension through the patellar ligament. flexors, or adductor longus all have an adverse effect Since it has been shown that the brain uses the rec- on achieving the necessary knee flexion. Since a trail- tus femoris to accelerate the thigh to selectively con- ing limb posture with hip extension to 10 degrees trol step length and cadence during swing (36), if hip past neutral amplifies the effect of the third rocker flexor angular velocity is initially slow and 40 degrees to shift the tibia forward, hip flexion contracture can of knee flexion was not achieved at the moment of also reduce the ability of the knee to passively flex foot-off, the rectus femoris may increase its activation to 40 degrees, despite the fact that such a contrac- in initial swing to serve as an auxiliary hip flexor. This ture often prevents the knee from fully extending at abnormal compensatory activity of the rectus femoris terminal stance. Furthermore, it is interesting that is in an effort to produce increased thigh acceleration, because of the hip extensor component of the biarticu- but because of its biarticular structure, it yields the late hamstrings, inappropriate activation or tightness negative effect of producing a larger knee extension of these open-chain knee flexors can inhibit passive moment, exacerbating the problem of insufficient knee knee flexion in pre-swing by resisting the hip flexors flexion in swing. Whether the rectus femoris is firing and adductor longus as they attempt to accelerate the as a compensatory mechanism or because of incorrect thigh. Problems with this critical event can be identi- motor control associated with upper motor neuron fied from the sagittal plane knee kinematics, the hip injury, if it continues to be active at the end of initial moments and powers, and the hip knee and ankle swing, it may contribute to the abnormality known dynamic EMG. Problems with rapid plantar flexion, as stiff-knee gait, the common name given to the gait which is necessary to produce sufficient knee flexion abnormality of insufficient knee flexion in swing in pre-swing, are also evident from the ankle kine- period. If kinematic and electromyographic evidence matics, kinetics, and dynamic EMG. Since the critical (reduced knee flexion peak and\/or slope and pro- events in this phase are so dependent upon concentric longed activation) exist, then a rectus femoris transfer contraction and power generation at the hip and ankle, to the semimembranosus or sartorius may harness this interventions to replace hip flexor and ankle plantar inappropriate activity, or more likely, prevent concen- flexor strength are somewhat limited to AFOs that can tric knee extension from limiting peak knee flexion in return plantar flexion moment in pre-swing or enhance swing and thereby disrupt swing limb advancement. the third rocker, or stretching, lengthening, or weak- The rectus femoris transfer for the treatment of stiff- ening muscles that may be inhibiting hip flexion using knee gait is a surgical procedure that was conceived neurolytic agents or surgical procedures (42).","Chapter 16 The Assessment of Human Gait, Motion, and Motor Function 481 as a direct result of using IGA techniques (43) and has The final critical event in the gait cycle is knee been supported by a series of laboratory investigations extension to neutral during terminal swing. This rep- and long-term follow-up (44,45,46,47,48,49). It is now resents the last opportunity of the swinging limb to considered the standard of care for the treatment of reposition the foot prior to weight acceptance, and if stiff-knee gait when evidence from IGA confirms that this critical event is achieved, a sufficiently long step the rectus femoris is responsible for failure to achieve length will result. In typically developing children and the critical event of obtaining maximum knee flexion normal adults, hamstring activity will begin during of 60 degrees during initial swing. this phase to decelerate the swinging lower limb so that a small amount of knee flexion (<4 degrees) is The two critical events during mid-swing are both present at initial contact. In some cases during slow related to achieving toe clearance as the limb swings speed walking, the quadriceps will contract concen- through the lowest point in its arc of motion and it trically to assist with final knee extension, but in gen- is at greatest risk to inadvertently make contact with eral, this is unnecessary if the subject displays proper the ground. These critical events are maximum hip motor control. In addition to kinematic recordings to flexion to 30 degrees and neutral ankle dorsiflexion. confirm final position and dynamic EMG recordings to The hamstrings may fire near the end of mid-swing determine if there is excessive hamstring activity, large to begin decelerating the forward movement of the hip extensor and knee flexor moments with power thigh or to slow down the cadence, but generally these absorption just prior to initial contact may be indica- muscles should be silent until terminal swing. Note tors that the hamstrings are tight or display increased that after the swinging limb clears the floor, there is tone. Lack of full knee flexion in terminal swing is typically no further need for hip flexion, and add- one of the most common gait abnormalities in cerebral itional hip flexion will only decrease the likelihood palsy (50), and may require neurolytic injections or of achieving the final critical event during terminal surgical lengthening of the hamstrings and adductors swing: knee extension to neutral. Children with cere- when the physical exam and gait measurements pro- bral palsy and other patients with upper motor neu- vide appropriate evidence. As in the previous sections, ron disease have a difficult time motor programming a table has been prepared to summarize the gait mea- the previous two phases of motor activity, and often surements that are useful in detecting abnormalities display excessive knee and hip flexion with peak val- in the six critical events associated with swing limb ues later than normal during mid-swing. Kinematics advancement (Table 16.6). If all six of these critical and dynamic EMG can help identify these incor- events are performed successfully, the limb will be rect patterns, and the usual procedures of stretch- properly prepared for initial contact and ready to begin ing, lengthening, or injecting the offending muscles the cycle of gait events again. may be useful if they can permit the critical events in pre-swing and initial swing to occur. The critical The 8 phases and 13 critical events described in event of neutral dorsiflexion is usually the responsi- the previous sections and summarized in Table 16.3 bility of the ankle dorsiflexors, which typically ini- complete the functional decomposition of the gait tiate concentric activity in pre-swing. The pretibial cycle. Armed with this analysis framework, the pedi- muscles generally reduce their activity in this phase atric physiatrist can utilize IGA measurements, radio- since they no longer need to concentrically contract graphs, and a comprehensive physical exam to better from the plantar flexed position and are only needed understand the complex interactions of body structure to hold the foot against gravity. If they are weak or if and function that produce abnormal gait patterns in there is an upper motor neuron injury preventing nor- the pediatric patient. We will conclude this chapter mal motor control, foot drop will result, which will with a case study illustrating the use of this frame- adversely affect toe clearance and necessitate com- work in a subject with a common pediatric diagnosis pensatory mechanisms of circumduction at the hip, but a unique and challenging gait abnormality. increased ipsilateral pelvic obliquity (hip hiking) or contralateral early heel-off (vaulting). The most com- MOVEMENT ANALYSIS mon solution to this problem is to prescribe an AFO CASE STUDY\u2014DIPLEGIA with a plantar flexion stop to hold the foot in the correct position throughout swing period. In children Cerebral palsy is the most common cause of motor dis- and adults with TBI, dynamic EMG can be used to ability in children, with an incidence of approximately determine if the lack of dorsiflexion during swing is 2 to 3 per 1,000 live births in the United States. It is related to incorrect cortical control or an inability to most often associated with low birth weight, preterm correctly motor-plan the dorsiflexion activity. In the infants or with multiple births, and despite improved latter, training with biofeedback of muscle contrac- prenatal care, the incidence has not decreased in sev- tion may improve foot clearance during swing and eral decades. Of the four main types of cerebral palsy eliminate the requirement of using an AFO.","482 16.6 Gait Measurements Useful for Identifying the Cause of an GAIT PHASE CRITICAL EVENT PHYSICAL EXAM TEMPOR AL \/DIST. K (ABNORMAL OR MEASURES \u2022 ABSENT) \u2022 \u2022 Delayed foot-off Pre-swing Passive knee flexion Strength \u2022 Prolonged stance \u2022 to 40\u00b0 \u2022 Weak hip flexors \u2022 Initial swing ROM period Mid-swing Rapid ankle PF \u2022 Tight hip flexors \u2022 Terminal swing \u2022 Delayed foot-off \u2022 Maximum knee (limit hip extension) \u2022 Prolonged stance \u2022 flexion (>60\u00b0) Strength \u2022 \u2022 Weak ankle PF period \u2022 Maximum hip flexion ROM to 30\u00b0 \u2022 Excessive DF or \u2022 Asymmetric stance\/ \u2022 swing ratio Neutral DF reduced PF \u2022 Strength \u2022 High variability in \u2022 Knee extension to \u2022 Weak hip flexors swing period or step neutral ROM length \u2022 Tight rectus femoris \u2022 Asymmetric stance\/ Strength swing ratio \u2022 Weak hip flexors ROM \u2022 High variability in \u2022 Tight hamstrings swing period or step length Strength \u2022 Weak ankle DF \u2022 Asymmetric stance\/ ROM swing ratio \u2022 Tight ankle PF Strength \u2022 High variability in \u2022 Weak hip flexors or swing period knee extensors \u2022 Asymmetric stance\/ ROM swing ratio \u2022 Tight hamstrings Neurologic \u2022 High variability in \u2022 Hamstrings tone swing period or step length DF, dorsiflexion; PF, plantarflexion; ROM, range of motion.","Absent or Abnormal Critical Event During the Swing Limb Advancement Task K INEMATICS KINETICS DYNAMIC EMG \u2022 Insufficient hip extension \u2022 Reduced peak hip flexor \u2022 Reduced or absent at beginning of Pre-Swing moment and power adductor longus or hip (<10\u00b0) generation flexor activity \u2022 Incorrect slope, 2nd knee \u2022 Reduced knee extensor \u2022 Abnormal hamstring flexion peak power absorption activity \u2022 Abnormal 3rd rocker (heel \u2022 Reduced peak PF moment \u2022 Prolonged ankle PF rocker) at start of pre-swing activity into late Pre-Swing \u2022 Excessive DF early or \u2022 Reduced peak PF power \u2022 Inappropriate co- reduced PF late in pre- generation contraction of ankle PF, DF swing \u2022 Non-zero moments and \u2022 Reduced or absent \u2022 Reduced or delayed peak powers at hip, knee and adductor longus and hip knee flexion in swing ankle by end of Initial flexor activity Swing \u2022 Incorrect slope in knee \u2022 Reduced or absent ankle flexion wave \u2022 Non-zero moments and DF activity powers at the hip \u2022 Slow ankle DF \u2022 Prolonged rectus femoris \u2022 Max hip flexion late or in \u2022 Premature knee flexor activity power absorption next phase \u2022 Premature hamstring \u2022 Abnormal pelvic obliquity \u2022 Non-zero moments and activity powers at the ankle (hip hike) or hip abduction \u2022 Reduced or absent ankle (circumduction) \u2022 Large hip extensor and DF activity with foot drop \u2022 Sagittal plane ankle curve knee flexor moment with with excess DF or PF power absorption just \u2022 Any PF activity before initial contact \u2022 Knee flexion >4\u00b0 before \u2022 Excessive knee flexor initial contact activity \u2022 Compensatory and \u2022 Reduced or absent ankle excess hip flexion for limb DF activity clearance","Chapter 16 The Assessment of Human Gait, Motion, and Motor Function 483 (spastic, athetoid, ataxic, and mixed), more than 70% Figure 16.14 Bilateral A\/P radiograph of the feet of the are classified as having spastic cerebral palsy, as is the subject described in case study. This radiograph is commonly subject of this case study. required when the subject presents with pes planus, to better understand the structural alignment of the foot. \u201cLD\u201d is a nonverbal 13.5-year-old male with spastic diplegia and developmental delays. His mother had an the laboratory showed a stiff-knee gait pattern during uncomplicated pregnancy, and he was born full-term, initial swing phase, reduced peak knee flexion in mid- but in his first year of life he demonstrated delayed swing, insufficient knee extension during terminal developmental milestones and did not start walking swing, and a reduced dynamic knee range-of-motion until age 6. He is also hearing-impaired with cognitive, throughout the gait cycle, all observed bilaterally. LD behavioral, and oral motor dysfunction. Previous treat- shows a foot-flat initial contact bilaterally, with no ments included oral baclofen, which had little effect sign of a heel or first rocker (see Fig. 16.13). At the on gait performance, and bilateral hinged AFOs. He ankle, LD showed premature tibial advancement dur- had no neurologic or orthopedic surgical procedures ing loading response and mid-stance with delayed performed prior to his visit to the cerebral palsy clinic heel-off bilaterally. In the frontal plane, LD demon- at our institution, after which LD was referred to our strated moderate lateral trunk lean during loading motion laboratory for instrumented gait analysis. His response on both sides consistent with a compensated family reported an increased incidence of tripping and Trendelenburg\u2019s gait pattern, suggesting weakness of falling over the previous 15 months with fast walking the hip abductors. and a perceived reduction in overall gait performance. They also reported that the left leg was now turning The instrumented gait analysis included temporal- out more than in the past. spatial measures, 3D kinematics, 3D kinetics, and dynamic EMG recorded from six muscles bilaterally The physical examination performed on the day using bipolar surface electrodes. Because of the report of the gait analysis measured LD\u2019s height as 165 cm, of pes planus, a plantar pressure recording was included his weight as 63 kg, and he had equal leg lengths. No to document the existence of excessive pressure in fixed joint contractures were found, but he showed a any area of the foot. The temporal-spatial recordings popliteal angle of \u201365 degrees bilaterally, consistent showed an average cadence of 103 steps\/minute (88% with hamstrings tightness. We measured a thigh-foot normal) and an average walking speed of 51 meters\/ angle of 35 degrees external on the left, 25 degrees minute (65% normal). The left side average step length external on the right, slight hindfoot valgus, moderate was 0.54 meters (80% normal) and the right side was forefoot abduction, and moderate pes planus bilater- slightly less at 0.47 meters (70% normal). There were ally. Ely and Thomas tests were normal, and there was no appreciable differences in gait symmetry or timing no appreciable spasticity (1 on the Ashworth scale) in of gait events between the left and right sides, with the hamstrings, quadriceps, peroneals, tibialis poste- the exception of a slightly longer single limb support rior, toe flexors, or triceps surae bilaterally. Strength time on the left that was not considered clinically sig- information from manual muscle test of the major nificant (95% normal on the left, 89% normal on the muscle groups was inconclusive due to the inability right). of the subject to perform an isolated muscle contrac- tion and his difficulty understanding instructions due Kinematic, kinetic, and dynamic EMG data to cognitive limitations. However, the therapist per- from both legs for the barefoot trial are shown in forming the physical examination reported that most Figures 16.15, 16.16, and 16.17, respectively. On the muscle groups should be at least in the range of 3\u20134 by observing other functional activities and by noting that the subject is an independent, limited community ambulator. Radiographs taken at the time of the analysis showed slight adduction of the proximal femurs but no sign of femoral head uncovering and otherwise normal hip joints bilaterally. Standing anterior\/posterior (A\/P) and lateral radiographs of the foot showed forefoot abduction, uncovering of the talus, midfoot collapse, and a reduced height of the medial longitudinal arch (see Fig. 16.14). This was consistent with evidence of increased pressure at the navicular during the physical exam and redness caused by the orthotics in the same area. Observational gait analysis using slow-motion video recordings while the subject walked barefoot in","484 Pediatric Rehabilitation Kinematics Barefoot Walking Kinetics and Kinematics: Sagittal Pelvic Tilt Pelvic Obliquity Pelvic Rotation Hip Flex\/Ext 80 Knee Flex\/Ext AnkleDorsi\/Plantar 70 30 30 30 30 Ant deg Up Protr Flex Flex Dors Post \u221230 deg deg deg deg deg Down Retr Ext Ext Plan \u221230 \u221230 \u221220 \u221220 \u221230 Hip Flex\/Ext Hip Ad\/Abduct Hip Rotation Hip Flex\/ Knee Flex\/ AnkleDorsi\/ 70 30 30 Ext Moment Ext Moment Plantar Moment Flex 1.5 1.5 2.0 deg Ext Add Int Ext Ext Plan \u221220 deg deg Nm Nm Nm Knee Flex\/Ext 80 Abd Ext Flex Flex Dorsi Flex \u22121.5 \u22121.5 \u22121.5 deg \u221230 \u221230 2.5 Ext 2.5 5.0 \u221220 Distal Shank Hip Power Knee Power Ankle Power Rotation Knee Var\/Valgus 20 Gen Gen Gen 30 Var Int WW W deg deg Abs Abs Abs Val Extl \u22122.5 \u22122.5 \u22122.5 20 40 60 80 20 40 60 80 20 40 60 80 \u221230 \u221240 Percent Percent Percent Ankle Dorsi\/Planter Foot Progression Ankle Rotation Left BF OLG Right BF OLG Avg File 8 30 20 20 Figure 16.16 Three-dimensional graphs of sagittal plane kinematics, sagittal plane joint moments, and total joint Dors Int Int power for the hip, knee and ankle constructed from a representative trial from the instrumented gait analysis of deg deg deg the 13.5-year-old case-study subject, \u201cLD.\u201d The solid line describes the right side, the dashed line shows the left side, Plan Ext Ext and the gray band is from the age matched normal database collected in the laboratory and used as a reference. \u221230 \u221280 \u221240 20 40 60 80 20 40 60 80 20 40 60 80 Percent Percent Percent Left BF Right BF Avg File 8 Figure 16.15 Three-dimensional kinematic graphs then advancing to the next phase until the cycle is constructed from a representative trial from the instrumented completed. Which of these procedures to follow is a gait analysis of the 13.5-year-old case-study subject, \u201cLD.\u201d matter of personal preference, and is sometimes dic- The solid line describes the right side, the dashed line shows tated by the complexity of the case, but for the novice, the left side, and the gray band is from the age-matched it is a good idea to consistently follow the same proce- normal database collected in the laboratory and used as a dure or review sequence until you are comfortable rec- reference. ognizing the significance of each graph individually. We typically start with the kinematic graphs and work kinematic and kinetic curves, the right side is repre- distally from the pelvis, scanning the graphs across all sented by a solid line and the left side uses a dashed phases of the gait cycle to identify deviations from the line, and for comparison, a gray band is included on normal reference. We focus first on the portions of the each graph representing the ensemble averages from curve that have the largest deviation from the reference our typically developing child database for this age data and then attempt to describe these deviations in group. The gray bands correspond to +\/\u2013 1 standard the context of the 8 gait phases and 13 critical events deviation across the ensemble average for that graph. described previously and summarized in Table 16.3. For the EMG data shown in Figure 16.17, the right side As needed, we jump to the subject\u2019s kinetic and EMG is darker, the left side is lighter, and the black bar at the data for additional evidence to explain the absence of bottom of each graph is a normal timing reference. a critical event at a specific phase of the gait cycle, and using all of the evidence gathered in the analysis, There are a variety of ways to review these data develop a logical rationale for the subject\u2019s unique gait systematically, including evaluating each joint or seg- pattern or abnormality. ment in sequence starting either proximally or dis- tally, evaluating all graphs for a particular data type In the case of LD, we see evidence of slightly first and then moving on to the other categories, or increased anterior pelvic tilt starting during loading reviewing all data for a particular phase of gait and","Chapter 16 The Assessment of Human Gait, Motion, and Motor Function 485 EMGS Barefoot Walking L Rectus Femoris R Rectus Femoris 500 500 mv mv \u2212500 L Vastus Lateralis \u2212500 R Vastus Lateralis 500 500 mv mv \u2212500 L Medial Hamstrings \u2212500 R Medial Hamstrings 500 500 mv mv \u2212500 L Anterior Tibialis \u2212500 R Anterior Tibialis 500 500 mv mv \u2212500 L Peroneals \u2212500 R Peroneals 500 500 mv mv \u2212500 L Triceps Surae \u2212500 R Triceps Surae 500 500 mv mv \u2212500 \u2212500 20 40 60 80 20 40 60 80 Percent Percent Avg EMG Control Left BF Right BF Figure 16.17 Filtered and time normalized EMG for 12 muscles of the lower extremity for a representative trial from the instrumented gait analysis of the 13.5-year-old case-study subject, \u201cLD.\u201d The black bars at the bottom of each graph are constructed from published normal EMG activations and are used as reference values. The smooth curve above the EMG activation is a processed EMG signal obtained by rectifying and integrating the raw EMG. response and reaching a peak of approximately initial swing comes from the same mechanism occur- 18 degrees at mid-stance on the left and 14 degrees on ring at loading response on the contralateral side. It is the right (Fig. 16.15, first row). This gives rise to a pat- reflected in the ipsilateral pelvic tilt because the pelvis tern often seen in diplegia called a \u201cdouble bump\u201d as is, of course, a single segment and the graphs of each the pelvis tilts slightly forward during weight accept- hemipelvis section are 180 degrees out of phase. Pelvic ance on each side. It is often associated with weakness obliquity and pelvic rotation are near normal bilater- of the hip extensors and lack of shock absorption more ally until foot-off and the beginning of initial swing, distally, and can be attributed to reduced performance when the right hemipelvis drops and retracts slightly in the critical event of hip stability during loading compared to the normal reference and the left side. response. Another cause could be tight hip flexors, but This suggests that the compensated Trendelenburg\u2019s this is unlikely given that the Thomas test from the gait pattern observed is not completely effective at physical examination was negative. The existence of maintaining appropriate pelvic position on the right the second bump in the pattern during pre-swing and side during initial swing, possibly due to weaker hip","486 Pediatric Rehabilitation abductors on the left side during loading response. All tibial torsion and normally wouldn\u2019t include this off- of these compensations can be attributed to difficulty set. We prefer to include the tibial torsion in this curve achieving the critical event of hip stability during load- to better understand the contribution of tibial torsion ing response and are evidence of proximal weakness to the overall foot progression angle, and therefore, during the task of weight acceptance. call it the distal shank rotation to avoid confusion. It is good practice to have a clear understanding of how the Moving to the hip joint, LD shows increased link-segment model is calculating a particular quan- hip flexion during loading response, decreased hip tity before utilizing it for clinical decision-making, and extension during terminal stance and pre-swing, and this curve in particular is frequently affected by vague increased hip flexion at terminal swing bilaterally. or unstated model assumptions. To conclude the rota- Notice that the shape and range-of-motion for the hip tional assessment, we see a large peak in the external flexion curve is virtually the same as the average nor- foot progression angle (left approximately 70 degrees mal curve, except that it is shifted up toward increased external, right 50 degrees external) that corresponds flexion by about 10 degrees. This is approximately the to a lateral whip of the foot at foot-off, most likely as a same amount that the corresponding anterior pelvic compensatory mechanism to help with limb advance- tilt curve is offset from its normal value. These two ment. This large external foot progression angle with graphs are often coupled since hip joint angles are cal- the left about 20 degrees greater than right, is consis- culated relative to the pelvis, the more proximal seg- tent with the parents\u2019 description, and from the kine- ment. The lack of hip extension at terminal stance is matic analysis, can be attributed to both the thigh and the most significant limitation here, since it negatively shank on the left, and from compensatory mechanisms affects the ability to achieve a trailing limb posture at the foot and ankle bilaterally. during terminal stance, which is essential to achiev- ing maximum stride length on the contralateral side. The analysis now moves distally to the knee, Moving to Figure 16.16 and the sagittal plane kinetics where some of the most significant gait deviations at the hip joint, we see no significant deficits in the exist. In Figure 16.15, the bilateral knee flexion\/exten- hip moment curve bilaterally, but a reduced hip power sion curves show increased knee flexion (relative to the generation at pre-swing, approximately 70% normal on normal reference) during loading response, decreased the left and 50% normal on the right. Since sufficient knee extension during terminal stance, decreased and power generation at the hip is necessary to achieve delayed peak knee flexion during initial swing (left the critical event of passive knee flexion to 40 degrees more severe), and increased knee flexion during ter- during pre-swing, and is also a necessary precursor to minal swing and initial contact. This has the appear- accomplish the task of swing limb advancement (50), ance of compressing the knee sagittal plane curve into reduced power generation at the hip may contribute the middle range of the normal reference, with a shal- to LD\u2019s increased incidence of tripping when trying to low rising slope from mid-stance through initial swing walk at higher speeds. (left = 52 degrees\/second, right = 65 degrees\/sec, normal = 240 degrees\/sec), and decreased dynamic Returning to Figure 16.15, the transverse plane range at the knee over the entire gait cycle (left = 24 motion at the hip shows near normal hip rotation on degrees, right = 31 degrees, normal = 60\u201370 degrees). the right side, but increased hip external rotation of The existence of swing period gait deviations at the approximately 10 to 15 degrees on the left side. This knee prevents the most important critical event in suggests that some of the reported external foot posi- swing from being accomplished: achieving maximum tion on the left can be attributed to the hip. Looking knee flexion of at least 60 degrees. Their presence also distally down the kinematic chain, we see additional provides evidence of a bilateral stiff-knee gait pattern contribution to the final foot progression angle occur- that, as previously described, adversely affects the task ring at the knee (distal shank rotation, left approxi- of swing limb advancement. But when taken together, mately 20\u201325 degrees external, right approximately this combination of excessive knee flexion in stance 10\u201315 degrees) and to a much lesser extent at the ankle and insufficient knee flexion in swing has the effect bilaterally, yielding a final foot progression angle of of disrupting all other critical events associated with approximately 40 degrees on the left and 20 degrees on normal knee function, including controlled knee flex- the right during mid-stance and terminal stance. We ion during loading response, achieving trailing limb use the term \u201cdistal shank rotation\u201d here rather than posture during terminal stance, passive knee flexion to knee rotation to highlight that the recording includes 40 degrees during pre-swing, and finally reaching full the external \u201ctwist\u201d of the tibia or tibial torsion in the knee extension during terminal swing. With this many graph rather than just the amount of rotation occurring critical events absent, altered, or delayed, all three between the thigh and shank segment. The modified fundamental gait tasks are compromised. Therefore, Helen Hayes marker set used to produce these curves in order to see any significant improvement in walk- assumes that the ankle joint axes and knee joint axes ing ability, these critical events need to be restored, are offset in the transverse plane by the amount of the","Chapter 16 The Assessment of Human Gait, Motion, and Motor Function 487 which by necessity prioritizes any intervention directly to the hamstrings could be considered here, but with affecting knee range of motion during the gait cycle. strong evidence for rectus femoris transfer and the To find support for specific interventions, we return to ease of performing a hamstring lengthening at the the kinetic and EMG recordings shown in Figures 16.16 same time as the rectus procedure, the surgical path and 16.16, respectively. In the top row of Figure 16.17, seemed most appropriate for this patient. Furthermore, we see that both the left and right rectus femoris EMG the combination of these two procedures has the best recordings show muscle activation beginning late in chance of restoring all missing critical events at the initial swing and continuing until terminal swing, knee in the shortest amount of time to prevent con- with a small peak in initial swing slightly before peak tinued progression of the crouch gait deformity as LD knee flexion. This abnormal EMG activity in combi- grows larger through adolescence. nation with insufficient peak knee flexion in initial swing and a shallow slope of the knee curve during To complete the instrumented gait analysis, we move pre-swing provide strong evidence to support the distally once more to the remaining graphs describing use of a rectus femoris transfer procedure bilaterally the ankle and foot. The sagittal plane ankle kinematics 46,49). When successful, this procedure can improve graph in the lower-left corner of Figure 16.15 provides both the peak knee flexion in swing and the slope of evidence of what was seen during the observational the knee flexion wave starting in pre-swing, address- analysis: increased dorsiflexion at initial contact and ing two missing critical events at the knee. To address no sign of a first or heel rocker during loading response. the other affected critical events, we must review the This is consistent with the foot-flat initial contact kinetics and EMG recordings during initial contact, observed, and is shown on the kinematic graph as an loading response, mid-stance, and terminal swing increasing slope in the first 10% of the gait cycle start- phases. With greater than 20 degrees of knee flexion ing at 5 degrees of dorsiflexion, rather than a decreas- throughout stance period, there is a significant force ing slope starting from a near-neutral ankle position for demand on the knee extensors during weight accept- the normal reference. The right side shows increased ance and single limb support. Evidence of this can be dorsiflexion continuing into mid-stance, with a peak found in the large knee extensor moments during load- at about 15% of the gait cycle, after which the dorsi- ing response and terminal stance, shown in the middle flexion stabilizes and then increases at a more normal graph of Figure 16.16, and the prolonged stance phase rate (slope of the ankle curve) near the upper extreme EMG activity of the vastus lateralis and rectus femoris of the normal reference until the beginning of termi- shown in Figure 16.17. These findings are consistent nal stance. After beginning in a dorsiflexed position at with a mild \u201ccrouch gait\u201d deformity, set up by the limi- initial contact, the left side dorsiflexion increases at a tation in knee extension at terminal swing. normal rate, tracking closely the slope of the reference value and providing evidence of a near-normal second While LD is able to overcome this biomechanically or ankle rocker. Following peak dorsiflexion in terminal disadvantaged position and maintain an upright pos- stance, the period of rapid ankle plantar flexion during ture at this time, as he matures and grows heavier, any pre-swing begins, which is associated with the third or increase in knee flexion during stance may increase the forefoot rocker. Unfortunately, maximum plantar flex- demand to a level greater than he can withstand, which ion stops at a joint angle of approximately 8 degrees would severely limit his overall gait performance. It is dorsiflexion on the left and 2 degrees dorsiflexion on reasonable here to consider the more aggressive surgi- the right\u2014clearly insufficient compared to the normal cal procedures that have been shown to improve knee reference. The ankle then maintains a dorsiflexed posi- function in cases of persistent crouch gait, namely a tion throughout swing period bilaterally. Considering knee extension osteotomy to reduce knee flexion con- these elements together and describing them in terms tracture and patellar advancement to treat patella alta of fundamental gait tasks and critical events, we begin and improve the function of the quadriceps (51). Since to see a clear picture of the impact of these gait devia- LD showed no significant knee flexion contracture on tions at the ankle. First, we have evidence that during physical examination or radiographic signs of patella weight acceptance LD is missing a heel-first initial con- alta, and the crouch deformity was considered mild tact and controlled ankle plantar flexion (first rocker) since he could achieve 20 degrees of knee flexion at ter- bilaterally. Second, during single limb support, con- minal stance, these surgical procedures were deemed trolled tibial advancement (second rocker) is altered on unnecessary at this time. However, since there was the right and controlled ankle dorsiflexion (DF) with evidence of tight hamstrings on physical examination heel rise is delayed bilaterally. Finally, while start- (popliteal angles of \u201365 degrees) and the EMG record- ing the task of swing limb advancement, rapid ankle ing of the medial hamstrings (third row, Figure 16.17) plantar flexion (third rocker) in pre-swing is reduced showed premature onset in mid-swing, the team felt bilaterally. Fortunately, LD does maintain sufficient hamstring lengthening procedures would be appropri- dorsiflexion in mid-swing to clear his foot so as not ate. Nonsurgical techniques such as phenol injections to compound the lack of knee flexion and stiff-knee","488 Pediatric Rehabilitation pattern already affecting swing limb advancement. As The experienced gait analyst might cite the with the analysis at the knee, failure to achieve these delayed heel-off and short step length of this \u201ccalca- critical events at the ankle represents significant gait neal gait\u201d pattern as obvious indicators of calf weak- dysfunction and must be addressed. Additional insight ness. While this may be true, the ankle power data can be obtained from the kinetic graphs on the right- provides a strong quantitative justification for such a most column of Figure 16.16 and the EMG recordings in claim, and has the added benefit of gauging the degree the lower three rows of Figure 16.17. As is seen on the of dynamic plantar flexor weakness that occurs at this right side of Figure 16.16, the combination of foot-flat critical point in the gait cycle. This evidence, along initial contact, increased knee flexion, and increased with the excess dorsiflexion during stance period and ankle dorsiflexion during loading response places a our concerns about more severe crouch gait deformity large demand (external moment) on the ankle plantar as LD matured, eliminated any thoughts of a tendo- flexors, and they respond by increasing the net ankle achilles lengthening or intramuscular lengthening of plantar flexion moment (internal moment) during load- the gastrocnemius for this subject. ing response and the early portion of mid-stance. This is most likely a compensatory response to the external Based on the results of the instrumented gait ana- demand, and is accomplished by prematurely activat- lysis and the other physical examination and radio- ing the peroneals and triceps surae during terminal graphic evidence, and following consultation with the swing, initial contact, and loading response. Notice patient and his family, our clinical team recommended that the peak in right ankle dorsiflexion at approxi- that LD undergo bilateral rectus femoris transfers to mately 15% of the gait cycle is accompanied by a peak the semitendinosis, bilateral hamstring lengthenings, in the plantar flexion moment and just preceded by a bilateral Evans calcaneal lengthenings, and a left tibial small peak of ankle plantar flexor power absorption, osteotomy of approximately 20 degrees internal. The rec- shown in the lower-right graph of Figure 16.16. The tus femoris transfers were clearly indicated from both ankle power curve then reverses to produce a small kinematic and dynamic EMG evidence and the presence amount of power generation at the point in the cycle of a stiff-knee gait pattern. The hamstring lengthen- (mid-stance) when continued ankle dorsiflexion is ings were supported by physical examination and IGA briefly reversed and the ankle plantar flexion moment data, and could be efficiently performed in conjunction returns to normal levels. This suggests that although with the rectus transfers. Since there were no previous biomechanically disadvantaged by foot position and surgical procedures performed on the hamstrings, we excessive knee flexion, the ankle plantar flexors ini- prefer to transfer the rectus femoris to the semitendi- tially absorb energy during loading response as the nosis, although we have found no evidence to rule out tibia falls forward, but then limit excess dorsiflexion the other potential transfer sites of sartorius or gracilis with a brief burst of power generation at the ankle at (49). The Evans calcaneal lengthenings were primarily the beginning of mid-stance. Since the physical exam- supported by the radiographic evidence that showed ination was inconclusive, it isn\u2019t clear whether this is significant uncovering of the talus and forefoot abduc- due to true ankle plantar flexor strength or simply the tion with mid-foot collapse. While not always a part of resistance or viscoelastic behavior of the muscluloten- our IGA procedure, for this case, a foot plantar pres- don unit. Regardless, it does explain the early dorsiflex- sure measurement from each limb was recorded using ion peak in the ankle sagittal plane graph and suggests a two-meter pressure plate mounted in the motion lab- there is some eccentric control over tibial advancement oratory walkway after the force platform array. These during loading response and mid-stance. recordings confirmed the existence of pes planus and showed an increased pressure under the first metatarsal However, ankle function is not as good during heads and medial border bilaterally, with the pressures terminal stance and pre-swing, when the powerful higher under the left foot. This information, combined concentric contraction of the triceps surae is needed with concerns expressed by the family regarding LD\u2019s to produce rapid ankle plantar flexion. The strongest flat feet, as well as the clinical team\u2019s hope that a more evidence of this is shown in the reduced ankle power rigid and properly aligned foot could improve the power generation during pre-swing in Figure 16.16, where generation capability of the ankle plantarflexors during the power generation is approximately 25% normal pre-swing, convinced us to add this procedure to the on both sides. Since power generation is normally list. The left tibial osteotomy was warranted based on larger at the ankle than at any other joint, and sub- the rotational kinematic findings that showed a distal stantial power generation from both the hip flexors shank rotation of approximately 15\u201320 degrees greater and ankle plantar flexors is necessary to produce pas- than normal, a foot progression angle approximately sive knee flexion during pre-swing, this is a profound 25\u201330 degrees greater than normal (including the contri- deficit that affects both the knee and the hip, and is bution from the external hip rotation that was believed to the strongest evidence of plantar flexor weakness in be compensatory), and the family\u2019s concerns about the the analysis. limb asymmetry and increasing external foot position.","Chapter 16 The Assessment of Human Gait, Motion, and Motor Function 489 Finally, bilateral leaf-spring ankle foot orthoses were but doesn\u2019t replace a sound clinical and technical prescribed to provide some plantar flexor assist and to understanding of normal gait. help control tibial advancement in the presence of the \u25a0 Normal gait is naturally cyclical and symmetric, so weak plantar flexors that would most likely persist after any movement asymmetry should be investigated. LD recovered from his surgical procedures. However, \u25a0 There are 13 critical events that must occur during we are hopeful that the improved biomechanical posi- 8 distinct phases of the gait cycle to produce a normal tion, increased knee flexion in swing phase, increased gait pattern. Each critical event has functional sig- knee extension at initial contact, and more rigid foot nificance, and so provides a link between observed that we expect will result from these surgical interven- gait abnormalities and possible interventions. tions will reduce the physical demands of walking suf- \u25a0 IGA provides evidence of absent, altered, or delayed ficiently for the AFOs to be discontinued once LD fully critical events, and provides the framework for iden- recovers. While a follow-up gait analysis to confirm our tifying treatments to directly address these func- recommendations could not been included here since it tional limitations. had not been completed at the time of this writing, it \u25a0 While skill, experience, and practice are required to really isn\u2019t the purpose of this case study to demonstrate fully utilize IGA results for clinical interpretation, our gait analysis prowess using a single sample. Rather, by following the strategy outlined in this chapter, we hope this clinical example serves to illustrate how the process can be less intimidating and more clini- instrumented gait analysis and a systematic analysis cally relevant to the pediatric physiatrist. procedure based on functional decomposition of the gait cycle can be used to make complex clinical decisions for Resources the pediatric patient with gait dysfunction. Gage JR. The Treatment of Gait Problems in Cerebral SUMMARY Palsy. London: Mac Keith Press;2004. In this chapter we have attempted to provide an over- Inman VT, Ralston HJ, Todd F. Human Walking. view of the methods, procedures, and strategy for uti- Baltimore: Lippincott Williams & Wilkins;1981. lizing instrumented movement analysis to assist with the clinical interpretation of gait deformity in children. Kirtley C. Clinical Gait Analysis, Theory and Practice. Focusing on the functional subdivisions that naturally Philadelphia: Churchill Livingstone-Elsevier;2006. occur during normal walking, and identifying the specific critical events that must be accomplished in Perry J. Gait Analysis: Normal and Pathological each phase of gait, we have developed a framework Function. Thorofare, NJ: Slack, Inc.;1992. that can be used for both instrumented and observa- tional gait analysis and that can be applied to children Sutherland D. Gait Disorders in Childhood and Adolescence. and adults. By providing a brief description of modern Baltimore: Lippincott Williams & Wilkins;1984. computerized systems for movement analysis and link- ing measurements from these systems to functional Acknowledgments tasks and critical events, we hope that instrumented gait analysis will be less intimidating and more clini- The authors wish to gratefully acknowledge Laura cally relevant to the pediatric physiatrist. Controversy Borgstede, MS; Nancy Denniston, MS, MA; and the remains regarding the value of IGA and its place on the staff of the Center for Gait and Movement Analysis modern rehabilitation service, with staunch advocates (CGMA) at The Children\u2019s Hospital, Denver, for their (8,10,35,52,53) and ardent detractors alike (54,55). 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Kaufman KR, Shaughnessy WJ, Noseworthy JH. Use of 39. Pathokinesiology and Physical Therapy Department, motion analysis for quantifying movement disorders. Rancho Los Amigos Medical Center. Normal gait summary. In: Ruzicka E, Hallett M, Jankovic J, eds. Advances in In: Perry J, ed. Observational Gait Analysis. Downey, CA: Neurology, vol. 87. Philadelphia: Lippincott Williams & Los Amigos Research and Education Institute, 1996:24\u201329. Wilkins, 2001:71\u201381. 40. Perry J. Kinesiology of lower extremity bracing. Clinical Orthopedics. 1974;102:18\u201331. 17. Sutherland D. Laboratory methods and terminology. In: 41. Pathokinesiology and Physical Therapy Department Rancho Gait Disorders in Childhood and Adolescence. Baltimore: Los Amigos Medical Center. Gait deviations: Most likely Williams & Wilkins, 1984:1\u201313. causes and significance. In: Observational Gait Analysis. Downey, CA: Los Amigos Research and Education Institute, 18. Vaughan CL, Davis BL, O\u2019Connor JC. Commercial Equipment Inc., 1996:34\u201352. for Gait Analysis. Dynamics of Human Gait. Champaign: 42. Kerrigan DC, Bang M-S, Burke DT. An algorithm to assess Human Kinetics Publishers, 1992;107\u2013126. stiff-legged gait in traumatic brain injury. Journal of Head Trauma Rehabilitation. 1999:14(2):136\u2013145. 19. Winter DA. Biomechanics as an Interdiscipline. Biomechanics 43. Perry J. Distal rectus femoris transfer. Dev Med Child and Motor Control of Human Gait. New York: John Wiley & Neurol. 1987;29:153\u2013158. Sons, 1990:1\u201310. 44. Gage J, Perry J, Hicks R, et al. Rectus femoris transfer to improve knee function of children with cerebral palsy. Dev 20. Kirtley C. Theory (Pt I). In: Clinical Gait Analysis, Theory Med Child Neurol. 1987;29:159\u2013166. and Practice. Philadelphia: Churchill Livingstone-Elsevier, 45. Sutherland DH, Santi M, Abel MF. Treatment of stiff-knee 2006. gait in cerebral palsy: a comparison by gait analysis of dis- tal rectus femoris transfer versus proximal rectus release. 21. Commission for Motion Laboratory Accreditation. J Pediatr Orthop. 1990;10:433\u2013441. Application Guidelines. Available at www.cmlainc.org. 46. Miller F, Dias RC, Lipton G, et al. The effect of rectus EMG patterns on the outcome of rectus femoris transfers. 22. Ounpuu S. Joint kinetics: Interpretation and clinical decision J Pediatr Orthop. 1997;17:603\u2013607. making for the treatment of gait abnormalities in children with neuromuscular disorders. In: Harris GF and Smith PA. Human Motion Analysis: Current Applications and Future Directions. Piscataway, NJ: IEEE Press, 1996:268\u2013302. 23. Kirtley C. Power. In: Clinical Gait Analysis, Theory and Practice. Philadelphia: Churchill Livingstone-Eslevier, 2006. 24. Perry J. Phases of gait. In: Gait analysis: Normal and Pathological Function. Thorofare, NJ: Slack, Inc., 1992:9\u201316. 25. Carollo JJ, Kondraske GV. The prerequisite resources for walking: Characterization using a task analysis strategy. In: Proceedings of the Ninth Annual IEEE Engineering in Medicine and Biology Society Conference. Boston: IEEE, 1987;357\u2013358. 26. Stanhope SJ. Does clinical gait analysis meet the patient care needs of rehabilitation specialists? In: Aiona MD,","Chapter 16 The Assessment of Human Gait, Motion, and Motor Function 491 47. Chambers H, Lauer A, Kaufman K, et al. Prediction of out- 52. Lofterod B, Terjesen T, Skaaret I, Huse A-B, Jahnsen R. come after rectus femoris surgery in cerebral palsy: The Preoperative gait analysis has a substantial effect on ortho- role of co-contraction of the rectus femoris and vastus lat- pedic decision making in children with cerebral palsy: eralis. J Pediatr Orthop. 1998;18:703\u2013711. Comparison between clinical evaluation and gait analysis in 60 patients. Acta Orthopaedica. 2007;78(1):74\u201380. 48. Ounpuu S, Muik E, Davis III RB, et al. Rectus femoris sur- gery in children with cerebral palsy. Part II: A comparison 53. Chang FM, Seidl AJ, Muthusamy K, Meininger AK, between the effect of transfer and release of the distal rectus Carollo JJ. Effectiveness of instrumented gait analysis in femoris on knee motion. J Pediatr Orthop. 1993;13:331\u2013335. children with cerebral palsy: Comparison of outcomes. J Pediatr Orthop. 2006;26:612\u2013616. 49. Muthusamy K, Seidle AJ, Friesen RM, Carollo JJ, Pan Z, Chang FM. Rectus femoris transfer in children with cere- 54. Klenerman L, Dobbs R, Weller C, et al. Bringing gait ana- bral palsy: Evaluation of transfer site and preoperative indi- lysis out of the laboratory and into the clinic. Age and cators. J Pediatr Orthop. 2008;28(6):674\u2013678. Ageing. 1988;17:397\u2013400. 50. Valvano J, Carollo JJ, Lutz B, Chang F. Knee Extension 55. Narayanan UG. The role of gait analysis in the orthopae- at Terminal Swing: A Missing Critical Gait Event for dic management of ambulatory cerebral palsy. Curr Opin Children with Spastic Cerebral Palsy. First Joint ESMAC- Pediatr. 2007;19:38\u201343. GCMAS Meeting (JEGM06), Amsterdam, the Netherlands. September, 2006. 56. Simon SR. Quantification of human motion: Gait analysis\u2014benefits and limitations to its application to clin- 51. Stout JL, Gage JR, Schwartz MH, Novacheck TF. Distal fem- ical problems. Journal of Biomechanics. 2004;37:1869\u20131880. oral extension osteotomy and patellar tendon advancement to treat persistent crouch gait in cerebral palsy. J Bone Joint Surg. 2008;90:2470\u20132484.","This page intentionally left blank","17 Psychosocial Aspects of Pediatric Rehabilitation Lee Renee Lucas While many clinicians have heard the iconographic The scope of this chapter will encompass those illustration of childhood disability in the piece children with disabilities and their families within a \u201cWelcome to Holland\u201d (1), there persists a tendency medical rehabilitation context. This work will cover to ignore the vital lessons embedded there and go on those with congenital and acquired disabilities, with to \u201cpreach\u201d based on anecdote and stereotypes. This some relative focus on those with acquired disability chapter will seek to explore both the literature on the due to injury or illness. Many children now survive family experience with childhood disability and clin- what in times past would have been lethal assaults by ical experience of the author after almost decades in illness or injury and now mature into adulthood. So the field. The clinical experience enlivens and enlarges now the issue is quality of life for the 1 to 2 million on the existing body of literature, giving attention to children who have a severe chronic physical condition the vital aspect of the actual experience embodied in in the United States (2). work such as \u201cWelcome to Holland.\u201d Quality of life means several things in this con- OVERVIEW text. Good quality of life depends on the family\u2019s ability to maintain its own integrity by developing The focus of this chapter must be the family. Any cred- an idiosyncratic \u201cnormal\u201d from which to preserve its ible work in this field is based on the premise that the primary job of guiding the child with a disability (or family\u2019s adjustment underlies that of the child\/adoles- any child) to independence. In real terms, this means cent. This is consistent with the developmental under- performance of tasks unique to children with disabili- standing of the \u201ctypical\u201d child, and the added issue ties. These tasks include, but are not limited to, mas- of disability only magnifies this relationship between tery of the medical system, needed accommodations child and parent or caregiver. Issues of dependence from the educational setting, navigation of the \u201crough beyond more typical childhood limits often exist in waters\u201d of social acceptance, and integrating the real- addition to the added management and stress of ity of the disability into the family structure. Specific involvement with medical and social systems not to this is empowering the family by providing the nec- encountered to any similar degree with a more typical essary educational materials as well as mentoring to child. facilitate adept handling of the two behemoths of the medical and educational\/vocational bureaucracies. It is essential that the family remain the center of all","494 Pediatric Rehabilitation training and education of the child with a disabil- based on a collaborative relationship between family ity. The family is the expert on its own functioning, and health care practitioner. and without deliberately tapping that expertise, inap- propriate goals and agendas are developed. Without 1. Respect doing this, in trying to \u201chelp,\u201d the family is left feeling 2. Honoring racial, ethnic, cultural, and socioeco- isolated as they travel their journey of childhood dis- ability and injury. nomic diversity and its effect on the families\u2019 expe- rience and perception of care FAMILY-CENTERED CARE 3. Recognizing and building strengths of each child and family, even in difficult and challenging Across the country, hospitals and other medical situations institutions are acknowledging the importance of 4. Supporting and facilitating choices for the child and including the family in critical medical and mental family about approaches to care health decisions. Gone are the days where the clini- 5. Ensuring flexibility in organizational policies and cian makes decisions without the patient\u2019s and fam- procedures so services can be tailored to meet the ily\u2019s input. In essence, there has been a paradigm needs, beliefs, and cultural values of the family shift, where the cultures of many health care orga- 6. Sharing honest and unbiased information with nizations are not only inclusive of families, but also families on an ongoing basis in ways that are use- are actively recruiting their involvement. The goal ful and affirming is to empower families to ask direct and courageous 7. Providing and\/or ensuring formal and informal questions by giving them access to medical infor- support for the child and parent\/caregiver during mation and placing more emphasis on the impor- each developmental phase tance of human interactions among all health care providers (3). While patient satisfaction is the primary goal, the author also describes several benefits for the pedia- \u201cFamily-centered care within the nursing profes- trician (and other health care providers) as well (8). sion is not a new trend, with roots dating back as early These include but are not limited to improved clin- as the 1950s\u201d (4). However, it did not receive national ical decision-making from better information and a recognition until 1987, when former Surgeon General collaborative process; improved follow-through, as the Koop made it a primary initiative (5). These initiatives family has been consulted; improved communication broadened the definition of family and acknowledged among health care team members; and greater child the diverse cultural backgrounds that make up fami- and family satisfaction with the health care team. lies in our nation. Family-centered care also recognizes that insti- Smith, Terrel, and Conant (6) state in their article tutional leadership and policies must promote the \u201cMaking family-centered care a reality,\u201d that \u201cChildren family\u2019s best interests and support the activity of the get better faster when their emotional and social needs direct care clinician. Although family satisfaction has are met along with their medical needs\u2014a hospital- increased from such initiatives as specialty meals, ized child is still first and foremost a child.\u201d access to technology, and more inclusive visitor policies (eg, younger siblings), economic considerations exist. While this statement may ring true for most chil- \u201cHealth care decision makers, providers, and third- dren and families, the literature also suggests that pro- party payers require evidence that family-centered viding family-centered care may be daunting for some care is not only effective but cost-effective\u201d (9). practitioners. For example, Newton (7) states, \u201cThere is no consensus as to how much and what form of The Family and Health Care parental involvement should exist and how far that Team Partnership participation should extend.\u201d Barriers such as bal- ancing parental involvement and participation need \u201cYou are so strong\u201d . . . \u201cI don\u2019t know how you do to be addressed honestly and openly with the health it\u201d . . . \u201cI could never take care of a child with . . . .\u201d care team. Keeping the child\u2019s medical condition in the forefront of decision making will allow a positive In well-meaning attempts at support or solidarity, experience for all participants. friends, family, and health care providers offer such words to a family who is absorbing the impact of a In an effort to gain a better understanding of severe trauma or diagnosis of severe illness. Though family-centered care, Eichner and Johnson and The such sentiments are heartfelt, the net result is distanc- American Academy of Pediatrics have defined seven ing, with families feeling more isolated. core principles (8) for the practitioner to incorpo- rate into their interactions with families during each Families of children with disabilities or illness encounter to improve outcomes. Each principle is need ongoing knowledge, guidance, education, and training at each developmental milestone to prepare","Chapter 17 Psychosocial Aspects of Pediatric Rehabilitation 495 them for the road ahead. It is the responsibility of in which the parent or caregiver views the world is the clinician to assist the family in integrating their immediately changed. They lose their naivety and are child with special needs into a world that may be forced to recognize the unfairness of the world. The unprepared to meet them. Acknowledgement of the process of this change is at the same time very fast disability or illness in a respective and professional and in slow motion. A parent or caregiver must imme- manner, while at the same time maintaining the fam- diately begin to make sense of the medical information ily\u2019s perspective, is paramount to all involved with the presented to them, while at the same time devise a plan child\u2019s care. for siblings, spouses, or other family members. The family system as they knew it has been permanetly Resilience altered, and caregivers must now face the challenge of learning new tools to facilitate their understanding of In ecology, \u201cresilience\u201d has been defined as \u201ctwo com- the child\u2019s illness or disability. peting fashions that emphasize two different aspects of stability\u201d (10). It may be said that when a child is diag- Depending upon the diagnosis, the period of nosed with a serious illness or injury, the two \u201ccom- understanding the child\u2019s illness or disability may peting forces\u201d are the family system and the medical unfold within days, months, or years. Physical, emo- setting. The family system is trying to maintain their tional, and spiritual development will continue to take current homeostasis while allowing a new organism place, and the caregiver\u2019s role as parent will also con- into their system, and the medical setting is trying to tinue to evolve as they learn new facets of their child\u2019s maintain its current state while integrating the child life. Extended family members who may not have been into its system. as involved in the past may now join the new family system in order to care for the siblings of a child with In this section, the author explores the litera- an injury or disability. ture pertaining to resilience\u2014changes that occur in the family when their child has been diagnosed with Traditional family roles and finances may be a serious illness, disability, or injury, as well as the affected as the family prepares to accommodate the health care team\u2014and suggest interventions for the special needs of their child. Parents who in the past family to once again achieve homeostasis. There will never had to rely on social services agencies may be further exploration of a framework that will not now require the tools to apply for public assistance. only engage practitioners in using these models when Applications for Social Security disability; Women, a child or adolesencent is diagnosed with a serious ill- Infants, and Children (WIC); and food stamps may now ness or injury, but also assist families to anticipate and need to be made in order for the family to survive. This plan for the future (11). process is not easy, and parents will not only require specific information about local and national agencies, The challenge of keeping consistent schedules and but also emotional support so as not to feel \u201cguilty or balancing the predictability or unpredictability of the ashamed\u201d about applying for these services. child with illness or disability is not new. The fami- ly\u2019s life is often set between constancy and change, Days before the diagnosis, the family may have or between predictability and unpredictability. Roland been maintaining an organized schedule of work, and Walsh imply that \u201ca family resilience framework school, church, recreation, and minimal physical- is grounded in the recognition that crises and persis- or health-related issues. Now, the caregiver system tent challenges [affect] the whole family and, in turn, is engaged in learning about the special needs of key family processes mediate the adaptation of all their child, and at the same time, needing to rely on members and their relationships\u201d (11). Therefore, the a \u201chealth care team\u201d of individuals, none of whom family requires a new road map along this journey. A know their child or family history. One complaint that fluid road map, where there are resources along the parents have during these intial meetings with the way to provide information, guidance, and support, is health care team is that it is difficult for the parent to necessary. establish themselves as primary caregiver when other members of the team have so much influence upon The Family System how the child will be cared for. Parents may have the sense of being \u201csteamrolled\u201d over by the health care \u201cAfter hearing that my child was injured, I felt as if I team and will need to maintain their role as primary were slapped in the face; I felt the burning sensation caregiver (8). for several minutes. There are some days when I can still feel that sensation on my cheek.\u201d \u2013Mrs. S In order to prevent these feelings, a parent should be supported by the health care team to continue to be It is not uncommon for a parent to have such a vis- the \u201cexpert\u201d about their child and also be encouraged ceral reaction after hearing that their child has been to partcipate as a member of the health care team. diagnosed with a serious illness or disability. The way A parent or caregiver will be the most successful in caring for their child with an injury or disability if","496 Pediatric Rehabilitation they are given the opportunity to partner with the This change can occur within or without the hospital health care team. The parent of a child with special system. On the rehabilitation team, for example, the needs begins to develop new roles and learns how to parent communicates with team members from one be the child\u2019s advocate, broker, educator, and project hospital to another in order to prepare for discharge manager. and ancillary services. Advocate Educator. Parents begin their child\u2019s educational pro- cess even before the child is born, as soon as they In the article \u201cHow to advocate for your child,\u201d begin to read the book What to Expect When You Shekerjian (12) offers 10 tips to advocate for your child Are Expecting (15), and they continue the process as as follows: long they live. Parents of children with special needs are no different from those parents without children 1) Define and examine your concerns. with special needs, but from the time they hear that 2) Develop possible solutions. their child has been injured, diagnosed with a dis- 3) Prepare a written document. ability, or become seriously ill, these parents become 4) Meet with the teacher (case manager, staff experts regarding the child\u2019s health care. At the ini- tial team meeting, parents may have completed their member). own research on the diagnosis and may have found 5) Approach the meeting with a positive attitude. information unknown to medical staff. Members 6) Define the next step. of the rehabilitation team rely on parents to inform 7) Document events. and educate them about a patient in order to give 8) Follow the chain of command. the child the best care. Parents\u2019 knowledge of the 9) Consider all educational options. child\u2019s likes, dislikes, and temperament are invalu- 10) Never forget that you are responsible for the edu- able to the staff. cation (treatment, success) of your child. Further, Faust (13) believes advocacy to be \u201ca vital Project Manager. \u201cParents of children with disabili- element because systems are not always responsive ties do not see their children\u2019s needs dividing neatly to the individual client.\u201d Parents, as advocates, take along program lines\u201d (16). However, the roles that on the role of negotiating home care services, educa- parents take on should be on their own terms and tional plans, and other social systems when their child should be evaluated periodically with staff. This has been diagnosed with a serious illness or injury. evaluation should include the successes as well as Parents have become more and more influential as the challenges faced by the family members. A care- social change agents, and advocacy is one way in ful and honest negotiation is necessary to clarify the which they make change. For example, a parent may needs of the patient and their caregivers. A parent need to call the administrator for their health care who becomes a skillful advocate, broker, and edu- policy or legislator in order for their child to receive cator is first and foremost a parent and should be specialized equipment that may not otherwise be cov- supported in that role, not evaluated on their effec- ered. The parent\u2019s opinion and understanding of her tiveness in other roles (17). child\u2019s illness or disability may have more influence than the medical team has on the insurance system. The Health Care Team System One caveat to this example, however, is that parents may not have the energy or expertise to navigate this \u201cEvery wise physician knows that the best he system without supports. can do for a patient [family] is to assist nature in healing\u201d (18). Broker. To manage, or to \u201cbroker,\u201d is the process in which a parent acts as a link or bridge to services (14). It is important to keep in mind that the best health Parents with children with special needs are often care is given when both the parent and the health care the primary bridge between the medical staff and team work in conjuction with one another. As in any ancillary staff in the hospital, community resources, relationship, communcation and mutual respect are and the educational system. This role is necessary to essential. Fallowfield (19) reminds us that parents may ensure that services are appropriate and accessible to have difficulty hearing the information regarding their their child. This role also involves the parent or care- child and that information from the caregiver may giver being concerned with the \u201cquality and quantity often need to be repeated. Furthermore, when giving of services.\u201d In other words, a parent will not rely on critical information regarding the patient\u2019s illness or only the services that are offered, but will challenge disability, it is practical for the practioner to have a the system to communicate in order to create change. \u201cplan\u201d to reinforce that the family has heard\/under- stood the information that is being presented (19).","Chapter 17 Psychosocial Aspects of Pediatric Rehabilitation 497 Davis (17) offers suggestions to organizing your within a holistic approach, acknowledging that as a \u201cplan\u201d when giving critical information to a family team we are separate and at the same time equal. member or caregiver: TASKS OF THE FAMILY 1. Begin with what the parent\/family knows; ask specific questions, such as: After either the initial diagnostic period or initial conversations about the child\u2019s injury or disability, \u201cWhen we spoke last, you asked . . .\u201d the family\u2019s goal must be to return to \u201clife as it was.\u201d \u201cWhat is your understanding of your child\u2019s Often, one parent must return to work, siblings must return to school, and the diagnosis or disability begins disability?\u201d to integrate into the family\u2019s world. It is suggested \u201cWhat did the emergency department physician tell here that a parent will have a better opportunity to achieve a new sense of \u201cnormalcy\u201d and get their needs you about the accident?\u201d met when they are able to approach the child\u2019s illness or disability with a sense of confidence and inherent 2. Present the information. Facts and data are impor- understanding that they will adapt and cope with an tant in this segment of the conversation, but in uncertainty that life may bring. Sandler (22), in her small, digestible parts that parents can integrate book Living with Spina Bifida, describes nine tasks into their knowledge base. that resilient parents of special-needs children learn. They are as follows: 3. Check the result. Observe the family and their reaction to the information that is currently being \u25a0 Balance the disability with other family needs. presented. Invite the family at this time to ask ques- \u25a0 Maintain clear family boundaries. tions or receive clarification. \u25a0 Become competent at communication. \u25a0 See situations in a positive light. 4. Ensure retention. \u25a0 Maintain family flexibility. \u25a0 Be committed to the family unit. It is also wise to offer written information about \u25a0 Engage actively in coping strategies. the specific topic, and refer to appropriate members \u25a0 Be well-integrated socially. of health care team (ie, case manager, social worker, \u25a0 Develop cooperative relationships with professionals. psychologist) who can continue to process this infor- \u25a0 Obtain information\/education. mation with the family. Many families may request \u25a0 Learn new parenting skills. an audiotape of the interview with the physician \u25a0 Achieve equilibrium or homeostasis. to share with other family members. The authors suggest that this process be established before the Working Toward a New \u201cNormal\u201d interview begins to ensure the privacy of the people involved. While loss is pivotal in a person\u2019s experience, it is not the loss of a child that these families are When an audiotape is not appropriate, Cunningham experiencing. Rather, it is the \u201closs\u201d of the way in and Newton (20) reported that using a written con- which their child experienced the world. It is the sultation questionnaire was also highly effective in loss of what was \u201cnormal\u201d and the comfort of what confirming that families understood the medical used to be. information being presented. This tool became valu- able to the parents as an effective means to commu- After her child was injured and began to use a nicate with the medical team and offered a voice to wheelchair, a parent spoke about missing walking parents who were not confident to prepare individual with her child through the leaves in the autumn. questions themselves. The mother felt sad that she could no longer hear her son\u2019s footsteps crunch underfoot, but after a period Stille and Antonelli (21) summarize in their arti- of adjustment, was able to feel a new kind of hap- cle, \u201cCoordination of care for children with special piness watching her son role himself through the health care needs,\u201d that coordination is highly depen- leaves. Instead of giving up on a favorite pastime, the dent upon communication.\u201d They go on to explain that family learned that pushing the child in the wheel- \u201ca team approach involving nonphysican staff and chair was fulfilling, just different from their previous families as primary partcipants to be the best option experience. in health care.\u201d Furthermore, it is the responsibilty of all members of the health care team to assist patients and families during all aspects of the child\u2019s illness or disability. The hope for all members of the health care team is that we view children and their families","498 Pediatric Rehabilitation Family members and caregivers are subjected to Information on local community support groups, as multiple tasks at the time of diagnosis, and one of these well as resource information on funding opportuni- tasks is how to reframe their child\u2019s experience and ties, will be helpful to the family. Concrete assistance, create an experience that not only meets the child\u2019s such as filling out a Medicaid application or arranging needs, but also that of the family. The following are a Social Security interview, will relieve the family\u2019s some examples of how families have reframed those stress greatly. initial negative feelings into feelings that are more pro- ductive or healthy: Communication is also an essential intervention when working with any family, regardless of their child\u2019s Helplessness Empowerment diagnosis. Most families may not remember the exact Fear Cautious optimism phrases or words that the practitioner uses to dissem- Sadness Openness of feelings inate information, but the family will often remember Anger Advocacy the tone, setting, and approachability of the practitioner during the interview. The physician\u2019s ability to restore TASKS OF THE PRACTITIONER competence in the family by acknowledging and vali- dating their fears or concerns will ensure that the family feels as if they are a member of the health care team. Families with children with disabilities face the simi- SELECTIVE TIMELINE OF THE HISTORY lar, mundane, everyday life struggles of families with OF DISABILITY RIGHTS typical children, yet there are volumes of research material investigating the differences between coping A great deal of change has occurred within the last styles and functions in the family of a child with a dis- 40 years with regard to people with disabilities, and ability, illness, or injury. \u201csome of the factors influencing the success are the nature and severity of the disabilities, accommoda- A study in Pediatrics (23) \u201cprovided a compare and tions available in society, and attitudes toward the contrast\u201d of children with chronic illness to those chil- disabled\u201d (25). What follows is a selective timeline of dren without. This study revealed that while all children the disability rights movement and how key pieces of and families should receive a psychosocial assessment, legislation broke down the barriers of society in order practitioners should not \u201cassume that dysfunction\u201d exists to allow all individuals the right to education, accom- because of the disability in the family. It appears from modations, and freedom (26,27). this study that assessment of the family\u2019s needs should come first and then a look at the family\u2019s strengths and 1964: Civil Rights Act passed outlawing discrimina- weaknesses in order to devise a support plan. tion on the basis of race in public accommodations and employment, as well as in federally assisisted pro- Similar research conducted by Press and Nolan grams. This law became the model for subsequent dis- (24) found that disease or disability does not predict ability rights laws. adaptation to disability and that the psychosocial adjustment of family life before the illness or injury 1965: Autism Society of America is founded by par- was the same as the psychosocial adjustment after the ents of children with autism in response to the lack illness or injury. The predictors for positive outcome of services. Parents found their children were being included good communication between family mem- discriminated against by the medical \u201cexperts\u201d who bers, low conflict in the home setting, and the positive believed autism was the result of poor parenting as expression of emotion. opposed to a neurological disability. With that being stated, the role of the practi- 1968: The Architectural Barrier Act was passed, man- tioner and the interventions offered to the family must dating that federally constructed buildings and facili- always \u201cstart where the family is.\u201d In other words, the ties be accessible to people with physical disabilities. practioner must listen to the family\u2019s needs and offer This act is generally considered to be the first ever emotional support at all developmental milestones or federal disability legislative law. turning points in the family\u2019s life. The practitioner can act as a positive role model for the family by acknow- 1970: The Physically Disabled Students Program (PDSP) ledging changes in the family dynamics or community was founded by Ed Roberts, John Hessler, Hale Zukas, systems and reframe these changes so that the family and others at the University of California in Berkley. can maintain function. With its provisions for community living, political advocacy, and personal assisted services, it became However, in order for a family to function at an the nucleus for the first Center for Independent Living, optimal level, one must provide the family with the founded two years later. information and resources necessary to succeed. The practitioner or medical staff member should investigate information and resources in the family\u2019s community.","Chapter 17 Psychosocial Aspects of Pediatric Rehabilitation 499 1973: Passage of the Rehabilitation Act of 1973 enrolled in private programs during litigation under marked the greatest achievement of the disability the Education for All Handicapped Children Act of rights movement. In particular, Title V and especially 1975 if the court rules such placement is needed for Section 504, with the first line confronting discrimina- the child to receive education in the least restrictive tion against people with disabilities. Litigation arising environment. out of Section 504 generated such concepts as \u201crea- 1988: The U.S. Supreme Court in Honing v. Doe affirms sonable modification,\u201d \u201creasonable accommodations,\u201d the \u201cstay-put rule\u201d established under the Education for and \u201cundue burden.\u201d This act became the framework All Handicapped Children Act of 1975, under which for federal law (ie, Americans with Disability Act school authorities cannot expel, suspend, or otherwise of 1990). move disabled children from the setting agreed upon in the child\u2019s Individual Education Program (IEP) with- The Education for All Handicapped Children Act out a due-process hearing. (Pub. Law 94\u2013142) was passed establishing the rights for children with disabilities, including a public edu- The National Parent Network on Disabilities was cation in an integrated environment. The act is a cor- established as an umbrella organization for the Parent nerstone of federal disability legislation. Over the next and Training Information Centers. 20 years, millions of children with disabilities were educated under its provisions, radically changing the 1990\u2013present: The Americans with Disabilities Act lives of people in the disability community. is signed by President George H.W. Bush and wit- nessed by thousands of disability rights activists. 1975: The first Parent and Training Information Center The law is the most sweeping disability rights leg- is founded to help parents of disabled children exer- islation in United States history, giving people with cise their rights under the Education for Handicapped disabilities full legal privileges. This law mandates Children Act of 1975. that local, state, and federal programs become access- ible; that businesses with more than 15 employees 1976: Passage of an amendment to the Higher Education make \u201creasonable accommodations\u201d for disabled Act of 1972 to provide services to physically disabled workers; and that public areas such as restaurants students entering college. and stores make \u201creasonable modifications\u201d to ensure access for all disabled citizens. Finally, this 1980\u20131983: The parents of \u201cBaby Doe\u201d in Bloomington, act also mandated access to public transportation Indiana, are advised by their physicians to forego and communication. a surgical procedure to unblock the baby\u2019s esopha- gus due to the fact that the baby had Down\u2019s syn- The Education for All Handicapped Children drome. \u201cBaby Doe\u201d starved to death before legal Act is amended and renamed the Individuals with action could be taken. However, this case prompted Disabilities Act (IDEA). the Reagan administration to issue legislation calling for \u201cBaby Doe squads\u201d to safeguard the civil rights of The final federal appeals court ruling in Holland newborns. v. Sacramento City Unified School District affirms the right of disabled children to attend public school clas- 1984: The \u201cBaby Jane Doe\u201d case, like the previous baby ses with nondisabled children. The ruling is a major in Bloomington, Indiana, involved an infant being denied victory in the ongoing effort to ensure enforcement of medical care because of the infant\u2019s disability. This case the IDEA. resulted in litigation argued before the U.S. Supreme Court in Bowen v. American Hospital Association and, in PEARLS AND PERILS turn, led to the passage of The Child Abuse Prevention and Treatment Act Amendments of 1984. \u25a0 Start where the family is. Allow them time and space to integrate the diagnosis or situation. The U.S. Supreme Court rules in Irving Independent School District v. Tatro that those school districts are \u25a0 Look to the family\u2019s strengths. Allow them to show required under the Education for All Handicapped you what works well. Children Act of 1975 to allow a school nurse or an aide to perform intermittent catheterization as a \u201crelated \u25a0 Never say \u201cI know how you feel.\u201d Each individual service to a disabled student.\u201d School districts can no experience is different. longer refuse to educate a disabled child because they might need such a service. \u25a0 Set limits and be consistent. Families need to know that someone is in charge and is an expert. They rely 1985: The U.S. Supreme Court rules in Burlington on that when they are confused or overwhelmed. School Committee v. Department of Education that pub- lic schools must pay expenses of disabled children \u25a0 There is nothing that kindness and compassion can\u2019t help. Even in the worst situation, a family will appreciate it if kindness was demonstrated to their child.","500 Pediatric Rehabilitation REFERENCES Director and Deborah Valentine, MSSW, Ph.D. Director School of Social Work Section II of the BSW Program on 1. Kingsley EP. Welcome to Holland (essay). 1987. Available at: pg. 11. Accessed 7\/21\/09. http:\/\/www.ssw.cahs.colostate. www.journeyofhearts.org\/kirstimd\/holland.htm. edu\/bsw\/files\/BSW_Handbook_2007\u201308.pdf. 15. Eisenberg A, Muroff HE, Sandler H. What to Expect When You 2. Wallander J, Thompson R, Alriksson-Schmidt J. Psychosocial are Expecting. 3rd ed. New York: Workman Publishing, 1991. adjustment of children with chronic physical disabilities. In: 16. Aron LY, Loprest PJ. Meeting the Needs of Children with Roberts M, ed. Handbook of Pediatric Psychology. New York: Disabilities. Washington, DC: Urban Institute Press, 1996. Guildford Publications, 2003;141\u2013144. 17. Davis H. Communication and Counseling in Health Care. Baltimore: Paul H. Brookes Publishing Co, Inc., 2003. 3. Institute of Medicine. Crossing the quality chasm: A new 18. Viscott D. Emotional Resilience. New York: Three Rivers health care system for the 21st century. Washington DC: Press, 1996. National Academies of Science, 2001. 19. Fallowfield L. Giving sad and bad news. Lancet. 1993;341: 476\u2013478. 4. Darbyshire L. Parents, nurses, and paedeatric nursing: 20. Cunningham C, Newton R. A question sheet to encourage A clinical review. J Adv Nurs. 1993;18:1970\u20131680. written consultation questions. Qual Health Care. 2000: 9(1):42\u201346. 5. Massachusetts Department of Mental Retardation. Family- 21. Antonelli RC, Stille CJ, Antonelli DM. Care coordination centered care. Available at www.communitygateway.org\/ for children and youth with special health care needs: a faq\/fcc.htm. descriptive, multisite study of activities, personnel costs, and outcomes. Pediatrics. 2008;122:e209\u2013e216. 6. Smith A, Terrel B, Conant H. Making family-centered care 22. Sandler A. Living with Spina Bifida: A guide for Families a reality. Semin Nurse Manage. 2000;8:136\u2013142. and Professionals. Chapel Hill: University of North Carolina Press, 1997. 7. Newton NS. Family-centered care: Current realities in par- 23. Cadman D, Rosenbaum P, Boyle M, Offord DR. Children ent participation. Pediatr Nursing. 2000;26:164\u2013168. with chronic illness: family and parent demographic characteristics and psychosocial adjustment. Pediatrics. 8. Eichner J, Johnson B. Family-centered care and the pedia- 1991;87:884\u2013889. trician\u2019s role. J Pediatr. 2003;112:691\u2013696. 24. Pless IB, Nolan T. Revision, replication and neglect: Research on maladjustment in chronic illness. J Child Psychol Psychiat. 9. Institute for Family-Centered Care. Briefing paper: Family- 1991;32:347\u2013365. centered health care. 1997. Bethesda: Institute for Family- 25. Molnar G, Alexander M. Pediatric Rehabilitation. 3rd ed. Centered Care, 1997. Philadelphia: Hanley and Belfus, Inc., 1999. 26. Americans With Disabilities Act Questions and Answers. 10. Wikipedia. Resilience. Available at: http:\/\/en.wikipedia. http:\/\/www.ada.gov\/quadaeng.htm. Accessed 7\/21\/09. org\/wiki\/Resilience. Accessed 2\/09. 27. Michigan Disability Rights Coalition. Disability History. Available at copower.org\/leader\/disabilityrightshistory.htm 11. Roland JS, Walsh F. Facilitating family resilience with Accessed 7\/8\/09. childhood illness and disability. Curr Opin Pediatr. 2006;18: 527\u2013538. 12. Parent Power Helping you make sense of Schooling Today: How to Advocate for your Child. August 2001, Vol.3. Issue 5. http:\/\/ www.edreform.com\/_upload\/01august.pdf. Accessed 7\/21\/09. 13. Faust JR. Clinical social worker as patient advocate in community mental health center. Clin Soc Worker J. 2008;36:293\u2013300. 14. Baccalaureate Social Work Program Student Handbook 2006\u20132009 by Victor A. Baez, AM, Ph.D. BSW Program","Index Page numbers in boldface type indicate complete chapters; f indicates a \ufb01gure; t indicates a table. AAAD. See American Athletic Association of the Deaf \u03b1-Adrenergic blockers AAASP. See American Association of Adapted Sports Programs for bladder dysfunction, 212 AAC. See Augmentative and alternative communication AACPDM. See American Academy of Cerebral Palsy and Adulthood, psychosocial development in, 118 Adventure activities, 87 Developmental Medicine Advocacy for child with spinal cord injury, 496 AAMR. See American Association on Mental Retardation AFO. See Ankle-foot-orthosis ABAS-2. See Adaptive Behavior Assessment System-2 Age- and grade-equivalent scores, 24 Abductor pads, for wheelchair, 112 Aging Access techniques, 121 Accommodations, 26 with cerebral palsy, 190 Accutane. See Isotretinoin with neural tube defect, 224\u2013225 ACE. See Antegrade continence enema Aging, with pediatric onset disability and diseases, 425\u2013452 Acetabular index, 394f access to health care, 450 Acetylcholinesterase de\ufb01ciency, 142, 152, 311 disability-speci\ufb01c health, 429, 430\u2013435t Achenbach System of Empirically Based Assessment, 44, 46t Achievement tests, 38\u201340 cerebral palsy, 429, 436\u2013439 Achondroplasia, 405\u2013406 childhood-onset spinal cord injury, 444\u2013446 Acquired childhood aphasia, 64 Down syndrome, 447\u2013449 Acquired language disorder, 64, 67t intellectual disabilities, 446\u2013447 Activities of daily living (ADLs), 6 limb de\ufb01ciency, 446 spina bi\ufb01da, 440\u2013444 with burn injuries, 382 spinal cord dysfunction, 439\u2013440 in juvenile idiopathic arthritis, 373 Williams\u2019 syndrome, 449 after spinal cord injury, 268, 397 health and performance, 428\u2013429 Acupuncture, in cerebral palsy, 186t health and wellness agenda, 450\u2013452 Acute illness, in primary care of\ufb01ce, 17 lifespan perspective, 427\u2013128 Acute in\ufb02ammatory demyelinating polyradiculoneuropathy transition of care to adult services, 449\u2013450 Agitation, after traumatic brain injury, 243 (AIDP), 312\u2013313 AIDP. See Acute in\ufb02ammatory demyelinating electrodiagnostic evaluation of, 146\u2013147 Acute motor axonal neuropathy, 147 polyradiculoneuropathy electrodiagnostic evaluation of, 147 AIMS web assessment system, 40 Acute transient synovitis (ATS), 384\u2013385 Allergies, history of, 3 Adapted physical education (APE), 80, 82, 87 Alpha feto-protein (AFP), in spina bi\ufb01da diagnosis, 203 Adapted SPORTS Model, 84\u201385 Alpine skiers, 87t Adaptive Behavior Assessment System-2 (ABAS-2), 41, 41t Alternate-form reliability, 24 Adaptive behavior, assessment of, 40\u201341 Amateur Softball Association, 96 Adaptive equipment. See Assistive devices Amateur Sports Act, 80 Adaptive interfaces, 117 Ambulation Adaptive sports and recreation classi\ufb01cation systems, 86\u201387 in juvenile idiopathic arthritis, 373\u2013374 exercise in pediatrics, psychologic impact of, 80\u201381 in spina bi\ufb01da, 204, 218\u2013220 fun and competition, sports for, 91\u201398 American Academy of Cerebral Palsy and Developmental history, 79\u201380 injury, in disabled athlete, 85 Medicine (AACPDM), 185 physical activity, participation in, 83\u201385 American Academy of Pediatrics, 184, 187 professionals, 82\u201383 recreation opportunities, adapting, 87\u201391 Committee on Children with Disabilities, 187 Adductors, 112, 480 American Academy of Pediatrics, 13, 16, 17 Adeli suit therapy (AST), in cerebral palsy, 185\u2013187, 186t American Amateur Racquetball Association, 94 ADHD. See Attention-de\ufb01cit hyperactivity disorder American Association of Adapted Sports Programs (AAASP), 84 Adjustment problems and psychiatric disturbance, 22\u201323 American Association on Mental Retardation (AAMR), 40 ADLs. See Activities of daily living American Athletic Association of the Deaf (AAAD), 80 Adolescence American Dietetic Association, 75 examination in, 6 American Speech-Language-Hearing Association (ASHA), 123 psychosocial development in, 118 American Spinal Injury Association (ASIA), 156 impairment scale, 262\u2013264 Americans with Disabilities Act, 84, 87, 450, 499 American Therapeutic Recreation Association, Code of Ethics, 83 American Wheelchair Bowling Association (AWBA), 80 501","502 Index Ataxia telangiectasia, 148 Ataxic movements, 166 Amnesia, posttraumatic (PTA), 34, 235 Athetosis, 172, 183 Amniotic band syndrome, 336f Atlantoaxial instability, 364\u2013365 Amputations. See also Limb de\ufb01ciencies ATS. See Acute transient synovitis Attention acquired, 337 Amputees, athletes, classi\ufb01cation of, 86 assessment of, 30 Anesthesia, for nerve conduction studies, 137 impairment of, after traumatic brain injury, 239 Ankle Attention-de\ufb01cit hyperactivity disorder (ADHD), 231, 292 Augmentative and alternative communication (AAC), 118\u2013123 assessment of, in cerebral palsy, 173, 438 devices, 118 Ankle-foot-orthosis (AFO), 107t, 325, 463, 478 resources for, 122\u2013123 Aural\/oral method, 65 in cerebral palsy, 184 Autism, 66 in clubfoot, 217 diagnostic criteria for, 65, 68 in spina bi\ufb01da, 220 and language disorders, 63 Ankle rocker, 475\u2013476, 476f Autistic syndrome, 68 Ankylosing spondylitis, 3, 372 Autoimmune myasthenia gravis, 311\u2013312 Annulus \ufb01brosis, 393 Automated feeders, 123 Anosmia, after traumatic brain injury, 238 Autonomic dysre\ufb02exia (AD), 271\u2013272 Anoxic brain injury, 252 Automobile accidents, 250 Antegrade continence enema (ACE), 270 Autophagy, 202 Anterior cord syndrome, 264 Autosomal-dominant episodic ataxia 1 (EA1), 321 Anterior \ufb02oor reaction\/ground reaction ankle foot orthosis, 107t Awareness through movement, 345 Anterior pituitary dysfunction, after traumatic brain injury, AWBA. See American Wheelchair Bowling Association Axillary crutches, 110 241\u2013242 Axonal Guillain\u2013Barr\u00e9 disorder Antibiotic prophylaxis and bacteriuria treatment electrodiagnostic evaluation of, 147 Azathioprine, 312 in neurogenic bladder, 212 Anticholinergic agents, for bladder dysfunction, 211 Bacitracin, for burn injuries, 379 Anticonvulsants Back assessment, in cerebral palsy, 89 Baclofen (Lioresal), 181, 182 in cerebral palsy, 181 in brachial plexus palsy, 370 for spasticity, 180t, 237 for seizures, 443 Bad Ragaz aquatic therapy, 90 Antidiuretic hormone (ADH) Balance, after traumatic brain injury, 236 in diabetes insipidus, 241 Balance forearm orthosis (BFO), 124 Banana arm, 343f syndrome of inappropriate secretion of. See Syndrome of Barium swallow, 17, 243 inappropriate antidiuretic hormone secretion Barlow\u2019s sign, 388 BASC-2. See Behavior Assessment System for Children-2 AOS. See Apraxia of speech Baseball, 91 APE. See Adapted physical education Basketball, 92 Apoptosis, 202 Battelle Developmental Inventory, 187 Apraxia of speech (AOS), 57, 58 Bayley Scales of Infant and Toddler Development, 46t Aquatic therapy, 90 Archery, 91 3rd edition (Bayley-III), 37, 43 Architectural Barrier Act, 498 Bayley Scales of Infant Development, 187 ARM. See Assistive Robotic Manipulator Becker muscular dystrophy, 293\u2013295 Arnold\u2013Chiari malformation, 3 Arousal impairment, after traumatic brain injury, 239 age of transition to wheelchair, 294 Arteriovenous shunt, 6 cardiomyopathy, 294\u2013295 Arthritis characteristics of, 288t clinical course of, 294 associated with in\ufb02ammatory bowel disease, 372 cognition, 295 infectious, 376 contractures, 294 psoriatic, 372 diagnostic evaluation, 293 reactive, 376 epidemiology, 293 septic, 376 genetic elements, 293 Arthrogryposis malignant hyperthermia and, 278 appearance in, 6 onset age and signs, 294 multiplex congenital, 366 pseudohypertrophy in, 279 Articulation, 57f pulmonary function, 294 Articulatory\/resonatory system, 57 spine deformity, 294 ASHA. See American Speech-Language-Hearing Association weakness, pattern and progression of, 294 ASIA. See American Spinal Injury Association Behavior Assistive devices, 103\u2013126 history of, 4 in cerebral palsy, 104, 111, 112 observation of, in psychological assessment, 40\u201341 for driving with prosthetics, 354 after traumatic brain injury, 240 for juvenile idiopathic arthritis, 373 in spina bi\ufb01da, 441 after spinal cord injury, 125 Assistive Robotic Manipulator (ARM), 124\u2013125 Assistive Technology Act, 103 Asymmetric tonic neck re\ufb02ex, 169, 218 Ataxia, 6","Index 503 Behavior Assessment System for Children-2 (BASC-2), 44, 46t Bulbar palsy, 2 Behavior Rating Inventory of Executive Functions (BRIEF), 31, 32, Burn-associated polyneuropathy (BAPN), 148 Burn injuries 45, 47t, 240 Bellows failure, 266 acute burn management, 379\u2013381 Benign focal amyotrophy. See Juvenile segmental SMA assessment, 378 Benzodiazepines, 181 chronic burn management, 381\u2013382 classi\ufb01cation of, 379f for spasticity, 237 dressing for, 379 BFO. See Balance forearm orthosis epidemiology of, 378 Big Keys Plus USB keyboard, 122 hospitalization, 381 Biofeedback, in therapeutic exercise, 27, 214, 481 outcome, 382\u2013383 Bisacodyl (Dulcolax), for bowel dysfunction, 214, 270t pain management with, 379\u2013382, 383f Bladder, neurogenic. See Neurogenic bladder positioning of patient, 381t Bladder function, 444, 448 prevention of, 384 Bladder management rehabilitation, 381 scar, classi\ufb01cation of, 382 after spinal cord injury, 269 severity, 379f after traumatic brain injury, 244 surgery for, 338\u2013339 Bladder training, in spina bi\ufb01da, 440 topical agents for, 379 Bladder volume, 244 BlazeSports America, 84 CAD. See Central autonomic dysfunction Blink Twice\u2019s TANGO!, 120f CAF. See Challenged Athletes Foundation Blood pressure, 7 Calcaneus foot Blount\u2019s disease, 385\u2013396 BNAS. See Brazelton Neonatal Assessment Scale in spina bi\ufb01da, 214, 217 Body composition, 322 California Verbal Learning Test-C (CVLT-C), 35t Bone conditions, 405 Calorie requirements Bone and mineral density (BMD) disorders, in cerebral palsy, 173 Bone mineralization, 80 in Duchenne muscular dystrophy, 328 Borrelia burgdorferi, 376 in neuromuscular diseases, 293 Boston Diagnostic Aphasia Examination, 34 CAMA. See Communication Aid Manufacturers Association Botulinum toxin (Botox), for spasticity, 212, 273t Camping, 87 Botulinum neurotoxin (BoNT), 179 Campylobacter, and reactive arthritis, 376 Botulism, 140t Canes, 110 acquired, noninfantile, 312 Carbamazepine, 305, 307 infanttile, 150\u2013151 Carbon dioxide suppositories (Ceo-Two), 270t Cardiac abnormalities electrodiagnostic evaluation of, 151 in Becker muscular dystrophy, 294\u2013295 and hypotonia, 312 in Emery-Dreiffuss muscular dystrophy, 302 Bowel management in fascioscapulohumeral muscular dystrophy, 301 after spina bi\ufb01da, 213\u2013214 in neuromuscular diseases management, 277, 329 after traumatic brain injury, 243\u2013244 in scoliosis, 400 Bowel medications, 270t Cardiorespiratory endurance, 392 Bowel training, in spina bi\ufb01da, 443 Carpal tunnel syndrome (CTS), in children, 149 Bowling, 92 Car seats, 117 Brachial plexus injury, 367 Caster cart, for child with spina bi\ufb01da, 115t complications, 368\u2013369 CAT. See Children\u2019s Apperception Test electrodiagnostic evaluation of, 143\u2013146 Catheterization. See Clean intermittent catheterization evaluation, 367\u2013368 Cattell-Horn-Carroll psychometric model, 36 pain, 370 Cauda equina syndrome, 264 SSEPs in, 158 Caudal regression syndrome, 203 surgery, 369\u2013370 Cavous feet, 366 surgical indications, 369 Cavus foot, 325 with traumatic brain injury, 368\u2013369 in spina bi\ufb01da, 204, 217 treatment, 368 CBCL. See Child Behavior Checklist Brain injury CDI. See Children\u2019s Depression Inventory in cerebral palsy, 165 Centers for Disease Control (CDC), 199, 231 nursing care for, 249 Central auditory processing impairment, 238 and SSEPs, 156 Central autonomic dysfunction (CAD), after traumatic brain injury, 244 traumatic. See Traumatic brain injury Central cord syndrome, 264 Brainstem malformations, in spina bi\ufb01da, 208 Central core myopathy, 303 Branched-chain ketoacid supplementation, in neuromascular Central nervous system malformations, in spina bi\ufb01da, 206, 206t cerebellum and hindbrain, 208 disease, 328\u2013329 forebrain, 209 Brazelton Neonatal Assessment Scale (BNAS), 37 malformations, 209 Brevicollis, 364 spinal cord, 206\u2013208 Brief Smell Identi\ufb01cation, 35 ventricles, 208\u2013209 BRIEF. See Behavior Rating Inventory of Executive Functions Central ray syndrome, 341 British Society of One-Armed Golfers, 79 Central ventilatory dysfunction (CVD), 3 Brown\u2013Sequard syndrome, 264 Bruininks-Oseretsky Test of Motor Pro\ufb01ciency, 236","504 Index Chemotherapeutic agents, 317 Chest harnesses, for wheelchairs, 112, 117 Central visual dysfunction, 239 Child abuse, 381 Centronuclear (myotubular) myopathy (non-X-linked), 303 Cerebellum malformations, in spina bi\ufb01da, 208 musculoskeletal pain and, 410\u2013412, 414\u2013415 Cerebral atrophy, after traumatic brain injury, 245\u2013246, 245f Child Abuse Prevention and Treatment Act Amendments of 1984, 499 Cerebral palsy (CP), 64\u201365, 80, 165, 481, 483 Child Amputee Prosthetic Project\u2013Functional Status Index, 346 Child Behavior Checklist (CBCL), 44 aging with, 429, 430\u2013431t, 436\u2013439 Child Health Questionnaire, 189, 407 cause of, 166, 170 Childhood aphasia, 64 classi\ufb01cation, 166\u2013168 acquired, 64 functional, 166\u2013167 and language disorders, 67t neurologic, 166 Childhood neuromuscular diseases, management of, 322 complementary and alternative treatments for, 186t Childhood-onset spinal cord injury, 444\u2013446 course and prognosis Child life specialist, 83 aging, with cerebral palsy, 190 Child Memory Scale (CMS), 35t outcome measures, 187\u2013189, 188t Children with special health care needs (CSHCN), 13 prognosis for ambulation, 189\u2013190 Children\u2019s Apperception Test (CAT), 44, 46t quality of life, 189 Children\u2019s Depression Inventory (CDI), 45, 47t criteria for diagnosis of, 165 Children\u2019s Orientation and Amnesia Test (COAT), 34, 235 diagnostic imaging in, 169\u2013170, 171f Children\u2019s Paced Auditory Serial Addition Test (CHIPASAT), 31t differential diagnosis, 170 Chloral hydrate, for anesthesia in nerve conduction studies, 137 disorders, associated Chlorpromazine, for spasticity, 237 bone and mineral density disorders, 173 Chlorpromazine hydrochloride, for anesthesia in nerve conduction cognitive impairments, 172 epilepsy, 172 studies, 137 gait impairments, 175\u2013176 Chondrodystrophic myotonia. See Schwartz\u2013Jampel syndrome genitourinary disorders, 173 Chondromalacia, 391 hearing impairments, 172 Chorea, 321 musculoskeletal disorders, 173\u2013175 Chronic illness, 21, 42 nutritional disorders, 172\u2013173 Chronic in\ufb02ammatory demyelinating polyradiculoneuropathy (CIDP) oromotor impairments, 172 psychological impairments, 172 electrodiagnostic evaluation of, 147 respiratory disorders, 173 Chronic in\ufb02ammatory demyelinating polyradiculoneuropathy, 313 sensory impairments, 170 Chronic kidney disease (CKD), 409 visual impairments, 170\u2013172 CIC. See Clean intermittent catheterization dyskinetic, 166, 169 Cisapride (Propulsid), for bowel dysfunction, 270t early intervention for, 179 Clavicle orthosis, 105t epidemiology, 165 Claw toe, in spina bi\ufb01da, 204, 217 evaluation of child with, 189 Clean intermittent catheterization (CIC) functional training in, 177 laboratory tests in, 170, 171f in spina bi\ufb01da, 212 mixed types of, 190 in spinal cord injury, 266, 269 pathology, 168\u2013169 primary care treatment of children managed with, 212 prognosis for, 188\u2013189 Clonidine, for spasticity, 180t, 237 psychosocial issues in, 189 Clostridium botulinum, 396 risk factors, 165\u2013166 Clubfoot, 365 signs and symptoms, 169 in spina bi\ufb01da, 217 spastic, 166 CMAP. See Compound muscle action potential speech disorders in, 172 CMS. See Child Memory Scale therapeutic exercise in, 176 COAT. See Children\u2019s Orientation and Amnesia Test therapeutic management of, 178\u2013179 Cobb method of curvature measurement, 398, 399f treatment Cochlear implant, 65 adaptive equipment, 184 Cocktail party syndrome, 223 alternative therapy, 184\u2013187 Cognitive assessment, 25, 27, 36\u201337 general principles, 176 alternative tests, 37\u201338 hypertonia management, 178\u2013183 instruments in orthopedic surgery, 183\u2013184 orthoses, 184 with young children, 37 physical and occupational therapy, 176\u2013178 Cognitive de\ufb01cits, after traumatic brain injury, 239 speech therapy, 178 Cerebral salt wasting syndrome, after traumatic brain injury, 241 attention and arousal, 239 Cervical nerve root lesions behavioral problems, 240 electrodiagnostic evaluation of, 143\u2013146 communication de\ufb01cits, 240 Cervical spine, juvenile idiopathic arthritis of, 374 executive function, 240\u2013241 Challenged Athletes Foundation (CAF), 85 memory impairment, 239\u2013240 Charcot\u2013Marie\u2013Tooth (CMT) neuropathy, 313\u2013316 social functioning, 241 Chemical denervation, 179 Cognitive function, in spina bi\ufb01da alcohol blocks, 179 neuropsychology and learning problems associated with spina botulinum neurotoxin (BoNT), 179 bi\ufb01da, 222\u2013224 Cognitive impairments after traumatic brain injury, 238 in cerebral palsy, 172","Index 505 Cold therapy, for juvenile idiopathic arthritis, 373 Constitutional\/intrinsic bone conditions (cont.) Collagen myopathy, 299\u2013300. See also Ullrich CMD disorganized cartilage and \ufb01brous components, 406 Coma\/Near-Coma Scale, 249 extraskeletal disorders, 409 Commission for Motion Laboratory Accreditation (CMLA), 465 tubular bone\/spinal growth, defects of, 405\u2013406 Communication. See also Augmentative and alternative Constraint-induced movement therapy (CIMT), 177\u2013178 communication Construct validity, 25 de\ufb01cits, after traumatic brain injury, 240 Content, 24 de\ufb01nition of, 53 Continuous Performance Tests, 31t disorders, 2, 55\u201369 Contour seating systems, 112 Control, in therapeutic exercise, 81 in cerebral palsy, 172 Controlled knee \ufb02exion, 475 intentional, 53 Communication Aid Manufacturers Association (CAMA), 123 walkers, 464 Communicative\u2013cognitive disorders, 67t Coordination, impaired, in movement disorders, 9 Community reintegration, of children with traumatic brain injury, Corpus callosum malformations, in spina bi\ufb01da, 209 Cortical sensory function, 10 248 Corticosteroids, 15 community support, 248\u2013249 individual educational plans, 248 in Duchenne muscular dystrophy, 325 in-home services, 249 Coup de sabre, in scleroderma, 377 long-term needs, planning for, 249 CP. See Cerebral palsy out-of-home services, 249 Coxa valga, 9, 204, 215, 393 school services, 248 Coxa vara, 393 sports and recreational activities, returning to, 249 Craig Hospital Inventory of Environmental Factors, 83 Community support Craniosacral technique, 185, 186t, 187 for child with traumatic brain injury, 248\u2013249 Creatine kinase, in neuromuscular diseases, 283 Compartment syndromes, 148, 149 Criterion, 24, 25 Compound muscle action potential (CMAP), 129 Critical events, of gait cycle, 474, 474t amplitudes, in children, 130t recording of, 136, 137, 141, 151 during single limb support task, 476\u2013478, 479t Complementary and alternative medicine (CAM), in cerebral during swing limb advancement task, 478\u2013481 during weight acceptance task, 475\u2013476, 477t palsy, 184, 186t Crutches, 110, 220 additional therapies, 187 CSHCN. See Children with special health care needs Adeli suit therapy (AST), 185\u2013187 CT. See Computed tomography conductive education, 185 C-TONI. See Comprehensive Test of Nonverbal Intelligence hyperbaric oxygen therapy (HBOT), 185 Culture-sensitive assessment, 28\u201329 Compound muscle action potential (CMAP), in children, 129, 130t Cups, adaptive, 104, 391 Comprehensive Test of Nonverbal Intelligence (C-TONI), 38, 39t CVD. See Central ventilatory dysfunction Computed tomography (CT) CVLT-C. See California Verbal Learning Test-C in cerebral palsy, 170 Cycling, 93 of traumatic brain injury, 233 Cyclophosphamide, for juvenile idiopathic arthritis, 312 Computer access, 121\u2013122 Cyclosporine, for juvenile idiopathic arthritis, 312 Computer-assisted rehabilitation, in traumatic brain injury, 247 Cystic \ufb01brosis, 81 Concentration, assessment of, 30 Concussion, in sport, management guidelines for, 250, 250t DAAA. See Dwarf Athletic Association of America Conductive education (CE), in cerebral palsy, 185, 186t Dance, 88 Conductive hearing loss, 238 Dantrolene sodium (Dantrium), 180 Congenital conditions of musculoskeletal system, 362, 364\u2013367 side effects of, 180t, 237 Congenital \ufb01ber-type size disproportion, 304 for spasticity, 180t, 182, 237 Congenital hypomyelinating neuropathy, 140t, 141, 146, 315t DAOS. See Developmental apraxia of speech Congenital kyphosis, 400 DAS. See Dynamic Arm Support Congenital muscular dystrophy (CMD), 298 DDH. See Developmental dysplasia of the hip with early spine rigidity, 300 Deconditioning, 3, 81, 267 Fukuyama CMD, 298\u2013299 Deep vein thrombosis, 272 merosin-de\ufb01cit CMD, 298 De\ufb02azacort, for neuromuscular diseases, 290, 291, 325, 329 merosin-positive CMD, 298 Dejerine-Sottas disease, 146, 279, 313, 315 muscle-eye-brain disease, 299 Delis\u2013Kaplan Executive Function System (D-KEFS), 32t Ullrich CMD, 299\u2013300 d-EMG. See Dynamic electromyography Walker-Warburg syndrome (WWS), 299 Demyelinating diseases, SSEPs in, 158 Congenital myasthenic syndrome (CMS), 152\u2013153, 311 Dental health, 15\u201316 Congenital myopathies, 302\u2013303 Dental problems, in cerebral palsy, 172 electrodiagnostic evaluation of, 153 Denver II (developmental screening test), 187 Congenital scoliosis, 400 Depression, disabilities and, 444, 448 Consonant sounds, acquisition of, 61t Dermatome, 361, 362f Constitutional\/intrinsic bone conditions, 405 Dermatomyositis, electrodiagnostic evaluation of, 153 abnormal bony density or structure, 406\u2013407 Development, 21 calcium\/phosphorus metabolism, metabolic conditions Developmental apraxia of speech (DAOS), 58 Developmental conditions, of musculoskeletal system, 384\u2013397 affecting, 407\u2013409 Developmental dysplasia of the hip (DDH), 386\u2013388, 387t, 388f","506 Index Duchenne muscular dystrophy (DMD) (cont.) cardiomyopathy, 291\u2013292 Developmental history, 2\u20133 characteristics of, 288t Developmental language disorder, 63, 67t cognition and behavioral phenotype, 292 Developmental milestones, 13\u201319, 218 contractures, 290 Developmental Test of Visual-Motor Integration (VMI), 33t diagnostic evaluation, 288\u2013289 Developmental verbal apraxia, 58 epidimeology, 289 Deviation IQ, 24 genetic elements of, 288 Diabetes, maternal, and limb de\ufb01ciency, 2, 335 incidence of, 288t Diabetes insipidus (DI) malignant hyperthermia and, 289 onset and early signs, 289 after traumatic brain injury, 241 palpation in, 7 Diabetic polyneuropathy, 148 pseudohypertrophy in, 279 Diaphysis, 393, 406, 412 pulmonary function, 291 Diastematomyelia, 206 scoliosis in, 326f Diazepam (Valium), 181 spine deformity, 290\u2013291 therapeutic exercise for, 322 for spasticity, 18, 180t weakness, 289 DIBELS. See Dynamic Indicators of Basic Early Literacy Skills and weight loss, 328 Diethylene triamine pentaacetic acid (DTPA) scan, of renal Duchenne-Erb\u2019s palsy, 144, 145 function, in spina bi\ufb01da, 211 Durable medical equipment, 14 Dimercaptosuccinic acid (DMSA), of renal function, in spina Dwarf Athletic Association of America (DAAA), 80 Dynamic Arm Support (DAS), 124 bi\ufb01da, 211 Dynamic electromyography (d-EMG), 468 Diparetic CP, 166, 167f Dynamic Indicators of Basic Early Literacy Skills (DIBELS), 40 Diplegia, 481\u2013489 Dynamic WHO, 184 DynaVox, 120, 121, 121f spastic, 396, 483 Dysarthria, 57\u201358 Diplopia, after traumatic brain injury, 239 Disability(ies) types, 58t Dyskinetic cerebral palsy, 166 acquired, AAC in, 55, 68, 364, 390 Dysphagia, diet levels, 76t children with, health promotion for, 7, 14\u201318, 87 Dysphonia, 57, 75 legislation associated with, 498\u2013499 Dysplasia rights, history of, 498\u2013499 school environment and, 22, 26, 274 de\ufb01nition of, 386 Disability-speci\ufb01c health, 429, 430t\u2013435t of hip, developmental cerebral palsy, 429, 436\u2013439 childhood-onset spinal cord injury, 444\u2013446 classi\ufb01cation, 387t Down syndrome, 435t, 447\u2013449 risk factors, 387t intellectual disabilities, 446\u2013447 Dystonia limb de\ufb01ciency, 433t\u2013434t, 446 after traumatic brain injury, 237 spina bi\ufb01da, 431t\u2013432t, 440\u2013444 Dystonic cerebral palsy, 167f spinal cord dysfunction, 439\u2013440 Dystrophenopathies Williams\u2019 syndrome, 449 Becker muscular dystrophy, 293\u2013295 Disabled Sports USA (DSUSA), 80 characteristics of, 288t Discharge planning, after traumatic brain injury, 247\u2013248 Duchenne muscular dystrophy, 287\u2013293 Discipline, family counseling on, 218 Dystrophic myopathies Discitis, 393 electrodiagnostic evaluation of, 153\u2013154 Distal motor latencies (DMLs), in children, 128\u2013129, 129t Dystrophic myopathies, 287 Distal spinal muscular atrophy, 320 Dystrophin-glycoprotein complex, diseases of, 287 Distance measurements, in nerve conduction studies, 133 Ditropan. See Oxybutynin chloride Early intervention programs, 4, 341 D-KEFS. See Delis\u2013Kaplan Executive Function System effects of, 90, 407 DMD. See Duchenne muscular dystrophy DMSA scan. See Dimercaprolsuccinic acid scan EasyStand, 110f Docusate (Colace: Sufak), for bowel dysfunction, 244, 270t ECEQ. See European Child Environment Questionnaire Dolichocephaly, 6 Ecological validity, 25 Doman Delacatto method, 187 Education. See also Schooling Down syndrome (DS), 447\u2013449 aging with, 435t of child with spina bi\ufb01da, 221, 225, 443 atlantoaxial instability in, 364\u2013365 after spinal cord injury, 265, 271, 273\u2013274 Williams\u2019 syndrome (WS), 449 Education for All Handicapped Children Act, 499 DPT, for anesthesia in nerve conduction studies, 137 EEG. See Electroencephalography Driving, 31\u201332, 354 Elbow Drooling, 17 injuries to, 340, 364, 390 in cerebral palsy, 172 juvenile idiopathic arthritis in, 374 Drosophila, 201 orthosis, 105t, 106t DSUSA. See Disabled Sports USA Elbow \ufb02exor contractures, 300, 322, 381t DTPA scan. See Diethylenetriamine pentaacetic acid scan in Duchenne muscular dystrophy, 324 Duchenne muscular dystrophy (DMD), 16, 287\u2013293 in Emery-Dreifuss muscular dystrophy, 302 ambulation loss, 289\u2013290 in neuromuscular disease, 290, 293 anthropometric changes, 292\u2013293 appearance in, 6, 7","Index 507 Elbow \ufb02exor contractures (cont.) Energy supplementation, in neuromuscular diseases, 328 in spasticity, 175 Enterobacter, and septic arthritis, 378 Enthesitis-related arthritis, 372\u2013373 Elbow-wrist-hand orthosis, 105t Entrapment mononeuropathies, in children, 149\u2013150 Electrical stimulation, in cerebral palsy, 178, 186t Electrodes, 136 carpal tunnel syndrome (CTS), in children, 149 neuropathies with limb-lengthening procedures, 150 recording, 134\u2013135 peroneal mononeuropathies in children, 149 motor conduction, 135 radial mononeuropathies, in children, 149 sensory conduction, 134\u2013135 sciatic mononeuropathies in children, 149\u2013150 ulnar mononeuropathies, in children, 149 stimulating, 133\u2013134 Ephedrine, for bladder dysfunction, 212 Electrodiagnosis, in pediatrics, 127 Epilepsy in cerebral palsy, 172 clinical problems in after traumatic brain injury, 244\u2013245 acute onset infantile hypotonia, 142 Epiphyseal, 242 brachial plexus and cervical nerve root lesions, 143\u2013146 dysplasia of, multiple, 384, 414 common polyneuropathies, 146\u2013148 injuries to, Salter\u2019s classi\ufb01cation of, 386 early respiratory distress in infancy, differential Equinovalgus foot deformity, in cerebral palsy, 173, 174f diagnosis for, 141 Equinus deformity entrapment mononeuropathies, in children, 149\u2013150 in cerebral palsy, 173 facial paralysis, in neonate, 146 in spina bi\ufb01da, 204, 217 \ufb02oppy infant, electrodiagnostic evaluation of, 138\u2013141 Erythema migrans, in Lyme disease, 376 motor neuron disorders, 142\u2013143 Escherichia coli, and septic arthritis, 378 myopathies, 153\u2013155 Esophageal phase, of swallowing, 74f, 75 neuromuscular junction disorders, 150\u2013153 Etretinate, 203 neuropathies associated with infections, 148\u2013149 European Child Environment Questionnaire (ECEQ), 83 somatosensory-evoked potentials, 155\u2013158 Evan\u2019s Blue Dye Test (MEBD), 73 spinal cord injury, 143 EVA walker, 111 Evoked potentials, 141, 143, 146, 147, 155\u2013158, 399 electromyography Ewing\u2019s sarcoma, 338, 351, 411 motor unit con\ufb01guration and amplitude, 130\u2013131 Examination, 5 motor unit duration, 131 by age, 5 motor unit recruitment, 131\u2013132 functional evaluation, 10 growth, 6 infantile nerve conduction studies, technical factors with inspection, 6\u20137 distance measurements\/measurement error, 133 musculoskeletal system, 9 nerve conduction studies, special considerations for, 135\u2013136 neuromuscular system, 7\u20139 recording electrodes, 134\u2013135 observation, 5 repetitive nerve stimulation studies, 136 organ systems, 7 shock artifact, 133 palpation, 7 stimulating electrodes, 133\u2013134 school-aged and adolescent patients, 6 temperature, 132 sensory, 9\u201310 volume conduction, 132 tone of, 1 Executive function, 240\u2013241 maturational factors in, 127 assessment of, 30\u201332 nerve conduction studies, 128\u2013130 Exercise, 80, 452 in DMD, 322 needle electromyography, technical factors of in juvenile idiopathic arthritis, 373 electrodes, 136 in neuromascular diseases, 322\u2013323 optimal muscles, for evaluation, 137 physiologic impact on, 80\u201381 optimal muscles to study for rest activity, 136\u2013137 psychosocial impact on, 81\u201382 sedation, 137\u2013138 Expressive Production Rating Scale. See ExPRS single-\ufb01ber EMG, limitations of, 138 ExPRS (Expressive Production Rating Scale), 65, 65t External moments, 467 Electroencephalography (EEG) Extraskeletal disorders, 409 of traumatic brain injury, 234 Facial appearance Electromyography (EMG) in myotonic muscular dystrophy, 28, 154, 304\u2013307 brachial plexus palsy, 368 in Schwartz-Jampel syndrome, 149, 154, 308 motor unit con\ufb01guration and amplitude, 130\u2013131 motor unit duration, 131 Facial palsy, 6 motor unit recruitment, 131\u2013132 in neonate, electrodiagnostic evaluation of, 146 muscle and neurologic function evaluation, 468\u2013469 needle, technical factors in, 136\u2013138 Facial paralysis, in neonate, electrodiagnostic evaluation of, 146 single-\ufb01ber, limitations, in pediatric populations, 138 Facial Recognition Tests, 33t in therapeutic exercise, 307 Facial weakness, in facioscapulhumeral muscular dystrophy, Electron microscopy, in neuromuscular diseases, 152, 287 300, 300f EMD. See Emery-Dreifuss muscular dystrophy Facioscapulohumeral muscular dystrophy (FSHD), 300\u2013301 Emerin, 302 Family counseling, after traumatic brain injury, 248 Emery-Dreifuss muscular dystrophy (EMD), 302 EMD1, 302 EMD2, 302 EMG. See Electromyogrphy EMLA cream, for anesthesia in nerve conduction studies, 137\u2013138 Endoscopic third ventriculostomy (ETV), 209 Endurance, cardiovascular, 400","508 Index Family environment Freiberg\u2019s disease, 391 assessment of, 45\u201346 Friedreich\u2019s ataxia, 148, 321 spina bi\ufb01da and, 45 Friendships, development of, 41 FSHD. See Facioscapulohumeral muscylar dystrophy Family Environment Scale (FES), 45 Full-scale IQ, 26 Family history, 5 Functional behavior assessment (FBA), 42\u201343, 46t Functional electrical stimulation (FES), 104, 178 in neuromuscular diseases, 279 Functional evaluation, 10 Fanconi anemia, 341 Functional Independence Measure (FIM), 250 Fascioscapulohumeral muscular dystrophy (FSHD), 300\u2013301 Functional Independence Measure for Children (WeeFIM), 250 Fazio-Londe disease. See Progressive bulbular paralysis of Functional limitation conditions, 426, 426t Functional neuromuscular stimulation, 186t childhood Functional scoliosis, 403 FBA. See Functional behavior assessment Fecal incontinence, in spina bi\ufb01da, 213 leg length inequality, 403\u2013405 Feeding F-waves, 129\u2013130 adaptive equipment for, 123 Gabapentin (Neurontin), for spasticity, 181, 273t assessment of, 73, 293 Gait aids, 110\u2013111 development of, 53, 71t Gait analysis, in cerebral palsy, 189 disorders of, 69\u201376 Gait assessment, 461 feeders, automated, 123 milestones, 71t critical events, 478\u2013481 oral gait cycle, subdivision, 469\u2013474 instrumented gait analysis, 464\u2013469 with dysphagia, 67t kinematics, 465\u2013466 transition to, after traumatic brain injury, 243 maturity, 464 oral motor dysfunction with, 2 movement analysis, case study, 481\u2013489 team members, 72t normal gait, 461\u2013464 tube feeding, 243 Gait cycle, 469 FEES. See Fiber-optic endoscopic evaluation of swallowing critical events, 474t, 478\u2013481 Feet phases of, 462f, 463f, 472t, 472\u2013474 assessment of, in cerebral palsy, 173 subdivision, 469\u2013474, 471t burns and, 381 walking, functional prerequisites for, 469\u2013472 juvenile idiopathic arthritis in, 375 Gait impairments, in cerebral palsy, 175\u2013176, 175t prosthetic, 351, 354 Gait trainers, 111 Feldenkrais method, 186t, 187 Galveston Orientation and Amnesia Test, 34 FES. See Family Environment Scale, Functional electrical Gastrocnemius\/soleus contracture, 179, 295 ankle-foot orthoses for, 173, 175t, 325 stimulation Gastroesophageal re\ufb02ux disease, 439 Fiber-optic endoscopic evaluation of swallowing (FEES), 75 management of, 243 Fiber-type disproportion, congenital, 304 after traumatic brain injury, 243 Fibrodysplasia, 406 Gastrointestinal dysfunction, after spinal cord injury, 266, Fibrous dysplasia, 406 Figure-eight harness, 344f 269\u2013270 FIM. See Functional independence measure Gastrointestinal system, 280, 287, 398 Fine motor\u2013adaptive behavior, assessment of, 37, 41 Gastrostomy, 17, 208, 243 Finger orthosis, 105t GCS. See Glasgow Coma Scale Fishing, 87\u201388 GDS. See Gesell Developmental Schedules; Gordon Diagnostic Fitness System components of, 449 Genitourinary disorders, in cerebral palsy, 173 in juvenile idiopathic arthritis, 374 Genu valgum, 396 Fixed battery, 27, 28 Gesell Developmental Schedules, Revised, 187 Flat feet, 304, 385, 395 Girl Scouts of America, 87 Flexible endoscopic examination of swallowing, 75t Glasgow Coma Scale (GCS), 234 Flexibility, 365 Floor hockey, 93 for children, 156 Floppy infant, electrodiagnostic evaluation of, 138\u2013141, 139t, 140t posttraumatic amnesia (PTA), 235 Fluency disorders, 67t Glasgow Outcome Scale, 250 Fluency Tasks Verbal and Design, 32t modi\ufb01ed, 250t Focal brain injuries, 235\u2013236 Glue-snif\ufb01ng neuropathy, 317 Fontanelles, palpation of, 7 Gluteus medial lurch. See Trendelenburg\u2019s gait pattern Football, 93 Glycerine suppositories, for bowel dysfunction, 270t Foot deformities, in spina bi\ufb01da, 217 GMFCS. See Gross Motor Function Classi\ufb01cation System Forebrain malformations, in spina bi\ufb01da, 209 GMFM. See Gross Motor Function Measure Forced vital capacity, in Duchenne muscular dystrophy, 391 Golden Opportunities funds, 85 Forebrain malformations, in spina bi\ufb01da, 209 GoLYTELY. See Polyethylene glycol Forefoot rockers, 476f, 478 Gordon Diagnostic System (GDS), 28, 31t Forward walkers, 111 Gowers\u2019 sign, 318t Fractures, 18\u201319 Grafting, 339, 352, 369, 379, 382, 386, 390 Frantz classi\ufb01cation system, 336 Gravity-eliminating orthoses, 123\u2013124 Frataxin, 321 Freeman-Sheldon syndrome, 366","Greenspan Social-Emotional Growth Chart, 43 Index 509 GRF. See Ground reaction force Gross Motor Function Classi\ufb01cation System (GMFCS), 166, 168f Hip (cont.) Gross Motor Function Measure (GMFM), 90, 177, 187, 189 dysplasia of Gross Motor Performance Measure, 187 acquired, 9, 174 Gross motor skills acquisition, 219t bilateral, 216f Ground reaction force (GRF), 466 congenital, 9 Growth traumatic, 389 juvenile idiopathic arthritis in, 371, 372, 373, 374 charts, 6, 14 orthosis for, 108t Duchenne muscular dystrophy and, 290 in examination, 6 Hip knee ankle foot orthosis (HKAFO), 108t with juvenile idiopathic arthritis, 371, 373, 374 for spina bi\ufb01da, 219 musculoskeletal system, 361\u2013362, 363f and nutrition, 14\u201315 Hippo Car Seat, 117 and scoliosis, 214, 398 Hippotherapy, 89, 186t Guillain\u2013Barr\u00e9 syndrome. See Acute in\ufb02ammatory demyelinating Hip spica\/hip abduction splint, 108t Hirayam disease. See Juvenile segmental SMA polyradiculoneuropathy Histology, in neuromuscular diseases, 286 History, 1 Habilitation, 21 Halliwick method, 90 adaptive sports and recreation, 79\u201380 Hallux valgus deformity, in cerebral palsy, 173 of behavior, 4 Halstead Category Test (HCT), 32t in cerebral palsy, 169 Halstead Neuropsychological Test Battery (HRNB), 29 developmental history, 2\u20133 Hamstring, 487\u2013488 of disability rights, 498\u2013499 Hand orthosis, 105t, 106t educational and social history, 4\u20135 Handicapped Scuba Association, 80, 88 family history, 5 Hands general health history, 3\u20134 in neuromuscular diseases, 278\u2013279 juvenile idiopathic arthritis in, 374 perinatal history, 1\u20132 orthosis, 106t, 184 prenatal history, 1\u20132 Handy 1 device, 123 in scoliosis, 398 HBRT. See Horseback riding therapy HIV infection, in children, 148\u2013149 HCT. See Halstead Category HKAFO. See Hip-knee-ankle-foot orthosis Head circumference, 6, 14, 208, 406, 414 Hockey, 93\u201394 HeadMinder Concussion Resolution Index (CRI), 35 Holt-Oram syndrome, 341 Headrests, for wheelchairs, 112\u2013113 HOME. See Home Observation for Measurement of the Healing, orthoses for, 104 Health history, 3\u20134 Environment Scale Health preventive screening services, 451t Home environment, 45\u201346 Health-related quality of life (HRQOL), 47 Home Observation for Measurement of the Environment Scale Hearing impairment, 3, 4, 16\u201317 in cerebral palsy, 172 (HOME), 45 facioscapulohumeral muscular dystrophy, 301 Home services, for child with traumatic brain injury, 249 after traumatic brain injury, 238 Horner\u2019s syndrome, 6, 144 Heart rate, 7, 83 Horseback riding therapy (HBRT), 89, 89 Heat therapy, for juvenile idiopathic arthritis, 373 Housemaid\u2019s knee, 6 Heel rocker, 475, 476f Hoyer lift, 109 Height, 6, 14, 361 H re\ufb02ex, 130, 134t Hemianopsia, 239 HRNB. See Halstead Neuropsychological Test Battery Hemiparetic CP, 166, 167f HRQOL. See Health-related quality of life Hemiplegia, 6, 95 Human gait assessment. See Gait assessment Hemophilia, 377 Hunting, 88 Hemorrhage, intraventricular, and cerebral palsy, 168, 170 Hurler\u2019s syndrome, 409 Hensen\u2019s node, 200 Hydrocephalus Hereditary motor sensory neuropathy (HMSN), types, 314\u2013315t. development of, 223 See also Charcot\u2013Marie\u2013Tooth (CMT) neuropathy, 313\u2013316 endoscopic management of, 209 III, and infantile hypotonia, 315t management of, 442 Hereditary neuropathies, electrodiagnostic evaluation of, 146 pathogenesis of, 208 Heterotopia, in spina bi\ufb01da, 209 in spina bi\ufb01da, 203, 205, 208\u2013209, 223 Heterotopic ossi\ufb01cation, after traumatic brain injury, 244 symptoms of, 208\u2013209 Higher Education Act, Amendment to, 499 after traumatic brain injury, 245\u2013246 Highly active antiretroviral therapy (HAART), 203 Hydromyelia. See Syringomyelia High tetraplegia, 268, 275 Hydrotherapy, 373 Hilgenreiner\u2019s line, 388f Hydroxychloroquine, for systemic lupus erythematosus, 377 Hinged (or articulated) ankle foot orthosis, 106t Hyoscyamine, for bladder dysfunction, 269 Hip Hyperbaric oxygen therapy (HBOT), in cerebral palsy, 185, 186t assessment of, in cerebral palsy, 174, 174f Hypercalcemia, after spinal cord injury, 272 deformities in spina bi\ufb01da, 215\u2013216, 442 Hypercapnia, 3 Hyperlordosis, in facioscapulohumeral muscular dystrophy, 301, 301f Hyperthermia, malignant, and neuromuscular diseases, 16, 278\u2013279, 303","510 Index Injury severity, morbidity by, 250\u2013252 anoxic brain injury, 252 Hypertonia management, in cerebral palsy, 178 concussions, 250\u2013251 chemical denervation, 179 mild to moderate injury, 251\u2013252 intrathecal baclofen (ITB), 181\u2013182 moderate to severe injury, 252 oral medications, 179\u2013181 profound injury, 252 selective dorsal rhizotomy (SDR), 182\u2013183 Injury severity, of traumatic brain injury Hypomyelinating neuropathy, congenital, 140t, 141, 287, 315 Children\u2019s Orientation and Amnesia Test, 235 Hypopharynx, 54 Glasgow Coma Scale, 234 Hypothalamo-pituitary dysfunction, 221, 241\u2013242 Posttraumatic Amnesia, 235 Hypotonia, infantile unconsciousness, duration of, 235 acute-onset, electrodiagnostic evaluation of, 142 InMotion Robots, 125 differential diagnosis, 139t Inpatient rehabilitation, in traumatic brain injury, 246\u2013248 electrodiagnostic evaluation of, 138\u2013140, 140t Insomnia, 3 in neuromuscular diseases, 280f, 289 Inspection, in examination, 6\u20137 Hypotonic bladder, 269 Instrumented gait analysis (IGA), 464\u2013469 urodynamic study in, 210 Intellectual assessment, 36\u201337 Hypotonic cerebral palsy, 166 Intellectual disabilities (ID), 446\u2013447 Hypotonicity, 8 aging with, 434t Ibuprofen, 244, 379, 391 Intelligence quotient (IQ) IDEA. See Individuals with Disabilities Education Act Idiopathic scoliosis, 400\u2013403 in Becker muscular dystrophy, 295 IEP. See Individualized education program in cerebral palsy, 172 Imaginative play, 66 versus cognitive assessment, 25 Imipramine, for bladder dysfunction, 212, 269 in Duchenne muscular dystrophy, 292 Immediate Post-Concussion Assessment and Cognitive Testing in myotonic muscular dystrophy, 307 performance, after traumatic brain injury, 26, 234 (ImPACT), 35 in spina bi\ufb01da, 222\u2013223 Immunization history, 4 testing, 25, 26 Immunizations, 15 after traumatic brain injury, 234 Immunoblotting, 286\u2013287 Intentional communication, 53 Immunostaining, 286\u2013287, 293 Interactive play, 5 Immunosuppressive agents, 377 Interface, adaptive, 117 ImPACT. See Immediate Post-Concussion Assessment and Intermediate SMA type II, 319t Internal moments, 467 Cognitive Testing Internal stability, in test, 24 Incontinence, 439, 441 International Shriners Hospitals, 261, 268, 269 International Silent Games, 79 in spina bi\ufb01da, 211, 213 International Society for Augmentative and Alternative Independence, after spinal cord injury, 268t Individualized education program (IEP), 4, 26, 82 Communication (ISAAC), 123 International Society for Prosthetics and Orthotics, 336 for child with limb de\ufb01ciency, 246 International Sports Organized for the Disabled (ISOD), 86 for child with traumatic brain injury, 248 International Stoke Mandeville Wheelchair Sport Federation Individuals with Disabilities Education Act (IDEA), 39, 64, 82, (ISMWSF), 79 248, 499 Intrathecal baclofen (ITB), 181\u2013182 Indomethacin, 244 Intervertebral disc injuries, 392 Infantile botulism, 150\u2013151, 312 IQ. See Intelligence quotient ISAAC. See International Society for Augmentative and Alternative electrodiagnostic evaluation of, 150\u2013151, 150f Infantile nerve conduction studies, technical factors with Communication ISMWSF. See International Stoke Mandeville Wheelchair Sport Federation distance measurements\/measurement error, 133 ISOD. See International Sports Organized for the Disabled recording electrodes, 134\u2013135 ISPO. See International Society for Prosthetics and Orthotics Isotretinoin, 203 motor conduction, 135 Ixodes dammini, and Lyme disease, 376 sensory conduction, 134\u2013135 repetitive nerve stimulation studies, 136 Jebsen-Taylor Hand Function Test, 187 shock artifact, 133 JIA. See Juvenile idiopathic arthritis special considerations for, 135\u2013136 Joint contractures, 323 stimulating electrodes, 133\u2013134 temperature, 132 in Becker muscular dystrophy, 294 volume conduction, 132 in congenital muscular dystrophy, 298 Infants in Duchenne muscular dystrophy, 290 examination of, 5, 6 in Emery-Dreifuss muscular dystrophy, 302 psychosocial development in, 81, 118 in juvenile idiopathic arthritis, surgery for, 375, 376 Infections, 4, 17 in limb girdle muscular dystrophy, 295 and limb de\ufb01ciencies, 338 Joint moments, 467 neuropathies associated with, 148\u2013149 Joint power, 467\u2013468 In\ufb02ammatory bowel disease, arthritis associated with, Juvenile idiopathic arthritis (JIA), 370\u2013376 cervical spine, 374 372, 373 Information processing, assessment of, 30 Informing interview, 10 In-home services for child with traumatic brain injury, 249","Index 511 Juvenile idiopathic arthritis (JIA) (cont.) Language features, of AAC devices, 118\u2013121 clinical features Language functioning of enthesitis-related arthritis, 372\u2013373 of oligoarthritis, 371 assessment of, 33\u201334 of polyarthritis, 371\u2013372 pragmatic, 119t of psoriatic arthritis, 372 Larsen syndrome, 366 of systemic-onset JIA, 371 Larynx, 56, 56f of undifferentiated arthritis, 373 Later stages of recovery, 255 differential diagnosis of, 372t Latex allergy lower extremities, 374\u2013375 in spina bi\ufb01da, 220\u2013221, 443 rehabilitation in, 373\u2013374 after spinal cord injury, 273 treatment, medical and surgical, 375\u2013376 Latex allergy, in spina bi\ufb01da, 220\u2013221 upper extremities, 374 clinical signs of, 220 Latex-fruit syndrome, 220 Juvenile segmental SMA, 320 Lead polyneuropathy, 317 Learned helplessness, 103 KABC-II. See Kaufman Assessment Battery for Children, Learning process, 26 2nd Edition Legg\u2013Calv\u00e9\u2013Perthes disease, 384 Leg length discrepancy (LLD), 352, 403\u2013405 KAFO. See Knee ankle foot orthosis Leiter International Performance Scale-Revised (Leiter-R), 38, 39t Kaufman Assessment Battery for Children, 2nd Edition (KABC-II), Les autres athletes, 86t Leukodystrophy, metachromatic, and infantile hypotonia, 140t 36, 38, 39t Leukomalacia, periventricular, 168, 168f Kaufman Test of Educational Achievement, 2nd Edition Lidocaine, for anesthesia in nerve conduction studies, 137 Limb de\ufb01ciencies (K-TEA-II), 39, 40t acquired amputations Kearns\u2013Sayre syndrome, 310 Kenney crutch, 110 classi\ufb01cations of, 337 Ketamine, for pain control in burn injuries, 309, 379 incidence and etiologies, 337 KidSwing, 85 infections, 338 Klippel\u2013Feil syndrome, 364 traumatic, 337 Klumpke\u2019s palsy, 144, 367 tumors, 337\u2013338 Knee aging with, 433\u2013434t congenital de\ufb01ciencies assessment of, in cerebral palsy, 173 classi\ufb01cation, 336\u2013337 contractures of, 375, 437 etiology, 335\u2013336 injuries to, 8 infections, 338 juvenile idiopathic arthritis in, 373, 374, 375 longitudinal, 337t orthoses for, 106t lower limb, 346\u2013347 Knee ankle foot orthosis (KAFO), 107t, 396 advancements, 355 bracing, 324\u2013325 amputation in children, 351 for spina bi\ufb01da, 219 common, 347\u2013350 Knee \ufb02exion contractures \ufb01tting timetable, 353 in cerebral palsy, 173\u2013174 intervention, prosthetic treatment and adaptive equipment, in spina bi\ufb01da, 216 Knee hyperextension splint, 107t 351\u2013352 Kohler\u2019s disease, 391 training, 353\u2013355 Krabbe disease, 148 uncommon, 350\u2013351 K-TEA-II. See Kaufman Test of Educational Achievement, 2nd Edition surgical approaches Kugelberg\u2013Welander syndrome. See Spinal muscular atrophy III general principles, 338\u2013339 Kyphosis phantom sensation, 339 in cerebral palsy, 174 transverse, 337t in spina bi\ufb01da, 204, 224 upper limb advancements, 346 Lactate, in neuromuscular diseases, 284 common, 339\u2013340 Lactic acidosis, 310 intervention, prosthetic treatment and adaptive equipment, Lactulose, 270t Lambert\u2013Eaton syndrome, 153 341\u2013345 LaNec disease, 391 therapy and training, 345\u2013346 Language uncommon, 340\u2013341 Limb deformity components, 59\u201363 contractures and, management of, 323\u2013324 de\ufb01nition of, 54, 59 with distal lower extremity weakness, management of, 325 spontaneous, observation of, 43 with proximal weakness, management of, 324\u2013325 Language ability, assessment of, 67 Limb girdle muscular dystrophy (LGMD), 295 Language behavior, assessment of, 66 calpainopathies, 295\u2013298 Language development, 53 characteristics of, 296\u2013297t Language disorders, 63\u201366 dysferlinopathies, 295 acquisition, 63 fukutin-related protein, 298 assessment of, 66\u201368 sacroglycanopathies, 295 in cerebral palsy, 64\u201365 Limb, development of, 361 congenital, 64 treatment for, 68\u201369","512 Index Medical care, of disabled children (cont.) respiratory complications Linear seating systems, 112 drooling, 17 Lioresal. See Baclofen respiratory distress, 17\u201318 Lite Gait, 111 routine health maintenance, 14 Literacy, in children with disabilities, 118\u2013121 dental, 15\u201316 Little League baseball, 91 growth and nutrition, 14\u201315 LLD. See Leg length discrepancy hearing, 16\u201317 Lobster claw. See Central ray syndrome immunizations, 15 Locomat, 125 vision, 16 Lofstrand crutches, 110 Long-term needs planning Medical conditions, associated with traumatic brain injury, 241 anterior pituitary dysfunction, 241\u2013242 for child with traumatic brain injury, 249 bladder management, 244 Lordosis, in spina bi\ufb01da, 214, 224 bowel management, 243\u2013244 Lower airway, 55 central autonomic dysfunction, 244 Lower extremities, 355\u2013356 cerebral salt wasting, 241 heterotopic ossi\ufb01cation, 244 weakness, distal, 325 neuroendocrine dysfunction, 241 de\ufb01ciency, congenital, 352 nutritional management, 242\u2013243 juvenile idiopathic arthritis in, 374\u2013375 gastroesophageal re\ufb02ux disease, 243 musculoskeletal conditions of, 446 oral feedings, transition to, 243 orthoses for, 184 tube feedings, 243 prosthetics, advancements in, 355 posttraumatic epilepsy, 244\u2013245 Lower limb posttraumatic hydrocephalus and cerebral atrophy, 245\u2013246 amputations, in children, 351 precocious puberty, 242 de\ufb01ciencies, common respiratory dysfunction, 242 femoral abnormalities, 348\u2013349 Memory longitudinal de\ufb01ciency of the \ufb01bula, 347\u2013348 assessment of, 34 longitudinal de\ufb01ciency of the tibia, 350 disorder, 67t de\ufb01ciencies, uncommon, 350\u2013351 impairment of, after traumatic brain injury, 239\u2013240 orthoses, 106t\u2013109t Lower motor neuron disorder, 7, 8, 141, 142, 280 Mental retardation, 299 Lund and Browder burn chart, 378, 380f with cerebral palsy, 165 Lung disease, 55 in facioscapulohumeral muscular dystrophy, 301 Meningococcemia, 338 in myotonic muscular dystrophy, 306 Meperidine hydrochloride, for anesthesia in nerve conduction in scoliosis, 320, 443 Luria neuropsychological model, 36 studies, 137 Lyme disease, 149 Mercury poisoning, 317 arthritis, 376 Metabolic myopathies erythema migrans in, 376 electrodiagnostic evaluation of, 154 Mafenide acetate, for burn injuries, 379 Metaclopramide (Reglan), 270t Magnesium citrate, for bowel dysfunction, 270t Metanolic myopathies, 308 Magnetic resonance imaging (MRI) acid maltase de\ufb01ciency, 308\u2013309 in cerebral palsy, 169, 170 myophosphorylase de\ufb01ciency, 308 in discitis, 393 Metaphysis, 385, 386 of growing skull fracture, 233 Methotrexate, 203 in juvenile idiopathic arthritis, 401 for juvenile idiopathic arthritis, 375 in scoliosis, 400 for scleroderma, 377 of traumatic brain injury, 233 Methylprednisolone, for spinal cord injury, 266 Malignant hyperthermia, and neuromuscular diseases, 278\u2013279, MFFT. See Matching Familiar Figures Microcephaly, 6, 169, 299 289, 303 Micrognathia, 308, 371, 374 Manual muscle testing, 8 Microsomia, after traumatic brain injury, 238 Marital arts, 88 Midazolam hydrochloride, for anesthesia in nerve conduction Maroteaux\u2013Lamy, type VI, 409 Massage technique, 382 studies, 137 Matching Familiar Figures (MFFT), 32t Milk of magnesia, for bowel dysfunction, 270t MCA. See Motor conduction velocities Mineral oil, for bowel dysfunction, 270t Measurement error, in nerve conduction studies, 133 Minicore disease, 304 MEBD. See Evan\u2019s Blue Dye Test Minnesota Multiphasic Personality Inventory (MMPI), 42, 43 Medical care, of disabled children, 13 Minnesota Multiphasic Personality Inventory-Adolescent acute illness, in primary care of\ufb01ce, 17 (MMPI-A), 42, 43, 46t medical home, 13\u201314 Miracle League, 91 neurological complications Mitochondrial disorders, 309\u2013310 Mitochondrial encephalopathy, 310 seizure activity, 18 Mitochondrial neurogastrointestinal encephalopathy, 310 spasticity, 18 Mitrofanoff procedure, 212 orthopedic complications Mixed connective tissue disease, diagnostic criteria for, 372t fractures, 18\u201319 MMD. See Myotonic muscular dystrophy palliative care, 19 MMPI. See Minnesota Multiphasic Personality Inventory","MMPI-A. See Minnesota Multiphasic Personality Index 513 Inventory-Adolescent Musculoskeletal conditions (cont.) Mobile arm support, 124 evaluation, 367\u2013368 Mobility pain, 370 surgery, 369\u2013370 aids, 104\u2013111 surgical indications, 369 guidelines, 267t treatment, 368 in neuromuscular diseases, 326\u2013327 in spina bi\ufb01da, 218\u2013220, 440 burn injuries after spinal cord injury, 267\u2013268 acute burn management, 379\u2013381 Moebius syndrome, 335, 336f burn assessment, 378 Molecular genetic studies, in neuromuscular diseases, 285 chronic burn management, 381\u2013382 Moro re\ufb02ex, 8, 169, 368 epidemiology, 378 Morphine, 244 outcome, 382\u2013383 for pain control in burn injuries, 379 prevention, 384 Morphology, 60 Morquio\u2019s disease, 409 child with rheumatic disease, rehabilitation of, 370 Motion assessment. See Gait assessment hematological disorders, 377\u2013378 Motion laboratories, 463, 464f infectious disease with arthritis, 376 Motor conduction velocities (MCVs), in children, 128, 128t, 135 juvenile idiopathic arthritis, 370\u2013376 Motor de\ufb01cits, after traumatic brain injury, 235 rheumatic diseases, 376\u2013377 balance, 236 diffuse damage, 236 congenital conditions, 362, 364\u2013367 focal damage, 235\u2013236 constitutional\/intrinsic bone conditions, 405 tone abnormalities, 236\u2013237 abnormal bony density or structure, 406\u2013407 dystonia, 237 calcium or phosphorus metabolism, metabolic conditions rigidity, 237 spasticity, 237 affecting, 407\u2013409 tremor, 236 disorganized cartilage and \ufb01brous components, 406 Motor development, in spina bi\ufb01da, 218, 441 extraskeletal disorders, 409 Motor disabilities, children with, 82 tubular bone\/spinal growth, defects of, 405\u2013406 Motor function assessment, 461, 483 developmental conditions, 384\u2013397 Motor learning, 177 growth and development, 361\u2013362, 363f Motor neuron disorders, 142\u2013143 musculoskeletal pain and child abuse, 410 spinal muscular atrophy (SMA), 317\u2013319 back pain, 410\u2013411 Motor speech disorders, 57\u201359 child abuse, 411 acquired, 57t, 67t complex regional pain syndrome, 410 developmental, 57t, 37t \ufb01bromyalgia, 410 Motor unit action potentials (MUAPs), in children tumors of bone, 411\u2013412 amplitude, 130\u2013131 scoliosis con\ufb01guration, 130\u2013131 functional scoliosis, 403 duration, 131 idiopathic scoliosis, 400\u2013403 recruitment, 131\u2013132 leg length inequality, 403\u2013405 MPS. See Mucopolysaccharidoses overview, 397\u2013399 MRI. See Magnetic resonance imaging types, 400 MS. See Multiple sclerosis Musculoskeletal deformities, in spina bi\ufb01da, 218, 440 MUAPs. See Motor unit action potentials Musculoskeletal disorders, in cerebral palsy, 173\u2013175 Mucopolysaccharidoses (MPS), 408\u2013409 foot\/ankle, 173 Multicore disease. See Minicore disease hip, 174 Multiple epiphyseal dysplasia, 384, 414 knee, 173 Multiple pterygius syndrome, 366 spine, 174\u2013175 Multiple sclerosis (MS), pediatric, SSEPs in, 158 upper extremity, 175 Muscle biopsy, in neuromuscular diseases, 139\u2013140 Musculoskeletal injuries, treatment of, 368 site selection for, 285\u2013286 Musculoskeletal pain, 370 technique for, 285 Musculoskeletal system Muscle-eye-brain disease, 299 in cerebral palsy, 179 Muscles examination of, 9 nerve conduction studies of, 137 in spina bi\ufb01da, rehabilitation for, 218 palpation of, 7 Myasthenia gravis Muscular dystrophy, 3 autoimmune, 311\u2013312 congenital, 298\u2013300 electrodiagnostic evaluation of, 153 differential diagnosis of, 393 transient neonatal, 151\u2013152 limb girdle, 295\u2013298 Myasthenic syndromes, congenital, 138, 152\u2013153, 311, 327 myotonic. See Myotonic muscular dystrophy Myelomeningocele, 201, 208\u2013209 Musculocutaneous nerve, conduction study of, 136f Myoclonus epilepsy with ragged-red \ufb01bers, 310 Musculoskeletal conditions, 361\u2013409 Myopathic stance, 284f brachial plexus palsy, 367 Myopathies complications, 368\u2013369 electrodiagnostic evaluation of, 153\u2013155 congenital, 153 dystrophic, 153\u2013154 metabolic, 154 myotonic disorders, 154\u2013155","514 Index Myopathies (cont.) Nerve conduction studies (NCSs), in pediatric electrodiagnosis (cont.) polymyositis\/dermatomyositis, 153 of rest activity, muscles for, 136\u2013137 sensory nerve conduction, 129 infantile hyptonia, 138 technical factors in, 132\u2013135 Myotomes, 361, 362f Myotonia Nerve stimulation studies, repetitive, 136 stimulator, 135f congenita, 307 in myotonic muscular dystrophy, 305, 307 Neural tube defects (NTDs), 199 in neuromuscular diseases, 305 clinical types of Myotonic disorders caudal regression syndrome, 203 electrodiagnostic evaluation of, 140t spina bi\ufb01da cystica, 203 Myotonic dystrophy spina bi\ufb01da occulta, 203 appearance in, 5, 6 congenital, and infantile hypotonia, 153 Neuroendocrine dysfunction, after traumatic brain injury, 241 Myotonic muscular dystrophy, 154 Neuro\ufb01bromatosis, appearance in, 6 Myotonic muscular dystrophy 1 (DM1), 304\u2013307 Neurogenic bladder Myotonic muscular dystrophy 2 (DM2). See Proximal myotonic in spina bi\ufb01da, 210\u2013213 myopathy (PROMM) after spinal cord injury, 269 Myotubular myopathy Neurogenic bowel bowel management, 213\u2013214 severe X-linked (congenital), 303\u2013304 neurogenic bowel dysfunction, 213 orthopedics, 214\u2013217 NAHRA. See North American Riding for the Handicapped in spina bi\ufb01da, 213 Association in spinal cord injury, 269\u2013270 Naproxen (Naprosyn), 391 bowel medications, 270t Nasopharynx, 54 Neuroimaging National Amputee Golf Association, 80 National Collegiate Athletic Association (NCAA), 92 of cerebral palsy, 169\u2013170 National Dysphagia Diet (NDD), 75 of congenital scoliosis, 400 National Handicapped Sports and Recreation Association of traumatic brain injury, 233\u2013234 Neurological system (NHSRA), 80 in spinal cord injury, 265 National Hockey League (NHL), 94 examination of, in cerebral palsy, 169 National Park Service, 87 Neurological complications National Pressure Ulcer Advisory Classi\ufb01cation, 272t seizure activity, 18 National Spina Bi\ufb01da Association, 199 spasticity, 18 National Wheelchair Athletic Association (NWAA), 79\u201380 Neuromuscular diseases (NMDs), 277\u2013278 National Wheelchair Basketball Association (NWBA), 92 aerobic exercise, 323 National Wheelchair Softball Association, 96 cardiac complications, management of, 329 Naturally Speaking, 122 diagnostic evaluation, 278\u2013285 NCAA. See National Collegiate Athletic Association electrodiagnostic studies, 284\u2013285 NCSs. See Nerve conduction studies functional mobility, 326 NDD. See The National Dysphagia Diet history in, 278\u2013279 NDT. See Neurodevelopmental treatment approach molecular genetic studies, 285 Neater Eater, 123, 124f muscle biopsy evaluation, 285\u2013287 Neck \ufb02exor weakness, in Duchenne muscular dystrophy, 289, 309 nerve biopsy evaluation, 287 Necrosis, avascular, in sickle cell anemia, 378 nutritional management Needle electromyography, technical factors of branched-chain ketoacid supplementation, 328 electrodes, 136 energy and protein supplementation, 328 optimal muscles, to study for rest activity, 136\u2013137 for swallowing problems, 328 optimal muscles, for evaluation, 137 for weight reduction, 328\u2013329 sedation, 137\u2013138 pharmacologic intervention, 329 single-\ufb01ber EMG, limitations of, 138 physical examination, 279\u2013283 Negative pressure ventilators, 18, 291, 327 serum laboratory studies in, 283\u2013284 Nemaline myopathy, 303 speci\ufb01c disease conditions Neonatal vs childhood treatment, 212\u2013213 dystrophic myopathies, 287 in neurogenic bladder, 212\u2013213 dystrophenopathies, 287\u2013288 NEPSY, 28, 29 strengthening exercise, 322 Developmental Neuropsychological Assessment, 29 Neuromuscular electrical stimulation (NMES), 178 NEPSY-II, 29 Neuromuscular junction disorders, 150\u2013153 Nerve biopsy, in neuromuscular diseases, 287 autoimmune myasthenia gravis, 311\u2013312 Nerve conduction studies (NCSs), in pediatric electrodiagnosis, congenital myasthenic syndrome (CMS), 311 congenital myasthenic syndromes, 152\u2013153 128\u2013130 electrodiagnostic evaluation of, 152 compound muscle action potential (CMAP), 129 infantile botulism, 150\u2013151 considerations in, 135\u2013136 Lambert\u2013Eaton syndrome, 153 distal motor latencies (DMLs), 128\u2013129 myasthenia gravis, 153 F-waves, 129\u2013130 toxic, 152 H re\ufb02ex, 130 transient neonatal autoimmune myasthenia gravis, 151\u2013152 motor nerve conduction, 128 transient neonatal myasthenia, 310\u2013311 neuromuscular transmission, 130","Neuromuscular system, examination of, 7\u20139 Index 515 Neuromuscular transmission, in newborns, 130 Neurontin. See Gabapentin Obesity, 80 Neuropathic recruitment in Down syndrome, 449 in intellectual disabilities, 446\u2013447 studies of, muscles for, 134f in spina bi\ufb01da, 221 Neuropathies Observation associated with central disorders, 147\u2013148 in examination, 5 associated with infections, 148\u2013149 in psychological assessment, 27, 42 HIV infection, 148\u2013149 Occupational therapy, in spina bi\ufb01da, 209 Lyme disease, 149 Of\ufb01ce environment, tone of, 1 hypomyelinating, and infantile hypotonia, 315t OI. See Osteogenesis imperfecta with limb-lengthening procedures, 150 Olfactory dysfunction, after traumatic brain injury, 238 metabolic, 317 Oligoarthritis, 371 toxic, 316\u2013317 Ophthalmologic disorders, 16 Neuropathy ataxia, 310 Oral apraxia, 58 Neuropsychological evaluation, 29 Oral feeding attention, concentration, and information processing, 30 \ufb02exible approach to, 27\u201328 with dysphagia, 67t problem-solving and executive functioning tests, 30\u201332 transition to, after traumatic brain injury, 243 test batteries, 29 Oral medications, to treat spasticity, 179\u2013181 Neurosurgical treatment, to spina bi\ufb01da, 210 baclofen, 181 Newborn benzodiazepines, 181 developmental milestones in, 218 dantrolene sodium, 181 facial paralysis in, electodiagnostic evaluation of, 146 Oral motor dysfunction, 2, 53 nerve conduction studies in, 128\u2013130, 132\u2013136 Oral sensorimotor, in feeding, 71t NHL. See National Hockey League Oral\u2013pharyngeal phase, swallowing, 74f NHSRA. See National Handicapped Sports and Recreation Oral phase, of swallowing, 74f Organophosphate poisoning, 148, 317 Association Organ systems, examination of, 7 Nifedipine, 372 Orlau Para Walker, in spina bi\ufb01da, 219 Night sweating, 3 Oromotor impairments, in cerebral palsy, 172 Nightmares, 3 Oropharynx, 54 Nitrofurantoin, for urinary tract infection prophylaxis, 212 Orthopedic complications NMDs. See Neuromascular diseases fractures, 18\u201319 Nodules, subependymal, 206t, 209 Orthopedic surgery, in cerebral palsy, 183\u2013184 Nonaccidental traumatic brain injury, 233 Orthopedics, in spina bi\ufb01da, 214\u2013217 Noninfantile acquired botulism, 312 feet, 217 Nonsteroidal anti-in\ufb02ammatory drugs (NSAIDs) hips, 215\u2013216 knees, 216 for juvenile idiopathic arthritis, 375 overview, 214 for Legg\u2013Calv\u00e9\u2013Perthes disease, 384 spine, 214\u2013215 for musculoskeletal injuries, 377, 448 tibia, 216\u2013217 for pain control in burn injuries, 384 Orthosis, 103 for systemic lupus erythematosus, 377 in cerebral palsy, 184 Nonverbal learning disorder (NVLD), 223 Nonverbal\/visual\u2013perceptual function tests, 32\u201333 lower extremity (LE) orthoses, 184 Normal curve, 23, 23f spinal orthoses, 184 Normative data, 44 upper extremity (UE) orthoses, 184 Norm-referenced measurement, 23\u201325 for positioning, range of motion, and healing, 104 reliability, 24 Orthotics validity, 24\u201325 and assistive devices, 103 Norms, 23, 28, 29 for limb deformity in neuromuscular diseases, 323 North American Growth in Cerebral Palsy Project (NAGCPP), 173 for spina bi\ufb01da, 217, 219 North American Riding for the Handicapped Association after spinal cord injury, 374\u2013375 Ortolani\u2019s sign, 388 (NAHRA), 89 Osgood\u2013Schlatter disease, 391 Nose, 54 Ossi\ufb01cation, heterotopic, after traumatic brain injury, 244 NSAIDs. See Nonsteroidal anti-in\ufb02ammatory drugs Ossur Modular Flex Foot, 354f Nucleus pulposus, 393 Osteochondritis dissecans, 391 Nutrition Osteochondrosis, 391 Osteogenesis imperfecta (OI), 81, 406\u2013407 alteration in intake, 3, 202 appearance in, 6 with burn injuries, 381 types of, 408t in cerebral palsy, 172\u2013173 Osteomyelitis, 368, 372t, 376, 378 growth and, 14\u201315 Osteoporosis history of, 3 in cerebral palsy, 438 in neuromuscular diseases, 327\u2013329 in spina bi\ufb01da, 221 after spinal cord injury, 266, 271 treatment, 222 after traumatic brain injury, 242\u2013243 OttoBock KIMBA, 113f NWAA. See National Wheelchair Athletic Association Outcome algorithm, 28 NWBA. See National Wheelchair Basketball Association","516 Index Periventricular leukomalacia (PVL), 168f Perkin\u2019s vertical line, 388f Outdoor adventure, 87 Peroneal mononeuropathies in children, 149 Out-of-home services, for child with traumatic brain injury, 249 Peroneal muscles, 173, 365, 395 Outriggers, 95 Personality Inventory for Children-2 (PIC-2), 42, 44, 46t Overuse syndromes, 389\u2013390 Pes planus. See Flat feet Oxybutynin chloride (Ditropan), for bladder dysfunction, 212, Pet\u00f6, Andras, 185 Phantom sensation, with limb de\ufb01ciency, 339 213, 269 Pharyngeal phase, of swallowing, 74f Pharynx, 54, 69f, 70f Paced Auditory Serial Addition Test (PASAT), 31t Phenol, for spasticity, 237 Pain management, with burn injuries, 379\u2013382 Phenylephrine hydrochloride, for anesthesia in nerve conduction Pain relief, in juvenile idiopathic arthritis, 373 Paley height myultipliers, 363f studies, 137 Palliative care, 19 Phenytoin, 15 Palmar grasp re\ufb02ex, 169 Palpation, 7 for posttraumatic epilepsy prophylaxis, 245 Paralympics, 80 Phonation, 56 Parachute reaction, 169 Phonemic acquisition, 60t Paralympics, 80, 85, 88 Phonological process, resolution of, 62 Paramyotonia congenita, 307\u2013308 Phonology, 59 Parapodium, 108t Phonological process, 62t Parapodium with ORLAU swivel modi\ufb01cation, 108t Phrenic nerve, conduction study of, 137f Parents of Children with Disabilities Inventory (PCDI), 46, 48t Physical Activity Scale for Individuals with Physical Disabilities Partial body weight support treadmill training (PBWSTT), 177 PASAT. See Paced Auditory Serial Addition Test (PASIPD), 83 PASIPD. See Physical Activity Scale for Individuals with Physical Physical and occupational therapy, in cerebral palsy, 176\u2013178 Disabilities constraint-induced movement therapy (CIMT), 177\u2013178 Patched (PTC) gene, 201 electrical stimulation, 178 Patella, position of, 391 partial body weight support treadmill training (PBWSTT), 177 Patterning, in cerebral plasy, 186t strengthening, 176\u2013177 Pavlick harness, 108t, 388\u2013389 stretching, 176 PCDI. See Parents of Children with Disabilities Inventory therapy methods, 176 PDPAR survey. See Previous Day Physical Activity Recall survey PIAT-R. See Peabody Individual Achievement Test-Revised Peabody Developmental Motor Scales, 187 PIC-2. See Personality Inventory for Children-2 Peabody Individual Achievement Test-Revised (PIAT-R), 39, 40t PINS. See Pediatric Inventory of Neurobehavioral Symptoms Peabody Picture Vocabulary Test-III (PPVT-III), 33, 38, 39t Plasticity, implications of PEDI. See Pediatric Evaluation of Disability Inventory after traumatic brain injury, 233 Pediatric brain injury, stages of recovery in, 68 Polyarthritis, 371\u2013372 Pediatric Evaluation of Disability Inventory (PEDI), 250 Polyarticular juvenile idiopathic arthritis, 81 Pediatric Inventory of Neurobehavioral Symptoms (PINS), 47, 48t Polyethylene glycol (GoLYTELY), for bowel dysfunction, 270t Pediatric limb de\ufb01ciencies. See Limb de\ufb01ciencies Polymicrogyria, in spina bi\ufb01da, 209 Pediatric Pain Questionnaire (PPQ), 47, 48t Polymyositis, electrodiagnostic evaluation of, 153 Pediatric rehabilitation, psychosocial aspects of, 493\u2013494 Polyneuropathies, electrodiagnostic evaluation of, 146\u2013148 acquired toxic neuropathies, 148 disability rights, history of, 498\u2013499 acute in\ufb02ammatory demyelinating polyradiculoneuropathy, family and health care team partnership, 494 146\u2013147 resilience, 495 axonal Guillain\u2013Barr\u00e9\/acute motor axonal neuropathy, 147 family-centered care, 494 burn-associated neuropathies, 148 family system, 495\u2013496 chronic in\ufb02ammatory demyelinating polyradiculoneuropathy, 147 health care team system, 496\u2013497 diabetic polyneuropathy, 148 tasks of family, 497 hereditary neuropathies, 146 neuropathies associated with central disorders, 147\u2013148 working toward new normal, 497\u2013498 Polyphasic motor unit action potential, 145f tasks of practitioner, 498 Polyradiculoneuropathy Pediatric rehabilitation population, psychological, acute in\ufb02ammatory demyelinating (AIDP), 312\u2013313 assessment in, 37 electrodiagnostic evaluation of, 312 PedsQL, 47, 48t chronic in\ufb02ammatory demyelinating (CIDP), 313 Penicillamine, 316 Percentile ranks, 23, 24 electrodiagnostic evaluation of, 313 Percutaneous gastronomy (PEG) tubes, 243 Popliteal pterygium syndrome, 366 Performance IQ, 223 Population-speci\ufb01c assessments, 46\u201348 Perinatal history, 1\u20132 Positioning Peripheral nerve disorders with burn injuries, 381t acute in\ufb02ammatory demyelinating polyradiculoneuropathy, components, 112\u2013116 312\u2013313 orthoses for, 104 Posterior leaf spring, 107t Charcot\u2013Marie\u2013Tooth (CMT) neuropathy, 313\u2013316 Posterior tibialis muscle, assessment of, 173, 324 chronic in\ufb02ammatory demyelinating polyradiculoneuropathy, Post-traumatic amnesia (PTA), 34 Posttraumatic epilepsy 313 after traumatic brain injury, 244\u2013245 metabolic neuropathies, 317 toxic neuropathies, 316\u2013317 Peripheral sensory modalities, examination of, 9","Posttraumatic hydrocephalus, after traumatic brain injury, Index 517 245\u2013246 Puberty, precocious. See Precocious puberty Posture, assessment of, 5, 8 Pulmonary problems, 75, 266, 270\u2013271 Posture control walkers. See Reverse walkers Push N Power Baseball, 91 Pott\u2019s disease, 393 Pyruvate, in neuromuscular diseases, 284, 308, 309 Powered overhead transfer lift systems, 109 Power wheelchairs, 113 Quad cane, 110 PPQ. See Pediatric Pain Questionnaire Quadriplegia, 264, 271 PPVT-III. See Peabody Picture Vocabulary Test-III Quad rugby, 94 Pragmatic language functions, 119t Quality of life, 493\u2013494 Pragmatics, 62 Precocious puberty in cerebral palsy, 189 in spina bi\ufb01da, 221 Racquetball, 94 after traumatic brain injury, 242 Radial mononeuropathies, in children, 149 Prednisone, 290, 291, 312, 313, 329 Radiography, in juvenile idiopathic arthritis, 301 Prematurity, and cerebral palsy, 165, 166, 169 Range of motion (ROM) Prenatal history, 1\u20132 Prenatal screening, of spina bi\ufb01da, 203 with burn injuries, 381 Prentke Romich Vantage, 121f orthoses for, 104, 180 Preschool children, psychosocial development in, 10, 37 progressive. See Progressive range-of-motion exercise Pressure mapping systems, 112 Ratio IQ, 24 Pressure ulcers, 205, 431t, 433t Raven\u2019s Progressive Matrices, 38, 39t classi\ufb01cation of, 271t, 272t RCMAS. See Revised Children\u2019s Manifest Anxiety Scale for Children after spinal cord injury, 267, 271, 443, 445 Rear-entry hinged \ufb02oor-reaction AFO, 107t Previous Day Physical Activity Recall (PDPAR) survey, 83 Reciprocating gait orthosis (RGO), 108t Prilocaine, for anesthesia in nerve conduction studies, 137 for spina bi\ufb01da, 219 Primary injury, 232 Recreation Problem solving, assessment of, 30\u201331 organizations for, 80 Progressive bulbular paralysis of childhood, 320\u2013321 professionals in, 82 Projective measures, 42, 44 therapeutic, 83 Prone standers, 110 after traumatic brain injury, 249 Propofol, for anesthesia in nerve conduction studies, 137, 138 Recreational equipment, 117 Proprioceptive neuromuscular facilitation, 90 Recreational vehicles (RVs), 87 Prosthetics Reduced range of motion, 371 acceptance, 339, 341, 342 Re\ufb02ex assessment, in cerebral palsy, 169 for acquired amputations, 351 Re\ufb02ex sympathetic dystrophy, 272 for bilateral upper extremity de\ufb01ciency, 109 Re\ufb02ux and small neurogenic bladders, surgical management for \ufb01tting for, 341, 351, 356 in neurogenic bladder, 213 for lower extremity de\ufb01ciency, 351, 355 Reglan. See Metaclopramide swimming equipment, 96 Rehabilitation training with, 345, 353 bone tumors, 42 transfemoral, \ufb01tting time-table for, 353 in juvenile idiopathic arthritis, 373\u2013374 for upper-limb de\ufb01ciency, 341\u2013345, 346 mucopolysaccharidoses, 409 Protective extension response, 8 osteogenesis imperfecta, 407 Protein supplementation, in neuromuscular diseases, 328 psychosocial aspect, 493\u2013499 Proximal femoral focal de\ufb01ciency (PFFD), 348 in spina bi\ufb01da, 218\u2013220 Proximal myotonic myopathy (PROMM), 307 after spinal cord injury, 266\u2013267 Proximal spinal muscular atrophy (SMA), 318t in traumatic brain injury, 246\u2013247 Pseudohypertrophy, in neuromuscular diseases, 279, 279f, Rehabilitation Act, Section 504, 26, 499 Rehabilitation Engineering and Assistive Technology Society of 295, 320 Psoriatic arthritis, 372 North America (RESNA), 123 Psychiatric disturbance and adjustment problems, 22\u201323 Reitan Neuropsychological Test Battery, 29 Psychological assessment, 41 Reliability, 24 REO, 125\u2013126 adjustment problems and psychiatric disturbance, 22\u201323 Resilence, in pediatric rehabilitation, 495 caveats, 42 RESNA. See Rehabilitation Engineering and Assistive Technology family environment, 45\u201346 individual assessment tools, 42\u201345 Society of North America measurement in, 23\u201325 Respiration, 54, 266 nontraditional methods in, 368 Respiratory complications after spinal cord injury, 273 types of, 27\u201329 drooling, 17 uses of, 25\u201327 respiratory distress, 17\u201318 Psychological impairments, in cerebral palsy, 172 Psychosocial aspects, of pediatric rehabilitation, 493\u2013499 in infancy, differential diagnosis for, 141, 141f Psychosocial services, after traumatic brain injury, 247 history of, 3 Psyllium, for bowel dysfunction, 270t in cerebral palsy, 173 PTA. See Post-traumatic amnesia Respiratory dysfunction, 447 in neuromuscular diseases, management of, 327 and speech disorders, 55\u201356 after spinal cord injury, 266 after traumatic brain injury, 242","518 Index Rest, for juvenile idiopathic arthritis, 273 Sclerotomes, 361, 362f Retinis pigmentos, 310 Scoliosis, 397\u2013399 Retrograde amnesia, 34 Reverse walkers, 111 appearance in, 7 Revised Children\u2019s Manifest Anxiety Scale for Children (RCMAS), in cerebral palsy, 172, 174, 175, 184 curvature measurement, 399f 45, 47t in Duchenne muscular dystrophy, 290\u2013291, 326f Rey-Osterreith Complex Figure Test (ROCF), 33t in facioscapulohumeral muscular dystrophy, 301 RGO. See Reciprocating gait orthosis functional scoliosis, 403 Rheumatic disease, appearance in, 6 idiopathic scoliosis, 400\u2013403 Rheumatic diseases in children, rehabilitation of leg length inequality, 403\u2013405 progressive, 291, 300 hematological disorders, 377\u2013378 in spina bi\ufb01da, 442 infectious disease, 376 types, 397t, 400 juvenile idiopathic arthritis, 370\u2013376 Scuba diving, 88 systemic lupus erythematosus, 376\u2013377 SDMT. See Symbol Digit Modalities Rheumatic fever Seating, 111 differential diagnosis of, 372t Second impact syndrome, 232\u2013233 Rhizotomy, selective dorsal, 65, 178, 182\u2013183, 273 Sedation, for nerve conduction studies, 137\u2013138 Ribs, \ufb02aring of, 7 Seizures, 18 Rickets, 407\u2013408 in cerebral palsy, 166, 172 hypophosphatemic, 395 after traumatic brain injury, 245 nutritional, 408 Selective dorsal rhizotomy (SDR), 182\u2013183 Rifton Gait Trainer, 111f Self-care, in spina bi\ufb01da, 221, 442 Rifton Adaptive Tricycle, 117 Semantics, 37, 54, 59, 60, 61, 62 Rigidity, after traumatic brain injury, 237 Senna (Senokot), for bowel dysfunction, 270t Rigid spine syndrome, 300, 302, 304 Sensorineural hearing loss, 238 Risser\u2019s lines, 398 Sensory conduction velocities, in children, 129, 131t, 132t, 134\u2013135 Rivermead Behavioral Memory Test, 34, 35t Sensory de\ufb01cits Road racing, 95 in cerebral palsy, 170 Robert\u2019s syndrome, 339f, 341 in spina bi\ufb01da, 204 Robots, 124\u2013125 after traumatic brain injury, 238\u2013239 therapy robots, 125\u2013126 Sensory examination, 9\u201310 ROCF. See Rey-Osterreith Complex Figure Test Sensory nerve action potential (SNAP), 368 Rockers, 475 amplitudes, 143 Rod body myopathy, 303 Sensory stimulation, in traumatic brain injury, 246\u2013247 Roller racer, 117 Sensory\u2013perceptual and motor tests, 34 ROM. See Range of motion computerized assessment, 35\u201336 Rooting re\ufb02ex, 69 Sequential Swim Techniques (SST), 90 Rorschach Inkblot Technique, 44, 46t Serial casting, 176 Rule of 9s, 378 Severe childhood autosomal recessive muscular dystrophy, 280 RVs. See Recreational vehicles Severe X-linked centronuclear (myotubular) myopathy, 303\u2013304 Sever\u2019s disease, 391 SAARDs. See Disease-modifying antirheumatic drugs Sexuality SACH foot, 354, 355 in childhood-onset spinal cord injury, 446 Sacral lesions, in spina bi\ufb01da, 204 with cerebral palsy, 439 Safety in Down syndrome, 449 in intellectual disabilities, 447 family counseling on, 249 with spina bi\ufb01da, 443\u2013444 after traumatic brain injury, 253 after spinal cord injury, 446 in wheelchair use, 220 SGDs. See Speech-generating devices Saline enemas (Fleet\u2019s enemas), for bowel dysfunction, 270t Shaken baby syndrome, 233 Salmonella, 378 Shea Classi\ufb01cation of Pressure Ulcers, 271t SB. See Spina bi\ufb01da Shenton\u2019s line, 216f SBAA. See Spina Bi\ufb01da Association of America Shock artifact, 133 Scanogram technique, 403, 403f Shoe inserts, 104 Scar management, with burn injuries, 381 Shoulder SCD. See Spinal cord dysfunction disarticulation, 340\u2013341 SCFE. See Slipped capital femoral epiphysis injuries to, 85, 391 Scheuermann\u2019s disease, 391 orthoses for, 105t atypical, 392 Sickle cell anemia, 409 School-aged children, examination of, 6 Sickle cell disease, 377\u2013378 School services. See also Education Silvadene. See Silver sulfadiazine for children with traumatic brain injury, 248 Silver nitrate, for burn injuries, 379 Schwartz\u2013Jampel syndrome, 154, 308 Silver sulfadiazine (Silvadene), for burn injuries, 379 SCI. See Spinal cord injury Sinding\u2013Larsen\u2013Johansson syndrome, 391 Sciatic mononeuropathies in children, 149\u2013150 Single-construct measures, 45 SCIWORA. See Spinal cord injury, without radiographic Single-\ufb01ber, limitations, in pediatric populations, 138 abnormality Scleroderma, 372t, 377","Index 519 Single limb support task, 476\u2013478, 479t Speech therapy, in cerebral palsy, 178 Single photon emission computed tomography (SPECT), 292 Speech-generating devices (SGDs), 118 Single tests, 27 Skeleton, development of, 361\u2013362 categories, 119t Skiing, 95 Sphincter dyssynergia, 205f Skin urodynamic study in, 210, 211, 21f assessment of, 383, 389 Spina bi\ufb01da (SB), 199, 431t\u2013432t, 440\u2013444 care of, after spinal cord injury, 271 inspection of, 6 aging with, 431\u2013432t Skin breakdown, 104, 205 central nervous system malformations, 206\u2013209 Skull fracture, growing, 233 clinical pearls, 217 Slalom, 95, 98 clinical signs and course of, 204, 205f SLE. See Systemic lupus erythematosus cognitive function, 222\u2013224 Sleep apnea, 3 complications of, 204\u2013205, 214 SLI. See Speci\ufb01c language impairment cystica (aperta), 203 Slipped capital femoral epiphysis (SCFE), 385\u2013386 denervation in, 205 SNAP. See Sensory nerve action potential diagnosis of, prenatal, 203 Snapping hip syndrome, 390 epidemiology, 199\u2013200 Snorkeling, 88 etiology, 200\u2013203 Soccer, 95\u201396 folic acid supplements, guidelines for, 199 Social history, 4\u20135 latex allergy, 220\u2013221 Social isolation, 5, 81, 383, 427 musculoskeletal, 218 Social issues. See Psychosocial issues long term, 224\u2013225 Societal factors, interaction of, 66 neural tube defects, clinical types of, 203 Softball, 96 neurogenic bladder, 210\u2013213 Solid ankle foot orthosis, 106t neurogenic bowel, 213\u2013217 Somatosensory-evoked potentials (SSEP), 155\u2013158 obesity, 221 clinical applications, in children, 156\u2013158 occulta, 203 brachial plexus injury, 158 appearance in, 6 brain injury in SSEPs, 156 osteoporosis, 221 demyelinating diseases, 158 intraoperative spinal monitoring, 158 treatment, 222 tethered cord syndrome, 157\u2013158 outcomes in, 199, 204 traumatic spinal cord injury, 156\u2013157 pathogenesis of, 200 median nerve, 155 precocious puberty, 221 principles of, 155, 156f rehabilitation in, 218\u2013220 tibial nerve, 155, 156, 157f self-care, 221 Sorbitol, for bowel dysfunction, 270t treatment of Spastic cerebral palsy, 166 Spastic hypertonicity, 8 neurosurgical treatment, 210 Spastic quadriparetic CP, 166, 167f team approach, 209\u2013210 Spasticity, 18, 402 Spina Bi\ufb01da Association of America (SBAA), 225 de\ufb01nition of, 166 Spinal cord, in spina bi\ufb01da dystonia, 166 L1\u2013L3 segment, 204 management of L4\u2013L5 segments, 204 pharmacologic, 237 Spinal cord dysfunction (SCD), 439\u2013440 physical, 237 Spinal cord injuries (SCI), 261\u2013275, 432\u2013433t medications, 180t, 273t aging with, 432\u2013433t and spinal cord injury, 273 anterior cord syndrome, 264 after traumatic brain injury, 237 autonomic dysre\ufb02exia (AD), 271\u2013272 Special Olympics, 85, 92, 96, 98 Brown\u2013Sequard syndrome, 264 Speci\ufb01c language impairment (SLI), 61\u201362 cauda equina syndrome, 264 SPECT. See Single photon emission computed tomography cause of injury, 262 Speech central cord syndrome, 264 components of, 54, 54t classi\ufb01cation of, 262\u2013264 de\ufb01nition of, 54 deep vein thrombosis, 272 development of, 3, 65, 66 demographics of, 261\u2013262 intelligibility, 61 early treatment, 265\u2013266 Speech disorders, 63\u201366 electrodiagnostic evaluation of, 143 acquisition, 63 epidemiology of, 261 articulatory\/resonatory dysfunction, related to, 57 equipment and environment, 274\u2013275 congenital, 64 and gastrointestinal function, 266 diagnosis and treatment of, 66\u201369 functional dependence after, 268t motor speech disorders, 57\u201359, 67t hypercalcemia, 272 phonatory dysfunction, related to, 57 incidence of, 261 respiratory dysfunction, related to, 55\u201356 long-term follow-up in, 275 Speech recognition software, 122 and mobility, 267\u2013268 nutrition, 271 prevalence of, 261 prevention of, 265 prognosis for neurologic recovery, 265"]