100 a. Useful for superior structural imaging of soft tis- sues and for flow of blood within medium and 10. Examine gait. larger arteries and veins; bone is poorly imaged. a. Kinematic gait analysis. b. Timed walking test: patient is asked to walk at b. Allows three dimensional localization with preferred pace or as fast as possible over a set high spatial resolution. distance, e.g., 10 m walk test. c. Primary method of examination of tumors, M. Review Medical Record for Diagnostic Procedures! demyelination, and va cular abnormalities. Results 1. Radiological procedures: skull x-rays. d. Contraindications: metal implants, pacemakers. a. Delineates lesions of bone. 7. Positron emission tomography (PET): neuroimag- b. Tomograms (tomography) are layered x-ray exposures, either vertical or horizontal. ing technique in which radioisotopes are inhaled 2. Ventriculography: x-rays of skull following injec- or injected, and emi sions are measured with a tion of air into lateral ventricles. gamma- ray detector sy tern. a. Delineates ventricle , helps localize tumors. a. Allows physiological mapping; a major clinical b. Useful with increased intracranial pressures. 3. Myelography: x-rays of spine following injection research tool for imaging cerebral blood flow, of air or dye into spinal subarachnoid space. brain metabolism. a. Delineates abnormalities impinging on sub- b. Lacks detailed resolution of CT or MR!. arachnoid space. 8. Electroencephalography (EEG): ongoing electrical b. Complications: dye may result in meningeal activity of brain is recorded, appearing as periodic irritation. waves. 4. Cerebral angiography: x-rays of skull following a. Provides useful information about structural injection of dye into carotid and/or vertebral arteries. disease of the brain, especially when seizures a. Useful in showing areas of increased and are present or likely. decreased vascularity. b. Can assist in localization of intracranial Ie ion b. Detects displacement of vessels by masses, in the brain. occlu ions, malformations and aneurysms. 9. Evoked potentials/evoked responses (EP): external c. Provides information about dynamics of circu- visual, auditory, or somatosensory stimuli are u ed lation time. to evoke potentials in brain, Visual Evoked d. Complications: invasive technique; may cause Potential (VEP); Brainstem Auditory Evoked meningeal irritation, hemorrhage, vasospasm, anaphylactic reaction to dye. TABLE 2-6 - FUNCTIONAL BALANCE GRADES 5. Computerized tomography (CT, CAT): neuro- imaging technique in which narrow x-ray beams Normal Patient is able to maintain steady balance without are transmitted through tissues of varying densities Good handhold support (static). and precisely measured; allows cross sections Fair Accepts maximal challenge and can shift weight easily (slices) of the brain to be visualized with three Poor and full range in all directions (dynamic). dimensional localization. a. Contrast agents (intravenous iodinated agents) Patient is able to maintain balance without handhold can be used to increase diagnostic sensitivity, support, limited postural sway (static). detect brain abnormalities (tumor, calcifica- Accepts moderate challenge; able to maintain balance tions, etc.). while picking object off floor (dynamic). b. Useful for demonstrating presence of abnormal changes in tissue density: areas of hyperemia Patient is able to maintain balance with handhold support; (hemorrhage) appear more dense, edematous may required occasional minimal assistance (static). tissue less dense. Accepts minimal challenge; able to maintain balance 6. Magnetic resonance imaging (MRI): neuroimag- while turning head/trunk (dynamic). ing technique in which nuclear particles (protons and neutrons) are depicted in a strong external Patient requires handhold support and moderate to magnetic field; no radiation is used. maximal assistance to maintain position (static). Unable to accept challenge or move without loss of balance (dynamic). From: O'Sullivan S and Schmitz T (200 I). Physical Rehabilitation: Assessment and Treatment. Philadelphia. FA Davis Co. p 196. with permission.
Potential (BAEP), Somatosensory Evoked Neuromuscular Physical Therapy 101 Potential (SEP). a. Potentials are recorded from surface electrodes (2) Insertional activity (burst of action poten- tials when EMG needle is inserted into nor- and processed by computer. mal muscle) is increased in denervated b. Delineates conduction times along these senso- muscle and many muscle diseases. ry pathways. (3) Number of motor unit potentials (MUP) is c. Detects lesions if responses are delayed or decreased in LMN injury (denervated mus- cles); overall configurations remain normal. absent. 10. Echoencephalogram (ultrasound/Doppler tech- (4) Alterations in MUP configurations (increased in size and duration, polyphasic niques): reflected ultrasonic waves are recorded shape) occur with re-innervation of previ- and analyzed. ou ly denervated muscles. a. Useful for imaging lumen of carotid artery and (5) Spontaneous, ongoing EMG activity. analyzing flow, detection of plaques in carotid (a) Fibrillation (spontaneous independent arteries. contractions of individual muscle b. Measures position and shifts of midline struc- fibers) evident with denervation for 1- tures, e.g., tumors or hematomas. 3 weeks after losing nerve. II. Lumbar puncture (LP): insertion of spinal needle (b) Fasciculations (spontaneous contrac- below level of Ll-2. tions of all or most of the fibers in a a. Purposes. motor unit; muscle twitches that can be (1) Withdraw CSF for chemical analysis and observed or palpated) are present with LMN disorders and denervation. cytologic examination: measurement of (c) Complete LMN lesions show only fib- protein, glucose, immunoglobulin content, rillation potentials; partial LMN cell count. lesions show both fibrillation and fas- (2) Mea ure intracranial pressures and spinal ciculation potentials. fluid dynamics. (3) Injection of contrast medium for radiologic b. Nerve conduction velocity (NCV): conduction examination. velocities are obtained by stimulating peripher- (4) Injection of therapeutic agents, e.g., treat- al nerves through the skin and recording mus- ment of cancer, meningitis. cle and sensory nerve action potentials. b. Complications: severe headache caused by (I) Distance between two points (conduction dis- CSF leakage (relieved by lying down); more tance) is divided by the difference between severe complications include infection, epidur- the corresponding latencies (conduction al hematoma, uncal herniation. time), expressed as meters/second (mls). c. Normal CSF: clear and colorless. (2) Decreased conduction velocities are seen in (1) Manometric pressure CSF: 70-200 mm of peripheral neuropathies characterized by water (avg. of 125). demyelination, e.g., Guillain-Barre syn- (2) Normal protein: 20-40 mg/dl. drome, chronic demyelinating polyneu- d. Pathological CSF findings. ropathy, Charcot-Marie-Tooth disease. (I) RBCs indicate hemorrhage or traumatic (3) Slowed conduction velocitie seen with tap; elevated WBC indicate significant focal compression of peripheral nerve. inflammation and infection. (2) Elevated proteins may indicate tumors or c. Strength-duration curve: representation by inflammation. graph of the relationship between the strength 12. Neuromu cular diagnostic procedures. (intensity) plotted on the Y axis and various a. Electromyography (EMG): detects electrical durations (time) plotted on the X axis of an activity arising from muscles, both resting applied electric current necessary to elicit a states and active contraction. threshold response from nerve and muscle. (I) Useful in diagnosing LMN disease or pri- (1) Position of the curve on the graph will vary mary muscle disease, defects in transmis- according to innervation status of muscle; an sion at neuromuscular junction. impulse oflong duration, and greater amplitude is required to stimulate denervated muscle.
102 the frontal or temporal lobes, or cerebellum. c. Treat infective organism, surgical intervention. (2) Rheobase: the intensity of an electric cur- d. Provide supportive symptomatic therapy. rent necessary to produce a minimal con- 4. Acquired Immunodeficiency Syndrome (AIDS). traction (visible twitch) of a muscle when a. Viral syndrome characterized by acquired and an electric current of infInite duration (300 ms) is applied. severe depression of cell-mediated immunity. b. Symptoms: wide-ranging; II3 of patients (3) Chronaxie: duration of an electric stimulus of twice the rheobase value that will elicit a exhibit CNS or PNS deficits. minimal response (muscle twitch). (1) AIDS dementia complex (ADC). (4) The chronaxie of an intact nerve and Symptoms range from confu ion and mem- healthy, innervated muscle is much lower ory loss to disorientation. (approximately 0.03ms) than that of a den- (2) Motor deficit : ataxia, weakness, tremor, ervated muscle (approximately 10 ms or loss of fine motor coordination. more). Refer to Chapter 10, Physical (3) Peripheral neuropathy: hypersensitivity, Agents and Figure 10-2. pain, sensory loss. c. Treat with antiHIV drugs. Refer to Chapter 6 III. Neurological Dysfunction Infectious Diseases. d. Take appropriate standard precautions. Refer to (Table 2-8) Neuromuscular Practice Patterns Table 6-1. A. Infectious Diseases e. Provide palliative and supportive therapy. B. Cerebral Vascular Accident (CVA, Stroke): sudden, Examine for signs of CNS infection, meningeal irrita- focal neurologic deficit resulting from ischemic or tion. hemorrhagic lesions in the brain. 1. Etiologic categories. Examine for signs of increased intracranial pressure. a. Cerebral thrombosis: formation or develop- 1. Meningitis: inflammation of the membranes of the ment of a blood clot or thrombus within the cerebral arteries or their branches. spinal cord or brain. b. Cerebral embolism: traveling bits of matter a. Etiology: can be bacterial (E. Coli, H. (thrombi, tissue, fat, air, bacteria) that produce occlusion and infarction in the cerebral arteries. Influenzae, S. Pneumoniae, streptococcus) or c. Cerebral hemorrhage: abnormal bleeding a a viral. Patients with bacterial meningitis are result of rupture of a blood vessel (extradural, usually sicker with more rapid time course. subdural, subarachnoid, intracerebral). b. Treat infective organism (bacterial meningitis) 2. Risk factors: with antibacterial therapy (antibiotic, antipyret- a. Atherosclerosis. ic). Maintain fluid and electrolyte balance. b. Hypertension. c. Provide supportive symptomatic therapy, c. Cardiac disease (rheumatic valvular disease, including bed positioning, PROM, skin care to endocarditis, arrhythmias, cardiac surgery). prevent complications of immobility; safety d. Diabetes. measure if confusion is present. e. Transient ischemic attacks (TIAs): brief warn- 2. Encephalitis: severe infection and inflammation of ing episodes of dysfunction (Ie s than 24 the brain. hours); a precursor of major stroke in more a. Etiology: arboviruses, or a sequela in influenza, than 1/3 of patients. (Reye's syndrome, eastern equine encephalitis, 3. Pathophysiology. measles), chronic and recurrent sinusitis, otitis a. Cerebral anoxia: lack of oxygen supply to the or other infections; bacterial encephalitis, prion brain (irreversible anoxic damage to the brain caused disease (Kuru, Mad Cow disease). begins after 4 to 6 minutes). b. Treat infective organism (bacterial encephalitis). b. Cerebral infarction: irreversible cellular damage. c. Provide supportive symptomatic therapy. c. Cerebral edema: accumulation of fluids within 3. Brain Abscess: infectious process in which there is brain; causes further dysfunction; elevate a collection of pyogenic material in the brain parenchyma. a. Signs and symptoms: headaches, fever, brain stem compression, focal signs CN II, VI. b. Can be a extension of an infection, e.g., menin- gitis, otitis media, sinusitis, post TEl; typically
intracranial pressures, can result in herniation Neuromuscular Physical Therapy 103 and death. 4. Neurovascular clinical syndromes: characteristics (2) Lateral medullary (Wallenberg's) yn- igns and symptoms associated with occlusion of drome (vertebral, posterior inferior cerebel- specific cerebral ve sels. lar or basilar artery occlusion): produces a. Internal carotid artery syndrome: ICA arises ipsilateral cerebellar symptoms (ataxia; off the common carotid and internal carotid vertigo, nausea and vomiting; nystagmus), arteries, gives off an ophthalmic branch and Homer's syndrome (miosis, ptosis, terminates in the anterior and middle cerebral decreased sweating); dysphagia, impaired arteries; occlusions commonly produce signs speech, diminished gag reflex; sensory loss and symptoms of middle cerebral artery of ipsilateral arm, trunk, or leg; contralater- involvement with reduced levels of conscious- al loss of pain and temperature of half of ness; anterior cerebral artery may also be body, sometimes face. affected; lesions involving both MCA and ACA distributions may produce massive edema, (3) Basilar artery syndrome: produces brain- brain herniation, and death. stem signs and symptoms and posterior (1) Anterior cerebral artery syndrome: ACA cerebral artery signs and symptoms. Locked-in syndrome (basilar artery occlu- supplies anterior two thirds of the medial sion at the level of the pons): occlusions cerebral cortex; occlusions produce con- produce quadriplegia and bulbar paralysis; tralateral ensory loss and hemiparesis, anarthria with preserved consciou ness; with leg more involved than arm. thus, the patient is unable to move or speak Occlusions proximal to anterior communi- but has full cognitive function; often fatal. cating artery produce minimal deficits due Sensation may be intact. to collateral circulation (Circle of Willis). (2) Middle cerebral artery syndrome: MCA (4) Mernal inferior pontine syndrome (occlu- supplies lateral cerebral cortex, basal gan- sion of paramedian branch of basilar glia, and large portions of the internal cap- artery): produces (1) ipsilateral signs and sule; occlusions produce contralateral sen- symptoms: cerebellar (nystagmus, ataxia), sory loss and hemiparesis, with arm more paralysis of conjugate gaze (to the side of involved than leg; may also produce motor the lesion), diplopia and (2) contralateral speech dy function (Broca's area); percep- signs and symptoms: hemiparesis, tual dysfunction (parietal sensory associa- impaired sensation. tion cortex); homonymous hemianopsia (optic radiation, internal capsule); loss of (5) Lateral inferior pontine syndrome (occlu- conjugate gaze to the opposite side (frontal sion of the anterior inferior cerebellar eye fields); sensory ataxia (parietal lobe). artery): produces (1) ipsilateral signs and b. Vertebrobasilar artery syndrome: two VAs arise symptoms: cerebellar (nystagmus, vertigo, off the subclavian arteries and supply the ven- nausea, vomiting, ataxia), facial paralysis, tral urface of the medulla and the posterior paralysis of conjugate gaze to the side of inferior aspect of the cerebellum before joining the lesion, deafness, tinnitus, impaired to form the basilar artery at the junction of the facial sensation and (2) contralateral signs pons and the medulla; the basilar artery sup- and symptoms: hemi impairment of pain plies the ventral portion of the pons and termi- and temperature. nates in the posterior cerebral artery. Numerous syndromes may occur. (6) Posterior cerebral artery syndrome: PCA (1) Medial medullary syndrome (vertebral and posterior commumcating arteries sup- artery occlusion or branch of lower basilar ply the midbrain, temporal lobe, dien- artery): produces ipsilateral paralysis of cephalon, and posterior third of cortex; tongue, contralateral paralysis of arm and occlusions may produce contralateral leg with impaired sensation. homonymous hemianopsia, contralateral sensory loss; thalamic syndrome, involun- tary movements (choreoathetosis, intention tremor, hemiballismus), transient contralat- eral hemipareses, Weber's syndrome (ocu- lomotor nerve palsy with contralateral
104 reflexes. (Table 2-4). (2) Loss of selective movements, pre ence of hemiplegia), and visual symptoms (paraly- sis of vertical eye movements, miosis, pto- basic limb synergies. (Table 2-5). sis, decreased pupillary light reflex). (a) Upper extremity flexion ynergy. Occlusions proximal to posterior commu- (b) Upper extremity extension ynergy. nicating artery produce minimal deficits (c) Lower extremity flexion ynergy. due to collateral circulation (same as for (d) Lower extremity extension synergy. ACA). (3) Presence of paresis, incoordination, motor 5. Sequential recovery stages. programming deficits (apraxia). a. Stage 1: initial flaccidity, no voluntary move- (4) Postural and balance deficits. ment. (5) Gait: typical deficits. b. Stage 2: emergence of spasticity, hyperreflexia, (a) Hip: poor hip position (retracted, synergies (mass patterns of movement). c. Stage 3: voluntary movement possible but only flexed); Trendelenburg limp (weak in synergies, spasticity strong. abductors); scissoring (spastic adduc- d. Stage 4: voluntary control in isolated joint tors); insufficient pelvic rotation dur- movements emerging, corresponding decline ing swing. of spasticity and synergies. (b) Weak hip flexors during swing may e. Stage 5: increasing voluntary control out-of- yield circumducted gait, external rota- synergy; coordination deficits present. tion with adduction, backward leaning f. Stage 6: control and coordination near normal. of trunk, or exaggerated flexion synergy. 6. Examine. (c) Knee: weak knee exten or (knee flex- a. Generalized signs of increased intracranial es during stance) may result in com- pressure. b. Level of consciousness, cognitive function. Figure 2-1 Schematic synopsis of somatosensory c. Speech and communication. pathways and their clinical syndromes. From Young, (1) Check for aphasia with lesions of pari- P and Young, P: Basic Clinical Neuroanatomy, etooccipital cortex of dominant hemisphere Williams & Wilkins, Baltimore, 1997, p. 147, (typically the left hemisphere). with permission. (2) Check for perceptual deficits with lesions of parietal lobe of the nondominant hemi- sphere (typically the right hemisphere). d. Behaviors. (1) Patients with lesions of the left hemisphere (right hemiplegia) are slow, cautious, hesi- tant and insecure. (2) Patients with lesions of the right hemi- sphere (left hemiplegia) are impulsive, quick, indifferent; often exhibit poor judg- ment and safety, overestimating their abili- ties while underestimating their problems. e. Sen ory deficits. (Figure 2-3). (1) Superficial, proprioceptive and combined sensations of contralateral extremities and trunk, face. (2) Hearing, vision; check for homonymous hemianopsia. (3) Cranial nerve function with brainstem, ver- tebrobasilar strokes (pseudobulbar palsy). f. Motor function. (Figure 2-2). (1) Presence of abnormal tone and primitive
pensatory locking of knee in hyperex- Neuromuscular Physical Therapy 105 tension; spastic quadriceps may also yield a hyperextended knee. (f) Decreased cadence, uneven timing. (d) Ankle: foot drop; equinus gait (heel g. Function: functional mobility skills (FMS), does not touch down); varus foot (weight i borne on lateral side of activities of daily living (ADLs). foot); or equinovarus position. h. Standardized tests and measures for examina- (e) Unequal tep lengths: hemi leg does not advance through the end of stance tion of patients with stroke. into toe off. (1) Fugl-Meyer Assessment of Physical Performance (FMA) (1980); expands on work of Brunnstrom; provides objective criteria for scoring of movements (0 cannot perform to 2 fully performed). Includes UPPER MOTOR Useful localizing features Lesion site (not always present) NEURON Impairment of conscious level. } CONTRALATERAL UMB WEAKNESS Visual field deficit. HEMISPHERE - UNILATERAL { Dysphasia (if dominant hemi- LESION . •.... Face (upper sphere). motor CONTRA- neuron pattern) Alert. . (1'f . } LATERAL No . dysphas1a dommant _INTERNAL CAPSULE arm hem1sphere). LESION . \"Leg Visual field deficit rare. CMOIDNBTRRAAILNALTEESRIAOLN HEMIPLEGIA Contra1ateraI CN III paIsy. Conjugate gaze deviation to- •..-Face (lower wards the weak limbs (impaired '-----\"\"' motor neuron movement towards the 'normal' pattern) limb). CONTRALATERAL .- ..•. Lower motor neuron facial PONTINE LESION \"Arm •Leg weakness on side opposite the HEMIPLEGIA weak limbs. CONTRA- Visual field deficit. LLATERAL- JDiscriminatory sensory deficit. CORTEX r Pain and temperature loss on} LESION Arm f---~ the same side as the weakness CONTRALATERAL ..-c .~' and a Horner's syndrome and MEDULLARY weak palate and tongue on the LESION ···Leg opposite side. Pain and temperature loss on} the opposite side to the limb IPSILATERAL Cl weakness and a Horner's syn- SPINAL LESION I drome and proprioception loss C4 Arm :i: Face on the same side. _ _ _ _ _ { Visual field deficit. } CONTRALATERAL ,) ~ :::---- Dysphasia (if dominant hemi- CORTEX ',_ .. \" .! LESION sphere). I, i'(, \"- ,/ - ' \\(v ~J\\\\._:' ',··.i)/L.) Discriminatory sensory deficit. SDiscriminatory sensory deficit. \"\" .•' '-., J Pain and temperature loss in the} opposite leg, proprioception loss -I-P-SI-LA-T-E-RA-L---f\"'Iir\"I MONOPLEGIA Leg on the same side. SPINAL LESION Figure 2-2 Localizing features of damage to s'pecific areas of brains and spinal cord. From Lindsay KW. Bone I. Callander R: Neurology and Neurosurgery Illustrated. Churchill Livingston. New York. 1986. p. 181, with permission.
106 (2) Oromotor training. (3) Exercise conditioning: cycle ergometry, subtests for UE function, LE function, bal- ance, sensation, ROM and pain. walking. (2) Motor Assessment Scale (MAS) developed g. Additional training modes. by Carr and Shephard (1985); measures functional capabilities using 8 categories of (1) Isokinetic training: useful to improve tim- movements; provides objective criteria for ing deficits, velocity control of movement. scoring performance. 7. Physical therapy goals, outcomes, and interventions. (2) Body weight-supported treadmill training a. Monitor changes associated with recovery and (BWSTT): the patient walks with assis- inactivity. tance on a treadmill with body weight par- (1) Prevent or minimize indirect impairments/ tially supported. Slow treadmill speeds secondary complications. (typically 0.01-2.25 mls) and light support (a) Maintain ROM and prevent deformity using an overhead harness (typically 30% of body weight to start) are used. One or through optimal positioning, PROM, two therapists provide manual a sistance in and mobilization. stabilization of trunk/pelvis and in move- (b) Maintain skin integrity. ment of the paretic limb. (c) Avoid traction injuries to arm, develop- ment of painful shoulder. (3) EMG - biofeedback training: useful to (2) Teach sensory compensation strategies for decrease firing in spastic mu cles, increase sensory and perceptual losses. firing in paretic muscles, improve motor b. Promote awareness, active movement, and use control. of hemiplegic side (remediation-facilitation approach). (4) Functional electrical stimulation (FES): (1) Promote normalization of tone through useful to stimulate muscle action, reduce tone reducing activities and techniques. spasticity, substitute for an orthosis. (2) Promote selective movement control (out- of-synergy movements) of involved (5) Constraint-induced Movement Therapy extremities; emphasize functional patterns (CI): the unaffected UE i restrained with of movement. the use of an arm sling and resting hand c. Improve postural control, symmetry, and balance. splint while training i focused on the d. Task specific training: (motor control/motor affected UE. Uses massed practice (up to 6 learning approach). (Table 2-5). hours/day) with repetitive training of func- (1) Promote active problem solving independ- tional tasks. Operant conditioning tech- ence. niques are used to shape re ponses. (2) Focus on goal directed tasks, functional mobility skills: e.g., rolling, supine-to-sit, h. Provide emotional support, encourage social- sitting, sit-to-stand, transfers, wheelchair ization and motivation. mobility, ambulation. (1) Reorient and reassure. (3) 'Focus on adapting movements to specific (2) Provide patient and family education. environmental demands. (4) Organize feedback inputs (knowledge of 8. Guidelines to promote learning with hemispheric results, knowledge of performance) and differences. practice schedules to facilitate learning. a. Patients with left hemisphere lesions (right e. Promote independence in activities of daily liv- hemiplegia). ing/self-care. Compensatory training as appro- (1) Develop an appropriate communication priate. base: words, gestures, pantomime; assess f. Improve respiratory and oromotor function; level of understanding. promote functional cardiorespiratory endurance. (2) Give frequent feedback and support. (1) Improve chest expansion, diaphragmatic (3) Do not underestimate ability to learn. breathing pattern. b. Patients with right hemisphere lesions (left hemiplegia). (1) Use verbal cues; demonstrations, gestures may confuse patients with visuospatial deficits. (2) Give frequent feedback: focus on slowing
euromuscular Physical Therapy 107 down and controlling movement. (2) Secondary brain damage. (3) Focu on safety. (a) Hypoxic-ischemic injury (HIT): result (4) Avoid environmental (spatial) clutter. from systemic problems (respiratory or (5) Do not overestimate ability to learn. cardiovascular) which compromises C. Trauma cerebral circulation. I. Traumatic brain injury (TBI). (b) Swelling/edema: can result in mass a. Etiology: mechanism of injury is contact forces effect with increased intracranial pres- to skull and rotational acceleration forces caus- sures (ICP), brain herniation (uncal, ing varying degrees of injury to the brain. central, or tonsillar) and death. b. Pathophysiology. (c) Electrolyte imbalance and mass release (l) Primary brain damage. of damaging neurotransmitter . (a) Diffuse axonal injury (DAI): disruption (3) Concussion: loss of consciousness, either and tearing ofaxons and small blood temporary or permanent, resulting from vessels from shear-strain of angular injury or blow to head with impaired func- acceleration; results in neuronal death tioning of the brainstem reticular activating and petechial hemorrhages. system (RAS); may see changes in HR, RR,BP. (b) Focal injury: contusions, lacerations, (a) Mild concussion syndrome: only mass effect from hemorrhage and momentary loss of consciousness or edema (hematoma). confusion after TBI; may see retro- grade amnesia (loss of memory that (c) Coup-contracoup injury: injury at point goes back in time before the injury of impact and oppo ite point of impact. occurred). (d) Closed or open injury (with fracture of the skull). SPINAL CORD SYNDROME CONTRALATERAL ,ill.;.,-_____ Loss of pain, temperature and} SPINOTHALAMIC . ,,;~-':~~S light touch below a specific TRACT LESION l{ dermatome .level (may sp~~~ . (Partial spinothalamic sacral sensatlOn). --tract lesio_n) { Loss of all modalities at one or several dermatome levels. . ~nd BROWN-SES~UARRODME Loss of temperature pam { below a speCific dermatome _ level. Loss of proprioception and 'dis- (Partial cord lesion) 1criminatory' touch up to similar level and limb weakness. IBilateral loss of all mOdalities.} .- - - - - - { Bilateral leg weakness. Bl'IateraI Ioss f0 p'am and COMPLETE CORD LESION _ { tPermespere~raattui?ren.. of proprioce?tion - - ~;0 ~::., and 'dlscnmmatory' sensatlon. ..\", \".. 'SUSPENDED' , SENSORY CENTRAL CORD LESION LOSS Figure 2-3 Spinal Cord Syndromes: patterns of sensory loss and weakness. From Lindsay, KW, Bone I, Callander R: Neurology and Neurosurgery Illustrated. Churchill Livingston, New York, 1986, p. 188, with permission.
108 (b) Classical concussion: moderate in (3) Rappaport's Disability Rating Scale severity, with loss of consciousness (DRS): classifies levels of disability using a that is transient and mostly reversible wide range of functional behaviors. in 24 hours; may see both retrograde and post-traumatic amnesia (PTA: loss (4) Glasgow Outcome Scale (GaS): expands of memory for events after the trau- original scale; includes major disability matic event). categories for outcome assessment. (c) Severe concussion: loss of conscious- d. Recovery stages from diffuse axonal injury ness for longer than 24 hours; associat- (Alexander): ed with diffuse axonal injury and coma. (l) Coma: a state of unconsciousness in which there is neither arousal nor awareness; eyes c. Diagnosis/clinical rating scales. remain closed, no sleep/wake cycles. (1) Glasgow coma scale (GCS): allows classi- (2) Unresponsive vigilance/vegetative state: fication into mild (scores of 13-15), moder- marked by the return of sleep/wake cycles ate (9-12), or severe (8 or less) head injury and normalization of vegetative functions (coma). (respiration, digestion, BP control); persist- (2) Rancho Los Amigos Levels of Cognitive ent vegetative state is determined if patient Functioning (LOCF): delineates 8 general remains in vegetative state one year or cognitive and behavioral levels. more after TBI. TABLE 2-7 - SIGNS ASSOCIATED WITH LOCALIZED LESIONS OFTHE CORTEX LOBE STRUCTURE FUNCTION DESTRUCTIVE LESION Frontal Area 4 Discrete volitional Contralateral paralysis and paresis (most pronounced in distal movements parts of limbs and lower part of face) Area 8 Conjugate eye movements Transitory paralysis of conjugate eye movements to opposite side Broca Speech (areas 44 and 45) Language production Nonfluent aphasia Prefrontal Cortex: Dorsolateral Motivation, problem solving, Bilateral lesions: Impaired ability to concentrate, easily distracted, judgment loss of initiative, apathy, cannot make decisions Orbitofrontal Emotions, behavior Unstable emotions; unpredictable and frequent unacceptable behavior Orbital Gyri (posterolateral part) Olfaction Inability to discriminate odors Parietal Areas 3,1,2 Somesthetic sensations Loss of contralateral stimulus location and intensity; severe impairment of two-point and limb position senses Area 43 Taste Impairment of taste in contralateral side of tongue Superior and Inferior Parietal Processing of somatic and Tactile and visual agnosia, visual disorientation, neglect of Lobules visual information especially contralateral self and surroundings related to use of hands Temporal Area 41 Hearing Subtle decrease in hearing and ability to localize sounds, both contralaterally Wernicke Speech (area 22) Language understanding Fluent aphasia and formulation Middle Inferior, and Occipito- Storage of auditorially Impairment of learning and memory temporal Gyri (dominant side) presented information Temporal Cortex Storage of visually Impairment of learning and memory (nondominant side) presented information Parahippocampal Region Recent memory Bilateral lesions: Profound memory loss of recent events and no new learning Occipital Area 17 Vision Contralateral homonymous hemianopsia Parastriate and Peristriate Visual association Bilateral lesions: Color agnosia and loss of spatial relationships (areas 18 and 19) (cannot draw floor plan of home, map of route to work or church, etc.) From Gilroy, J: Basic Clinical Neurology, ed. 2. Pergamon Press, Elmsford, NY, 1990, p. 228-229, with permission.
(3) Mute respon iveness/minimally respon- Neuromuscular Physical Therapy 109 sive: tate in which patients are not vegeta- tive and do show signs, even if intermittent, use atrophy, contractures and deformity, of fluctuating awareness. skin breakdown). f. Physical therapy goals, outcomes, and inter- (4) Confusional tate: mainly a disturbance of ventions. attentional mechanisms; all cognitive oper- (1) Monitor changes associated with recovery ations are affected, patient is unable to and inactivity. form new memories; may demonstrate (2) Management based on decreased response either hypo or hyperarousal. level (LOCF I - ill). (a) Maintain ROM, prevent contracture (5) Emerging independence: confusion is clearing and some memory is possible; sig- development: PROM, positioning, nificant cognitive problems and limited splinting, serial casting. insight remain; frequently disinhibited (b) Maintain skin integrity, prevent decu- social behaviors. biti development through frequent position changes. (6) Intellectual/social competence: increasing (c) Maintain respiratory status, prevent independence though cognitive difficulties complications: postural drainage, per- (problem solving, reasoning) persist along cussion, vibration, suctioning to keep with behavioral and social problems airway clear. (enhancement of premorbid traits, mood (d) Provide sensory stimulation for arous- swing ). al and to elicit movement: environmen- tal and direct stimulation (auditory, (7) Patient can plateau at any stage or regress visual, olfactory, gu tatory, tactile under conditions of stress or repetitive stimuli). brain injury. (e) Promote early return of functional mobility skill : upright positioning for e. Examine. improved arousal, proper body align- (1) For generalized signs of increased intracra- ment. nial pressure. (3) Management based on mid-level recovery (2) Level of consciousness (GCS), cognitive (LOCF IV-VI). function (LOCF), check for disorders of (a) Provide structure, prevent over stimu- learning, attention, memory, and complex lation for the confused, agitated patient: closed, reduced stimulus envi- information proces ing. ronment, daily schedules, and memory logs; relaxation techniques. (3) Cranial nerve function. (b) Provide consistency: use team-deter- (4) For changes in behavior: check for inap- mined behavioral modification tech- niques, give clear feedback, written propriate physical, verbal, sexual behav- contracts. iors; poor judgment; irritability, low frus- (c) Engage the patient in task-specific tration tolerance, and aggression; impulsiv- training; limit activities to familiar, ity and safety issues; depressed mood; well-liked ones; offer options; break restricted affect. down complex tasks into component (5) Speech and communication. parts. (6) Sensory deficits. (d) Provide verbal or physical assistance. (7) Motor function: check for paresis, apraxia (e) Control rate of instruction; provide fre- (dyspraxia), reflexive behaviors, balance quent orientation to time, place, your deficits, ataxia and incoordination (cerebel- name, task. lar damage is common). (f) Emphasize safety, behavioral manage- (8) Functional mobility skills, activities of ment techniques. daily living. (g) Model calm, focused behavior. (9) Level of general deconditioning; after pro- longed hospitalization (comatose, vegeta- tive, decreased response levels), patients experience evere deconditioning and effect of prolonged immobilization (dis-
110 occurs between Cl and C8, involves all four extremities and trunk. (4) Management based on high-level recovery (c) Paraplegia: injury occurs between Tl (LOCF VII & VIII). and T12-Ll, involves both lower (a) Allow for increasing independence: extremities, trunk (varying levels). wean patient from structure (closed to (2) Degree of injury. open environments); involve patient in (a) Complete: no sensory or motor func- decision making. tion below the level of lesion. (b) Assist patient in behavioral, cognitive, (b) Incomplete: preservation of sensory or emotional reintegration: provide hon- motor function below the level of est feedback, prepare for community injury; spotty sensation, some muscle re-entry. function (less than 3+/5 grades). (c) Promote independence in functional (c) American Spinal Injury Association tasks: mobility skills, activities of daily (ASIA) Impairment Scale. living, in real-life environments. A = Complete, no motor or sensory (d) Improve postural control, symmetry, and balance. function is preserved in the sacral (e) Encourage active lifestyle, improved segments S4-S5. cardiovascular endurance. B =Incomplete: sensory but not motor (5) Provide emotional support, encourage socialization, behavioral control, and moti- function is preserved below the neu- vation. rologic level and includes the sacral (a) Reorient and reassure. segments S4-S5 (b) Provide patient and family education. C = Incomplete: motor ~nction is pre- served below the neurologic level, 2. Spinal cord injury (SCI). and the majority of key muscles a. Etiology: partial or complete disruption of below the neurological level have a spinal cord resulting in paralysis, sensory loss, muscle grade less than 3. altered autonomic and reflex activity. (1) Traumatic causes: motor vehicle accident D =Incomplete: motor function is pre- (most common cause of SCI), jumps and falls, diving, gunshot wounds. served below the neurological level, (2) Mechanisms of injury: flexion (most com- and the majority of key muscles mon lumbar injury), flexion-rotation (most below the neurological level have a common cervical injury); compression, muscle grade greater than or equal hyperextension. to 3. (3) Spinal areas of greatest frequency of injury: E = Normal: motor and sensory func- C5, C7, T12 and Ll. tion is normal. (4) Non-traumatic causes: disc prolapse, vas- (3) Syndromes. (Figure 2-3). cular insult, infections. (a) Anterior cord syndrome: damage is b. Pathophysiology. mainly in anterior cord resulting in loss (1) Primary injury, interruption of blood supply. of motor function and pain and temper- (2) Secondary sequelae: ischemia, edema, ature with preservation of light touch, demyelination and necrosis ofaxons, pro- proprioception, and position sense. gressing to scar tissue formation. (b) Brown-Sequard syndrome: hemisection c. Classification. of SC resulting in ipsilateral weakness (1) Level of injury: upper motor neuron and loss of position and vibration sense (UMN) injury. below the level of lesion, with contralat- (a) Lesion level indicates most distal unin- eral loss of pain and temperature a few volved nerve root segment with normal segments below the level of lesion. function; muscles must have a grade of (c) Central cord syndrome: loss of more at least 3+/5 or Fair + function. centrally located cervical tracts/arm (b) Tetraplegia (quadriplegia): injury function with preservation of more peripherally located lumbar and sacral
tracts/leg function; early loss of pain Neuromuscular Physical Therapy 111 and temperature. (d) Cauda equina: injury below L1 results (c) Autonomic dysreflexia (hyperreflex- in injury to lumbar and sacral roots of ia): an emergency situation in which a peripheral nerves (LMN) with sensory noxious stimulus precipitates a patho- loss and paralysis and some capacity logic autonomic reflex with symptoms for regeneration; LMN, autonomous or of paroxysmal hypertension, bradycar- nonreflex bladder. dia, headache, diaphoresis (sweating), (e) Sacral sparing: sparing of tracts to flushing, diplopia, and/or convulsions; sacral segments, with preservation of check for irritating stimuli; treat as a perianal sensation, rectal sphincter medical emergency, elevate head, tone, and/or active toe flexion. check/empty catheter fIrst. d. Examine. (1) Vital signs. (d) Heterotopic bone formation (ectopic (2) Respiratory function: action of diaphragm, bone): abnormal bone growth in soft respiratory muscles, intercostals; chest tissues; check for early changes: soft expansion; breathing pattern; cough, vital tissue swelling, pain, erythema, gener- capacity; respiratory insufficiency or fail- ally near large joint; late changes: cal- ure occurs in lesions above C4 (phrenic cifIcation, initial signs of ankylosis. nerve, C3-5 innervates diaphragm). (3) Skin condition, integrity: check areas of (e) Deep venous thrombosis (DVT): check high pressure. LEs for edema and tenderness. (4) Muscle tone and DTRs. (5) Sensation/SC level of injury: check to see if (2) Improve respiratory capacity: deep breath- sensory level corresponds to motor level of ing exercises, strengthening exercises to innervation (may differ in incomplete respiratory muscles; assisted coughing, res- lesions). piratory hygiene (postural drainage, per- (6) Muscle strength (MMT)/SC level of injury: cussion, vibration, suctioning) as needed to lowest segmental level of innervation keep airway clear; abdominal support. includes muscle strength present at a Fair+ grade (3+/5); use caution when doing (3) Maintain ROM, prevent contracture: MMT in acute phase with spinal immobi- PROM, positioning, splinting; selective lization. stretching to preserve function, e.g., ten- (7) Functional status: full functional assess- odesis grasp. ment only possible when patient is cleared for activity and active rehabilitation. (4) Maintain skin integrity, free of decubiti and e. Physical therapy goals, outcomes, and inter- other injury: positioning program, pres- ventions. sure-relieving devices (e.g., cushions, gel (1) Monitor changes associated with recovery cushion, ankle boots), patient education: and inactivity. pressure relief activities (e.g., pushups) and (a) Spinal shock: transient period of reflex skin inspection; provide prompt treatment depression and flaccidity; may last of pressure sores. several hours or up to 24 weeks. (b) Spasticity/spasms: determine location (5) Improve strength: strengthen all remaining and degree of tone. Check for nocicep- innervated muscles; use selective strength- tive stimuli that may trigger increased ening during acute phase to reduce stress tone (e.g., blocked catheter, tight on spinal segments; resistive training to clothing or straps, body position, envi- hypertrophy muscles. ronmental temperature, infection, decubiti). (6) Reorient patient to vertical position: tilt table, wheelchair; use of abdominal binder, elastic LE wraps to decrease venous pool- ing; check for signs and symptoms of orthostatic hypotension, (lightheadedness, syncope, mental or visual blurring, sense of weakness). (7) Promote early return of functional mobility skills, activities of daily living: emphasis on independent rolling and bed mobility,
112 gait orthoses with walker with or with- out FES system (Functional Electrical assumption of SlttlOg, transfers, sit-to- Stimulation). Typically independent stand, and ambulation as indicated. See household ambulators; wheelchair use section on transfer training in Chapter 11. for community ambulation. (8) Improve sitting tolerance, postural control, (c) Patients with low lumbar lesions (L4- symmetry and balance; standing balance as L5); can be independent with bilateral indicated. AFO and crutche or cane . Typically (9) Appropriate wheelchair (w/c) prescription. independent community ambulators; (a) Patients with high cervical lesions (Cl- may still use wheelchair for activities with high endurance requirements. C4): will require electric w/c with tilt- (d) High rate of rejection of orthoses/ in space seating or reclining seat back; ambulation in favor of w/c mobility microswitch or puff & sip controls; and energy conservation. portable respirator may be attached. (12)Improve cardiovascular endurance: (b) Patients with cervical lesions, shoulder (a) Methods: arm crank ergometry (ACE); function, elbow flexion (C5): can use a functional electrical stimulation (FES)- manual chair with propulsion aids (e.g., leg cycle ergometry; hybrid: ACE and projections); independent for short dis- FES-leg cycle ergometry; wheelchair tances on smooth, flat surfaces; may propulsion (WERG). choose electric w/c for distances, ener- (b) Precautions: individual with tetraple- gy conservation. gia and high-lesion paraplegia experi- (c) Patients with cervical lesions, radial ence blunted tachycardia, lack of pres- wrist extensors (C6): manual chair sor re ponse and very low V02 peak, with friction surface handrims; inde- substantially higher variability of mo t pendent. respon es. (d) Patients with cervical lesions, triceps (c) Trunk tabilization and kin protection (C7): same as for C6, but with important. increased propulsion. (d) Vascular support may be needed (elas- (e) Patient with hand function (C8-Tl and tic stockings, abdominal binder). below): manual w/c, standard handrims. (e) Absolute contraindication to exercise (f) Significant changes in lighter, more testing and training of individuals with durable, sports oriented chairs. SCI (from American College of Sports (lO)Promote wheelchair skills/independence: Medicine, ACSM): management of w/c parts, turns, propulsion • autonomic dysreflexia all surfaces indoors and outdoors, safe fall • severe or infected skin on weight- out of and return to w/c. (ll)Appropriate orthotic prescriptionlambula- bearing surfaces tion training. • symptomatic hypotension (a) Patients with mid thoracic lesions (T6- • urinary tract infection (UTI) T9): supervised ambulation for short • uncontrolled spasticity or pain distances (physiological, limited • unstable fracture household ambulator); requires bilater- • uncontrolled hot and humid environ- al KAFOs and crutches, swing-to gait pattern; requires assistance; may prefer ments standing devices/standing w/c s for • insufficient ROM to perform exer- physiological standing. (b) Patients with high lumbar lesions cise task (Tl2-L3): can be independent in ambu- (l3)Body weight support treadmill training lation all surfaces and stairs; using a swing-through or 4 point gait pattern (BWSIT). and bilateral KAFOs and crutches. (a) Indications: incomplete cervical/tho- Patients may also use reciprocating racic injuries (ASIA levels B, C, D). (b) Promotes spinal cord learning/activa-
tion of spinal locomotor pools. Neuromuscular Physical Therapy 113 (c) Uses body harnes to support weight; benign, exacerbating-remitting, remitting- variable levels of loading from 45% progressive, progressive. decreasing to 10% to full loading. (7) Categories of MS. (d) Early training: therapists assist with (a) Relapsing-remitting MS: characterized foot placement. (e) TM speed: low progre sing to near by relapses with either full recovery or normal (1.5-2.5 mph). Progress to some remaining neurological signs/ overground walking. symptoms and residual deficit upon (f) High frequency (4 days/week); moder- recovery. Periods between relapses ate duration (30 min); typically for 8- characterized by lack of di ea e pro- 12 weeks. gression. (14)Promote maximum mobility in home and (b) Primary-progressive MS: character- community environment; assist patient in ized by disease progre sion from onset, community reintegration; ordering of prop- without plateaus or remissions or with er equipment, home modification. occasional plateaus and temporary f. Provide psychological and emotional support, minor improvements. encourage socialization and motivation. (c) Secondary-progre sive MS: character- (1) Reorient and reassure. ized by initial relapsing-remitting (2) Promote independent problem solving, course, followed by progression at a elf-direction. variable rate that may also include (3) Provide patient and family education. Focus occasional relapses and minor remis- on strategies to prevent skin breakdown, sions. maintain ROM, trength, and function. (d) Progressive-relapsing MS: characterized D. Degenerative Disorders by progressive disease from onset but I. Multiple Sclerosis (MS): a chronic, progressive, without clear acute relapses that mayor demyelinating disease of the CNS affecting large- may not have some recovery or remis- ly young adults. sion; commonly een in people who a. Etiology: unknown; most likely viral, auto- develop the disease after 40 years of age. immune, (active immune responses detected in c. Diagnostic tests: lumbar puncture/cere- cerebrospinal fluid). brospinal fluid (LP/CSF) elevated gamma b. Characteristics. globulin, CT or MRI, myelogram, EEG. (\\) Demyelinating lesions (plaques) impair d. Examine. neural transmission, cause nerves to fatigue (1) History: symptoms, disease progression, rapidly. functional deficits. (2) Variable symptoms: lesions scattered (2) Cognitive/behavioral status: mild to moder- throughout CNS, common in pyramidal ate cognitive impairment common; also tract, dorsal columns, and periventricular euphoria, emotional dysregulation. areas of cerebrum, cerebellar peduncles. (3) Communication: dysarthria and scanning (3) Variable course with fluctuating periods: speech common; dysphasia. exacerbations (worsening of symptoms) (4) ROM, deformity: associated with disuse and remissions, progressing to permanent and inactivity. dysfunction. Lesions are cattered \"in time (5) Sensation: sensory symptoms common, and place\". e.g., paresthesias, hyperpathia (hypersensi- (4) Precipitating or exacerbating factors: infec- tivity to sensory stimuli), dysesthesias tion , trauma, pregnancy, stress. (abnormal sensations), trigeminal neural- (5) Transient worsening of symptoms: adverse gia, Lhermitte's sign (electric shock-like reactions to heat, hyperventilation, dehy- sensation throughout the body produced by dration, fatigue. flexing the neck). (6) Variable course: four main types identified- (6) Vision: diplopia or blurred vi ion common; also optic neuritis, scotoma (blind spot), nystagmus.
114 (2) Rehabilitation goals. (a) Restorative: intensive, time-limited (7) Skin integrity and condition. rehab services designed to improve/ (8) Muscle tone, DTRs: spasticity and hyper- stabilize patient status after a relapse. (b) Functional maintenance: services reflexia are common (pyramidal tract designed to manage effects of progres- lesions). sive disease, and prevent/minimize (9) Muscle strength and control: paresis is indirect impairments associated with common; if spasticity is severe, MMT may disuse and inactivity. be invalid. (lO)Coordination: ataxia is common; intention (3) Maintain ROM, prevent contracture. tremors, dysmetria, dysdiadochokinesia. (4) Maintain skin integrity, free of decubiti and (11)Balance: vestibular involvement common, with vertigo, dizziness, unsteadiness, other injury. paroxysmal or sudden onset of symptoms. (5) Improve respiratory function. (12)Gait: ataxic gait is common. (6) Improve sensory awareness, sensory com- (13)Fatigue patterns: early afternoon fatigue and exhaustion common with high energy pensation to prevent injury; consider eye periods in early morning, and some recov- patching with diplopia. ery in early evening. (7) Improve strength. (14)Respiratory status. (8) Improve motor control, coordination: teach (15)Functional status: functional mobility tone reduction techniques, compensatory skills, activities of daily living. strategies, safety. (16)Standardized tests and measures for (9) Improve postural control, symmetry, and patients with MS. balance; teach compen atory strategies and (a) Expanded Disability Status Scale safety, provide assistive devices for gait. (1 0)Promote independence in functional mobil- (EDSS)- Kurtzke. ity skills and activities of daily living; (b) Minimum Record of Disability (MRD)- supervise family/home health aides in assisting patient. International Federation of MS societies. (11)Promote maximum mobility in home and (c) Modified Fatigue Impact Scale. community; provide appropriate mobility e. Medical management. aids and adaptive equipment (wheelchair (1) Immunosuppressant drugs: treats acute use common); anticipate changes, rate of flare-ups and shortens duration of episode; disease progression. ACTH and steroids, e.g., Prednisone, (12)Teach energy con ervation techniques, Dexamethasone, Betamethasone, Methyl- activity pacing. prednisolone. (13)Avoid precipitating exacerbations: sched- (2) Interferon drugs: slow progression of dis- ule therapy sessions during optimal times ease, decrease symptoms, e.g., Avonex, for function; minimize fatigue, establish Betaseron, Copaxone. schedule of rest and moderate exercise; (3) Symptomatic management of spasticity: avoid stressors, overheating. drugs (e.g., Baclofen, Valium, Dantrium), g. Provide psychological and emotional support. Baclofen pump, phenol block surgery. (1) Emphasize realistic expectation; focus on (4) Symptomatic management of urinary remaining abilities. problems: anticholinergic drugs. (2) Provide patient, family, caregiver educa- f. Physical therapy goals, outcomes, and inter- tion. ventions. (3) Teach problem solving skills, emphasize (1) Monitor changes associated with disease coping skills. progression; revise rehabilitation plan 2. Parkinson's disease (PD): a chronic, progressive accordingly; develop/supervise mainte- disease of the CNS with degeneration of dopamin- nance program. ergic SN neurons and nigrostrial pathways. (a) Check for signs of urinary tract infec- a. Etiology: several different causes identified: tion, respiratory infection (common causes of death).
infectious/postencephalitic, atherosclerosis, Neuromuscular Physical Therapy 115 idiopathic, toxic, drug induced. (1) Deficiency of dopamine within the basal aching and stiffness, abnormal sensations (cramplike sensations, poorly localized), ganglia corpus striatum with degeneration problems in spatial organization, percep- of substantia nigra. tion of vertical, extreme restlessness (2) Los of inhibitory dopamine results in (akathisia). exce sive excitatory output from choliner- (8) Vision: check for blurring, cogwheeling gic system (acetylcholine) of basal ganglia. eye pursuit, eye irritation from decreased b. Characteristics. blinking, decreased pupillary reflexes. (1) Classic symptoms: rigidity, (leadpipe, cog- (9) Skin integrity and condition, circulatory wheel), bradykinesia (hypokinesia), resting changes: edema may occur in lower tremor (resting), impaired postural reflexes. extremities; increased sweating (ANS dys- (2) Slowly progressive with emergence of sec- function); decubitus ulcers in late stages. ondary impairments and permanent dys- (lO)Muscle tone: check for rigidity including function. location, distribution and symmetry (3) Stages (Hoehn and Yahr Classification): between two sides of body, type (cogwheel I. Minimal or absent disability, unilateral or leadpipe). (11)Muscle strength: weakness is associated symptoms. with disuse and atrophy; assess torque out- II. Minimal bilateral or midline involve- put at varying speeds (isokinetics). (12)Motor function: check for bradykinesia ment, no balance involvement. (slowed movement) or akinesia (absent ill. Impaired balance, some restrictions in movement), ability to initiate movement (number of freezing episodes, precipitating activity. factors); assess reaction time versus move- IV. All symptoms present and severe. ment time, overall poverty of movement. (13)For innvoluntary movements: check for Stands and walks only with assistance. presence, location of tremor, precipitating V. Confinement to bed or wheelchair. factors; resting tremor common, especially c. Examine. pill-rolling of hands; tremors during move- (1) History: symptoms, disease progression, ment may occur in advanced stages; pos- functional deficits. tural tremors. (2) Cognitive/behavioral status: intellectual (14)Balance: impaired postural reactions are impairment/dementia occur in advanced common (worse with severe rigidity of stages; check for memory deficits, trunk, lack of trunk rotation); check for bradyphrenia (slowing of thought process- ability to maintain both static and dynamic es), depression. balance, reactive adjustments and anticipa- (3) Communication: dysarthria, hypophonia tory adjustments. (decreased volume) are common; mutism (15)Gait: characterized by poverty of move- in advanced stages; masklike face with ments, with generalized lack of extension; infrequent blinking and expression, writing festination cornmon (an abnormal, involun- becomes progressively smaller. tary increase in the speed of walking, often (4) Oromotor control, nutritional status: dys- with forward acceleration but may occur phagia is common, problems in chewing with backward progression). and swallowing. (16)Functional status. (5) Respiratory status: breathing patterns, vital (17)Overall level of endurance: fatigue and capacity; decreased chest expansion com- inability to sustain performance is common, mon. affected by stress, high effort; cardiovascu- (6) ROM, deformity associated with disuse lar deconditioning occurs with long-standing and inactivity: contractures common in disease. flexor, adductors; persistent posturing in (18)Patients on Levadopa: check for fluctua- kyphosis with forward head; many patients o teoporotic with high risk of fracture. (7) Sensation/perceptual function: check for
116 technique). (5) Teach relaxation skills. tions in symptoms related to dosing (end of (6) Improve postural control, symmetry and dose deterioration, on-off phenomenon, dyskinesia); common with disease progres- balance; teach compensatory strategies, sion and long-term use of L-dopa, e.g., 2-3 safety. years. (7) Promote independence in functional mobil- (19)Standardized tests and measures for ity skills, activities of daily living; super- patients with PD. vise family/home health aides in assisting (a) Unified Rating Scale for Parkinsonism. patient. d. Medical management. (8) Promote maximum mobility and safety in (1) Sinemet (carbidopa), or sustained-release home and community, improve gait: pro- Sinemet: provides dopamine (crosses vide appropriate aids and adaptive equip- blood-brain barrier) and decreases effects ment; anticipate changes, progression of of disease; effect is prolonged with low- disease. protein diet. Numerous adverse effects (9) Improve cardiovascular endurance. including nausea and vomiting, orthostatic (lO)Teach energy conservation techniques, hypotension, cardiac arrhythmias, involun- activity pacing. tary movements (dyskinesias), and psy- (1 1)Provide psychological and emotional sup- choses and abnormal behaviors (hallucina- port (see section on MS). tions are quite common). In on-off phe- 3. Myasthenia gravis (MG): a neuromuscular junc- nomenon, patients experience sudden tion disorder characterized by progressive muscu- changes from normal function to immobility lar weakness and fatigability on exertion. to severe dyskinetic movements. a. Etiology: autoimmune antibody-mediated (2) Dopamine agonist drugs: enhance the attack on acetylcholine receptors at neuromus- effects of Sinemet therapy (Bromocriptine, cular junction. Pergolide mesylate). b. Characteristics. (3) Anticholinergic drugs: for control of (1) Muscular strength worse with continuing tremor. contraction, improved with rest. (4) Amantidine: enhances dopamine release. (2) Classified into four types: ocular myasthe- (5) Selegiline (deprenyl): an MAO inhibitor nia (confined to extraocular muscles), mild increases dopamine; used during early generalized myasthenia, severe generalized disease to slow progression. myasthenia, and crisis. (6) Surgery: thalamotomy, pallidotomy, deep (3) Generalized myasthenia: usually involves brain stimulation in thalamus or subthalam- bulbar (extraocular, facial, and muscles of ic nucleus, cell transplant. mastication) and the proximal limb-girdle e. Physical therapy goals, outcomes, and inter- muscles. ventions. (4) Course is variable: may progress from mild (1) Monitor changes associated with disease to severe, typically within 18 months. progression and pharmacological interven- (5) Myasthenic crisis: myasthenia gravis with res- tions; revise rehabilitation plan according- piratory failure; treat as medical emergency. ly; develop/supervise maintenance pro- c. Examine. gram. (1) Cranial nerves: check for diplopia and pto- (2) Prevent or ffilnlIillze secondary impair- sis; progressive dysarthria or nasal speech; ments associated with disuse and inactivity difficulties in chewing and swallowing; dif- (refer to section on MS). ficulties in facial expression, drooping (3) Teach compensatory strategies to initiate facial muscles. movement (unlock freezing episodes); (2) Respiratory function: breathing difficulties, repetitive auditory stimulation (RAS). hoarse voice. (4) Improve strength: emphasis on improving (3) Muscle strength: proximal more involved overall mobility, rotational patterns (con- than distal. Fatigability is characteristic of sider PNF patterns, rhythmic initiation
this di ease; repeated muscle use results in Neuromuscular Physical Therapy 117 rapid weakness. (4) Functional mobility skills: common diffi- sudden attack of anxiety, tachycardia, culties with climbing stairs, rising from sweating, piloerection, abnormal sensation chair or lifting (similar to myopathies). rising up in upper abdomen and chest. (5) EMG and repetitive nerve stimulation stud- (5) Cognitive phenomena: sudden failure of ies conclusive: shows abnormal responses comprehension, inability to communicate, to repetitive nerve stimulation (failure of intrusion of thought, illusions, hallucina- transmission, decreased EMG-recorded tions, affective disturbances (intense feel- re ponses). ings of fear, anger and hate). d. Medical interventions. c. Primary, generalized seizures: bilateral and (1) Acetylcholinesterase (ACE) inhibitors: symmetrical, without local onset. e.g., pyridostigmine. (1) Tonic-clonic (grand mal): dramatic loss of (2) Corticosteroids: e.g., prednisone, methyl- consciousness, with a cry, fall, and tonic- prednisolone. clonic convulsions of all extremities; often (3) Immunosuppressants: e.g., Azathioprine, with tongue biting and arrested breathing, intravenous immunoglobulin (IVIG). urinary and fecal incontinence; after 2 to 5 (4) Alternate treatments include: IV minutes, contractions subside and con- immunoglobulin, plasmapheresis (removal sciousness is gradually regained; the of blood with filtering and separation of cel- patient is confused, drowsy, and amnesiac lular element from plasma); thymectomy. about the event; full recovery may take sev- e. Physical therapy goals, outcomes, and inter- eral hours; some attack are preceded by a ventions. brief aura. (1) Monitor changes in patient's condition for (2) Absence seizures (petit mal): brief, almost complication: vital signs, respiration, imperceptible lapse of consciousness, fol- swallowing. lowed by immediate and full return to con- (2) Promote independence in functional mobil- sciousness; posture is maintained, with no ity kills and activities of daily living. convulsive muscle contractions; may occur (3) Teach energy conservation techniques; as often as a hundred times a day. activity pacing: promote optimal activity d. Partial seizures. with rest as indicated. (1) Simple partial seizures: focal, begin local- (4) Provide p ychological and emotional sup- ly, limited to a portion of the body, usually port. have an identifiable structural cause. E. Epilepsy: abnormal and excessive neuronal discharges (a) Focal motor: clonic activity involving a due to disturbances of CNS I. Characteristics. specific area of the body. a. Etiology: brain tumor; trauma; stroke; progres- (b) Focal motor with march (Jacksonian): sive neurologic disease; hereditary disorders, congenital anomalies; febrile states; idiopathic. an orderly spread or march of clonic b. Symptoms. movements from initial muscles to (1) Altered consciousness. involve adjacent muscles, with spread (2) Altered motor activity (convulsion): char- to the entire side. acterized by involuntary contractions of (c) Temporal lobe seizure: characterized mu cle ; tonic activity (stiffening and by episodic changes in behavior, with rigidity of muscles); clonic activity (rhyth- complex hallucinations; automatisms mic jerking of extremities). (e.g., lip smacking, chewing, pulling (3) Sensory phenomena: the experiencing of on clothing); altered cognitive and omato ensory, visual, auditory, olfactory, emotional function (e.g., sexual arous- gustatory, vertiginous sensations. al, depression, violent behaviors); pre- (4) Autonomic phenomena: associated with ceded by an aura. (2) Complex partial seizures: simple partial seizures followed by impairment of con- sciousness. f. Status epilepticus: prolonged seizure or a series
118 dysmetria, poor eye pursuit, dysfunc- tional vestibular ocular reflex (VOR), of seizures (lasting more than 30 min.) with impaired eye-hand coordination. very little recovery between attacks; may be (b) Gait and trunk ataxia: poor postural life-threatening, consider as medical emer- control and orientation, wide-ba ed gency (generalized status epilepticus). gait. 2. Examine/determine. (c) Little change in tone or dyssynergia of a. Time of onset, duration, type of seizure, extremity movement. sequence of events. (2) Lesions of the paleocerebellum. b. Patient activity at onset, presence of aura. (a) Hypotonia. c. Sensory elements, motor activity: type, degree (b) Truncal ataxia: dysequilibrium, static and location of involvement. postural tremor, increased sway, wide d. Presence of tongue biting, incontinence, respi- BOS and high guard arm position. ratory distress. Posture worse with eyes closed, narrow e. Behavioral elements, changes in mood, percep- BOS (Romberg, Sharpened Romberg). tion. (c) Ataxic gait: unsteady, increased falls, f. Patient responses after the seizure. uneven/decreased step length, increased 3. Medical interventions. step width. a. Antiepileptic medications, e.g., phenytoin (2) Lesions of the neocerebellum produce (Dilantin), carbamazepine (Tegretol), pheno- ataxic limb movements. barbital, etc. (a) Intention tremor: irregular, oscillatory b. Surgical intervention: lobe resection, hemi- voluntary movements. spherectomy. (b) Dysdiadochokine ia: impaired rapid 4. Physical therapy goals, outcomes, and interven- alternating movement (RAM). tions. (c) Dysmetria: hypermetria (overshoot- a. Protect patient from injury during seizure: ing), errors or force, direction, ampli- remain with patient, remove potentially harm- tude, rebound phenomenon (Holmes). ful nearby objects, loosen restrictive clothing, (d) Dyssynergia: abnormal timing (errors do not restrain limbs. of velocity, on et and top), movement b. Establish airway, prevent aspiration: turn head decomposition of agonist/antagonist to side or position in sidelying; check to see if interactions. Impairments of multi- airway is open, wait for tonic-clonic activity to joint coordination, movement sequences, subside before initiating artificial ventilation if complex motor tasks. needed. (e) Errors in timing related to perceptual c. Promote regular routines for physical activity tasks. and emotional health. (3) Additional impairment. F. Cerebellar Disorders (a) Asthenia: generalized weakness (F to a. Diseases/lesions of the cerebellum. G muscle grades). (1) Hereditary ataxia, Friedreich's ataxia. (b) Hypotonia: especially in acute cerebel- (2) Neoplastic or metastatic tumors. lar lesions, difficulty with postural (3) Infection. control of proximal (axial) muscles. (4) Vascular: stroke. (c) Motor learning impairments: decreased (5) Developmental: ataxic cerebral palsy, anticipatory control, feedback and learning delays. Arnold-Chiari syndrome. (d) Cognition: deficits in information pro- (6) Trauma: TBI. cession, attention deficits. (7) Drugs, heavy metals. (e) Emotional dysregulation: changes in (8) Chronic alcoholism. emotional behaviors. b. Lesions/impairments of the cerebellum. Cerebellar c. Examine. lesions tend to produce ipsilateral signs and (1) Muscle strength, tone. symptoms. (1) Lesions of the archicerebellum. (a) Central vestibular symptoms: ocular
(2) Range of motion. Neuromuscular Physical Therapy 119 (3) Coordination: determine abnormalities of enhance stability and postural control (i.e. coordinated movement. balance training platform). (4) Balance: determine abnormalities of pos- (11)Energy conservation techniques, assistive devices as needed. tural control and balance. G. Vestibular Disorders (5) Gait: determine abnormalities of gait 1. Characteristics. a. Dizziness: sensation of lightheadedness, giddi- (ataxic gait). ness, faintness; increased risk of falls. (6) Motor function: determine abnormalities of b. Vertigo: sensation of moving around in space, or having objects move around a person; tends motor learning. to come in attacks; if severe, accompanied by (7) Functional status. nausea and vomiting. (8) Endurance and fatigue level: fatigue is c. Visual changes. (1) Nystagmus: involuntary, cyclical move- common with dysmetric patients. ment of the eyeball, e.g., horizontal, rotary. d. Phy ical therapy goals, outcomes, and inter- (2) Blurred vision: gaze instability secondary to vestibular ocular reflex (VOR) dysfunction. ventions. d. Dysequilibrium or postural instability: vestibu- (1) Goals. lar spinal reflex (VSR) dysfunction; ataxia, gait disturbances; increased risk of falls. (a) Improve accuracy of limb movements. e. Anxiety, fear, depression. (b) Improve postural stability and dynam- f. Indirect impairments: physical deconditioning, decreased cervical ROM. ic postural control. 2. Etiology: unilateral vestibular disorders (UVD). (c) Improve functional mobility and safe- a. Trauma: vestibular symptoms seen in 30% to 65% of patients with traumatic brain injury. ty: transfers and gait. b. Vestibular neuronitis, labyrinthitis: an acute (d) Stabilize VORlvision. infection with prolonged attack of symptoms, (2) Eye-head coordination exercise: slow head persisting for several days or several weeks; movements with visual fixation; active eye caused by viral or bacterial infection. and head movements. c. Meniere's disease: recurrent and usually pro- (3) Stability exercises: use of weight-bearing gressive vestibular disease; episodic attacks po tures, carefully graded resistance and may last from minutes to several hours with approximation to promote steady holding. severe symptoms; usually associated with tin- Use of theraband, weights (ankle and wrist nitus, deafness, sensation of pressure/fullness cuffs), weighted waist belts and walkers to within ear; etiology unknown, edema of mem- decrea e ataxic movements. branous labyrinth is a consistent finding. (4) Dynamic stability exercises: promote small d. Benign paroxysmal positional vertigo (BPPV): range control, smooth reversals of move- brief attacks of vertigo and nystagmus that ments, movement transitions, using care- occur with certain head positions (lying down, fully graded resistance. turning over in bed, tilting head back); may be (5) Balance training: compensatory training/ related to degenerative processes, mechanical safety important. Standing balance and gait impairment of peripheral vestibular system. activities. e. Tumor: acoustic neuroma, gliomas/brainstem (6) Therapeutic pool: water provides graded or cerebellar medulloblastoma. resistance, decreases ataxic movements and 3. Etiology: bilateral vestibular disorders (BVD). postural instability. a. Toxicity: ototoxic drugs. (7) Coordination exercises: PNF patterns, b. Bilateral infection: neuritis, meningitis. Frenkel's exercises, ball gymnastics to pro- c. Vestibular neuropathy, oto clerosi (Paget's mote balance. disease). (8) Stationary bike: assists timing of reciprocal movements. (9) Motor learning strategies: low stimulus environment (closed environment) ideal; focus on practice and repetition; distributed practice (endurance may be low). (10)Biofeedback: augmented feedback to
120 VSR as much as possible. (a) Eye and head exercises, e.g., eye 4. Examine. a. History: determine type, nature, duration of movements up and down, side to side; symptoms, triggering stimuli/activity. head movements up and down, side to b. Subjective assessment: Dizziness Handicap side progressing slow to fast. Inventory (DHI). (b) Exercises to improve postural stability: c. VOR function: check for nystagmus, blurred sitting and standing, static and dynam- vision with head and total body movements. ic activitie , e.g., bending forward, d. Sensory function. turning, Swiss ball exercises. (1) Check for intact vision, proprioception (3) Empha ize functional mobility skills: especially of feet/ankles. Important for walking, turning, stairs, community activi- compensatory postural adjustments with ties, activities with spatial and timing con- vestibular losses. straints. (2) Clinical Test for Sensory Interaction in (4) Relaxation training: to decrea e anxiety Balance (CTSIB): check for instability levels. when vision and support surface are altered (5) Begin conservatively, avoid excessive exac- (conditions 5 + 6). erbation of symptoms. e. VSR function: examine posture and balance; d. Recovery is better, generally faster in unilater- check for instability in sitting, standing, during al than bilateral ve tibular dysfunction. functional activities and gait. e. Provide psychological support and reassur- f. Responses to positional changes. ance. (1) Hallpike maneuver: from sitting, move H. Cranial and Peripheral Nerve Disorders patient quickly back to supine, with head 1. Peripheral nerve disease/injury. extended back 30 degrees over end of table; a. Etiology: wide range of etiologic factors (more elicits vertigo and ny tagmus; tests for than 100 distinct disea es). benign paroxysmal positional vertigo. b. Basic pathologic proce e. (2) Check responses to head movements, (1) Wallerian degeneration: tran ection (neu- movement tran itions. rotrnesis) result in degeneration of the g. ROM: special attention to cervical ROM. axon and myelin sheath di tal to the site of h. Vertebral artery compression: can produce axonal interruption. ve tibular symptoms (i.e., in supine, extend, (a) Chromatolysis and repair processes laterally flex, and rotate head, hold for 30 sec- occurs in nerve cell body. onds; each side tested separately). (b) Endoneurium (sheath) does not degen- I. Functional status: determine current level of erate but forms a tube directing regen- activity. eration. (2) Segmental demyelination: axons are pre- 5. Medical interventions: vestibular suppressant served (no Wallerian degeneration); medications; prolonged use may delay recovery; remyelination restores function (e.g., severe cases may require ablative surgery. Guillain-Barre Syndrome). (3) Axonal degeneration: degeneration of axon 6. Physical therapy goals, outcomes, and interven- cylinder and myelin, progressing from di - tions. tal to proximal, \"dying back\" of nerves a. Bedrest: brief, useful during initial stages only; (e.g., peripheral neuropathy). prolonged bedrest may delay recovery. c. Terminology. b. Implement safety measures: teach sensory sub- (1) Neuropathy (peripheral neuropathy): any stitution, compensatory trategies; provide disease of nerve characterized by deterio- ambulatory aids as indicated, e.g., cane, walker. rating neural function e.g., diabetic neu- c. Provide active exercises to promote vestibular ropathy, alcoholic neuropathy. adaptation (recalibration of ystem). (a) Polyneuropathy: bilateral symmetrical (1) Habituation training: repetition of move- involvement of peripheral nerves, usu- ments and position that provoke dizziness and vertigo. (2) Encourage movement, engage VOR and
ally legs more than anns, di tal seg- Neuromuscular Physical Therapy 121 ments earlier and more involved than proximal. dence of reinnervation (low amplitude, (b) Mononeuropathy: involvement of a short duration, polyphasic motor unit ingle nerve. potentials). (2) Radiculopathy: involvement of nerve roots. 2. Trigeminal neuralgia (tic douloureux): neuralgia (3) Traumatic nerve injury. of the trigeminal nerve (C.N.V). (a) Neurapraxia (Class I): injury to nerve a. Etiology: results from degeneration (etiology that causes a transient loss of function unknown) or compression (tortuous basilar (conduction block ischemia); nerve artery or cerebellopontine tumor); occurs in older dysfunction may be rapidly reversed or population (mean age around 50); abrupt onset. persist a few weeks, e.g., compression. b. Characteristics: brief paroxysms of neurogenic (b) Axonotmesis (Class 2): injury to nerve pain (stabbing and/or shooting pain); reoccur- interrupting the axon and causing loss ring frequently. of function and Wallerian degeneration (1) Occurs along the distribution of the trigem- distal to the lesion; with no disruption inal nerve, mandibular and maxillary divi- of the endoneurium, regeneration is sions (involvement of ophthalmic division pos ible, e.g., crush injury. is rare); restricted to one side of the face. (c) Neurotme is (Class 3): cutting of the (2) There is autonomic instability: exacerbated nerve with everance of all structures by stress, cold; relieved by relaxation. and complete loss of function; reinner- c. Examine/determine. vation typically fails without surgical (1) Pain: location, intensity. intervention because of aberrant regen- (2) Trigger points: light touch to face, lips, or eration (failure of regenerating axon to gums will cause pain. find it terminal end). (3) Triggering stimuli: extremes of heat or d. Clinical symptoms LMN syndrome (Table 2-3). cold, chewing, talking, brushing teeth, (1) Weakness/paresis of denervated muscle, movement of air across the face. hyporeflexia and hypotonia, (rapid) atrophy, (4) Motor function: control is normal. fatigue. d. Medical: medications (anticonvul ants, vita- (2) Sensory loss: corresponds to motor weak- min B12); alcohol injections, surgery ( ection- ne ; proprioceptive losse may yield sensory ing of nerve, permanent anesthesia). ataxia; in en itivity may yield limb trauma. e. Transcutaneous nerve stimulation (TENS) can (3) Autonomic dysfunction: vasodilation and be effective for pain relief. 10 s of vasomotor tone (dryness, wann 3. Bell's Palsy (Facial Paralysis): a LMN lesion skin, edema, orthostatic hypotension). involving C.N. VII (facial nerve), resulting in uni- (4) Hyperexcitability of remaining nerve lateral facial paralysis. fibers. a. Etiology: acute inflammatory process of (a) Sensory dysesthesias: hyperalgesia, unknown etiology (immune or viral disease) pins and needles, numbness, tingling, resulting in compression of the nerve within burning. the temporal bone. (b) Motor: fasciculations, spasms. b. Characteristics. (5) Muscle pain (myalgia) with inflammatory (1) Muscles of facial expression on one side myopathies (e.g., post polio syndrome). are weakened or paralyzed. e. Diagno tic tests. (2) Lo s of control of salivation or lacrimation. (1) erve conduction studies (NCV): conduc- (3) Onset is acute, with maximum everity in a tion times (motor, sensory) are slowed or few hours or days; commonly preceded by complete conduction block may be evident. a day or two of pain behind the ear; most (2) EMG (motor nerve function): check for recover fully in several week or months. signs of widespread denervation atrophy (4) Sensation is normal. (pontaneous fibrillation potentials); evi- c. Examine/determine. (1) Drooping of comer of mouth, eyelids that don't close.
122 e. Physical therapy goals, outcomes, and inter- ventions. (2) Function of muscles of facial expression: (1) Suctioning, oral care. have patient wrinkle forehead, raise eye- (2) Maintenance of respiratory function, open brows, frown, smile, close eyes tightly, puff airway. cheeks. (3) Elevate head of bed. (4) Dietary change: oft food, liquids. (3) Taste of the anterior 2t3s of tongue. d. Medications: corticosteroids (prednisone); 5. Guillain-Barre syndrome (GBS, acute ascending, symmetrical polyneuropathy): polyneuritis with pro- analgesics. gressive muscular weakness that develops rapidly. e. Physical therapy goals, outcomes, and inter- a. Etiology: unknown; associated with an autoim- mune attack, usually occurs after recovery ventions. from an infectious illness (respiratory or gas- (1) Protect cornea (artificial tears or temporary trointestinal). b. Characteristics. patching) until recovery allows for eyelid (1) Involves acute demyelination of both cra- closure. nial and peripheral nerves (LMN disease). (2) Electrical stimulation to maintain tone, (2) Sensory loss, paresthesias (tingling, burn- support function of facial muscles. ing), pain; sensory loss is typically less (3) Provide active facial muscle exercises. than motor loss. (4) May require face sling to prevent over- (3) Motor paresis or paralysis: relative sym- stretching of facial muscles. metrical distribution of weakness; pro- (5) Provide functional retraining: foods that gresses from lower extremities to upper can be easily eaten, chewing with opposite (ascending pattern) and from distal to prox- side. imal; may produce full tetraplegia with res- (6) Provide emotional support and reassurance. piratory failure. 4. Bulbar Palsy (bulbar paralysis): refers to weakness (4) Dysarthria, dysphagia, diplopia, and facial or paralysis of the muscles innervated by the weakness may develop in severe cases. motor nuclei of the lower brainstem, affecting the (5) Progression evolves over a few days or muscles of the face, tongue, larynx, and pharynx. weeks; recovery usually slow (6 months to a. Etiology: the result of tumors, vascular or degen- 2 years) and usually complete (85% of erative diseases of lower cranial nerve motor cases); some mild weakness may persist; nuclei, (e.g., amyotrophic lateral sclerosis). 3% mortality. b. Examine/determine. (6) Complications. (1) Glossopharyngeal and vagal paralysis: (a) Respiratory impairment and failure. phonation, articulation, palatal action, gag (b) Autonomic instability: tachycardia, reflex, swallowing. arrhythmias, BP fluctuations. (2) Changes in voice quality: dysphonia (c) Pain: myalgia. (hoarseness or nasal quality). (d) Risk of pneumonia. (3) Bilateral involvement: severe airway (e) Prolonged ho pitalization and immobil- restriction with dyspnea, difficulty with ity: DVT, skin breakdown, contracture. coughing. (f) Relapse: if treatment is inadequate. (4) Possible complications: aspiration pneu- c. Examine. monia. (1) Cardiac and respiratory status, vital signs. c. Pseudobulbar palsy: bilateral dysfunction of (2) Cranial nerve function (VII, IX, X, XI, corticobulbar innervation of brainstem nuclei; XIl). a central or UMN lesion analogous to corti- (3) Motor strength (serial MMTs indicated). cospinal lesions disrupting function of anterior (4) Reflexes: decreased or absent tendon horn cells. reflexes. (1) Produces similar symptoms as bulbar palsy. (5) Sensation: changes can include paresthe- (2) Check for hyperactive reflexes: increased jaw jerk, and snout reflex (tapping on lips produces pouting of lips). d. MedicaUsurgical treatment of underlying cause.
sias, anesthe ias, hyperesthesias, pain euromuscular Physical Therapy 123 (muscle aching, burning); may have stock- ing and glove distribution (anesthesia of (3) Spasticity, hyperreflexia (UMN signs). distal extremities in a pattern as if the (4) Dysarthria, dysphagia, dysphonia second- patient were wearing long gloves and stockings). ary to pseudobulbar palsy and progressive (6) Functional tatus. bulbar palsy. d. Medical. (5) Usually absence of ensory changes; small (1) Good nursing care. number (20%) may show sensory deficits. (2) Plasmapheresis. (6) Autonomic dysfunction in about one third (3) Intravenous immunoglobulin (IVIG). of patients. (4) Analgesics for relief of pain. (7) Pain due to spasticity, cramping, postural e. Physical therapy goals, outcomes, and inter- stress syndrome, joint hypomobility or ventions. instability. (1) Maintain respiratory function: may require (8) Respiratory impairments:weakness >paral- endotracheal intubation, tracheotomy and ysis, nocturnal difficulty, exertional dysp- ventilation; pulmonary physical therapy. nea, accessory muscle use; paradoxical (2) Prevent indirect impairments: PROM with- breathing, ventilator dependent; poor in pain tolerance, positioning and skin care. cough, clearance of secretions. (3) Prevent injury to denervated muscles: mon- (9) Typical sparing of bowel and bladder func- itor recovery; splinting, positioning. tion. (4) Provide muscle reeducation, moderate (lO)Cognition is normal, similar to locked-in exercise program (active assistance and syndrome (CVA). active exercise progressing to resistive), (ll)Depression common. functional training as recovery progresses. c. Stages of ALS. (5) Teach energy conservation techniques and (1) Stage I: early disease, mild focal weakness, activity pacing: avoid overuse and fatigue asymmetrical distribution; symptoms of which may prolong recovery. hand cramping and fasciculations. (6) Improve cardiovascular fitness following (2) Stage II: moderate weakne s in groups of prolon&ed bedrest and deconditioning. muscles, some wasting (atrophy) of mus- (7) Provide emotional support and reassurance cles; modified independence with assi tive to patient and family. devices. 6. Amyotrophic lateral sclerosis (ALS, \"Lou (3) Stage ill: severe weakness of specific mus- Gehrig' disease\"): a degenerative disease affecting cles, increasing fatigue; mild to moderate both upper and lower motor neurons (degeneration functional limitations, ambulatory. of anterior hom cells and descending corticobulbar (4) Stage IV: severe weakness and wasting of and corticospinal tracts). LEs, mild weakness of UEs; moderate a. Etiology: unknown (viraVautoimmune, toxic); assistance and assistive devices required; 5-10% genetic (autosomal dominant). wheelchair user. b. Characteristics. (5) Stage V: progressive weakness with deteri- (1) Progressive disease, often leading to death, oration of mobility and endurance, typically in 2 to 5 years; highly variable increased fatigue, moderate to severe symptoms. weakness of whole limbs and trunk; spas- (a) Bulbar onset (progressive bulbar palsy). ticity, hyperreflexia; loss of head control; (b) Spinal cord onset (progressive muscu- maximal assist. (6) Stage VI: bedridden, dependent ADL, lar atrophy). FMS; progressive respiratory distress. (2) Mu cular weaknes that spreads over time: d. Examine. (1) History: varied pattern of onset. early onset involves limbs progressing to (2) Vital signs, respiratory function. whole body; atrophy, cramping, muscle (3) Cranial nerve function: especially lower fasciculations or twitching (LMN signs). cranial nerves (VII, IX, X, XI, XII). (4) Motor function.
124 (avoid exercise if less than 113 of motor units are functioning); limited posi- (a) Check for atrophy, widespread weak- tions with decreased pulmonary func- ness; a symmetrical distribution, mus- tion. cle cramping, and muscle twitching. (d) As disease progre es, replace resist- ance exercises with functional training (b) Check for spasticity, hyperreflexia. activitie . (c) Coordination tests: manual skills. (5) Teach energy conservation activity, pacing (5) Sensory function. techniques, e.g., balance activity with rest. (6) Gait: timed walk (10m walk test). (6) Maintain maximal functional independ- (7) Functional status: monitor closely for over- ence: provide appropriate assistive devices, work fatigue, persistent weakness follow- orthotic support, wheelchair, environmen- ing exercise or activity, e.g., keep activity tal adaptations; anticipate needs. log. (7) Symptomatic treatment of pain, spasms, (8) ALS Functional Rating Scale (ALSFRS): spasticity. assesses di ease progre sion and function (8) Teach patient, family, caregivers all care, acros 10 functional categories; scored 0 activities of daily living; assist in utilization (los of function) to 4 (normal function); 40 of community re ource . maximal score. (9) Provide psychological upport and reassur- e. Medical management: there is no effective ance, maximum comfort; los of control is treatment for this disease. an important issue. (1) Riluzole, a glutamate antagonist, may slow 7. Post-polio syndrome, PPS (Progre ive Post-Polio progression, prolong survival especially muscular atrophy, PPPMA): new, slowly progres- with bulbar onset disease. sive muscle weakness occurring in individuals (2) Symptomatic relief: i.e., spasticity, pain, with a confirmed history of acute poliomyelitis; respiratory failure. follows a stable period of functioning. f. Physical therapy goals, outcomes, and inter- a. Etiology: unknown; possible hyperfunctioning ventions. of motor neurons, long term overuse at high (1) Maintain respiratory function: may require levels resulting in new denervation. airway clearance techniques, cough facili- b. Characteristics: tation, breathing exercises, chest stretching, (1) New weakness and atrophy, a ymmetrical suctioning, incentive spirometry, long-term in distribution. Occur in both initially mechanical ventilation. weak and uninvolved muscle . (2) Provide for nutritional needs: assist in man- (2) Abnormal fatigue: may not be related to agement of dysphagia; may require naso- activity levels, doesn't recover easily with gastric tube or percutaneous gastrostomy in usual rest periods. later stages. (3) Pain: myalgia, cramping pain, joint pain (3) Prevent indirect impairments: maintain with repetitive injury, hypersen itivities. activity levels as long as possible, PROM, (4) Decreased function with reduced positioning, skin care. endurance for routine activities. (4) Provide moderate exercise program. (5) Slow progression, either steady or stepwise. (a) Prevent further deconditioning and dis- (6) Environmental cold intolerance. (7) Difficulty in concentration, memory, atten- use atrophy while avoiding overwork tion; damage to reticular formation, hypo- damage in weakened, denervated mus- thalamus, dopaminergic neurons (brain cle; e.g., mild resistive exercises if fatigue generator model). muscles are in good to normal ranges; (8) Sleep disturbance . active exercises or functional activities (9) Decreased functional mobility, aerobic as weakness progresses. capacity, labile exercise blood pressures. (b) Mild aerobic activities: e.g., swim- (10)Slow progression, can be steady or stepwise. ming, walking stationary bike (sub- maximal levels). (c) Exercise precautions: monitor fatigue levels closely; avoid overwork injury
c. Examine. Neuromuscular Physical Therapy 125 (I) History: confirm original acute polio ill- ness; document onset of present symptoms, activity pacing: balance activity with fre- presentation, course, chronology. quent rest periods to decrease fatigue, pre- (2) Motor function: strength, atrophy, muscle vent overwork damage in weakened, dener- fatigue, muscle twitching and cramps. vated muscle. (a) Identify problem musculature, weak- (a) Teach relaxation techniques to maxi- ness found in both new muscles and muscles previously affected by polio. mize rest. (b) Identify functional contractions (fair (b) Avoid unnecessary activities to maxi- grades or above). (c) Look for spotty involvement, asym- mize important work. metrical paralysis. (3) Preserve or increase muscle strength. (3) ROM and deformity. (4) Pain. (a) Provide moderate exercise program (a) Muscle pain: check tenderness to (nonexhaustive exercise): modified touch. strengthening and conditioning; use (b) Skeletal, soft tissue pain: chronic over- low intensity, discontinuous non-fatigu- use, poor alignment. ing exercise with increased rest periods. (5) Sensory function: any sensory deficit is due to other etiology (sensation is unaffected in (b) Caution against widespread use of PPS). strength training. (6) Respiratory function: check for dyspnea, difficulty in speaking, weak cough. (c) Consider pool programs: minimizes (7) Functional status: functional mobility overwork, relieves pain; general body skills, activities of daily living. conditioning. (8) Endurance, activity levels: fatigue is a pri- mary symptom. (d) Foster weight control and reduction. (9) Aerobic capacity: use ergometer that (4) Aerobic conditioning: moderate to low involves both upper and lower extremities, e.g., Schwinn Air-Dyne, discontinuous pro- level training depending upon class of dis- tocol, submaximal test (ACSM recommen- ease, discontinuous protocol. In severe dation). atrophic polio, exercise is contraindicated. (lO)EMG to identify prior anterior horncell (5) Maintain or increase function: provide rec- (AHC) disease and new motor unit pathol- ommendations for lifestyle modification; ogy. See denervation changes, fascicula- minimize abnormal postures, gait deviations. tions, fibrillations, increased motor unit (6) Prescribe appropriate orthoses, mobility amplitude and duration. aids (motorized cart), assistive devices, (l1)Check for presence of depression or anxiety. environmental modifications. (7) Eliminate or control pain: provide options d. Medical management. for pain control, foster self-control. (1) Antidepressants: e.g., Elavil, Prozac. (8) Teach patient and family all care, activities (2) Neurotransmitter inhibitors: decreases of daily living; lifestyle modifications. fatigue and sleep disorders, e.g., serotonin, (9) Provide psychological support and reas- nor-epinephrine. surance. I. Pain: the sensory and emotional experience associated e. Physical therapy goals, outcomes, and inter- with actual or potential tissue damage (International ventions. Association for the Study of Pain) (1) Maintain respiratory function: teach 1. Pain pathways/neurophysiology. breathing exercises, supportive cough a. Fast pain: transmitted over A delta fibers (poly- maneuvers, postural drainage as indicated. modal, nonmyelinated), processed in spinal (2) Teach energy conservation techniques, cord dorsal hom lamina (I & V), crosses to excite lateral (neo) spinothalamic tract; terminates in brainstem reticular formation and thalamus with projections to cortex; functions for local- ization, discrimination of pain. b. Slow pain: transmitted over C fibers, processed in spinal cord lamina (II & ill to V), cross to excite anterior (paleo) spinothalamic tract; ter-
126 eral nerve or nerve root distribution. (a) Typically worse in distal limb than minates in brainstem reticular formation; excites reticular activating system (RAS), func- proximal. tions for diffuse arousal (protective/aversive (b) Precipitating trauma can be minor with reactions), affective and motivational aspects of pain; also terminates in thalamus with pro- time of onset of CPRS variable. jections to cortex. (c) Pain is severe, out of proportion to c. Intrinsic inhibitory mechanisms. (1) Gate control theory: transmission of sensa- original injury. (d) Early symptom include: vasodilation tion at spinal cord level is controlled by balance between large fibers (A alpha, A in skin, abnormal weating, edema, beta) and small fibers (A delta, C); activity and skin atrophy. of large fibers at level of first synapse can (e) Late changes include: atrophy of skin, block activity of small fibers and pain muscles, and joints; osteoporosis. May transmission (counter-irritant theory). develop muscles pare is and spasm (2) Descending analgesic systems: endogenous (3) Reflex sympathetic dystrophy, (RSD) (al 0 opiates (endorphins, enkephalins) pro- known a Causalgia, Shoulder-Hand duced throughout CNS (e.g., periaqueduc- Syndrome, and Sudeck's Atrophy): diffuse, tal gray, raphe nuclei, pituitary gland/hypo- persistent pain involving central reorgani- thalamus, SC laminae I and II); can depress zation of sensory systems. Typically devel- pain transmission at various sites through ops as a result of trauma to a peripheral mechanisms of presynaptic inhibition. pathway with sympathetic overactivity. 2. Acute pain: pain provoked by noxious stimulation, Categorized as a syndrome under CPRS. associated with an underlying pathology (injury or Three stages have been defined acute inflammation/disease); signs include sharp (a) Acute or early stage: characterized by pain and sympathetic changes (increased heart diffuse, severe burning or aching pain; rate, increased blood pressure, pupillary dilation, increases with emotional stress; allo- sweating, hyperventilation, anxiety, protective/ dynia (pain on light touch) and hyper- escape behaviors). pathia (increased sensitivity to normal 3. Chronic pain: pain that persists beyond the usual stimuli); vasomotor instability with course of healing; symptoms present for greater dusky mottling, cool skin, swelling and than 6 months for which an underlying pathology edema. is no longer identifiable or may never have been (b) Dystrophic or middle stage: kin present. change with thin, pale, cyanotic kin; 4. Pain yndromes: ces ation of hair and nail growth; a. Neuropathic pain: pain as a result of lesions in hyperhidrosis; muscle atrophy and some part of the nervous system (central or osteoporosis. peripheral); usually accompanied by some (c) Atrophic or late stage; decreased degree of sensory deficit. hypersensitivity; normal blood flow (1) Thalamic pain: continuous, intense, central and temperature; smooth, glossy skin; pain occurring on the contralateral hemi- severe muscles atrophy; pericapsular plegic side; the result of a stroke involving fibrosis; diffu e osteoporosis; develop- the ventral posterolateral thalamus; auto- ment of claw hand may occur. nomic and vasomotor dysfunction common. (4) Disorders of peripheral roots and nerves. (2) Complex regional pain syndrome (CRPS): (a) Neuralgia: pain occurring along the a complex disorder or group of disorders branches of a nerve; frequently parox- that develop as a consequence of trauma ysmal. affecting body partes) and disuse. The term (b) Radiculalgia: neuralgia of nerve roots. regional indicates signs and symptoms are (c) Paresthesias, allodynia: with nerve present throughout the limb (upper or injury or transection. lower limb) and not occurring in a periph- (5) Herpes Zoster (shingle ): an acute, painful mononeuropathy caused by the varicella-
zoster virus; characterized by vesicular Neuromuscular Physical Therapy 127 eruption and marked inflammation of the posterior root ganglion of the affected (3) Numerical rating scales (rate pain on a spinal nerve or sensory ganglion of the cra- scale of 1 to 10, e.g., 8/10). nial nerve; ventral root involvement (motor weakness) in 5%-10% of cases; infection (4) Visual analog scale (e.g., bisect line where can last from 10 days to 5 weeks; post-her- your pain falls, from mild to severe pain). petic neuralgia pain may persist for months or years. (5) Spatial distribution of pain: using drawings (6) Phantom limb pain: in a limb following to plot location, type of pain. amputation of that limb; differentiate from far more common phantom limb sensation. c. For underlying pathology (cause of pain); b. Musculoskeletal pain. objective physical findings are usually not (1) Fibromyalgia: widespread pain accompa- readily identified. nied by tenderness of muscles and adjacent (1) All systems: musculoskeletal, neurologic, soft tissues, a nonarticular rheumatic dis- cardiopulmonary. Check for muscle guard- ease of unknown origin. ing. (2) Myofascial pain syndrome (MPS): persist- (2) Check for postural stress syndrome (PSS). ent, deep aching pains in muscle, nonartic- (3) Check for movement adaptation syndrome ular in origin; characterized by well- (MAS): habituated movement dysfunction. defined, highly sensitive tender spots (trig- (4) Check for autonomic changes (sympathetic ger points). activity): typically present with acute pain (3) Postural Stress Syndrome (PSS): postural but not for chronic pain. malalignment produces chronic muscle lengthening and/or shortening and stress to d. Degree of suffering. soft tissues. (1) Verbal complaints are out of proportion to c. Pain with psychiatric disorders (psychosomatic degree of underlying pathology; include pain): the origin of the pain experience is due emotional content. to mental or emotional disorders. (2) Exhibits a stooped posture, antalgic gait. d. Headache and craniofacial pain, e.g., temporo- (3) Exhibits facial grimacing. mandibular joint syndrome (TMJ). e. Referred pain: pain arising from deep visceral e. Functional changes, abnormal movements. tissues that is felt in a body region remote from (1) Check for self-imposed limited activity; the site of pathology, resulting in tenderness, disrupted lifestyle; disuse syndrome. and cutaneous hyperalgesia; e.g., medial left (2) Check for avoidance of work, social inter- arm pain with heart attack; right subscapular actions, or sexual activity. pain from gallbladder attack. 5. Examine. f. Consequences of pain, behavioral impact, sec- a. History: determine chief complaints, descrip- ondary gains. tion of onset, mechanism of injury, localization (1) Monetary benefits (malingering, insurance (chronic pain is poorly localized, not well claims). defined); nature of pain (constant, intermit- (2) Sympathy and attention. tent); irritating stimuli/activities. (3) Avoidance of undesirable work. b. Subjective assessment using pain intensity rat- ing scales. g. Depression, anxiety. (1) Simple descriptive scales: verbal report h. Prescription drug misuse. (e.g. select the words that best describe i. Dependence on health care system: multiple your pain). (2) Semantic differentiation scales: McGill health care providers, clinical services; \"shop- Pain Questionnaire. ping around\" behaviors. j. Responsiveness of pain to physiological inter- ventions/treatments: chronic pain is often unre- sponsive. k. Motivational/affective components (sick role). (1) Previous experience with pain. (2) Learned responses to pain. (3) Perception of control over pain. (4) Ethnicity/cultural aspects of pain. 6. Physical therapy goals, outcomes, and interventions. a. Assist patient in identifying pain behaviors,
Indications: an inability to initiate move- Neuromuscular Physical Therapy 129 ment, hypotonia, weakness, marked imbal- ances between antagonists. around a longitudinal axis with passive (6) Hold-relax (HR): a relaxation technique movements into newly gained range. u ually performed at the point of limited Active holding in the new range is then ROM in the agonist pattern; an isometric stressed. Indications: hypertonia with limi- contraction of the range-limiting antagonist tations in function or ROM; e.g., patients pattern is performed against slowly with Parkinson's disease. increa ing resistance, followed by volun- (12)Rhythmic stabilization (RS): simultaneous tary relaxation, and passive movement into i ometric contractions of both agonist and the newly gained range of the agonist pat- antagonist patterns performed without tern. Active contraction (HRAC) into the relaxation using careful grading of resist- newly gained range of the agonist pattern ance; results in cocontraction of opposing can also be performed and serves to main- muscle groups; RS emphasizes rotational tain the inhibitory effects through recipro- stability control. Indications: instability in cal inhibition. Indications: limitations in weight-bearing and holding, poor antigrav- ROM caused by muscle tightness, muscle ity control, weakness, ataxia; also limita- spasm, and pain. tions in ROM caused by muscle tightness, (7) Maximal resistance: resistance to stronger painful muscle splinting. muscles to obtain overflow to weaker mus- (13)Slow reversals (SR), Slow reversal hold cles. Indications: weakness, muscle imbal- (SRH): slow isotonic contractions of first ances. agonist, then antagonist patterns using care- (8) Repeated contractions (RC): repeated iso- ful grading of resistance and optimal facili- tonic contractions induced by quick tation; reversal of antagonists. In SRH, an stretches and enhanced by resistance per- isometric hold is added at the end of the formed through the range or part of range range at a point of weakness (the hold may at a point of weakness; RC is a unidirec- be added in both directions or only in one tional technique; an isometric hold can be direction). Indications: inability to reverse added at a point of weakness. Indications: directions, muscle imbalances, weakness, weakness, incoordination, muscle imbal- incoordination, lack of endurance. ances, lack of endurance. (l4)Timing for emphasis (TE): use of maxi- (9) Re isted progression (RP): stretch and mum resistance to elicit a sequence of con- tracking resistance is applied to facilitate tractions of major muscle components of a progres ion in walking, creeping, kneel- pattern of motion; allows overflow to occur walking, or movement transitions. Indi- from strong to weak components; can be cations: impaired strength, timing, motor performed within a limb (ipsilateral from control and endurance. one muscle group to another) or using over- (lO)Rhythmic initiation (RI): Voluntary relax- flow from limb to limb (contralateral) or ation followed by passive movement trunk to limb. Typically combined with through increasing ROM, followed by repeated contractions to the weaker compo- active-as isted contractions progressing to nents, TEIRC. Superimposed upon normal tracking resistance (light, facilitatory resist- timing: timing of muscle components in a ance) to isotonic contractions; RI may be distal to proximal equence occurring dur- unidirectional or bidirectional. Indications: ing PNF diagonal patterns; proximal spasticity, rigidity, inability to initiate motion is delayed until distal component movement (apraxia), motor learning approaches full range. Indications: weak- deficits, communication deficits (aphasia). ness, incoordination. (11)Rhythrnic rotation (RRo): voluntary relax- (l5)Traction: a distraction force applied to ation combined with slow, passive, rhyth- joints. Indications: stimulate afferent nerve mic rotation of the body or body part endings and facilitate flexor muscles, mobilizing patterns. c. Diagonal patterns of movement: upper extremity
130 (2) Original approach from Bobaths was based on hierarchical motor control theory (levels (UE) named for motions occurring at the prox- of reflex integration within the eNS). imal joint (shoulder); intermediate joint Abnormal reflexes (e.g., ATNR, STNR), (elbow) may be straight, flexing, or extending obligatory synergies, and spasticity were (intermediate pivot). inhibited; normal postural reflexes (higher- (1) Flexion-adduction-external rotation (D 1F, level righting, equilibrium, and protective extension reactions) were facilitated. These diagonal 1 flexion) e.g., close your hand, concepts have been modified in favor or turn, and pull your arm across your face. more recent motor control theorie . (2) Extension-abduction-internal rotation (D IE) e.g., open your hand, turn and push your (3) Distributed control! dynamical systems arm down and out. model of motor control. Multiple factors (3) Flexion-abduction-external rotation (D2F) contribute to movement dysfunction. e.g., open your hand, turn, and lift your arm up and out. (4) Focus is on facilitation of normal move- (4) Extension-adduction-internal rotation (D2E) ment patterns, avoidance of abnormal and e.g., close your hand, turn, and pull your compensatory patterns of movement. arm down and across your body. d. Diagonal patterns of movement: lower extrem- (5) Motor learning (or relearning) of patterns ity (LE) named for motions occurring at the of movement can be facilitated by appro- proximal joint (hip); intermediate joint (knee) priate handling techniques, a combination may be straight, flexing, or extending (interme- of inhibition/facilitation techniques, repeti- diate pivot). tion, and experience in the environment. (1) Flexion-adduction-external rotation (DIF) e.g., bring your foot up, turn and pull your (6) Focus is on functional skills. leg up and across your body. b. Techniques of treatment. (2) Extension-abduction-internal rotation (D 1E) e.g., push your foot down, turn, and push (1) Guided movement (guiding): active move- your leg down and out. ments are guided or assi ted. Focus on: (3) Flexion-abduction-internal rotation (D2F) (a) Assisted movement; assistance is given e.g., lift your foot up, turn, and lift your leg only as needed. up and out. (b) Task understanding, voluntary control (4) Extension-adduction-external rotation (D2E) of movement. e.g., push your foot down, turn, and pull (c) Low effort: maximizes performance in your leg down and in. the presence of tonal disorders; high e. Diagonal patterns: head and trunk. effort, maximal resistance results in (1) Supine or sitting, chop: upper trunk flexion unwanted activity, and is avoided. with rotation to right or left; lead arm moves (d) Avoidance of substitution movements. in DIE, assist arm holds on top of wrist. (e) Minimizing verbal instructions or (2) Supine or sitting, lift: upper trunk extension feedback during movement. with rotation to right or left; lead arm moves (f) Ensuring movement success, avoid- in D2F, assist arm holds beneath the wrist. ance of repeated failures. (3) Supine, lower trunk flexion with rotation to right or left; knees flexing. (2) Normalization of postural tone. (4) Supine or sitting, head and neck flexion (a) Efforts are made to increase tone if tone with rotation to right or left. is too low (hypotonia), or decrease 3. Neurodevelopmental Treatment (NDT). tone if tone is too high (spasticity), a. Basic concepts. e.g., rhythmic rotation or tapping. (1) Focus is on enhancing motor skills, bal- (b) Abnormal patterns of movements, and ance, and quality of movements. Accurate reflexes are inhibited or prevented. analysis of the patient's movement patterns is essential. (3) Normalization of sensory/perceptual expe- riences. c. Patterns of movement. (1) Resumption of normal functional activities that are meaningful, goal-oriented, e.g.,
euromuscular Physical Therapy 131 rolling, sitting up, standing, walking. movement in synergy, a concept now (2) Development or retraining of balance reac- viewed as inappropriate. 5. Sensory Stimulation. tions: righting, equilibrium, and protective a. General concepts. reactions (normal postural reflex mecha- (1) Indications: patients who demonstrate nism). absent or disordered motor control, i.e., dif- (3) Selective limb movements, e.g., UE func- ficulty initiating movement (initial mobili- tional tasks. ty) or sustaining movement (stability), who (4) Integrated movements utilizing both affect- would benefit from the use of augmented ed and intact body segments. feedback; most useful in the early stages of 4. Movement Therapy in Hemiplegia. motor learning. a. Basic concepts. (2) Contraindications: patients who will not (1) Based on work of Signe Brunnstrom. benefit from a hands-on approach, who (2) Sen orimotor recovery occurs in a sequen- demonstrate sufficient motor control to per- tial recovery pattern (see Stroke section); form and refine a motor skill, and the abil- recovery can vary between limbs (typically ity to self-correct based on intrinsic feed- leg more advanced than arm), and even back mechanisms; e.g., later stage of within limbs (typically shoulder more motor learning. advanced than hand); recovery can plateau (3) Response to stimulation is dependent upon at any stage. multiple factors, including level of intact- (3) Careful examination can delineate the stage ness of CNS, initial central statellevel of of recovery, and provide an accurate CNS arousal, type and amount of stimula- description of the pathokinesiology of tion, specific activity of alpha motoneuron stroke. (the development of an accurate pool. stroke asse ment tool is a major contribu- tion of Brunnstrom). TABLE 2-8 - NEUROMUSCULAR PREFERRED b. Techniques. PRACTICE PATTERNS (1) Volitional control of movement can be facilitated through use of: Pattern A: Primary Prevention/Risk Reduction for Loss of Balance (a) Reflexes: now a concept discarded as Pattern B: and Falling Pattern C: inappropriate. Impaired Neuromotor Development (b) Proprioceptive inputs: resistance, weight Pattern D: Impaired Motor Function and Sensory Integrity bearing, stretch, tapping, manipulations. Pattern E: Associated with Nonprogressive Disorders of the (c) Exteroceptive inputs: rubbing, stroking. Pattern F: Central Nervous System - Congenital Origin or (d) Eye contact, appropriate verbal com- Pattern G: Acquired in Infancy or Childhood Pattern H: mands. Pattern I: Impaired Motor Function and Sensory Integrity (e) Use of sound side to facilitate herniside: Associated with Nonprogressive Disorders of the Central Nervous System - Acquired in Adolescence transfer effects. or Adulthood (2) Control is progressed from small range to Impaired Motor Function and Sensory Integrity large; isometric and eccentric contractions Associated with Progressive Disorders of the Central to i otonic contractions. Nervous System (3) Fatigue, pain, or heavy resistance are avoided since control decreases. Impaired Peripheral Nerve Intergrity and Muscle (4) Positive reinforcement and repetition are Performance Associated with Peripheral Nerve Injury key to successful motor learning. c. Patterns of movement. Impaired Motor Function and Sensory Integrity (1) Training activities focus on the out-of-syn- Associated with Acute or Chronic Polyneuropathies ergy combinations needed for every day function (e.g. hand function, walking). Impaired Motor Function, Peripheral Nerve Integrity, (2) Patients with very little recovery and limit- and Sensory Integrity Associated with Nonprogressive ed movement (stages 1 and 2) first practice Disorders of the Spinal Cord Impaired Arousal, Range of Motion, and Motor Control Associated with Coma. Near Coma or Vegetative State From APTA Guide for Physical Therapist Practice, 2nd ed, 200 I
132 (b) Maintained touch (maintained pres- sure): produces calming effect, gener- (4) Early use of sensory stimulation techniques alized inhibition. should be phased out as soon as possible in favor of active control by the patient; (c) Slow troking (continuous, slow important to avoid feedback/therapist stroking to spinal posterior primary dependence. rami): produces calming effect, gener- alized inhibition. (5) Spatial summation (multiple techniques) or temporal summation (repeated application (d) Prolonged icing (ice packs, ice bath): of the same technique) may be necessary to produce inhibition of muscle tone, produce the desired response in some low- spasm, and pain. level patients, e.g., sensory stimulation pro- gram for patients in coma or early recov- (e) Neutral warmth (retention of body heat ery following TBI. through wrapping, air splint, tepid bath): produces generalized inhibition (6) Consider cumulative effects: the total envi- of tone, relaxation, calming effect, ronment along with the effects of sensory decreased pain. stimulation techniques. (a) Avoid bombardment (overload): may (3) Vestibular stimulation techniques. prove harmful; CNS shut down is like- (a) Slow, maintained vestibular stimula- ly in the face of over-stimulation, or tion (slow, repetitive rocking): pro- sympathetic fight-or-flight reactions. duces generalized inhibition of tone, (b) Consider what stimuli may yield the relaxation, calming effect. desired performance and optimum (b) Fast, irregular ve tibular tirnulation learning. (spinning, fa t rolling): produces gen- eralized facilitation of tone, improved b. Techniques. motor coordination, improved retinal (1) Proprioceptive timulation techniques. image stability. (a) Quick stretch, tapping of muscle belly or tendon: facilitates agonist muscle, B. Motor Control/Motor Learning Approach inhibits antagonist. 1. General concepts. (b) Prolonged, slowly applied stretch (manu- a. Incorporates theorie of motor control and al, positioning, inhibitory casts): inhibits motor learning. agonist muscle, dampens high tone. b. Used in combination with task-related training. (c) Resistance: recruits motor units, both c. Consideration is given to both intrinsic neuro- alpha and gamma motoneurons; facili- muscular control processe and environmental tates, strengthens agonist contraction. constraints. (d) Joint approximation: enhances joint 2. Motor control strategies. awareness, facilitates cocontraction, a. General concepts - motor control. action of postural extensors, stabilizing (1) Motor program: a set of prestructured mus- muscles. cle commands that, when initiated, results (e) Joint traction: enhances joint aware- in the production of a coordinated move- ness, action of flexors; relieves muscle ment sequence (learned task); can be carried spasm (joint mobilization). out largely uninfluenced by peripheral (f) Inhibitory pressure (firm pressure on feedback. long tendons): inhibits muscle, damp- (2) Motor plan: an overall strategy for move- ens tone, e.g., weightbearing on an ment; an action sequence requiring the coor- extended open hand (spastic hand) or dination of a number of motor programs. kneeling (spastic quadriceps). (3) Feedback: afferent information sent by var- (2) Exteroceptive stimulation techniques. ious sensory receptor to control center . (a) Light, quick touch: initiates phasic, (a) Feedback update control centers withdrawal reactions, e.g., quick stroke about the correctne of movement to palm of hand can produce withdraw- while it progre es; hapes ongoing al of th hand away from the stimulus. movement.
(b) Feedback allows motor responses to be Neuromuscular Physical Therapy 133 adapted to the demands of the environ- ment. (c) Knowledge of results (KR): augmented feedback about the outcome of a move- (4) Feedforward: readies the system in advance ment. of movement; anticipatory responses that adjust the ystem for incoming sensory (d) Knowledge of performance (KP): aug- feedback or for future movements; e.g., mented feedback about the nature of preparatory po tural adjustments. the movement produced, e.g., move- ment characteristics. (5) Motor kill acquisition. (a) Behavior is organized to achieve a (e) Feedback schedules: feedback given goal-directed task. after every trial; feedback summed (b) Active problem solving/processing is (after set number of trials), fading required for the development of a (decreasing) or bandwidth (if responses motor program/motor plan, motor outside a designated range). learning; improves retention of skills. (c) Adaptive to specific environmental (4) Practice. demands (regulatory conditions). (a) Blocked practice: practice of a single Clo ed environment: fixed, nonchang- motor skill repeatedly; repetitive practice. ing. Open environment: variable, (b) Variable practice: practice of varied changing. motor skills in which the performer is required to make rapid modifications (6) CNS recovery/reorganization is dependent of the skill in order to match the upon experience. demands of the task. (c) Random practice: practice of a group 3. Motor learning strategies. or class of motor skills in random order a. General concepts - motor learning. (no predictable order). (l) A change in the capability of a person to (d) Serial practice: practice of a group or perform a skill; the result of practice or class of motor skills in serial or pre- experience. dictable order. (2) Measures of motor learning include: (e) Mas ed practice: relatively continuous (a) Performance: determine overall quality practice in which the amount of rest of performance, level of automaticity, time is small (re t time is less than the level of effort, speed of decision making. practice time). (b) Retention: the ability to demonstrate (f) Distributed practice: practice in which the skill after a period of no practice. the rest time is relatively large (prac- (c) Generalizability: the acquired capabili- tice time is less than rest time). ty to apply what has been learned to (g) Mental practice: cognitive rehearsal of other similar tasks (transfer tests), e.g., a motor skill without overt physical transfers wheelchair to mat, to toilet, performance. and to car. (d) Re istance to contextual change: (5) Transfer: the effects of having previous acquired capability to apply what has practice of a skill or skills upon the learn- been learned to other environmental ing of a new skill or upon performance in a contexts, e.g., clinic, home, work. new context; transfer may be either positive (3) Feedback. (assisting learning) or negative (hindering (a) Intrinsic feedback: sensory informa- learning). tion normally acquired during per- (a) Part-whole transfer: a learning tech- formance of a task. nique in which a complex motor task is (b) Augmented feedback: externally pre- broken down into its component or sented feedback that is added to that subordinate parts for separate practice normally acquired during task per- before practice of the integrated whole. formance, e.g., verbal cueing. (b) Bilateral transfer: improvement in movement skill performance with one limb results from practice of similar
134 movements with the opposite limb. (4) Supportive feedback (reinforcement) can b. Strategies for effective learning. (Table 2-9). be used to shape behavior, motivate patient. (1) Feedback given after every trial improves (5) Assist learner in recognizing/pairing intrin- performance while variable feedback sic feedback with movement responses. improves learning and retention. (6) Provide augmented feedback: knowledge (2) Early training should focus on visual feed- of results, knowledge of performance. back (cognitive phase of learning) while (a) Early in learning, focus feedback on later training should focus on proprioceptive correct aspects of performance. feedback (associative phase of learning). (b) Later in learning, focus feedback on errors as they become consistent. (3) Reduce extraneous environmental stimuli (c) Feedback after every trial improves per- early in learning (e.g., closed environment) formance, useful during early learning. while later learning focuses on adaptation (d) Use variable feedback (summed, fad- to environmental demands (e.g., open envi- ing, bandwidth) to improve retention, ronment). TABLE 2-9 - STAGES OF MOTOR LEARNING AND TRAINING STRATEGIES CHARACTERISTICS TRAINING STRATEGIES Cognitive Stage Highlight purpose of task in functionally relevant terms The learner: Demonstrate ideal performance of task to establish a reference of correctness develops an understanding of task: Have patient verbalize task components and requirements cognitive mapping Point out similarities to other learned tasks assesses abilities, task demands Direct attention to critical task elements identifies stimuli, contacts memory Select appropriate feedback selects response, performs initial • Emphasize intact sensory systems, intrinsic feedback systems approximations of task • Carefully pair extrinsic feedback with intrinsic feedback structures motor program • High dependence on vision: have patient watch movement modifies initial responses • Knowledge of Performance (KP): focus on errors as they become consistent; do not \"What to do\" decision cue on large number of random errors • Knowledge of Results (KR): focus on success of movement outcome Ask learner to evaluate performance, outcomes; identify problems, solutions Use reinforcements (praise) for correct performance, continuing motivation Organize feedback schedule • Feedback after every trial improves performance during early learning • Variable feedback (summed, fading, bandwidth designs) increases depth of cognitive processing, improves retention; may decrease performance initially; can begin to use by end of stage Organize initial practice • Stress controlled movement to minimize errors • Provide adequate rest periods (distributed practice) if task is complex, long, or energy costly or if learner fatigues easily, has short attention, poor concentration • Use manual guidance to assist as appropriate • Break complex tasks down into component parts, teach both parts and integrated whole • Utilize bilateral transfer as appropriate • Use blocked (repeated) practice of same task to improve performance • Use variable practice (serial or random practice order) of related skills to increase depth of cognitive processing and retention; may decrease performance initially • Use mental practice to improve performance and learning, reduce anxiety Assess, modify arousal levels as appropriate • High or low arousal impairs performance and learning (inverted U theory) • Avoid stressors, mental fatigue Structure environment • Reduce extraneous environmental stimuli, distractors to ensure attention, concentration • Emphasize closed skills initially gradually progressing to open
euromuscular Physical Therapy 135 increase depth of cognitive processing. improve learning (promotes retention and (e) Avoid feedback dependence: reduce generalizability). (9) Use random or serial practice order, rather augmented feedback as soon as possi- than blocked practice, in order to improve ble; foster active introspection, deci- learning (retention). sion making by learner. (10) Use mental practice to improve learning; (7) Establish practice schedule: use distributed have patient verbalize task components, practice when superior performance is requirements for performance; effective desired, when motivation is low, or when when task has a large cognitive component the learner has short attention, poor con- or to decrease fear and anxiety. centration, or fatigues easily. (1l)Use parts to whole transfer when task is (8) Use variable practice of a group of func- complex, has higWy independent parts or tional ta ks rather than constant practice to TABLE 2-9 - STAGES OF MOTOR LEARNING AND TRAINING STRATEGIES CONT. CHARACTERISTICS TRAINING STRATEGIES Associated Stage The learner: Select appropriate feedback practices movements • Continue to provide KP; intervene when errors become consistent refines motor program: spatial and temporal • Emphasize proprioceptive feedback, \"feel of movement\" to assist in establishing an organization decreases errors, extraneous movements internal reference of correctness dependence on visual feedback decreases, • Continue to provide KR; stress relevance of functional outcomes increases for use of proprioceptive • Assist learner on improving self-evaluation, decision making skills cognitive monitoring decreases • Facilitation techniques, guided movements may be counterproductive during this \"How to do\" decision stage of learning Organize feedback schedule • Continue to provide feedback for continuing motivation; encourage patient to self- assess achievements • Avoid excessive augmented feedback • Focus on use of variable feedback (summed, fading, bandwidth) designs to improve retention Organize Practice • Encourage consistency of performance • Focus on variable practice order (serial or random) of related skills to improve retention Structure environment • Progress toward open, changing environment • Prepare the learner for home, community, work environments Autonomous Stage Assess need for conscious attention, automaticity of movements The learner: Select appr.opriate feedback: • practices movements • Learner demonstrates appropriate self-evaluation, decision-making skills • continues to refine motor responses, spatial • Provide occasional feedback (KP, KR) when errors evident Organize practice and temporal highly organized • Stress consistency of performance in variable environments, variations of tasks • movements are largely error-free • minimal level of cognitive monitoring (open skills) • High levels of practice (massed practice) are appropriate \"How to succeed\" decision Structure environment • Vary environments to challenge learner • Ready the learner for home, community, work environments Focus on competitive aspects of skills as appropriate, e.g., wheelchair sports From O'Sullivan, S and Schmitz, T: Physical Rehabilitation - Assessment and Treatment, ed 4. F.A. Davis Co., Philadelphia, 200 I, p. 368, with permission
136 2. Constraint-induced Movement Therapy (CI). a. A task-oriented training approach for patients when learner has limited memory or atten- recovering from stroke in which the unaffected tion, difficulty with a particular part. Practice UE is restrained with the use of an arm sling both the parts and the integrated whole. and resting hand splint while training is (12)Lirnit information with learners who have focused on the affected UE. . attention deficits, mentally fatigue easily; b. Use massed practice (up to 6 hours/day) with focus on key task elements; give frequent repetitive training of functional tasks. rest periods. c. Operant conditioning techniques are used to (13)Tasks that have highly integrated compo- shape responses. nents should be practiced as a whole, e.g., gait. 3. Body weight-supported treadmill training (BWSTT). (14)Transfer of learning is optimized when a. Task-oriented training approach in which the tasks are higWy similar (similar stimuli, patient walks with assistance on a treadmill similar responses), e.g., bilateral transfer, with body weight partially supported. one arm to the other. b. Slow treadmill speeds (typically 0.01-2.25 m/s) (15)Use guided movement early in learning, and light support using an overhead harne not late; most effective for slow postural or (typically 30% of body weight to start) are used positioning tasks. during initial practice; speeds are gradually (16)Optimal arousal is necessary for optimal increased and weight support is gradually learning; low arousal or intense arousal reduced. yield poor performance and learning. c. One or two therapists provide manual assis- (Inverted U theory). tance in stabilization of trunk/pelvis and in (17)Involve learner in goal setting; task should movement of the paretic limb. be desirable, functionally relevant, impor- d. Progression is to overground walking; body tant to learn. weight support can be used to start with pro- C. Task-Related Training Approach gression is to no weight support. 1. General concepts. a. Emphasis is on forcing use of the affected body D. Compensatory Training Approach segmentsllimbs using task-related experiences 1. General concepts. and training. a. Indications: to offset or adapt to residual (1) Patients practice important functional tasks impairments and disabilities. essential to independence, e.g., stand up b. Focus is on early resumption of functional inde- and sit down; balance, walking and stair pendence with reliance on uninvolved segments climbing, reaching and manipulation. for function, e.g., functional training with an (2) Patients practice tasks in appropriate and individual with complete spinal cord injury. safe environments; focus is on anticipated c. Changes are made in the patient's overall environments for daily function. approach to tasks. b. Patients practice under therapist's supervision (1) Patient is made aware of movement defi- and independently. ciencies, alternate ways to accomplish tasks. (1) Therapists provide assistance through guid- (2) Patient relearns functional patterns and ed movement and verbal cueing. habitual ways of moving. (2) Therapists serve as motor learning coaches, (3) Patient practices functional skills in a encouraging correct performance. variety of environments. (3) Exercise/activity logs can help organize the 2. Issues with the compensation approach. patient's self-monitored practice. a. Focus on uninvolved egments to accomplish (4) Repetition and extensive practice are daily tasks (e.g., stroke, traumatic brain injury) required. may suppress recovery and contribute to c. Promotes use-dependent cortical reorganization learned nonuse of the impaired egments. (neural plasticity) and recovery. b. Focus on task specific learning may lead to the d. Prevents learned non-use of the affected body development of splinter skills in patients with segments/extremities. brain damage; skills cannot be easily general-
euromuscuJar Physical Therapy 137 ized to other ta ks or environmental situations. c. May be the only approach possible. (1) If no additional recovery is anticipated (e.g., complete spinal cord injury). (2) If evere motor deficits are present or if sensorimotor recovery has plateaued (e.g., stroke). (3) If patient exhibits extensive co-morbidities and poor health. 3. Strategies. a. Simplify activities. b. Establish a new functional pattern; identify key task elements, residual segments available for control of movements. c. Repeated practice; work toward consistency, efficiency. d. Energy conservation and activity pacing tech- niques are important to ensure completion of all daily movement requirements. e. Adapt environment to facilitate relearning of kills, ease of movement. (1) Simplify; set up for optimal performance. (2). U e environmental adaptations to enhance performance, e.g., color code stairs, grab bar ,etc.
CHAPTER 3 CARDIOVASCULAR PHYSICALTHERAPY Susan B. O'Sullivan and Raymond P. Siegelman I. Anatomy and Physiology of the Cardio- 120 vascular System 100 A. The Heart and Circulation 80 1. Heart tissue. a. Pericardium: fibrous protective sac enclosing \" ' -~~C) 60 Isovolumetric heart. b. Epicardium: inner layer of pericardium. \"'I - t - - - - relaxation c. Myocardium: heart muscle, the major portion of the heart. 0~. .EE_ d. Endocardium: smooth lining of the inner sur- face and cavities of the heart. 40 2. Heart chambers. a. Right atrium (RA): receives blood from sys- 20 temic circulation, from the superior and inferi- or vena cavae. 0 Left atrium b. Right ventricle (RY): receives blood from the RA and pumps blood via the pulmonary artery \"'1:: \"0 '-....--' to the lungs for oxygenation; the low-pressure 41 pulmonary pump. I''\"\"&'c\"j: c. Left atrium (LA): receives oxygenated blood Diastole ~ I ~ Systole from the lungs and the four pulmonary veins. 23 d. Left ventricle (LY): receives blood from the A ~ I~ Diastole LA and pumps blood via the aorta throughout the entire systemic circulation; the high-pres- p sure systemic pump. The walls of the LY are thicker and stronger than the RY and forms C) most of the left side and apex of the heart. u UJ QS Figure 3-1 Events of the cardiac cycle. Electrical depolariza- tion of the ventricle (represented by the QRS) precedes mechanical systole (contraction), which begins with the first heart sound (S I) and ends with the second heart sound (S2).The amount of blood ejected with one contraction (stroke volume) times the number of contractions per minute (heart rate) deter- mines the cardiac output for one minute. From Pocket Guide to Cardiovascular Care, 1990 by Susan Stillwell and Edith Randall, CV Mosby Company, p2. with permission.
3. Valves: provide one-way flow of blood. Cardiovascular Physical Therapy 139 a. Atrioventricular valves: prevent backflow of blood into atria during ventricular systole; empties into the right atrium. anchored by chordae tendineae to papillary c. Distribution of blood supply is variable from mu cle ; valve close when ventricular walls contract. individual to individual. (1) Tricuspid valve (three cusps or leaflets): d. Myocardial oxygen supply and myocardial right heart valve. (2) Bicu pid or mitral valve (two cusps or oxygen demand (MV02) should be in balance. leaflets): left heart valve. 6. Conduction. b. Semilunar valves: prevent backflow of blood from aorta and pulmonary arteries into the ven- a. Specialized conduction tissue: allows rapid tricles during diastole. transmission of electrical impulses in the (1) Pulmonary valve: prevents right backflow. myocardium (normal sinus rhythm, NSR). (2) Aortic valve: prevents left backflow. (1) Nodal tissue. (2) Purkinje fibers: specialized conducting tis- 4. Cardiac cycle: the rhythmic pumping action of the sue of both ventricles. heart. a. Systole: the period of ventricular contraction. b. Sinoatrial (SA) node. End-systolic volume is the amount of blood in (1) Located at junction of superior vena cava the ventricles after systole, about 50 ml. and right atrium. b. Diastole: the period of ventricular relaxation (2) Main pacemaker of the heart, initiates the and filling of blood. End-diastolic volume is impulse. the amount of blood in the ventricles after dias- (3) Has sympathetic and parasympathetic tole, about 120 mI. innervation affecting both heart rate and c. Atrial contraction occurs during the last third strength of contraction. of diastole and completes ventricular filling. c. Atrioventricular (AV) node. 5. Coronary circulation. (1) Located at the junction of the right atrium a. Arteries: ari e directly from aorta near aortic and the right ventricle. valve; blood circulates to myocardium during (2) Has sympathetic and parasympathetic diastole. innervation. (1) Right coronary artery (RCA): supplies (3) Merges with bundle of His. right atrium, most of right ventricle, and in most individuals the inferior wall of left d. Purkinje tissue. ventricle, atrioventricular (AV) node and (1) Right and left bundle branches of the AV bundle of His; 60% of time supplies the node are located on either side of intraven- sinoatrial (SA) node. tricular septum. (2) Left coronary artery (LCA): supplies most (2) Terminate in Purkinje fibers, specialized of the left ventricle; has two main divisions. conducting tissue of the ventricles. (a) Left anterior descending (LAD): sup- plie the left ventricle, and the inter- e. Conduction of heart beat. ventricular septum, and in most indi- (1) Origin is in the SA node; impulse spreads viduals the inferior areas of the apex; it throughout both atria which contract may also give off branches to the right together. ventricle. (2) Impulse stimulates AV node, is transmitted (b) Circumflex (Circ): supplies blood to down bundle of His to the Purkinje fibers; the lateral and inferior walls of the left impulse spreads throughout the ventricles ventricle and portions of the left atri- which contract together. um; 40% of time supplies SA node. b. Veins: parallel arterial system; the coronary 7. Myocardial fibers. sinus receives venous blood from the heart and a. Muscle tissue: striated mu c1e fiber but with more numerous mitochondria; exhibits rhythmic- ity of contraction; fibers contract as a functional unit (sliding filament theory of contraction). b. Myocardial metabolism is essentially aerobic, sustained by continuous O2 delivery, from the coronary arteries. c. Smooth muscle tissue is found in the walls of blood vessels.
140 (2) MV02 is increased with actlVlty and increases with HR and/or BP. 8. Hemodynamics. a. Stroke volume (SV): the amount of blood B. Peripheral Circulation ejected with each myocardial contraction, 1. Arteries: transport oxygenated blood from areas of about 70 m\\. Influenced by: high pressure to lower pressures in the body tissues. (1) Left ventricular end diastolic volume a. Arterial circulation maintained by heart pump. (LVEDV): the amount of blood left in the b. Influenced by elasticity and extensibility of ventricle at the end of diastole. Also known vessel walls, and by peripheral resistance, as preload. The greater the diastolic filling amount of blood in body. (preload), the greater the quantity of blood 2. Capillaries: minute blood ve el that connect the pumped (Frank-Starling law). ends of arteries (arteriole ) with the beginning of (2) Contractility: the ability of the ventricle to veins (venules); forms an ana tomosing network. contract. a. Functions for exchange of nutrients and fluids (3) Afterload: the force the LV must generate between blood and tissues. during systole to overcome aortic pressure b. Capillary walls are thin, permeable. to open the aortic valve. 3. Veins: transport dark, unoxygenated blood from b. Cardiac output (CO): the amount of blood dis- tissues back to the heart. charged from the left or right ventricle per a. Veins have larger capacity, thinner walls than minute. arteries; greater number. (1) For average adult at rest it is approximate- b. Veins have one-way valves to prevent backflow. ly 4 - 6 L per minute. c. Venous system includes both uperficial and (2) Determined by multiplying stroke volume deep veins (deep vein accompany arterie times heart rate. while superficial do not). c. Left ventricular end-diastolic pressure (LVEDP): d. Venous circulation influenced by muscle con- pressure in the left ventricle during diastole. traction, gravity, respiration (increased return d. Ejection fraction (EF): percentage of blood with inspiration), compliancy of right heart. emptied from the ventricle during systole; a 4. Lymphatic system. clinically useful mea ure of LV function. a. Drains lymph from bodily tissues and returns it (1) EF = stroke volume (SV)/left ventricular to the venous circulation. end diastolic volume (LVEDV). b. Lymph travels from lymphatic capillaries to (2) Normal EF averages 60% to 70%; the lymphatic vessels to ducts to left subclavian lower the EF, the more impaired the LV. vein. e. Atrial filling pressure: the difference between c. Major lymph nodes are submaxillary, cervical, the venous and atrial pressures. axillary, mesenteric, iliac, inguinal, popliteal, (1) Right atrial filling pressure is decreased and cubital. during strong ventricular contraction and d. Contributes to immune system function: lymph atrial ftlling is enhanced. nodes collect cellular debris and bacteria and (2) Right atrial ftlling pressure is affected by produce antibodies. changes in intrathoracic pressure; decreased during inspiration and increased during C. Neurohumoral Influences coughing or forced expiration. 1. Parasympathetic stimulation (cholinergic). (3) Venous return is increased when blood vol- a. Control located in medulla oblongata, cardioin- ume is expanded and decreased during hibitory center. hypovolemic shock. b. Via vagus nerve (C.NX), cardiac plexus; inner- f. Diastolic filling time is decreased with vates all myocardium; relea e acetylcholine. increased heart rate and with heart disease. c. Slows rate and force of myocardial contraction; g. Myocardial oxygen demand (MV02) repre- decreases myocardial metabolism. sents the energy cost to the myocardium. d. Causes coronary artery vasoconstriction. (1) Clinically measured by the product of heart 2. Sympathetic timulation (adrenergic). rate (HR.) and systolic blood pressure (SBP), a. Control located in medulla oblongata, cardio- known as the rate pressure produce (RPP). acceleratory center.
b. Via cord segments TI-T4, upper thoracic to Cardiovascular Physical Therapy 141 superior cervical chain ganglia; innervates all but ventricular myocardium; releases epineph- (widened PR interval and QRS, tall T rine and norepinephrine. waves). (2) Hypokalemia: decreased concentration of c. Causes an increase in the rate and force of myocar- potassium ions produces EKG changes dial contraction, and myocardial metabolism. (flattened T wave , prolonged PR and QT intervals); arrhythmias, may progress to d. Causes coronary artery vasodilation. ventricular fibrillation. e. The kin and peripheral vasculature receive (3) Hypercalcemia: increased calcium concen- trations increases heart actions. only po t ganglionic sympathetic innervation. (4) Hypocalcemia: decreased calcium concen- Causes vasoconstriction of cutaneous arteries; trations depresses heart actions. sympathetic inhibition must occur to obtain 4. Peripheral resistance. vasodilation. a. Increased peripheral resistance increases arteri- f. Drugs that increase sympathetic functioning al blood volume and pressure. are sympathomimetics; drugs that decrease b. Decreased peripheral resistance decreases arte- sympathetic functioning are sympatholytics. rial blood volume and pressure. 3. Additional control mechanisms. c. Influenced by arterial blood volume: viscosity a. Baroreceptors (pressoreceptors): main mecha- of blood and diameter of arterioles and capil- nisms controlling heart rate. laries. (I) Located in walls of aortic arch and carotid II. Cardiovascular Examination: History, sinus; via vasomotor center. Systems Review, Tests and Measures (2) Circulatory reflex: respond to changes in A. Patient Interview blood pressure. 1. Health history. (a) Increased BP results in parasympathetic a. Presenting symptoms. Note on et, progression, nature of symptoms, insight into one's medical stimulation, decreased rate and force of condition. cardiac contraction; sympathetic inhibi- (I) Chest pain, palpitation, hortness of tion, decreased peripheral resistance. breath. (b) Decreased BP results in sympathetic (2) Fatigue: generalized feeling of tiredness, timulation, increa ed heart rate, blood weakness. pressure and vasoconstriction of (3) Palpitations: awareness by patient of heart peripheral blood vessels. rhythm abnormalities; e.g., pounding, flut- (c) Increased right atrial pressure causes tering, racing heart beat, skipped beats. reflex acceleration of heart rate. (4) Dizziness, syncope (transient loss of con- b. Chemoreceptors. sciousness) due to inadequate cerebral (I) Located in the carotid body. blood flow. (2) Sensitive to changes in blood chemicals: (5) Edema: retention of fluid in the tissues; 02' CO2, lactic acid. swelling, especially in dependent body (a) Increased CO2 or decreased 02' or parts/lower extremities; sudden weight gain. decreased pH (elevated lactic acid) b. Positive risk factors (ACSM Risk Stratification results in an increase in heart rate. in ACSM's Guidelines for Exercise Testing and (b) Increased O2 levels result in a decrease Prescription, 6th edition, p. 24). in heart rate. (I) Hypercholesterolemia. c. Body temperature. (2) Hypertension. (I) Increa ed body temperature causes heart (3) Cigarette smoking. rate to increase. (4) Impaired fasting glucose: fasting blood (2) Decreased body temperature causes heart glucose of ~ 110 mgldL. rate to decrease. (5) Obesity: body mass index (BMI) of ~ 30 d. Ion concentrations. kg, or waist girth of> 100 cm. (I) Hyperkalemia: increased concentration of potassium ions decreases the rate and force of contraction, produces EKG changes
142 dorsal medial aspect of foot; used to moni- tor lower extremity circulation. (6) Sedentary lifestyle. c. Determine heart rate (HR). (7) Family history. (1) Normal adult HR i 70 beats per minute c. Negative risk factor . (bpm); range 60-80 bpm. (1) High serum HDL cholesterol: > 60 mg/eIL. (2) Pediatric: newborn average is 120 bpm; 2. Past medical history: other diagnoses, surgeries, normal range 70-170 bpm. medications. (3) Tachycardia: greater than 100 bpm. 3. Social history: current living situation, family/ Exercise commonly results in tachycardia. social support, education level, employment, Compensatory tachycardia can be seen lifestyle, risk factors. with volume 10 (surgery, dehydration). 4. Risk factors. (4) Bradycardia: less than 60 bpm. a. Focus on social habits: smoking, diet. d. Pulse abnormalities. b. Past and present level of activity. (1) Irregular pulse: variations in force and fre- B. Physical Examination - Cardiovascular System. quency; may be due to arrhythmias, 1. Examine pulse: rhythmical throbbing of arterial myocarditis. wall as a result of each heartbeat; note rate and (2) Weak, thready pulse: may be due to low rhythm. stroke volume, cardiogenic shock. a. Influenced by force of contraction, volume and (3) Bounding, full pulse: may be due to short- viscosity of blood, diameter and elasticity of ened ventricular systole and decreased vessels; emotions, exercise, blood temperature, peripheral pressure; aortic insufficiency. and hormones. 2. Examine heart sounds. b. Palpate pulses; palpate for 30 seconds with reg- a. Auscultation: the process of listening for ular rhythm, 1-2 minutes with irregular rhythm. sounds within the body; stethoscope is placed (1) Apical pulse or Point of Maximal Impulse directly on chest. Note intensity and quality of heart sounds. (PMI): patient is supine, palpate at 5th b. Auscultation landmarks. interspace, midclavicular vertical line (1) Aortic valve: locate the 2nd right inter- (apex of the heart; may be displaced costal space at the sternal border. upward by pregnancy or high diaphragm; (2) Pulmonic valve: locate the 2nd left inter- may be displaced laterally in congestive costal space at the ternal border. heart failure, cardiomyopathy, ischemic (3) Tricuspid valve: locate the 4th left inter- heart disease. costal space at the sternal border. (2) Radial: palpate radial artery, radial wrist at (4) Mitral valve: locate the 5th left intercostal base of thumb; most common monitoring space at the midclavical area. site. c. S1 sound (\"lub\"): normal closure of mitral and (3) Carotid: patient is lying down with head of tricuspid valves; marks beginning of systole. bed elevated; palpate over carotid artery, on Decreased in first-degree heart block. either side of anterior neck between stern- d. S2 sound (\"dub\"): normal closure of aortic and ocleidomastoid muscle and trachea. pulmonary valves; mark end of systole. (a) Assess one side at a time to reduce the Decreased in aortic stenosi . e. Murmurs: extra sounds. risk of bradycardia through stimulation (1) Systolic: falls between Sl and S2. May of the carotid sinus baroreceptor which indicate valvular disease (e.g., mitral valve produces a reflex drop in pulse rate or prolapse) or may be normal. blood pressure. (2) Diastolic: fall between 52 and 51. Usually (4) Brachial: palpate over brachial artery, indicates valvular di ea e. medial aspect of the antecubital fossa; used (3) Grades of heart murmur: grade I (softest to monitor blood pressure. Best in infants. audible murmur) to grade 6 audible with (5) Femoral: palpate over femoral artery in stethoscope off the che t). inguinal region. (6) Popliteal: palpate over popliteal artery, behind the knee with the knee flexed slightly. (7) Pedal: palpate over dor alis pedis artery,
(4) Thrill: an abnormal tremor accompanying a Cardiovascular Physical Therapy 143 vascular or cardiac murmur; felt on palpation. (b) Premature ventricular contractions f. Bruit: an adventious sound or murmur (blow- (PVCs): a premature beat arising from ing sound) of arterial or venous origin; com- the ventricle; occurs occasionally in mon in carotid or femoral arteries; indicative of the majority of the normal population. atherosclerosis. On ECG: no P wave; a bizarre and wide QRS that is premature, followed g. Gallop rhythm: an abnormal heart rhythm with by a long compensatory pause. Serious three sounds in each cycle; resembles the gallop PVCs: >6 per minute, paired or in of a horse. sequential runs, multifocal, very early (1) S3; associated with ventricular filling; occurs PVC (R on T phenomena). soon after S2; in older individuals may be indicative of congestive (LV) heart failure. (c) Ventricular tachycardia: a run of three (2) S4: associated with ventricular filling and or more PVCs occurring sequentially; atrial contraction; occurs just before S 1. S4 very rapid rate (150-200 bpm); may is indicative of pathology, e.g., CAD, MI, occur paroxy mally (abrupt onset); aortic stenosis, or chronic hypertension. usually the result of an ischemic ven- tricle. On ECG: wide, bizarre QRS 3. Examine heart rhythm. waves, no P waves. Seriously compro- a. Electrocardiogram (ECG): 12 lead ECG pro- mised cardiac output. vides information about rate, rhythm, conduc- tion, area of i chemia and infarct, hypertrophy, (d) Ventricular fibrillation: chaotic activ- electrolyte imbalances. ity of ventricle originating from mul- b. Normal cardiac cycle (normal sinus rhythm). tiple foci; unable to determine rate. (1) P wave: atrial depolarization. On ECG: bizarre, erratic activity (2) P-R interval: time required for impulse to without QRS complexes. No effective travel from atria through conduction sys- cardiac output; clinical death within tem to Purkinje fibers. 4-6 minutes. (3) QRS wave: ventricular depolarization. (4) ST segment: beginning of ventricular repo- (3) Atrial arrhythmias (supraventricular): rapid larization. and repetitive firing of one or more ectopic (5) T wave: ventricular repolarization. foci in the atria (outside the sinus node). (6) QT interval: time for electrical systole. (a) On ECG, P waves are abnormal (vari- c. Calculate heart rate: count number of intervals able in shape) or not identifiable (atrial between QRS complexes in a 6 second strip and fibrillation). multiply by 10. (b) Rhythm may be irregular: chronic or d. Assess rhythm: regular or irregular. occurring paroxysmally. e. Identify arrhythmias (dysrhythmias): abnormal, (c) Rate: rapid with atrial tachycardia disordered rhythms. (140-250 bpm), atrial flutter (250-350 (1) Etiology: ischemic conditions of the bpm); fibrillation (>300 bpm). myocardium, electrolyte imbalance, acidosis (d) Cardiac output is usually maintained; or alkalosis, hypoxemia, hypotension, emo- may precipitate ventricular failure. tional stre s, drugs, alcohol, caffeine. (2) Ventricular arrhythmias: originate from an (4) Atrioventricular blocks: abnormal delays ectopic focus in the ventricles (outside the or failure to conduct through normal con- normal conduction system). ducting system. (a) Significant in adversely affecting car- (a) First, second, or third (complete) diac output; ventricular fibrillation is a degree atrioventricular blocks; bundle pulseless, emergency situation requiring branch blocks. emergency medical treatment: car- (b) If ventricular rate is slowed, cardiac diopulmonary resuscitation (CPR), output decreased. defibrillation, medications. (c) Third degree, complete heart block is life threatening: requires medications (Atropine), surgical implantation of pacemaker.
144 g. ECG changes with MI: present in leads over the infarcted area. (Figure 3-2). f. Determine ST segment changes. (1) With impaired coronary perfusion (ischemia (1) Abnormal Q waves (central zone of infarc- or injury) the ST segment becomes depressed. (2) ST segment depression can be upsloping, tion). horizontal or downsloping. (2) ST elevation (zone of injury). (3) ST segment depression or elevation greater (3) T wave inversion (zone of ischemia). than 1 mrn measured 0.8 sec. from the J h. Metabolic and drug influences on the ECG. point is considered abnormal. (1) Potassium levels. Zone of ischemia Zone of infarction and necrosis Zone of hypoxic injury Normal Ischemia Injury Infarction/necrosis 1\\;\"\"\"\"~w\", '\",m'\" Abnormal a - - ~ AB C D Figure 3-2 ECG changes after Myocardial Infarction From Pathology: Implications for the Physical Therapist by Catherine Goodman and William Boissonnault,WB Saunders CO, 1998, p282, with permission. Pulmonary veins Pulmonary artery Left main Great Superior vena cava coronary artery cardiac vein Right - Area of sinus node coronary artery Left circumflex Circumflex branch of left Inferior vena cava Left anterior coronary artery descending artery Right coronary Coronary sinus artery Diagonal branches Posterior descending branch of right coronary artery ANTERIOR VIEW POSTERIOR VIEW Figure 3-3 Areas of myocardium affected by arterial insufficiency of specific coronary arteries From Pathology: Implications for the Physcial Therapist by Catherine Goodman and William Boissonnault, WB Saunders CO, 1998, p28D, with permission.
(a) Hyperkalemia: widens QRS, flattens P Cardiovascular Physical Therapy 145 wave, T wave becomes peaked. (4) Hypotension: a decrease in BP below nor- (b) Hypokalemia: flattens T wave (or mal; blood pressure is not adequate for inverts), produces a U wave. normal perfusion/oxygenation of tissues. May be related to bedrest, drugs, arrhyth- (2) Calcium levels. mias, blood loss/shock, or myocardial (a) Hypercalcemia: widens QRS, shortens infarction. QT interval. (b) Hypocalcemia: prolongs QT interval. (5) Orthostatic hypotension: sudden drop in BP that accompanies change in position. (3) Hypothermia: elevates ST segment; slows (a) Take BP in lying (5 minutes). Repeat rhythm. BP at 1 and 3 minutes after moving into standing or sitting position. (4) Digitalis: depresses ST segment, flattens T (b) Common symptoms include lighthead- wave (or inverts), QT shortens. edness, dizziness, loss of balance. (c) Drop in systolic BP of more than 20 (5) Quinidine: QT lengthens, T wave flattens mmHg or standing BP less than 100 (or inverts), QRS lengthens. mmHg systolic BP is significant and should be reported. (6) Beta Blockers (e.g., Propranolol/Inderal): decreases heart rate, blunts heart rate (6) Pediatric BP. response to exercise. (a) Infants less than 2 years (95 percentile): 106-110 systolic; 59-63 diastolic. (7) Nitrates (nitroglycerin): increases heart rate. (b) Children 3-5 years: 113-116 systolic, (8) Antiarrhythmic agents: may prolong QRS 67-74 diastolic. and QT intervals. b. Mean arterial pressure (MAP): the arterial i. Holter monitoring: continuous ambulatory pressure within the large arteries over time; dependent upon mean blood flow and arterial ECG monitoring via tape recording of cardiac compliance. rhythm for up to 24 hours. (1) Calculated by taking the sum of SBP and (1) Used to evaluate cardiac rhythm, transient twice the DPR, divided by 3. (2) An important clinical measure in critical care. symptoms, pacemaker function, effect of medications. 5. Examine respiration. (2) Allows correlation of symptoms with activ- a. Determine rate, depth of breathing. ities (activity diary). (1) Normal adult respiratory rate (RR) is 12 to 4. Examine blood pressure (BP). 20 breaths per minute. a. Determine blood pressure (2003 Joint National (2) Pediatric: newborn RR is between 30-60 Committee on Prevention, Detection, breaths per minute. Evaluation, and Treatment of High Blood (3) Tachypnea: an increase in rate of breathing, Pressure Guidelines). greater than 20 breaths per minute. (1) Normal adult BP: <120 mmHg systolic; (4) Hyperpnea: an increase in depth and rate of <80 mmHg diastolic. breathing. (2) Prehypertension: 120-139 mmHg systolic; b. Dyspnea: shortness of breath. 80-89 mmHg diastolic. (1) Dyspnea on exertion (DOE): brought on by (3) Hypertension. exercise or activity. (a) Stage 1: 140-159 mmHg systolic; 90- (2) Orthopnea: inability to breathe when in a reclining position. 99 mmHg diastolic. (3) Paroxysmal nocturnal dyspnea (pND): sudden (b) Stage 2: ~160 mmHg systolic; dOO inability to breathe occurring during sleep. (4) Dyspnea Scale: mmHg diastolic. +1 mild, noticeable to patient but not (c) Primary or essential hypertension: no observer. +2 mild, some difficulty, noticeable to identifiable cause for elevated BP. observer. (d) Secondary hypertension: cause can be determined; may be related to arte- -' riosclerosis and vascular disorders, renal disease, endocrine disorders, pregnancy, drug-related. (e) Majority of patients with hypertension are asymptomatic.
146 (PVD); check bilaterally. +3 moderate difficulty, but can continue. (1) Lower extremity: position patient supine, +4 severe difficulty, patient cannot continue. c. Auscultation of the lungs: assess respiratory check femoral, popliteal, dorsalis pedis, sounds. (1) Normal breath sounds. posterior tibial pulse . (2) Assess for adventitious sounds. (a) Crackles (rales): rattling, bubbling sounds; (2) Upper extremity: check radial, brachial, may be due to secretions in the lungs. and carotid pulses. (b) Wheezes: whistling sounds. d. Assess cough: productive or nonproductive. (3) Grading scale. 6. Examine oxygen saturation. a. Use pulse oximetry, an electronic device that 4+ Bounding. measures the degree of saturation of hemoglo- bin with oxygen (SaOz). 3+ Increased. b. Provides an estimate of PaOz based on the oxy- hemoglobin desaturation curve. 2+ Brisk, expected. c. Hypoxemia: abnormally low amount of oxygen in the blood. I+ Diminished, weaker than expected. d. Hypoxia: low oxygen level in the tissues. 7. Examine for pain. o Absent, unable to palpate. a. Chest pain may be cardiac or non-cardiac in origin. (4) Listen for bruit: femoral artery. b. Ischemic cardiac pain (angina or myocardial infarction): diffuse, retrosternal pain; or a sen- c. Examine skin color. sation of tightness, achiness, in the chest; asso- ciated with dyspnea, sweating, indigestion, (1) Cyanosis: bluish color related to decreased dizziness, syncope, anxiety. (1) Angina: sudden or gradual onset; occurs at cardiac output or cold; especially lips, fin- rest or with activity; precipitated by physi- cal or emotional factors, hot or cold tem- gertips, nail beds. peratures; relieved by rest or nitroglycerin. (2) Myocardial infarction pain: sudden onset; (2) Pallor: absence of rosy color in light pain lasts for more than 30 minutes; may have no precipitating factors; not relieved skinned individuals, associated with by medications. (3) Anginal Scale. decreased peripheral blood flow, PVD. 1+ light, barely noticeable. 2+ moderate, bothersome. (3) Rubor: dependent redness with PVD. 3+ severe, very uncomfortable. 4+ most severe pain ever experienced. d. Examine skin temperature. c. Referred pain. (1) Cardiac pain can refer to shoulders, arms, e. Examine for kin changes. neck, or jaw. (2) Pain referred to the back can occur from (1) Clubbing: curvature of the fingernails with dissecting aortic aneurysm. C. Physical Examination - Peripheral Vascular System soft tissue enlargement at base of nail: 1. Examine condition of extremities. a. Check for diaphoresis: excess sweating associ- associated with chronic oxygen deficiency, ated with decreased cardiac output. b. Check arterial pulses: decreased or absent pulses heart failure. associated with peripheral vascular disease (2) Pale, shiny, dry kin, with 10 of hair, asso- ciated with PVD. (3) Abnormal pigmentation, ulceration, der- matitis, gangrene, associated with PVD. f. Examine for intermittent claudication: pain, cramping, and fatigue occurring during exer- cise, and relieved by rest, associated with PVD. (1) Related to arterial insufficiency: pain is typically in calf; may also be in thigh, hips, or buttocks. (2) Patient may experience pain at rest with severe decrease in arterial blood supply; typically in forefoot, worse at night. g. Examine for edema. (1) Check girth mea urements u ing a tape, or volumetric measurements u ing a volumeter (useful with irregular body parts, such as hand or foot). (2) Pitting edema (indentation): depression is maintained when finger is pressed fLfrnly; grading scale. Mild 1+ <V4\" depth of depression. Moderate 2+ V4\" to 1;2\" depth of depre ion.
Severe 3+ 112\" to 1\" depth of Cardiovascular Physical Therapy 147 depression. 3. Tests of peripheral arterial circulation. a. Rubor of dependency. Check color changes in (3) Bilateral edema is associated with conges- skin during elevation of foot followed by dependency (seated, hanging position). tive heart failure. (1) With insuffiency, pallor develops in elevat- ed position; reactive hyperemia (rubor of (4) Unilateral edema is associated with local dependency) develops in dependent posi- tion. factors, thrombophlebitis, PVD. (2) Changes that take longer than 30 seconds are also indicative of arterial insufficiency. 2. Tests of peripheral venous circulation. b. Venous filling time. Check time necessary to refill veins after emptying. a. Examine venous system before arterial; venous (1) With patient supine, leg elevated about 60° for I minute, then place leg in dependent insufficiency can invalidate some arterial tests position. Note time for veins to refill. (2) Greater than 10-15 seconds is indicative of (Table 3-4). arterial insufficiency. c. Examine for intermittent claudication: exer- b. Percussion test: determines competence of cise-induced pain or cramping in the legs that is absent at rest. Usually calf pain, but may also greater saphenous vein. occur in buttock, hip, thigh, or foot. (1) Have the patient walk on level grade, I (1) In standing, palpate one segment of vein milelhour, e.g., treadmill. Test is stopped with claudicatory pain. while percussing vein approximately 20 cm (2) Note time of test. Use subjective ratings of pain to classify degree of claudication. higher. Grade I: minimal discomfort or pain. Grade II: moderate discomfort or pain, (2) If pulse wave is felt by lower hand, the patient's attention can be diverted. Grade ill: intense pain, patient's attention intervening valves are incompetent. cannot be diverted. Grade IV: excruciating and unbearable c. Trendelenburg's test (retrograde filling test): pain. (3) Check for coldness, numbness, or pallor in determiJ;les competence of communicating the legs or feet; loss of hair over anterior tibial area. veins and saphenous system. (4) Leg cramps may also result from diuretic use with hypokalemia.. (1) Patient is positioned in supine with legs 4. Examine lymphatic system. elevated to 60 degrees (empties venous a. Palpate superficial lymph nodes: cervical, axil- lary, epitrocWear, superficial inguinal. blood). b. Check for edema. (1) Visual inspection: note swelling, decreased (2) Tourniquet is then placed on proximal thigh range of motion, loss of functional mobility. (2) Check girth measurements. (occludes venous flow in the superficial c. Paresthesias may be present. d. Lymphoscintigraphy using radioactive agents veins). (x-ray of lymph vessels): provides information about lymph flow, lymph node uptake, and (3) Patient is then asked to stand. backflow. (4) Examiner notes if veins fill in normal pat- tern. Should take approximately 30 seconds. d. Doppler ultrasound: examination using an ultrasonic oscillator connected to earphones. (1) Determines blood flow within a vessel, useful in both venous and arterial disease. (2) Doppler probe placed over large vessel; ultrasound signal given transcutaneously; movement of blood causes an audible shift in signal frequency. (3) Useful in locating nonpalpable pulses, measuring systolic BP in extremities. e. Air plethysmography (APG): pneumatic device calibrated to measure patency of venous system; volume. (1) Cuff is inflated around calf, attached to a pressure transducer and microprocessor. (2) Occludes venous return, permits arterial inflow; recorder registers increasing vol- ume with cuff; time to return to baseline with cuff deflation. (3) Comparison tests performed in sitting, standing, and up onto toes.
148 a. Cholesterol: desirable: <200, borderline: 200- 230, high risk: >240. C. Diagnostic Tests 1. Chest x-ray: will reveal abnormalities of lung flu- b. High-density lipoprotein (HDL): low risk: >60, ids, overall cardiac shape and size (cardiomegaly), moderate risk: 35-60, high risk: <35. aneurysm. 2. Myocardial perfusion imaging: used to diagnose c. Low density lipoprotein (LDL): >100 with mul- and evaluate ischemic heart disease, myocardial tiple risk factors, > 160 for low risk individuals. infarction. a. Thallium-201 scan: thallium (or other radioiso- d. Triglycerides: desirable: <165. tope) is injected into blood via IV; radioisotopes e. LDLIHDL ratio: low risk: 0.5-3.0, moderate concentrate in normal tissue but not in ischemic or infarcted tissues (cold spots). risk: 3.0-6.0; high risk: >6.0. b. Used to identify myocardial blood flow, areas of stre s-induced ischemia (exercise test), old III. Coronary Artery Disease (CAD) infarcts. c. Thallium stress test: used with exercise test Definition: an athero clerotic disea e process that (treadmill or bicycle ergometer); injected at narrows the lumen of coronary arteries, resulting peak exercise. in ischemia to the myocardium; can progress to d. Positron emission tomography (PET); uses injury and death. radio-active marker (18F-fluorodeoxyglucose A. Atherosclerosis (FDG). 1. Disease of moderate and large arteries; not limited 3. Echocardiogram: noninvasive test that uses ultra- to the coronary arteries. sound to visualize internal structures (size of 2. Characterized by thickening of the intimal layer of chambers, movement of valves, septum, abnormal the blood ve el wall from focal accumulation of wall movement). lipids, platelets, monocyte , plaque and other debris. 4. Cardiac catheterization or cath: passage of a tiny 3. Multiple risk factors are linked to atherosclerosis. tube through heart into blood vessels with intro- a. Non-modifiable risk factors: age, sex, race, duction of a contrast medium into coronary arteries and subsequent x-ray. family history of CAD. a. Provides information about anatomy of heart b. Modifiable risk factors: cigarette smoking, and great vessels, ventricular function, abnor- mal wall movements. high blood pressure, elevated chole terollevels b. Allows determination of ejection fraction (EF). and LDL levels, elevated blood homocystine, 5. Central line (Swan Ganz catheter): catheter insert- obesity, inactivity, stress. ed through vessels into right side of heart. c. Contributory di ea e : diabetes. Measures central venous pressure (CVP), pul- d. Two or more risk factors multiplies the risk of monary artery pressure (PA), pulmonary capillary CAD. wedge pressures (PCWP). B. Main Clinical Syndromes of CAD 1. Angina pectoris: substernal chest pain or pressure; D. Laboratory Tests and Values may be accompanied by Levine sign (patient 1. (Table 3-1). clenches fist over sternum). 2. Enzyme changes associated with myocardial a. Represents imbalance in myocardial oxygen infarction. supply and demand; brought on by: a. Elevations in SGOT (serum glutamic- (1) Increased demand on heart: exertion, emo- oxaloacetic transaminase) (peaks 24-48 hr). b. Elevations CK or CPK (serum creatine phos- tional tress, moking, extremes of temper- pho kinase) (peaks at 24 hr), CK-MB (serum ature especially cold, overeating, tach- creatine kinase MB) (peaks 12-24 hr). yarrhythmias. c. Elevations in LDH (serum lactate dehydroge- (2) Vasospasm: symptoms may be present at nase) (peaks 3-6 days). rest. 3. Serum lipids (Lipid Panel) (mgldl): used to deter- b. Types of angina. mine coronary risk. (1) Stable angina: classic exertional angina; occur at a predictable rate-pressure prod- uct, RPP (HR x BP), relieved with rest and/or nitroglycerin. (2) Unstable angina (preinfarction, crescendo angina): coronary insufficiency with risk
Cardiovascular Physical Therapy 149 for myocardial infarction or sudden death; a. Precipitating factors: atherosclerotic heart disease pain is difficult to control; doesn't occur at with thrombus formation, coronary vasospasm or predictable RPP. emboli m; cocaine toxicity. 2. Myocardial infarction, MI: prolonged ischemia, injury, and death of an area of the myocardium b. Zones of infarction. (Figure 3-2). caused by occlusion of one or more of the coro- (1) Central zone: consists of necrotic, noncon- nary arteries. tractile tissue; electrically inert; on EKG, see pathological Q waves. TABLE 3-1 - LABORATORY TESTS &VALUES NORMALVALUES CLINICAL SIGNIFICANCE NORMAL VALUES CLINICAL SIGNIFICANCE Arterial Blood Gases (ABGs) Complete Blood Cell Count (CBC), adult values SaO. :> 95% SaO> below 88-90% usually requires Leukocytes (WBCs) Indicative of status of immune system. supplemental 0, t in infection: bacterial, viral; inflammation, Male & Female: hematologic malignancy, leukemia, lymphoma, PaO, 80-1 OOmmHg t in hyperventilation 5,000-10,000 cellslmm3 drugs (corticosteroids) -I, in aplastic anemia, B12 or folate deficiency + in cardiac decompensation, COPO and some With immunosuppression: t risk of infection Exercise considerations: neuromuscular disorders > 5000 use light exercise only < 5000 with fever exercise is contraindicated PaCo, 35-45mmHg t in COPO < 1000 use mask, standard precautions + in pregnancy, pulmonary embolism and anxiety pH, whole blood 7.35-7.45 below 7.35 is acidotic, above 7.45 is alkalotic t in Respiratory alkalosis: hyperventilation, sepsis, liver disease, fever Erythrocytes (RBCs) t in polycythemia t in Metabolic alkalosis: vomiting, potassium Male: 4.7-6.1106/mm3 depletion, diuretics, volume depletion Female: 4.2-5.4 106/mm3 + in anemia + in Respiratory acidosis: COPO, respiratory Erythrocyte Sedimentation t in infection and inflammation: rheumatic or Rate (ESR) pelvic inflammatory disease, osteomyelitis depressants, myasthenia Male up to 15mm/hr Used to monitor effects of treatment, e.g. RA, Female up to 20 mm/hr SLE, Hodgkin's disease + in Metabolic acidosis (bicarbonate deficit): Hematocrit (HeI) % of RBC t in erythrocytosis, dehydration, shock increased acids (diabetes, alcohol, starvation); of the whole blood vol. renal failure, increased acid intake and loss of Male 42-52% + in severe anemias, acute hemorrhage alkaline body fluids Female 37-47% (age dependent) Exercise considerations: Hemostasis (ClottingIBleeding times) > 25% but less than normal:light exercise only < 25% exercise is contraindicated Prothrombin time (PT) Prolonged in factor X deficiency, hemorrhagic 11-15 sec disease, cirrhosis, hepatitis drugs (warfarin) Hemoglobin, total t polycythemia, dehydration, shock Male: 14-18 g/dL If clotting time is t 2.5 times or more normal: Female: 12-16 g/dL + in anemias, prolonged hemorrhage, RBC physical therapy is contraindicated (age-dependent) destruction (cancer, sickle cell disease) Partial Thromboplastin t in factor VIII, IX, and X deficiency Exercise considerations: Time(PTI) 25-40 sec Low values (8-1 Og/dL) resu~ in + exercise tolerance, International normalized ratio INR < 2 desirable (INR): Ratio of individual's INR > 2: consult with M.D. for t risk of bleeding t fatigue, and tachycardia: use light exercise only PTto reference range INR > 3 t risk of hemarthrosis 0.9-1.1 (ratio) < 8g/dL exercise contraindicated Platelet count t chronic leukemia, hemoconcentration 150,000450,000 cellslmm3 + thrombocytopenia, acute leukemia, aplastic Bleeding time t in platelet disorders, thrombocytopenia anemia, cancer chemotherapy 2-10 min Exercise considerations: < 20,000: AROM, AOLs only 20,000-30,000: use light exercise only 30,000-50,000: use moderate exercise Fibrinogen, plasma t in inflammatory states, pregnancy, oral 175-433 mg/dL contraceptives + in cirrhosis, hereditary diseases Nicoll D, McPhee S, Chou T, Detmer W (eds) (1997). Pocket Guide to Diagnostic Tests, 2nd ed. Stamford CT, Appleton & Lange. Goodman D, Boissonnault W (1998). Pathology: Implications for the Physical Therapist. Philadelphia, w.G. Saunders Co.
150 (2) Zone of injury: area immediately adjacent flex artery. to central zone, tissue is noncontractile, (c) Anterior MI, disturbances of lower cells undergoing metabolic changes; elec- trically unstable; on EKG, see elevated ST conduction sy tem: left anterior segments in leads over injured area. descending artery. d. Impaired ventricular function results in: (3) Zone of ischemia: outer area, cells also (1) Decreased stroke volume, cardiac output under-going metabolic changes, electrically and ejection fraction. unstable; on EKG, ee T wave inversion. (2) Increased end diastolic ventricular pressures. e. Electrical instability: arrhythmias, present in c. Infarction sites. injured and ischemic areas. (1) Transmural (Q wave infarctions): full 3. Heart failure, H.E (cardiac failure): a condition in thickness of myocardium. which the heart is unable to maintain adequate cir- (2) Nontransmural (non Q wave infarctions): culation of the blood to meet the metabolic needs subendocardial, subepicardial, intramural of the body. Termed conge tive heart failure infarctions. (CHF) when edema is present. (Table 3-2). (3) Sites of coronary artery occlusion. (Figure a. Etiology: results from impairment of left ven- 3-3). tricular functioning; from coronary artery dis- (a) Inferior MI, right ventricle infarction, ease, valvular disease, congenital heart disease, disturbances of upper conduction sys- hypertension, or infection. tem: right coronary artery. b. Physiological abnormalities: decreased cardiac (b) Lateral MI, ventricular ectopy: circum- output, elevated end diastolic pressures (pre- load); increased heart rate; impaired ventricular TABLE 3-2 - POSSIBLE CLINICAL function which, over time, may progress to car- MANIFESTATIONS OF CARDIAC FAILURE diomyopathy. c. Left heart failure (forward H.E): blood is not SIGNS ASSOCIATED WITH RIGHT-SIDED HEART FAILURE adequately pumped into systemic circulation; due to an inability of left ventricle to pump, Nausea Increase in RAP, CVP increases in ventricular end-diastolic pressure Anorexia and left atrial pres ures, with: Weight gain Jugular venous distention (1) Increased pulmonary artery pressures and Ascites pulmonary edema. Right upper quadrant + hepatojugular reflex (2) Pulmonary signs and symptoms: cough, dyspnea, orthopnea. pain Right ventricular heave (3) Weakness, fatigue. d. Right heart failure (backward heart failure): Murmur of tricuspid insufficiency blood is not adequately returned from the sys- Hepatomegaly temic circulation to the heart; due to failure of Peripheral edema right ventricle, increased pulmonary artery pressures, with: SIGNS ASSOCIATED WITH LEFT-SIDED HEART FAILURE (1) Peripheral edema: weight gain, venous stasis. (2) Nausea, anorexia. Fatigue Tachycardia e. Compensated heart failure: symptoms are con- trolled by medical therapy. Cough S3 gallop f. Sympathetic stimulation results in tachycardia. g. Decreased cardiac output results in pre-renal Shortness of breath Crackles failure. 4. Sudden death. DOE Increased PAP, PAWP, SVR C. Medical and Surgical Management of Cardiovas- cular Disease Orthopnea Laterally displaced PMI 1. Diet: low salt, low chole terol, weight reduction. PND Left ventricular heave Diaphoresis Pulsus Alternans Confusion Decreased urine output Cheyne-Stokes respirations (advanced failure) Murmur of mitral insufficiency RAP, right atrial pressure. CVP, central venous pressure. PAP, pulmonary artery pressure. PAWP, pulmonary artery wedge pressure. SVR, systemic vascular resistance. DOE, dyspnea on exertion. PND, paroxysmal noctumal dyspnea. PMI, point of maximal impulse. From Pocket Guide to Cardiovascular Care, 1990 by Susan Stillwell and Edith Randall, CV Mosby Company, p19, with permission.
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