Spinal Manual Therapy SECOND EDITION by M. Howard

94 Chapter 11 Figure 11-10. Example of weak deep neck flexors. Figure 11.11a. Training of deep neck flexors phase I. Becau c the postcrior scalene and levator scapulae stretches incorporate lower cervic;)l f lexion, the therapist and patient need to exercise caution. It is possible to exacer­ bate a latent derangement on the stretched side. Therefore, the patient must not overstretch, stop at the first indication of peripheral symptoms, return slowly to the start position, and perform a few prophylactic neck retractions to protect against disc disturbance. Cervical Strengthening Exercises The phasic muscles that require strengthening and Figure 11-11b. Training of deep neck flexors phase 2. endurance training in the head-neck region are the upper cervical or deep neck flexors and the lower cervical segmen­ (CCFr), using the Stabilizer pre sure biofeedback device tal extensors. It is only when these muscles are strong and (Chattanooga Group Inc, Chattanooga, TN) or the flexor possess good endurance that the tendency towards FHP (ie, endurance test, which demonstrated excellent intratester \"backward head/forward neck\") can be overcome. When these muscles are weak, the patient demonstrates occipital reliability (intraclass coefficient of 0.92 for women and 0.93 extension upon attempting to flex the head-neck region, rather than flexion, suggesting that substitution with the for men).21 The flexor endurance test21 involves the follow­ sternocleidomastoid muscles is taking place (Figure 11-10). ing steps: To strengthen the occipital or upper cervical flexors 1. The subject assumes the supine hook-lying position (ie, rectus capitis anterior, longus capitis, and rectus capi­ with hands resting on his or her abdomen. tis lateralis muscles), the supine patient is instructed to perform passive upper cervical spine f lexion followed by 2. The subject is then asked to raise his/her head just lower cervical f lexion (phase 1) with his or her fingers inter­ locked behind the occiput (Figure 11-l1a). The patient then enough to allow the tester to slide the widths of the progresses from passive to active assisted to active f lexion index and middle finger of one hand, one on top of the other, under the subject's head at the most poste­ (phase 2) without the assist from his or her hands (Figure rior aspect of the occiput. Ll-11b). The deep neck flexor of the lower cervical spine, 3. The subject is allowed to rest his/her head-neck on the longus colli, is recruited when the lower cervical spine is flexed with the head in the chin-tuck position. the examiner's fingers. A deficiency in endurance of the deep neck (cervi­ 4. The subject is then asked to \"tuck the chin com­ cal) flexor muscles (longus capitis, rectus capitis anterior, pletely\" (craniocervical f lexion) and to raise the head rectus capitis lateralis, and longus colli) is associated with just off the examiner's fingers (cervical flexion). The neck pain, forward head posture, as well as cervicogenic examiner gently moves his or her fingers side to side and tension-type headache.20,47,51,87-90 Endurance of these under the subject's head, providing a tactile reminder muscles can be tested with the craniocervical flexion test20 for maintaining proper head-neck position during the test (Figure II-lIe). Copyrighted Materail

Therapeutic and Home Exercises for the Cervical Spine 95 figure ll-11c. The flexor endurance test. figure 11-11d. Training of deep neck flexor muscle endur­ ance. figure 11-12a. Tr,lining lower cervical' extensors w hile prone. 5. Time is started when the subject's head is raised off figure 11-12b. Training lower cervical the tester's fingers and ended when any of the follow­ extensors while sitting. ing conditions are met: head-neck region is placed over the end of the table as a. The subject experiences pain and is unwilling to the therapist localizes axial extension to the C4 through continue. C7 levels, one segment at a time (Figure 11-12a). Once properly localized to the barrier of bilateral apophyseal b. The subject reaches the end of endurance and is joint extension, the therapist withdraws his or her forehead unwilling to continue. support and the patient performs an isometric contraction of the segmental extensor muscles. Through bilateral facet c. The examiner determines that the chin-tuck has palpation, the therapist ensures that the patient activates been lost. the desired segmental extensor muscles. Similar segmental extensor training can be performed in sitting as well (Figure d. The examiner determines that the subject raises 11-12b). the head (flexes the neck while still in a chin­ tuck) such that the tester's fingers no longer For either the upper cervical flexors or the lower cervical maintain contact. segmental extensors, the patient, following competency in the clinic, can perform self-strengthening at home. He or Endurance of the deep neck flexors is trained by having she can do 10 repetitions, holding each repetition for 5 to the patient maintain a chin-tuck position over the end of 10 seconds, repeating 3 times per day. the table for progressively longer periods of time (Figure ll-lld). In the beginning, therapist support will be needed. However, with improvement, the patient should be able to maintain this position for at least 10 seconds without shak­ ing or anxiousness. To strengthen the lower cervical segmental extensors (ie, semispinalis cervicis and multifidus), the prone patient's Copyrighted Materail

96 Chapter 1 I In addition to the postural realignment function of the Occivator mentioned previou.,ly in this chapter, it is also used to enhanc e the strength of the occipital flexor muscles, lower cervical segmental extensors, and the lower scapular stahilizt'rs, simultaneously. A second device developed by this author, the Posture)ac, has the advantage of being a portahle posture-retraining device and will he covered in detail in Chapter 25. Lastly, the Stabi,lizer alluded to previously, has an air­ filled pressure sensor that monitors the slight flattening of the cl'1'vical lordosis (Figure 11-13). In addition to its role in the CCFT,20 the Stabilizer is also useful as a biofeedback tool in the retraining of motor control, strength, and endur­ ance of the deep neck flexors. 20 Figure 11-13. B iofccdback of the deep neck flexors with the Stabilizer. Copyrighted Materail

The Role of the Cervical Spine in Headache and DizzinessF==========+====== L-__-=============__ ==__________________________==== - he head and neck are areas of intense postural and pars caudalis (Figure 12-l). The pars caudalis is the most -9 caudal of the 3 and merges imperceptibly with the dorsal 99-1 Treflex activitylO Examples include the tonic neck, horns of the upper 3 cervical spinal cord segments, consist­ cervicocollic, cervicorespiratory, cervicosympa­ ing of the marginal zone, substantia gelatinosa, and the thetic, cervico-ocular, and trigeminocervical reflexes to nucleus proprius. The spinal tract of the trigeminal nerve name a few9! Consequently, in the presence of cervical descends caudally through the medulla oblongata as far as spine impairment, particularly in the uppermost segments, the C4 level. Fibers from the spinal tract terminate in the there is the potential for many systems to be adversely gray matter of the pars caudalis and upper 3 cervical cord impactedIO,91 segments. Bogduk921, 02 dizziness are common features of cervical impairment, of interconnecting gray matter of the pars caudalis and injury, or disease. Their cervical causes are of great interest the upper cervical dorsal horns as the \"trigeminllcervical to manual therapists. In this chapter, the role of the cervi­ nucleus.\" This nucleus is defined not by intrinsic features, cal spine in both headache and dizziness will be explored. but by the afferent input it receives from the spinal tract of Porterfield and DeRosa95 state, \"The neurosciences of the the fifth cranial nerve. Because it incorporates the neuro­ cervical spine have a degree of complexity found in no anatomic structures responsible for pain transmission and other region of the axial skeleton.\" We will certainly be receives afferent input from trigeminal and upper cervical exposed to some of this complexity in this chapter. nerves, the trigeminocervical nucleus can be seen as the nociceptive nucleus for the entire head and upper neck. Headache In addition, Mannheimer and Rosenthal94 report that the entire trigeminocervical complex includes not only the fifth Headache of cervical origin (ie, cervicogenic headache cranial nerve, but also receives input from the 7th, 9th, [CGH]) accounts for 15% to 20% of all chronic and recur­ lOth, 11th, and 12th cranial nerves as well. The clinical ring headaChes, and up to 70% of individuals with frequent significance of these scientific discoveries is summarized by intermittent headaChe (eg, 50 million in the United States) Jull,103 who states, 'Through the convergence of cervical and trigeminal afferents on common neurons in the rigemi­ report associated neck pain 88.96-lJS nal nucleus, any structure innervated by any of the upper three cervical nerves may refer pain into the head and face.\" To better understand the role of the cervical spine Furthermore, Ju1l88 describes \"bi-directional illlcractions\" between trigeminal and upper cervical afferents within the ll1 GH88, and its contribution to other forms of trigeminocervical nucleus. Consequently, this may explain not only head and face pain of upper cervical origin, but also chronic headaChe, it is necessary to review our current neck symptoms of trigeminal origin (eg, migraine). understanding of the neuroanatomy of the upper cervical spinal cord. The spinal nucleus of the trigeminal nerve (ie, fifth cra­ nial nerve) consists of 3 parts: pars oralis, pars interpolaris, 97 1\\l.lkfJi':'ik)'IIW Spiprtrl MlIrrrM/ rI'('rrtp)', but rd. (pp 97·IO ) C) 2010 SLj\\( K IncMplJI.lkJ Copyrighted Materail

98 Chapter 12 v C 1 =-:-< \\ LI pars caudalls spinal tract C2 C3 Figure 12-2. Head and temporomandibular j oint/facial pain Figure 12-1. The trigeminocervical n ucleus. of cervical origin . (Reprin ted with permission from Okeson (Reprinted with permission from Bogduk N. J. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Cervical causes of headache and dizziness. Management. Chicago, II: Quintessence Publishing; 1996.) In: Grieve's Modern Manual Therapy. 2nd ed. New York, NY: Churchill L ivin gston e; 1994.) indirect role of the upper cervical region in other forms of chronic headache, including tension-type, migraine with Although the pathophysiology of CGH is not completely and without aura, posttraumatic headache (PTH), and understood, Bogduk92 believes that there is sufficient \"cir­ analgesic rebound headache. The role of the cervical spine cumstantial evidence\" pointing to the convergence between in temporomandibular disorders (TMD) will be addressed nerves that innervate the head and nerves that innervate in a subsequent chapter. the cervical spine as the \"foundational mechanism.\" He goes on to say that this is not simply convergence between CGH is a form of secondary headache arising from pain­ trigeminal and cervical afferents, for in addition to innerva­ ful dysfunction or disease of the cervical spine, particularly tion by the trigeminal nerve, the head is also innervated by cervical nerves. For example, the occiput and regions as far the upper 3 segments. In 2004, the International Headache forward as the coronal suture are innervated by the greater occipital nerve, the lesser occipital nerve, and the greater Society (IHS) accepted CGH as a discrete hC<lJache auricular nerve, whereas the forehead and orbital regions type, as published in the 2nd edition of the International are innervated by the trigeminal nerve. Consequently, Classification of Headache Disorders.104 Prior to that, the CGH perceived anterior to the coronal suture implies Cervicogenic Headache International Study Group estab­ convergence between cervical and trigeminal afferents; CGH posterior to the coronal suture suggests convergence lished diagnostic criteria for CGH in 1990 and again in between certain cervical and other cervical afferents.92 1998105 The following are the current IHS diagnostic crite­ To support the concept of upper cervical pain referral ria for CGH89,98-101: into the head and face, Bogduk102 cites several studies in this regard and then states the following, 'These experi­ 1. Pain localized in the neck and occiput, which can ments clearly demonstrate the capacity of experimental painful stimuli in the upper neck to produce pain in the spread to other areas in the head, such as the fore­ head. It is possible, therefore, that pathological painful head, orbital region, temples, vertex, or ears, usually lesions of any of the structures innervated by the upper cer­ unilateral. vical nerves are equally capable of producing such referred pain\" (Figure 12-2). 2 . Pain preCipitated o r aggravated b y specific neck move ­ ments or sustained postures. When considering the role of the cervical spine in head­ ache, there are 2 possible connections. The first involves 3. At least one of the following: direct pain referral from upper cervical spine disease or somatic impairment (ie, CGH). The second involves the a. Resistance to or limitation of passive neck move­ ments, b. Changes in neck muscle contour, texture, tone, or response to active and passive stretching and contraction, and/or c. Abnormal tenderness of neck musculature. 4. Radiological examination reveals at least one of the following: Copyrighted Materail

The Role of the Cervical Spine in Headache and Dizziness 99 a. Movement abnormalities cervical origin. In addition to the role of manual therapy in the management of headaches of cervical spine origin, b. Abnormal posture Ju1l20,lll emphasizes the importance of specific retraining of the upper cervical flexor muscles, the lower trapezius, and c. Fractures, congenital abnormalities, bone tumors, serratus anterior, combined with postural retraining as well rheumatoid arthritis, or other distinct pathology as ergonomic and lifestyle advice. (not spondylosis or osteochondrosis). There is some controversy regarding the role of the In addition, the presence of painful upper cervical joint cervical spine in such primary headache conditions as dysfunction, accompanied by impairments in the deep migraine and tension-type headache. However, several stud­ cervical flexors, scapular postural muscles, and cervical ies have established a correlation between chronic tension­ kinaesthesia, suggests that the headache is of cervical origin.97,106 Headache characteristics include moderate to type headache and 1) FHp49,SO; 2) neck mobilitySO,90,ll2; severe, nonthrobbing, and nonlancinating pain, usually starting in the neck and eventually spreading to the ocu­ 3) reduced deep cervical muscle strength and endur­ lofrontotemporal area on the symptomatic side. CGH is, in principle, a unilateral headache, but it may become bilateral ance4S,llJ; and 4) active myofascial trigger points in the over time. The frontotemporal pain may at times exceed the neck/occipital pain. In the initial phase, the headache is suboccipital muscles, upper trapezius, SCM, and temporalis usually episodic; later it becomes chronic with a fluctuating muscles.49,ll4 Regarding episodic tension-type headache, quality. Occasionally, patients with CGH also report nau­ the following somatic features have been identified versus sea, phonophobia/photophobia, dizziness, blurred vision, difficulty swallowing, and ipsilateral edema in the periocu­ a healthy nonheadache control groupllS: 1) smaller cra­ lar area. However, these \"attack-related phenomena\" are not the major features of this headache. Diagnostic anesthetic niovertebral angle (ie, FHP); 2) decreased neck mobility; blockade of the greater/lesser occipital nerves, C2 and C3 and 3) more active myofascial trigger points in the upper roots, third occipital nerve, facet joints, and lower cervical trapezius, SCM, and temporalis muscles. roots and branches on the symptomatic side should tem­ porarily abolish the pain of CGH. However, Ju1l88 suggests In addition, there is a growing body of knowledge sug­ that there are problems of specificity with diagnostic blocks gesting that the musculoskeletal system does in fact play a and are therefore \"not fail-safe for the diagnosis of CGH.\" role in the pathogenesis and management of migraine,ll6 Of the 3 spinal segments involved with CGH (ie, OA, AA, including a recent study showing that subjects with unilat­ and C2,3), the C2,3 facet joints are thought to play the eral migraine had a significantly greater number of active most significant role.107 Having said that, other researchers trigger points on the same side as the migraine as well provide upport for the role of C1,2 segmental dysfunction as a greater forward head posture in both the sitting and in CGH. Specifically, Hall and Robinson found that sub­ standing positions versus healthy controls.ll7 As far back as jects with CGH have an average of 17 degrees less rotation 1995, Hack et al1l8 identified a fibrous connection between toward the headache side in the flexion-rotation test (FRT) the rectus capitis posterior minor muscle and the posterior in contrast to subjects with no headache. T he FRT, which atlanto-occipital membrane, which attaches to the cranial identifies restriction of rotation at the Cl,2 segment, has a dura mater. This proposed \"myodural bridge\" shed light on the connection between subcranial muscle tension and sensitivity of 86% and a specificity of 100% for detecting migraine. In a study by Marcus et al,ll9 postural abnormali­ ties were more prevalent in patients with migraine and ten­ CGH.108 Studies have also shown a connection between sion-type headache than in the controls. Karpouzis et all20 CGH, FHP, weak and poor endurance of the deep cervical showed that a history of head, neck, and back injury was the flexors, facet joint arthropathy, cervical spine trauma, and most commonly reported circumstance related to the onset joint hypo/hypermobility including clinical cervical spine of chronic headache in 1013 patients; Silberstein et ajl21 instability.20,42,47,89,109 Consequently, the role of spinal demonstrated a clinically favorable response to pericranial manual therapy and specific exercise as an intervention for injection of botulinum toxin type A with reduced migraine CGH is gaining momentum. In fact, the Evidence Report: frequency, severity, acute medication usage, and associ­ Behavioral and Ph)'sical Treatments for Tension-Type and ated vomiting. Whereas most neurology-based textbuoks and articles view muscle contraction as a consequence Cervicogenic Headache from the Duke University Evidence­ of migraine, Silberstein et all21 raise the possibility that muscle contraction may play a role in migraine pathogen­ Based Practice Center published in 2001 concluded the fol­ esis through some \"as of yet unknown effect on the sensory system.\" Thus, we see an increasingly important role of lowing: \"Cervical spine manipulation was associated with the cervical spine in headache diagnosis and management significant improvements in headache outcomes in trials emerging in the scientific literature. Whether this role is involving patients with neck pain and/or neck dysfunction as an etiologic factor in primary headache pathogenesis or secondary to the neurochemical pain pathophysiology and headache.\"llO Schoensee et aI,lO7 investigating the effect expressed in migraine and tension-type headache remains to be determined. of upper cervical mobilization on the frequency, duration, and intensity of cervical headaches, concluded that manual Moskowitzl22 proposed a mechanism whereby an upper therapy was effective as an intervention for headaches of cervical impairment can give rise to a throbbing vascu­ Copyrighted Materail

1 00 Chapter 72 lar headache. This mechanism involves the activation of from an impaired upper cervical region is one of many fac­ trigeminal sensory fibers in the brainstem, which in turn . tors. Migraine, whether with or without aura, is primarily a trigger an efferent pathway through the facial nerve to disturbance within the trigeminal system, with the greatest the greater superficial petrosal nerve. The greater super­ pathophysiology emanating from the trigeminov;]scular ficial petrosal nerve provides the autonomic connection junctions at the base of the brain and in the dura mater. 109. by innervating autonomic pathways in the cranial vascu­ 121,122.125.128 Supporting the role of the trigeminal system in lature. Some have used this and other similar physiologic migraine, DaSilva et al129 recently demonstrated structural mechanisms12.3 to suggest a major role of the cervical spine changes with MRI (eg, thickness) in the somJtosensory in migraine. However, the literature does not support this cortex of migraine sufferers compared to Jge and gender­ concept. A more plausible argument, and the one to which matched controls. The most significant thickness changes the author subscribes, is that upper cervical spine impair­ were noticed in the caudal somatosensory cortex, where the ment (eg, OA, A A, and/or C2,3 joint dysfunction, forward trigeminal area is somatotopically represented. The authors head posture, myofascial trigger points, greater occipital conclude that, \"Repetitive migraine attacks may lead to, or nerve entrapment) is one of many factors in migraine be the result of neoplastic changes in cortical and subcor­ pathogenesis leading to what is known as central sensitiza­ tical structures of the trigeminal somatosensory system.\" tion109,114.117.124-126 (ie, somatosensory hypersensitivit y). There appears to be little to no benefit of manual therapy Similar to the role of emotional stress, dietary triggers, sleep during an attack of migraine, but between episodes there deprivation, hypoglycemia, hormonal factors in women, is Significant benefit. By correcting somatic impairment etc, the presence of chronic upper cervical spine impair­ throughout the head, neck, TMJ, and upper back,130 there ment, leading to nociceptive-neuronal hyperexcitability of will be less nociceptive input into the trigeminocervical the trigeminocervical nucleus, has the potential to trigger a nucleus. This \"de-facilitation\" will have the net effect of migraine attack. Nocturnal bruxisml27 and fibromyalgia124 raising the central pain threshold for the head and upper are thought to trigger migraine in a similar manner. neck region and hopefully have a beneficial effect on the W hereas migraine was once thought to be a function of frequency, duration, and severity of migraine. intracranial/extracranial vasodilatation (ie, Wolff's vascular There is an effective nonmedicinal strategy that can theoryI25.128), it is now believed that migraine is a complex be employed to abort an extracranial vascular headache. disorder of CNS regulation of pain-producing intracranial According to Willis,131 a tourniquet is applied around the structures (ie, neurovascular malregulation leading to neu­ head just above the ears. The best time to use this method rogenic inflammation125.129 of the trigeminovascular com­ is just prior to the headache, but it can be used during the plex). Based upon this neurovascular theory 109.125.128 and migraine, providing that the scalp is not overly sensitive to given that migraine in known to run in families and affect pressure (ie, allodyniaI25). The tightness of the tourniquet is a large segment of the population (30 million Americans), to be moderate in nature and it can be left in place for sev­ this author considers the following the best definition of eral hours. The principle behind this method is based upon migraine to date, \"A common, disabling malfunction of Laplace's law, where T = Pr. T represents the circumferential the pain-regulating mechanism of the brain.\" It is beyond tension within the vessel wall, P represents the pressure gra­ the scope of this chapter to provide a detailed analysis of dient across the vessel, and r stands for the radius of the ves­ migraine pathophysiology. However, it is important for sel. Because vasodilatation increases T during migraine, the manual therapists to realize that migraine is enormously arterial wall is stretched and becomes inflamed and painful. complex and that the presence of cervical impairment is When T is decreased with the tourniquet, by decreasing not the \"whole ball of wax.\" In addition to abnormal affer­ P and r, the stretch on the vessel wall is lessened and the ent input from the upper cervical area (mainly through the headache diminishes. This is a useful method in patients opthalmic division of the trigeminal nerve92.94.102.103), the who cannot tolerate migraine medication. trigeminocervical nucleus receives afferent input from the Regarding PTH,109,125.128 the role of the cervical spine extensive trigeminovascular system, which is thought to cannot be ignored. Although there is a strong correlation be abnormal in patients suffering from migraines. There is between mild head injury and PTH, there is also a large strong evidence to suggest that a neurochemical imbalance percentage of PTH patients who have a history of cervical in serotonin (5-HT) plays a key role in this abnormal­ spinal injury as well. The term posttraumatic migraine has ity.I09.J25.128 Plasma serotonin has been shown to fall at the been used to describe the onset of migraine following mild onset of a migraine attack, and the fact that reserpine (a head injury. However, according to Packard,132 \"trauma serotonin-depleting agent) precipitates migraine is further probably never causes migraine.\" Instead he attributes the evidence that falling serotonin and migraine are related.128 onset of migraine following head injury to a temporary In addition, the relief that migraine sufferers obtain from worsening of preexisting migraine related to a nonspecific the 5-HT agonists is another indication of the serotonin­ stress reaction or to a \"complicating neck sprain,\" which migraine connection.J25.128 may aggravate pre-existing migraine as well. Because the The ta ke-home message from this crash-course in brain symptoms of PTH include physical, psychological, and neurochemistry is that migraine is multifactorial. The input cognitive aspects, its management must involve a multidis­ Copyrighted Materail

The Role of the Cervical Spine in Headache and Dizziness 101 ciplinary approach. Jensen et al133 demonstrated a superior Dizziness effect of manual therapy over cold packs in the treatment of PTH. Using a combination of pinal mobilization, high Dizziness associated with cervical spine movement velocity thrust, and muscle energy techniques, the manual impairments may be secondary to VBI, the vestibular sys­ therapy group demonstrated a more rapid decline in the tem, the visual system, or from cervical spine structures (ie, pain index and overedl use of analgesics compared with the cold pack group. cervicogenic dizziness [CD] 137,138). The term dizziness will There are 2 remaining chronic headache types to dis­ be used, generically, in this chapter to include the following cuss relative to the role of the cervical spine. The first is symptoms: cluster headache and the second is analgesic abuse head­ ache.109,128,[30 Alrhuugh the exact ml'chanism of cluster > Vertigo: A sensation that the environment is spin­ headache remains uncerr<lin, Hildebrandt and Jansen134 ning (external), or that the individual is spinning reported on 2 middle-age males in whum chronic intermit­ (internal). tent hemicrania associated with ciliary injections, lacrima­ tion, and rhinorrhea (typical symprollls of cluster headache) > Presyncopal lightheadedness: A feeling that one is were successfully trcared' with surgical decompression of the about to pass out. C2 and C3 nerve roots. In one case, a pannus-like layered network of veins with arterial supply was the culprit; in the > Disequilibrium: A sensation of imbalance or unsteadi­ other case, it was a network of veins. This study illustrates ness (more prominent in standing). the point that there may be an upper cervical component in some cases of cluster headache. Whether somatic impair­ Dizziness can have central, peripheral, or systemic ment can cause the symptom complex noted in the above causes139-141 Peripheral causes include peripheral vestibu­ 2 cases of vascular compression is unknown, but certainly lopathy, peripheral vestibular disorder (eg, benign parox­ the possibility exists. ysmal positional vertigo), Meniere's disease, labyrinthitis, labyrinthine concussion, vestibulotoxic drugs, perilymph The abuse of both over-the-counter and prescription fistula, etc. Central causes include demyelinating disease, analgesics for chronic headache management is a serious tumors, seizures, VB!, migraine-related vertigo, transient health problem. Although not always to blame, drug­ ischemic attack, minor brain injury, and CD. Systemic mduced factors arc often the cause of what has been referred causes of dizziness include endocrine disease (hypothyroid­ to as transformational migraine135 (ie, the transformation ism, diabetes), pharmacologic side effects (anticonvulsants, of periodic migraine, that over time, takes on a more antihypertensives, tranquilizers, analgesics, muscle relax­ frequent and then continuous pattern). Srikiatkhachorn ants, etc), and the many causes of presyncope (eg, hypo­ et al136 demonstrated that chronic paracetamol admin­ glycemia, panic, vasovagal episode, hypotension, cardiac Istration in laboratory animals resulted in 5-HT deple­ arrhythmias, Valsalva's maneuver, etc). tion that, in turn, produced readaptation of the 5-HT 2a receptor. This change in the 5-HT 2a serotonin receptor Generally, true vertigo indicates a disorder of the inner may be an important mechanism related to the loss of ear, vestibular nerve, brainstem, or cerebellum, whereas VBI analgesic efficacy, ultimately resulting in the daily com­ presents with presyncope and CD with disequilibrium. plaints associated with analgesic abuse. Analgesic abuse headache is finally receiving the attention it deserves and The diagnOSis of VBI is straight forward when the 5 Os, may be prevented or reversed by avoiding the chronic use of analgesic medication. This means that therapists must 3 Ns, and 1 A139,140,142 are present (see special tests section of do a better job of providing nonmedicinal headache relief Chapter 8). However, when only dizziness is present (which to their patients. The normalization of head, neck, TMJ, and spinal function[JO will go a long way toward achiev­ is sometimes the case) diagnosis is difficult. The diagnosis of ing this goal and consequently spare at least some, if not BPPV is also straight forward. It is common in middle age, many, the nightmare of the chronic head, neck, and face pain, in addition to the many other adverse effects associ­ but in about 15% of cases there is a relationship to head ated with analgesic abuse (eg, gastrointestinal, kidney, and liver damage). trauma.19,139,142,143 The patient typically develops severe vertigo when turning over or first lying in bed. The episodes The author, as with much of this textbook, has inten­ last less than a minute and the patient can find another tionally not included an extensive review of the basic sci­ position in which he or she is asymptomatic. As soon as he ence material on this topic. The reader is encouraged to or she moves, however, another attack is provoked. There scan the references in order to broaden his or her knowledge are 2 theories as to how BPPV occurs. One is canalithiasis of the subject. and the other cupulolithiasis.19,140,142 Canalithiasis, caused by free-floating otoconia in one of the semicircular canals, is thought to be the more common of the two. Clinically, the onset of vertigo associated with cupulolithiasis has less latency due to the fact that the otoconia are deposited directly on the cupula (ie, vertigo occurs without significant delay when provoked as compared to canalithiasis). The Hallpike-Dix maneuver (88% sensitivity, 100% specificity) is used to test patients suspected of having BPPV affecting the posterior or anterior canals, whereas the roll test detects horizontal canal BPpv.19,144,145 The treatment of BPPV is Copyrighted Materail

1 02 Chapter 12 best managed with physical procedures geared toward either Figure 12-3a. The Fitz-Ritson or removing debris from the affected canal or decreasing symp­ neck torsion test with the head­ toms through habituation.19 neck turned to the left. demonstrated efficacy with BPPV affecting the anterior and posterior canals, whereas the log roll maneuver is effective ocular and vestibular sensations. Wapner et aP48 discovered in managing horizontal canal BPPV.19,145 lithiasis (especially of the posterior semicircular canal) is that the sensation of tilting or falling could be evoked by suspected, the Semont (\"Liberatory\") maneuver is the tech­ electrical stimulation of the cervical muscles. Grayl49 found nique of choice. The Brandt-Daroff habituation exercises that CD could be relieved by injecting local anesthetic into are a useful tool for those who have difficulty tolerating the canalith repositioning maneuvers mentioned above.19,141,145 the posterior cervical muscles. A detailed description of the above-mentioned diagnostic claim that abnormal afferent input from the cervical region and treatment procedures for BPPV is beyond the scope of results in patient-perceived dizziness. this text. The reader is directed to the references provided. that she doubts whether cervical lesions have a \"profound effect\" on the oculomotor and vestibular systems, but goes CD is a sensation of altered orientation in space and on to say, \"There is evidence that treatment of cervical dys­ di sequilibrium originating from abnormal afferent activity functions can lead to decreased symptoms of dizziness and from the neck.19,1J improvements in postural stability.\" vesti bular dysfunction and, therefore, rarely results in true vertigo. Signs and symptoms of CD include the following: This discussion will conclude with a description of a clinical assessment tool for CD known as the neck torsion Intermittent positioning-type dizziness precipitated by testI9,144,145 (90% sensitivity, 91% specificity), which is head and neck movement. similar to the test developed by Fitz-Ritson.150 seated on a stool that rotates (Figures 12-3a and 12-3b). The No latency period (ie, onset of symptoms is immediate therapist stands behind the patient and holds the patient's upon assuming the provoking position). head steady. tion to prestretch the cervical musculature. With the patient's The duration is anywhere from minutes to hours. eyes closed, the body is rotated to either side with the feet. This motion essentially rotates the neck to either side while Dizziness is fatigable with repeated motion. the semicircular canals are motionless. ness must therefore be of cervical spine origin. Fitz-Ritson Associated signs and symptoms include nystagmus, found that the patients who responded best to manipulative neck pain, suboccipital headaches, and occasionally treatment were those who suffered upper cervical joint prob­ paresthesia in the trigeminal di stribution. lems, along with muscle trauma in that region. the theory that CD arises from abnormal afferent input from Possible head-neck malalignments, such as forward the receptors of the upper cervical spine. head and torticollis. According to Jull and colleagues,20 patients presenting with neck pain, with or without complaints of dizziness, Segmental impairment of the upper cervical spine. lightheadedness, or feelings of unsteadiness, should be examined for impairments in the postural control system. Positive neck torsion test. CD is often associated with whiplash-associated disor­ ders,20 which can make diagnosis difficult as BPPV and VBI can also be trauma related146,147 CD has also been reported in advanced cases of cervical arthritis, herniated cervical discs, and head trauma. In the latter, complaints of ataxia, unsteadiness of gait, and/or postural disequilibrium are the most common. The pathophysiology of CD appears to involve abnor­ mal afferent input to the vestibular nuclei from damaged joint receptors in the upper cervical region, resulting in a false sense of motion. Aspinall 139 attributes CD to a disturbance of the tonic neck reflexes from a distortion of the normal afferent input to the vestibular nuclei from the neck. Herdman19 suggests that inflammation or irritation of the cervical roots or facet joints would lead to a mismatch among vestibular, visual, and cervical inputs. This \"multi­ sensory mismatch\" would then give rise to the symptoms of CD, especially during movements of the head-neck region. Isaacs and BookhoutlZ relate CD to abnormal muscle tone in cervical musculature or following mobilization of the cer­ vical spine, when proprioceptive feedback does not match Copyrighted Materail

The Role of the Cervical Spine in Headache and Dizziness 103 the postural control system20 (ie, sensorimotor control). Regarding the complexity of the cervical spine from a neuroanatomical perspective, the clinician must be cogni­ zant of the multiple inputs and inf luences that affect the somatic structures of the neck. They include, at a minimum, vestibular,19 visual,20,151 limbic,152 craniomandibular,153,154 respiratory,57,155 and visceralll [n addition, migraine head­ ache is believed to cause pain and muscle hypertonicity in the head-neck regionI2:, Consequently, all potential SOurces of cervical spine pain, including pathological causes (eg, undiagnosed fractures), must be identified :md managed if the patient's condition is to improve. This may necessitate referral to a neurologist, neurosurgeon, orthopedic surgeon, internist, ophthalmologist, ear, nose and throat specialist, dentist, dental surgeon, psychiatrist, etc. Figure 12-3b. The Fitz-I\\itson or Section III: Key Points neck tors i on test with the head­ neck turned to the right. 1. The cervical spine is the most mobile region of the vertebral column and is prone to developing clinical This examination includes the following: spinal instability (Panjabil. >- Tests of cervical joint position sense 2. McKenzie's derangement syndrome occurs often in >- Balance the cervical spine, primarily at C5,6 and C6,7. >- Oculomotor control 3. Upper cervical spine impairment may cause headache The oculomotor assessment incorporates the assessment and dizziness, whereas lower cervical impairment may of all aspects of eye movement including the ability to be the source of referred pain into the scapula, chest maintain gaze while moving the head (gaze stability), eye wall, and upper limb. follow while keeping the head still (smooth-pursuit), and maintaining g:nc when the eyes and head are moving (eye­ 4. Avoid performing thrust manipulation in the upper head coordination). The reader is referred to the text by Jull, Sterling, Falla, Treleaven, and O'Leary for more infor­ cervical spine. The benefit does not justify the riskl mation on the assessment and treatment of disturbances in 5. Forward head posture has been lmked to many condi­ tions and needs to be taken seriously. Copyrighted Materail

References �=----- = 1. Cook CE, Hegedus EJ. Orthopedic Physical Examination Tests: 14. McKenzie R A. The Cervical and Thoracic Spine, Mechanical An Evidence-Based Approach. Upper Saddle River, NJ: Pearson Diagnosis and Therapy. Waikanae, New Zealand: R. A, McKenzie; Prentice Hall; 2008. 1990. 2. Cleland J, Orthopaedic Clinical Examination: An Evidence-Based 15. Kramer J, Intervertebral Disc Diseases: Causes, Diagnosis, Approach for Physical Therapists, Carlstadt, NJ: Icon Learning Treatment, and Prophylaxis, 2nd ed. ('w York, NY: Thieme Systems; 2005. Medical Publishers; 1990. 3. Huijbregts PA. Clinical prediction rules: time to sacrifice the holy 16. Rocabado M. Biomechanical relationship of the cranial, cervi­ cow of specificity? I Manual Manipulative Ther, 2007;'15(1):5-8. cal, and hyoid regions. I Craniomandib Pract, '1983;1(3):61-66. 4. Childs JD, Fritz JM, Piva SR, Whitman JM. Proposal of a classifi­ 17. Vidal P, Huijbregts p, Dizziness in orthopaedic physical ther­ cation system for patients with neck pain. I Orthop Sports Phys apy practice: history and physical examination. I Manual Ther. 2004;34(11):686-700. Manipulative Ther. 2005;13(4):221-250, 5. Kendall FP, Kendall McGreary E, Provance PG, Mcintyre Rodgers 18. Ono K, Ebara S, Fuji T, Yonenobu K, Fujiwara K, Yamashita K, M, Romani WA. Muscles: Testing and Function With Posture and Myelopathy hand: new clinical signs of cervical cord damage. Pain. 5th ed. Baltimore, MD: Williams & Wilkins; 2005. I Bone loint Surg. 1987;69B(2):215-219. 6. Andrade GH, Azevedo DC, Lorentz I, et al. Influence of scapular 19. Herdman SJ. Vestibular Rehabilitation. 3rd ed, Philadelphia, PA: position on cervical rotation range of motion. I Orthop Sports F. A. Davis Company; 2007. Phys Ther. 2008;38(11):668-673. 20, Jull G, Sterling M, Falla D, Treleaven L O'Leary S, Whiplash, 7. Rocabado M. Diagnosis and treatment of abnormal craniocervi­ cal and craniomandibular mechanics, In: Solberg WK, Clark Headache, and Neck Pain: Research-Based Directions for GT, eds. Abnormal law Mechanics: Diagnosis and Treatment, Physical Therapies. Edinburgh: Churchill Livingstone; 2008. Chicago, IL: Quintessence Publishing; 1984. 21. Olson LE, Millar AL, Dunker L Hicks L Glanz D, Reliability of a clinical test for deep cervical flexor endurance. I Manipulative 8. Hickey ER, Rondeau MJ, Corrente JR, Abysalh L Seymour CJ. Physiol Ther, 2006;29(2):134-138, Reliability of the cervical range of motion (CROM) device and 22. Fitz-Ritson D. Assessment of cervicogenic vertigo, I Manipulative plumb-line techniques in measuring resting head posture (RHP). Physiol Ther. 1991;14(3):193-198, I Manual Manipulative Ther. 2000;8(1):10-17, 23. Jansson A, Saartok T, Werner S, Renstrom p, General joint laxity in 1845 Swedish school children of different ages: Age and gen­ 9. Fletcher JP, Bandy WD. Intrarater reliability of CROM measure­ der-specific distributions. Acta Paediatr. 2004;93(9):1202-1206. ment of cervical spine active range of motion in persons with and 24. Savitz SI, Caplan LR. Vertebrobasilar disease. N Engl I Med. without neck pain, I Orthop Sports Phys Ther. 2008;38(10):640­ 2005;352:2618-2626. 645. 25. Coman WB. Dizziness related to ENT conditions. In: Grieve GP, ed. Modern Manual Therapy of the Vertebral Column. 10. Dutton M. Orthopaedic Examination, Evaluation, and Edinburgh, UK: Churchill Livingstone; 1986, Intervention, 2nd ed. New York, NY: McGraw-Hili Companies, 26. Kerry R, Taylor AL Mitchell L McCarthy C, Brew J, Manual ther­ Inc; 2008. apy and cervical arterial dysfunction, directions for the future: a clinical perspective. I Manual Manipulative Ther, 2008;16(1 ):39­ 11. Greenman PE. Principles of Manual Medicine. 3rd ed. 48. Philadelphia, PA: Lippincott Williams & Wilkins; 2003. 27. Huijbregts P, Vidal p, Dizziness in orthopaedic physical ther­ apy practice: classification and pathophysiology. I Manual 12. Isaacs ER, Bookhout MR. Bourdillon's Spinal Manipulation. 6th Manipulative Ther. 2004;12(4):199-214. ed. Boston, MA: Butterworth-Heinemann; 2002. 13. McKenzie R, May S. The Lumbar Spine, Mechanical Diagnosis & Therapy. Volume /, Waikanae, New Zealand: Spinal Publications New Zealand Ltd; 2003. 104 Copyrighted Materail

References 105 28. Magee DJ. Orthopedic Physical Assessment. 5th ed. St. Louis, 50. Fernandez-de-Ias-Penas C, Alonso-Blanco C, Cuadrado ML, MO: Saunders Elsevier; 2008. Pareja JA. Forward head posture and neck mobility in chronic tension-type headache: a blinded, controlled study. Cephalalgia. 29 Konin JG, Wiksten DL, Isear JA, Brader H. Special T('sts in Orthopedic Examination. 3rd ed. Thorofare, NJ: SLACK, 2005;26:314-319. Incorporated; 2006. 51. Falla D, Jull G, Hodges PW. Feedforward activity of the cervical 30. Gross), Fetto Rosen E. Musculoskeletal ExaminaLion. 2nd ed. flexor muscles during voluntary arm movements is delayed in Cambridge, MA: Blackwell Science; 2002. chronic neck pain. Exp Brain Res 2004;15743-48. 31. Richter RR, Reinking MF. Clinical question: How does evidence 52. Kreig L. Thoracic outlet syndrome: Pathology and treatment. on the diagnostic accuracy of the vertebral artery test influence I Manual Manipulative Ther. 1993;1(2):52-59. teaching of the test in a professional physical therapist education 53. Keller TS, Harrison DE, Colloca C), Harrison DD, Janik program? Phys Ther. 2005;85(6):589-599. TJ. Prediction of osteoporotic spinal deformity. Spine. 32. Meadows J. Orthopedic Differential Diagnosis in Physical 2003;28(5):455-462. Therapy: A Case Study Approach. New York, NY: McGraw-Hili; 54. Ludewig PM, Cook TM. Alterations in shoulder kinematics and 1999. associated muscle activity in people with symptoms of shoulder 33. Zaina C, Grant R, Johnson C, Dansie n. Taylor L Spyropolous P. impingement. Phys Ther. 2000;80(3):276-289. The effect of cervical rotation on blood flow in the contralateral 55. Solem-Bertoft E, Thuomas K-A, Westerberg C-E. The influence of vertebral artery. Man Ther. 2003;8(2):103-109. scapular retraction and protraction on the width of the subacro­ 34. Kuether TA, Clark WM, Barnwell SL. Rotational vertebral mial space. Clin Orthop Relat Res. 1993;296:99-103. artery occlusion: a mechanism of vertebrobasilar insufficiency. 56 . Cacciatore TW, Horak FB, Henry SM. Improvement in automatic postural coordination following Alexander technique lessons in a Neurosurgery. 1997;41(2):427-433. person with low back pain. Phys Ther. 2005;85(6):565-578. 35 Di Fabio RP. Manipulation of the cervical spine: Risks and ben­ 57. Jankelson RR. Posture, Airway & the Tongue in Clinical Dentistry. Kent, WA: Myotronics, Inc; 2006. efits. Phys Ther 1999;79(1):50-65. 58. McMaster M), Glasby MA, Singh H, Cunningham S. Lung func­ 36 Haldeman S, Kohlbeck F), McGregor M. Unpredictability of tion in congenital kyphosis and kyphoscoliosis. I Spinal Disord cerebrovasular ischemia associated with cervical spine manipu­ Tech. 2007;20(3):203-208. lation therapy. Spine. 2002;27(1):49-55. 59. Wright EF, Domenech MA, Fischer JR. Usefulness of posture 37. Ernst E. Adverse (,ffects of spinal manipulation: a systematic review. I R Soc Med. 2007;100:330-338. training for patients with temporomandibular disorders. IADA. 38. Kasai Y, Morishita K, Kawakita E, Kondo T, Uchida A. A new evaluation method for lumbar spinal instability: passive lumbar 2000;131:202-210. extension test. Phys Ther. 2006;86(12):1661-1667. 39. Weinstein IN, Rydevik BL, Sonntag VKH, eds. Essentials of the 60. Evcik D, Aksoy O. Relationship between head posture and Spine. New York, NY: Raven Press; 1995. temporomandibular dysfunction syndrome. I Musculoskel Pain. 40. Panjabi MM. Clinical spinal instability and low back pain. I Electromyogr and Kinesiol. 2003;13:371-379. 2004;12(2):19-24 41. Rocabado, M. The importance of soft tissue mechanics in stabil­ ity and instability of the cervical spine: a functional diagnosis for 61. Hiemeyer K, Lutz R, Menninger H. Dependence of tender points treatment planning. I Craniomandib Pract. 1987;5(2):130-138. upon posture - a key to the understanding of fibromyalgia syn­ 42. Olson KA, Joder D. Diagnosis and treatment of cervical spine drome. I Manual Medicine. 1990;5:169-174. clinical instability. I Orthop Sports Phys Ther. 2001;31(4):194- 62. Lennon), Shealy CN, Cady RK, Matta W, Cox R, Simpson WF. 206. Postural and respiratory modulation of autonomic function, pain, and health. Amer I Pain Management. 1994;4(1):36-39. 43. Pettman E. Stress tests of the craniovertebral joints. In: Boyling JD, Palastanga I',), eds. Crieve's Modern Manual Therapy: The 63. Freeman JT. Posture in the aging and aged body. lAMA. Vertebral Column. 2nd ed. Edinburgh: Churchill Livingstone; 1957;165(7):843-846. 1994. 64. Calliet R. Soft Tissue Pain and Disability. 3rd ed. Philadelphia, 44. Mintken PE, Metrick L, Flynn T. Upper cervical ligament testing PA: FA Davis; 1996. in a patient with os odontoideum presenting with headaches. I Ortlwp Sports Phys Ther. 2008;38(8):465-475. 65. Conable B, Conable W. How to Learn the Alexander Technique: A Manual for Students. 2nd ed. Columbus, OH: Andover Road 45. Fernandez-de-Ias Penas C, Perez-de-Ia-Heredia M. Performance Press; 1992. of the craniocervical flexion test, forward head posture, and hean.1Che clinic)1 parameters in patients with chronic ten­ 66. Chaitow L, DeLany JW. Clinical Application of Neuromuscular sion-type headache: a pilot study. I Orthop Sports Phys Ther. Techniques. Vol. 2, The Lower Body. Edinburgh, UK: Churchill Livingstone; 2002. 2007;37(2):33-39. 67. Paris SV. Course Notes, The Spine. Etiology and Treatment of 46. San Agustin CT, Wilmarth MA, Raymond 1. Hilliard TS. The Dysfunction Including loint Manipulation. Atlanta, GA: 1979. amount and variation of craniovertebral angle changes in col­ 68. Chaitow L. Positional Release Techniques. Edinburgh, UK: Churchill Livingstone; 2002. lege-aged students using one-strapped and two-strapped back­ packs and bags. Orthop Pracl. 2003;15(3):30-33. 69. Kaltenborn FM. Manual Mobilization of the loints, Vol. I, The 47. Watson DH, Trott PH. C{'rvical headache: an investigation of Extremities, 6th ed. Minneapolis, MN: OPTP; 2002. natural head posture and upper cervical flexor muscle perfor­ 70. Evjenth 0, Hamberg J. Muscle Stretching in Manual Therapy. A Clinical Manual. Vol. 1/ The Spinal Column and mance. Cepha/J/giJ. 1993;13:272-284. Temporomandibular loinl. Alfta, Sweden: Scand; 1984. 48. Paris SV. Cervical symptoms of forward head posture. Top 71. Simons DG, Travell JG, Simons LS. Travel/ & Simoll5' Myofascial Ceriatr Rehabil. 1990;5(4):11-19. Pain and Dysfunction: The Trigger Point Manual. Vol I. Upper 49 Fernandcz-de-Ia-Penas C, Alonso-Blanco C, Cuadrado ML, Half of Body. Baltimore, MD: Williams & Wilkins; 1999. Gerwin RD, Pareja JA Trigger points in the subOCCipital muscles 72. Schmitt L, Snyder-Mackler L. Role of scapular stabilizers in etiol­ and forward head posture in tension-type headache. Headache. ogy and treatment of impingement syndrome . I Orthop Sports 2006;464.14-460. Phl's Ther. 1999;29(1):31-38. 73. Tubbs RS, Tyler-Kabara EC, Aikens AC, et al. Surgic al anatomy of the dorsal scapular nerve. I Neurosurg. 2005;102:910-911. Copyrighted Materail

106 References 74. Kuzmich D. The levator scapulae: making the con-neck-tion. 98. van Duijn J, van Duijn A, \\Jihch W. Orthopaedic manu,ll physi­ J Manual Manipulative Ther. lQ94;2(2):43-54. cal therapy including thrust Illc1l1ipulatioll and exercise ill the management of .) pctient with e crviCQgc:nic headache: a Cil5e 75. Diener I. The dfect of levator sc pula tightness on the cervical report. J Manual Manipulative' TilC'r. 2007;15( 1):10-24. spine: proposal of another length test. J Manual Manipulative Ther. 1998;6(2):78-86. 99. Hanten WP, Olson SL, LinelSJy Wi\\, LounsiJerry KA, Stewart IK. The effect of manual thf'r,lpy and a homf' exercise progr<lm on 76. Butlcr DS. Mobilization of the Nervous System. Melbourne, cervicogenic headaches: a case report. J Manual Manipulativp Australia: Churchill Livingstone; 1991. Ther. 2005;13(1):35-43. 7 7. Butler DS. Ihe Sensitive Nervous System. Adelaide, Australia: 100. Horn C, Smith KL. Cervicflgpnic he,1elache part II: clinical Noigroup Publlications; 2000. examination, findings, and approaches to manClgement. J Manual Manipulative Ther. 1997;5(4):171-175. 78. Herrington L. Effect of different neurodynamic mobilization technique's on knee extension range of motion in the slump posi­ 101. Hall T, Briffa K, Hopper D. Clinical evaluation of cervicogenic tion. J Manual MallJpulative Ther. 2006;14(2):101-107. headache: a clinical perspective. J Manual Manipulative Ther. 2008;16(2):73-80 79. Hammer WI. Functional 50ft (issue Examination and Treatment by Manual Methods: New Perspectives. 2nd ed. Gaithersburg, 102. Bogduk I\\J. Cervical causes of hcadache and dizziness. In: Grieve MD: Aspen Publishers; 1999. GP, ed. Modem M\"1Ilual Ihrrd/'Y o( the Vcrtebral Column. 2nd ed. Edinburgh: Churchill Livingstone; 1994. 80. Conable B, Concble W. How to Learn the Alexander Technique: A Manual for Students. 2nd ed. Columbus, OH: Andover Road 103. Jull GA. Headaches of cerviCill origin. In: Grant R, ed. Physical Press; 1992. Therapy of the Cervical and Thordcic Spine!: Clinics in Physical Therapy. London: Churchill Livingstone; 1988. 81. Brennan R. The Alexander Technique Workbook, Your Personal System for Health, Poise, and Fitness. London: Element Books 104. IHS: Headache Classification Suhcommittee of the Intel'llationJl Ltd; 2002. Headache SOCiety. The Internati()nal Classification of Headache Disorders. 2nd ed. Cephalalgia. 2004;24(Suppl 1):':1-160 82. Caplan D. Back Trouble: A New Approach to Prevention and I emvery. Gainesville, F L: Triad Publishing; 1987. 105. Sjaastad 0, Fredriksen A, PfJflellr:lth V. Cervicogenic headache: diagnostic criteria. Headache. 1998;38:442-446. 83. Goldstein LB, Makofsky HW. TMD/facial pain and forward head posture. Practical Pain Management. 2005;5(5):36-39. 106. McDonnell MK, Sahrmann SA, Van Dillr'n L. A spccific C'xercise program and modific,ltion of Jlustural alignment lur trc\"ltment 84. Augustine C, Makofsky HW, Britt C, et al. Use of the Occivator of cervicogenic hc'aelJche: a case' report. J Orthop Sports Phys for the correction of forward head posture and thf' implications Ther. 2005;35(I ):3-15. for tpmporomandibular disorders: a pilot study. J Crdniomandib Pract. 2008;26(2):1-8. 'j(j7. Schoensce' SK, lensen G, Nicholson G, Gossman M, Katholi C. The efteet of mobilization on cervical headaches. J Orthop 85. Curic D, Adamson T. Minimally invasive cervical microendo­ Sports Phys Ther. lQQ5;21(4):184-190. scopic laminoforaminotomy. Neurosurg Focus . 2008;25(2):E2. 108. Hall T, Robinson K. The flexion rotation test and active cervical 86. Li J, Yan DL, Zhang ZH. Percutaneous cervical nucleoplasty mobility: a comparative measurement study in cervicogenic in the treatment of cervical disc herniation. Eur Spine /. headache. Manual Therapy. 2004;9:197-202. 2008;17(12):1664-1669. 109. Swerdlow B. Whiplash and Related Heilciaches. B()ed Raton, FL: 87. Fernandez-de-Ias-Penas C, Perez-de-Heredia M, Molero­ CI,C Press; 1999. Sanchc'z A, Miangolarra-Page Jc. Performance of the craniocC'r­ vic.ll fllexion test, forward head posture, and headache clinical 110. McCrory DC, Penzien DB, Hasselblad \\I, Gray RN. Lvicil'llce parameters in patients with chronic tension-type headache: A Report: Behavioral and Physical TrefJ1menls for Tcnsion-IYfJC' pilot study. J Orthop Sports Phys Ther. 2007;37(2):33-39. and Cprvicogenic Headache. Durham, C: Duke University Evidence-Rased Practice (center; 200'1. 88. lull G. Diagnosis of cervicogenic headache. J Manual Manipulative Ther. 2006;14(3):136-138. 111. lull G. Management of cervical headache. Manual Therapy. 1997;2(4) :182-190. 89. Petersen SM. Articular and muscular impairments in cervico­ genic headache. J Orthop Sports Phys Ther. 2003;33(1):21-30. 112. Kidd RF, Nelson R. Musculoskeletal dysfunction of Ihe neck in migraine and tension headache. Headache. 1993;33(10):566-569 90. Harris KD, Heer DM, Roy TC, Santos DM, Whitman 1M, Wainner I'S. Reliability of a measurement of neck flexor muscle 113. Morask,l A, Chandler C. Changes in clinical parameters in endurance. Phys Ther. 2005;85(12):1349-1355. patients with tension-type headache following mass:1ge therapy: A pilot study. J Manual Manipulative Ther. 2008;16(2):106-'112 91. Murphy DR. l\\Jorrnal function of the cervical spine II, neu­ rophysiology and stability. In: Murphy DR, ed. Conservative 114. Fernandez-de-Ias-penas C, Arendt-Nic'lsGn L, Simons D. Management of Cervical Spine Syndromes. New York, NY: Contributions of myoi,lscial trigger points to chronic tension-type McGraw-Hili Companies, Inc; 2000. headache. J Manual MallJpulative 7 her. 2006;14(4):222-231. 92. Bogduk N. Cervicogenic headache: anatomic basis and patho­ 115. Ff'rnandez-de-Ias-penas C, Cuadrildo ML, PareJa JA. Myofascial physiologic mechanisms. Current Pain and Headache Reports. trigger points, neck mobility, and forward head posture in epi­ 2001;5:382-386. sodic tension-type headache. He!adacllC'. 2007;47(5):662-672. 9J') . Wrisley DM, Sparto PJ, Whitney SL, Furman JM. Cervicogenic 116. Saper JR. Chronic daily headache: a clinician's perspective dizziness: a review of diilgnosis and treatment. J Orthop Sports Headache'. 2002;42(6):538-542. Phys Ther. 2000;30(12):75\"-766. 117. Fernandez-de-lils-J\"enas C, Cuadrado ML, Parej,l JA. Myofascial 94. tvtannheimer JS, Rosenthal RM. Acute and chronic postural triggcr points, neck mobility, and forward head posture in unilat­ abnormalities as related to craniofacial pain and temporoman­ eral migraine. Cephalalgia. 2006;26:1061-1070. dibular disorders. Dent Clin North Amer. 1991;35(1):185-208. 1113. Hack GD, Koritzer RT, Robinson WL, Hallgren RC, Crccnman 95. Porterfield JA, DeRosa C. Mechanical Neck Pain. Perspectives in Functional Anatomy Philadelphia, PA: WB Saunders; 1995. PE. Anatomic relation between the rectus capitis post 'rior minor muscle and the dura mater. Spine. 1995;20(13):2484-24116 96. Hall T, Chan HT, Christensen L, Odenthal B, Wells C, Robinson 119. Marcus DA, Scharff L, Mercer S, Turk DC Musculoskeletal 1<. Efficacy of a Cl-C2 self-sustained natural apophyseal glide abnormalitips in chronic hedelilche: a controllpel cotllp;lrison of (SNAG) in the management of cervicogenic headache. J Orthop headache diagnostic groups. /-Ie,luache. 1999;1'):2127. Sports Phys Ther. 2007;37(3):100-107. 120. Karpouzis KM, Spierings E. Circumstances of onset of chronic headache in patients attending a specialty practice 1i(\"Ic/,I( he. 97. Zito G, Jull G, Story I. Clinical tests of musculoskeletal dysfunc­ 1999;39:317-320. tion in the diagnosis of cervicogenic headache. Manual Therapy. 2006;11 :1113-129. Copyrighted Materail

References 107 121. Silberstein S, Mathew N, Saper J, Jenkins 5 Botulinum toxin type 140. Meadows J. Orthopedic Differential Diagnosis in Physical A as a migraine preventive treatment. Headache. 2000;40:445- Therapy. New York, NY: McCraw-Hili, '1999, 450 122. Moskowitz MA. The neurobiology of vascular head pain. Ann 141. Yardley L, Donovan-Hall M, Smith HE, Walsh BM, Mullee Neurol.1984;16:156-168. M, Bronstein AM. Effectiveness of primary care-based ves­ 123. Olesen J Clinical and pathophysiological observations in tibular rehabilitation for chronic dizziness. Ann Intern Mecl. migraine and tension-type headache explained by integration of 2004 ;141(8):598-605. vascular, supraspinal, and myofascial inputs. Pain. 1991;46:125- 142. Huijbregts P, Vidal P. Dizziness in orthopaedic physical ther­ 132. apy practice: classification and pathophysiology. ) Manual l24. Wood P. Proposed models of fibromyalgia sub-types. Practical Manipulative Ther. 2004;12(4):199-214. Pain Management. 2008;8(5):70-75. 125. Young WH, Silberstein SD. Migraine and Other Headaches. New 143. Willis Cc. Acoustic Nerve.' Deafness, Tinnitis, and Vertigo. York, NY: Demos Medical Publishing LLC; 2004. Neuroanatomy of the VIII Cranial Nerve and Connections. 126. Bendtsen L. Central sensitization in tension-type headache: Lecture Notes. Maizuru Ceneral Hospital, Kyoto P refecture, Possible patho-physiological mechanisms. Cephalalgia. Japan, 1990. 144. Vidal P, Huijbregts P. Dizziness in orthopaedic physical ther­ 2000;29:486-508. apy practice: history and physical examination, } Manual 127. Shankland WE. Migraine and tension-type headache reduction through pericranial muscular suppression : a preliminary report. Manipulative Ther. 2005;13(4):221-250. } Craniomandib Pracl. 2001;19(4):269-278. 145. Vidal P. Examination and Intervention of Dizziness: The Veslibular 128. Saper JR, Silberstein S, Cordon CD, Hamel RL, Swidan S. System and Orthopaedics. Brentwood, TN: Paul Vidal & Cross Handbook of Headache Management: A Practical Cuide to Diagnosis and Treatment of Head, Neck, and Facial Pain. 2nd ed. Country Education, Inc; 2005. Baltimore, MD Lipincott Williams & Wilkins; 1999. 146. Oostendorp R, VanEupen A, VanErp L Elvers H. Dizziness fol­ 129. DaSilva AF, Cranziera C, Snyder J, Hadjikhani N. Thickening in lowing whiplash injury: a neuro-otological study in manual ther­ the somatosensory cortex of patients with migraine. Neurology. apy practice and therapeutic impliccltion. } Manual ManipulativI' 2007;69:19 0-199';. Ther. 1999;7(3):123-130. 130. Morrone L. Overcoming Headaches and Migraines: Clinically 147. Endo K, Ichimaru K, Komagata M, Yamamoto K, Cervical vertigo Proven Cure for Chronic Pain. Eugene, OR: Harvest House and dizziness after whiplash injury. Eur Spine }. 2006;15:886- IJublishers; 2008. 131. Willis Cc. Headache. Lecture Notes. Maizuru Ceneral Hospital, 890, Kyoto Prefecture, Japan, 1990. 148. Wapner S, Werner H, Chandler KA. Experiments on the sensory­ 132. P ackard RC. Post-traumatic headache: more than just a head­ tonic field theory of perception: effect of extraneous stimulation ache, Headache Quarterly. 2001;12:99-100. of the visual perception of verticality. } Exp Psych. 195'1;42:351- 133. knsen 0, Nielsen F, Vosmar L. An open study comparing 357. m,lnual therapy with the use of cold packs in the treatment of 149. Cray LP. Extralabyrinthine vertigo due to cervical muscle lesions. posttraumatic headache. Cephalalgia. 1990;10:241-250. } Laryngology. 1956;70:352-361. 134. Hildebrandt J, Jansen J. Vascular compression of the C2 and C3 150. Fitz-Ritson D, Assessment of cervicogeni vertigo, } Manipulative roots-yet another cause of chronic intermittent hemicrania? Physiol Ther. 1991;14(3):193-198 CephalalgiJ.1984;4:167-170, 151. Vernon H. Upper Cervical Syndrome: Chiropractic Diagnosis 135 Mathew NT, Stubits E, Nigam M. Transformation of episodic and Treatment, Baltimore, MD: Williams & Wilkins; 1988. migraine into daily chronic headache: an analysis of factors. 152. Janda v. Muscles and motor control in cervicogenic disorders. Headache.1982;22:fifi-68. In: Crant R, ed. Physical Therapy of the Cervical and Thoracic 136. Srikiatkhachorn A, Tarasuh N, Covitrapong P. Effect of chronic Spine. 3rd ed. New York, NY: Churchill Livingstone; 2002, analgesic exposure on the cl'ntral serotonin system: a pos­ 153. Urbanowicz M. Alteration of vertical dimension and it effect on sible mechanism of analgesic abuse headache. Headache. head and neck posture. } Craniomandib PraCl. 1991;9(2):174- 2000;40 341-350. 137. Wrisley OM, Sparto PJ, Whitney SL, Furman JM, Cervicogenic 179. dizzines : d review of diagnosis and treatment. } Orthop Sports 154. Chakfa AM, Mehta NR, Forgione AC, AI-Badawi EA, Lobo S, Phys Ther. 2000;30(12):755-766 Zawawi KH. The effect of stepwise increases in vertical dimen­ 138. Kondratek M, Creighton D, Krauss J. Usc of translatoric mobiliza­ sion of occlusion on isometric strength of cervical flexors and tion in a patient with cervicogenic dizzin ss and motion restriction: deltoid muscles in nonsymptomatic females, } Craniomandib a case report. } Manual Manipulativp Ther, 2006;'14(3):140-151. 139. Aspinall W. Clinical testing for cervical mechanical disorders PraCl. 2002;20(4) 264-273. which produce ischemic vertigo. } Orthop Sports Phys Ther. 1989;11(5):176-182, 155. Makofsky HW. Snoring and obstructive slcrr apnea: does head posture play a role? } Craniomandib PraCl. 1<)'17;15(1):68-73. Copyrighted Materail

Section TEMPOROMAND1BULAR J01NT F== --- \"---- \"'\"--=' Copyrighted Materail

Examination and Evaluation of the Temporomandibular J�o�in�t�!=; Posture hypomobility; the left towards hypermobility upon opening of the mouth. he analysis of craniomandibular alignment or pos­ As mentioned, the examination of dent,ll ucclusion is beyond the scope of this introductory textbouk. However, T ture is a complex science that requires expertise certain dental concepts)-3 are useful in terms of understand­ in general dentistry, orthodontics, oral and maxil­ ing the role of head-neck posture in both craniom mdibular lofacial surgery, as well as in physical medicine.l-3 For those kinesiology and pathokinesiology. The term maximum therapists with advanced training in the TMJ, including an interwspation (MIP) refers to the position of the upper and understanding of cranial osteopathy, the analysis of cranio­ lower teeth in the fully clenched state of the upper and facial structure is an essential component of the examina­ lower jaws. It is a function of tooth anatomy and geometry tion. However, at the introductory level, more emphasis is and is unaffected by transient changes in head-neck posi­ placed on the analysis of mandibular range of motion, soft tion. The term vertical dimension of occlusion (VDO) refers tissue palpation, and the influence of the cervical spine and to the distance from the nose to the chin with the teeth in posture on the craniomandibular region then on structural MIP. It, too, is a structurally determined dental relationship alignment, including the assessment of dental occlusion. that is unaffected by anything other than occlusion. The That being said, the basic examination of the TMJ/facial dental profession alone has exclusive rights by virtue of region should note the following: their training and expertise to manage pathology, impair­ ment, functional limitation, and disability related to MIP > Facial type (eg, a longer dolichocephalic face versus a and VDo. Having said that, there are other dental con­ rounder brachicephalic one) cepts that are influenced by functional factors, including head-neck posture, that clearly fall within the domain of > Deviations from the normal orthognathic position, the physical therapy profession. Five such concepts that are including horizontal deficiency of the lower jaw related and that clearly fall within the functional realm are (ie, retrognathia) as well as horizontal excess of the mandibular rest position, interocclusal or freeway space, the mandible (ie, prognathia), as observed from the habitual pathway of closure, initial tooth contact position, side. Whereas the orthognathic profile has a straight and the vertical dimension of rest (VDR). Though many appearance, the retrognathic mandible appears con­ would argue that these concepts are also dental in nature, vex; the prognathic jaw concave. there is no doubt that extradental factors (eg, head-neck posture) also play a role. For example, it has been estab­ > From the front, the height of the mandibular ramus lished that head-neck extension exerts a posterior force on (from gonial angle to the head of the condyle) should the mandible, which changes the pathway of mandibular be compared from left to right for asymmetry. If for example, the left ramus is longer, the patient's face will appear convex on the left; concave on the right. This may predispose the patient's right TMJ toward 777 ,\\l;lkof ky HW Spinal Malltlal Therapy. lud I'd. (w II t-IIR) \" 1010 SLJ\\CK Incorpor:ttnl Copyrighted Materail

1 1 2 Chapter 13 Figure 13-1a. TMJ palpatation during mandibular Figure 13-1b. Active mandibular depression from the depression. side. Figure 13-1c. Measuring mandibular depression. 2. Ohserve for mandibular deflections and deviations closure and shifts the initial tooth contacts posteriorly.4 (see Figure 13-13) from the front. With regard to head-neck posture, it has been demonstrated that FHP exerts a superiorly directed force on the mandible 3. Observe for premature and/or excessive anterior man­ which alters the rest position of the mandihle and decreases freeway space as well as VDR.5 Consequently, the basic dibular translation from the side (Figure 13-1b). examination of mandibular posture must include an inspec­ tion of the influences from below, namely an examination 4. Measure (Figure 13-1c) the maximal interincisal of the cervical and scapulothoracic region as previously covered in this text. opening (M]O). Active Mandibular Movements The normal TMJ (Figure 13-2) is freely moveable, friction­ There are 4 active movements of the mandible that will free, and noise-free6 However, in the impaired TMJ there are basically 3 types of joint sounds that can be palpated. They be assessed. They include mandibular depression (opening), lateral excursion to the right and left, and protrusion. are clicking, crepitus, and a popping sound or \"thud.\" Most clicks are Single, short duration noises associated with a reduc­ When assessing depression of the mandible, the exam­ iner must do the following: ing disc displacement. Tiley can be palpated during opening 1. Palpate the lateral poles of the mandibular condyles or closing and may occur at any point in the opening/closing for joint sounds (Figure 13-1a). cycle. When a TMJ demonstrates both opening and closing clicking, the term reci/)1'Ocal clicking is used. This is a sign of an anterior disc displacement (ADD) with reduction (Figure 13­ 3a). The opening click is typically more pronounced than the closing click, which may require auscultation with a stetho­ scope in order to be heard. This is in contrast to an ADD without reduction (ie, a closed-lock of the TMJ) in which joint clicking is absent (Figure 13-3b). Reciprocal clicking must he distinguished from the clicking that occurs secondary to an articular surface defect. Whereas an articular surface defect click will occur at the same point in the opening and closing cycle, reciprocal clicking rarely occurs at the same point in both opening and closing. The opening click usually occurs beyond 20 mm and the closing click occurs Just before the teeth meet in occlusion. Crepitus is a grating or gravelly noise associated with degenerative joint disease of which the TMJ is not excluded. A loud popping noise or thud palpated at the end of opening indicates TMJ hypermohility. This occurs as the disc and mandibulm condyle, together, translate past the articular eminence of the temporal bone. This hypermobil­ ity can be confined to the TMJ or be a generalized state of increased motion throughout the body. When the elisc/con­ dyle complex translates anterior to the articular eminence and cannot return to its normal anatomic position, it is considered dislocated or an open-lock (Figure 13-4). Copyrighted Materail

Examination and Evaluation of the Temporomandibular Joint 113 Figure 13-2. The TMJ at rest and in mouth opening. (Reprinted from Morrone L, Makofsky H. The TMJ home exercise program. Clinical Management in Physical Therapy. 1991 ;11 [2] :20-26, with permission of the American Physical Therapy Association.) Figure 13-3a. Right TMJ anterior disc displacement with Figure 13-3b. Right TMJ anterior disc displacement without I'eduction. reduction (closed-lock). Figure 13-4. f(ight TMJ dislocation (open-lock), The second aspect of examining depression involves observing deflections and deviations of the mandible. The mandible is said to deflect when it shifts from its midline position to either the right or the left side and fails to return to the midline (Figure 13-5). Deflections occur when the mandibular condyle has restricted anterior translation on the ipsilateral side or excessive translation on the contra­ lateral side. For example, if translation is restricted on the right, a deflection will occur to the right; if excessive on the right, a deflection will occur to the left (usually toward the end of range). The pathology leading to impairment of translation is most often due to either unilateral capsular tightness or an ADD without reduction, Although the underlying pathology is different (ie, capsular versus intra­ capsular), the deflection of the depressing mandible to the side of impairment is the same, Copyrighted Materail

1 1 4 Chapter 13 20 ! 20 L L Figure 13-5. Mandibular deflection to the right. 60 Figure 13-6. Mandibular deviation to the right. Figure 13-7a. Lateral excursion left. Figure 13-7b. Lateral excursion right. The mandible is said to deviate when it shifts to one side that rotational motion within the TMJ occurs in the infe­ of midline during opening but then returns to the midline rior joint compartment between the head of the condyle as opening continues (Figure 13-6). Deviations during and the articular disc, whereas translation or sliding motion opening, when correlated to ipsilateral reciprocal clicking, occurs in the superior compartment of the TMJ between are usually secondary to an ADD with reduction. Whereas the disc and articular eminence of the temporal bone . A the anteriorly displaced disc causes a shift of the lower jaw common pattern seen in patients with TMD is premature to the affected side (due to a momentary interruption of or excessive translation. It is this premature or excessive mandibular translation), the return of the mandible to translation that causes mechanical stress and strain within midline occurs when the displaced disc is reduced. This the tissues of the TMJ, leading to the common development disc reduction (ie, normalization of position) produces the of hypermobility. characteristic opening click. The closing click occurs when the condyle slips off the posterior aspect of the disc, usually The normal range of mandibular depression MIO is at the end of closing. between 40 and 50 mm, as measured between the upper and lower anterior incisors (see figure 13-lc). In the absence of a Mandibular depression should also be assessed from the metric ruler, the patient is askeJ to place his or her knuckles side (see Figure 13-1b). For simplicity's sake, depression between the upper and lower teeth in a sideways manner. of the mandible can be divided into 3 phases. The initial One knuckle opening is hypomobile, 2 is low normal, 3 is phase of opening consists of an X-axis rotation. The middle high normal, and 4 tends toward hypermobility. phase consists of a combination of X-axis rotation and translation of the mandible along the Z or anteroposterior Normal range for mandibular lateral excursion is 8 mm to axis, and the final phase of opening consists primarily of either side. A metric ruler can be used, but an easier method further anterior translation along the Z axis. It is believed involves observing the lower lip frenulum as the lower jaw moves from side to side (Figures 13-7a and 13-7b). The Copyrighted Materail

Examination and Evaluation of the Temporomandibular Joint 115 therapist's gloved hand pulls the lower lip down to expose the Figure 13-8. Mandibular protrusion. frenulum. With the teeth slightly apart, the p,ltient moves his or her mandible to the right and then to the left. Since the tion in the normal range of depression, lateral excursion to anterior Up[1Cr incisor is approximately 8 mm in width, nor­ either side, and protrusion. mal lateral excursion involves the lower hp frenulum clearing the upper anterior incisor on each respective side. Thus the The indications of an intracapsular closed-lock are a patient's lateral excursions can be evaluated without the lise prior history of reciprocal clicking and intermittent closed of a ruler if desired. If impairment of moti()(1 is pre.'ient, it can locking. Though a closed-lock can occur following a single be described as minimal, moderate, or severe. Conversely, macrotrauma, it usually occurs in response to cumulative excessive motion should also be noted. For those patients microtrauma over a period of time and is associated with who have difficulty coordinating lateral excursion of the such parafunctional activities as bruxism, nail biting, gum mandible, placing the tongue on the upper back molar will chewing, and other nonessential activities that stress and assist with lateral motion to that side. A distinction should be strain the internal supportive structures of the TM]. made between restricted mobility and incoordination. Consequently, intraoral joint play testing of the TMJ is The final active mandibular movement to assess is pro­ helpful in confirming the diagnosis of TMJ hyp, mobility trusion (Figure 13-8). The examination of mandibular pro­ and is useful in distinguishing a tight capsule from a non­ trusion includes palpating the lateral poles of the condyles reducing disc displacement (though a closed-lock results for joint sounds, observing the motion for deflections and in hypomobility, its precursor, the ADD with reduction, is deviations, and measuring the quantity of motion present. actually a form of hypermobility between the condyle and Normal protrusion should obtain to 8 mm. A simple way of articular disc). Though an MRI examination is the gold assessing this is to ask the patient to place his or her lower standard for the diagnosis of a closed-lock, the MRI should teeth anterior to the upper teeth. If this can be achieved, not be ordered unless TMJ surgery is being considered. The then the motion has normal range. Abnormal motion can difference between a tight capsule and a closed-lock rela­ be described as minimal, moderate, or severe limitation or tive to intraoral joint play testing is twofold. The trained hypermobility. The clinical interpretation of joint sounds manual therapist is usually able to detect a difference in and deflections/deviations in protrusion is similar to the the end-feel. Whereas the tight capsule has a slight degree same findings in the opening and closing cycle of the man­ of \"creep\" or \"give\" at the end-range, the nonreducing disc dible as discussed previously. derangement is less yielding and is often associated with muscle splinting, which makes the end-feel even firmer. Mandibular retrusion is not tested actively, but it can be However, the more significant distinction between the two assessed passively as a TMJ provocation test. This can be is found in the response to manipulation. Whereas the done in supine or sitting by means of a gentle up and back tight capsule gains millimeters, the closed-lock gains cen­ motion of the mandible. Pain in one or both TMJs suggests timeters of increased motion. This distinction holds true the presence of inflammation. Easy does itl whenever an internal derangement is reduced and a joint is \"unlocked\" (eg, the knee, spine, elbow). Intraoral Joint Play Motion There are 3 joint play motions of the TMJ that will be There are 2 indications for the use of intraoral joint play assessed intraorally. They are long axis distraction, lateral motion testing. One is suspected capsular hypomobility and glide, and anterior glide. The therapist stands on the side the other is the likelihood of an ADD without reduction opposite the joint to be mobilized and stabilizes the head or a closed-lock (see Figure 13-3b). Because the TMJ is while monitoring the affected joint with either the middle more often a disorder of hypermobility than hypomobility, or index finger. The gloved thumb of the other hand is manual therapists must be careful not to subject these tis­ placed intraorally on the mandibular arch with the index sues to unnecessary mechanical stress. finger alongside the body of the mandible extraorally. This The indications of capsular hypomobility are as follows: » A history of macrotrauma to the jaw with subsequent inflammation and/or a history of jaw immobilization following surgery, infection, or as an intervention for TMD. » The presence of a capsular pattern when impairment is unilateral (ie, restricted depression associated with deflection to the affected side, restricted lateral excur­ sion to the contralateral side, and restricted protru­ sion with mandibular deflection to the affected side). In the presence of bilateral impairment, the mandible will not deflect nor deviate, but will demonstrate limita- Copyrighted Materail

1 1 6 Chapter 13 Figure 13-9. RightTMJ intraoral mobility testing. Figure 13-lOa. Temporalis muscle. Figure 13-10b. Masseter muscle. Figure 13-10c. Medial pterygoid muscle. examination technique is demonstrated with the patient without associated hypertonicity, whereas an increase in in the supine position (Figure 13-9), but it can also be per­ tone (eg, splinting, guarding, bracing) is neuroreflexive in formed with the patient sitting. nature and points to the presence of increased tissue reac­ tivity as discussed previously in Chapter 3. Extracapsular For each of the intraoral movements tested, the quality, impairment of the TMJ (ie, myofascial pain) is common in patients suffering from TMD. It can occur in conjunction quantity (0 to 6 scale covered previously), tissue reactivity, with a capsular impairment, intracapsular derangement, or be found in the presence of a normal TMJ. and end-feel are assessed. Long axis distraction involves sep­ aration of the mandibular condyle away from the temporal The basic evaluation of the TMJ soft tissues consists of fossa in a caudal direction, lateral glide involves t ranslatoric an ext raoral examination (Figures 13-1Oa to 13-1Oe) of the motion in a straight lateral direction, and anterior glide following structures: consists of a translatoric motion in a forward or protrusive direction. Because of the potential for the cusps of the man­ >- Temporalis muscle (anterior, middle, and posterior dibular teeth to cause discomfort to the therapist's thumb, it fibers) is suggested that a sterile gauze pad be used as a cushion. >- Masseter muscle (no distinction made between super­ Soft Tissue Palpation ficial and deep fibers) As with the palpation of other regions of the mus­ >- Medial pterygoid muscle (deep to the gonial angle) culoskeletal system, the 3 markers of soft tissue impair­ ment include an assessment of tenderness, tightness, and >- The soft tissues lateral and posterior to the lateral tone. Tightness involves an increase in myofascial density pole of the mandibular condyle (ie, TMJ ligament, joint capsule laterally and posteriorly, lateral collat­ eralligament, and the periosteum) in both the closed and open mouth positions. Copyrighted Materail

Examination and Evaluation of the Temporomandibular Joint 117 Figure 13-10d. Lateral pole in the closed Figure 13-1 Oe. Lateral pole in the open mouth mouth position (lateral structures). position (posterior and lateral structures). Some examiners assess for posterior TMJ capsulitis by it can be very uncomfortable for the patient and, in this placing their fifth digits in the patient's ear canal (finger author's opinion, unnecessary. pads facing anteriorly) with the mouth open and then have the patient close against this anteriorly directed pressureo For an overview of the differential diagnosis of mechani­ Although this method will detect TMJ pain/inflammation, cal TMD, the reader is referred to Figure 13-11. Copyrighted Materail

r Temporomandibula rl 1--t i1 Capsular Disorders 1. History of craniofacial l. History of cumulative 1. Hi story of mic macrotrauma common. microtrauma common. and/or macrotr 2. Reduced mandibular 2. Increased mandibular 2. ReCiprocal cli mobility with deflec­ mobility with deflec­ affected side. tion to the affected tion away from affected side. side. 3. Mandibular d on affected sid 3. Capsular tissues short­ 3. Capsular tissues lax with ened with reduced increaseJ mobility. 4. Full mandibul mobility. of motion. 4. Muscle splinting to li­ 4. Pain at end-range of mit excessive motion. mandibular motion. Capsular Capsular Amerlur Disc Dis Hypomobility Hvpermobility With Reciu Figure 13-11. Differential diagnosis of mechanical TMD. Copyrighte

ar Disorders (TMD) l CD C) ::T­ Q -0 ar .., tv Intracapsular Disorders crotrauma 1. History of microtrauma l. History of emotional trauma. and/or macrotrauma. streS·5, hruxism, fibm­ icking on myalgia, etc. 2. History of reciprocal deviation clicking and intermit­ 2. Myofascial trigger/ten­ de. tent locking. der points of the masti­ lar range catory muscles. 3. Mandibular deflection to affected side. 3. Upper quarter imbal­ ances including forward 4. Reduced mandibular head/rounded shoulders range of motion. posture, reduced freeway space, altered tongue pos­ ition, mouth breathing, etc. splacement Anterior Disc Displacement 1 uc(io[l Wit:hullt Redllcrion (Closed-Lock) Extracapsular I mpai fmcnt (Myofascial Pain) ed Materail

Conn ective Tissue Techniques for th e Temporomandibular F==� Joint/Facia l Region I Ii. = he utilization of direct fascial techniques for the epicranial muscle, along with the connecting temporopari ­ et dis, can bring significant relief to patients suffering from T purpose of achieving myofascial relaxation and relief of TMD symptoms is strongly recommended chronic and episodic tension-type headache. Figure 14-1 in cunjunction with trilditiunal physical therapy modali­ ties (eg, ice, heat, electrical stimulation, ultrasound). This illustrates a connective tissue technique that separates the chapter will begin with the more basic extraural approach muscle fibers of the frontalis in a medial to lateral direction. to treatment followed hy a description of intraural direct This approach can be extended posteriorly to include the Llscial technique. When rerforming myofascial massage occipitalis and laterally to include the temporoparietalis. to the TMJ/facial area, the therapist must be mindful of the emotions related to a patient's facial area. For those Corrugator, Orbicularis Oculi, individuals with histories of physical abuse, touching the (ace lLlay evoke unpleasant memories. The key to effective and Procerus faciaI techniquc is a ,gentle and caring touch. Once the The corrugator supercilii muscle (Figure 14-2) runs from patient grows accustomed to having the suft tissues of the the medial end of the superciliary arch to the deep surface jaw and face massaged, the therapist is then ahle to explore of the skin above the middle of the orbital arch. It can be the release of deep ti:;sue tension, myo(ascial trigger points, a source of pain at the medial and inferior aspect of the and muscle-holding Slates. For a review of the principles of eyebrows and is overworked in patients who are habitual frowners. The orbicularis oculi is the closing muscle of the direct fascial technique, the reader is referred to Chapter 5. eye and is often tender and tight in patients who habitually A small amount of massage or hand crC3m is helpful when squint. Proper eyeglasses and sunglasses will often remedy this problem. Direct fascial technique of these muscles must working in the craniufacial region. be performed with sensitivity, especially when releasing the taut fibers of the orbicularis oculi as they insert into the Frontalis orbit and frontal bone above the eye. While in the upper nasal region, the procerus muscle shoulJ also be treated The fronmlis muscle, 3S with many of the TMJ/facial with gentle direct fascial technique, if necessary. It arises muscles, is overactive in many patients, uften resulting in from either side of the nasal bone and runs upward to insert forehead wrinkles, frontal headache, and at times com­ into the skin over the lower part of the forehead between pression of the supraorbital nerve. Because the frontalis is the eyehrows. When the procerus muscles contract, the contiguous with the occipitalis muscle (occipitofrontalis), skin of the nose is pulled upward as the lower forehead is this cutaneous muscle of the scalp will often require treat­ ment of both components. Direct fascial technique of this Makofsky HW Spinal Mrw/l(// Th('f(lPY(pP 119-124) 02010 SLACK Incorporated Copyrighted Materail

1 20 Chapter 14 Figure 14-1. Frontalis. Figure 14-2. Corrugator, orbicularis oculi, procerus. Figure 14-3. Temporalis. Figure 14-4. Masseter. pulled down, forming horizontill wrinkles between the eye­ painful symptoms :lOd restoring normal function. It is also brows and over the bridge of the nose. It is the (.!Cial muscle important that the therapist identify and correct all related responsible for the expression of distaste. impairments (eg, posture, jaw parafunction, stress) so thClt temporalis tone can return to a normal level. Temporalis Masseter The temporalis muscle (Figure 14-3) is commonly The masseter muscle (Figure 14-4) is a powerful elevator involved in patients with TMD, especially in those suffer­ of the mandible and is commonly involved in the presence ing from extracapsular/myofascial impairment associated of restricted jaw opening. Myofascial trigger points of the with bruxism and emotiunal stress. It is ,11so a source of superficial fibers result in facial pain. Involvement of the symptoms in patients suffering from tension-type headache. deep layer can be a cause of TMJ and ear symptoms. In In :.Iddition, there appears to be a correbtion between FHP addition to ipsilateral ear pain, the deep fibers c:.ln also be and increased temporalis activity in which the mandible is a source of tinnitus. displaced posterior and superior, thus reducing the inter­ occlusal freeway space.? Consequently, treatment of the There is no attempt to differentiate the superficial from temporalis muscle with direct fascial technique is beneficial the deep layer when performing direct fascial technique in a variety of musculoskeletal conditions related to the to the masseter muscle. The therapist will find the most TMJ/facial region. myofascial impairment (ie, tenderness, tightness, and tone) along the inferior aspect of the zygomatic arch and all along The therapist works in a direction perpendicular to the angle and ramus of the mandible. Digital oscillations the fibers and addresses all aspects of the muscle, includ­ along these hony landmarks is quite effective in achieving ing the anterior, middle, and posterior fihers. As with all the desired release of tension in this area. soft tissue mobilizations, the goal is to soften, relax, and improve local circulation to the area in hopes of relieving Copyrighted Materail

Connective Tissue Techniques For the Temporomandibular Joint/Facial Region 121 Figure 14-5. Suprahyo ids. Figure 14-6. Medial pterygoid. Suprahyoids diminishing tone and restoring extensibility to the medial pterygoid muscle. The suprahyoids (Figure 14-5) include the mylohyoid, In addition to manual therapy interventions, including stylohyoid, geniohyoid, and dig<Jstric muscles (anterior and the connective tissue techniques described previously, other posterior bellies). With FHP, the infrahyoids are under nonsurgical options such as electrothcrapeutic modalities stretch but the suprahyoids tend to shorten as their origin (eg, iontophoresis, low-level bser therapy), TMJ occlusal and insertion approximate. This shortening will retrude splint therapy, heat or ice, biofeedback, spray and stretch the mandible and elevate the hyoid bone, hoth of which with fluorimethane spray, and acupuncture, have demon­ can adversely affect swallowing and the rest position of the strated effectiveness when dealing with TMD of som3tic mandible. Whereas myufascial trigger points in the mylo­ origin1,3,9-11 If indicated, the use of trigger point injections hyoid mu cle can refer pain to the tongue, trihohner points in and short-term muscle relaxants should he discussed with the stylohyoid and posterior belly of the dig<Jstric can cause the patient's dentist or physician. With regard to the role head and neck pain. In addition, dentists should be aware of intraoral devices, the Nociceptive Trigemin<ll lnhibitiun that myofascial dysfunction of the anterior belly of the Tension Suppression System (NTITSS) has shown promise digastric can refer pain into the lower incisors.S for the management of nocturnal bruxisml2 and may be an effective nonmedicinal intervention in the treatment Medial Pterygoid of primary headache.l3 By disoccluding the posterior teeth, the clenching muscles are inhibited. Therefore, bruxism is The medial pterygoid (Figure 14-6) along with the mas­ also controlled, and the entire trigeminal afferent system is \"defacilitated,\" explaining the therapeutic role of the NTl­ seter and temporalis muscles is an elevator of the mandible. TSS in both migraine and tension-type headaches. In patients who clench and grind their teeth, these muscles are prone to developing myofascial pain. Because of the Lateral Pole proximit y to the tensor palati muscle, hypertrophy of the medial pterygoid muscle may contribute to barohypoacusis There are several soft tissue attachments into the lateral (ie, ear stuffiness). Other myofascial symptoms include referred mouth, jaw, and ear pain.S pole of the mandibular condyle (Figure 14-7) that respond Palpation for examination and intervention can be well to soft tissue mobilization. The author finds circular accomplished either intraorally or extraorally. Palpation friction to be the intervention of choice in this region. The extraorally is accomplished by having the patient tilt his or structures from superficial to deep include the TMJ liga­ her head to the ipsilateral side in order to slacken the tissues ment (outer-oblique and inner-horizontal fibers); the articu­ and permit greater access. The inner aspect of the angle lar capsule, which is reinforced by the TMJ ligament; and of the mandible is explored with the palpating fingcr(s) as the lateral collateral ligament, which secures the TMJ disc it presses in a superior and medial direction. The inferior to the lateral pole. Circular friction around the lateral pole fibers of the muscle's mandibular attachment are thereby assists with decongestion of venous and lymphatic stasis, accessed and treated with the appropriate direct fascial an increase in arterial f low, and relief of painful symptoms procedure. Strumming over taut fibers is especially useful in through the stimulation of various mechanoreceptors. Copyrighted Materail

122 Chapter 14 Figure 14-7. Lateral pole. Figure 14-8. Intraoral tempora1lis fascial technique. Figure 14-9. Intraoral lateral pterygoid fascial technique. Figure 14-10. Intraoral medial pterygoid fascial technique. Intraoral motion is then applied to the temporalis tendon for Direct Fascial Technique 30 to 60 seconds. The desired response is a softening If the extraoral approach fails to achieve satisfactory of the tissues. results, the therapist should consider working within the oral cavity to eradicate painful myofascial trigger points8 of the 2. lnferior head of the lateral pterygoid - the therapist now stands on the opposite side of the treated area as masticatory muscles. The 4 intraoral techniques described in illustrated (Figure 14-9). The therapist's 5th digit is this section are for the temporalis, inferior head of the lateral pterygoid, the medial pterygoid, and masseter muscles (all again placed above the maxillary teeth on the buccal intraoral procedures are performed using a sterile glove). surface, as far distal as possible, between the mandible and maxilla (active lateral excursion to the treated 1. Temporalis - the patient is treated in supine with side creates more space for the therapist's 5th digit as above). The palmar surface of the 5th digit is then the therapist standing on the same side as the treat­ directed superiorly and medially (\"up and in\") against ed area. The therapist's fifth digit (palmar surface the lateral pterygoid plate of the sphenoid. This is directed toward the therapist) is positioned above also quite sensitive to touch and the technique must the maxillary teeth on the buccal surface, as far distal as possible, between the mandible and maxilla be performed slowly and gently. A massaging motion (more space is created by having the patient actively is applied to this area of myofascial insertion for 30 to displace the mandible toward the therapist in lateral 60 seconds. excursion). The therapist's fifth digit is then directed in a superior and lateral direction (\"up and out\") 3. Medial pterygoid - the therapist, standing on the towards the coronoid process (Figure 14-8). This is same side of the treated area, places his or her index finger along the occlusal surface of the mandibular the site of insertion of the temporalis tendon and can teeth and proceeds distally until the vertical man­ be extremely sensitive to touch. A gentle massaging dibular ramus is encountered (Figure 14-10). The medial pterygoid is found on the medial side of the Copyrighted Materail