__Spinal_Manual_Therapy__An_Introduction_to_Soft_Tissue_Mobilization__Spinal_Manipulation__Therapeutic_and_Home_Exercises

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

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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