R e v i e w A r t i c l e C e r v ic o g e n ic H e a d a c h e Pa r t 1: a n A n a t o m ic a n d C l i n i c a l O v e r v ie w ( a w a r d e d t h e O P T P A w a r d f o r E x c e l l e n c e in a P u b l i s h e d r e v i e w o f t h e L i t e r a t u r e * * ) A B S T R A C T : C ervicogen ic headache is a headache arising fro m painful dysfunction o f the upper cervical spine. This p a p e r review s current literature on the anatomy, etiology, clinical presentation an d differential diagnosis o f cervicogen ic headache. L ow er c e rv i­ cal spine levels an d cervica l soft tissue com ponents w ill be incorporated where they have a d irect influence on the upper three segm ents. K EY W ORDS: CERVICOGENIC HEADACHE, HEADACHE, N E C K PAIN, PATHOLOGY K A T H R Y N L S M IT H , PT CLAIRE H O R N , PT INTRODUCTION Cervicogenic headache (CGH) is a headache (HA) arising from painful dys­ function of the cervical spine, particular­ ly the upper three segments. Studies have shown that a connection exists between HA and poor posture, weak cervical flex­ ors, facet joint athropathy, cervical joint traum a, and jo int hypom obility and hypermobility1'7. The term cervicogenic headache is recognised but not yet offi­ cially accepted by the International Headache Society (IHS) Classification Committee8-9. For the purposes of this paper, the term cervicogenic headache will be used as it is in current literature. This paper will focus on CGH as it emanates from the upper three cervical segments. ANATOMY AND ETIOLOGY Many pain sensitive structures in and around the upper cervical spine may be implicated in CGH. These structures can be broadly categorized into joints (occiput to C3), ligaments, nerve roots and nerves, and muscles and their attach­ ments to bone. Vascular components may also be implicated; these will be dealt with briefly later in this paper. UPPER CERVICAL SPINE DYNAMICS The upper cervical spine is the transi­ tional area between the fixed skull and mobile lower cervical spine. Transitional areas are subject to greater static and dynam ic strain than other vertebral levels10. The cervical area has two nor­ mally occurring curves: the larger lordot­ ic curve in the lower cervical area and a reversal of this in the upper cervical spine, observed when the head and neck are in a neutral position. The persistence of the upper cervical curve is responsible for maintaining the horizontal line of CORRESPONDENCE: Claire Horn, PT / Kathryn L, Smith, PT 3221 Kansas Street Oakland, CA 94602 vision. This makes possible flexion and extension of the upper cervical spine independent of the lower cervical spine, and vice versa11. The cervical spine has divisions occur­ ring both morphologically and histologi­ cally at the C2/3 level". (The occipito- ’ axial (CO/1. C l/2 ) articulation is well recognised as a transitional area between the fixed skull and m obile cervical spine10. I ’he concept of two transitional areas in the upper cervical region is sup­ ported by a study by Jull10. Two hundred and twenty-five volunteers (92 males and 133 females) 10 to 65 years of age par­ ticipated in the study. No prior mention was made of either headaches or neck pain. Passive accessory and physiologi­ cal inter vertebral movements of all the cervical spine joints were m anually examined by two experienced manual therapists who performed a total of 78 separate tests on each patient. Results of each test were graded according to per­ ceived mobility on a scale of 1-5,1 being classified as hypermobile and 5 as very limited to no movement. There was com­ plete agreement in 88% of cases and only minor discrepancies in the other 12%. [Stiffness was the most common f in d in g / w itirhyperm obility being rare. The per­ centage incidence of involvement was highest at CO/1, followed by C2/3, then C l/2. There was a rapid decrease in com­ parable joint signs opposite C3/4 (Fig. 1). RANGE OF MOTION Marked variability exists in the report­ ed ranges of motion at the cranio-verte- bral joints. This reflects various methods of describing movements, different mea­ suring techniques, lack of reliability and validity studies, and errors in measure­ ment. In a literature review Bogduk12 concludes that it is not worth pursuing intervertebral range of motion as a diag­ nostic test. Intersegm ental range of motion is an unstable parameter, with the uncertainty of any measurement being approximately 5 degrees. The movement of greatest amplitude at the 'C 0/lj joints is flexion/extenlion or nodding. Literature -varies in_ measure­ ment from ;i 0 to 35 degrees ifor this jo in t". Lateral flexion- here is often described as a lateral tilt with a simulta­ neous contralateral rotation within this jo in t" 13. Penning and W ilmink13 in a CT study of normal subjects, describe a lat­ eral displacement of 4.4 mm of the atlas relative to the foramen magnum. This lat­ eral displacement occurred contralateral to the direction o f rotation. R otation is described as a slipping movement of one occipital condyle forwards and the other backwards1" 3. Jull10 reports an essentially equal division between subjects in rela­ tion to symmetry and asymmetry, and left and right asymmetry of the trans­ verse process of the atlas. No correlation was found between those subjects with abnormal accessory movement of CO/1, C l/2 , C2/3 and asymmetry at the atlas. Also within the population with asymme­ try, no relationship could be determined between the findings of abnormality of the left or right joint tests in the presence of left or right asymmetrical prominence or non-prominence. Jull concludes that this anomaly of the atlas has no apparent effect on upper cervical joint mobility and should be interpreted as an incidental finding. The movement of greatest amplitude at the /C l/2 joints is rotation,? L iterature, ~ in_jneasurement here from ^9 to ) 40.5 d eg rees"13.R otation is accompanied__________ -t by a screw-like action, accounting for vertical translation of the atlas in relation to the axis. Rotation to the left is checked by the tension of those fibres of the left alar ligament which are attached to the dens in front of the axis of movement and those of the right alar ligament which are attached to the process behind the axis of varies^ ** Republished from : The Journal o f M anual and M anipu la tive Therapy Vol 5. No 4 (1997) 158-170. 12 SA J o u r n a l o f Ph y sio t h er a py 1998 V o l 54 No 3 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. ) m ovem ent11. Flexion and extension are seen by the relative separation and approximation of the spinous process of the axis relative to the posterior arch of the atlas. This movement also involves gliding of the atlantal arch superiorly on the odontoid in extension and inferiorly in flexion. A pproxim ately the same amount of lateral flexion occurs between the axis and atlas (4.07° ± 2.01°), and the occiput and atlas (3.97° ± 1.54°). This lat­ eral flexion is coupled with contralateral axial rotation between the atlas and axis11. Saldinger and Dvorak14 investigated the histology of the transverse and alar ligaments. They conclude that collagen, as the most exclusive constituent together with the fiber orientation determine the mechanical properties of these ligaments. This supports the hypothesis that the liga­ ments can be irreversibly over-stretched or even ruptured when the head is rotat­ ed, and, in addition, flexed by impact trauma as in unexpected rear-end colli­ sions. Structurally _ and biomechanically the Cervical intervertebral joints, including C2/3, are saddle joints^ blow ing m ove­ ments in only two planes at right angles to each other12. The uncinate processes form a concave jo int surface facing upwards and forwards in the plane of the facet joints. The upper vertebral body has a concave lower surface in the sagittal plane. Movement can only occur in the plane of the facet joints and in the sagit­ tal plane. It is well established tlmf la te r-f a f Ifexion results in a coupled range of Pte M rotation aPfach of the cervical, fm segments. jThisls usu- _________aljy compensated for by_ r rotation of the atlanto-axial j ( level. J ’his explains why it is possible for the face to remain in the frontal plane w hile side flexion is per­ formed and coupled range of ipsilateral rotation below the atlanto-axial level still occurs11. The instantaneous axis of rotation (IAR) is a mathemat­ ical concept that has been used to describe motion in contemporary cervical spine biomechanical studies1215. It is the centre about which a moving vertebra appears to rotate if its motion during flexion and extension is per­ ceived as a uniform arcuate movement. The IAR can be located by simple goniometric means if radiographs showing the starting and ending positions of the moving vertebra are superim- p o sed 12. May er, e/_ a /'-, reported -that- ! patients with cervical headache exhibited ' abnormal IARs, particularly at C2/3. There was also~a~small widening of the C2/3 joint in extension as compared to flexion. Pain was elicited by pressure to the cervical spine in this area; therefore, M ayer et al- suggested, a -correlation__ between "clinical symptomatology and radiographic findings^at_th&_same_loc; tion. jArnevcTe? a717 found 72% of 109 "Symptomatic patients exhibited at least one clearly abnormal IAR at or above the symptomatic- segment. The mechanical (disturbances were_most common at C2/3 and C3/4, implicating symptomatic joints at C l /2 and C2/3./They concluded that abnormal lARs were, therefore, a valid marker of neck pain. Bogduk12 hypothe­ sizes that the IAR changes are brought about by muscle spasm secondary to the pain. This mayjvelLsuggesLthaLa lower j cervical injury may cause upper cervica^ /'segm ents to become symptomatic .jit thus__ follows thatjthe headache that commonly accom panies C5/6 pain may not be directly related to that segment but may arise as a result of secondary m echanical - [disturbances at C2/3 or C3/413- jWorth11 writes that abnormal patterns of m ove­ ment may cause persistent irritability in the joint above. This irritability may be temporarily relieved by treatment but is likely to recur unless the motion seg- '! ments are restored to as normal a pattern of movement as possible. -------- HEADACHE, UN ILAT ERAL S IG N S -------- HEADACHE, CENTRAL S IG N S --------NON-HEADACHE,U NILATERAL S IG N S ........... N O N-H EA DACH E.CENTRAL S IG N S "J -J " j - 4 ”4*5 "5 -6 6-7 IN T E R V E R T E B R A L L E V E L Fig 1: The percentage incidence o f p o sitive jo in t signs fo u n d in the le ft or right apophyseal jo in ts and the central interverte­ bral jo in ts fo r the 96 headache and the 107 non headache sub­ jects (from Jull GA. Headaches associated w ith the cervical spine - a clinical review. In Grieve GP (ed), M o d em m anual th era p y o f the vertebral colum n, Edinburgh, Churchill Livingstone, 1986:323) FACET JOINTS Recent and current research has been directed at investigating cervical facet joint pain referral patterns3-618'20. The pres- — ence o f m echanoreceptive and noci- eepive endings in cervical facet joint cap- .7 sules proves that these tissues are moni­ tored by the central nervous system20. This implies that neural input from the facets is important to proprioception and pain sensation in the cervical spine. In a study published in 1990, Dwyer, Aprill and Bogduk3 present a composite map of characteristic pain distribution from facets C2/3 to C6/7 (Fig. 2). Normal cer­ vical facets in five volunteers were stim­ ulated by distending the joint capsule with injections o f contrast medium. As joints from above downward were stimu­ lated, the evoked areas of pain were centered over progressively more caudal levels, and pain from the lower cervical joints extended laterally into the shoulder girdle. Pain from C2/3 was distinguished from C3/4 by its extension into the head. The authors report that pain from the C2/3 area resembled the distribution of pain reported by patients with headaches Jstem m ing from the C2/3 facet joint. C In a follow-up study the same year, •j Aprill, Dwyer and Bogduk tested the pre- ' dictive value of the facet joint segmental pain chart4. Predictions were made as to the segmental location of the sympto­ matic segment in ten patients with sus­ pected cervical facet pain. Correct pre­ dictions were made in all nine patients shown to have symptomatic joints on the basis of diagnostic jo int blocks. The remaining patient was not relieved by blocks of either of the joints pre­ dicted. The authors claim that the results vindicate the accuracy of pain charts for predicting the seg­ mental location of symptomatic joints. D reyfuss et al6 investigated atlanto-occipital and lateral atlanto-axial joint pain patterns. CO/1 and C l/2 join ts of five asymptomatic individuals were isolated and stimulated through mechanical distention of the joint capsules via intra-articular fluo- roscopically guided injections. Head and/or neck pain was gener­ ated by each injection. All joint referral patterns were ipsilateral. The evoked referral pattern for all C l/2 joints was primarily lateral and slightly posterior at the C 1/2 level. Evoked referral patterns SA J o u r n a l o f Ph ysio t h er a py 1998 V o l 54 No 3 13 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. ) from CO/1 varied considerably; inferiorly from the C5 vertebral level to superiorly approaching the vertex of the skull. The authors were unable to chart a composite pain referral map because of the variabil­ ity of referred pain produced, and the small sample size. They did note that the perceived pain/sensation was greater, and that the referral pain patterns were broad­ er, with the CO/1 joint injections. CERVICAL NERVE ROOTS The cervical nerve roots exit from each intervertebral foramen and split into a posterior and anterior division (Figs. 3- 5). The anterior divisions of the four upper cervical nerves form the cervical plexus21. The first and second cervical nerve roots emerge from behind the lat­ eral articular pillars of C l and C2. The roots are not protected posteriorly by the pedicles and facets present in the rest of the vertebral colum n15. The ganglion of the first two cervical nerve roots are found on the vertebral arches of C l and C2 and not inside the intervertebral fora­ men. The nerves travel upward and later­ ally and split into two primary divisions. The anterior primary ramus of the first cervical root passes over the posterior arch of C l. The anterior primary ramus o f the second cervical root passes between the arches of C l and C2; the posterior primary ramus passes back­ ward between the posterior arches of C l and C2 and extends to the soft tissues of the neck15. The posterior primary ramus of the third cervical root proceeds obliquely downwards and outwards. It gives rise to the third occipital nerve which pierces trapezius and supplies the skin on the lower and back part of the head15-2'. The second cervical root supplies the C2 dermatome, myotome and the C l/2 joint. The third cervical root supplies the C3 dermatome, myotome and C2/3 joint (Fig. 6). The first cervical root’s function is controversial. Classically, it has been described as a pure motor root supplying the C l myotome, which are the muscles around the CO/1 joint. Gray however, describes a small sensory root consisting of three rootlets21. Orbital, frontal and occipital pain may be produced on stim­ ulation of a specific rootlet15. This may be explained by the neural anastomosis of the occipital and supraorbital nerves. The greater and lesser occipital nerves origi­ nate in the C l to C3 region. The trigemi­ nal tract extends down to, and synapses between, C l and C4. The auriculotempo­ ral and zygom aticotem poral nerves, which supply the side of the head, are branches of the trigeminal nerve. Any problem in the suboccipatal spine can, therefore, produce any combination of headache, facial, or cervical pain. It is generally agreed that neck trauma, such as whiplash, is one of the most com­ mon causes of chronic headache21-1518. Nerve root compression as well as disc herniation may occur. M ark15 reports that the occipital nerve can become entrapped or com ­ pressed from a hyperflexion injury by the sem ispinalis and possibly the splenius capitus muscles, but he does not specify greater occipital nerve, lesser occipital nerve, or both. Tearing o f these muscles may occur causing muscle guarding, pulling the cranium down and compress­ ing the suboccipital region. The posterior prim ary ramus of the second cervical root, which continues into the scalp as the greater occipital nerve, may be injured by the approximation of the bony arches of C l and C2, or by excessive m obility at this joint. With a forward head posture, posterior rotation of the cranium on the cervical spine may cause compression o f the spinal tract o f the trigeminal nerve, which can in turn give rise to facial or head pain separate from trigger points or any lesion occurring on the head or facial areas. Lord et aP reports that third occipital nerve headache is a common condition in patients with chronic neck pain and headache after whiplash. One hundred patients with at least a three month histo­ ry of post-whiplash neck pain participat­ ed in this double-blind study. Seventy- Fig 3: Deep dissection o f the le ft cervical dorsal rami. The superficial posterior neck muscles have been resected. The lateral branches (lb) o f the dorsal rami and the nerves to the intertransversarii (ni) have been transected, leaving only the m edial branches (m) intact. The Cl dorsal ram us su p p lies the obliquus superior (os), obliquus inferior (oi) and rectus capitis (re) muscles. The m edial branches o f the C2 and C3 dorsal rami, respectively, form the greater occipital (gon) and third occipital (Ion) nerves. Com m unicating loops (c) connect the C l, C2 and C3 dorsal rami. Three m edi­ al branches (nnS) o f the C2 innervate the sem i-spinalis capitis, w h ile the C3 to C8 m ed ia l branches send articu la r branches (a) to the zyg a p o p h o sea l jo in ts before innervating the m ultifid u s (M) and sem ispinalis cervicis (SSCe), and those a t C4 and C5 from superficial cutaneous branches (s). TP, transverse process o f atlas; SP, spinous process o f T l. (From Bogduk N. Innervation and pain patterns o f the cervical spine, In G rant R. (ed), P hysical therapy o f the cervical and thoracic spine, 2nd edition, N e w York, C hurchill L ivin g sto n e 1994.-66) Fig. 2: A c o m p o site map o f the results in all volunteers depicting the p u ta tiv e characteristic distribution o f pain from zygapophoseal jo in ts a t segments C2-3 to C6-7. (From D w yer A , A p rill C, Bogduk N. Cervical zygapophoseal jo in t pain patterns 1; a stu d y in nor­ m a l volunteers. Spine 1990; 15(6):453-457) 14 SA J o u r n a l o f Ph ysio t h er a py 1998 V o l 54 No 3 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. ) Fig 4: D istribution o f the upper three cervical sinuvertebral nerves and the in n erva tio n o f the a tla n to -o c c ip ita l and a tla n to a x ia l jo in ts. A rticu la r branches (arrowed) to the a tlanto-occipital and atla n to a xia l jo in ts arise from the C l and C2 ventral rami, respectively. The C l to C3 sinuvertebral nerves (svn) pass through the foram en magnum to innervate the duram ater over the clivus. En route, they cross and supply the transverse ligam ent o f the atla s (TL). The dura m ater o f the more lateral parts o f the posterior cranial fo ssa is innervated by meningeal branches o f the hypoglossal (xii) and vagus (x) nerves. (From Bogduk N. Innervation and pain patterns o f the cervical spine, In Grant R. (ed), P hysical therapy o f the cervical and thoracic spine, 2nd ed itio n , N e w York, Churchill Livingstone 1994.-67) Fig 5: The innervation o f a cervical intervertebral disc. Nerve fibres enter the anterior and anterolateral aspect o f the annulus fibrosus from branches o f the cervical sym pa th etic trunk (st) th a t form a plexus accom panying the anterior longitudinal lig­ a m ent (all). Nerve fibers enter the posterolateral aspect o f the annulus fibrosus from branches o f the vertebral nerve, w hich accompanies the vertebral artery (va). From this nerve arise the cervical sinuvertebral nerves (svn), w hich from a plexus accom panying the posterior longitudinal ligam ent (pll) and from w hich branches enter the posterior aspect o f the annulus fibrosus. (From Bagduk N. Innervation and pain p a tterns o f the cervical spine, In G rant R. (ed), Physical therapy o f the cer­ vical and thoracic spine, 2nd edition, N ew York, Churchill L ivingstone 1994:67) one complained of headache associated with their neck pain; for 40 it was the dominant complaint; for 31 a secondary problem. Diagnostic blocks of lignocaine and bupivacaine were administered in random order to the third suboccipital nerve. The diagnosis of third suboccipital nerve headache was made only if both blocks completely relieved the patient’s upper neck pain and headache and the relief lasted longer with bupivacaine. The prevalence of third occipital nerve HA in the 100 patients was 27%. Among those with dominant HA (40 patients), the prevalence was 53%; the cause of HA in the other 47% of these patients was not explained. This study also found that patients with a positive diagnosis were significantly more tender over the C2/3 facet joint in comparison to other cervi­ cal levels. SOFT TISSUE The associated soft tissues undoubtedly play an integral role in cervicogenic headaches. Janda22 writes that muscle dysfunction is closely related to joint dysfunction, and that treatm ent of impaired muscle function is a most effec­ tive way to restore normal functioning of a particular joint. He also emphasises that it would be wrong to consider mus­ cle dysfunction independently o f the functional status of other structures. It is important as well not to focus only on a symptomatic area but rather to consider it in relation to the functional status of the whole motor system. The “proximal or shoulder crossed syndrome” describes the most important muscle imbalance syndrome in the upper body (Fig.7). This is characterized by tightness in the upper trapezius, levator scapulae, and pectoral muscles, and weakness of the lower sta­ bilizers of the scapula and the deep neck flexors. When the weakened muscles and shortened muscles are linked, they form a cross. In addition, the sternocleidomas­ toid and suboccipital muscles are tight in this syndrome. A forward head posture would also be observed. From a muscu­ lar point o f view, a forward head posture is due to weakness of the deep neck flex­ ors and dominance or even tightness of the sternocleidomastoid. A forward head posture particularly stresses the cervic- ocranial and cervicothoracic junctions and may case painful symptoms in these areas. Watson and Trott7 investigated nat­ ural head posture and upper cervical flex­ or muscle performance. Sixty female subjects were divided into two equal groups on the basis of the absence or presence o f headache. The headache group had confirm ed upper cervical articular cause and was found to be sig­ nificantly different from the non­ headache group in respect to forward head posture; they also had less isometric strength and less endurance of the upper cervical flexors. Myofascial pain patterns should also be considered in soft tissue evaluation. Travell23 describes several cervical mus­ cles that refer to pain specifically to the cranial area, and may be implicated as a cause of pain the cervicogenic headache.1 Recent literature indicates that muscles SA J o u r n a l o f Ph y sio th era py 1998 V o l 54 No 3 15 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. ) may directly influence the pain sensitive dura mater24, thus suggesting an alterna­ tive mechanism for headache generation. Anatomical research has shown that a connective tissue band exists between the rectus capitus posterior minor muscle and the posterior atlanto-occipital mem­ brane24. This membrane is attached to the underlying spinal dura, thus contraction of the rectus capitus posterior minor can exert tension on the dura, thus producing headache. CLINICAL PRESENTATION Cervicogenic headache is referred to as a “syndrom e” rather than a single headache entity2128. Clinical manifesta­ tions vary in terms of pattern and may present in acute, sub-acute or commonly chronic form s1. Sjaastad et aP describe clinically con­ sistent characteristics for CGH and pro­ pose diagnostic criteria. The presentation of CGH with the major signs and symp­ toms as outlined by Sjaastad et al are referred to consistently by several authors in discussion and research on dif­ ferent headache types15 28'32. The criterion of unilaterality is discussed by Jull33 as being significant in terms o f onset pain, which is usually in the neck of CGH. Jull" refers to the fact that Sjaastad et al8 first characterized CGH as strictly unilat­ eral, but she reports that subsequent stud­ ies have shown that the headache can be unilateral, unilateral with spread, or bilat­ eral34. Jull1 confirms unilaterity in that she describes the CGH as not changing sides after onset. Robarth35 reports that the N orth A m erican Cervicogenic Headache Society has adopted a defini­ tion which addresses cause rather than symptoms for CGH. A shortened version o f this understanding o f CGH presenta­ tion is “Referred pain perceived in any region of the head caused by a primary nociceptive source in the muscule skele­ tal tissues innervated by cervical nerves”. D ’Amico et a P examined side-locked unilaterality and pain distribution at onset and at peak headache in 74 patients with different form s o f long-lasting headache: migraine, tension-type, and cervicogenic headache as described by Sjaastad et al8. The findings o f the D ’Amico et al study showed that side- locked unilaterality in m igraine was 20,8%, in tension-type HA 12.5%, and in CGH 100% (only 4% of the entire sam­ ple). Pain localization described for migraine was initially anterior and then spread over the entire hemicranium. In tension type HA pain was more variable around central sides, tending to localize anteriorly; and in CGH, the pain always began in the occipito-nuchal region, and it could shift to the peri-orbital area or could remain confirmed posteriorly. Jull1 states that one established diag­ nostic criterion for cervical headache is the presence of symptomatic articular dysfunction m anifested as a painful abnormality of motion at a relevant seg­ ment in the cervical spine. A primary diagnosis of cervical headache is consis­ tent with an abnormality within the upper cervical join ts (occiput to C3). The motion abnormality may result from joint trauma, chronic strain, degenerative joint disease, or inflammatory joint disease. The motion abnormality may present as symptomatic joint hypomobility, hyper- momobility, or instability. Fig 6: Derm atom ic pattern o f the anteri­ or and posterior branches o f C2 and C3 (according to Maigne) (From the Quebec Headache Stu d y Group: M eloche e t al: P a in fu l In terverteb ra l D ysfu n ctio n : R obert M aigne's Original C ontribution to H eadache o f Cervical Origin. Headache 33:328-334,1993) Jull34 developed a cervical headache profile after reviewing 203 patients, 96 of whom had CGH. This study demon­ strated that the headaches were either unilateral or bilateral. Pain was described as being in any area o f the head or face but was commonly occipital, subocipital, frontal, or retro-orbital. A common histo­ ry was one o f trauma, but the headaches would also be related to prolonged pos­ tural and functional strain. Dizziness, nausea, lightheadedness, inability to con­ centrate and visual disturbances are dis­ cussed as being common34-36-31 as opposed to “minor” by Sjaastad et aP”. The diagnostic criteria as outlined by Sjaastad et aP are as follows: M a jo r S ig n s a n d S y m p t o m s i Unilaterality o f the head pain (defined as no change in side from onset)31. ii Neck involvement: a Provocation o f attacks: - Pain, seemingly o f a similar nature, triggered by neck move- Fig 7: Schematic representation o f the proxim al crossed syndrome. The thick lines connect shortened and w eakened muscles. The short, tig h t muscles are the levator scapulae, upper trapezius, and pectorals; the w ea k muscles are the deep neck flexors and low er stabilizers o f the scapula. (From JandaV: M uscles and Cervicogenic Pain Syndromes. In Grant (ed), P hysical Therapy o f the Cervical and Thoracic Spine, Ch 9. Edinburgh: Churchill Livingstone, 1988.) 16 SA J o u r n a l o f P h ysio t h er a py 1998 V o l 54 No 3 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. ) ment and/or sustained awkward head positioning. - Pain similar in distribution and character to the spontaneously occurring pain elicited by exter­ nal pressure over the ipsilateral upper, posterior neck region or occiput. b) Ipsilateral neck, should and arm pain of a rather vague, non-radi- cular nature. c) Reduced ROM in the cervical spine. P a in C h a r a c te r is tic s iii Non-clustering pain episodes. iv Pain episodes o f varying duration or fluctuating continuous pain. v Moderate, non-excruciating pain, usually o f a non-throbbing nature. vi Pain starting in the neck, eventually spreading to oculo-frontal-temporal areas, where the maximum pain is often located. O th e r im p o r t a n t c rite ria vii Anesthetic blockades o f the major occipital nerve and/or of the C2 root on the symptomatic side abolish the pain transiently, provided complete anesthesia is obtained. viii Affects more women than men. ix A history of head and/or neck trauma (whiplash). M in o r, m ore ra rely occurring, n o n -o b lig a to r y s y m p to m s a n d sig n s Various attack related phenomena: x Autonomic: a) Nausea b) Vomiting c) Ipsilateral edema and less fre­ quently flushing, mostly in the periocular areas. xi Dizziness. xii Phono-and photophobia xii “Blurred vision” in the eye ipsila teral to the pain xiv Difficulty swallowing Classic areas o f pain referral from spinal segments are described34 3638 and represented in figure 8. CO/1 - Occipital, ear pain. CI/2 - Suboccipital, posterior head to forehead, into and behind the eye, temporal pain, band around head. C2/3 - May irritate C2 or C3 nerve root, anterior neck pain, top of head, neck tongue syndrome (transient). D iffe r e n tia l D ia g n o s is Headache is one of the most frequent­ ly reported symptoms in the general adult population13. Grieve39 describes cranial and facial pain as a frequent complaint in cervical spine disorders but points out that headache may be the presenting symptom of disorders not involving the musculoskeletal tissues. Pain sensitive structures need to be considered in dif­ ferential diagnosis; these include blood vessels, dura, ligaments, fascia, perios­ teum, muscles, joints, skin, subcutaneous tissues, glandular tissue, sinus and nasal mucosa, dental pulp, gums in the lining of the oropharynx, endoneurium , epineurium, and perineurium of the cra­ nial and cervical nerves40. Pain can also be referred into the cranium from struc­ tures located elsewhere, but pain sensi­ tive structures are primarily involved41. M ig r a in e , T e n s io n -ty p e , a n d C lu s te r h e a d a c h e s y n d r o m e s Jull1 states that clinical physical thera­ pists who are consulted on a first-contact basis by a patient with headache symp­ toms must decide whether cervical dys­ function is a primary cause, a partial cause in a headache continuum , is enhancing symptoms o f other forms of headache, or has no role in the patient’s headache. Headache types overlap with­ in the classification o f varying headache sy n d ro m es'915-40'42. D ifferentiation o f headache type is typically by area and behaviour o f symptoms ‘•29-31-34-43. (Table 1). D ’Amico el a P found that unilaterity is characteristic of all forms of long last­ ing headache (>4 hours) but to differing ' extents in different headache categories. Localization of pain, particularly at the beginning of an attack, can assist with differentiation as CGH pain is typically felt in the posterior parts o f the head or neck (occipitonuchal) region at onset. The pain may remain posteriorly or shift to the peri-orbital area, and will be asso­ ciated with a cervical spine movement dysfunction pattern1'29. Migraine pain is often located in the anterior regions of the head initially (periorbital-frontal) and then spreads over the entire hemicrani- um29. M igraine is differentiated from CGH in that there is marked associated autonomic symptoms of nausea/vomit­ ing, photo and phonophobia40. Migraine may be influenced by movement of the craniovertebral region 40 whereas CGH is typically triggered by neck move­ ment31. Migraines are episodic, have a reasonably consistent duration for a par­ ticular individual and frequently termi­ nate within 24 hours. Periods between headaches are usually pain free1. Tension -type headache is differentiated from CGH in that pain tends to localize in the anterior regions. Pain is variable, may be present in the occipical region and is more typically bilateral with a descrip­ tion of a tight band around the head30-32-34. Tension headaches are usually long last­ ing and protracted and may be further differentiated from CGH in that m ove­ ment dysfunction patterns in the cervical spine are not typically aggravating. Muscle skeletal dysfunction may be a contributory factor to the etiology o f both m igraine and tension headaches3044. Limitation o f ROM and prevalence of trigger points in the cervical musculature in these types o f headaches have been described44, Vernon et al30 challenge the “narrow prescriptive definition o f cer­ vicogenic headaches”. They report find­ ings o f occipital and neck pain during headaches, tender points in the upper cer­ vical spine region, greatly reduced or absent cervical curve and X-ray evidence of joint dysfunction in the upper and lower cervical spine in migraine and ten­ sion-type headaches. Leone et aP' inves­ tigated the identification o f CGH am ongst patients with m igraine analysing 374 headaches. In the migraine group, 44.6% experienced side-locked unilateral headaches; in these cases the pain was not precipitated by trauma or associated with neck movements and, therefore, did not fully meet the criteria of Sjaastad8. Leone et aP' suggest that additional clinical and instrumental crite­ ria are required to distinguish migraine from CGH. Cluster headaches are more easily dif­ ferentiated from CGH as the typical clus­ ter pattern of pain is not found in C G H 115. Cluster headaches are typically short- lasting and episodic. Pain is predom i­ nantly ocular/periocular and may be associated with a H orner’s syndrome (ocular sym pathetic paresis, ptosis). There is no palpable neck muscle tight­ ness11532. (Table 1). H e m ic r a n ia C o n tin u a a n d C h ro n ic P a r o x y s m a l H e m ic r a n ia Hemicrania continua is a unilateral headache syndrome similar in presenta­ tion to CGH, however it differs in that it has no mechanical precipitator, it starts in the front-tem poral region and it is stopped typically with indomethacin42. Chronic paroxysmal hemicrania differs SA J o u r n a l o f Ph ysio t h er a py 1998 V o l 54 No 3 17 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. ) from CGH as it has a modified cluster pattern of pain. Symptoms can be bilater­ al, occur in the ocular/periocular area and may be diffuse in the ipsilateral shoulder and arm, and it may have a mechanical precipitator. There may be signs o f cervi­ cal spine involvement but ROM is nor­ mal. Chronic paroxysm al hem icrania also responds well to indomethacin'5. S e rio u s P a th o lo g y M akofsky40 outlines the follow ing headache danger signals: • Sudden onset o f new severe headache (subarachnoid hemorrhage, meningoen­ cephalitis, vertebral artery dissection45,- internal carotid artery dissection46); • Progressively worsening headache (advancing intracranial process, brain tumor, subdural haematoma or extracra- nial process of temporal arthritis); • Onset after physical exertion, strain­ ing, coughing or sexual activity (worsen­ ing vascular headaches, increasing intracranial pressure); • A ssociated sym ptom s such as drowsiness, confusion, loss of memory, focal neurological signs, fever, arthral­ gia, myalgia; • Onset after 50 years o f age (most benign recurrent headaches begin before middle age, patient should be referred to a physician immediately). Headache can be the presenting feature in the presence of ominous disease, and serious consideration must be given to the history40. Early diagnosis of vertebral artery dissection (VAD) or internal carotid artery dissection (ICAD) is essen­ tial due to the progressive nature of these disorders and the potential for delayed cerebral lesion4546. Sturzenegger15 reports that VAD presents in a similar way to CGH with unilateral head and neck pain (always on the side of the dissection). Sudden onset, severe sharp nature of pain with no previous history of HA are dif­ ferentiating factors. VAD is usually apparent only when focal ischaem ia develops. Prior to this stage these headaches can be misdiagnosed as mus­ cle contraction or CGH46. ICAD46 also initially manifests with sharp ipsilateral HA but is differentiated from CGH by site of pain. Head pain is predominantly anterior or on one entire side (frontal, temporal, parieto-occipital), is constant, steady, aching and is associated with a H om er’s syndrome o f oculosympathetic paresis46. Presentation of headache due to brain tumor is possible®41. Symptoms may include a deep, steady, dull, aching pain which is sometimes severe but not as intense as migraine, can be relieved by cold packs or aspirin, and does not usual­ ly interfere with sleep. Pain occurs from distortion o f pain sensitive structures such as dural membranes, blood vessels, and periosteum. In contrast to CGH it may be provoked by coughing, straining at stool, or postural changes, and the increase in intracranial pressure can cause vomiting but no nausea. Blurred vision, and a loss of lateral gaze with eyes deviated medially (cranial n.VI) may occur depending on location of the tumor. Headache is rarely caused early on by a tumor. Symptoms o f neurologic CNS dysfunction are more frequent41. T rig e m in a l N e u r a lg ia (tic d o lo u r o u x ) Trigeminal neuralgia16 affects the cra­ nial nerve which is responsible for sensa­ tion to the face and anterior scalp and for motor innervation of the muscles o f mas­ tication41. Pain occurs in this distribution with sudden, intense, superficial shoot­ ing or stabbing pain which immobilizes the face (cheek, chin, lips, and tongue). It is triggered by light touch, may come interm ittently with one or two paroxysms, may last a minute only or come with repeated paroxysms giving the feeling o f continuous pain. Post­ herpetic neuralgia commonly involves the opthalmic branch of the trigeminal nerve and is associated with annoying parasthesias or sharp jabbing pain on a background o f steady burning or aching. Post-herpetic neuralgia is easily differen­ tiated from CGH by the behaviour, onset and area of pain. Physical therapy has no described role in the treatment of post­ herpetic neuralgia. T e m p o r o m a n d ib u la r J o in t Tem porom andibular disorders (TMD) are frequently the cause o f headaches and facial pain3747"19 and can be both m yo­ genic or arthrogenic. Arthrogenic pain may radiate to the temple, zygoma, ramus of the m andible or the ear. Myogenic pain may result in tenderness on palpation to masseter, temporalis and pterygoid muscles. TMD patients may have associated craniovertebral and pos­ tural dysfunction3749. Grieve39 comments that patients with or without upper cervi­ cal joint problems may have cheek, ear, temporal and postauricular pain. Origin o f these symptoms can be either cervical, TMD or a combination. TMD can be dif­ ferentiated from CGH in that TMD is aggravated by chewing hard foods or anything with excessive overuse o f the jaw, and by clenching or grinding of teeth (this may be evident on intraoral exami­ nation). It may wake the person at night with jaw pain and may be associated with sleep disorders49. Haley et al47 compared patients suffering from TMD and a gen­ eral HA population; both groups demon­ strated pericranial tenderness although the TMD patients had significantly more jaw dysfunction and the HA patients exhibited more neck muscle tenderness. MYOFASCIAL TRIGGER POINTS Janet Travell et a P describes myofas­ cial trigger points that refer pain to the head and neck region. Muscles to consid­ er are the sternocleidomastoid (SCM) trapezius, temporalis, splenius capitus and cervicus, multifidus, scalenes, the suboccipital group, masseter, and medial and lateral pterygoid. These muscles may be implicated in classic CGH as a prima­ ry or secondary cause. OTHER Grieve39 describes the list o f possible cause o f headaches (ocular, aural, nasal, dental structures and sinuses) as “formi­ dable”. Other types o f headaches which the clinician may be faced with can be vascular in origin in the form of essential hypertension: can be related to pre-men- strual tension, temporal arthritis, dilata­ tion o f cranial arteries due to infections, poisons, or foreign protein reactions 3 7 , 39,41 CONCLUSION The upper cervical spine is a complex region. A good understanding o f the local anatomy and biomechanics will enhance the ability o f the clinician to identify dysfunction and the tissues responsible for the generation of pain. Recognising and understanding the clin­ ical presentation of headaches em anat­ ing from this region will direct the clini­ cian in examine and treatment. The clin­ ician should also be aware o f the many other causes o f headache and that other headache presentations may have a cer­ vicogenic component. 18 SA J o u r n a l o f Ph y sio th era py 1998 V o l 54 No 3 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. ) T A B L E 1 : H e a d a c h e s CERVICAL TENSION MIGRAINE CLUSTER Area of symptoms • frontal, retro-orbital, temporal, occipital, assoc with subocc & neck pain (Sx usually start in neck subocc or occipital) • unilateral spread to other side or bilateral does not change sides • frontal, retro-orbital, temporal, occipital; may have cervical Sx • bilateral • frontal, retro-orbital, temporal, occipital; may have cervical Sx (usually start in frontal & temporal then spread to other areas) • unilateral, can change sides • frontal, retro-orbital, temporal, occipital: may have cervical Sx (neck pain is more of an ache compare to the excruciat­ ing head pain) • unilateral, can change sides Quality of symptoms • Dull boring pain • can have shooting pain (deep) • Moderate to severe level (20%) • tight band or heavy weight around the head • moderate to severe level • throbbing bursting boring • moderate to severe level (if uncontrolled can reach disabling) • significant ocular Sx & intense pressure behind the eye • typically excruciating Associated symptoms • nausea, vomiting & photophobia (ipsilateral to side of pain) • nausea, vomiting & photophobia • nausea, vomiting & photophobia (no correla­ tion between side of pain & neurological features) • autonomic disturbances (forehead sweating, tearing of the eye, ipsilateral ptosis, 7 nasal stuffiness or secretion) Neurolo­ gical signs • not common (tongue neck syndrome occipital pain radiating to ear with ipsilateral tongue numbness: abnormal sublux of lat A A joint) • surgically confirmed compression of C2 C3 C4 NR Frequency and duration • can be episodic (few hrs to few days) or chronic (semi-conti­ nuous or 2-3/ week) • can be episodic (few hrs to few days) or chronic (semi-conti­ nuous or 2-3/week) • few hrs - days but generally less than 24 hrs • 1 /yr - several per week (distinct periodicity appropriate assoc fea­ tures with painfree periods) • 15 min - 2 hrs • 1/2/24 hr period but can range from 2 week to 8/24 hrs • typically last 1 -2 mnths: chronic up to 1 yr, Remis­ sion 6 months - 2 yrs Time and Mode of Onset • m a y b e p re s e n t w h e n w a k in g & w o rs e n a s d a y g o e s o n : a c tiv ity d e p e n d e n t • less fr e q u e n tly w a k e s w ith h e a d a c h e • w a k e s w it h h e a d a c h e • w a r n in g o r a u r a o f fo c a l n e u r o S x p r io r to h e a d a c h e • n e c k m o v e m e n ts c a n t r ig g e r h e a d a c h e s Precipi­ tating Factors & Relieving • s u s ta in e d n e c k p o s tu re s o r m o v e m e n ts • m a y n o t k n o w p a r t i­ c u la r p a tte r n • stress o r te n s io n m a y in c re a s e h e a d a c h e • stress o r te n s io n • stress in d u c e d o r stress re le a s e d s itu a tio n s • fo o d a lle r g ie s , b r ig h t lig h ts , e x e r t io n , n o is e e tc . • n e c k m o v e m e n ts c a n t r ig g e r h e a d a c h e s General Medical History • n o fa m ily h is to r y m o r e c o m m o n fr o m 20- 5 0 a g e g r o u p • F>M • familial te n d e n c y • F>M • familial te n d e n c y • F>M • n o f a m ilia l h is to r y • M>F History of Onset • tr a u m a o r DJD o r U C x jo in ts • c la s s ic a lly n o t r e la te d to c e r v ic a l t r a u m a o r s tr a in • onset related to puberty • c la s s ic a lly n o t r e la te d to c e r v ic a l t r a u m a o r s tr a in A d a p t e d fr o m J u ll, C A : C e r v ic a l H e a d a c h e a R e vie w . In G r ie v e G P (e d ), M o d e m M a n u a l T h e r a p y o f th e V e r t e b r a l C o lu m n , p 3 3 3 - 3 4 7 , N e w Y o rk , C h u r c h ill L iv in g s to n e , 1 9 9 4 . SA J o u r n a l o f Ph ysio t h er a py 1998 V o l 54 No 3 19 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. ) Fig 8: Cervical headache pain patterns SITE 1-CO/l, SITE 2-CO/1, SITE 3-C1/2, C2/3, SITE 4-C1/2, C2/3, SITE 5-C1/2, C2/3, SITE 6-C2/3, SITE 7-C1/2, C2/3, SITE 8-C2/3, SITE 9-C1/2, C2/3, SITE 10-C1/2, C2/3, SITE U -C 5 /6 Discogenic, SITE 12-T4, Lumbar (From Bang M. From Kaiser Northern California region. Teleconference: S ink or S w im -strea m lin in g the in itia l evaluation, 1996) 20 SA J o u r n a l o f Physiotherapy 1998 V o l 54 No 3 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. ) ACKNOWLEDGMENTS This paper was part of a project com­ pleted in partial fulfilment of the require­ ments for the Kaiser Permanent Physical Therapy R esidency Program in Advanced Orthopaedic Manual Therapy: 27400 Hesperian Boulevard, Hayward. CA 94545. The authors o f this literature review would like to acknowledge Judy Sills, MS, PT and Allen Bernstein MD for their advice and guidance during the preparation of this manuscript. REFERENCES 1. Jull G A : H e adaches o f C ervical O rigin. In: G ra n t R (e d ), P h y s ic a l T h e ra p y o f the C e n ’ica l a n d Thoracic Spine, C h 13. N ew York: C hurchill L ivingstone, 1994 2. 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Barnsley L, Lord S, Wallace B, Bogduk N: The Prevalence o f Chronic Zygapophyseal Joint Pain After Whiplash. Spine 2 0 (l):2 0 -2 6 , 1995 19. B ovim G, Berg R, Gunnar D ale L: C e rv ic o g en ic Headache: A n esth etic Blockades o f Cervical N erves (C2-C 5) and Facet Joint (C 2/3). P ain 49:315-320, 1992. 20. M clain R: M echanoreceptor Endings in Human C ervical F acet Joints. S p in e 19(5):495-501, 1994 21. Gray H: G r a y ’s A n a to m y: The C lassic C o llectors E dition, p 758-764. N ew Jersey: Crown Publishers, 1977 22. Janda V: M uscles and C ervicogenic Pain Syndromes. In Grant (ed), P h ysic a l T herapy o f the C e rv ic a l a n d T h o ra cic Spine, Ch 9. Edinburgh: Churchill Livingstone, 1988 23. Travell JG, Sim ons DG: M y o fa scia l P ain a n d D y sfunction. The Trigger P o in t M a n u a l Volume 1. Baltimore, W illiams and W ilkins, 1993. 24. 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Isaacs ER, Bookhout MR: Screening for Pathologic Origins o f Head and Facial Pain. In B o isse n a u lt W (ed), E x a m in a tio n in P h ysic a l T h e ra p y P ractice, nd Edition, Ch 8. N ew York: Churchill L ivingstone, 1995 42. Sjaastad O, Joubert J, Elsas T, B ovim G, Vincent M: H em icrania Continua and C ervicogenic Headache. Separate Headaches or T w o F aces o f the Sam e H eadache? F u n ctio n a l N e u ro lo g y 8(2):79-83, 1993 43. Kaiser Advanced Orthopaedic manual Therapy R esidency Program Syllabus Notes, Union City, California, p 117-118, 1996 44. Kidd R, N e lso n R: M u scu losk eletal Dysfunction o f the N eck in Migraine and Tension Headache. H e a d a c h e 33:566-569, 1993 45. Sturzenegger M: Headache and N eck Pain: The Warning Sym ptom s o f Vertebral Artery D issection . H e a d a c h e 3 4 :1 8 7 -1 9 3 , 1994 46. Silbert P, M okri B , S c h ie v in k W: Headache and N eck Pain in Spontaneous Internal Carotid and Vertebral Artery D issec tio n s. N e u ro lo g y 4 5 ( 15): 151 7 -1 5 2 2 , 1995 47. Haley D, Schiffman E, Baker C, Belgrade M: The Comparison o f Patients Suffering from Temporomandibular Disorders and a G eneral H eadache P opulation. H e a d a c h e 33:210-213, 1993 48. Talley R, Murphy G, Smith S, Baylin M, H aden J: Standards for the H istory, Examination, D iagnosis, and Treatment o f Temporomandibular Disorders (TM D): A P osition Paper. T h e J o u r n a l o f C ra n io m a n d ib u la r P ra c tic e 8 (l):6 0 -7 7 , 1990 49. Trott P: E xam ination o f the Temporomandibular Joint. In: G rieve GP (ed ), M o d e rn M a n u a l T h e r a p y o f the V erte b ra l C o lu m n , Ch 4 8 . Edinburgh: Churchill L ivingstone, 1986 SA J o u r n a l o f Ph y sio th era py 1998 V o l 54 No 3 21 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 3. )