The World Cervicogenic Headache Society defines. Articular and Muscular Impairments in Cervicogenic Headache: A Case Report

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1 Articular and Muscular Impairments in Cervicogenic Headache: A Case Report Shannon M. Petersen, MPT, OCS, COMT 1 Journal of Orthopaedic & Sports Physical Therapy Study Design: Case report. Objectives: To describe the use of manual therapy and muscle re-education for an individual with suspected cervicogenic headache. Background: This patient was a 27-year-old woman with complaint of headache. She was functionally limited with prolonged postures and lifting. She also demonstrated impairments in cervical mobility and muscular performance. Methods and Measures: This patient was treated 8 times over an 8-week period. Intervention included manual upper cervical spine mobilization techniques, muscle re-education for the deep neck flexor muscles, and scapular stabilization exercises. Results: Following treatment, the patient demonstrated an increase in cervical mobility, improved muscular performance, a decrease in headaches, and complete resolution of functional limitations. Conclusion: The combination of manual therapy and muscle re-education was successful in relieving headaches and improving function in this patient. J Orthop Sport Phys Ther. 2003;33: Key Words: cervical spine, deep neck flexors, manual therapy The World Cervicogenic Headache Society defines cervicogenic headache (CGH) as referred pain perceived in any part of the head caused by a primary nociceptive source in the musculoskeletal tissues innervated by cervical nerves. 38 These structures may include muscles, facet joints, capsules, ligaments of the upper 3 cervical segments, nerves, dura mater, spinal cord, or vertebral artery. 4,24 The International Headache Society (IHS) has established criteria for diagnosis of CGH. These criteria are presented in Table 1. To make a diagnosis, all of the letter headings in the IHS diagnostic criteria must be met. 13,18,24,25 Symptoms Individuals with CGH present with a pattern of characteristic symptoms, however, there can be some degree of variance in their complaints. The location of symptoms is usually unilateral and does not change sides; they begin in the neck and spread to the head. Pain can range from a dull, deep ache to a heavy pressure of moderate or severe intensity (Table 2). 7,9,18,32,33 Cervicogenic headaches may be present 1 Instructor, Division of Physical Therapy, Des Moines University/Osteopathic Medical Center, Des Moines, IA. Send correspondence to Shannon M. Petersen, Division of Physical Therapy, Des Moines University/ Osteopathic Medical Center, 3200 Grand Avenue, Des Moines, IA, Shannon.Petersen@ dmu.edu upon waking or can begin or worsen in intensity as the day goes on, especially with sustained neck postures or movements. While this type of headache can begin at any age, it often increases in frequency and intensity over a period of years and may or may not accompany a history of neck trauma or cervical joint degenerative disease. 9,31,36 Articular Dysfunction Cervical facet joints have been recognized as a source of CGH. 10 Several studies have documented cervical pain referral patterns through use of fluoroscopically guided facet injections. 7,8,10 The upper 3 cervical segments are capable of referring pain to the head. The typical referral patterns include symptoms in the occipital region, upper posterolateral and upper posterior cervical region, temporal area, and vertex of the head. 7,8,10 Cervical zygapophyseal joint blocks have been used to identify the source of referred pain. 3,10 Because this invasive procedure is inappropriate in the physical therapy setting, manual examination is performed in an attempt to reproduce the headache and identify dysfunction that correlates with symptoms. Jull et al 17 found physical examination by a skilled manual therapist to be as accurate as radiologically controlled diag- CASE REPORT Journal of Orthopaedic & Sports Physical Therapy 21

2 TABLE 1. Criteria established by the International Headache Society for the diagnosis of cervicogenic headache. All of the letter headings must be met to make a diagnosis. 13,18,24,25 A. Pain is localized to the neck and occipital region and may project to forehead, orbital region, temples, vertex, and ears B. Pain is precipitated or aggravated by special neck movements or sustained neck posture C. At least 1 of the following: 1. Resistance to or limitation of passive neck movements 2. Changes in neck muscle contour, texture, tone, or response to active and passive stretching and contraction 3. Abnormal tenderness of neck muscles D. Radiological exam reveals at least 1 of the following: 1. Movement abnormalities in flexion/extension 2. Abnormal posture 3. Fractures, congenital abnormalities, bone tumors, rheumatoid arthritis, or other distinct pathology except spondylosis and osteochondrosis TABLE 2. Headache classification criteria. 8,11,15,30 Headache Type Onset Symptom Area Frequency Cervicogenic With or without trauma; any age Unilateral and does not change sides; frontal, retro-orbital, temporal, occipital Migraine Puberty Unilateral and can change sides; frontal, retro-orbital, temporal, occipital Tension Not related to trauma Bilateral; frontal, retro-orbital, temporal, occipital Episodic or chronic; 2 3/wk; may last hours to days Last less than 24 h; 1/y to several/wk Episodic or chronic; may last hours to days nostic blocks in detecting symptomatic joints in the cervical spine. Manual examination of intersegmental mobility has been used to identify symptomatic cervical joints including those of the upper cervical segments that may refer pain to the head. 11,17,20 It is the belief of some textbook authors that passive accessory and passive physiologic motion assessment of the involved joints can reveal altered quality of movement, abnormal end feel, and reproduction of headache pain. 9,18,22 Passive mobilization or manipulation of the cervical spine has been shown to be effective in relieving or reducing the occurrence of CGH. 26,32,37 Improvements occur in the areas of headache frequency, duration, and intensity following mobilization treatments. 15,26,33,37 Reduction in the use of pain medication for headaches has also been reported following cervical manipulation/mobilization treatments. 26,32,37 Muscle Dysfunction Although muscle tightness has not been shown to be a strong feature in CGH, 16 limitations in cervical muscle strength, endurance, and control have been associated with CGH. 1,16,31,35 Studies by Treleaven et al 34 and by Jull et al 16 used an inflatable pressure sensor to indirectly assess deep cervical flexor muscle activation, and both studies found significantly inferior performance in subjects with CGH compared to control subjects. Others have found subjects with neck pain and headache to demonstrate 43% to 46% less isometric cervical flexor muscle strength than control subjects. 1,35 Others have also shown that general cervical flexor muscle strength was significantly lower in individuals with cervicogenic headache. 31,36 Jull et al 16 describe a cranio-cervical flexion test used to assess upper cervical flexion muscular control/performance. In this low-load test, the subject must perform upper cervical flexion slowly and precisely without substitution strategies involving the middle and lower cervical muscles. Although studies have been done to assess the effectiveness of manual therapy on headaches, 15,26,32,37 few have incorporated muscle re-education of the deep neck flexors. 2,19 The purpose of this case study was to report the effects of cervical joint mobilization and deep neck flexor muscle training in an individual with suspected CGH. Aggravating Factors Sustained postures, neck movements, trauma Physical exertion; certain foods; environmental stresses (light or noise) Emotional stress; muscle tension Associated Symptoms Neck pain or stiffness; phonophobia or photophobia may be present; may or may not have nausea or vomiting Aura; phonophobia; photophobia; nausea or vomiting Phonophobia or photophobia may be present; may or may not have nausea or vomiting Pain Intensity Moderate to severe Moderate to severe Moderate to severe 22 J Orthop Sports Phys Ther Volume 33 Number 1 January 2003

3 CASE DESCRIPTION The patient was a 27-year-old female with a primary complaint of left-sided suboccipital headache. She was referred to physical therapy by her family physician. History Chief Complaint The patient described her symptoms as an aching pressure on the back of her neck at the base of the skull that extended into the occipital region. Pain intensity ranged from 5/10 to 8/10 with 0 being no pain and 10 being the worst pain imaginable. Nausea and vomiting were not associated with her headaches. She denied having dizziness, diplopia, dysarthria, dysphagia, drop attacks, or paresthesias. She had no difficulty chewing and no difficulty sleeping. The patient denied complaints of visual or aural disturbances, and photophobia or phonophobia. Aggravating Factors The headache was continuously present, but would increase in intensity as the day went on. Her neck felt as though it may pop with movement and fatigued after about 2 hours of computer use or paper work at her desk. She was employed as an office clerk which required her to work at a computer most of the day, however, about 1 to 2 hours 3 times per week was spent lifting 11-kg (25-pound) file boxes from the floor to waist height. The most intense headaches would come on about 3 times per week and would last 2 to 6 hours. She attributed these more severe episodes to lifting boxes on those days. Past History and Intervention The patient stated that the headaches began insidiously in childhood. Approximately 8 years prior to this physical therapy consultation, the headaches increased in intensity and frequency to such a degree that she sought treatment. Symptoms with that episode partially resolved with osteopathic manipulation but were never completely eliminated. At that time, her job involved frequent lifting. She denied having any other health problems. She was not participating in a regular exercise program. Present History and Intervention Symptoms had insidiously become more intense and more frequent over the past 6 months. Intervention for this episode included 2 treatments of osteopathic manipulation, which did not change the symptoms. Medication included an over-the-counter pain reliever containing acetaminophen, aspirin, and caffeine. She would take medication only when the headaches were at their worst and this helped to decrease pain intensity. The patient did not have any imaging studies or any other special medical tests done for her current problem. Her goals were to decrease the frequency of the intense headaches and to be able to tolerate computer work, desk work, and lifting without increased pain. Differential Diagnosis Based on the Subjective Examination A headache in the suboccipital region is consistent with IHS criteria for cervicogenic headache but may also be characteristic of other headache types (Table 2). 7,9,13,18,33 This patient s complaint of unilateral neck pain in addition to the headache is also consistent with the IHS criteria for CGH. 13 While the pain intensity and the semicontinuous nature of the headache that this patient presented with could be a quality of various headache types (Table 2), 7,9,13,18,33 the complaint of symptoms increasing in intensity with sustained postures is consistent with IHS criteria for CGH. 13,18,24,25 The patient s neck fatigue with prolonged postures and pain with lifting lead to the impression that muscle strength, endurance, or control limitation may be present, as well as possible problems with functional work postures and ergonomics. 12,13,14,18,24,25 The complaints of unilateral pain and popping in the neck could suggest that cervical articular dysfunction may be associated with the patient s symptoms. 22,30,33 Although phonophobia, photophobia, nausea, and vomiting may be associated with CGH, these symptoms are more commonly present in individuals with migraines (Table 2). 9,13,18 This patient did not have these associated symptoms so it was felt that she probably did not have migraine headaches. Because of the patient s symptom location, frequency, aggravating factors, and associated symptoms, the general impression following the subjective examination was that this patient was most likely having cervicogenic headaches. A physical examination focusing on the cervical spine was planned to confirm this hypothesis and further localize the source of the disorder. There were no contraindications to proceeding with physical therapy examination and intervention. Physical Examination Observation The patient did not appear to be in acute physical distress. Seated and standing subjective postural assessment revealed flattened cervical lordosis and thoracic kyphosis, slight forwardrounded shoulders with the right being greater than the left, and moderate forward head held with the chin extended forward into moderately excessive upper cervical extension. Range of Motion (ROM) Shoulder ROM was normal and did not reproduce symptoms. Full active cervical ROM for flexion and extension was present based on visualization, however, left-sided upper cervical pain was reproduced at end range extension. No signs or symptoms of vertebrobasilar artery insufficiency (VBI) were present with sustained cervical extension. Testing was performed to differentiate between upper and lower cervical extension ROM in accordance CASE REPORT J Orthop Sports Phys Ther Volume 33 Number 1 January

4 with Maitland. 22 Upper cervical spine extension mobility was tested with the patient s chin guided out forward while allowing the lower cervical spine to flex and the upper cervical spine to extend. Lower cervical spine extension mobility testing was performed with the upper cervical region maintained in a relatively flexed position and the chin nodded down toward the throat. The headache was reproduced with upper cervical spine extension ROM, but not with isolated lower cervical spine extension. Active cervical rotation ROM measurements were 80 to the left and 85 to the right. No complaints of pain and no signs and symptoms of VBI were present with sustained rotation. Cranio-vertebral stress tests were negative for alar ligament and transverse ligament laxity. Passive ROM for cervical rotation was slightly limited to the left compared to the right. This asymmetry was more pronounced when rotation was localized to the upper cervical spine with the lower cervical spine held in full flexion. Cervical lateral flexion ROM and thoracic AROM were not assessed at this time. Muscle Testing Upper extremity strength assessed with manual muscle testing was 5/5 throughout myotomes C2 through T1. Strength of the middle trapezius muscle was 4+/5 bilaterally and the lower trapezius muscle was 4/5 on the right and 4 /5 on the left. Cervical extension strength was 5/5 without symptoms. Manual muscle testing for upper cervical flexor muscles was not done, however, performance of these muscles was assessed using the pressure biofeedback method described by Jull et al. 16 This patient was able to hold an increase in pressure of 2 mm/hg for 10 seconds 1 time but demonstrated significant substitution with the sternocleidomastoid (SCM) muscle. This substitution was evident through visual observation and palpation of the SCM muscle as it contracted. Flexibility of the upper trapezius muscle was slightly limited bilaterally, however, the patient did not complain of discomfort in this area and testing did not reproduce the patient s headache. Tenderness was present with moderately deep palpation to the left upper cervical extensor muscles. Moderate limitation in length of these muscles was also noted during passive upper cervical flexion with the C2 vertebra stabilized. There were no significant flexibility limitations found in the levator scapula or scalenae muscles and they were not tender to palpation. Manual Assessment Passive physiologic intervertebral movement (PPIVM) was assessed in the supine position by passively moving the patient s neck through lateral flexion and rotation while palpating over the articular pillar for resistance or pain. PPIVM for cervical lateral flexion left and cervical rotation right revealed hypomobility and reproduction of headache at onset of resistance (R1) at C0-1, C1-2, and C2-3. Passive mobilization at C2-3 produced the patient s headache to the greatest degree. Posterior to anterior (PA) intervertebral pressures revealed moderate hypomobility and reproduction of neck pain and headache at R1 unilaterally on the left at C0-1 and C1-2, with marked hypomobility at C2-3. PA at C2-3 most closely reproduced the patient s headache. Upper limb tension tests were found to be negative. 5 Differential Diagnosis Based on the Physical Examination The finding of reproduction of headache obtained during the physical examination supported the diagnosis of cervicogenic headache. Impairments were found in posture, cervical ROM, muscle performance, and accessory motion. 13,18,24 Although studies attempting to link forward head posture to headaches have been inconclusive, this patient demonstrated a posture with excessive upper cervical extension. This could have closed down the upper cervical facets and may have contributed to her symptomatic state, especially during sustained postures and cervical extension ROM. 9,12,31,36 The weakness in this patient s middle and lower trapezius could have contributed to her limited endurance and tolerance of sustained postures and lifting. Poor function of these scapular stabilizers may also have lead to excessive strain on the cervical spine and muscles, which could have contributed to symptoms during work activities. 2,14 Significant limitation was found in upper cervical flexor muscle performance. Poor strength, endurance, or control of these deep neck flexors could have contributed to the patient s neck pain and headache during sustained postures and lifting. 16,23 Tenderness of the upper cervical extensor muscles may have been related to their length position secondary to the patient s postural deviation. These muscles, when dysfunctional, can refer pain to the head. 4,21,25 Passive physiological and passive accessory intervertebral motion testing revealed hypomobility and reproduction of the patient s headache symptoms, which could indicate articular involvement. 3,7,9,18,22 The prognosis seemed good at this point for the patient to return to the level she was at just prior to the most recent flare-up 6 months ago. Her strength deficits could be addressed through exercise and joint hypomobility could be treated by mobilization techniques. At this point, no contraindications to physical therapy intervention were identified and treatment was initiated. COURSE OF TREATMENT The patient was seen for a total of 8 visits over an 8-week period. Treatment consisted of patient 24 J Orthop Sports Phys Ther Volume 33 Number 1 January 2003

5 education, exercise, and manual therapy techniques to address impairments found during the examination as well as functional limitations. The goal was to decrease headache intensity and frequency and to increase tolerance for functional and work activities (see Table 3 for summary of treatment sessions). Patient Education Following the initial examination, the patient was educated in the proper posture and its potential impact on symptoms. She was also instructed in proper ergonomic setup for her desk and proper body mechanics for lifting. Therapeutic Exercise Instruction in home exercise program at the first visit included scapular retraction and a deep neck flexor exercise, which the patient was instructed to perform 2 times per day. Scapular retraction was done while pulling a resistive band held in both Journal of Orthopaedic & Sports Physical Therapy TABLE 3. Summary of treatment sessions. Session Subjective Report Manual Intervention Exercise 1 (day 0) See history Left PA* to R1 at C0-1, C1-2, C2-3 2 (day 3) Current headache 6/10 Onset after paperwork 3 (day 8) No longer had neck fatigue or popping 1 headache at end of work day 1 headache after waterskiing 4 (day 11) No headache since last report Neck feels looser 5 (day 16) 1 headache after driving go-carts 6 (3 wk after initial visit) No headache, even with lifting and sitting at work 7 (2 wk later) Did not exercise 2 wk while on vacation 1 headache after car travel 85% overall improvement 8 (2 wk later) Resumed home program No headaches * PA, posterior to anterior passive accessory intervertebral motion. RI, onset of resistance. PPIVM, passive physiologic intervertebral motion. Left PA to R1 at C1-2 and C2-3 (C0-1 not tender) Soft tissue mobilization to suboccipital muscles Hypomobility and tenderness left C2-3 Treated with left PA C2-3 grade IV Hypomobility and tenderness left C2-3 Treated with left PA C2-3 grade IV Hypomobility and tenderness left C2-3 Treatment as in session 4 Hypomobility and tenderness left PA C2-3 and PPIVM C1-2 and C2-3 Treated with left PA C2-3 grade IV and PPIVM for rotation right and for lateral flexion left C1-2 and C2-3 grade III Hypomobility and tenderness left PA and PPIVM C2-3 Treated with combined rotation right/lateral flexion left C2-3 grade III and IV No hypomobility detected with PA Slight hypomobility with PPIVM treated with combined rotation right/lateral flexion left C2-3 grade IV Scapular retraction Deep neck flexors Continued as in first session Deep neck flexors Instructed in prone middle trapezius strengthening and row Deep neck flexors Continued strengthening exercises As in session 4 Continued deep neck flexors Added prone lower trapezius strengthening Manual muscle test of middle and lower trapezius 4+/5 bilaterally Manual muscle testing middle and lower trapezius 5/5 Reassessment After Intervention Decreased pain with extension Decreased headache intensity Accessory motion increased Headache decreased to 1/10 Increased upper cervical rotation left Accessory motion increased with report of decreased tenderness Accessory motion increased with report of decreased tenderness No significant hypomobility No report of tenderness with PA or PPIVM No significant hypomobility No report of tenderness with PA or PPIVM No significant hypomobility No report of tenderness with PA or PPIVM CASE REPORT J Orthop Sports Phys Ther Volume 33 Number 1 January

6 hands. Two sets of 10 repetitions of this exercise were done in both sitting and standing positions. The deep neck flexor exercise described by Jull (Figure 1), 16 was performed with the patient supine with the cervical spine in a neutral position and a stabilizer pressure biofeedback unit (Chattanooga Group, Hixson, TN) placed under the cervical lordosis. The pressure sensor was inflated to 20 mmhg. The patient was instructed to slowly nod the head. As muscular activation of the deep cervical flexors occurs, the cervical lordosis slightly flattens and registers as an increase in pressure on the pressure sensor. The activation score is the pressure that can be achieved and held steadily for 10 seconds. The performance index of the muscles holding capacity is calculated by multiplying the target pressure by the number of successful repetitions. Ideal performance of the upper cervical flexor muscles would register on the pressure sensor as an increase in pressure of 10 mmhg held for 10 seconds, 10 times. 2,16 SCM and scalenae were monitored through observation and palpation for contraction, which indicates a substitution strategy because of their ability to flex the neck, though they do not have the stability role that the deep neck flexors have. 2,18,27,29 The deep cervical flexor muscles longus colli, longus capitus, rectus capitus anterior, and rectus capitus lateralis flex the upper cervical spine and provide segmental stability to the cervical spine during torqueproducing actions of the more superficial muscles. 16,23 Following instruction in the deep neck flexor exercise, the patient was able to perform 3 repetitions of 7-second holds. The patient did not use the pressure biofeedback unit when exercising at home but was educated in self-palpation of the SCM and scalenae to monitor substitution strategies. She was instructed to carry out the exercise 2 times per day, performing FIGURE 1. Deep neck flexor exercise with pressure biofeedback unit. at least 3 sets of 3 repetitions at each sitting while avoiding palpable substitution. She was instructed to increase the number of repetitions as she was able to without substitution. Graphs representing the patient s progress are presented in Figures 2, 3, and 4. The deep neck flexor exercise was continued at each physical therapy session. The exercise was progressed in number of repetitions and hold time (up to 10 seconds) as the patient s performance of the exercise improved and she was able to complete more repetitions while still avoiding palpable substitution (Figure 4). Exercises at the second treatment session were continued as in the first. She was now able to attain an increase of 2 mmhg with the pressure biofeedback unit 5 times with 10-second holds. Prone middle trapezius muscle strengthening and prone row exercises were introduced during the third treatment session. The patient was able to per- Average Headache Intensity FIGURE 2. Average headache intensity per week on a scale of 0 to 10 where 0 is no pain and 10 is the worst pain imaginable. Week 0 refers to symptoms reported at first physical therapy visit. The last physical therapy visit took place on week 8. Information for weeks 8 through 12 was obtained by follow-up phone call. Number of Days With Headache FIGURE 3. Number of headache days per week. Week 0 refers to patient report at first physical therapy visit. The last physical therapy visit took place on week 8. Information for weeks 8 through 12 was obtained by follow-up phone call Week 0 26 J Orthop Sports Phys Ther Volume 33 Number 1 January 2003

7 Performance Index of Deep Neck Flexors (mmhg) FIGURE 4. Average performance index of deep cervical flexor muscles, where performance index is the target pressure multiplied by the number of successful 10-second holds. Muscle performance was not measured on weeks 4, 5, and 7. form 2 sets of 10 repetitions with complaint of upper extremity fatigue during the second set. She was instructed to add these exercises to her home exercise program because of the muscle weakness found during the initial examination. During the fourth session, the patient was able to perform an increase of 6 mmhg with the pressure biofeedback unit, for 10 repetitions of 10-second holds. Scapular stabilization exercises were continued in the clinic and as part of the home exercise program. At the fifth physical therapy visit, scapular retraction exercises were progressed to 2 sets of 20. The deep neck flexor muscle exercise was continued, however, the patient was now able to perform an increase in pressure of 8 mmhg for 8 repetitions of 10-second holds. At the sixth visit, deep neck flexor exercises were continued and prone lower trapezius muscle strengthening was added to the patient s home program. She was able to perform 5 repetitions correctly before substituting with trunk extension and rotation. She was advised to perform 3 sets of 5 repetitions of this exercise 2 times per day. A hand-held 0.45-kg weight was added to the prone middle trapezius and row exercises. During the deep neck flexor muscle test at the seventh physical therapy session, the patient was able to hold an increase of 8 mmhg for 10 seconds, 10 times without palpable substitution with SCM or scalenae muscles. The patient was now able to perform 2 sets of 10 repetitions of the lower trapezius exercise. Strength in the middle and lower trapezius muscles was assessed with manual muscle testing and found to be 4+/5 bilaterally. Two weeks later, at the eighth session, manual muscle testing of the middle and lower trapezius muscles revealed strength to be 5/5. The weights used with the middle trapezius exercise were increased by 0.45 kg, and a 0.45-kg weight was added to the lower trapezius exercise as a progression because the patient had gained strength. At this time, Week deep neck flexor muscles were assessed. The patient was able to hold an increase in pressure of 10 mmhg for 10 repetitions of 10-second holds without demonstrating substitution patterns. This would be considered ideal muscle performance according to Jull et al. 17 Manual Intervention Manual intervention at the first session consisted of PA mobilization to R1. Mobilizations were performed as described by Maitland to the left C0-1, C1-2, and C2-3 segments to decrease pain and increase ROM. 8,20,22 Mobilizations were continued as above for session 2 at the C1-2 and C2-3 segments. No symptoms were reported at C0-1 and no significant hypomobility was noted, so this segment was not mobilized at session 2. Soft tissue mobilization to the upper cervical extensor muscles was performed due to their shortened length found upon examination. Soft tissue mobilization was performed in the supine position. At the third session, full cervical ROM was present and asymptomatic both with active ROM and with overpressure. Passive ROM for rotation localized to the upper cervical spine was slightly limited to the left as compared to the right, but no symptoms were reproduced. Mobilizations for sessions 3 through 5 were continued at C2-3 because of continued mild tenderness at this segment. The headache was not reproduced with PA motion assessment, so the grade of mobilization was increased to a grade IV which Maitland describes as a small-amplitude mobilization into 50% resistance. 22 The sixth session was 3 weeks after the initial evaluation. PA accessory motion assessment revealed only slight stiffness on the left at C2-3 with mild local tenderness. Stiffness was present with PPIVM for rotation right and for lateral flexion left at C1-2 and C2-3 with greater hypomobility into rotation. Because the patient had been improving with PA mobilization but continued to have some limitation, treatment at this visit included PPIVM for rotation right and for lateral flexion left with a large-amplitude movement into 50% resistance (Maitland s grade III) 22 at C1-2 and C2-3 followed by left PA at C2-3 grade IV. PA motion assessment on visit 7 revealed slight stiffness at C2-3 on the left with mild local tenderness. By visit 8, there was no stiffness or tenderness detected with PA motion. PPIVM for rotation right and lateral flexion left was slightly hypomobile at visits 7 and 8. The patient s symptoms had decreased by this point in time, yet some hypomobility remained at the level that had been symptomatic, so movements were combined and the mobilization was taken further into resistance. PPIVM treatment at these sessions was a combined movement for rotation right and lateral flexion left at C2-3. PA mobilizations were also performed. CASE REPORT J Orthop Sports Phys Ther Volume 33 Number 1 January

8 The patient s goals were met at this point and it was mutually decided between patient and therapist to discontinue formal physical therapy in the clinic. The patient was advised to continue her home exercise program at least 3 to 4 times per week and she expressed motivation to do this. At a 1-month follow-up phone call, patient reported that she had been performing her home exercise program 2 to 3 times per week and had experienced no headaches. DISCUSSION This patient met the criteria for cervicogenic headache as defined by the International Headache Society. 13,25,37 Pain was localized to the suboccipital region and aggravated by sustained neck postures. Limited passive neck movement was present physiologically and segmentally, and tenderness was present in the upper cervical extensor muscles. No radiological examination was done, so it is unknown whether criteria D was met (Table 1). The characteristics of this patient s headaches were consistent with a diagnosis of CGH as described by other authors. 7,9,32,33 Various investigators have studied the anatomic basis for cervicogenic headache including the distribution of referred pain to determine the segmental location of symptomatic joints. Through the use of fluoroscopically guided intra-articular injections, these authors have shown that C0-1, C1-2, and C2-3 are the segments most likely to refer pain into an area that would be perceived as a headache. 4,7,8,10 Articular dysfunction in the patient in this paper appeared to be local to the upper 3 cervical segments, which is consistent with the findings of these studies on referral patterns. Manual assessment at these segments did reproduce the patient s headache symptoms. Manual therapy has been shown to be effective in reducing the frequency, duration, and intensity of headaches. 15,26,32,37 Whorton and Kegerreis 37 and Nilsson et al 26 also found a reduction in use of analgesics following manual therapy intervention. In the current case report, manual therapy was used to increase mobility and decrease pain. 9,15,22,26,32,37 As segmental mobility increased through the course of treatment, the accessory movements became less provocative. By the fourth session, altered quality of movement detected manually was only slight and manual assessment no longer reproduced headache symptoms. At this point, the headaches had considerably decreased in frequency (Figure 3). There was 1 intense headache reported at week 6, however, it lasted only 2 hours and resolved on its own without the use of medication. Contributing factors to that headache may have been that the patient had not been doing her exercises for 2 weeks and that she had spent several hours traveling in a car while on her vacation. Significant limitation was present in this patient s deep cervical flexor muscles. Although deficiency in cervical flexor muscle control has been associated with CGH, 1,16,31,34,35,36 few studies have been done to determine if training the deep neck flexors to improve their performance would have an influence on headache frequency and intensity. 2,19 In a case report, Beeton and Jull 2 incorporated the use of muscle re-education exercises for the lower trapezius and deep neck flexors in addition to manipulative techniques to treat a man with cervicogenic headache. They found significant improvements in frequency of headache, active and segmental mobility, and muscle length and endurance. More recently, Jull et al 19 reported on the effectiveness of manipulative therapy and a low-load exercise program for individuals with cervicogenic headache. They found that both manipulative therapy and specific exercise was effective in reducing headache frequency and intensity. In this current case, improvements were also seen in mobility and muscle performance that correlated with decreases in headache intensity (Figures 2 and 4). The patient in this study also had weakness in the scapular stabilizing muscles, which could lead to increased strain on the cervical spine and cervical muscles. This patient complained of neck fatigue with sustained postures and increased headache with lifting. As improvements in strength and muscle performance occurred, these complaints decreased. Following the first week of therapy the patient reported that she no longer felt neck fatigue at work. This could be attributed to her significant improvement in deep cervical flexor muscle performance (Figure 4) or changes in her workstation set up. During week 3, she reported no longer having increased symptoms with lifting at work. This could be due to her continued gains in deep cervical flexor muscle performance or gains in strength of the scapular stabilizers. The pattern of presentation fits that described by Panjabi, 28,29 with a stabilizing system of the spine involving active, passive, and neural control subsystems. When joints of the symptomatic region are dysfunctional (the passive subsystem), the muscular component (the active subsystem) must compensate for the loss of integrity of the passive structures. The active subsystem responds to changes in load and is responsible for controlling motion within the neutral zone. If these muscles are dysfunctional, this can contribute to limited control and has the potential to compound symptoms. If there is a limited ability to hold and control a low level of contraction of the deep upper cervical flexor muscles, this will affect the individual s ability to hold static postures and to control functional movements. 6,16,23,27,28,29 The patient did improve at a higher rate and to a greater extent than originally anticipated due to the 28 J Orthop Sports Phys Ther Volume 33 Number 1 January 2003

9 chronicity of the problem. She did attain full strength in the muscle groups that were limited and gained pain-free cervical ROM. The physical therapy intervention had a profound effect on subjective complaints of headache. Because the symptoms had not changed to this degree prior to initiation of physical therapy, it was felt that improvement was not due merely to the passage of time. Because of the chronicity of the problem, the patient could benefit from continuation of a regular exercise program as a measure to prevent reoccurrence of symptoms. CONCLUSION This case report provides a detailed account of manual therapy treatment for a patient with cervicogenic headache presenting with articular and muscular dysfunction. A combination of manual therapy and muscle control exercises were used to address her limitations. This study was a case report with only 1 subject so the results cannot be generalized to the entire CGH population. This report also did not assess long-term results of the treatment. The results of a recently published randomized controlled trial provide further evidence to the use of manual therapy and exercise for the treatment of cervicogenic headache. 19 REFERENCES 1. Barton PM, Hayes KC. Neck flexor muscle strength, efficiency, and relaxation times in normal subjects and subjects with unilateral neck pain and headache. Arch Phys Med Rehabil. 1996;77(7): Beeton K, Jull G. Effectiveness of manipulative physiotherapy in the management of cervicogenic headache: a single case study. Physiotherapy. 1994;80: Bogduk N, Marsland A. On the concept of third occipital headache. J Neurol Neurosurg Psychiatry. 1986;49(7): Bogduk N. The anatomical basis for cervicogenic headache. J Manipulative Physiol Ther. 1992;15(1): Butler DS. Mobilisation of the Nervous System. London, UK: Churchill Livingstone; Conley MS, Meyer RA, Bloomberg JJ, Feeback DL, Dudley GA. Noninvasive analysis of human neck muscle function. Spine. 1995;20(23): Dreyfuss P, Michaelsen M, Fletcher D. Atlanto-occipital and lateral atlanto-axial joint pain patterns. Spine. 1994;19(10): Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns. I: A study in normal volunteers. Spine. 1990;15(6): Edeling J. Manual Therapy for Chronic Headache. 2nd ed. London, UK: Butterworth Heinemann; Fukui S, Ohseto K, Shiotani M, et al. Referred pain distribution of the cervical zygapophyseal joints and cervical dorsal rami. Pain. 1996;68(1): Hanten W, Oslon S, Ludwig GM. Reliability of manual mobility testing of the upper cervical spine in subjects with cervicogenic headache. J Man Manipulative Ther. 2002;10(2): Haughie LJ, Fiebert IM, Roach KE. Relationship of forward head posture and cervical backward bending to neck pain. J Man Manipulative Ther. 1995;3: International Headache Society Headache Classification Committee. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia. 1988;8(suppl 7): Janda V. Muscles and cervicogenic pain syndromes. In: Grant R, ed. Physical Therapy of the Cervical and Thoracic Spine. New York, NY: Churchill Livingstone; 1988: Jensen OK, Nielsen FF, Vosmar L. An open study comparing manual therapy with the use of cold packs in the treatment of post-traumatic headache. Cephalalgia. 1990;10(5): Jull G, Barrett C, Magee R, Ho P. Further clinical clarification of the muscle dysfunction in cervical headache. Cephalalgia. 1999;19(3): Jull G, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygapophysial joint pain syndromes. Med J Aust. 1988;148(5): Jull GA. Cervical headache: a review. In: Boyling JD and Palastanga N, eds. Grieve s Modern Manual Therapy. New York, NY: Churchill Livingstone; 1994: Jull G, Trott P, Potter H, et al. A randomized controlled trial of exercise and manipulative therapy for cervicogenic headache. Spine. 2002;27(17): ; discussion Jull G, Zito G, Trott P, Potter H, Shirley D. Interexaminer reliability to detect painful upper cervical joint dysfunction. Aust J Physiother. 1997;43(2): Lord SM, Barnsley L, Wallis BJ, Bogduk N. Third occipital nerve headache: a prevalence study. J Neurol Neurosurg Psychiatry. 1994;57(10): Maitland G, Hengeveld E, Banks K, English K. Maitland s Vertebral Manipulation. 6th ed. London, UK: Butterworth Hinemann; Mayoux-Benhamou MA, Revel M, Vallee C, Roudier R, Barbet JP, Bargy F. Longus colli has a postural function on cervical curvature. Surg Radiol Anat. 1994;16(4): Nicholson GG, Gaston J. Cervical headache. J Orthop Sports Phys Ther. 2001;31(4): Nilsson N. The prevalence of cervicogenic headache in a random population sample of year olds. Spine. 1995;20(17): Nilsson N, Christensen HW, Hartvigsen J. The effect of spinal manipulation in the treatment of cervicogenic headache. J Manipulative Physiol Ther. 1997;20(5): O Sullivan PB, Twomey L, Allison G. Dynamic stabilization of the lumbar spine. Crit Rev Phys Rehabil Med. 1997;9: Panjabi MM. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J Spinal Disord. 1992;5(4): ; discussion Panjabi MM. The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis. J Spinal Disord. 1992;5(4): ; discussion Pfaffenrath V, Kaube H. Diagnostics of cervicogenic headache. Funct Neurol. 1990;5(2): Placzek JD, Pagett BT, Roubal PJ, et al. The influence of the cervical spine on chronic headache in women: a pilot study. J Man Manipulative Ther. 1999;7: Schoensee SK, Jensen G, Nicholson G, Gossman M, Katholi C. The effect of mobilization on cervical headaches. J Orthop Sports Phys Ther. 1995;21(4): CASE REPORT J Orthop Sports Phys Ther Volume 33 Number 1 January

10 33. Sjaastad O, Bovim G, Stovner LJ. Laterality of pain and other migraine criteria in common migraine. A comparison with cervicogenic headache. Funct Neurol. 1992;7(4): Treleaven J, Jull G, Atkinson L. Cervical musculoskeletal dysfunction in post-concussional headache. Cephalalgia. 1994;14(4): ; discussion Vernon HT, Aker P, Aramenko M, Battershill D, Alepin A, Penner T. Evaluation of neck muscle strength with a modified sphygmomanometer dynamometer: reliability and validity. J Manipulative Physiol Ther. 1992;15(6): Watson DH, Trott PH. Cervical headache: an investigation of natural head posture and upper cervical flexor muscle performance. Cephalalgia. 1993;13(4): ; discussion Whorton R, Kegerreis S. The use of manual therapy and exercise in the treatment of chronic cervicogenic headaches: a series of case studies. J Man Manipulative Ther. 2000;8: World Cervicogenic Headache Society. Cericogenic headache definition. Available at: definit2.html Journal of Orthopaedic & Sports Physical Therapy Invited Commentary Headache is a prevalent complaint in modern-day society. The most common chronic or recurrent forms are migraine and tension-type headaches. Nevertheless, headaches arising from cervical musculoskeletal disorders, termed cervicogenic headache, 21 are also common and are estimated to account for 15% to 20% of chronic headaches. Petersen has presented a case history of successful physical therapy management of a typical patient with cervicogenic headache. The case highlights some important factors in diagnosis and management of cervicogenic headache, which are worthy of comment. Petersen has illustrated the use of established headache classification criteria in the clinical reasoning process in patient assessment, a process that should be adopted routinely by physical therapists. Accurate differential diagnosis of chronic headache is a first and fundamental step towards successful treatment outcomes. The initial task for physical therapists is to identify those patients with headaches for whom management methods of manual therapy and exercise are most appropriate, rather than treating all patients with headaches indiscriminately. Symptomatically there is an overlap between cervicogenic, migraine without aura, and tension-type headaches. The presence of neck pain with headache has no discriminatory value, as up to 70% of persons with headache report associated neck aching, pain, or stiffness, 12 and neck tenderness has low specificity in the diagnosis of headache. Rather, as illustrated in this case study, the physical therapist should seek a pattern of symptoms that are associated with relevant signs of cervical musculoskeletal impairment or dysfunction to confirm a diagnosis of cervicogenic headache. The physical characterization of cervicogenic headache described in the International Headache Society classification criteria 11 is nonspecific. But recent research is beginning to better define specific related physical impairments, especially as they pertain to the muscular system. The presence of painful cervical joint dysfunction, particularly within the upper cervical joints, which have access to the trigeminocervical nucleus, is well established in cervicogenic headache. 5 7,16 In association with the joint dysfunction, Petersen also identified several problems in the patient s muscular system, which is in accord with findings of recent research. While clinically there is a good understanding of factors of muscle strength, endurance, and flexibility, Petersen elected to use a low-load test of control of a cranio-cervical flexion action to establish poor muscular performance. This test is quite different from traditional strength tests and is a test that may be described as a clinical test of neuromuscular control. Testing aspects of cervical neuromuscular control is a comparatively new field of clinical measurement in cervicogenic headache. Those aspects include investigations into the control of the cranio-cervical flexion movement, EMG measurement of muscle activity in defined tasks, and tests of cervical kinaesthesia. This newer mechanistic approach appears to be better at defining the problems in the muscular system, which, as demonstrated in Petersen s case report, quite precisely directs the treatment approach. The development of the cranio-cervical flexion test was stimulated by knowledge of the importance of the deep segmental muscles for control of the cervical curve and segments. 17,18,23 Our studies using the cranio-cervical flexion clinical test have demonstrated disturbances in the neck flexor synergy in patients with cervicogenic headache and whiplash-associated disorders In our studies, patients with neck pain, as compared to asymptomatic control subjects, were less able to perform and hold progressively increasing ranges of cranio-cervical flexion (the action of longus capitus in synergy with longus colli). Petersen reported similar findings in this case example. We were able to determine that this deficit in the deep neck flexors was accompanied by increased 30 J Orthop Sports Phys Ther Volume 33 Number 1 January 2003

11 activity in the superficial neck flexors, 14 inferring the presence of altered strategies of neuromuscular control in the cervical region seemingly as a reaction to pain and pathology that may disturb muscle control strategies. Other studies have also documented changes in the deep suboccipital extensors (atrophy and fatty infiltration), which may further compound problems of control of the upper cervical segments. 1,8,19 Likewise these changes would be in concert with the deficits in cervical kinaesthetic sense (joint position error) that have been documented in patients with idiopathic neck pain and whiplashassociated disorders 9,10,20,22 and that relate to the not infrequent reports of dizziness and light-headedness by patients with cervicogenic headaches. The muscular dysfunction also involves the axioscapular muscles. Petersen, in this patient s case, found slight tightness in the upper trapezius muscle and a reduction in strength of the middle and lower components of the muscle. Such changes in the muscle control or coordination strategies may lead to inappropriate loads on the cervical joints. 3 Abnormal patterns of muscle use have been demonstrated in the research arena. For example, Bansevicius and Sjaastad 2 demonstrated increased EMG activity in the upper trapezius in patients with cervicogenic headache while they performed a computer-based task requiring concentration. We have also demonstrated increased activity of the sternocleidomastoid and anterior scalene muscles during a low-load repetitive upper limb task in patients with whiplash and idiopathic neck pain. 4 What are the implications of this knowledge of muscle system dysfunction for the management of cervicogenic headache? There has been an emphasis placed on the manual therapy treatment of cervical joint dysfunction for the management of cervicogenic headache, as indicated by Petersen in her review. Implicit in this approach is an erroneous assumption that the problems in the muscular system will automatically resolve with relief of pain. 15 The merit in Petersen s management of this patient was that it addressed, in a multimodal approach, the precise problems presenting in the articular and muscular systems while also providing education in posture and ergonomics. A point I would emphasize, based on the evidence of the nature of the muscular system dysfunction in cervicogenic headache, is that it is vital for clinicians to assess and focus initially on rehabilitation of the altered patterns of muscle activity and neuromuscular control that are being demonstrated in patients with cervicogenic headache. It is notable from research that these coordination problems are demonstrable under low-load rather than high-load conditions. It is possible that if we progress to a focus on muscle strengthening too soon, we may not adequately address these fundamental problems of muscle coordination and control. As reflected in Petersen s case report, cervicogenic headache often has a prolonged history. The challenge for clinicians, which has not been satisfactorily met in neck pain syndromes, is prevention of symptom recurrence. More detailed attention to re-eduction of muscle control may provide one answer. Petersen is to be congratulated on presenting a detailed account of a well-reasoned approach to assessment and management of a patient with cervicogenic headache. While it is not possible to extrapolate the results of a case report to a total population, a recent randomised controlled trial 15 provides further evidence for the long-term efficacy of the management approach described in this case. Gwendolen Jull, M Phty, Grad Dip Manip Ther, PhD, FACP Associate Professor, Department of Physiotherapy University of Queensland, Queensland, Australia REFERENCES 1. Andary MT, Hallgren RC, Greenman PE, Rechtien JJ. Neurogenic atrophy of suboccipital muscles after a cervical injury: a case study. Am J Phys Med Rehabil. 1998;77(6): Bansevicius D, Sjaastad O. Cervicogenic headache: the influence of mental load on pain level and EMG of shoulder-neck and facial muscles. Headache. 1996;36(6): Behrsin JF, Maguire K. Levator scapulae action during shoulder movement: a possible mechanism for shoulder pain of cervical origin. Aust J Physiother. 1986;32(2): Bilenkij G, Falla D, Jull G. An EMG analysis of neck muscle activity during a repetitive upper limb task in patients with whiplash and idiopathic neck pain. [in review]. 5. Bogduk N, Marsland A. Third occipital headache. Cephalalgia. 1985;3(suppl 5): Bovim G, Berg R, Dale LG. Cervicogenic headache: anesthetic blockades of cervical nerves (C2 C5) and facet joint (C2/C3). Pain. 1992;49(3): Dreyfuss P, Michaelsen M, Fletcher D. Atlanto-occipital and lateral atlanto-axial joint pain patterns. Spine. 1994;19(10): Hallgren RC, Greenman PE, Rechtien JJ. Atrophy of suboccipital muscles in patients with chronic pain: a pilot study. J Am Osteopath Assoc. 1994;94(12): Heikkila H, Astrom PG. Cervicocephalic kinesthetic sensibility in patients with whiplash injury. Scand J Rehabil Med. 1996;28(3): Heikkila HV, Wenngren BI. Cervicocephalic kinesthetic sensibility, active range of cervical motion, and oculomotor function in patients with whiplash injury. Arch Phys Med Rehabil. 1998;79(9): International Headache Society HCC. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Headache Classification Committee of the International Headache Society. Cephalalgia. 1988;8(suppl 7):1 96. CASE REPORT J Orthop Sports Phys Ther Volume 33 Number 1 January