Toby Hall, Darren A. Rivett, Mark A. Jones Jean is a 42-year-old female working part-time from home as an information technologist managing a small website business. She does this while looking after her two young children (aged 6 and 4 years), one of whom had some early developmental delay but was now progressing well. Jean had previously been very active, with a rigorous exercise routine and regularly swimming in a swim club, but this stopped just before the birth of her first child and had not resumed due to time constraints, so she was no longer physically active. Her young children had previously caused her to wake frequently during the night, which had led to a poor pattern of sleep, which had been maintained in recent times. Jean had a 5-year history of left-sided-dominant daily frontal headache together with a general non-specific headache, which made her head feel tight (Fig. 16.1). She had an episodic history of neck pain prior to the headache onset related to a whiplash injury 10 years ago, which is also shown in Fig. 16.1. Headache and neck pain now both occur together. Symptoms had plateaued in the previous few years and were rated at 58/100 on the Headache Disability Inventory, indicating a substantial burden. Headache, rather than neck pain, was the major complaint and reason for physiotherapy consultation. Jean found that sitting for more than 30 minutes while working on her laptop with the laptop resting on her lap provoked the headaches. Lifting and carrying her children, heavy shopping bags or other loads also provoked her headache. Self-reported stress was also a factor, particularly associated with managing a small business with two young children. She had also been stressed by the developmental delay in her younger child. This was not helped by the fact that her husband was not able to help her with household duties or child care due to his long work hours. There were no associated features such as aura, nausea or photophobia, but she occasionally had light-headedness, which she could not relate to a specific aggravating activity or movement. It did not appear to be postural related, nor was it a feeling of vertigo. Medical investigations included a computed tomography (CT) scan of the brain 5 years previously and x-rays of her neck after the whiplash injury 10 years ago. Her general practitioner (GP) had referred her to a neurologist 5 years ago, who had arranged the CT scan and who also diagnosed tension-type headache. Medication had been trialed at that time, but Jean self-medicated with over-the-counter analgesics (Panadol), often on a daily basis. Despite this, the headache had increased to the point that it occurred daily, with an average intensity of 5/10. Jean was otherwise healthy, and there were no other features indicating red or yellow flags apart from the stress that she was undergoing while managing a family and working from home. When questioned about associated features in the jaw, she denied any difficultly with jaw function or any symptoms associated with jaw movement. On physical examination, Jean sat with a kyphotic thoracic and lumbar spine and forward head posture. When standing, she adopted a swayback posture with generally low muscle tone. Her scapulae were bilaterally depressed with both clavicles horizontal, well below the normal 10-degree angle to the horizontal (Ha et al., 2013). The scapulae were also bilaterally protracted to approximately 45 degrees and tilted forward to 30 degrees, both more than optimal. Correcting her sitting posture, by altering the pelvis, spine, scapular and head position, felt ‘easier’, and Jean’s headache/neck pain were immediately reduced but not eliminated. Furthermore, neck movement increased in the range of lateral flexion and rotation when the scapular and spine position was corrected (Ha et al., 2011). It was decided that a Mulligan Headache SNAG (Hing et al., 2015) would be trialed early in the physical examination. The rationale for the Mulligan approach is to determine whether manual glide force applied to the symptomatic motion segment can eliminate pain. The Headache SNAG involves the therapist contacting the C2 spinous process with the little finger of one hand while gentle horizontal pressure is applied by the opposite arm through the thenar eminence applied directly to the finger overlying the spinous process (Fig. 16.2). It is important to stabilize the patient’s head during the sustained pressure on C2. Pressure is maintained for at least 10 seconds. This technique caused an immediate increase in symptoms. A Reverse Headache SNAG (reversing the Headache SNAG direction of glide) had no effect on symptoms, whereas applying a modified Headache SNAG at C3 with pressure directed at 45 degrees to the horizontal plane immediately reduced the symptoms. Active head retraction was reduced to half the expected normal range of movement (ROM) and provoked neck pain which was increased with gentle overpressure into retraction (Fig. 16.3). Protraction range was increased and was also symptomatic. These movements predominantly occur in the upper cervical spine, with maximal movement occurring at C0/C1 and C1/C2 into flexion during retraction and extension during protraction (Ordway et al., 1999; Takasaki et al., 2010). Hence pain provocation increases suspicion of an upper cervical movement problem. Plane axial cervical movements were also problematic. Extension of the whole cervical spine caused localized neck pain, and there was poor control of movement, with a tendency to ‘collapse’ the neck, associated with a focus of movement in the mid- and upper cervical spine with lack of movement in the cervicothoracic junction. Supporting Jean’s head during extension and controlling the movement reduced the pain associated with extension. Similarly, correcting the spine and scapula posture also improved extension control and reduced symptoms. Cervical lateral flexion and rotation bilaterally gave a feeling of tightness in the neck muscles contralaterally and appeared restricted in range. Correcting the scapular and spine posture improved the cervical rotation and lateral flexion movement markedly to near full range, which was pain-free (Fig. 16.4). This information, taken together with the evidence of poor extension control, indicated that the symptoms might be associated with issues of motor control of the spine and scapulae, although it did not discount articular impairment. It is possible that cervical segmental movement impairment may be compensated for by movement at adjacent vertebral levels (Bogduk, 2002). This might explain why a large survey of 4293 adults failed to find any difference in cervical ROM when comparing those with chronic neck pain to those without (Kauther et al., 2012). There was little movement in the upper thoracic spine during any cervical movement. Combined movement testing of the upper cervical spine revealed increased neck pain on retraction with left rotation (Fig. 16.5A). This movement is thought to bias the C0/C1 motion segment (Edwards, 1992) due to the predominance of sagittal movement at this level (Karhu et al., 1999). Hence pain provocation during this movement indicates the need for further testing at this level and the potential for symptom provocation. Further testing also identified that rotation to the left with C2 stabilized with the addition of upper cervical flexion was also provocative (Fig. 16.5B). The movement of head and upper neck rotation with C2 fixed predominantly occurs at C1/C2 (Takasaki et al., 2011; Osmotherly et al., 2013). Hence, further tests are required to evaluate symptoms arising from C1/C2. Finally, with C3 stabilized, the addition of upper cervical extension and ipsilateral lateral flexion also increased neck pain. Due to the ipsilateral nature of coupling in the cervical spine (Cook et al., 2010), the possibility of C2/C3 segmental involvement is further raised. In a seated position, examination of upper cervical left rotation with C2 stabilized was reduced in range to approximately 5 degrees (Fig. 16.6AB). The segmental range of rotation for this test is reported as approximately 10 degrees when measured using magnetic resonance imaging (MRI) in a laboratory setting (Osmotherly et al., 2013). However, typically, in a clinical test environment, the normal rotation range is 10–15 degrees to each side. Stabilizing C3 also gave a similar range of rotation. Segmental examination revealed hypomobility at C0/C1, C1/C2 and C2/C3 vertebral levels. The flexion-rotation test was positive, with a subjective estimate of 20 degrees to the left side, which is much less than the expected range of 44 degrees to each side (Ogince, 2003; Hall and Robinson, 2004). A positive test is reported as range less than 33 degrees (Hall et al., 2010). Palpation of the C2 spinous process indicated that it was centrally located, not deviated. It has been suggested that a deviated C2 spinous process is indicative of dysfunction of the C2/C3 vertebral segment and is associated with headache (Macpherson and Campbell, 1991). Passive accessory movements were performed in both prone and supine positions. Headache was reproduced on palpation of the left posterior arch of C1 when the neck was positioned in upper cervical spine retraction with a few degrees of left rotation (Fig. 16.7). Local neck pain only was reproduced on palpation of the C2 and C3 articular pillars on the left side, despite the neck being placed in a provocative position for the C1/C2 and C2/C3 vertebral segments. This indicates the greater potential for C0/C1 segmental involvement over C1/C2 and C2/C3. Caution is required when interpreting headache reproduction on palpation. Recently it was shown that headache could be provoked from palpation of the neck in people with migraine and tension-type headache (Watson and Drummond, 2012). The preliminary observation of posture and movement control indicated potential for impairment of motor control as a contributing factor to the patient’s symptoms. The cranio-cervical flexion test has been shown to be a valid (O’Leary et al., 2007) and reliable (Chiu et al., 2005) measure of function of the anterior neck muscles. Research has established that patients with neck pain disorders, including CGH (Jull et al., 2007), when compared with controls, have altered motor control during cranio-cervical flexion characterized by reduced activity in the deep cervical flexors and increased activity in the superficial flexors. In Jean’s case, there was a reduction in her ability to perform the cranio-cervical flexion test, with marked substitution of superficial muscles, particularly the hyoid muscles and sternocleidomastoid. Even the smallest movement of the head induced inappropriate superficial neck flexor muscle activity. This information, taken together with the apparent lack of neck movement and pain on palpation of the upper cervical spine, is highly diagnostic of CGH (Jull et al., 2007). In that study, the presence of these three factors had very high levels of sensitivity and specificity in identifying people with CGH from those with migraine, tension-type headache or asymptomatic controls. In addition to the poor deep neck flexor muscle control, Jean was also unable to correctly position the scapulae unilaterally or bilaterally without inappropriate muscle activity of the latissimus dorsi and rhomboid muscles. Muscle length was reduced in the sub-occipital extensors and pectoralis minor bilaterally, and there were trigger points provoking headache in the levator scapulae, as well as tender points in the sternocleidomastoid and upper trapezius bilaterally. Prevalence of trigger points in neck muscles is not isolated to people with CGH; these occur in many other headache forms, including tension-type headache, migraine and cluster headache (Calandre et al., 2006, 2008; Alonso-Blanco et al., 2011). Neurodynamic tests were carried out in both sitting and supine positions. With the patient seated, upper cervical spine retraction was assessed with the patient’s knees flexed to 90 degrees and then in a slumped spine position with her knees fully extended. Retraction was more painful and restricted in range in the slumped position compared to upright position. This is a useful screening tool to identify neural tissue mechanosensitivity as the limiting factor for retraction. Cervical flexion during retraction elongates the cervical neuromeningeal tract; hence, increased neural tissue mechanosensitivity is likely to be identified quickly by this test. Confirmation of a neural tissue pain disorder requires further neurodynamic tests and supporting evidence of pain on palpation of upper cervical neural tissue (Hall et al., 2008). While testing passive range of upper cervical spine flexion in supine, positioning the arms in a neural provocative position of bilateral shoulder abduction to 90 degrees increased Jean’s neck pain and also reduced available range, but headache was not provoked. The greater occipital nerve at the occiput was moderately sensitized bilaterally to gentle non-noxious mechanical pressure. The prevalence of neural tissue mechanosensitivity in people with CGH is approximately 8% (Zito et al., 2006), but it also appears in people with migraine (von Piekartz et al., 2007). Temporomandibular dysfunction is common in people with CGH (von Piekartz and Ludtke, 2011). Such dysfunction is usually associated with impairment of upper cervical spine movement (Grondin and Hall, 2015). Hence, evaluation of the jaw region is important in the clinical evaluation of headache. Evaluation for temporomandibular dysfunction was carried out by evaluating range of movement, joint sounds and symptoms associated with jaw opening as well as sensitivity to palpation of the jaw muscles. No significant features of temporomandibular dysfunction were identified. Due to the subjective report of light-headedness, tests for cervical arterial dysfunction were performed according to the current International Federation for Orthopaedic Manipulative Physical Therapists (FOMPT) guidelines (Rushton et al., 2014), and these tests were unremarkable. Furthermore, in light of the history of neck trauma and light-headedness, tests for cranio-cervical ligament integrity were also performed and revealed no abnormality. One study found evidence of significant ligament damage of the tectorial membranes, alar and transverse ligaments in up to one-third of cases of people who had suffered whiplash injury on average 6 years after trauma (Kaale et al., 2008). Smooth pursuit eye tests and tests for proprioception and head repositioning were not conducted at this time due to time constraints and were planned for subsequent follow-up sessions if required. Reasoning Question: Answer to Reasoning Question: Headache is both a symptom and a disease (Dodick, 2010); hence, diagnosis can be challenging. Differential diagnosis based on symptoms alone can be problematic, and there is often misdiagnosis (Pfaffenrath and Kaube, 1990; Moeller et al., 2008). To explain this, it has been postulated that headaches form a spectrum, with shared common pathophysiological mechanisms (Cady et al., 2002). It has also been suggested that CGH forms part of this spectrum (Watson and Drummond, 2012). Despite the similarity in the mechanisms underlying different headache forms, it appears that physical treatment is not effective for all forms of headache (Biondi, 2005; Bronfort et al., 2010). Manual therapy can be effective for tension-type headache and CGH, but there is less evidence for effect in migraine (Chaibi and Russell, 2012; Sun-Edelstein and Mauskop, 2012). It appeared clear to me that Jean had a number of issues that were contributing to her chronic headache symptoms and that she should respond to physical intervention. The common difficulty in diagnosis is distinguishing between migraine without aura and CGH. Making diagnosis even more challenging is that an individual patient typically has more than one type of headache (Amiri et al., 2007). In Jean’s case, there was substantial evidence supporting a diagnosis of CGH together with medication-overuse headache and potentially tension-type headache. With respect to potential physical contributing factors identified in the physical examination, there was a clear link between her less-than-optimal spine and scapular posture and neck symptoms. Previous studies have raised questions regarding the link between posture and headache, with some studies reporting an association (Watson and Trott, 1993; Budelmann et al., 2013), which is not substantiated by others (Treleaven et al., 1994; Dumas et al., 2001; Zito et al., 2006). One explanation for this might be the wide variation in cervical posture seen in asymptomatic people (Miyazaki et al., 2008). Hence, a common postural abnormality is unlikely to be seen in headache. Despite this, a clear link was established between Jean’s posture and pain by examining the effect of altering her posture on symptoms and neck movements, which were positively influenced by the correction. There was also clear evidence of movement impairment in the cervical vertebral segments capable of provoking referred head pain (Bogduk and Govind, 2009). Palpation of these impaired motion segments induced neck pain and headache. In addition, it was possible to alleviate neck pain and headache by manual therapy techniques. As well as the evidence of articular and myofascial dysfunction, there was also evidence of neural tissue mechanosensitivity. Table 16.1 defines the International Headache Society diagnostic criteria for CGH (Sjaastad et al., 1998). Based on these criteria, Jean satisfies the majority of requirements for a diagnosis of CGH (Antonaci et al., 2001) as indicative of ‘probable’ CGH. TABLE 16.1
Cervicogenic Headache
Subjective Examination
History
Physical Examination
Active and Combined Cervical Movements
Upper Cervical Spine Retraction and Protraction
Cervical Spine Flexion and Extension
Cervical Spine Rotation and Lateral Flexion
Cervical Spine Combined Movement
Segmental Mobility and Pain Provocation Tests
Segmental Movement Tests
Segmental Pain Provocation Tests
Muscle Function
Cranio-cervical Flexion Test
Neurodynamic Tests
Temporomandibular Joint
Special Tests
Cervicogenic Headache
16
Fig. 16.1 Body chart detailing location of symptoms.
Fig. 16.2 Headache SNAG: The head is fixed while horizontal posteroanterior pressure is applied through the spinous process of C2.
Fig. 16.3 Active upper cervical spine retraction guided by the therapist to ensure pure retraction to minimize flexion occurring in subaxial segments.
Fig. 16.4 Scapula correction with hand contact on the inferior angle and acromion: Correction is based on the individual patient presentation and response.
Fig. 16.5 Combined movement evaluation. (A) C0/C1 combining flexion with rotation to the left. (B) C1/C2 combining left rotation with flexion.
Fig. 16.6 Hand placement for fixation of C2 vertebra during axial rotation in the upper cervical spine.
Fig. 16.7 Palpation over the C1 left posterior arch with the neck in flexion.
