Abstract
The contribution of cervical musculoskeletal structures to the pathogenesis of headache is a topic of ongoing clinical and scientific debate. Whereas trigeminovascular mechanisms and especially brainstem alterations (1), as well as genetic factors, seem to play a dominant role for the development of migraine (2), the mechanisms of tension-type headache (TTH) are less clear. Furthermore, the transition from episodic to chronic headache states remains an area of speculation rather than knowledge. The use of analgetic medication with its associated neurotransmitter actions (3), especially the use of NSAIDS and triptans (4) but also comorbidities (5), and the presence of trigger points (6) as well as many other external or internal factors have been proposed as contributing factors to chronicity.
In the present study ‘Correlation between chronic headaches and the rectus capitis posterior minor muscle: A comparative analysis of cross-sectional trail’, Yuan et al. (7) investigated the magnetic resonance imaging (MRI) images of the rectus capitis posterior minor muscle (RCPmi) of 115 chronic headache patients (diagnosis not further specified) and of 120 age- and gender-matched headache-free participants, for changes in cross-sectional size (7). The results indicated that male participants in both groups showed larger RCPmi and, more to the point, that the RCPmi in the headache group was significantly larger than in the non-headache group. The authors concluded that this RCPmi hypertrophy could contribute to the pathogenesis of chronic headache by influencing the so-called ‘myodural bridge’, i.e. a connection between the RCPmi and the spinal dura (8). Recently, similar connections have been identified between the RCPma or the obliquus capitis inferior muscle and the spinal dura (9). The suggested role of these connections is to prevent an infolding of the dura during cervical extension and to protect the spinal dura from excessive loading or tension.
Does that mean that the book is closed and that enlarged neck muscles are the cause of headache? Certainly not.
The authors themselves do not provide an explanation why the RCPmi of chronic headache patients should be enlarged. A simple suggestion from a physiotherapy point of view would be habitual posture changes. An EMG study has shown that the RCPmi is activated during ventral translation of the head (10). Ongoing activity during positions that involve ventral translation of the head (e.g. during computer work) could therefore result in hypertrophy of the RCPmi. Previous publications indicated a correlation between ventral translation of the head and chronic headaches supporting this hypothesis (11,12). However, physiotherapy aiming at posture corrections is not effective for the reduction of chronic headaches and this theory seems somewhat simplistic.
A more likely explanation is that central effects of the headache syndrome itself are responsible for a hyperactivity of the neck muscles: increased muscle size might not be limited to RCPmi but may constitute a general phenomenon in specific headache types. Headache patients have generally shown higher EMG activity in the neck muscles (13), especially during mental activity (14), but also during specific exercises (15). This has been specifically demonstrated for the scaleni muscles and the sternocleidomastoid muscles in boys and girls with migraine (compared with TTH) (16). Heightened muscle activity will lead to muscle hypertrophy. If the hypothesis is true that a connection between the RCPmi and the spinal dura via the myodural bridge can influence headaches by either increasing the tension on the cranial dura or interfering with the cerebro-spinal fluid circulation through the subarachnoid space (8), muscle hypertrophy due to excessive muscle tension may be a contributing factor to the chronification of symptoms. However, currently, the only proof for this hypothesis is a case study of a patient with headaches following a traumatic event. This patient showed hypertrophy of the RCPmi and a surgical release of the myodural bridge relieved the symptoms (17).
An alternative hypothesis is that RCPmi hypertrophy is a protective mechanism for a sensitized nervous system, including the spinal dura mater. Central sensitization has been shown in two-thirds of the migraine population (18) and in TTH (19), and is an explanation for a range of clinical phenomena including scalp tenderness and tender points. Following this hypothesis, an increased muscle size might be beneficial for the patient. However, to date, this has not been proven.
In conclusion, the current study provides sound evidence for muscle alterations in patients with chronic headache by using a double-blind approach and including a sufficiently large number of MRIs. This is particularly important, as previous authors had reported statistically significant side-by-side differences in healthy participants in the cross-sectional analysis of RCPmi (20). It demonstrates a clinical connection between trigeminovascular symptoms and an extracranial musculoskeletal phenomenon, but it cannot provide evidence for a contribution of the neck to chronic headache symptoms, as cause–effect relations cannot be clarified by the cross-sectional approach. Only longitudinal studies demonstrating that persons with larger RCPmi muscles are more likely to develop chronic headache or studies influencing the hypertrophy of the RCPmi and showing reduced headache would answer this question.