Review articleThe neck and headaches
Section snippets
Historical background
Documented interest in cervicogenic headaches can be traced at least as far back as 1913 when Gordon Holmes reported that headaches could arise from the neck [11]. He described headaches associated with tender nodules in the posterior neck muscles, which he attributed to fibrositis. This gave rise to the notion of “rheumatic headache,” which contemporaries of Holmes also described [12], [13]. Approximately 30 years later this notion was resurrected [14] and extended to include headaches caused
Neuroanatomic basis
The pars caudalis of the spinal nucleus of the trigeminal nerve is continuous longitudinally with the outer laminae (laminae I to V) of the dorsal horns of the upper three to four segments of the cervical spinal cord [55], [56], [57], [58]. Collectively, this column of gray matter constitutes the trigeminocervical nucleus. This nucleus, however, is not defined by any distinctive cytoarchitecture or by any intrinsic boundaries. Rather, it is defined by its afferents. This column of gray matter
Peripheral anatomy
The possible sources of cervical spinal pain that might be referred to the head are dictated by the distribution of the upper three cervical spinal nerves. Through their various branches, these nerves innervate the joints and ligaments of the median atlantoaxial joint [59], the atlanto-occipital [60] and lateral atlantoaxial joints [60], [61], the C2-3 zygapophysial joint [62], the suboccipital and upper posterior neck muscles [62], the upper prevertebral muscles [63], the spinal dura mater and
Experimental evidence
Studies in laboratory animals demonstrate convergence between cervical and trigeminal afferents in the spinal cord. In the cat, various sites in the spinal cord at the C1-2 level respond to electrical stimulation of either the trigeminal nerve or the roots of the C1 or C2 spinal nerve [69]. Neurons in the lateral cervical nucleus respond to electrical stimulation of either the superior sagittal sinus or the greater occipital nerve [70].
In studies of human volunteers, electrical stimulation of
Vertebral and internal carotid artery aneurysm
Because the vertebral artery and the internal carotid artery are innervated by cervical nerves, disorders involving these vessels are possible causes of cervicogenic headache. Because there are no means by which arteries can be selectively anaesthetized, however, there are no data that directly implicate such disorders in the cause of headache. Nevertheless, there is circumstantial evidence.
Headache is the most common presenting feature of internal carotid artery dissection [88], [89] and may
Discussion
The concept of cervicogenic headache does not enjoy universal, or even widespread, acceptance. Indeed, eminent authorities seem staunchly opposed to the concept [156]. The cardinal argument seems to be that no one has demonstrated the pathology of the cause of pain, either by medical imaging or by other means. Paradoxically, the same reasoning applies to all common forms of headache—migraine, tension-type headache, and cluster headache—but does not prevent those entities from being recognized.
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2021, Musculoskeletal Science and PracticeCitation Excerpt :It is well established that autonomic dysfunction can enforce pain perception, like in headache [Benarroch, 2006]. Both hypo and hyperfunction of the autonomic nervous system (ANS) have been reported in patients with recurrent headache [Bogduk, 2004][Cady, 2007]. Pain perception processes and the ANS correspond at the dorsal horn, nucleus of the solitary tract, parabrachial nucleus, thalamus, hypothalamus, amygdala, insular cortex, lamina-I neurons and sympathetic cell columns of the thoraco-lumbar segments [Bogduk, 2004].
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2020, Journal of Bodywork and Movement TherapiesCitation Excerpt :It is believed that during migraine attacks, the headache is triggered by activating the trigeminovascular neuroinflammatory cascade (Puledda et al., 2017) and meningeal nociceptors (Cutrer, 2010). The presence of nociceptive afferents and inputs from the C1-C3 roots and pericranial muscles converge in the nucleus of the trigeminovascular system (Robertson and Morris, 2008), thereby leading to an increase in the excitability of the first-order neuron located in the trigeminal ganglion; its permanence makes the second order neuron, located in the caudal nucleus of the trigeminal and dorsal horn of the C1-C3 roots, more sensitive, thus contributing to the pain process (Bogduk, 2004; Bartsch and Goadsby, 2005). In addition, the prolonged presence of these inputs in migraineurs may contribute to developing allodynia (cephalic and extra-cephalic), restriction of cervical mobility (Grossi et al., 2011; Ferracini et al., 2017) and kinesiophobia during the pain attack (Martins et al., 2006), which could lead to altered motor control.
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