307.81 Tension headache
339 Other headache syndromes
339.0 Cluster headaches and other trigeminal autonomic cephalgias
339.1 Tension type headache
339.2 Post-traumatic headache
339.3 Drug induced headache, not elsewhere classified
339.4 Complicated headache syndromes
339.8 Other specified headache syndromes
G44 Other headache syndromes
G44.009 Cluster headache syndrome, unspecified, not intractable
PREFERRED PRACTICE PATTERN
4E: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Localized Inflammation
Brain stem pathways that modulate sensory input. The key pathway for pain in migraine is the trigeminovascular input from the meningeal vessels, which passes through the trigeminal ganglion and synapses on second-order neurons in the trigeminocervical complex (TCC). These neurons in turn project in the quintothalamic tract and, after decussating in the brain stem, synapse on neurons in the thalamus. Important modulation of the trigeminovascular nociceptive input comes from the dorsal raphe nucleus, locus coeruleus, and nucleus raphe magnus. (From Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.)
Positron emission tomography (PET) activation in migraine. In spontaneous attacks of episodic migraine there is activation of the region of the dorsolateral pons; an identical pattern is found in chronic migraine (not shown). This area, which includes the noradrenergic locus coeruleus, is fundamental to the expression of migraine. Moreover, lateralization of changes in this region of the brain stem correlates with lateralization of the head pain in hemicranial migraine; the scans shown in panels A and B are of patients with acute migraine headache on the right and left side, respectively. (From Afridi SK, et al. Brain. 2005;128:932.)
Central and peripheral nervous system sites proposed to be involved in migraine pathogenesis. During the aura phase, a reduction in cortical blood flow spreads anteriorly from the occipital cortex (large arrow), which is thought to be due to spreading depression. During the headache phase, sterile inflammation in the meninges may activate trigeminal (V) nerve sensory fibers that project to the nucleus caudalis, periaqueductal gray, sensory thalamic nuclei, and primary somatosensory cortex (small arrows). Alternatively, this central sensory pathway may convey normal afferent signals that are interpreted as noxious. (From Greenberg DA, Amnioff MJ, Simon RP. Clinical Neurology. 8th ed. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.)
Posterior hypothalamic gray matter activation on positron emission tomography ...
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