Cephalalgia : an international journal of headache
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A controversial entity, Eagle's syndrome, is reviewed. After an anatomical description of the maxillo-vertebro-pharyngeal region we summarize the causative, diagnostic and therapeutic aspects of the syndrome. ⋯ We believe that the term "Eagle's syndrome" is legitimate only in the first case and in those "atypical" painful head and neck conditions related to an elongated styloid process and relieved by styloidectomy. We believe Eagle's syndrome deserves consideration in the International Headache Classification.
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Two mechanisms have been proposed to explain the primary mode of action of sumatriptan: vasoconstriction, and trigeminal nerve terminal inhibition. Sumatriptan is a potent vasoconstrictor of intracranial arteries. It has been shown to increase blood flow velocity in large intracranial arteries in man in a dose-dependent fashion both during and between migraine attacks. ⋯ Experimental data from animal studies have shown that following electrical stimulation of the trigeminal ganglion there is a neurogenic inflammatory response with plasma protein extravasation from dural blood vessels. This response can be significantly reduced by sumatriptan at a dose level similar to that used in clinical treatment. This finding is further supported by the clinical observation that sumatriptan reduces the plasma levels of calcitonin gene-related peptide which are raised during a migraine attack.
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The cerebral circulation is invested by a rich network of neuropeptide Y (NPY) and noradrenaline containing sympathetic nerve fibers in arteries, arterioles and veins. However, the nerve supply of vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) containing fibers is sparse. While noradrenaline and NPY cause vasoconstriction, VIP, SP and CGRP are potent vasodilators. ⋯ Subjects with spontaneous attacks of migraine show release of CGRP in parallel with headache. Cluster headache patients have release of CGRP and VIP during bouts. Treatment with sumatriptan aborts headache in migraine and cluster headache as well as the concomitant peptide release.
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Exteroceptive suppression of temporalis muscle activity was proposed by Schoenen and co-workers in 1987 as a tool in headache diagnosis and research. Their finding of a decreased or abolished second silent period (ES2) in chronic tension-type headache sufferers has been confirmed by several independent laboratories during the last five years. ⋯ The pathophysiological concept of muscle contraction in tension-type headache has been challenged by studies using temporalis silent periods. The exteroceptive suppression of temporalis muscle activity points unequivocally towards a central pathogenetic mechanism, although it remains unclear whether the abnormalities of temporalis ES2 represent the primary dysfunction or a secondary phenomenon in chronic tension-type headache.
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About half of the aneurysm patients admitted to neurosurgical departments experience warning symptoms in the form of minor bleeding episodes days or even several months before a major haemorrhage occurs. Headache is the most common symptom of this warning leak, occurring in 9 out of 10 patients. The onset of headache is sudden and is unusual in severity and location, being unlike any headache the patient has otherwise experienced. ⋯ It is misinterpreted as attacks of migraine, tension headache, the 'flu, sinusitis, or a "sprained neck". A more vigilant attention to the presence of a warning headache probably offers the greatest opportunity for altering the otherwise serious natural history of aneurysmal subarachnoid haemorrhage. If a warning headache is suspected, lumbar puncture is the examination of choice, once CT scanning has ruled out an intracranial mass lesion.