Cases reported "Migraine Disorders"

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1/29. migraine with aura-like headache associated with moyamoya disease.

    A 49-year-old woman was admitted to our hospital because of severe headache. She had a 10-month history of migraine with aura-like headache that occurred every 7 to 10 days and was preceded by photopsia. Brain CT showed cerebral infarction of the left occipital lobe. Bilateral carotid angiograms showed vascular occlusions in the supraclinoid portion of the bilateral internal carotid arteries with telangiectatic vessels acting as collateral channels to the occluded distal carotid arteries, which were consistent with the diagnosis of moyamoya disease. headache resolved gradually and has never developed again after the infarct of the left occipital lobe. Pathophysiological mechanisms of migraine-like headache were discussed. We conclude that borderline perfusion of occipital lobe cortex could be a trigger for the development of migraine with aura-like headache in susceptible patients. In the case of atypical attack of migraine detailed investigation should be done to detect underlying vascular diseases such as moyamoya disease.
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2/29. Migraine associated bilateral intracerebral haemorrhages.

    The authors report a case of bilateral basal ganglionic haemorrhages which occurred during an attack of classical migraine. The patient had a history of migraine associated with aura of neurological deficit for 10 years and a history of arterial hypertension for 20 years, which was treated with propranolol. Intracerebral haemorrhage during an attack of migraine is very rare and up to now the existence of true migraine-induced intracerebral haemorrhage has been controversial. Our case of bilateral occurrence of the haemorrhages supports the theory of the existence of migraine-induced damage of the wall of intraparenchymal vessels during vasoconstriction and focal ischaemia at the beginning of a migraine attack. Subsequent vessel rupture may occur during the following period of increased cerebral blood flow especially with coexisting arterial hypertension. The terminology of the syndrome of migraine associated with intracerebral haemorrhage is reviewed.
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3/29. Migraine and Raynaud phenomenon: possible late complications of Kawasaki disease.

    Migraine and Raynaud phenomenon often coexist and may reflect similar vascular reactions. Both have been associated with vascular endothelial cell dysfunction. Kawasaki disease is a systemic vasculitis of unknown etiology that affects children and may lead to the formation of coronary artery aneurysms. Endothelial cell dysfunction has been demonstrated late in Kawasaki disease and is not restricted to coronary vessels. We report the case of a patient who developed typical migraine with aura and Raynaud phenomenon at the age of 14, 12 years after onset of Kawasaki disease. His migraine responded well to pizotifen, and both migraine and Raynaud phenomenon improved after initiation of treatment with valproic acid. We postulate that both migraine and Raynaud phenomenon in this case represent late consequences of Kawasaki disease and result from extracoronary endothelial dysfunction.
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4/29. Parry-Romberg syndrome with migraine and intracranial aneurysm.

    Parry-Romberg syndrome or progressive facial hemiatrophy (PFH) is a rare disease of unknown etiology characterized by atrophy of the skin and subcutaneous tissue on one side of the face. The authors present the case of a 32-year-old woman with PFH who had migraine and an intracranial aneurysm. The findings support the hypothesis that the disease could be related to a neural crest migration disorder, from which both fronto-nasal mass and cranial vessels take origin.
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5/29. Serial MRI in a case of familial hemiplegic migraine.

    We report MRI findings in a patient with familial hemiplegic migraine (FHM) with repeated episodes of hemiparesis. FHM is caused by a penetrant autosomal dominant genetic mutation; several mutations have been genotyped, involving brain-expressed ion channels. We found cerebral oedema, dilatation of intracerebral vessels and decreased water diffusion contralateral to the hemiparesis, not respecting vascular territories, with subsequent complete resolution of both clinical and imaging abnormalities. These results are thought to be consistent with an underlying primary neuronal pathology with secondary vascular effects, as opposed to the traditional, primarily vascular, model of migraine aetiology.
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6/29. Reversible conduction block in human ischemic neuropathy after ergotamine abuse.

    Conduction block [a significant reduction in compound muscle action potential (CMAP) amplitude after proximal compared to distal stimulation] is often found in demyelinating neuropathies, including inflammatory neuropathies and degenerative neuropathies, such as "liability to pressure neuropathy." There is experimental evidence that a transient conduction block can occur in rats after ischemic lesions of peripheral nerves are induced either by ligation of arterial vessels supplying nerve trunks, or by injection of arachidonic acid into peripheral arterial vessels. Conduction block has also recently been described in cases with necrotizing vasculitis. To date, however, no example of a reversible conduction block has been reported in human ischemic neuropathy.
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7/29. Systemic lupus erythematosus associated with familial moyamoya disease.

    We report on a 13-year-old female with systemic lupus erythematosus (SLE) who exhibited symptoms of severe migraine and familial moyamoya disease. Cerebral magnetic resonance angiography (MRA) showed stenosis and occlusion of the bilateral internal carotid arteries associated with the development of collateral circulation (moyamoya vessels). In a child, as in this case, headaches with cerebral infarction associated with moyamoya disease are unusual. Few cases of SLE associated with familial moyamoya disease have been reported, with no previous reports of such cases from korea. There were no evidences of antiphospholipid syndrome, and activity of SLE or other risk factors for cerebral occlusion were also absent.
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8/29. ophthalmoplegic migraine.

    ophthalmoplegic migraine is a rare presentation of migraine complicated by an isolated oculomotor paresis. vasodilation of extracranial vessels is believed to underlie the headache, and vasoconstriction to account for the ophthalmoplegia. Whether the vascular insult involves the central or peripheral portions of the oculomotor nerve is still uncertain. We describe a child who presented with ophthalmoplegic migraine and was demonstrated to have a deficiency of the near triad documented by eye movement and pupillary recordings. Voluntary conjugate eye movements--saccades, smooth pursuit, and optokinetic nystagmus--were normal. Vergence amplitudes appropriate to fixation distance were elicited for Snellen optotypes but not to a point source of light. Concurrent measures of pupillary diameter failed to reveal significant modulation to either stimulus. Brain magnetic resonance imaging scan was normal, and there was no contrast enhancement of the oculomotor nerve at its exit from the midbrain. Both the oculomotor paresis and concurrent presence of a deficiency of the near triad localized the vascular insult to the oculomotor nerve complex in the brainstem.
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9/29. Acute migraine attack, angina-like chest pain with documented ST-segment elevation and slow coronary flow.

    Slow flow of dye in epicardial coronary arteries is not an infrequent finding in patients during routine coronary angiography. The coronary slow flow phenomenon is an angiographic finding characterized by delayed distal vessel opacification in the absence of significant epicardial coronary artery disease. It is speculated that coronary slow flow is a new disease characterized by acute but recurrent perturbations of microvascular function. There are many theories concerning the pathogenesis of migraine. The clinical effectiveness of vasoactive drugs and many investigations on the cerebral blood flow in patients with migraine, strongly support a vascular theory. The relationship between migraine and cardiopathy has not been sufficiently established and controversy exists concerning its favouring role in coronary artery disease. We report a case of an acute migraine attack in a patient who uses triptans (5-HT(1B/1D) receptor agonists). The attack was accompanied by angina-like chest pain with documented ST-segment elevation and slow coronary flow in the absence of any significant obstructive coronary artery disease and no evidence of any major epicardial coronary arterial spasm.
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10/29. Which triptan for which patient?

    The triptans were developed for the acute treatment of a migraine attack and have revolutionised the treatment of this disorder since their introduction in the early 1990s. Although their mechanisms of actions are similar and based on the stimulation of specific serotonin (5-hydroxytryptamine) receptors including peripheral 1B and central and peripheral 1D subtypes, each triptan has its own distinctive pK properties that result in different profiles of efficacy and tolerability. Triptans work by decreasing neurogenic inflammation peripherally in the meninges, vasoconstriction of meningeal vessels and by modulating secondary-order neurons in the brain stem. Studies of patient attitudes towards their acute care regimens reveal that they are often unhappy with some aspect of their treatment-usually the speed of action, degree of efficacy, presence of adverse events and the need for additional doses due to frequent and/or rapid recurrence. The majority of patients, when asked in a clinical trial performed at tertiary care headache centres, are willing to try another triptan. The aim of this article is to review the pK and clinical characteristics of these acute care, migraine-specific triptan medications and discuss how their individual characteristics lead to their preferred choice in various clinical scenarios. The pK and clinical efficacy data presented are taken from older published studies in which triptans were compared to placebo or each other, but the patients were asked to wait till the headache reached moderate or severe intensity prior to taking study medication. New studies have looked at early treatment paradigms and result in better efficacy data, but are difficult to compare due to different endpoints.
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