Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

NeuroSPECT of regional cerebral blood flow (rCBF) with Tc-99m HMPAO demonstrated left temporoparietal hyperemia in two patients with acute receptive aphasia. This finding prompted further testing with electroencephalography that added to the impression of ictal dysphasia. The differential diagnosis in one case included complicated migraine. NeuroSPECT depicts blood flow abnormalities in acute aphasic disorders, either due to ischemia, which is most commonly the cause, or due to hyperemia secondary to migraine or epilepsy. The treatment and prognosis of these latter conditions differ from stroke, and thus SPECT plays a role in patient management.
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PMID:Hyperemic receptive aphasia on neuroSPECT. 850 76

Ergot's derivatives are widely used in the treatment of migraine and in the prophylaxy of deep venous thrombosis in association with heparin. Clinical ergotism is rarely observed and can affect all the arteries, especially of the inferior limbs. Vasospasm of the peripheral arteries and collateral formation are specific findings on angiography. We report the illustrative case of a 38 years old woman hospitalized for a small bowel occlusion. She suffers from chronic migraine treated by ergotamine tartrate. During her hospitalization, she develops an acute ischemia of the lower limbs. An ergotism was clinically suspected and confirmed by Duplex sonography which demonstrate multiple vasospasm. Under iv sodium nitroprusside and peridural analgesia the spasm resolved in 24 hours. The control Duplex sonography confirm the normality of the lower limb arteries. This examination modality allow a non-invasive diagnosis and evolution control of arteriospasm.
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PMID:[Value of duplex ultrasound in diagnosis of ergotism of the legs]. 858 19

Sumatriptan, a 5-hydroxytryptamine1, (5-HT1) receptor agonist is an effective abortive agent for migraine headaches. A common side effect in 3% to 7.9% of patients is chest pain. Although most cases of chest pain are not thought to be of cardiac origin, its mechanism is not entirely understood. Rare examples of electrocardiogram changes consistent with transient ischemia have been reported. Isolated instances of angina, arrhythmia, myocardial infarction, and death have been temporally associated with sumatriptan administration. In most cases, it is unclear whether underlying cardiovascular disease existed or contributed to this adverse event. We report the history of a 56-year-old female patient with migraine who experienced a myocardial infarction shortly after using sumatriptan, despite having had a normal cardiovascular evaluation. As she had a normal cardiac catheterization after the event, we find it probable that sumatriptan induced coronary vasospasm and myocardial infarction.
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PMID:Vasospasm-induced myocardial infarction with sumatriptan. 868 77

Endothelin-1 is a recently discovered peptide mainly released from endothelial cells. Hypoxia and ischemia as well as numerous factors such as angiotensin 11, thrombin and transforming growth factor beta 1 stimulate the formation of the peptide. On the other hand the synthesis of endothelin is inhibited by nitric oxide and atrial natriuretic peptide via the formation of cyclic guanosine monophosphate. Released from endothelial cells endothelin-1 mediates transient vasodilation followed by a profound and longlasting vasoconstriction. Endothelin is also a mitogen for smooth muscle proliferation. Endothelins exert their biological effects via activation of specific receptors. Two different receptors have been cloned from mammalian tissues (ET(A) and ET(B) receptors). On vascular smooth muscle cells both receptors mediate contractions. Endothelial cells only express ET(B) receptors linked to the formation of nitric oxide and/or prostacyclin formation. Increased plasma concentrations of endothelin-1 have been described in a variety of diseases such as pulmonary hypertension, arteriosclerosis, renal failure, acute coronary syndromes, heart failure, migraine and vascular diseases. Recently an increasing number of endothelin receptor antagonists have been synthetized, which have been shown to inhibit endothelin-mediated vasoconstriction. Clinical studies are now ongoing to elucidate the pathophysiologic role of endothelin and the potential benefit of the blockade of the system in different disease states.
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PMID:Endothelin and endothelin antagonists: potential role in cardiovascular and renal disease. 873 56

We described a 67-year-old right handed man with a left internal carotid artery occlusion, who developed monocular photopsia that supervened neovascular glaucoma. He had an antecedent transient motor aphasia. His photopsia, exaggerated by light, persisted intermittently. Orbital bruit was obtained on the left, more clearly during the photopsia. Brain MRI, cerebral angiography, and duplex sonography of carotid and ophthalmic arteries indicated left internal carotid artery (ICA) occlusion with collateral circulation through the ophthalmic artery. Visual evoked potentials (VEPs) revealed a prechiasmal disturbance of the optic pathway of the left side. The patient had carotid endarterectomy of the left ICA, and his visual disturbance has gradually improved. Ocular symptoms due to ICA ischemia are commonly transient visual loss with dark background known as amaurosis fugax. Neovascular glaucoma is sometimes complicated with carotid artery occlusion. However, photopsia associated with carotid artery occlusion is rare. Photopsia mimics scintillating scotomata, but the latter precedes migraine and is biocular and homonymous, ascribable to spreading depression from the occipital lobe. Retinal or prechiasmal optic pathway might be influenced by poor circulation of the ophthalmic artery. In addition, disturbance of light adaptation due to retinal hypoperfusion may be possible reason. Neovascular glaucoma is intractable, once developed. Therefore, atypical scintillating visual disturbance must be recognized as a sign of carotid artery insufficiency and supervened glaucoma to prevent it.
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PMID:[Monocular photopsia preceding with neovascular glaucoma due to internal carotid artery occlusion; a case report]. 874 54

Previous studies have shown that migraine with aura is associated with the reduction of regional cerebral blood flow (rCBF). However, the question of whether the reduction of rCBF during migraine aura is caused by cerebral vasospasm or is secondary to the neural depression (spreading depression) is still disputed. We measured rCBF by high resolution SPECT method during the attack of migraine and examined whether the reduction in flow corresponds to the cerebral vascular territory. Fourteen patients with migraine with aura (7 men and 7 women, 34.7 +/- 17.8 years) were studied. In all the patients rCBF was measured during the interictal period and in four patients rCBF was measured during the aura of migraine. SPECT measurements of rCBF was performed using Tc-99m-PAO (740 MBq) as a tracer. During the aura of scintillation scotoma in the unilateral visual field rCBF was reduced in the opposite occipital, temporal and thalamic regions which corresponded clearly to the region of the posterior cerebral arterial territory. The reduction of rCBF was by 31 approximately 49% compared with the opposite hemisphere. Cerebral spinal fluid lactate level during the headache measured in one patient was higher (38 mg/dl) than the interictal period (12 mg/dl). Our data indicated that the reduction of rCBF during the aura is caused by ischemia probably due to the cerebral vasospasm and is not secondary to the neuronal depression. It was also suggested that the primary site of rCBF reduction during the visual aura is the occipital association cortex which is reported to be responsible for the visual hallucination.
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PMID:[Regional cerebral blood flow during migraine]. 875 89

Ergotamine tartrate (ET) and dihydroergotamine mesylate (DHE) have been widely and effectively used in the treatment of migraine for many decades, although few randomized, controlled clinical trials have been conducted with these compounds. To compare their safety profiles, the world literature on the two agents was surveyed. The results are summarized, along with a critical analysis of the strengths and limitations of the various sources of safety data (in vitro research, animal studies, Phase I and II studies, controlled clinical trials, and postmarketing surveillance). Significant pharmacologic and safety differences exist between ET and DHE. Dihydroergotamine mesylate is a less potent arterial vasoconstrictor than ET, although nearly equipotent as a venoconstrictor. It is a more potent alpha-adrenergic antagonist, but is much less emetic, has less effect on the uterus, and is not associated with rebound headache. Adverse effects associated with ET (which are often due to excessive dosage and/or chronic usage) include nausea, acroparesthesia, ischemia, habituation and overuse headache, and, rarely, overt ergotism. Reports of serious adverse effects following recommended doses of DHE are rare. As with most antimigraine drugs, the most frequent adverse effect with intravenous (i.v.) DHE is nausea; however, following intramuscular (i.m.) or intranasal (IN) administration, the incidence of nausea is low and concomitant administration of an antiemetic is not needed. In patients without contraindications, both DHE and ET are safe and effective when used in recommended doses. Nearly 50 years of clinical experience without major safety problems allows a high level of confidence in their clinical use.
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PMID:Ergotamine tartrate and dihydroergotamine mesylate: safety profiles. 900 72

Vestibular symptoms frequently occur in patients with migraine headache. The common migraine is defined in neurology as a unilateral, pulsating headache, which may be associated with nausea and vomiting, and lasts one or several days. In the classic form patients have visual prodromal symptoms. Focal neurological signs in the migraine complique include, for example, oculomotor palsy and vestibular abnormalities. This so-called vestibular migraine is different from basilar migraine, which involves the irritation of the cervical sympathetic system, and can cause symptoms that resemble transient brainstem ischemia. In order to evaluate vestibular dysfunction electronystagmography (ENG) was used. Patients frequently had abnormal caloric test responses, especially with a directional preponderance, and most had a spontaneous nystagmus. In the migraine attack the patients are presumed to have hypersensitivity of the labyrinth with nausea and vomiting, while in the headache-free period the ENG was almost normal. At present, we have had a high success rate in treating patients with pyracetam. Diazepam was used to treat basilar migraine and flunarizine to prevent vestibular migraine.
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PMID:Vestibular disorders in patients with migraine. 906 28

The authors report two cases of a particular type of migraine with aura, known as familial hemiplegic migraine (FHM). According to the International Headache Society (IHS) diagnostic criteria, the FHM can be diagnosed with the exception of organic causes, in a patient with migraine with aura including emiparesis of anything severity and with an end occurring a member of the family with similarity in the attach pattern. The two clinical cases reported clearly show these features and they can be considered exemplary for this type of pathology. This rare type of migraine has an unknown etiology, it seems to depend on a decreases of cerebral blood flow originative on the occipital lobe, over the subsequentially spreading anteriory region temporal and parietal lobe. The hypoperfusion with the next following neural ischemia is related to the variation of blood flow and/or "the spreading depression" supported by Leao and Olesen recently. We wanted to show these two cases so that the psychiatrist, the pediatrician, and the neurologist can be able to refer parents to the right approach, considering possibility of a pathology rare but benign; this is the FHM.
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PMID:Familial hemiplegic migraine in developmental age: report of two cases. 917 12

Neurologic and visual symptoms frequently occurred in 56 reported patients with essential thrombocythemia (ET). They may either precede or follow the well-known microcirculatory complications of ET of acroparesthesias, erythromelalgia, and acrocyanosis or ischemia of one or more toes. In comparison with transient ischemic attacks in patients with vascular risk factors, the usual neurologic presentation of ET consists of brief attacks of sudden cerebral or visual dysfunction, which can be either well localized or diffuse and entirely nonspecific. A dull and throbby headache usually lasting for several hours frequently accompanies the neurologic symptoms. Visual symptoms are less frequent and include transient monocular blindness and global symptoms such as scintillating scotomas and attacks of blurred vision. Neurologic and visual symptoms may leave minor sequelae but are generally nondisabling. The striking similarity to migraine, together with the absence of vascular risk factors and the striking efficacy of aspirin treatment supports the hypothesis that the ischemic neurologic and visual symptoms in ET are caused by shear rate-induced intravascular activation and aggregation of platelets with subsequent transient sludging or occlusion of the cerebral arterial microvasculature. Available data show that both the erythromelalgic distress and the ischemic neurologic attacks in ET are completely abolished by control of platelet function with low dose aspirin alone or reduction of platelet counts to normal as well as by the combination of platelet reducing therapy and low-dose aspirin. Early recognition and appropriate treatment of neurologic symptoms in patients with ET is therefore of great clinical relevance.
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PMID:Neurologic and visual symptoms in essential thrombocythemia: efficacy of low-dose aspirin. 926 53


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