Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report 22 cases of transient ischemic attacks (TIA's) manifested by amaurosis fugax or hemiparesis or paresthesia of less than 24 hours' duration. None of the patients demonstrated 1) evidence of atherosclerotic cerebral vascular disease on angiography, 2) evidence of intracranial lesion on brain scan, 3) cardiac source of emboli, 4) arteritis or collagen disease, or 5) history of migraine. The only abnormalities found to explain the TIA's were abnormally increased platelet adhesiveness and/or aggregation. All of these patients were followed from 1 to 5 years, and had repeated coagulation studies. Treatment with antiplatelet drugs showed an excellent clinical response with associated decrease in platelet adhesiveness and aggregation. Discontinuance of the antiplatelet drug resulted in a recurrence of the TIA's which coincided with an increase in aggregation and adhesiveness. In two cases the platelet morphology was studied by transmission and scanning electron microscopy. It appears that there is a specific group of patients with TIA's in whom the sole cause of the attack is an abnormality of platelet function. For these people there is a specific therapy and a method monitoring the treatment.
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PMID:Transient ischemic attacks due to increased platelet aggregation and adhesiveness. Ultrastructural and functional correlation. 42 99

An uncommon consequence of intracranial vascular disease is the intramural dissection of blood or "dissecting aneurysm". A 69-year-old man with chronic subarachnoid hemorrhage from a posterior fossa mass lesion and a 30-year-old man with migraine and a brain stem stroke illustrate the diverse etiologic, clinical, radiographic, and pathologic characteristics of this unusual lesion.
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PMID:Dissecting aneurysms of the basilar artery in 2 patients. 46 17

Ischaemic optic neuropathy is a well recognised cause of sudden visual loss in middle and late life. It is characterised by painless visual impairment, pale swelling of the optic disc and nerve fibre bundle field defects. Although some cases are due to cranial arteritis, the majority of patients suffer from non-arteritic diseases, particularly hypertension. The present study consists of a reveiw of 22 cases of ischaemic optic neuropathy. Apart from cranial arteritis and vascular disease, migraine and trauma appear to have a causal relationship to the disorder.
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PMID:Ischaemic optic neuropathy. 55 Sep 42

Extensive plexuses of serotonin axons form a supra- and subependymal system in the walls of the ventricles, in the arachnoid sheath around major cerebral blood vessels, and in the pia over the spinal cord. These have been demonstrated by autoradiography after continuous intraventricular perfusions of exogenous [3H]5-HT in rats and monkeys. The axons accumulate 5,6-DHT rendering them electron opaque, but have no uptake systems for [3H]NE. After treatment with MAO inhibitors and [3H]5-HT, the axonal boutons contain large (70nm) variably dense synaptic vesicles, and small (35 nm) vesicles each equipped with a dense dot. The latter vesicles are not seen in untreated controls. Electrical stimulation in the raphe nuclei causes significant increases in axonal [3H]5-HT uptake indicating that the fibers originate in the raphe. Quantitatively, the supraependymal plexus is variable, profuse over the dorsal and ventral aqueductal surfaces, sparse over the lateral aspects. Individual raphe neurons have their specific uptake affinities for [3H]5-HT that are independent of tracer concentration or diffusion gradient. It is suggested that raphe neurons with low 5-HT uptake may utilize other neurotransmitters. Two new functional roles are proposed: (1) the serotonin ventricular and pial axons are probably important modifiers of local cerebrospinal fluid (CSF) composition so that regional CSF variations in 5-HT and its metabolites are highly probable; (2) the subarachnoid plexus around major cerebral vessels may contribute to local vasomotor action, thus affecting the cerebral blood flow. The possible significance of these serotonin systems for an understanding of certain neurological entities such as migraine and hemodynamic regulation in cerebral vascular disease is indicated.
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PMID:Serotonin axons in the supra- and subependymal plexuses and in the leptomeninges; their roles in local alterations of cerebrospinal fluid and vasomotor activity. 81 16

Thirty-three of 129 patients who incurred isolated ophthalmic migraine had monocular attacks of scotomatous visual field loss. Fifteen of 33 patients with monocular attacks had immediate or remote evidence of vascular disease. Four patients had carotid bruits on the same side as the monocular attacks and low ophthalmodynamometer readings. One patient had ischemic optic neuropathy and two had atheromatous disease (advanced stage in one patient). Forty-five percent of the patients with monocular attacks and only 13% of the remaining patients with homonymous attacks had vascular complications. This represents an important finding even in such a small group of patients. It is felt that, whether the vascular problems are trigger mechanisms or coexistence pathology to the migraine-type attack, one should strongly suspect such an association when a patient describes a monocular attack and one should look for a possible vascular explanation other than migraine.
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PMID:Isolated ophthalmic migraine in the differential diagnosis of cerebro-ocular ischemia. 96 Jan 57

The author reviews the pertinent literature and the results of own investigations in migraine. EEG changes in migraine are observed in nearly 50% of cases during attacks as well as in the periods free of pains. Most investigations were done in the periods between attacks. The H response characteristic of migraine was found by the author in 25% of cases only. Focal changes were present in 30% of cases. They were not related to the side of the pain, its duration and the form of migraine. Seizure activity was never observed. The author regards isolation of the so-called dysrhythmic form of migraine as not justified. EEG changes suggest--according to the author--that migraine is a primary cerebral and only secondarily a vascular disorder.
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PMID:[Electroencephalographic studies in migraine]. 115 64

Forty migraine patients were examined by means of 3D-transcranial Doppler scanning (TCD). The complete circle of Willis was investigated in all patients during headache-free intervals. TCD investigations were repeated in 10 patients during a migraine attack, in one patient twice. Based on the diagnostic criteria of the "headache classification committee of the international headache society" 23 patients were assigned to a "migraine without aura" group and 17 to a "migraine with aura" group. Twenty age-matched volunteers, not suffering from headache or any vascular disease, served as a control group. No significant differences were detected between the hemodynamic data of the control group and the migraine groups both with respect to the headache-free interval and the attack. No hemodynamic changes in keeping with the pathophysiologic hypothesis of vasospasm were found in the proximal segments of the basal cerebral arteries.
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PMID:Hemodynamic findings in migraine patients on transcranial Doppler sonography. 144 59

Subdural hematomas many sometimes clinically resemble Transient Ischemic Attacks (TIA's). We present three cases which were initially evaluated for, diagnosed as having and were treated for TIA's, but later were found to have subdural hematomas. As in case one, patients with subdurals may have antecedent head trauma which they may or may not recall. Patients presenting with symptoms resembling TIA's need a complete neurologic evaluation. The differential diagnosis for TIA's includes arteriosclerotic extracranial vascular disease, cardiac emboli, migraine, seizure disorder, and mass lesions. Since the prognosis and treatment differs one needs to determine the etiology of the symptoms before treatment is initiated. Specifically, other diagnoses must be excluded prior to anticoagulation therapy, as evidenced by case 2.
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PMID:Transient ischemic attack (TIA) secondary to subdural hematoma. 145 13

Distension of dural sinuses in man produces migraine-like pain. In eight alpha-chloralose anaesthetized cats mechanical distension of the superior sagittal sinus with a small intraluminal device was used to activate single units in the dorsolateral C2 spinal cord. Units in this region have been shown to respond to electrical stimulation of the superior sagittal sinus in the cat model. Linked responses to mechanical dilatation could only be obtained with very rapid stretching stimuli or high amplitudes of distension of the vessel. Lower thresholds for transduction of distension in the vessel wall may depend on transferral to the dura or biochemical or neural pre-sensitization of the superior sagittal sinus. These data are consistent with the view that migraine is not primarily a vascular disorder but requires at least humoral or neural facilitation.
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PMID:Activation of the trigeminovascular system by mechanical distension of the superior sagittal sinus in the cat. 162 3

I studied 9 patients with migraine and posterior circulation ischemia. Inclusion criteria were (1) brainstem or cerebellar infarcts or transient ischemic attacks, (2) satisfactory vertebrobasilar angiograms, and (3) migraine. Excluded were patients with only occipital lobe ischemia, known arteriosclerosis, or other nonmigrainous vascular disease. Two women and 7 men, ages 6 to 58 years (mean, 34.7), had transient attacks only (2), single strokes (4), single stroke followed by attacks (1), or multiple strokes (2). Five had antecedent classic, 2 common migraine, and classic migraine began only after the initial ischemic event in the other two. The 7 stroke patients all had CT- or MRI-documented brainstem (4) or cerebellar (6) infarcts. Angiography was normal (3) or demonstrated basilar artery (BA) narrowing (2) or occlusion (4), or branch occlusion (1). In 3 patients the initially occluded BA later reopened. At follow-up (average 4.3 years, range 1 to 9 years), 5 were normal and 4 had important clinical deficits. I conclude that (1) "basilar migraine" is not always benign; it affects both sexes and a wide age range; (2) the pattern of headaches, attacks, and strokes varies; (3) migraine may appear only after ischemia; (4) some patients have BA occlusion or diffuse narrowing; and (5) BA occlusion can be temporary.
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PMID:Migraine and vertebrobasilar ischemia. 192 34


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