Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 42-year-old black man, a physician, presented with a three week history of intermittent right arm and leg numbness and weakness, lasting about five minutes. This was not associated with headache, visual changes, seizures, aphasia or loss of consciousness. There was no history of head trauma, migraines, or previous attacks. Positive findings on physical examination were confined to a blood pressure of 182/80; evidence of hypertensive retinopathy; normal carotid pulses without bruits; and a Grade II/VI systolic ejection murmur with normal sinus rhythm. Initial hematocrit was 25.7%; white blood cell count 14,000 cu/mm with a normal differential; platelet count 532,000 cu/mm. An electrocardiogram showed left ventricular hypertrophy. Duplex scan demonstrated normal carotid bifurcations bilaterally, and arteriogram revealed no carotid or intracranial pathology. Hemoglobin electrophoresis revealed sickle cell disease of the SS type. He was treated with transfusion therapy and has remained asymptomatic at 40 months. Approximately 20% of children with the SS type sickle cell disease will have cerebrovascular symptoms caused by small intracranial artery occlusion due to sludging of the abnormal hemoglobin. This unusual cause of transient ischemic attacks can occur in older patients of African-American ancestry and must be recognized to enable early and effective therapy with exchange transfusion.
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PMID:An unusual cause of transient ischemic attacks: case report. 187

An 18-year-old female presented with two seizures induced by photic stimulation. She had a positive family history for migraine and a history of febrile convulsions. Since the age of 13 she had suffered from migraine attacks with aura. A brain computerized tomography with contrast enhancement was negative and several electroencephalograms showed a photoparoxysmal response. At the age of 18 she had a partial secondary generalized seizure after photic stimulation during routine electroencephalogram. The onset of seizure was in the occipital region. Two days later, the patient presented with a typical migrainous attack with aura. Interictal apomorphine test (1.5 mg s.c.) blocked the photoparoxysmal response. According to Quesnay, dopaminergic failure of the occipital cortex may account for both epileptic and migraine features.
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PMID:Migraine with aura and photosensitive epileptic seizures: a case report. 188 72

Occipital epileptiform activity that is almost continuous and reactive to eye opening has been associated with a childhood epilepsy syndrome and basilar migraine with seizures. An association of these syndromes with a benign course had been disputed. In this study, a retrospective investigation of reactive occipital epileptiform activity (ROEA) was performed to determine the prognostic value of this distinctive EGG pattern. The EEG and hospital record of patients with ROEA were reviewed with an observation period of 6 months to 8 years. The patients were divided into good and poor outcome groups based on response to treatment. Of 33 patients, 12 (36.4%) had complete seizure control; 21 (63.6%) continued to have poorly controlled seizures. Only 3 (9.1%) patients were able to discontinue antiepileptic drugs (AEDs) without seizure recurrence. Analysis of clinical and EEG variables showed that a history of perinatal difficulties, abnormal neurologic findings, and abnormal EEG background activities occur significantly more frequently in the poor outcome group. This study suggests that ROEA is not uniformly associated with a benign course and that other factors are involved in determining prognosis of the epilepsy.
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PMID:Reactive occipital epileptiform activity: is it benign? 189 22

A 24-year-old male had a deficiency of the complex I (NADH coenzyme-Q-reductase) of the mitochondrial respiratory chain, which clinically presented as a mitochondrial encephalomyopathy, with lactic acidosis and stroke-like episodes (MELAS syndrome). The encephalopathic episodes were preceded by migraine and were characterized by focal deficit signs, motor partial seizures and hypodense areas in the CT scan. An echocardiographic diagnosis of hypertrophic cardiomyopathy without intracavitary thrombi was made. It is suggested that hypertrophic cardiomyopathy is caused by the mitochondrial abnormalities that have been reported in the myocardium, and that migraine and cerebral infarctions are associated with abnormalities in the mitochondria from the endothelium and smooth muscle fibres of the cerebral small arteries and arterioles.
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PMID:[Complex I (NADH coenzyme-Q-reductase) deficiency, MELAS syndrome and hypertrophic cardiomyopathy]. 190 55

Despite the high prevalence of psychic symptoms in lupus patients, there are few systematic studies in this area. Through a multidisciplinary approach, the authors developed a prospective study to characterize and correlate psychopathological aspects with clinical and laboratory data concerning neural manifestations of the disease. Out of 23 patients studied, 12 showed psychic alterations, which were interpreted as primary manifestations of the disease. All of them presented organic mental syndromes (DSM-III-R) in which cognitive symptoms were the most prominent, followed by affective, catatonic and hallucinatory features. The neurologic findings (seizure, migraine and muscular atrophy), as well as the ophthalmologic alterations (hemorrhage and soft exudates) were frequent and concomitant with the psychic features. The laboratory findings were: LE cells 50%; anti-Sm: 16%; anti-U1 RNP: 50%; anti-Ro/SS-A: 50%; anti-nDNA: 58%; decreased CH50 or fractions (C3, C4): 67%; anti-P: 18%; antigangliosides IgG: 67%; antigangliosides IgM: 78%. The cerebrospinal fluid analysis showed: increased cellularity: 18%; elevated protein: 36%; antigangliosides IgG: 67%; antigangliosides IgM: 33%; immunocomplexes: 36%. In spite of the absence of an adequate control group and of the small number of patients, the multidisciplinary approach leads to a better characterization of the nervous system involvement in this disease.
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PMID:[Psychic changes in systemic lupus erythematosus: a multidisciplinary prospective study]. 196 71

EEG abnormalities in migraine have been reported by a number of authors during the last 50 years. Prevalences vary considerably in the older literature. A number of unspecific rhythms related to drowsiness or hyperventilation have probably been counted as "abnormal", and the reported numbers of definitely abnormal EEG rhythms have been consistently low. In a few controlled and blinded studies, however, slight excess of various EEG rhythms has been found in migraine patients. Similar prevalences of interictal EEG abnormalities have generally been found in patients with classic and common migraine, but the diagnostic classification may not have been precise enough in some studies. During visual aura, either slow waves, depression of background activity amplitude or normal EEG have been reported. The most definitely abnormal EEGs with unilateral or bilateral delta activity have been recorded during attacks of hemiplegic migraine, and during attacks of migraine with disturbed consciousness. The relationship between migraine and epilepsy has still not been adequately clarified. The connection seems to exist in several small entities (e.g. migraine-like headache as an epileptic manifestation, epileptic seizures triggered by epileptic attacks, and possibly in epilepsies with occipital spike waves), but it is seemingly not "fundamental". Newer methods, i.e. EEG frequency analysis and topographic brain mapping, are promising tools in this field. So far, mostly small studies have been published with somewhat inconsistent results. A pattern of increased alpha rhythm variability (and/or asymmetry) in the headache-free phase seems to emerge, however. Significant asymmetry of alpha and theta during headache has been reported in one topographic brain mapping study. Magnetoencephalographic studies of migraine patients have demonstrated slow wave-shifts (similar to those observed in animals with spreading depression). The EEG patterns observed in migraine patients seem to suggest a possible physiological connection between sleep, hyperventilation and migraine. The study of such relationship may shed new light on migraine pathophysiology.
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PMID:EEG in migraine: a review of the literature. 205 54

Breathing rate (RR), end-tidal percent CO2, and EEG were obtained in three groups: psychiatric referral subjects presenting with anxiety, panic phobia, depression and migraine; a group of idiopathic seizure sufferers; and a group of asymptomatic controls. Virtually all the noncontrol subjects were found to show moderate to severe hyperventilation and the accompanying EEG dysrhythmia. The seizure group subjects were taught diaphragmatic respiration with end-tidal percent CO2 biofeedback. The training normalized their respiration and altered their EEGs and seizure frequency.
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PMID:Effect of diaphragmatic respiration with end-tidal CO2 biofeedback on respiration, EEG, and seizure frequency in idiopathic epilepsy. 212 89

Fourty epileptic and 66 migraine patients were examined. The differences in clinical features of headache paroxysms, consciousness disorders, psycho-sensory++, viscero-autonomic++ and affective spells were determined. The elements of confused consciousness, short-lived and local autonomic responses were characteristic of seizure-free epileptic attacks. Migrainous paroxysms were multiform and pronounced in terms of autonomic disorders, had lesser depth and incidence of consciousness disorders with longer lasting vaso-autonomic++ crises.
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PMID:[Seizure-free paroxysms in epilepsy and migraine]. 217 Dec 68

To better understand and treat painful conditions, one needs to identify the cause, discover the source, and develop knowledge of peripheral and central pain transmission; headaches are no exception. The development of appropriate animal models is important. Accordingly, we have reviewed the anatomy, neurochemistry, electrophysiology, and pharmacology of the trigeminovascular system in experimental animals and emphasized whenever possible the relevance of this final common pathway to migraine, cluster, and other headache syndromes in humans. For example, based on recent anatomic dissections, the pericarotid cavernous sinus plexus was suggested as an important focus to investigate cluster headache pathophysiology. This plexus is an anatomic point of convergence for the nerves giving rise to the signs of sympathetic and parasympathetic activity and sensory symptoms that develop in cluster patients. As in other nociceptive systems, trigeminovascular axons assume at least two important roles. One concerns the transmission of nociceptive information. Electrophysiologic evidence supports the trigeminal nucleus caudalis as an important site for the convergence of visceral (vessel) and somatic (forehead) inputs to mediate the referral of vascular pain to superficial tissues. A second important role concerns the initiation of local increases in blood flow and enhanced protein permeability (sterile inflammation) via the axonal release of vasoactive neuropeptides. Plasma extravasation develops within the dura mater following trigeminal stimulation. Extravasation can be blocked by the administration of ergot alkaloids or sumatriptan, a new serotonin-like agonist, and a prejunctional (neuronal) mechanism of action for these drugs (such as blockade of release) was suggested based on experimental evidence. Whether vasoconstriction also relates to the therapeutic efficacy remains to be determined. As in other organ systems, real or threatened tissue injury provides an important stimulus for depolarizing sensory fibers. The stimulus may come from external conditions such as reduced blood flow or hypoglycemia. The brain may also possess intrinsic neuronal mechanisms by which nociceptors may be synthesized (e.g., glutamate-induced neurotoxicity, seizures). Molecules of relevance include bradykinin, prostaglandins, leukotrienes, and potassium. Experimental evidence was presented demonstrating that the trigeminal nerve mediates hyperemia within cortical gray matter by axon-reflex like mechanisms. An important role for this nerve was established during the hyperemic period of recirculation after ischemia or during severe hypertension above the limits of autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Basic mechanisms in vascular headache. 217 82

Transient global amnesia is often attributed to a seizure, vascular cause, or migraine, but the outcome is usually benign. The presence of migraine and important risk factors for stroke necessitates close patient monitoring. Anti-platelet therapy should be considered.
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PMID:Transient global amnesia. 219 58


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