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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Migraine is conventionally regarded as a specific type of headache with a small set of associated neurologic symptoms. Yet, the true scope and frequency of migrainous phenomena are much greater than is generally acknowledged. Six cases are presented to illustrate some of the diverse manifestations of migraine: (1) transient global amnesia, (2) persistent visual phenomena, (3) migraine and seizures, (4) vestibular dysfunction, (5) hearing loss, and (6) migraine masquerading as multiple sclerosis. These and other migraine-associated neurologic symptoms are discussed in relation to previous reports in the literature. Pitfalls in recognizing the diverse manifestations of migraine, which are often underdiagnosed or misdiagnosed, are reviewed. Whether or not the established diagnostic criteria for migraine are too strict, other factors contributing to failure to identify migraine when it causes nonclassic neurologic symptoms include: (1) the belief that these are rare, (2) lack of an objective measure for migraine, (3) inadequate attention to the positive diagnostic features of migraine in the absence of headache, (4) confusion regarding prior migraine history, and (5) dismissing the diagnosis because of reported failure of prior migraine treatment. Recognition of the diversity of migraine helps avoid unnecessary testing and opens the door to effective treatment.
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PMID:The menagerie of migraine. 887 61

Patients who experience episodes with a transient disturbance in perception, memory, mood, and level of anxiety are frequently encountered by neurologists, psychiatrists, and psychologists. The possibilities for differential diagnosis of these episodes include partial complex epilepsy, psychogenic seizures, panic disorder, dissociative states, migraine, and transient global amnesia, among others. The clinical history may be vague and confusing, making it difficult to determine definitively the etiology of the events. This article describes a spectrum of paroxysmal disorders involving limbic structures, highlighting the clinical features and assessment techniques that aid in diagnosis and treatment. Clinical-anatomic correlations are provided whenever possible.
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PMID:Paroxysmal limbic disorders in neuropsychiatry. 927 42

The pathophysiology of transient global amnesia (TGA) has been obscure since the definition of this syndrome more than 30 years ago. Current hypotheses include migraine, seizure, or transient cerebral arterial ischaemia. However, none of these potential mechanisms explain both the absence of other neurological signs or symptoms during TGA, and its frequent precipitating activities: many of which would be expected to result in marked increases in venous return from the arms to the superior vena cava. Patients with TGA also commonly have a Valsalva manoeuvre at the onset of attacks. I suggest that a Valsalva manoeuvre, blocking venous return through the superior vena cava, may allow brief retrograde transmission of high venous pressure from the arms to the cerebral venous system, resulting in venous ischaemia to the diencephalon or mesial temporal lobes and to TGA.
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PMID:Aetiology of transient global amnesia. 1155 19

The transitory memory disturbance known as transient global amnesia (TGA) remains an enigma from a pathogenic point of view. In spite of its typical benign prognosis, TGA is a frightening experience for patients and their relatives. Moreover, a TGA episode usually leads to extensive investigation of patients in search of organic alterations that might be responsible for the event. Finally, TGA generates queries about therapeutic choices. In this review, we critically re-evaluate the evidence in support of and against the three main pathogenic hypotheses (i.e. ischemia, seizure discharge, and migraine), and we conclude that none of these appears completely convincing. Given the good prognosis and the lack of association with organic and instrumental abnormalities, we advance the hypothesis that TGA may be related to psychological disturbances causing transient alteration in brain metabolism and, consequently, amnesia. Our conclusion has relevant consequences in the evaluation of patients with TGA.
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PMID:Transient global amnesia: a review emphasizing pathogenic aspects. 1108 3

This article addresses syndromes that clinically and/or radiologically resemble acute stroke. These syndromes generally fall into four categories. (1) Patients with acute neurological deficits with nonischemic lesions and no acute abnormality on diffusion-weighted images. These patients may have peripheral vertigo, migraines, seizures, dementia, functional disorders, amyloid angiopathy, or metabolic disorders. When these patients present, we can confidently predict that they are not undergoing infarction. (2) Patients with ischemic lesions with reversible clinical deficits. Nearly 50% of patients with transient ischemic attacks have lesions with restricted diffusion. Patients with transient global amnesia may have punctate lesions with restricted diffusion in the medial hippocampus, parahippocampal gyms, and corpus callosum. (3) Vasogenic edema syndromes that may mimic acute infarction clinically and on conventional imaging. These include eclampsia/hypertensive encephalopathy, other posterior leukoencephalopathies, human immunodeficiency virus encephalopathy, hyperperfusion syndrome following carotid endarterectomy, venous sinus thrombosis, acute demyelination, and neoplasm. These syndromes demonstrate elevated diffusion rather than the restricted diffusion associated with acute ischemic stroke. (4) Entities in which restricted diffusion may resemble acute infarction. These include pyogenic infections, herpes virus encephalitis, Creutzfeldt-Jakob disease, diffuse axonal injury, tumors with dense cell packing, and rare acute demyelinative lesions.
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PMID:Diffusion-weighted imaging as a problem-solving tool in the evaluation of patients with acute strokelike syndromes. 1114 28

Disorders or complaints of memory are a frequent cause of consultation in depression, major anxiety and psychiatry disease with personality disorders. We report 3 patients with obsessive compulsive disorder (OCD), without diagnosis and treatment, examined in a specialized memory consultation. They always had OCD with cognitive checking. Diagnosis of transient global amnesia and temporal complex seizure were discussed in 2 cases. Psychometric impairment only was observed in first free recall of a verbal memory task and was no specific. Behavioural during testing seemed to be very important to analyse. First, a 49-year-old man consulted because he had stereotyped transient amnesia lasted one minute, 2 or 3 times a week, since 6 months. He was a teacher. Transient amnesia always occurred during lessons. Suddenly he didn't know where he was or what he was speaking about. Episodes lasted one minute. After them, he had no confusion and no difficulty in concentration but intense anxiety. In an another hand, when he was in his car, after lessons, he could forget where he was during some minutes. CT scan and EEG were normal. Neuropsychological tests only objectived impairment in first free recall of Grober and Buschke's words. Patient explained that he could not prevent to check responses. He told us checking obsessive compulsive disorder during since long time ago. We discussed clear differences which existed between seizure and ruminations or preoccupations. Secondly, a 55-year-old woman was afraid of her memory performances. She was medical secretary and had no problem in her work but she would like a memory consultation to reassure herself. She was neither depressed nor anxious. She presented curious production in fluency task. She had to produce as many animals's names as possible: she could say 35 names which was an excellent performance but only in alphabetic order! Neuropsychological tests objectived impairment in her first free recall of Grober and Buschke's words. She tried in her first free recall to remember words in alphabetic order. She explained how she was bound to range everything in alphabetic order! She had a lot of rituals. She thought that she had an obsessive compulsive disorder but never consulted about this. The observation illustrated suspiscions about memory operations which could be observed in patients group with obsessive compulsive disorders. Finally, a 62-year-old man told us that he had presented a transient global amnesia during 4 hours. He had an important appointment and was upset about that. He didn't go to it and wandered in his flat. He always asked the same questions and forgot everything. He had no neurological deficit. He was anxious, sad and cried several times. He perfectly remembered the episod and thought that he had a panic attack! Verbal memory tests only objectived difficulties in his first free recall of Grober and Buschke words as the two others patients. He had a story of obsessive compulsive disorder with checking and rituals. In this observation, we discussed clear differences which existed between panic attacks and global transient amnesia. We analyzed patterns of neuropsychological performances which illustrated clinical features of obsessive compulsive disorder. These three patients impaired in their first free recall of verbal memory task. It is not a specific result. We observed during psychometric evaluation, strategic processing which impaired episodic memory: patients tried to check their performances. Memory complaints only were observed in checking obsessive compulsive disorder. It is a difficulty or a doubt about memory capacities. Difficulties could be due to particular cognitive processes who pertubate normal memory capacities.
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PMID:[Amnesic presentations of the compulsive obsessional confusions (about 3 patients appearing in a consultation of memory)]. 1197 42

The etiology of transient global amnesia is poorly understood, particularly in children and young adults. Transient global amnesia may follow a wide range of precipitating events. Proposed causes have included vascular event, seizure, and migraine. A young man with cyanotic congenital heart disease experienced an episode of transient global amnesia in the setting of polycythemia. Differential diagnosis of acute confusional episodes in children should include transient global amnesia, as well as confusional migraine, and should include evaluation for underlying coagulation abnormalities and polycythemia.
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PMID:Transient global amnesia in a young adult with cyanotic heart disease. 1464 97

Numerous studies have shown the pathological influence anti-phospholipid antibodies (APLA) have on the physiology of the single neuron as well as the function of the entire human nervous system. The influence is well demonstrated in the antiphospholipid syndrome (APS). This syndrome is characterized by a triad of arterial or venous thrombotic events, recurrent fetal loss and thrombocytopenic purpura. The syndrome exhibits different neurological pathologies such as: chorea, seizures, transverse myelopathy, migraine, cerebral ataxia, hemiballismus and transient global amnesia, which are not fully explained by the procoagulopathic trait of APLA. A study on mice induced with APS demonstrated hyperactive behavior when compared to the control group. The information gathered from these different studies raised the question whether APLA has any part in the etiology of Attention Deficit/Hyperactive Disorder (ADHD) in children. We compared 41 children diagnosed with ADHD to a control of 28 healthy children. Blood drawn from the two groups was screened using ELISA for the presence of anti-cardiolipin antibodies, anti-beta2GP antibodies, anti-phosphatidyleserine antibodies and anti-ethanolamine antibodies. The results show no significant difference in the level of antiphospholipid antibodies (APLA) measured between the children diagnosed with ADHD and the control group.
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PMID:Lack of association between anti-phospholipid antibodies (APLA) and Attention Deficit/Hyperactivity Disorder (ADHD) in children. 1476 40

The emergence of a sudden, global, and fully reversible amnestic state during an intracarotid amobarbital procedure (IAP) performed in a patient with a right temporal tumor is described. Forms of amnesia during the IAP are discussed, and it is argued that because of its appearance, the associated behavioral abnormalities, and EEG findings, this state was a transient global amnesia (TGA). In addition to other origins such as bitemporal lesions, increased barbiturate levels, seizures, and epileptic amnesia, TGA may triggered by stress or angiography during the IAP.
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PMID:Transient global amnesia triggered by the intracarotid amobarbital procedure. 1571 Mar 18

Transient global amnesia (TGA) is a disorder of unknown aetiology, characterized by sudden loss of anterograde memory, in the absence other neurological signs or symptoms, followed by complete recovery in less than 24h. Precipitating actions such as strenuous physical activity or valsalva-like manoeuvres are frequently reported. Since first described in 1958, by Fisher and Adams, the possible pathophysiology has undergone much speculation. Nonconvulsive epileptic seizures, migraine, paradoxical embolism thorough a patent foramen ovale, and transient ischemic attacks have been proposed as potential mechanisms. One of the latest hypotheses is that venous congestion causes either ischemia or induces spreading depression in the medial temporal lobes. It has been demonstrated that retrograde flow in the internal jugular veins occurs more frequently during valsalva manoeuvres in TGA patients than in controls, supporting a dysfunctional venous circulation as part of the pathogenesis. However, earlier hypotheses typically fail to explain the relatively low recurrence rate of TGA, lack of comorbidity and the relation to precipitating events. If cerebral venous hypertension was the solely cause of TGA it would presumably be much more common with very high recurrence rates among those predisposed of the condition. Structural changes observed in MRI and SPECT studies along with reports of mild cognitive impairment lasting much longer than the amnestic episodes, indicate that TGA is less transient and perhaps somewhat less benign than earlier believed. Many cases of TGA seem to be associated with factors of increased risk of cerebral venous thrombosis, such as polycythemia, antiphospholipid antibodies, venous hypertension, female sex and more. We suggest that most cases of TGA may be due to small thrombi in the deep cerebral venous system. Small venous thrombi may difficult to visualize even when using modern imaging technology. Further studies of TGA patients with for example blood analysis of D-dimer together with MR venography or CT venography could be done to evaluate this new hypothesis.
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PMID:Transient global amnesia may be caused by cerebral vein thrombosis. 1606 28


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