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

Transient global amnesia is a clinical syndrome characterized by sudden onset of short-term memory loss followed by retrograde amnesia in an otherwise healthy subject. During the attack, the patient remains alert and retains much of his personal identity. The patient usually becomes upset and concerned about his memory loss. This condition may be diagnosed incorrectly as hysteria, psychosis, or temporal lobe seizure, despite its unique clinical features.
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PMID:Transient global amnesia. 42 19

The postconcussion syndrome refers to a large number of symptoms and signs that may occur alone or in combination following usually mild head injury. The most common complaints are headaches, dizziness, fatigue, irritability, anxiety, insomnia, loss of consciousness and memory, and noise sensitivity. Mild head injury is a major public health concern because the annual incidence is about 150 per 100,000 population, accounting for 75% or more of all head injuries. The postconcussion syndrome has been recognized for at least the last few hundred years and has been the subject of intense controversy for more than 100 years. The Hollywood head injury myth has been an important contributor to persisting skepticism and might be countered by educational efforts and counter-examples from boxing. The organicity of the postconcussion syndrome has now become well documented. Abnormalities following mild head injury have been reported in neuropathologic, neurophysiologic, neuroimaging, and neuropsychologic studies. There are multiple sequelae of mild head injury, including headaches of multiple types, cranial nerve symptoms and signs, psychologic and somatic complaints, and cognitive impairment. Rare sequelae include hematomas, seizures, transient global amnesia, tremor, and dystonia. Neuroimaging and physiologic and psychologic testing should be used judiciously based on the problems of the particular patient rather than in a cookbook fashion. Prognostic studies clearly substantiate the existence of a postconcussion syndrome. Manifestations of the postconcussion syndrome are common, with resolution in most patients by 3 to 6 months after the injury. Persistent symptoms and cognitive deficits are present in a distinct minority of patients for additional months or years. Risk factors for persisting sequelae include age over 40 years; lower educational, intellectual, and socioeconomic level; female gender; alcohol abuse; prior head injury; and multiple trauma. Although a small minority are malingerers, frauds, or have compensation neurosis, most patients have genuine complaints. Contrary to a popular perception, most patients with litigation or compensation claims are not cured by a verdict. Treatment is individualized depending on the specific complaints of the patient. Although a variety of medication and psychologic treatments are currently available, ongoing basic and clinical research of all aspects of mild head injury are crucial to provide more efficacious treatment in the future.
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PMID:The postconcussion syndrome and the sequelae of mild head injury. 143 59

Thirteen patients with "epileptic amnesic syndrome" (EAS) presented with adult-senile onset of a severe memory complaint that started before or at the same time as seizures. All were diagnosed as temporal lobe epilepsy (TLE). The seizures were stereotyped, with only short loss of contact and oral automatisms, and because they were not obvious or disturbing, they remained underdiagnosed for a long time. Nine cases also presented attacks of transient anteroretrograde amnesia after the seizures--called "epileptic amnesic attacks" (EAA)--during which the patients were able to perform complex actions. EAA are similar to the attacks of transient global amnesia (TGA) but are more frequent, shorter, accompanied by clear-cut clinical and electroencephalographic epileptic manifestations, and respond favorably to antiepileptic therapy. Neuropsychological investigation ruled out global mental deterioration, showing only selective memory impairment in a few long-term tasks and dissociation between formal findings and the relevant memory complaint. These cases have uniform anamnestic, clinical, and neuropsychological characteristics and represent a particular clinical expression of TLE, namely EAS. We suggest that an epileptic origin be entertained in patients presenting repeated amnesic attacks resembling TGA or who complain of persistent memory disturbance, after more common etiologies have been excluded.
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PMID:Epileptic amnesic syndrome. 148 32

A case control study of transient global amnesia (TGA), transient ischaemic attacks (TIA) and normal controls is described. Each of the 51 TGA patients, selected between January 1985 and March 1990, was compared with four controls (two TIAs and two normals) for the presence of vascular risk factors (hypertension, diabetes, smoking habits, cholesterol, triglycerides and haematocrit levels, heart disease, previous stroke), previous TGA, migraine, psychiatric illness and recent head trauma. Patients with TGA had less diabetes, hypercholesterolaemia and hypertriglyceridaemia than TIA. TGA subjects had significantly more hypertension (odds ratio = 3.31) and migraine (odds ratio = 8.67) than normal controls. During a mean of 17.4 mths of follow-up (range 1-96 mths), three subjects had recurrent TGA, one sustained a TIA and a minor stroke, but none had seizures. Thrombo-embolism and epilepsy are unlikely to be the cause of this benign disorder. The role is stressed of appropriate precipitants, including haemodynamic changes, and of individual susceptibility (of which migraine is probably a marker) in the genesis of TGA.
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PMID:Transient global amnesia. A case control study. 155 58

Pure amnestic seizures (PAS) sometimes occur in patients with temporal lobe epilepsy. They never represent the only type of seizures in these patients. Pure amnestic seizures are defined as seizures during which the only clinical manifestation is the patients' inability to retain in memory what occurs during the seizure coupled with the preservation of other cognitive functions and the ability to interact normally with their physical and social environment. It is postulated that PAS result from selective ictal inactivation of mesial temporal (MT) structures without isocortical involvement. This occurs most often in patients with neuropsychological and electroencephalographic (EEG) evidence of bilateral dysfunction of MT structures (six out of eight patients in this study). In the few patients without such evidence as well as in some with bilateral MT dysfunction, PAS may result from seizure discharge limited to the MT structures of both temporal lobes. In the light of current anatomical knowledge, contralateral spread of seizure discharge from the MT structures of one side to those of the other through the dorsal hippocampal commissure is the only likely explanation for this situation. One observation with depth electrode stimulation of MT structures supports this view. In patients with evidence for bilateral MT dysfunction, a unilateral seizure may presumably suffice to induce a PAS, the contralateral MT structures being unable to ensure normal memory function. In most instances PAS can be distinguished from episodes of transient global amnesia on clinical grounds.
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PMID:Pure amnestic seizures in temporal lobe epilepsy. Definition, clinical symptomatology and functional anatomical considerations. 162

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

The P3 evoked potential has been linked to memory mechanisms, but its neuronal generators are uncertain. Transient global amnesia (TGA) is a disorder of recent memory that has been postulated to result from ischemia or focal seizures in the medial temporal lobes and/or thalamus. To our knowledge, this is the first report of a recording of P3 evoked potential and sphenoidal electroencephalogram during TGA. The tonal P3 was not decremented in comparison to P3 recordings one month and two years after recovery. Sphenoidal electroencephalogram was normal. The results suggest that the neuronal networks which generate the tonal P3 are not involved in the part of the memory system affected by TGA.
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PMID:The P3 evoked potential and transient global amnesia. 312 55

Transient global amnesia (TGA) was formerly supposed to have an epileptic origin thought unlikely by more recent authors. Further, epileptic seizures rarely present transient memory dysfunction as prominent symptom. These particular cases of which we report here three examples were previously identified as epileptic amnesic attacks (EAA). They have uniform clinical characteristics quite different from TGA and respond favorably to antiepileptic therapy. The features differentiating these two conditions are discussed. The authors suggest that an epileptic origin should be considered in patients presenting frequent transient amnesic attacks.
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PMID:Epileptic transient amnesia. 317 Jan 70

Fifty-five patients admitted to hospital for 'pure' transient global amnesia (TGA) were studied and followed up for a period ranging from 12 to 67 months. The major pathogenetic theories of TGA (epileptic, thrombotic and migrainous) were investigated through the study of clinical histories and risk factors and the recurrences of neurological disturbances during follow-up. Seventy-one percent of the sample had one or more thrombotic risk factors (TRF), 2 patients had both TRF and a history of migraine, and none ever experienced a seizure. A computerized tomography (CT) scan was performed in 40 out of 55 patients to detect focal lesions: 3 patients (7.5%) had a lacuna in the deep structures of the brain. Over the follow-up period, 1 patient died from hepatic cirrhosis, 1 patient died from cerebral haemorrhage, 2 patients experienced transient ischaemic attacks and 3 patients had a total of 4 TGA recurrences. Our conclusion is that TGA represents a benign form of transient ischaemic cerebral disease.
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PMID:Transient global amnesia: pathogenesis and prognosis. 337 81

Electroencephalographic recordings were obtained during 13 episodes of transient global amnesia in 13 patients. Eight were entirely normal; none showed seizure discharges or other epileptiform activity. Electroencephalographic recordings were also obtained after 103 episodes of amnesia in 96 patients with transient global amnesia (TGA) alone, five patients who had both TGA and epilepsy independently, and three patients with amnesia related to epilepsy. The majority (60.8%) of waking records were normal during or after episodes of TGA. Mild or moderate and nonfocal abnormalities were found in a minority. Genuine epileptiform activity was observed only among patients who had seizure disorders. Amnestic episodes attributable to seizures were more brief and more apt to be repeated than TGA and usually responded to anticonvulsant drugs. Differentiation of TGA from epilepsy is essential for appropriate management.
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PMID:Transient global amnesia and epilepsy. Electroencephalographic distinction. 357 80


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