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

The cause of transient global amnesia (TGA) remains controversial. Focal cerebral ischemia, seizure, venous congestion, and migraine have all been proposed as underlying mechanisms. We describe a patient presenting with typical TGA who two days later developed a posterior circulation stroke due to basilar artery occlusion. He was treated successfully with intra-arterial thrombolytic therapy. Shortly thereafter, he had recurrent basilar artery thrombosis and jugular vein thrombosis, and was found to have a mucinous adenocarcinoma believed to be causing a hypercoagulable state. We believe this case supports the hypothesis that TGA can on occasion be caused by cerebral ischemia.
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PMID:Transient global amnesia heralding basilar artery thrombosis. 1631 Nov 49

The two main aetiologies of transient amnesia in the elderly are idiopathic transient global amnesia (TGA) and iatrogenic or toxic amnesia. Vascular and epileptic amnesia are less common. According to the literature, transient psychogenic amnesia, which is a frequent cause of amnesia at age 30 to 50, is very rare in the elderly. TGA is the prototypical picture of transient amnesia. It occurs more often after age 50, with no identified cause, even if some authors accept emotional stress or minor head trauma as occasional precipitants. The mechanism of TGA remains a matter of discussion. It may be the consequence of a spreading depression similar to that described in migraine with aura, but other arguments support an ischemic mechanism. Iatrogenic amnesias are mainly caused by benzodiazepines (BZs) or anticholinergics. The former may occur in a non-anxious subject, who is not a usual consumer of BZ and takes a single dose. The latter are more often due to a hypersensitivity to anticholinergic drugs, in particular in patients presenting with a covert, incipient Alzheimer's disease. A vascular origin must be considered when amnesia is accompanied by other neurological symptoms, and when the regression of the amnesic disorder is slow, lasting several days. It results from lesions involving various mechanisms and locations, mainly subcortical. Partial seizures, most often mesio-temporal, more rarely frontal, may be the cause of transient amnesia in the elderly, in the absence of a past history of epilepsy. The red flag supportive of an epileptic origin is the repetition of stereotyped amnesic episodes. EEG demonstration of seizures may be difficult and the response to antiepileptic drugs effective on partial seizures is usually good.
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PMID:[Transient amnesia in the elderly]. 1655 16

We describe 30 patients with "epileptic amnesic syndrome" (EAS) with adult-senile onset of a severe memory complaint that started before or at the same time as stereotyped seizures with only short loss of contact and automatisms. Because the seizures were not obvious or disturbing, they remained undiagnosed for a long time. Twenty-three patients also had attacks of transient anteroretrograde amnesia after the seizures: "epileptic amnesic attacks" (EAA). These are similar to attacks of transient global amnesia but are more frequent, shorter, accompanied by clear-cut clinical epileptic manifestations, and respond favorably to antiepileptic drug (AED) therapy. Interictal neuropsychological investigation ruled out global mental deterioration, showing only selective memory impairment in a few long-term tasks, and subjective and objective improvement after AED. Bilateral deep discharges involving the hippocampal-mesial temporal lobe regions may explain EAA, which is probably a postictal phenomenon. The interictal memory problems may be due to subclinical discharges causing difficulty in codification or consolidation of the amnesic trace. EAS patients having uniform anamnestic, clinical and neuropsychological features represent a particular type of temporal lobe epilepsy. We propose a definition of EAS, according to which cases can be classified as definite, probable or possible forms.
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PMID:Epileptic amnesic syndrome: an update and further considerations. 1710 76

Little is known about the pathophysiology of transient global amnesia (TGA) and how it is related to epilepsy. We report here five typical episodes of TGA, each occurring several years after surgery for epilepsy. In all cases, patients were seizure-free after a surgery consisting of anterior temporal lobectomy for refractory medial temporal lobe epilepsy associated with hippocampal sclerosis (n = 4) or linked with a dysembryoplastic neuroepithelial tumour (n = 1). Investigations, including MRI or CT scan, angio-MRI or echocardiogram or vascular echo Doppler, excluded a vascular origin. Using accepted criteria to distinguish between TGA and epileptic amnesic attacks--the typical clinical presentation, the long duration of the episode, the absence of other symptoms associated with seizures and the absence of recurrence--it is evident that these patients suffered a TGA. These studies suggest that hippocampal resection carried out therapeutically in some epileptic patients may be a precipitating factor for TGA.
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PMID:Is anterior temporal lobectomy a precipitating factor for transient global amnesia? 1803 54

Sildenafil, a phosphodiesterase-5 inhibitor commonly used for erectile dysfunction, may also have a beneficial therapeutic effect in the treatment of stroke, subarachnoid hemorrhage, dementia, learning, and neurodegenerative disorders by enhancing angiogenesis and neurogenesis. It also favorably influences the nitric oxide-cyclic guanosine monophosphate pathways, which are involved in the pathogenesis of a number of neurological diseases. Its potential therapeutic role in the treatment of the neurological disorders mentioned above is still under preclinical investigation. Sildenafil is currently being used to treat erectile dysfunction in patients with multiple sclerosis, Parkinson disease, multisystem atrophy, and spinal cord injury by improving their neurologically related erectile dysfunction. Conversely, it has been implicated in a number of neurological problems, such as intracerebral hemorrhage, migraine, seizure, transient global amnesia, nonarteritic anterior ischemic optic neuropathy, macular degeneration, branch retinal artery occlusion, and ocular muscle palsies. Thus, preclinical and very limited clinical data suggest that sildenafil may have therapeutic potential in selected neurological disorders. However, numerous reports are available regarding neurological adverse events ascribed to the drug. Although sildenafil shows some promise as a therapeutic agent in selected neurological disorders, well-designed clinical trials are needed before the agent can be recommended for use in any neurological disorder.
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PMID:Role of sildenafil in neurological disorders. 1905 Apr 13

Diagnosis of epileptic seizure may be difficult in older patients because seizure manifestations are often unusual: confusion, paresis... and because there are multiple differential diagnoses (syncope, transient ischemic attack, transient global amnesia...). To promote and facilitate the diagnosis of seizures in the elderly, neurologists and gerontologists must work together and focus their strategy on two points: firstly, the knowledge of the specific presentation of seizures in elderly patients, and secondly, the adoption of a reasoning based on seizures and not epileptic syndromes. A multidisciplinary group worked on epilepsy of the elderly to elaborate an electro-clinical score which aims to help establish the diagnosis of epilepsy in elderly patients in different clinical settings. This electro-clinical score is based on a systematic review of scientific literature and the recommendations are explicitly linked to supporting evidence. Further, clinical validation of the electro-clinical score is required.
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PMID:[Specificity of epileptic seizures in the elderly: A proposed electro-clinical scale]. 1915 Jul 24

We report the clinical findings and neuropsychological profiles of a sample of patients exhibiting a focal retrograde amnesia (FRA) seen consecutively during the period 1992-2007. The cohort comprised 13 patients, five males, with a mean age of 30 years (range 16-49). They were given a neurologic examination, psychiatric interview and formal neuropsychological examination (all but one) during the amnesic phase, underwent neuroimaging, and were followed up for six months to ten years. All presented with an acute amnesia characterized by an impaired recollection of memories predating the acute event, with spared or minimally and transiently affected anterograde memory, thus consistent with FRA. The events triggering FRA varied widely: mild to severe head injury, road accident without head injury, seizure, dissociative fugue, BDZ overdose, posttraumatic headache, syncope, migraine attack, acute distress. The neuropsychological hallmark of FRA was a selective or prominent impairment of autobiographical memory. The defect was often so severe as to cover most or all of the patients' lives and, in some cases, to erase the knowledge of their own identity. Conventional neuroimaging (brain CT and MRI) was unimpressive. Cerebral SPECT/PET disclosed unilateral frontal hypoperfusion in three (two left). All but one patient fully recovered, time of recovery ranging from three days to six months. FRA is a condition reflecting a block of memory function triggered by heterogeneous events, including both physical and psychic insults. Analogies shared with the more frequently encountered and better known condition of transient global amnesia suggests common pathogenetic mechanisms. A tentative nosographic classification of FRA is finally offered.
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PMID:When the past is lost: focal retrograde amnesia. Focus on the "functional" form. 1964 Dec 49

In this case report and review of the literature, transient global amnesia (TGA) is discussed. A 72-year-old physician presented to the emergency department with sudden loss of memory. In particular, he was unable to recall recent events. Other neurological examination was intact. The loss of recent memory was completely resolved, during the next 4 hours. This event (TGA) must be distinguished from other neurological events such as transient ischemic attacks, seizures, and cerebral vascular events. A literature review suggested that TGA is related to an acute loss of function in the temporal lobe. It is important for palliative medicine physicians to have this unusual syndrome in their differential diagnosis, as this cause of memory loss must be separated from more aggressive causes of memory loss, for example, stroke and seizure. Transient global amnesia is a self-limiting disorder without late consequences.
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PMID:Transient global amnesia: a case report and literature review. 2217 16

Transient amnesic syndromes are striking clinical phenomena that are commonly encountered by physicians in acute medical settings. Diagnosis of such syndromes can be challenging, and their causes have been debated for over 50 years. Critical clinical distinctions, such as between transient global amnesia (TGA) and transient epileptic amnesia (TEA), as well as important clues to the underlying pathophysiology, have recently been revealed. TGA is characterized by the sudden onset of a profound anterograde and retrograde amnesia that lasts for up to 24 h, with neuroimaging after an acute TGA event showing transient perturbation of specific hippocampal circuits that are involved in memory processing. Some cases of transient amnesia are attributable to focal seizure activity and are termed TEA, which has a clinical presentation similar to that of TGA, but can be distinguished from the latter by the brevity and frequency of amnesic attacks. Moreover, TEA carries a risk of persistent memory impairment that can be mistaken for dementia. Here, we summarize clinically relevant aspects of transient amnesic syndromes, giving practical recommendations for diagnosis and patient management. We describe results from imaging and epidemiological studies that have shed light on the functional anatomy and pathophysiological mechanisms underlying these conditions.
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PMID:Transient amnesic syndromes. 2329 43

Anti-glutamic acid decarboxylase directed antibodies are a rare cause of autoimmune limbic encephalitis that is relatively resistant to immunotherapy. Here we report a 15-year-old boy with nonparaneoplastic, anti-glutamic acid decarboxylase limbic encephalitis presenting with subacute headache, memory disturbance, psychiatric symptoms, and seizures. At onset, his memory disturbance manifested as transient global amnesia-like episodes. Clinical remission was achieved with rituximab, intravenous immunoglobulin, and corticosteroids.
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PMID:Anti-glutamic Acid decarboxylase antibody associated limbic encephalitis in a child: expanding the spectrum of pediatric inflammatory brain diseases. 2409 95


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