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

We investigated the efficacy of the intracarotid amobarbital procedure to accurately predict post-temporal lobectomy anterograde amnesia. We presented items at 2 separate times during amobarbital assessment; both early and late item recall were decreased during the injection contralateral to seizure onset indicating sensitivity to bilateral temporal lobe dysfunction. Ten patients for whom follow-up neuropsychological assessment was available failed either the early or late item recognition portions of their amobarbital evaluation ipsilateral to seizure onset, but had hippocampus included in the temporal lobectomy by virtue of satisfactory performance on other tests of hippocampal function. None of these 10 patients displayed postoperative anterograde amnesia, although there was a reduction in material-specific memory in some patients. These results indicate that relying solely on amobarbital memory testing to assess the functional ability of the contralateral temporal lobe to sustain global memory prior to temporal lobectomy may needlessly exclude patients from a viable therapeutic option.
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PMID:The intracarotid amobarbital procedure as a predictor of memory failure following unilateral temporal lobectomy. 232 Feb 33

Neurotoxic substances are discussed to cause neurodegeneration by acting as excitotoxins on glutamate receptors. We investigated the properties of L-beta-oxalyl-amino-alanine (L-BOAA) and 3,4, 6-trihydroxyphenlyalanine (6-OH-Dopa) at the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) glutamate receptor and that of L-BOAA and domoic acid at the kainate glutamate receptor in human hippocampus. (3H)AMPA binding in hippocampal subfields was inhibited by L-BOAA and 6-OH-Dopa with mean IC50-values in the low micromolar range. (3H)Kainate binding was inhibited by L-BOAA with similar potency as (3H)AMPA binding and by domoic acid with mean IC50-values in the low nanomolar range. These results support the notion that symptoms like anterograde amnesia and epileptic seizures seen in domoic acid intoxication and limbic symptoms, e.g. cognitive and mood impairment observed in neurolathyrism may be caused by excitotoxic action on non-NMDA receptors. The potent interaction of 6-OH-Dopa with the AMPA-receptor may point to a possible dopaminergic-glutamatergic interaction in the development of neurodegenerative diseases like Parkinson's and Huntington's disease.
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PMID:Interactions of neurotoxins with non-NMDA glutamate receptors: an autoradiographic study. 753 23

We report a patient with a generalized frontal-predominant nonconvulsive status epilepticus without clinically apparent altered consciousness. The patient was examined and EEG performed during and after the episode. Severe retrograde and anterograde amnesia during the seizure, contrasting with a preservation of ongoing memories formation that could be assessed only after its resolution, suggests a transient disconnection of access to stored representations. This unusual memory disorder is both clinically and electrographically dissimilar to other reported cases of transient epileptic amnesia. Although the patient probably had numerous episodes previously, there was no history of overt seizure.
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PMID:Failure to recall (but not to remember): pure transient amnesia during nonconvulsive status epilepticus. 919 4

Electroconvulsive therapy (ECT) is a highly effective treatment for major depression, but is also associated with characteristic cognitive side effects. Several reports document that endogenous opioids and their receptors are activated by electroconvulsive shock (ECS) and that naloxone in doses sufficient to block endogenous opioid receptors may reverse ECS-induced retrograde amnesia. This placebo-controlled, randomized, within-patient study was conducted to examine the potential of naloxone, given in doses sufficient to block opioid receptors (high dose), to ameliorate acute anterograde and retrograde memory impairments following ECT. Compared to placebo and low dose naloxone, high dose naloxone administered immediately before ECT resulted in significant reductions in anterograde amnesia, and better performance on an attention task. Both low and high dose naloxone improved verbal fluency. There were no beneficial effects of high dose naloxone on retrograde amnesia, and an indication that high dose naloxone may have worsened retrograde amnesia for shape stimuli. There were no effects of high dose naloxone on seizure duration, vital signs, and subjective side effects. The study is consistent with prior research in which change in behavioral and physiological measures was produced principally by naloxone doses sufficient to block endogenous opioid receptors and offers evidence of the potential for ameliorating some adverse cognitive effects associated with ECT.
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PMID:Naloxone in the prevention of the adverse cognitive effects of ECT: a within-subject, placebo controlled study. 1043 76

Classical benzodiazepine drugs are in wide clinical use as anxiolytics, hypnotics, anticonvulsants, and muscle relaxants. They act by enhancing the gamma-aminobutyric acid(A) (GABA(A)) receptor function in the central nervous system. The pharmacological relevance of the multitude of structurally diverse GABA(A) receptor subtypes has only recently been identified. Based on an in vivo point mutation strategy, alpha(1)-GABA(A) receptors were found to mediate sedation, anterograde amnesia, and part of the seizure protection, whereas alpha(2)-GABA(A) receptors, but not alpha(3)-receptors, mediate anxiolysis. Rational drug targeting to specific receptor subtypes has now become possible. Only restricted neuronal networks will be modulated by the new subtype-selective drugs. Promising new anxiolytics have already been developed. A new pharmacology of the benzodiazepine site is on the horizon.
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PMID:A new benzodiazepine pharmacology. 1175 90

Right unilateral (RUL) ECT is reported to have fewer memory side effects than bilateral (BL) ECT. We compared RUL ECT at eight times the seizure threshold (ST) against BL ECT at 1.5 times the ST. Adults with major depression were randomly assigned to RUL ECT at eight times ST or BL ECT at 1.5 times the ST. Blinded ratings of mood and memory were made before ECT, 1 to 3 days after the final ECT, and at 2 and 4 weeks after ECT. Forty patients received RUL and 37 received BL ECT. The antidepressant response rate was not significantly different for the RUL and BL groups (60% vs. 73%). Sustained antidepressant response, accompanied by recovery from anterograde memory side effects, was seen through the first month with both treatments. Measures of mood and memory were not significantly different for the two groups at any time point. The modest sample sizes of this study do not rule out a type II error in the detection of small but meaningful differences between assigned treatments. Also, the period of post-ECT observation consisted of 1 month of naturalistic treatment. Both RUL ECT at eight times the ST and BL ECT at 1.5 times the ST produce similar mood and memory effects. Both forms of ECT produced acceptable antidepressant response rates and only transient anterograde amnesia. No clear advantage emerged for either form of ECT, and both are justifiable as first-line techniques of ECT.
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PMID:Markedly suprathreshold right unilateral ECT versus minimally suprathreshold bilateral ECT: antidepressant and memory effects. 1279 64

Long-term amnesia is a slowly developing form of anterograde amnesia accompanied by retrograde amnesia of variable severity (Kapur, 1996; 1997) often associated with damage to the anterior temporal neocortex and epileptic seizures. The precise neural and functional deficits that underlie this condition are unknown. A patient, JL, who has this condition following a closed-head injury, is described in detail. Her injury caused bilateral anterior temporal neocortex damage that was more extensive on the left and right-sided damage to the perirhinal and orbitofrontal cortices. The hippocampus appeared to be intact bilaterally. Epilepsy developed within two years of JL's injury. Apart from her memory impairments, JL's cognitive functions, including high-level visual perception, attention, semantic memory and executive functions were well preserved. Her memory also seemed well preserved for at least 30 minutes following encoding. The one exception was the patient's relatively greater impairment at difficult visual recognition tests for which verbalization may not have been an effective strategy. This problem may have been caused by JL's right-sided perirhinal and orbitofrontal cortex damage. Her recall and recognition was clearly impaired after a three-week delay. She also showed a retrograde amnesia, which appeared to be milder than her remote post-morbid memory deficit. JL's remote memory was preserved for information first encountered in either the pre- or post-morbid period provided the information had received sufficient rehearsal over long periods of time. Her long-term amnesia may have been caused by anterior temporal neocortex damage, possibly in association with her epileptic seizures. Whether the condition is heterogeneous, involves a deficit in slow consolidation, disruption of unconsolidated memories, or blockage of maintenance or disruption of insufficiently rehearsed memories whether or not these have been slowly consolidated is discussed.
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PMID:Long-term amnesia: a review and detailed illustrative case study. 1458 44

Anterograde amnesia is a severely disabling state which has been reported as a consequence of bilateral mesiotemporal lesions in humans. In the present paper, recurrent epileptic seizures after temporal lobectomy are described as a rare cause of severe amnesia in two patients. Diffusion-weighted MRI in one patient showed cytotoxic edema during a nonconvulsive status epilepticus and subsequent progressive hippocampal atrophy within the following month. In the other patient, repeated conventional MRI revealed no structural abnormalities in the contralateral temporal lobe.
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PMID:Persistent severe amnesia due to seizure recurrence after unilateral temporal lobectomy. 1514 10

The authors report neuropsychological (NP) and serial quantitative magnetic resonance imaging (MRI) findings of a 29-year-old woman with lymphomatoid granulomatosis (LG). Disease course was characterized by acute psychosis, tremor, fever, seizures, and progressive cognitive impairment. At the time of symptom onset, brain MRI revealed mild lesion volume and normal parenchymal volume. This was followed by dramatic progression of brain lesions and atrophy over 2 years, at which point the patient expired. Atrophy was most prominent in the mesial temporal lobes. NP testing revealed marked amnesia and mild impairments in other cognitive domains. To our knowledge, this is the first recorded case of LG in which bilateral temporal lobe atrophy is evident and accompanied by anterograde amnesia. We speculate that temporal lobe atrophy was influenced by the established susceptibility of this region in various neurological diseases.
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PMID:Progressive cerebral disease in lymphomatoid granulomatosis causes anterograde amnesia and neuropsychiatric disorder. 1662 40

Cerebral amyloid angiopathy (CAA) can rarely be complicated by vascular and perivascular inflammation. Patients typically present with subacute cognitive decline, seizures, headaches, and hyperintensities on T2-weighted or fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) sequences. Little is known about the cause and natural history of inflammatory CAA, but recent case series show that some patients respond well to steroids. Here, we describe a patient who presented with severe subacute encephalopathy and was diagnosed with probable CAA-related inflammation based on characteristic MRI, showing subcortical FLAIR hyperintensities with mass effect and multiple cortical microbleeds, after excluding other possible causes of subacute delirium. Mental status examination markedly improved after a course of intravenous methylprednisolone, initially without significant change in MRI appearance. An MRI 4 months later, however, showed marked reduction in the volume of white matter T2 hyperintensities. Mental status remained improved with mild residual retrograde and anterograde amnesia. We propose that the diagnosis of CAA-related inflammation should be considered in patients with profound subacute mental status changes and typical MRI findings. In steroid-responsive patients, clinical improvement can precede radiographic improvement.
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PMID:MRI showing white matter lesions and multiple lobar microbleeds in a patient with reversible encephalopathy. 1849 80


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