Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014547 (focal epilepsy)
1,627 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent developments of benzodiazepine receptor imaging (123I-Iomazenil SPECT and 11C-Flumazenil PET) in neuropsychiatric disorders were reviewed. In focal epilepsy, a number of previous studies have reported a decreased benzodiazepine receptor binding in epileptic foci and greater sensitivity compared to regional cerebral blood flow imaging, especially for diagnosis of medial temporal lobe epilepsy. These findings indicate clinical validity of benzodiazepine receptor imaging in focal epilepsy and may be related to the "disinhibition mechanism" in GABA/benzodiazepine systems underlying epilepsy. In panic disorder, abnormal benzodiazepine receptor bindings are recently demonstrated in the temporal, parietal or frontal cortex. Further studies would clarify the "benzodiazepine dysfunction hypothesis" in panic disorder.
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PMID:[Benzodiazepine receptor imaging in the brain: recent developments and clinical validity]. 1039 Sep 53

In 20-30% of potential surgical candidates with refractory focal epilepsy, standard MRI does not identify the cause. gamma-Aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the brain. [(11)C]Flumazenil (FMZ) PET images most subtypes of GABA(A) receptors, present on most neurons. We investigated [(11)C]FMZ binding in grey and white matter in 16 normal controls and in 44 patients with refractory neocortical focal epilepsy and normal optimal MRI. Fourteen patients had unilateral frontal lobe epilepsy, five occipital lobe epilepsy (OLE), six parietal lobe epilepsy (PLE) and 19 neocortical epilepsy that was not clearly lobar. Parametric images of FMZ volume of distribution (FMZ-V(d)) were computed. Statistical parametric mapping (SPM99) with explicit masking, including the white matter, was used to analyse individual patients and groups. Thirty-three of the 44 patients showed focal abnormal FMZ-V(d); increases in 16, decreases in eight, and both increases and decreases in nine. In seven patients, the increases in FMZ binding were periventricular, in locations normally seen in periventricular nodular heterotopia on MRI. There were frontal and parietal increases in FMZ binding in grey and white matter in the PLE group and decreases in the cingulate gyrus in the OLE group. FMZ binding increases, particularly periventricular increases, were a prominent feature of MRI-negative focal epilepsies and may represent neuronal migration disturbances.
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PMID:Grey and white matter flumazenil binding in neocortical epilepsy with normal MRI. A PET study of 44 patients. 1276 53