Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMNESIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources

Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up.

Memory for past events was assessed in 43 patients who had been prescribed bilateral electroconvulsive therapy (ECT) for relief of depressive illness. Four memory tests of personal or public events were administered before ECT, shortly after the fifth treatment, one week after completion of treatment, and about seven months later. The results indicated that ECT can initially disrupt recall of events that occurred many years previously, but recovery of these memories was virtually complete by seven months after treatment. It was also clear that persisting memory loss for information acquired only a few days before treatment can occur. For information acquired one to two years prior to treatment, recovery was substantial, but the results suggested that some memory problems might persist for events that occurred during this time period.

Amnesia↗

Anterograde and retrograde amnesia after lormetazepam and flunitrazepam.

In a pharmacopsychological study, memory impairments after single oral doses of benzodiazepines or placebo were investigated in 40 healthy men aged 20-40 years. The study was designed as a double-blind and placebo-controlled trial. Four independent groups of 10 subjects randomly received either 1 mg lormetazepam, 2 mg lormetazepam, 2 mg flunitrazepam, or placebo. The tests consisted of word lists, picture tests, and syllable pairs (consonant-vowel-consonant trigrams). Tests were performed before drug ingestion, and 1, 2, 3, and 5 h after application. Different test versions were used on each occasion. The target variables were immediate recall (after presentation and a 10-s distraction task) and delayed recall and recognition (after 30 min). Recognition was also tested after 24 h for all five versions. A distinction must be made between anterograde amnesic effects and retrograde amnesic effects. The greatest anterograde memory impairments were observed after 2 mg flunitrazepam (p less than 0.05). Lormetazepam 2 mg produced less marked impairments than flunitrazepam. Results after 1 mg lormetazepam did not differ from those after placebo. Performance in the memory tests was better under benzodiazepines than under placebo as regards material learned before drug ingestion, i.e. the benzodiazepines had not negative retrograde amnestic effects, but rather "promnesic" effects. The results suggest that the extent of the benzodiazepines' amnesic effects--both negative (anterograde) and positive (retrograde)--depends on the dosage and type of substance.

Amnesia↗

Retrograde amnesia after electrical stimulation of the substantia nigra: mediation by the dopaminergic nigroneostriatal bundle.

Stimulation of the zona compacta of the substantia nigra (SNC) has been reported to impair the long-term retention of a passive avoidance step-down task. In the present experiments it was observed that previous ipsilateral lesions of the dopaminergic nigro-neostriatal bundle (NSB) with 6-hydroxydopamine blocked the stimulation-induced memory deficit. Unilateral or bilateral lesions of the dopaminergic NSB did not by themselves disrupt acquisition or retention of the passive avoidance task. In addition, the memory deficit observed after electrical stimulation of the caudate-putamen was not reduced by ipsilateral NSB lesions. These results indicate that the retention deficit produced by stimulation of the SNC was mediated by the dopaminergic NSB. However, in view of the fact that lesions of this projection did not affect acquisition or retention of the step-down task, it is suggested that this system is not critically involved in learning and memory. Rather, it is hypothesized that stimulation of the SNC results in an excess release of dopamine in the caudateputamen which interferes with neurochemical and neurophysiological events in this structure which are important substrates for long-term memory.

Amnesia↗