Search

P3(00) event-related brain potentials (ERPs) were recorded using auditory and visual stimuli from 5 amnesic patients with confirmed (n = 4) or suspected (n = 1) bilateral damage to the hippocampal formation without skull defects. Four normal control subjects were matched to each amnesic patient with respect to age, sex, education, and IQ subtest scores (n = 20 total controls). All 5 amnesic patients exhibited ERPs, and no reliable differences in P3 amplitude or latency could be detected between the patients and the control subjects in either modality. The findings indicate that the hippocampal formation does not contribute significantly to the scalp-recorded P3 from auditory and visual target stimuli, a conclusion also supported by additional recent findings from studies of patients with extensive bilateral medial temporal lobe damage studies. The significance of the P3 component for cognitive processing is discussed.

Inhibition of cerebral protein synthesis impairs long-term memory in a variety of species and tasks. Recently it was reported that subcutaneous injection of the protein synthesis inhibitor cycloheximide impaired short-term retention, measured 10 min after training in a passive avoidance task. To examine the possibility that inhibition of cerebral protein synthesis may sometimes disrupt short-term memory, mice were injected subcutaneously with cycloheximide (120 mg/kg) or anisomycin (150 mg/kg), or bitemporally with cycloheximide or anisomycin (100 mug/side) and given one training trial in a passive avoidance box. Subcutaneously injected cycloheximide reduced step-through latencies 10 min after training as reported previously, but anisomycin or bitemporally injected cycloheximide did not. All 4 drug groups exhibited impaired long-term memory. Since the results obtained at short intervals after training varied depending on the drug and route of injection, the impairment produced by subcutaneous cycloheximide at 10 min after training cannot be attributed to inhibition of cerebral protein synthesis. It is suggested that performance at short intervals after training reflects drug side effects on step-through behavior. By contrast, the impairment obtained at long intervals after training is consistent with the hypothesis that cerebral protein synthesis is required for formation of long-term memory.

Four patients with subcortical lesions and either aphasia or amnesia were compared to four patients with cortical lesions and aphasia. Each patient had [18F] fluorodeoxyglucose positron-emission computed tomography, language, and memory evaluations. Marked metabolic depression was found in the thalamus and caudate in all patients. The subcortical patients had only mild left-cortical changes, while the cortical patients showed marked cortical metabolic changes in the left hemisphere. Language changes were mild in the subcortical patients, while moderate to severe in the cortical patients. All patients showed severe verbal memory dysfunction. The only common abnormalities in the two groups were metabolic changes in the thalamus and severity of verbal memory dysfunction. These findings suggest a relationship between verbal memory and thalamic function.

Spontaneous firing rates and changes in firing rate in response to an intravenously administered dose of apomorphine were measured after various electroconvulsive shock (ECS) treatment regimens from dopaminergic cells of the substantia nigra in urethane-anesthetized rats. Similar measurements were obtained from noradrenergic neurons of the locus coeruleus before and after intravenous injection of clonidine. A significant decrement in the inhibition of spontaneous firing in response to intravenous administration of these agonists was observed following multiple or single ECS treatment in both substantia nigra and locus coeruleus cells. There was a consistent but nonsignificant tendency for cells in both areas of the brain from treated animals to display higher rates of spontaneous firing than their respective sham-shocked controls. Both the effects on base-line rates of spontaneous activity and on the depression of firing rate in response to drug administration were found to be independent of repeated treatment. A significant negative correlation was obtained between base-line firing rate and percentage depression to the autoreceptor agonist, but this correlation alone was insufficient to account for the observed differences in the drug response. These results are discussed with respect to possible mechanisms of action of electroconvulsive therapy in the treatment of depression.

Memory complaints before bilateral electroconvulsive therapy (ECT), 1 week after ECT, and 6 months after ECT were assessed in 35 patients using a newly developed self-rating scale. Memory complaints that occurred 1 week after ECT differed quantitatively and qualitatively from memory complaints that occurred before ECT. Six months later, memory complaints qualitatively resembled the complaints reported 1 week after ECT and differed sharply from those reported before ECT. It was suggested that a patient's impression of his memory is altered by bilateral ECT and that this altered impression persists in gradually diminishing form for at least 6 months after a typical course of treatment. Since the self-rating instrument used here appeared to differentiate between memory complaints associated with depression (before ECT) and memory complaints associated with amnesia (1 week after ECT), this instrument may be useful in a variety of settings where there is interest in human memory function.