Psychosurgery outcome and CNV asymmetry.
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Biomedical subjects
Publications and source records attributed to A F Mirsky.
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Two types of asphyxia were studied in monkeys, total asphyxia during mid-pregnancy (94--98 days gestation) and combined partial and total axphyxia at term (165 days gestation). Auditory evoked potentials and the acquisition of 2 auditory discrimination tasks were studied in asphyxiated animals as well as in group of controls. The brains of all asphyxiates were examined histologically. No auditory discrimination deficit was found in the asphyxiated animals; however, the auditory evoked potentials differentiated between control and asphyxiated animals, especially those with verified inferior colliculus damage.
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Precentral motor cortex neurons were studied under non-drug and drug conditions in three trained monkeys during the performance of a go-no go visual "attention" task. The two drugs studied, secobarbital and chlorpromazine, produced differing patterns of effect on components of the motor sequence involved in reaction time. The following components were considered: The SF interval or the period from stimulus onset to change in neuronal firing; the FR interval, which is the period from change in firing to the beginning of the task response; and MT or movement time, which is the time necessary to complete the response. Secobarbital produced an increase of 80% in SF and a relatively small average change in FR although there was considerable variability in the latter. MT was decreased in most secobarbital experiments. Anatomical factors relating to the FR variability were considered, and the MT decrease was discussed in terms of possible excitatory effects of the drug. Chlorpromazine produced small increases in SF, FR and MT, alternating with periods of complete abolition of performance. The results were discussed in terms of theories of attention deficit following administration of secobarbital and chlorpromazine.
The effects of secobarbital and chlropromazine upon behavior in a continuous, rapidly presented successive (go-no go) discrimination ("attention") task were evaluated in six Macaca mulatta monkeys. Simultaneous monitoring of EEG activity from epidural and subcortical electrodes permitted an evaluation of the nature of altered central nervous system events during erroneous performance (errors of omission) on this task. The computer-assisted analysis of pre-stimulus and post-stimulus EEG frequency activity (baseline crossings) suggests that the best measure of attentive behavior from the pre-stimulus EEG is percentage of beta 2 (25-40 cps) activity. No difference could be observed between drugs or among cerebral placements in this regard. This was determined by comparing measures of EEG frequency, pooled for a given test period, with performance from the same test period. On a trail-by-trail basis. however, the beta 2 measure in the pre-stimulus epoch failed to ditinguish correct responses from errors of omission. Separation between correct responses and errors of omission is possible if comparisons are made between the changes in percentage of beta 2 activity in the pre-stimulus vs. post-stimulus occurs with correct positive trials and the smallest change with correct negative trials. For secobarbital, no difference could be detected between correct and incorrect positive trials. For chlorpromazine, however, there was significantly less change in beta 2 for incorrect positive than for correct positive trials. The results were interpreted in terms of the hypothesis that secobarbital produces errors by depression of the general level of activation whereas chlorpromazine acts by reducing the sensory input which is necessary for correct discrimination performance.
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This is the first report in the literature of an application of the rigorous symptom-context method for determining the nature of the psychological antecedents of petit mal EEG paroxysmal activity. The activity is defined by the presence of a 3 cycle/second spike and wave on the EEG which is recorded concurrently while the patient is speaking his thoughts freely during interviews. The content of the patient's speech before each petit mal episode is compared with the content of speech during nonparoxysmal periods. Three petit mal patients were examined in this way for four sessions each. (Total petit mal EEG paroxysms for patient no. 1 were 19, patient no. 2 were 25, and patient no. 3 were 55.) For the first patient, strong psychological antecedents were found before petit mal EEG paroxysms as compared with comparison periods from the same patient. These consisted of such usual negative affects as feeling depressed and blocked. For the two other patients, only a few psychological antecedents discriminated significantly and these were not of the same type across the three patients. We conclude that the patients differ in amount and type of psychological antecedents. The differences may be attributed to differences in the type of petit mal and/or differences in the psychological component to the petit mal. The differences among the patients are probably not related to the average length of the paroxysms since we have shown that the relationships with the duration were generally silences than during the patient's speech (for two of the three patients)--talking probably requires more focused attention than silence; more focused attention or activity tends to reduce these episodes.
Ocular manifestations are prominent in petit mal attacks. The nuclei innervating the extraocular muscles lie in mesencephalic and pontine regions of the brainstem which have been regarded by some as critical areas in the generation of petit mal attacks. Ocular signs and their timing relative to spike-and-wave onset were studied cinematographically in 4 patients with petit mal epilepsy. Each patient showed a consistent pattern of eye deviation or fixation during spike-wave bursts. Neither the activation of oculomotor pathways, as indicated by eye deviation, nor their inactivation, as suggested by interruption of ongoing elicited ocular activity, preceded the appearance of spikewaves. Because ocular manifestations began only after the onset of spike-wave, this study provided no evidence that brainstem oculomotor regions were involved in the initiation of these petit mal attacks.
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