The application of pattern recognition techniques to the contingent negative variation for the differentiation of subject categories.
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In 27 normal adult subjects, pre- and postimperative phases of the CNV had an homogeneous pattern. The return to the baseline was of short duration (320 +/- 170 msec) whatever the amplitude and surface. This is in favor of an active mechanism terminating the CNV. In 27 schizophrenic and 13 schizoaffective patients, pre- and postimperative phases of the CNV were heterogeneous in character suggesting the possibility of multiple disturbances. When present, the preimperative negativity was of lower amplitude and had a delayed return to the baseline with a wider dispersion. In the patients with preimperative negativity followed by a PINV (postimperative negative variation), a linear relationship has been found between the amplitudes of the two waves.
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The aim of this study was to examine the influence of interfering stimuli on subjects' C.N.V. With a labyrinthic stimulation before association S1-S2 and arithmetic calculation task between S1 and S2, the C.N.V. showed a statistically significant variation (P less than 0.025): it became prolonged after the response to S2. Provocation of a prolonged C.N.V. could be used as criterion to determine an individual threshold of stress.
The CNVs of three disorganized schizophrenics and three paranoid schizophrenics were studied longitudinally over a 5-year period. The CNV of the disorganized-type schizophrenics reached its maximum decrease within 3 years of disease onset. A more gradual and less accentuated decrease was noted in the paranoid group within a span of 5 years.
CNV magnitude was studied in a task involving spatial localization and discrimination Subjects were 18 children 10 years of age. The CNV amplitude of half the subjects increased when the performance decreased and, in the other half, CNV amplitude decreased when the performance decreased. However, it seems that CNV magnitude increases as task difficulty increases but only above a minimal threshold varying with the subject. The results suggest that CNV amplitude cannot be related to a single psychological factor.
The present study was designed to investigate the effect of verbal information processing upon CNV, using a lexical decision task. Subjects performed a choice reaction time (RT) task under possible combinations of sense and nonsense syllables serving as warning (S1) and imperative (S2) stimuli. The results showed that CNV developed exclusively when the expectant information for motor response was given at S1. It was also found that CNV resolution time as well as RT was shorter in the near meaning condition than in the far meaning condition. These findings were discussed in relation to verbal information processing.
Slow EEG potentials were recorded during performance of a simple reaction task in which warning signal intensity was varied from trial to trial under foreperiod durations of 1, 3 and 8 sec. As shown by speed of reaction, the warning signal had an activating effect which increased with its intensity and decreased with foreperiod duration. This effect was related to the amplitude of a slow potential which appears in the EEG shortly after presentation of the warning signal. This potential is interpreted as a component of the orienting response regulating sensitivity to subsequent stimulation, so that reaction time is affected through change in the effective intensity of the imperative signal.
After a review of the literature stressing the biological factors underlying CNV genesis, the author sets up a tentative biological model of CNV, based on the neurophysiological and neurochemical findings of Skinner and Yingling (1977) and Marczynski (1978). In terms of balance between excitatory and inhibitory processes this model encompasses different CNV abnormalities in amplitude or duration frequently observed in mental pathology. The interest of such a model lies in the physiopathologic and therapeutic hypotheses it may lead to. In this respect, CNVs of prolonged duration, which would reflect a catecholaminergic hyperactivity, could constitute an indication for treatment by neuroleptics and/or benzodiazepines. CNVs with a weak amplitude would rather invite one to prescribe antidepressant drugs.
The effects of changes in pCO2 in the development and resolution of normal (return to base line within 2 sec after S2) and abnormal (return to base line in more than 2 sec after S2) CNVs were studied. Decreased pCO2 produced by hyperventilation induced a significant reduction in the duration of the post-imperative negative variation (PINV) without significantly affecting the amplitude of the CNV. Increased pCO2, by inhalation of 5% CO2, on the contrary, produced prolongation of the PINV in two subjects. Control subjects with normal CNVs did not show significant changes in the amplitude or in the duration of the CNV wave when pCO2 was altered. The results are discussed in terms of the possible independence and higher sensitivity to metabolic changes of the PINV brain generators compared with the generators of the CNV wave per se.
Nine subjects were given to breath 10%, 20%, 30% and 40% nitrous oxide in oxygen. The inhaled gas concentrations were monitored by a mass spectrograph. At each gas concentration the CNV was measured in a standard long S1-S2 CNV paradigm to a click and tone with a mandatory button press at S2. The results confirmed the previous observations of Lader and Morris (1974) that the cortical evoked potential decreases rapidly with increasing concentrations of nitrous oxide. The CNV, however, against prediction remains surprisingly well preserved up to the borders of unconsciousness. In this situation there is little correlation between CNV amplitude and attention, arousal or reaction time.
The early and late components of the CNV were measured in 18 stutterers and 18 non-stutterers, all dextral, prior to a manual and 3 speech tasks. It was hypothesized that, due to a proposed deficit in articulatory timing, prior to the more complex speech tasks, stutterers would show reduced late CNV amplitudes over Broca's area when compared to the non-stutterers. This hypothesis was not confirmed. In both groups, there was a finding of greater late CNV activity over the right hemisphere prior to speech responses. Explanations for this finding in terms of (a) CNV polarity, and (b) right hemisphere involvement in the speech responses used, are proposed. It is suggested that attention be paid to the nature of the response when attempting to record slow brain potentials prior to speech.
Early diagnosis of chronic hepatic encephalopathy (CHE) in the latent stage before the appearance of clinical signs, should reduce both morbidity and mortality as deterioration is often preventable by treatment. Since existing diagnostic procedures are inadequate, we have investigated a test in which morphine is used as a provocative agent and any resulting change in cerebral function assessed by measurement of the CNV in conjuction with a psychological trail test. Twenty six patients were studied, 6 of whom had clinically overt CHE. A significant correlation (P less than 0.05) between the change in CNV amplitude with morphine and the initial CNV amplitude, consistent with the theoretical model of Tecce (1972), was found. However, the CNV and trail test results taken as a whole did not allow even those patients with overt CHE to be distinguished and we conclude that it is unlikely that differing degrees of latent CHE could be detected.
Three groups, each comprising eight subjects, were twice tested with an interval of one week: one group receiving 10 and 20 mg chlordiazepoxide, another group receiving 150 and 300 mg caffeine and a control group receiving placebo and 'no-drug' treatment. During each session the CNV was determined five times: one pre-drug and four post-drug measurements, each divided in a condition with and one without 'white noise'. Based on Eysenck's theory it was predicted that the CNV would increase after administering chlordiazepoxide and would decrease after administering caffeine. Furthermore it was expected that 'white noise' would attenuate the CNV of introverts and would enhance the CNV of extraverts. The first hypothesis was significantly verified comparing the chlordiazepoxide group with the caffeine group. However, making comparisons within groups, only the decrease between the measurement before taking caffeine and the first one after administering was significant. The second hypothesis could be supported for introverts only.
Using a classical click/flash paradigm, the CNV was recorded from the following three groups of subjects at Broadmoor Hospital: (1) 14 'psychopathic' patients selected by use of the 4/9 MMPI profile and confirmed by independent clinical diagnosis; (2) 15 'non psychopathic' patients, all psychotic and mainly schizophrenic; (3) 14 healthy staff control subjects. All three groups were matched for age and sex; the two patients groups were also matched for length of stay. Two series of 32 paired stimuli were used, separated by an interval of 30 minutes. The mean CNV voltage was significantly lower in the 'non-psychopathic' patients. The amplitude of the 'psychopath's' CNV response did not differ significantly from that of the staff controls, but the response variability between the first and second series of trials was much greater in the 'psychopathic' patients than in the other two subject groups. The 'psychopathic' subjects tended to show more rapid initial development of the CNV.
Obsessional-compulsive disorder has been conceptualised in terms of overattention to irrelevant details. The aim of the present study was to investigate whether this feature would be reflected in the 'early' CNV component. Sixteen obsessional patients and matched controls were tested in a motor-set CNV paradigm with a 5 sec interval between S1 and S2. Patients exhibited a higher amplitude of the 'late' component and male patients prolonged negativity during the first half of trials. In addition, patients yielded lower levels of heart-period than controls. Results are accounted for better by the assumption of uncertainty and doubt in patients compared with controls.