ABSTRACT
OBJECTIVE: Speaking is hypothesized to generate a corollary discharge of motor speech commands transmitted to the auditory cortex, dampening its response to self-generated speech sounds. Event-related potentials were used to test whether failures of corollary discharge during speech contribute to the pathophysiology of schizophrenia. METHOD: The N1 component of the event-related potential elicited by vowels was recorded while the vowels were spoken by seven patients with schizophrenia and seven healthy comparison subjects and while the same vowels were played back. RESULTS: In the healthy subjects, the N1 elicited by spoken vowels was smaller than the N1 elicited by played-back vowels. This reduction in N1 elicited by spoken vowels was not observed in the patients with schizophrenia. CONCLUSIONS: These findings provide direct neurophysiological evidence for a corollary discharge that dampens sensory responses to self-generated, relative to externally presented, percepts in healthy comparison subjects and its failure in patients with schizophrenia.
Subject(s)
Auditory Cortex/physiopathology , Evoked Potentials, Auditory/physiology , Schizophrenia/physiopathology , Schizophrenic Language , Speech Perception/physiology , Verbal Behavior/physiology , Adult , Brain Mapping , Cerebral Cortex/physiopathology , Electroencephalography , Humans , Male , Middle Aged , Schizophrenia/diagnosisABSTRACT
In this study we report neuropsychological and brain-imaging findings in a patient with frontotemporal lobar degeneration. Brain imaging using registration of (18)fluorodeoxyglucose (FDG)-PET data to three-dimensional (3-D) magnetic resonance imaging showed atrophy and highly significant hypometabolism of the left temporal lobe and both frontal lobes. Volumetric measurements of the hippocampi/amygdala showed a reduction in volume of 25% on the left compared to right within cortical areas. Neuropsychological testing revealed semantic dementia with severe anomia as well as apraxia with impairment of both recognition and production of motor acts. The implications of this case of early manifestation of frontotemporal lobar degeneration for our knowledge of dementia are discussed.
Subject(s)
Dementia/psychology , Frontal Lobe/pathology , Pick Disease of the Brain/diagnosis , Pick Disease of the Brain/psychology , Semantics , Temporal Lobe/pathology , Anomia/etiology , Apraxias/etiology , Atrophy , Dementia/etiology , Dementia/pathology , Diagnosis, Differential , Fluorine Radioisotopes , Fluorodeoxyglucose F18 , Frontal Lobe/diagnostic imaging , Humans , Male , Middle Aged , Neuropsychological Tests , Pick Disease of the Brain/diagnostic imaging , Pick Disease of the Brain/pathology , Temporal Lobe/diagnostic imaging , Tomography, Emission-ComputedABSTRACT
BACKGROUND: The contingent negative variation (CNV) is considered to reflect prefrontal functioning and can be observed before manual and ocular motor responses. Schizophrenic patients exhibit reduced CNV amplitudes in tasks requiring manual motor responses. A number of studies has also found normal prosaccades, but delayed antisaccades and an augmented rate of erroneous prosaccades during the antisaccade task in schizophrenia. In this study we examined the CNV during pro- and antisaccade tasks in schizophrenic patients and healthy control subjects. METHODS: Data of 17 medicated schizophrenics (ICD-10, F20) and 18 control subjects, matched with patients for age, gender, and education were analyzed. Horizontal pro- and antisaccades were elicited in four blocks, each consisting of 80 trials. Electroencephalogram was recorded from 32 channels with a DC amplifier. RESULTS: Patients exhibited delayed correct responses and more erroneous prosaccades during the antisaccade task than control subjects, but normal prosaccadic reaction times. In control subjects, the vertex-predominant saccadic CNV was generally larger than in patients, and larger during the anti- than during the prosaccade task. This task-related amplitude augmentation was absent in patients. Analyses of additional components suggested specificity of impaired event-related potential modulation to the saccadic CNV. CONCLUSIONS: In accordance with the presumed prefrontal dysfunction, our results suggest deficient preparation and execution of antisaccades in schizophrenia.
