Plasma CPK levels in monozygotic and dizygotic twins discordant for schizophrenia.
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Biomedical subjects
Publications and source records attributed to P S Holzman.
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In a study of vestibular responses to caloric stimulation that controlled opportunity for fixation and state of alertness, we evaluated previous findings of diminished nystagmus in schizophrenia. We failed to replicate earlier reports in these respects: (1) None of the psychotic patient groups, when compared with normal controls, showed lower response intensity, latency, or culmination time of the nystagmic response. (2) The schizophrenic groups did not manifest a prevalence of clinically significant asymmetry. We did, however, observe that chronic deteriorated schizophrenics and recent schizophrenics have significantly greater dysrhythmic responses. This diminished orderliness of nystagmus may explain previous reports of absent or diminished nystagmus in the schizophrenics. The results are not compatible with peripheral vestibular disease in schizophrenia, but they may reflect state-related phenomena consistent with disturbances in alertness, which are not necessarily voluntary or motivational in origin.
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Eliminating opportunity for visual fixation as well as providing for the maintenance of an optimal degree of a patient's mental alertness are necessary for a valid assessment of nystagmic response to caloric stimulation. Controlling only for alertness can result in suppressed, absent, or dysrhythmic nystagmus. Data from four normal patients dramatically illustrate the suppressing effects of fixation opportunity despite an alert state. A new clinical instrument for obtaining optimal control over visual influences is described.
Disordered smooth-pursuit eye movements occur in a high percentage of schizophrenic patients and their first-degree relatives. A Test of the hypothesis that these disorders represent a genetic indicator of schizophrenia was undertaken by testing pursuit eye movements in a sample of monozygotic and dizygotic twins discordant for clinical schizophrenia. Deviant eye tracking is significantly concordant within monozygotic twin pairs, and less so with dizygotic twin pairs discordant for schizophrenia. A genetic interpretation is consistent with these results.
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The authors administered semi-structured interviews to 187 psychiatric inpatients to determine the role of anhedonia in schizophrenia. The interviews were taperecorded and then given blind ratings for anhedonia on a 7-point scale. Schizophrenic patients had significantly more anhedonia than nonschizophrenics, although many of the latter group had anhedonic tendencies. Most of the difference between the groups resulted from high anhedonia scores for chronic schizophrenics; less anhedonia was found in the acute schizophrenic patients. The data indicate that anhedonia is not necessary or unique to schizophrenia but is a prominent factor in chronic schizophrenia.
In previous studies, smooth pursuit eye movements (SPEM) have been shown to be disordered in about 70% of schizophrenics and about 45% of their first-degree relatives. In this report, the role of attention in these eye movements is addressed in three experiments (using as subjects schizophrenics, their first-degree relatives, and normals administered chloral hydrate) that recruit focused attention to the task. These studies show that voluntary attention in the form of inattention, "heedless negligence," or failure to cooperate, is not the specific attentional quality that is disordered in SPEM of schizophrenics and their relatives. Rather, the data both indicate that nonvoluntary attending is specifically disordered in these persons, and implicate a neurophysiological substrate that can be described as a failure of inhibitory, synchronizing integrating systems which may be located in the brain stem.
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This study examined the effects on smooth-pursuit eye tracking of single doses of CPZ (0.667 and 1.334 mg/kg), diazepam (0.071, 0.142, and 0.284 mg/kg), and secobarbital (100 mg). Only the barbiturate significantly affected the ability to follow a moving target with smooth-pursuit eye movements. In repeated testing of a single subject, 130 mg of secobarbital disrupted smooth-pursuit movements at least until 24 hrs after ingestion.
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