ABSTRACT
There is widespread evidence that schizophrenic symptomatology is best represented by three syndromes (positive, negative, disorganized). Both the disorganized and negative syndrome have been found to correlate with several neurocognitive dysfunctions. However, previous studies investigated samples predominantly treated with typical neuroleptics, which frequently induce parkinsonian symptoms that are hard to disentangle from primary negative symptoms and may have inflated correlations with neurocognition. A newly developed psychopathological instrument called the Positive and Negative and Disorganized Symptoms Scale (PANADSS) was evaluated in 60 schizophrenic patients. Forty-seven participants treated with atypical neuroleptics performed several neurocognitive tasks.A three-factor solution of schizophrenic symptomatology emerged. Negative symptomatology was associated with diminished creative verbal fluency and digit span backward, whereas disorganization was significantly correlated with impaired Stroop, WCST and Trail-Making Test B performance.Data suggest that disorganization is associated with tasks that demand executive functioning. Previous findings reporting correlations between negative symptomatology and neurocognition may have been confounded by the adverse consequences of typical neuroleptics.
Subject(s)
Affective Symptoms/drug therapy , Antipsychotic Agents/adverse effects , Neuropsychological Tests , Schizophrenia, Disorganized/drug therapy , Schizophrenia/drug therapy , Acute Disease , Adult , Affective Symptoms/diagnosis , Affective Symptoms/psychology , Antipsychotic Agents/therapeutic use , Diagnosis, Differential , Female , Humans , Male , Middle Aged , Psychiatric Status Rating Scales , Schizophrenia/diagnosis , Schizophrenia, Disorganized/diagnosis , Schizophrenia, Disorganized/psychologyABSTRACT
Beech et al. [Br. J. Clin. Psychol. 28 (1989) 109--116] previously reported attenuated negative priming in schizophrenic patients that was interpreted as a sign of dysfunctional cognitive inhibition. However, subsequent research has provided mixed results. In the present study, it was investigated whether reduced negative priming in schizophrenics may be an experimental artifact. Based on evidence from backward masking studies in schizophrenia, it was hypothesized that brief prime presentation times and pattern masking as used by Beech et al. and others may have impaired the visual perception of the prime display in schizophrenics. 20 schizophrenic patients and 20 matched healthy controls participated in the study. Subjects completed four negative priming experiments varying in prime presentation time (100 or 250 ms) and masking (a mask or a blank screen followed prime presentation). In line with prediction, reduced negative priming in schizophrenics only occurred for trials with 100 ms prime presentation time followed by a mask. Neither psychopathology nor any sociodemographic variable correlated substantially with negative priming. Results strongly suggest that reduced negative priming in schizophrenics may not be due to reduced cognitive inhibition but mirrors perceptual deficits.
Subject(s)
Cognition Disorders/diagnosis , Cognition Disorders/etiology , Perceptual Masking/physiology , Schizophrenia/complications , Adult , Female , Humans , Male , Neuropsychological Tests , Reaction Time , Severity of Illness Index , Visual Perception/physiologyABSTRACT
BACKGROUND: A number of studies have suggested that indirect semantic priming is enhanced in thought-disordered schizophrenics. However, research on direct semantic priming has produced conflicting results. The aim of the present study was to resolve some of the ambiguities of previous findings. METHODS: For the present study, 44 schizophrenic patients were split according to the presence of associative loosening into a positive thought-disordered (TD) and non-positive thought-disordered (NTD) group. Thirty healthy subjects and 36 psychiatric patients served as controls. RESULTS: Schizophrenics displayed increased indirect semantic priming compared with psychiatric controls. When subtyping the sample, TD-patients exhibited significantly enhanced indirect semantic priming compared with healthy and psychiatric controls as well as NTD-patients. Overall slowing was found to be independent of priming effects. Medication, age and chronicity of the schizophrenic illness did not modulate priming. CONCLUSIONS: In line with Spitzer and Maher it is inferred that disinhibited semantic networks underlie formal thought disorder in schizophrenia. For future research, it would be appropriate to: employ indirect semantic priming rather than direct semantic priming conditions; and, pay more attention to potential moderators of the priming effect, most importantly, the prime display duration and the length of the stimulus onset asynchrony.
