Eye-tracking dysfunction and birth-month weather in schizophrenia.

The prevalence of eye-tracking dysfunction (ETD) is significantly elevated in individuals with a diagnosis of schizophrenia and in their nonschizophrenic relatives, suggesting that ETD marks a familial (most likely genetic) risk factor for schizophrenia. Birth in a season with intemperate weather is also a widely reported risk factor for schizophrenia and is particularly marked for the subgroup with no family history of the disorder. This study examined how these two risk factors covaried in 78 patients with a Diagnostic and Statistical Manual of Mental Disorders (3rd ed., rev.; American Psychiatric Association, 1987) diagnosis of schizophrenia. Eye tracking and birth-month weather were independently assessed. As hypothesized, patients without ETD were significantly more likely to be born in months with intemperate weather (both hot and cold) than either patients with ETD or people in the general population. Etiologic factors associated with severe weather near birth may be important sources of nonfamilial schizophrenia.     

Emotional experience and expression in schizophrenia and depression.

The emotional responses of schizophrenic, depressed, and normal subjects and whether differences in the emotional responding of these groups depended on how emotional responses were elicited or measured were examined. Twenty-three blunted and 20 nonblunted schizophrenics, 17 unipolar depressed subjects, and 20 normal subjects were exposed to a series of affect-eliciting stimuli. The stimuli varied in valence (positive vs. negative) and in level of cognitive demand. Subjects reported their subjective experiences, and their facial expressions were videotaped. Blunted schizophrenics were the least facially expressive, although their reported subjective experiences did not differ from those of the other groups. The nonblunted schizophrenics were more responsive than the depressed subjects to the positive stimuli, although the two groups did not differ in their clinical ratings of affective flatness.     

Mentalising, schizotypy, and schizophrenia.

Despite accumulating evidence that patients with schizophrenia perform poorly in mentalising tasks, doubts remain about the primacy of the role played by defective mentalising in schizophrenia. This study investigated the relationship between mentalising ability and self-reported schizotypal traits in non-clinical adults who reported no history of psychiatric illness in order to test two counter-proposals: (1) defective mentalising is a primary cause of psychotic symptoms in schizophrenia; and (2) defective mentalising in schizophrenia is a secondary consequence of the chronic asociality that is typical of general psychiatric illness. Mentalising ability was tested using a false-belief picture sequencing task that has been used elsewhere to demonstrate poor mentalising in patients with schizophrenia. Evidence of selective mentalising deficits in high schizotypal non-clinical subjects discounted the view that defective mentalising is restricted to psychiatric illness and strengthened the case for continuity models of psychosis-proneness. Furthermore, evidence that poor mentalisers in the normal population are more likely to self-report psychotic-like traits, as well as asocial or idiosyncratic behaviours, refuted suggestions that defective mentalising is linked solely to asocial symptomatology and supported the view that defective mentalising may have a fundamental role to play in the explanation of psychotic symptoms. In order to specify what that role might be, alternative theoretical accounts of defective mentalising were tested. Neither executive planning deficits nor failure to inhibit cognitively salient inappropriate information could adequately explain the pattern of selective mentalising deficits found in high schizotypal non-clinical subjects. Our findings suggest that there exists a domain-specific cognitive module that is dedicated to inferring and representing mental states which, when dysfunctional, causes defective mentalising that manifests phenomenologically in psychotic-like traits and impoverished social awareness of variable expression and ranging severity.     

Forms of memory failure in schizophrenia.

Effortful and automatic memory task performances were examined in 36 schizophrenic patients and 18 normal control Ss. Tasks included free recall, recognition, and frequency estimation. Patients demonstrated impairment in recall, in recognition, in semantic encoding, and in frequency estimation. Deficits were observed across tasks despite differences in attentional demands. The results suggest a basic compromise of memory function, which is consistent with recent neuroimaging evidence of structural or physiological abnormalities in frontal and temporal lobe structures in schizophrenia.     

Interocular transfer of movement after-effects in schizophrenia.

A group of 16 chronic schizophrenic subjects were compared with 15 age-matched control subjects for interocular transfer of movement after-effects. Contrary to the hypothesis that schizophrenic subjects would show a deficit on this measure schizophrenics showed increased transfer compared to the controls. This effect is not due to response perseveration and is not correlated with length of hospitalization, age or dose of antipsychotic drugs. It is suggested that the effect reflects a deficit in 'inhibitory processes' in schizophrenia.     

Alexithymia in schizophrenia: an exploratory study.

This study assessed a relationship between alexithymia and schizophrenia suggested by reports based on small samples of patients. Here, 50 outpatients with a diagnosis of paranoid schizophrenia were compared with 50 pair-matched healthy subjects. Alexithymia was measured by the Polish version of the Toronto Alexithymia Scale-20. The mean total score was significantly higher in the schizophrenia group (M = 52.3, SD = 13.47) than in the healthy controls (M = 45.8, SD = 11.39, p < .02). This replicates earlier findings showing that a group of patients with paranoid schizophrenia have higher scores on alexithymia scales than healthy controls. There seems a need for a comprehensive examination of relations between alexithymia and other concepts denoting pathology of affect in schizophrenia.     

On the metapsychology of schizophrenia.

The author's point of departure is schizophrenic fragmentation, which has been considered here from a drive-economic and structural point of view, starting from Freud's prestructural conceptions and Jacobson's metapsychological formulations. The view is arrived at in the essay that the central psychological mechanism in the schizophrenic disorder is a drive-energetic decathexis of the basic psychic tissue, or the primal representative matrix, which has far-reaching consequences within the entire psychic organization. The basic psychic tissue corresponds to that area of inner reality which, according to Freud, remains beyond the primal repression and is made up of the first representations of the instinctual drive. The entire psychic organization has then been woven out of this representational tissue, binding drive energies in a preliminary way. According to the view put forward here, schizophrenic fragmentation does not primarily represent a disintegration of the psychic macrostructures or a consequence of the ego's resorting to primitive defences but is a consequence of a drive-energetic crisis at the level of the basic psychic tissue. The disorder manifests itself as the disappearance of inner liveliness and as a diffuse dissociation of the entire representional world, which I have characterized as the disappearance of psychic transparence. Its influences naturally also extend to the realm of the more advanced psychic functions and macrostructures and will invalidate in a radical way the person's drive economy. Reference is made in the article to the possibility that the central task of the primal representative matrix may be the creation of lively connexions and a striving for synthesis throughout the entire psychic organization and that the schizophrenic disorder may be intimately related to the decathexis of this function.