JoAnn Goodson

Natural killer cell activity in depressive illness: preliminary report.

The central nervous system and the immune system are closely interrelated. Stress and psychiatric illness have previously been associated with immune dysregulation (Calabrese et al. 1987). We reported earlier that patients with major depression manifested a reduction in mitogeninduced lymphocyte proliferation, a correlate of cellular immune function (Kronfol et al. 1983). These findings were later confirmed by other investigators (Schleifer et al. 1984). We now report our preliminary results on Natural-Killer (NK) cell activity, a more specific parameter of immune function directed against tumoror virus-infected cells, in 12 drug-free patients diagnosed with major depressive disorder and 12 ageand sex-matched normal controls.

Covariance of positive and negative symptoms during neuroleptic treatment in schizophrenia: A replication

Although poor response to neuroleptics has traditionally been considered a characteristic feature of negative schizophrenic symptoms (Crow 1980; Andreasen et aJ 1982), several recent studies have documented significant improvement in negative symptoms in schizophrenic patients treated with neuroleptics (Breier et al 1987; vanKammen et al 1987; Kay and Singh 1989; Tendon et al 1990; Meltzer, 1990, Serban et al 1992). The question of whether neuroleptic-induced improvement in negative symptoms is linked to concomitant improvement in positive symptoms (vanKammen et al 1987; Tendon et al 1990; Meltzer 1990) or occurs independently of such improvement (Breier et al 1987; Serban et al 1992) is unresolved. This issue has obvious pathophysiological and therapeutic relevance. in a previous study (Tendon et al 1990), we had observed a significant improvement in negative symptoms with four weeks of neuroleptic treatment in a sample of forty schizophrenic inpatients; a significant correlation between change in positive and negative symptoms was also noted, in an effort to replicate these findings and further evaluate to covariance of positive and neg, ative symptoms in the course of initial neuroleptic treatment, we assessed positive ~nd negative symptoms in another nonoveflapping sample of 80 schizophrenic inpatients at drug-free baseline and four weeks after clinically determined neuroleptic treatment.

Positive and negative symptoms in schizophrenia and the dexamethasone suppression test

Although the Dexamethasone Suppression Test (DST) was originally proposed as a specific marker for major depressive disorder (Carroll et al. 1981), several recent studies have reported high rates of DST nonsuppression in schizophrenic patients, ranging from 22% to 73%. DST nonsuppression in schizophrenia has been attributed to depressive symptomatology (Munro et al. 1983), negative symptomatology (Coppen et al. 1983; Shima et al. 1986), subtype differences (Banki et al. 1984), episodic course, and good prognosis (Targum 1983). Investigations have so far yielded discrepant findings, prompting at least one author (Myers 1984) to suggest

Biological predictors of suicidality in schizophrenia

The objective of this study was to determine whether polysomnographic rapid eye movement (REM) sleep abnormalities and cortisol response to the dexamethasone suppression test (DST) differentiate between schizophrenic patients with and without a history of suicidal behaviour. We assessed a sample of 96 schizophrenic in-patients at the end of a 2-week medication-free period with the DST, polysomnography, and an extensive clinical assessment battery. Patients exhibiting suicidal behaviour were significantly more likely to have increased total REM time and increased total REM activity. We found no significant relationship between suicidal behaviour and DST non-suppression. This study confirms a previous finding suggesting an association between REM sleep abnormalities and suicidal behaviour in schizophrenia. It is postulated that this observed association may be related to serotonergic dysfunction in schizophrenia.

Familial/sporadic schizophrenia: Differences in neuropsychological function

There is now substantial evidence that both genetic and environmental factors play a role in the etiology of schizophrenia; however, little is known about the relationships between these factors and known markers for schizophrenia. In this paper we apply the familial/sporadic subtyping method as a first step towards examining the contribution of familial (approximated to genetic in this study) and environmental factors to relevant neurobiological markers in schizophrenia. Specifically, we compare cerebral ventricular size and neuropsycho[ogical function in schizophrenic patients with and without a first-degree relative with schizophrenia. Family history was ascertained by interview with the patient and a family member and a review of the medical record in 48 schizophrenic inpatients diagnosed by SADS/RDC and DSM-III-R criteria. Seven patients had a first-degree relative with schizophrenia. Neuropsychological functions were measured on the Wechsler Adult Intelligence Scale-Revised (full scale IQ, verbal IQ, and performance IQ); Trail Making Test Part B; Reaction Time (choice); Wisconsin Card Sorting Test (WCST); and the Controlled Oral Word Association Test. IQ, Trails B, and WCST scores were standardized to acoount for differences in age, sex, and education levels. Ventricle-brain ratios (VBRs) were calculated from CT scans. Patients with positive (FHpos) and negative (FHneg) family histories did not differ on the severity of either positive or negative symptomatology. Our results showed that a negative family history was associated with increased VBR (means -FHpos: 0.06; FHneg: 0.09; p = 0.06); these findings are consistent with several other reports. Of the neuropsychological indicators, only scores on Trails B differed significantly in the FHpos and FHneg groups; positive family history was associated with worse functioning (FHpos: 62.7; FHneg: 84.1; Mann-Whitney U: p = 0.01). These data suggest that nonfamilial factors contribute to ventricular enlargement while familial factors contribute to frontal lobe deficits in schizophrenia. This might reflect the presence of ventricular enlargement and frontal lobe neuropsychological dysfunction on separate pathogenetic pathways in schizophrenia. The results support the utility of the familial/sporadic approach in studying the pathogenetic heterogeneity of schizophrenia.