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Biomedical subjects

J G Csernansky

Publications and source records attributed to J G Csernansky.

At least 109 records · Page 6Linked to original sources
PubMed1988

Luria-Nebraska performance and symptomatology in unmedicated schizophrenic patients.

Recent attempts at subgrouping schizophrenia have emphasized negative symptoms (e.g., blunted affect, emotional withdrawal), and several works have suggested that patients with negative symptoms show greater cognitive deficits and structural brain abnormalities. However, many of these studies have relied on screening devices or single measures of neuropsychological performance. Accordingly, the present study used the Luria-Nebraska Neuropsychological Battery (LNNB) in assessing 38 unmedicated inpatients with a diagnosis of schizophrenia. The results found no relationship between LNNB performance and symptom ratings derived from clinical interviews using the Brief Psychiatric Rating Scale. The findings show that cognitive performance may be unrelated to symptomatology when a complex battery type test is used.

Adult↗
PubMed1988

Dexamethasone nonsuppression in chronic schizophrenia.

It has been suggested that dexamethasone nonsuppression in schizophrenia is related to the presence of negative symptoms. In a sample of chronic schizophrenic outpatients we could find no relationship between dexamethasone nonsuppression and negative symptoms. In addition nonsuppression was not related to depressive symptoms, anxiety or age. The cause of hypothalamic pituitary adrenal dysregulation in schizophrenic patients remains unclear.

Adult↗
PubMed1987

A comparison of the neurochemical and behavioral effects of clenbuterol and desipramine.

Because both long-term adrenoceptor agonist administration and antidepressant treatment in animals down-regulate CNS beta-adrenoceptors and attenuate brain adenylate cyclase activity, beta-adrenoceptor agonists may also possess antidepressant properties. We compared the effects of the centrally acting beta-adrenoceptor agonist clenbuterol (5, 10 and 35 mg/kg per day), and the combination of propranolol (5 mg/kg per day) and clenbuterol (10 mg/kg per day), with desipramine (15 mg/kg per day) on forced swim test performance and on cortical beta-adrenoceptors in rats following 7 days of drug administration. Desipramine (15 mg/kg per day), and clenbuterol (10 and 35 mg/kg per day, but not 5 mg/kg per day) both significantly reduced immobility in the forced swim test. Frontal cortex beta-adrenoceptors were significantly down-regulated after desipramine and all 3 doses of clenbuterol. The co-administration of propranolol (5 mg/kg per day) blocked both the reduction in immobility and down-regulation of cortical beta-receptors induced by clenbuterol (10 mg/kg per day). Propranolol (5 mg/kg per day) alone up-regulated frontal cortex beta-adrenoceptors, but had no significant effect on swimming performance. These data suggest that the physiological consequences of beta-adrenoceptor down-regulation are important in the mechanism of action of antidepressants. The results also suggest that clenbuterol may be useful in the treatment of depression.

Animals↗
PubMed1987

Differential effects of proglumide on mesolimbic and nigrostriatal dopamine function.

Cholecystokinin octapeptide (CCK-8) is prevalent as a co-transmitter in the mesolimbic dopamine pathway. The effect of proglumide, a CCK-8 antagonist, on two acute and one chronic behavioral models of dopamine function was tested. First, haloperidol was used to inhibit stereotypies induced by apomorphine in rats. Pre-administration of proglumide significantly shifted the haloperidol dose response curve to the left. Second, rats were injected in the left caudate nucleus with kainic acid. Three weeks later, haloperidol was used to inhibit apomorphine-induced circling. Pre-administration of proglumide had no effect on this haloperidol dose response curve. Third, either proglumide, haloperidol, or combined treatment was administered to rats for 2 weeks. In proglumide-treated animals, a significant increase in 3H-spiperone binding sites in the nucleus accumbens was observed.

Animals↗
PubMed1987

Rating scales in research: the case of negative symptoms.

Two measures of negative schizophrenic symptoms, the Scale for the Assessment of Negative Symptoms and the withdrawal-retardation subscale of the Brief Psychiatric Rating Scale, are found to be redundant when used together. Studies incorporating redundant measures have numerous disadvantages. Using multiple scales increases the cost and effort for the investigator, places a greater burden on research subjects, and compromises the interpretability of findings by increasing the probability of both Type I and Type II errors. A strategy for evaluating the use of multiple rating scales is suggested, and the theoretical basis of this strategy is discussed.

Humans↗
PubMed1987

Depression, parkinsonian symptoms, and negative symptoms in schizophrenics treated with neuroleptics.

To determine whether depression and neuroleptic-induced parkinsonism confound the clinical assessment of negative symptoms in schizophrenics, we evaluated 45 outpatient schizophrenics for depression, parkinsonian symptoms, and negative symptoms using standard clinical rating scales. Neuroleptic and anticholinergic dose and plasma activity were also determined. Associations between negative symptoms and these clinical and drug variables were examined using a multivariate statistical model. Negative symptoms were significantly correlated with several parkinsonian symptoms, some vegetative features of depression, and with anticholinergic dose. No significant correlations were found between negative symptoms and cognitive features of depression, or neuroleptic and anticholinergic plasma activity. These findings suggest that assessment criteria for negative symptoms, depression, and drug-induced parkinsonism overlap in treated schizophrenics. Strategies for differentiating these clinical syndromes are discussed.

Adult↗
PubMed1987

Distinguishing depressive and negative symptoms in chronic schizophrenia.

In rating negative symptoms in chronic schizophrenia the Scale for the Assessment of Negative Symptoms showed less overlap with the Hamilton Rating Scale for Depression than the withdrawal-retardation subscale of the Brief Psychiatric Rating Scale. The distinction between depression and negative symptoms is best made by a careful evaluation of the patients' mood and thoughts.

Chronic Disease↗
PubMed1986

Possible associations among plasma prolactin levels, tardive dyskinesia, and paranoia in treated male schizophrenics.

To determine whether there is an association between prolactin (PRL) levels and psychopathology or tardive dyskinesia during neuroleptic treatment, we measured plasma prolactin levels and neuroleptic activity (NA) in 33 chronically treated male schizophrenics. Neuroleptic dose, plasma NA, and PRL were significantly intercorrelated. Plasma PRL levels were also measured in 8 male schizophrenics recently withdrawn from neuroleptics and in 18 normal male controls. In treated patients, but not in controls, PRL levels decreased with age and duration of illness, two variables that we interpreted as indirect measures of neuroleptic exposure. PRL levels in patients recently withdrawn from neuroleptics were lower than in treated patients or controls, which was suggestive of rebound hypoprolactinemia. A prolactin index, calculated as the ratio of PRL levels to NA, was inversely correlated with paranoid symptoms and tardive dyskinesia in younger treated patients. These results lead to speculation that tuberoinfundibular dopaminergic supersensitivity develops in chronically treated schizophrenics and that it is associated with nigrostriatal supersensitivity, manifested by tardive dyskinesia, and paranoid symptoms, which may reflect mesolimbic supersensitivity.

Adult↗