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Biomedical subjects

T B Horvath

Publications and source records attributed to T B Horvath.

At least 37 records · Page 2Linked to original sources
PubMed1987

Induction of depression with oxotremorine in patients with Alzheimer's disease.

Cholinergic neurotransmission has long been implicated in the development of depression. In this study seven patients with Alzheimer's disease were given oral oxotremorine, a long-acting cholinergic agonist, to assess the drug's effects on cognitive function. There were unexpected depressive reactions in five of the seven patients; three patients dropped out of the study because of the side effects. Cardiovascular effects of the drug were negligible, but its effect on memory and cognition remains unknown because of the small number of subjects who completed the study.

Aged↗
PubMed1987

Characteristics of very poor outcome schizophrenia.

The authors compared 21 "Kraepelinian" schizophrenic patients who had been ill and dependent on others for the past 5 years with 76 chronic schizophrenic patients in remission or with exacerbations requiring hospitalization. The Kraepelinian patients met the criteria for schizophrenia by more diagnostic systems than the exacerbated patients, were less responsive to haloperidol, had more severe negative symptoms, and had similarly severe positive symptoms. They had cerebral ventricles that were more asymmetrical and a greater family history of schizophrenia spectrum disorders than the other chronic patients. These data suggest that patients with 5 years of illness and complete dependency on others may represent a subgroup of schizophrenia.

Adult↗
PubMed1987

L-dopa challenge and relapse in schizophrenia.

Neuroleptic administration has been shown to be superior to placebo in prolonging schizophrenic remission. However, individual patients are able to maintain long periods of remission in the absence of neuroleptic treatment, while others relapse soon after neuroleptic withdrawal. This study attempted to predict time to relapse in 28 schizophrenic patients withdrawn from neuroleptics and challenged with L-dopa for 7 days, then followed until relapse. Time to relapse correlated significantly with L-dopa-induced increase in BPRS score (p = .006). Five of six patients who responded to L-dopa relapsed within 4 weeks after L-dopa administration, while only four of 22 who did not respond relapsed in a comparable period.

Adult↗
PubMed1986

Cortisol and Alzheimer's disease, I: Basal studies.

Patients with Alzheimer's disease and nondemented elderly control subjects participated in studies of cortisol secretion during sleep and at 9:00 a.m. and were given dexamethasone suppression tests (DSTs) and lumbar punctures. Nocturnal and 9:00 a.m. cortisol concentrations were significantly higher in the demented patients. CSF MHPG negatively correlated with mean nocturnal cortisol. The most severely demented patients had the highest 9:00 a.m. and mean nocturnal cortisol concentrations. DST results did not distinguish samples with substantially different nocturnal cortisol concentrations. These results suggest that measurements of basal plasma cortisol concentrations and dexamethasone suppression provide different information but support the notion of somewhat higher than normal cortisol concentrations in Alzheimer's disease patients.

Aged↗
PubMed1985

Plasma homovanillic acid concentration and the severity of schizophrenic illness.

Concentrations of plasma homovanillic acid before treatment were highly correlated with global severity of illness in schizophrenic patients, both before and after treatment. In contrast, a fixed dose of haloperidol did not affect those concentrations. Thus, in patients with a diagnosis of schizophrenia, plasma homovanillic acid may reflect the severity of illness, but not be influenced by short-term pharmacological perturbations by neuroleptics.

Adult↗
PubMed1985

Evaluating prolactin response to dopamine agonists in schizophrenia. Methodological problems.

Serum prolactin (PRL) level was assessed after challenges with apomorphine hydrochloride, saline, dopamine hydrochloride, or levodopa-carbidopa (Sinemet) in 19 control and 38 chronic schizophrenic subjects. Baseline PRL level varied inversely with age. High correlations existed between baseline PRL level and any subsequent absolute measure of PRL after administration of a dopamine agonist or placebo. Percent decrease was not a function of baseline concentrations and was therefore the only independent measure of drug response. Baseline PRL level was generally lower during exacerbation than remission in patients studied during two states of illness. Percent PRL level decrease after apomorphine administration was significantly greater in normal subjects than in schizophrenics. Correction of apomorphine responses for corresponding placebo (saline) values abolished differences between groups. Prolactin responses after dopamine or levodopa-carbidopa did not differ; however, placebo correction was not possible.

Acute Disease↗
PubMed1985

Apomorphine has no effect on plasma homovanillic acid in schizophrenic patients.

Previous experiments suggest that pharmacological perturbations of the brain dopaminergic system may be reflected by concentrations of plasma homovanillic acid. This study examined the ability of low-dose apomorphine to reduce plasma homovanillic acid concentrations in schizophrenic patients chronically treated with neuroleptics. The data suggest that apomorphine does not reduce plasma homovanillic acid in those patients.

Adult↗
PubMed1985

Clinical studies of the cholinergic deficit in Alzheimer's disease. I. Neurochemical and neuroendocrine studies.

Autopsy studies indicating that cholinergic neurons are selectively lost in patients with Alzheimer's disease (AD) and senile dementia of the Alzheimer type (SDAT) suggest that peripheral markers for central cholinergic activity would be useful in diagnosis. The present studies found that cerebrospinal fluid (CSF) concentrations of acetylcholine (ACh) correlated with the degree of cognitive impairment (r = .70) in a sample of carefully diagnosed patients with AD/SDAT, but metabolites of other neurotransmitters were not related to cognitive state; this suggests that CSF ACh may be a valid measure of cholinergic degeneration. Cortisol and growth hormone were measured in plasma samples drawn from patients and controls every 30 minutes from 2100 to 1100 hours the next day. Mean plasma cortisol concentrations were higher in patients with AD/SDAT than in controls and correlated inversely with CSF methoxy-hydroxyphenylglycol (MHPG) (r = .61) and positively with degree of cognitive impairment (r = +.53); as anticholinergic drugs suppress cortisol this finding indicates that cortisol dysregulation may be a marker for abnormalities in other neurotransmitter systems, particularly the noradrenergic system. Growth hormone secretion was not different in patients and controls but was positively correlated with CSF MHPG (r = +.63).

Acetylcholinesterase↗
PubMed1985

Clinical studies of the cholinergic deficit in Alzheimer's disease. II. Psychopharmacologic studies.

Two studies investigated the ability of physostigmine, given both intravenously and orally, to reduce symptoms of Alzheimer's disease. Intravenous physostigmine significantly and reliably enhanced memory in 13 of 16 patients tested, but the dose producing the improvement varied among patients. Oral physostigmine decreased overall symptom severity in a reliable way in seven of 12 patients tested. The extent of improvement was correlated with the increase in mean cortisol secretion produced by physostigmine, suggesting that the drug improved behavior and cognition only to the extent that it had a specific central cholinomimetic effect. There was no significant association between response to physostigmine and results of a dexamethasone suppression test and physostigmine had no effect on growth hormone secretion.

Administration, Oral↗
PubMed1985

Oral physostigmine treatment of patients with Alzheimer's disease.

Twelve patients with Alzheimer's disease received 0.0, 0.5, 1.0, 1.5, and 2.0 mg of oral physostigmine every 2 hours for 3-5 days; symptoms after each dose were assessed with the Alzheimer's Disease Assessment Scale. Placebo and the dose associated with the least severe symptoms were then readministered for 3-5 days each. Of the 10 patients who completed the study, three showed clinically significant improvement on the highest physostigmine dose in both phases, four more were marginally improved in both phases, and three had inconsistent responses to physostigmine. Cortisol measures obtained during a sleep study suggest that patients whose symptoms improved on physostigmine were those in whom oral physostigmine enhanced central cholinergic activity.

Administration, Oral↗
PubMed1984

Apomorphine and schizophrenia. Treatment, CSF, and neuroendocrine responses.

Previous studies have variably reported the efficacy of apomorphine in treatment of schizophrenia and tardive dyskinesia. Stimulation of dopamine neuron autoreceptors is the presumed mode of action. Low-dose apomorphine (0.75 mg subcutaneously) and placebo were administered to 25 male schizophrenics to evaluate the drug's effect on psychotic and tardive dyskinetic symptoms. No significant improvement or deterioration was seen. Concomitant measurements of plasma prolactin and growth hormone levels and CSF homovanillic acid level indicated that the dose used was centrally active. These results indicate that an active though nonsedating dose of apomorphine does not ameliorate symptoms of schizophrenia or tardive dyskinesia.

Adult↗
PubMed1984

Positive and negative symptoms in schizophrenia.

Negative and positive symptoms were determined for 46 drug-free patients who met Research Diagnostic Criteria (RDC) and/or Feighner criteria for schizophrenia. A modified version of the Scale for the Assessment of Negative Symptoms (SANS) was completed for each patient based on items from the Schedule for Affective Disorders and Schizophrenia (SADS) and other scales. Positive symptoms were scored from the SADS as well as from the following four diagnostic systems: RDC, Schneider's first-rank symptoms, the 12-point Flexible system, and Langfeldt's criteria for poor prognosis schizophrenia. For all patients, there was no correlation of negative symptoms and positive symptoms defined by any diagnostic system. Within the paranoid and undifferentiated subtypes, there was a positive correlation of positive and negative symptoms. Patients moving from stable to exacerbated states had an increase in both positive and negative symptoms, and patients with a poor history of treatment response had both more positive and more negative symptoms than responsive patients in a stable state. These results do not support the view that subgroups of patients have predominantly either negative or positive symptoms.

Adult↗
PubMed1984

A study of the reliability of reported premorbid adjustment in schizophrenic patients.

A study was conducted to determine the interrater reliability and the inter-informant reliability of two rating scales commonly used with schizophrenic patients. Both scales were completed by two informants for each of 45 schizophrenics. The Levels of Functioning Scale, which measures current social functioning, gave consistent results both between raters and between informants. The Premorbid Asocial Adjustment Scale, which measures social functioning during childhood and adolescence, produced very high reliability between raters but very poor reliability between informants. This suggests that much of the data collected about premorbid adjustment of schizophrenic patients are not accurate and that attempts to correlate reported premorbid adjustment with biological measures may be invalid. Ways of increasing the reliability and validity of premorbid adjustment measures are discussed.

Adult↗
PubMed1980

Cerebral ventricular size and neuropsychological impairment in young chronic schizophrenics. Measurement by the standardized Luria-Nebraska Neuropsychological Battery.

The relationship between size of cerebral ventricles in chronic schizophrenics and performance on a comprehensive neuropsychological battery, the Standardized Luria-Nebraska Neuropsychological Battery, was investigated. Ventricular size was determined by using a planimeter to measure the size of the lateral ventricles and the ventricular body, if present, on the computerized tomographic (CT) scan image that showed the largest lateral ventricles. This number was divided by the size of the brain as a whole on the same image of the CT scan to yield a ventricular brain ratio. This ratio was then correlated with the scores on the Luria-Nebraska Neuropsychological Battery. Eight of the 14 scales of the Luria-Nebraska Neuropsychological Battery correlated significantly at the .05 level with the ventricular brain ratio in a sample of 42 chronic schizophrenics with an average age of 32.3 years. Overall, there was a multiple correlation of .72 between the ventricular brain ratio and Luria scores. The overall ventricular brain ratio for the schizophrenics was significantly above that found in normal populations. Changes in the size of the ventricles in schizophrenics appear to have significant correlates with measures of neuropsychological performance.

Adult↗