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Biomedical subjects

D G Kirch

Publications and source records attributed to D G Kirch.

At least 55 records · Page 3Linked to original sources
PubMed1991

A clinical trial of nifedipine in schizophrenia and tardive dyskinesia.

Effects of the dihydropyridine calcium channel inhibitor nifedipine on chronic schizophrenia and tardive dyskinesia were studied in an 8-week double-blind crossover trial. Four of the ten patients had tardive dyskinesia, and three of these were not receiving neuroleptics. No effects on symptoms of chronic schizophrenia were found using Psychiatric Symptom Assessment Scale ratings. In the four patients with tardive dyskinesia, an average improvement in total Abnormal Involuntary Movement Scale scores of 57% was observed. These data suggest that dihydropyridine calcium channel inhibitors may be effective in the treatment of tardive dyskinesia in schizophrenic patients.

Adult↗
PubMed1991

The continued search for evidence of retroviral infection in schizophrenic patients.

Retroviral infection has been proposed as an etiologic factor in schizophrenia. In an effort to unmask a latent retrovirus, short term cultures of peripheral lymphocytes from 15 schizophrenic subjects and nine normal controls were exposed to ionizing radiation and co-cultured with indicator cells. Reverse transcriptase activity, a marker of retroviral infection, could not be detected in any of the cultures. Our findings are further evidence against a role for retroviral infection in the etiology of schizophrenia.

Adult↗
PubMed1991

When symptoms persist: choosing among alternative somatic treatments for schizophrenia.

Many patients with schizophrenia continue to have significant disabling symptoms despite adequate trials of different types and doses of traditional neuroleptics. Clinicians treating these neuroleptic-resistant patients must look to other treatments in the hope of providing some relief. The literature on many of the alternative treatments is too scanty for firm conclusions. We offer criteria for deciding which treatments may warrant consideration. We review the evidence for the eight treatments we found to meet these criteria and discuss clinical points salient to their use in this population. Although not always conclusive, the data do offer clues for treatment guidelines and an approach to choosing among the available treatments is suggested.

Anti-Anxiety Agents↗
PubMed1991

Commentary: the acquisition and use of human brain tissue in neuropsychiatric research.

Witelson and McCulloch (1991) report on the establishment of a collection of normal human brain tissue that was secured through a unique method of premortem and postmortem assessments. Their work highlights the growing need in neuro-scientific research for carefully characterized collections of human brain tissue from both normal control subjects and patients with specific neuropsychiatric disorders. Brain tissue of this type, however, has not been readily available. Patients with mental disorders may not be competent to consent to a postmortem brain donation; other obstacles include various socioeconomic and legal impediments to autopsies. In addition, a number of methodologic issues exist regarding human brain tissue collections, including the problem of standardized postmortem diagnostic assessment and difficulty in establishing uniform procedures for processing formalin-fixed and frozen tissue. Various proposals to enhance brain-tissue collections are discussed. These include the establishment of networks for tissue donation and use, the linking of ultimate postmortem brain tissue collection to prospective clinical studies, and promulgation of standardized procedures for methods of postmortem diagnosis and tissue handling.

Adult↗
PubMed1991

The nucleus basalis of Meynert, senile plaques, and intellectual impairment in schizophrenia.

The large, hyperchromic, cholinergic neurons of the nucleus basalis of Meynert (nbM) and the presence of senile plaques were quantified in postmortem brain tissue from 10 intellectually impaired schizophrenic patients, seven intellectually intact schizophrenic patients, seven control subjects, and three patients with Alzheimer's disease. The two groups of schizophrenic patients did not show any significant differences when compared with the control group in nbM cell density or in plaque frequency. The Alzheimer's disease patients showed the expected decrease in nbM neuronal density and increase in plaques compared with the controls. The data suggest that compromised cognitive function in schizophrenia is not associated with diffuse neuropathology of the basal forebrain cholinergic system.

Acetylcholine↗
PubMed1990

Effect of chronic caffeine administration on monoamine and monoamine metabolite concentrations in rat brain.

Caffeine was chronically administered in four doses (0, 10, 25, and 50 mg/kg/day) to rats via twice-daily intraperitoneal injections for 30 days. Concentrations of brain tissue monoamines, dopamine (DA), norepinephrine (NE), and serotonin (5HT), and monoamine metabolites, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-methoxy-4-hydroxyphenylglycol (MHPG), and 5-hydroxyindoleacetic acid (5HIAA), were determined. At the 10 mg/kg/day dose, no significant changes were found compared with controls. At 25 mg/kg/day and 50 mg/kg/day significant changes were observed within each monoamine system. In striatum, DA and 5HT were increased, while DOPAC was decreased. In frontal cortex, NE was increased. In cerebellum, 5HT and MHPG were increased.

Animals↗
PubMed1990

Polydipsia and hyponatremia in psychiatric patients: challenge to creative nursing care.

Among patients with psychiatric disorders, especially schizophrenia, a pattern of extreme polydipsia and polyuria sometimes emerges, usually without readily identifiable medical causes. Hyponatremia may develop and progress to water intoxication, with symptoms including restlessness, confusion, seizures, or even death. We review the clinical features and pathophysiology of this syndrome and discuss nursing roles in identifying and managing patients with polydipsia and hyponatremia. While the causes of polydipsia and hyponatremia are unclear, relevant factors seem to include a possible dysfunction in central nervous system (CNS) thirst and osmoregulatory centers, the inappropriate secretion of or sensitivity to antidiuretic hormone (ADH), and psychoactive drugs. Management techniques for affected patients concentrate on careful observation, fluid restriction, and the minimization of possible exacerbating factors such as high neuroleptic dosage and cigarette consumption.

Humans↗
PubMed1989

Lack of evidence for a role of T-cell-associated retroviruses as an etiology of schizophrenia.

The evidence that schizophrenia may involve infection by a virus (or viruses) has been indirect. The recent discovery, however, of the human retroviruses--human T-cell lymphoma-leukemia virus-I, and II (HTLV-I, -II) and human immunodeficiency virus (HIV)--now also known to affect the central nervous system (CNS), together with the development of new techniques in retrovirology, have made it possible to investigate more directly the role of this class of viruses as an etiology of schizophrenia. In our first effort to screen for the presence of a T-cell lymphotropic virus in schizophrenia, short-term tissue cultures of peripheral lymphocytes from 17 chronic schizophrenic patients and 10 normal controls were established. The cells were cultured in the presence of T-cell growth factor (TCGF, IL-2), and the culture supernatants were tested for the presence of the retroviral enzyme reverse transcriptase. No T-cell-associated reverse transcriptase activity was detected in cultures from patients or normal controls. Therefore, the data do not provide evidence for a role for T-cell lymphotropic retroviruses as an etiology of schizophrenia.

Adult↗
PubMed1989

Haloperidol and reduced haloperidol concentrations and psychiatric ratings in schizophrenic patients treated with ascorbic acid.

Recent reports have suggested an augmentation by ascorbic acid of haloperidol treatment of schizophrenic patients. This study was designed to examine whether pharmacokinetic interactions between ascorbic acid and haloperidol occur in this population. Eight male inpatients diagnosed as having chronic schizophrenia by DSM-III-R criteria and stabilized on a fixed dose of haloperidol were given oral doses of ascorbic acid, 4.5 grams daily, for 2 weeks in an open trial. Serum concentrations of haloperidol and is metabolite, reduced haloperidol, were measured by high performance liquid chromatography. Psychiatric symptoms were monitored using the Psychiatric Symptom Assessment Scale performed by nursing staff blind to the haloperidol status but not to the ascorbic acid dosage. The addition of ascorbic acid was not associated with any change in psychopathology in this group of patients, nor was there any apparent pharmacokinetic interaction with haloperidol.

Ascorbic Acid↗
PubMed1989

Haloperidol and reduced haloperidol concentrations in plasma and red blood cells from chronic schizophrenic patients.

In a double-blind, placebo-controlled study, 15 drug-free chronic schizophrenic inpatients were treated with a fixed dose of haloperidol for 6 weeks. Haloperidol and its metabolite, reduced haloperidol, were measured in plasma and red blood cells after 2, 4, and 6 weeks of treatment. Behavioral change was rated using the Brief Psychiatric Rating Scale (BPRS). Not only the raw concentrations, but also blood compartment sums and ratios of these four drug measurements were tested for their strength of association with behavioral improvement. Positive associations with some BPRS subscales at some time points emerged; however, no significant correlations were found to extend across all time points measured. There was a trend in this cohort for negative symptom improvement to be associated with the ratio of haloperidol to reduced haloperidol in red blood cells. The ratio of haloperidol to reduced haloperidol in plasma was always greater than that in the red blood cells for all patients, reflecting an accumulation of the metabolite in red blood cells.

Adolescent↗
PubMed1988

Hypothesis: a nicotine-dopamine interaction linking smoking with Parkinson's disease and tardive dyskinesia.

1. Nicotine, an important pharmacological component of cigarette smoke, is known to have significant effects on central nervous system (CNS) dopaminergic function. Although acute doses of nicotine have been shown to facilitate dopamine release, recent data indicate that chronic nicotine treatment may actually decrease CNS dopamine turnover in the striatum. 2. A number of epidemiological investigations have demonstrated that individuals who are or who have been smokers are less likely to develop idiopathic Parkinson's disease (a disorder involving a deficit in nigrostriatal dopaminergic neurotransmission). In addition, there is preliminary evidence that individuals with tardive dyskinesia (a hyperkinetic movement disorder observed in some cases of chronic neuroleptic treatment and thought by some to be associated with striatal dopamine receptor supersensitivity) are more likely to be smokers. 3. A unitary hypothesis is presented, proposing that smoking in early adult life may decrease CNS catecholamine turnover, thereby protecting against free radical formation from catecholamine oxidation that in turn damages striatal neurons. These individuals are thereby "protected" from the later development of Parkinson's disease. In this hypothetical scheme, individuals who are given neuroleptics and who also are smokers may develop a greater degree of dopamine receptor supersensitivity due to combined receptor blockade by neuroleptics and a decrease in CNS dopamine turnover caused by nicotine, resulting in an increased prevalence of tardive dyskinesia in this group.

Dopamine↗
PubMed1988

Plasma amine metabolites before and after withdrawal from neuroleptic treatment in chronic schizophrenic inpatients.

Plasma catecholamine metabolites were measured in paired blood samples from 22 subjects with chronic schizophrenia. One sample was drawn while patients were on a stable dose of neuroleptic medication; the second was drawn 6 weeks after discontinuation of medication. In comparison with baseline values during neuroleptic treatment, there was a significant increase in the plasma concentration of the norepinephrine metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), and a trend toward an increase in the plasma concentration of the dopamine metabolite, homovanillic acid (HVA), in the medication-free subjects. There were no significant correlations between plasma MHPG or HVA concentrations and the corresponding ratings of psychopathology for these patients.

Adolescent↗
PubMed1988

Serum haloperidol concentration and clinical response in schizophrenia.

Previous studies have reported a therapeutic window (i.e., a curvilinear relationship between clinical response and drug level) for haloperidol concentrations in serum or plasma. The authors treated 30 acutely decompensated schizophrenic inpatients with a fixed dose of haloperidol (.4 mg/kg/day). After 6 weeks there was no statistically significant correlation between clinical improvement and serum haloperidol concentration. Fifteen subjects with serum concentrations of 5-15 ng/ml did not differ in clinical improvement compared with 15 subjects who had concentrations above 15 ng/ml. These data are consistent with a therapeutic plateau, rather than a window, and suggest that in most cases there is no clinical advantage to the use of haloperidol doses greater than approximately 30 mg/day in schizophrenic patients.

Adult↗
PubMed1988

Polydipsia and hyponatremia in psychiatric patients.

Many psychiatric patients have polydipsia and polyuria without identifiable underlying medical causes. Hyponatremia develops in some polydipsic patients and can progress to water intoxication with such symptoms as confusion, lethargy, psychosis, and seizures or death. This syndrome is sometimes called "compulsive water drinking," "psychogenic polydipsia," and "self-induced water intoxication." Although the underlying pathophysiology of the syndrome is unclear, several factors have been implicated in producing polydipsia and symptomatic hyponatremia. These include a possible hypothalamic defect, the syndrome of inappropriate secretion of ADH (SIADH), and neuroleptic medication. Evaluation of psychiatric patients with polydipsia includes a search for other medical causes of polydipsia, polyuria, hyponatremia, and SIADH. Treatment modalities currently available include fluid restriction and medications.

Adult↗
PubMed1987

Effect of chronic nicotine administration on monoamine and monoamine metabolite concentrations in rat brain.

The effects on rat brain tissue monoamine and monoamine metabolite concentrations of chronic nicotine administration at two doses (3 and 12 mg/kg/day) using constant infusion were studied. After 21 days of treatment, tissue concentrations of dopamine (DA), norepinephrine (NE), 5-hydroxytryptamine (5-HT), and several metabolites in striatum, hypothalamus, and frontal cortex were determined by high performance liquid chromatography with electrochemical detection. Compared with a control group, nicotine treatment significantly decreased NE in frontal cortex but not in other regions. The concentration of 5HT also was decreased in frontal cortex but increased in the hypothalamus at the higher dose of nicotine. The 5HT metabolite 5-hydroxyindoleacetic acid (5-HIAA) was not significantly altered in any region. The 5HT index (5-HIAA/5-HT) was significantly decreased in the hypothalamus and increased in frontal cortex at the higher dose. Concentrations of DA and the metabolite homovanillic acid (HVA) were not significantly altered by nicotine. Nevertheless, significant decreases in the DA metabolite dihydroxyphenyl-acetic acid (DOPAC) were observed in both striatum and hypothalamus. Moreover, the DA index [(DOPAC + HVA)/DA] was significantly decreased in all three brain regions. In contrast to other studies using acute dose and in vitro perfusion paradigms that have reported increased CNS catecholamine release stimulated by nicotine, chronic administration appears to be associated with decreased catecholamine turnover in some brain regions.

Animals↗