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Biomedical subjects

D E Casey

Publications and source records attributed to D E Casey.

At least 91 records · Page 5Linked to original sources
PubMed1985

Spontaneous and tardive dyskinesias: clinical and laboratory studies.

Although rates of both tardive and spontaneous dyskinesia have increased by approximately 1% per year over the past 2 decades, the corrected tardive dyskinesia rate (with spontaneous dyskinesia subtracted) has remained fairly stable at 15% in comparisons of similar patient populations. In assessing rates of tardive dyskinesia, it is necessary to consider the influence of factors such as aging and the natural history of psychosis. Data are reviewed from clinical and animal studies that have addressed these and related factors in tardive dyskinesia. It is suggested that the competing needs to control psychosis and to manage tardive dyskinesia can be developed into a successful strategy for extended neuroleptic treatment.

Aged↗
PubMed1985

Five-year follow-up study of tardive dyskinesia.

A 5-year follow-up investigation of TD was carried out in 85 Hungarian schizophrenic out-patients. No substantial changes occurred during the 5 years in pharmacotherapy: most patients continued on neuroleptics and antiparkinson drugs. Comparison of 1978 and 1983 ratings revealed increased dyskinesia scores, which was statistically significant on the DRS Choreo-athetosis cluster. There was an increase in the number of patients with "moderately" severe TD from 4 in 1978 to 6 in 1981 to 10 (9 "Moderate" and 1 "Severe" TD) in 1983. The total number of TD cases as defined by research diagnostic criteria increased by only 3. The long-term trend in these neuroleptic-treated schizophrenics is for dyskinesia to plateau after reaching mild intensity, while in a minority of cases, the dyskinesia tends to extend from the oro-facial region to other body regions.

Antipsychotic Agents↗
PubMed1984

Effect of a cholinomimetic drug (RS 86) in tardive dyskinesia and drug-related parkinsonism.

RS 86, a specific muscarinic agonist, was evaluated in a blind, placebo-controlled, single-dose trial in 10 psychiatric patients with stable tardive dyskinesia (TD). RS 86, 0.5-4 mg orally, produced no significant effects in TD, although 4 mg caused a minimal aggravation in parkinsonism. Side effects of the highest dose (4 mg) included hypersalivation (eight patients), nausea (6), sweating (3), and vomiting (3). It is concluded that treatment with RS 86 and probably other cholinomimetics has no or only limited beneficial effect in TD.

Adult↗
PubMed1984

Sulpiride in tardive dyskinesia.

The pathogenesis of tardive dyskinesia (TD) appears to consist of a combination of a predisposing vulnerability of the patient and an antidopaminergic (neuroleptic) treatment. This combination may result in 1) a relative dopamine hyperreactivity associated with an increased number of dopamine receptors and/or a cholinergic hypo-function (reversible TD), and 2) in long-term treatment, degenerative phenomena leading to a decreased threshold for expressing dyskinetic symptoms (irreversible TD). Sulpiride, a selective D-2 dopamine receptor blocker, is able to suppress TD without producing a reciprocal aggravation in parkinsonism, although in vulnerable patients it may induce/aggravate parkinsonian symptoms. Animal data suggest that sulpiride has less TD-inducing effect than traditional neuroleptics, but long-term clinical studies are still needed to prove this suggestion.

Antipsychotic Agents↗
PubMed1983

Initial anticholinergic prophylaxis for neuroleptic-induced extrapyramidal syndromes.

Initial prophylaxis with anticholinergics for neuroleptic-induced extrapyramidal syndromes (EPSs) is controversial. Recommendations, based on conflicting research findings, vary from routine prophylactic use of anticholinergics to withholding these agents until dystonia, akathisia, or parkinsonism develops. To determine whether anticholinergic prophylaxis influenced EPS rates during the first 21 days of neuroleptic treatment, 215 psychotic inpatients were reviewed. Initial prophylaxis with anticholinergic drugs significantly reduced the occurrence of EPSs. This treatment's efficacy depended on a complex interaction of variables, including the patient's sex and age, antipsychotic drug type and dose, and treatment phase.

Adolescent↗
PubMed1983

Effect of gamma-vinyl GABA in tardive dyskinesia.

gamma-Vinyl GABA (gamma-aminobutyric acid), a drug that increases brain GABA via GABA transaminase inhibition, was evaluated in a blind, placebo-controlled trial in 10 patients with stable tardive dyskinesia. Drug effects during active treatment (2 to 6 g/day) and during pre- and posttreatment placebo periods were determined by scoring randomly sequenced videotapes of tardive dyskinesia and parkinsonian symptoms recorded weekly during standardized examinations. Tardive dyskinesia was significantly reduced, and correlated to increased parkinsonism. Eye blinking rates decreased, but psychiatric symptoms were unchanged during treatment.

Adult↗
PubMed1982

The effect of tetrahydroisoxazolopyridinol (THIP) in tardive dyskinesia: a new gamma-aminobutyric acid agonist.

gamma-Aminobutyric acid (GABA) agonists have been proposed for the treatment of tardive dyskinesia, but their therapeutic potential has been limited by side effects and toxicity. To elucidate further the role of GABA in neuroleptic-induced dyskinesias, we evaluated tetrahydroisoxazolopyridinol (THIP), a new, less toxic GABA analog and GABA receptor agonist, in both a dose-finding (single-dose) pilot study with five patients and a longer (four-week) placebo-controlled study with 13 patients. The patients were videotaped during a standardized examination; tardive dyskinesia, parkinsonian symptoms, and eye-blinking rates were rated blindly and randomly. The maximal short-term dose of THIP was 10 to 25 mg, whereas in the longer-term study the highest daily dose ranged from 20 to 120 mg. Tardive dyskinesia was unchanged during THIP treatment, but preexisting parkinsonism increased significantly and eye-blinking rates decreased. Psychiatric symptoms showed no significant changes, although tension and depression lessened. Side effects included sedation, confusion, dizziness, vomiting, and myoclonic jerks. Although THIP is not an effective new treatment for tardive dyskinesia, more specific GABA agonists should be evaluated in future studies of this syndrome.

Adult↗
PubMed1982

High-dose destyrosine-gamma-endorphin in tardive dyskinesia.

Destyrosine-gamma-endorphin (DTGE) has purported neuroleptic properties, although the findings have been conflicting. Four chronic psychotic inpatients with neuroleptic-induced dyskinesias were treated with single injections of placebo and DTGE in high doses (20-120 mg). No consistent differences were found in tardive dyskinesia, parkinsonism, eye-blinking rates, or mental status. Laboratory tests were unchanged. It is concluded that acute DTGE treatment has no beneficial effect in drug-induced dyskinesia.

Adult↗
PubMed1982

Levodopa and receptor sensitivity modification in tardive dyskinesia.

Tardive dyskinesia (TD), a syndrome of involuntary hyperkinetic movements, purportedly involves the development of dopamine (DA) receptor hypersensitivity following long-term receptor blockade with neuroleptic drugs. It has been proposed that through a process of receptor hypersensitivity modification, TD can be treated by reversing the receptor hypersensitivity with DA agonists. Thirteen patients with TD were treated for 4--8 weeks with levodopa plus benserazide, a peripheral decarboxylase inhibitor (Madopar, Roche, Basel, Switzerland) over a wide dose range corresponding to 3.0--9.0 g/day levodopa. Drug effects was assessed by blind evaluations of randomly sequenced videotapes made before, during, and for 6 weeks following treatment. TD scores moderately increased during levodopa. After the drug was discontinued, TD scores returned to pretreatment baseline levels without further improvement in those patients receiving concurrent neuroleptic medications (N = 9), but in the neuroleptic-free patient TD scores decreased 25% in three patients and were resolved in one younger patient. Psychological effects of depression or increased psychotic symptoms occurred at higher drug doses. These results do not support the proposal that receptor sensitivity modification with levodopa is an effective therapeutic approach to TD, though selected patient and drug treatment variables, including other DA agonists, are considerations for further investigation.

Adult↗
PubMed1981

Effect of des-tyrosine-gamma-endorphin in tardive dyskinesia.

The endorphin neuropeptides may have neuroleptic-like effects on dopamine function and may be antischizophrenic. Ten chronic psychotic patients with neuroleptic-induced tardive dyskinesia and parkinsonism received placebo and des-tyrosine-gamma-endorphin (DT gamma E). Drug effects on movement disorders and eye-blinking rates were assessed by blind evaluations of randomly sequenced videotapes made during standardized examinations before and 30, 60, and 120 minutes after each injection and at 24 hours postinjection on days of consecutive treatment. Changes in schizophrenic symptoms were evaluated openly with the schizophrenia subscale of the Comprehensive Psychiatric Rating Scale. There were no significant effects of DT gamma E on any parameter and no side effects. This suggests that DT gamma E, within the tested dose range, does not influence the pathophysiology of neuroleptic-induced dyskinesias or chronic schizophrenia or have neuroleptic properties. However, DT gamma E is well tolerated and should be tested with higher doses during prolonged treatment.

Blinking↗
PubMed1981

Vasopressin in anergic schizophrenia. A cross-over study with lysine-8-vasopressin and placebo.

Sixteen out of 19 patients suffering from chronic anergic schizophrenia completed a placebo-controlled cross-over study with lysine-8-vasopressin (LVP), following a schedule of 1 week of placebo, 3 weeks of LVP, starting with 22.5 IU/day, gradually increased to 67.5 IU/day, and finally 4 weeks of placebo. The psychic state was evaluated with the Brief Psychiatric Rate Scale (BPRS), during weekly live interviews, and following videotaped BPRS interviews at the beginning and end of the LVP period, and at the end of the final placebo period. Symptoms of parkinsonism and tardive dyskinesia were also videotaped during a standardized examination at the same intervals. The videotapes were subsequently randomized and evaluated blindly. The results of liver interviews showed a significant (P less than 0.05) decrease in the BPRS anergic factor after 2 and 3 weeks of LVP treatment, but there were no changes in any single item, other BPRS factors, or the BPRS total score. The results of the videotape evaluations showed that the BPRS thinking disorder factor was significantly (P less than 0.05) decreased after 3 weeks of LVP, whereas the BPRS score was unchanged. No consistent changes in parkinsonism or tardive dyskinesia were found. Although side effects were few, six patients became agitated or aggressive during the LVP treatment. The beneficial effect on thought disorder and anergia, but the absence of global effects on the schizophrenic syndrome, illustrates the need for further research with other vasopressin analogues. The advantages and disadvantages of live and videotaped psychiatric interviews are also discussed.

Adult↗
PubMed1981

The differential diagnosis of tardive dyskinesia.

The evaluation, diagnosis, and treatment of involuntary hyperkinetic movements can be a difficult challenge. A thorough history, including past and present drug use, and a complete physical, neurological, and psychiatric examination, accompanied by appropriate laboratory tests, are often necessary to make the correct differential diagnosis of dyskinesias. Movement disorders in psychiatric patients are usually related to neuroleptic medicines. Extrapyramidal syndromes related to starting these drugs include dystonia, akathisia, and parkinsonism, whereas dyskinesia occurs late in the course of the treatment. Involuntary movements may, however, be idiopathic, be caused by many other drugs, or occur as part of psychoses, hereditary neurodegenerative diseases, or other medical illnesses.

Attention Deficit Disorder with Hyperactivity↗