PubMed Health⌕ Search

Biomedical subjects

L D Alphs

Publications and source records attributed to L D Alphs.

26 records · Page 2Linked to original sources
PubMed1987

Brain gamma-aminobutyric acid abnormality in tardive dyskinesia. Reduction in cerebrospinal fluid GABA levels and therapeutic response to GABA agonist treatment.

A double-blind, placebo-controlled trial of gamma-vinyl gamma-aminobutyric acid (GVG) and 4,5,6,7-tetrahydroisoxazolo-(5,4-c) pyridine-3-ol (THIP) was carried out in drug-free schizophrenic patients with tardive dyskinesia. A significant decrease in dyskinetic symptoms occurred with the administration of GVG, associated with a twofold increase in cerebrospinal fluid levels of GABA; THIP produced a more moderate, yet consistent decrease in the involuntary movements. A pathophysiologic role for gamma-aminobutyric acid (GABA)-mediated neuronal transmission in tardive dyskinesia was explored by analyzing cerebrospinal fluid GABA concentrations in drug-free schizophrenic patients with and without tardive dyskinesia. A significant reduction in cerebrospinal fluid levels of GABA was observed in the dyskinetic schizophrenics compared with the nondyskinetic controls. These data compliment a growing body of experimental evidence suggesting a critical role for GABA-ergic neurons in the pathophysiology of tardive dyskinesia.

Adult↗
PubMed1986

Dopamine agonist treatment of schizophrenia with N-propylnorapomorphine.

We administered N-propylnorapomorphine, a potent aporphine-family dopamine (DA) agonist, to schizophrenic patients with active psychotic symptoms. After acute administration a significant antipsychotic action of N-propylnorapomorphine, maximal at an oral dose of 19 mg, was noted. The antipsychotic action predominated in subjects with neuroleptic-responsive symptoms, not in neuroleptic-nonresponders. However, when N-propylnorapomorphine was administered on a subchronic dosage schedule, no antipsychotic effect occurred. These observations suggest a rapid-onset tolerance phenomenon of psychosis to N-propylnorapomorphine and are consistent with results from preclinical experiments. These data support the idea that the acute antipsychotic response of DA agonists is mediated by the DA autoreceptor but fail to provide evidence for the potential clinical usefulness of this treatment approach.

Administration, Oral↗
PubMed1986

Neuronal cholecystokinin and schizophrenia: pathogenic and therapeutic studies.

Neuroleptic-free schizophrenic patients received caerulein, a potent analogue of cholecystokinin octapeptide, in a fixed- and rising-dose schedule. In addition, neuroleptic-treated patients received a single dose of the peptide with a 4-week follow-up. No significant change in mental status was observed after any of these administration schedules. Peak plasma levels of caerulein were noted at 20-30 min after IM administration; at this time no changes in cortical evoked potential were demonstrated. Furthermore, levels of cholecystokinin were not found to be reduced, but were in fact elevated in lumbar cerebrospinal fluid of schizophrenic patients. These data argue against the antipsychotic efficacy of systemic caerulein administration and, because evidence of CNS response to CCK is lacking, suggest that other pharmacologic strategies may be necessary to effectively modify central peptide systems with systemically administered drugs.

Adult↗
PubMed1985

Treatment of negative symptoms.

The rational treatment of the negative symptoms of schizophrenia requires a careful differentiation of those secondary to a range of other factors and those that constitute enduring primary or deficit symptoms. Secondary negative symptoms are usually responsive to treatment of the underlying cause. In contrast, there is no intervention currently available with established efficacy in treating deficit symptoms. These distinctions serve to reduce the heterogeneity of negative symptoms. A discussion of the diagnosis and treatment of the various forms of secondary negative symptoms is followed by suggestions for future research in the treatment of deficit symptoms.

Antipsychotic Agents↗
PubMedDate not supplied

Validation of the 16-item Negative Symptom Assessment.

The dimensional structure of the 16-item Negative Symptom Assessment (NSA-16) was validated in a sample of 223 unmedicated schizophrenic inpatients and cross-validated on an independent sample of 276 patients with schizophrenia. Using a confirmatory factor analytic procedure, a five factor model was found to best characterize the structure of this rating instrument. These factors include: Communication, Emotion/Affect, Social Involvement, Motivation, and Retardation. The latent structure of the NSA-16 is similar to the larger instrument from which it was derived. The findings provide support for a multidimensional model of negative symptoms in schizophrenia and offer a useful measure for their assessment.

Adult↗