ABSTRACT
Perseverative and intrusive behavior were studied in three psychiatric patients with toxic dementia associated with anticholinergic drugs. A mechanism was proposed attributing these behaviors to the delayed extinction (residual activation) of prior executive sets (or schema) in the context of sets containing nondissociated operations. Reutilization of these operations appeared to trigger the nonextinguished set back into executive status. It was hypothesized that set perseveration and intrusion reflect a defect in the set-scheduling process induced by loss of cholinergic function.
Subject(s)
Antiparkinson Agents/adverse effects , Cholinergic Fibers/drug effects , Extinction, Psychological/drug effects , Parasympatholytics/adverse effects , Psychoses, Substance-Induced/physiopathology , Receptors, Cholinergic/drug effects , Stereotyped Behavior/drug effects , Antiparkinson Agents/therapeutic use , Antipsychotic Agents/adverse effects , Antipsychotic Agents/therapeutic use , Attention/drug effects , Attention/physiology , Bipolar Disorder/drug therapy , Bipolar Disorder/physiopathology , Cholinergic Fibers/physiology , Extinction, Psychological/physiology , Female , Humans , Male , Middle Aged , Neuropsychological Tests , Parasympatholytics/therapeutic use , Psychomotor Performance/drug effects , Psychomotor Performance/physiology , Receptors, Cholinergic/physiology , Schizophrenia/drug therapy , Schizophrenia/physiopathology , Stereotyped Behavior/physiology , Verbal Behavior/drug effects , Verbal Behavior/physiologyABSTRACT
The emergence of depression, parkinsonism, and akathisia after neuroleptic therapy was associated with increased length of hospital-stay in schizophrenics with affective heredity only. In schizophrenics with schizophrenic heredity, increased length of hospital-stay was associated with residual hallucinations and apathy. In the former patients, findings were theoretically attributed to a putative biogenetic abnormality sensitive to the effects of neuroleptic drugs.
Subject(s)
Antipsychotic Agents/adverse effects , Depressive Disorder/genetics , Length of Stay , Schizophrenia/genetics , Schizophrenic Psychology , Antipsychotic Agents/therapeutic use , Chlorpromazine/adverse effects , Clinical Trials as Topic , Depressive Disorder/chemically induced , Double-Blind Method , Dyskinesia, Drug-Induced/genetics , Fluphenazine/adverse effects , Humans , Perphenazine/adverse effects , Random Allocation , Risk Factors , Schizophrenia/drug therapyABSTRACT
A psychopharmacogenetic strategy was used to investigate a genetic heterogeneity model of schizophrenia. This model consisted of various genetic subtypes represented by patients classified hypothetically according to the types and genealogical (Mendelian) patterns of illnesses in first-degree relatives. The effect of neuroleptics on these subtypes (drug x genetic subtype interactions) were tested for evidence of post-treatment responses which discriminated between them. The findings revealed that schizophrenics who had depressed relatives tended to exhibit (1) depression and more severe pseudoparkinsonism irrespective of types of neuroleptics, and (2) greater remission of paranoid-hostility symptoms when treated with neuroleptics of the aliphatic-piperadine type. Schizophrenics who had schizophrenic relatives failed to show these responses. Interpretation of these findings emphasized the recognition of these responses as arising from neuroleptic-induced alterations of defective neurologic-neurochemical systems underlying this subtype and as "pharmacogenetic criteria" by which it can be discriminated.
Subject(s)
Antipsychotic Agents/therapeutic use , Schizophrenia/drug therapy , Adolescent , Adult , Antipsychotic Agents/adverse effects , Humans , Middle Aged , Models, Genetic , Muscle Rigidity/chemically induced , Schizophrenia/geneticsABSTRACT
Alcoholism in the male relatives of patients with various (nonalcoholic) psychiatric disorders is consistently elevated above population risk. Over the years, this finding has given rise to theories which propose that some forms of alcoholism are attributable to the pleiotropic expression of genes underlying these disorders. This mechanism was tested in the fathers of patients from ethnic groups associated with culturally suppressed alcohol abuse where it was predicted that decreased alcoholism would be substituted for by increased psychiatric disorder. Results, however, failed to support such a mechanism. Other explanations of this elevated alcoholism were considered.
