2 results
2 - Aging and tardive dyskinesia
- from Part II - Clinical aspects of tardive dyskinesia
- Edited by Ramzy Yassa, Douglas Hospital, Quebec, N. P. V. Nair, Douglas Hospital, Quebec, Dilip V. Jeste, University of California, San Diego
-
- Book:
- Neuroleptic-induced Movement Disorders
- Published online:
- 09 October 2009
- Print publication:
- 28 October 1996, pp 13-25
-
- Chapter
- Export citation
-
Summary
Tardive dyskinesia, a syndrome of abnormal, involuntary body movements, is produced by administration of antipsychotic drugs. The movements can involve the face, lips, jaw, tongue, neck, trunk, upper extremities, and lower extremities. Less obvious internal body regions can also be involved, such as the muscles of respiration. “Dyskinesia” is a generic term, referring to excessive or abnormal movements of any etiology or character. Historically, it has been used predominantly to refer to choreoathetoid-type movements; more recently it has also been used to include tics, dystonia, akathisia, myoclonus, and ballismus. Although tremors are also, by definition, abnormal movements, they have traditionally been recorded as a separate form of movement disorder. When an antipsychotic drug is believed to be the cause of the dyskinesia, the term “tardive” is employed. When an antipsychotic drug is implicated in the appearance of tremors, the term “drug-induced parkinsonism” is used. In general, it has been the rule that at least 3 months of neuroleptic treatment should precede any attribution of these drugs as causative agents in the development of tardive dyskinesia (Schooler & Kane, 1982), although recent work with older individuals suggests that shorter exposure times may be sufficient. The abnormal movements themselves can be distinguished phenomenologically by their rhythmicity, speed, and repetition, as well as by the presence or absence of sustained postures at the termination of the movement. Combinations of different movements are frequently seen, with parkinsonism, choreiform dyskinesia, and akathisia being among the most common in elderly patients.
28 - Development of novel antipsychotic drugs with reduced extrapyramidal side effects
- from Part VII - Treatment of tardive dyskinesia
- Edited by Ramzy Yassa, Douglas Hospital, Quebec, N. P. V. Nair, Douglas Hospital, Quebec, Dilip V. Jeste, University of California, San Diego
-
- Book:
- Neuroleptic-induced Movement Disorders
- Published online:
- 09 October 2009
- Print publication:
- 28 October 1996, pp 427-453
-
- Chapter
- Export citation
-
Summary
The introduction of antipsychotic drugs such as chlorpromazine (CPZ) in the 1950s was a major advance in the treatment of schizophrenia and other psychotic disorders. Although CPZ and other typical antipsychotic drugs remain important, the limitations imposed by their adverse reactions and partial efficacy in a significant proportion of schizophrenic patients are widely recognized. The most prevalent and most troublesome adverse drug reactions associated with the typical antipsychotics are their acute and chronic extrapyramidal motor side effects (EPSEs). In contrast, the “atypical” antipsychotic drugs that have recently been marketed (e.g., clozapine, risperidone, and remoxipride) or that are in various stages of development are expected to entail significantly lower incidences of EPSEs and possibly offer greater therapeutic efficacy. This chapter focuses on how these new developments in antipsychotics will affect the incidence and severity of acute and chronic EPSEs.
Acute and Chronic EPSEs
The common acute EPSEs associated with typical antipsychotic treatment include drug-induced parkinsonism (characterized by tremor, rigidity, and bradykinesia), acute dystonic reactions, and akathisia (subjective and objective motor restlessness). Those side effects can lead to a wide range of deleterious clinical consequences: disruption of the doctor–patient therapeutic alliance; noncompliance with the prescribed treatment/medication (Van Putten, 1974; Kane, 1990); physical and emotional distress, resulting in a reduction in the overall quality of life and in poorer social and vocational functioning; behavioral toxicity (Van Putten & Marder, 1987), including “secondary” negative symptoms (Rifkin, Quitkin, & Klein, 1975; Van Putten & May, 1978) and cognitive impairment; cosmetic disfigurement, which can contribute to social isolation and stigmatization.