The status of late-onset vacuous chewing/perioral movements during long-term neuroleptic treatment in rodents: tardive dyskinesia or dystonia?

1987 ◽  
Vol 91 (1) ◽  
pp. 136-137 ◽  
Author(s):  
John L. Waddington ◽  
Anthony G. Molloy
Keyword(s):  
Tardive Dyskinesia ◽  
Late Onset ◽  
Neuroleptic Treatment ◽  
The Status ◽  
Vacuous Chewing

The Expression of Schizophrenia, Affective Disorder and Vulnerability to Tardive Dyskinesia in an Extensive Pedigree

1988 ◽  
Vol 153 (3) ◽  
pp. 376-381 ◽  
Author(s):  
John L. Waddington ◽  
Hanafy A. Youssef
Keyword(s):  
Family History ◽  
Tardive Dyskinesia ◽  
Movement Disorder ◽  
Affective Disorder ◽  
Psychiatric Illness ◽  
Late Onset ◽  
Psychiatric Morbidity ◽  
Neuroleptic Treatment ◽  
History Of

The demography, psychiatric morbidity, and motor consequences of long-term neuroleptic treatment in the 14 children born to a father with a family history of chronic psychiatric illness and a mother with a late-onset affective disorder resulting in suicide are documented. Twelve siblings lived to adulthood, nine of whom were admitted to a psychiatric hospital in their second or third decade, and required continuous in-patient care; five remaining in hospital, with long-term exposure to neuroleptics, had chroniC., deteriorating, schizophrenic illness and emergence of movement disorder. Two siblings showed no evidence of psychosis but developed a late-onset affective disorder. The implications for the issues of homotypia, vulnerability to involuntary movements, and interaction with affective disorder are discussed.

Treatment of tardive dyskinesia

1978 ◽  
Vol 16 (14) ◽  
pp. 55-56
Keyword(s):  
Tardive Dyskinesia ◽  
Late Onset ◽  
Psychiatric Patients ◽  
Term Treatment ◽  
Neuroleptic Drugs ◽  
Abnormal Movements ◽  
Long Term Treatment ◽  
The Face ◽  
Schizophrenic Patients

Neuroleptic drugs cause many forms of extra-pyramidal syndromes. One of these, tardive dyskinesia,1 occurs only after the patient has been taking the drug for some time (‘tardive’ refers to the late onset). The movements are involuntary and repetitive usually involving the face and tongue, but they may also affect the limbs and trunk. Tongue protrusion, licking and smacking of the lips, sucking and chewing movements, grimacing, grunting, blinking and furrowing of the forehead have all been described and attributed to long-continued medication with neuroleptic drugs of the phenothiazine, butyrophenone and thioxanthene groups. The patient can inhibit the movements, but anxiety makes them worse. Many of these symptoms were noticed in schizophrenic patients before neuroleptic drugs were introduced2 and they can occur in otherwise normal untreated elderly people. Nevertheless it is generally accepted that in most cases tardive dyskinesia is an unwanted effect of neuroleptic medication. Despite suggestions to the contrary, the abnormal movements are not necessarily associated with high dosage of neuroleptic drugs or with pre-existing brain damage.3 4 Tardive dyskinesia has been reported in 3–6% of a mixed population of psychiatric patients5 and over half of a group of chronic schizophrenics on long-term treatment.4 The more careful the neurological examination, the greater the apparent incidence.

scholarly journals Kindling: A Model for the Development of Tardive Dyskinesia?

1988 ◽  
Vol 1 (1) ◽  
pp. 29-40 ◽  
Author(s):  
B. Glenthøj ◽  
R. Hemmingsen ◽  
T. G. Bolwig
Keyword(s):  
Risk Factor ◽  
Tardive Dyskinesia ◽  
Repeated Administration ◽  
Substantia Nigra Pars Reticulata ◽  
Clinical Use ◽  
Neuroleptic Drugs ◽  
Neuroleptic Treatment ◽  
Gaba Transmission

Tardive dyskinesia (TD) from long-term neuroleptic treatment may be irreversible; therefore prevention has become a major concern. A controversial issue with regard to the clinical use of neuroleptic drugs is the possible influence on the development of TD of drug holidays. The major characteristics of kindling, theories of TD and the role of multiplicity in the development of TD are described. Some clinical studies point to interruption of neuroleptic therapy being a risk factor for development of irreversible TD. Induction of dyskinesia in non-human primates has been demonstrated after repeated administration of haloperidol. Rodent studies have not been conclusive. Several experimental results link TD with kindling: both conditions involve repeated stimulations, both seem to involve increased receptor responsiveness and in both conditions does depression in GABA transmission in SNR (substantia nigra; pars reticulata) play an important role. It is concluded that the kindling hypothesis is relevant to the investigation of TD.

The Current Status of Tardive Dyskinesia

2000 ◽  
Vol 34 (3) ◽  
pp. 355-369 ◽  
Author(s):  
Perminder S. Sachdev
Keyword(s):  
Risk Factors ◽  
Tardive Dyskinesia ◽  
Effective Treatment ◽  
Current Knowledge ◽  
Clinical Manifestations ◽  
Current Status ◽  
Neuroleptic Treatment ◽  
Duration Of Treatment ◽  
Schizophrenic Patients

Objective: This paper aims to provide an overview of the current knowledge on neuroleptic-induced tardive dyskinesia (TD) in relation to its clinical features, risk factors, pathophysiology and management. Method: The published literature was selectively reviewed and assessed. Results: Tardive diskinesia is a common neurological side-effect of neuroleptic medication, the cumulative incidence of which increases with increasing duration of treatment. Its clinical manifestations are diverse and subsyndromes have been described. Many risk factors for TD are now recognised, but increasing age remains pre-eminent as a risk factor. The pathophysiology of TD is not completely understood. Of the neurotransmitter hypotheses, the dopamine receptor supersensitivity hypothesis and the γ-aminobutyric acid insufficiency hypothesis are the main contenders. There is increasing recognition that TD may in fact be caused by neuroleptic-induced neuronal toxicity through free radical and excitotoxic mechanisms. The occurrence of spontaneous dyskinesias in schizophrenic patients and even healthy subjects suggests that neuroleptics act on a substratum of vulnerability to dyskinesia. As no effective treatment for TD is available, the primary emphasis is on prevention. Many drugs can be tried to reduce symptoms in established cases. The increasing use of atypical neuroleptics has raised the possibility of a lower incidence of TD in the future. Conclusions: After four decades of clinical recognition, the pathophysiology of TD is still not understood and no effective treatment is available. Its prevention with the optimal usage of currently available drugs and regular monitoring of patients on long-term neuroleptic treatment remain the best strategies to reduce its impact.

The Course of Tardive Dyskinesia in Patients on Long-Term Neuroleptics

1989 ◽  
Vol 154 (4) ◽  
pp. 523-528 ◽  
Author(s):  
J. A. Bergen ◽  
E. A. Eyland ◽  
J. A. Campbell ◽  
P. Jenkings ◽  
K. Kellehear ◽  
...  
Keyword(s):  
Tardive Dyskinesia ◽  
Psychiatric Patients ◽  
Involuntary Movement ◽  
Neuroleptic Treatment ◽  
Community Based ◽  
Abnormal Involuntary Movement Scale ◽  
History Of ◽  
Significant Change ◽  
Chronic Psychiatric Patients

Results are presented of five consecutive annual examinations using the Abnormal Involuntary Movement Scale for 101 community-based chronic psychiatric patients. These 101 patients had a history of longer and more consistent neuroleptic treatment than the 231 patients who initially entered the study, so no conclusions about prevalence of TD can be drawn. At each examination two-thirds of this group showed signs of TD; however, only 45% were TD positive at most examinations and 24% were best described as having fluctuating TD status. Of those patients who were consistently TD positive, 82% showed no overall significant change in summed AIMS scores, 11% improved and 7% became worse.

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