The management of tardive dyskinesia

1986 ◽  
Vol 24 (7) ◽  
pp. 27-28
Keyword(s):  
Tardive Dyskinesia ◽  
Antipsychotic Drugs ◽  
Disease Process ◽  
Neuroleptic Drug ◽  
Blocking Drug ◽  
Unwanted Effect ◽  
Difficult Condition ◽  
The Face ◽  
Schizophrenic Patients

Dyskinesias are involuntary movements usually of the face and tongue and sometimes of the limbs and trunk. Tardive (delayed) dyskinesia occurs in patients who have been taking an antipsychotic (neuroleptic) drug or, rarely, another central dopamine-receptor-blocking drug such as metoclopramide. It generally occurs only in those treated for longer than a year, although much shorter exposures have been implicated with the antipsychotics. A similar dyskinesia occurred in schizophrenic patients before antipsychotic drugs were introduced, and can occur in healthy untreated elderly people; risk factors include old age, brain damage1 and the schizophrenic disease process.2 Nevertheless, in most patients on an antipsychotic drug (whether psychotic or not), tardive dyskinesia is an unwanted effect of the drug. It occurs in 5–40% of patients on long-term antipsychotic medication.3–5 we discuss here advances in the management of this difficult condition since our last review.6

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.

Tardive Dyskinesia: A Concern for the Pediatrician

PEDIATRICS ◽  
1986 ◽  
Vol 77 (4) ◽  
pp. 553-556
Author(s):  
HARVEY S. SINGER
Keyword(s):  
Side Effects ◽  
Tardive Dyskinesia ◽  
Children And Adolescents ◽  
Behavior Disorders ◽  
Antipsychotic Drugs ◽  
Extrapyramidal Side Effects ◽  
Body Movements ◽  
Neuroleptic Therapy

Antipsychotic drugs, such as the phenothiazines (chlorpromazine, fluphenazine, thioridazine), butyrophenones (haloperiodol), and diphenylbutylpiperidines (pimozide) are used in children and adolescents to treat a variety of clinical entities including psychoses, tics, behavior disorders, and movement problems. Because virtually all of these drugs have a potential to affect body movements and posture, they have also been termed neuroleptics.1 Most physicians are aware of the more common acute extrapyramidal side effects of these drugs, such as oculogyria, pseudoparkinsonism, dystonia, and restlessness (akathisia). Despite the widespread use of neuroleptics, however, little is known about the long-term neurologic consequences of such treatment. Of particular concern, based originally on data in adults, is the risk of severe and persistent tardive dyskinesia developing in persons receiving neuroleptic therapy.

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.

scholarly journals What is the evidence on cholinergic medication for tardive dyskinesia?

2018 ◽  
Vol 24 (5) ◽  
pp. 289-294
Author(s):  
Vishal Bhavsar
Keyword(s):  
Tardive Dyskinesia ◽  
Movement Disorders ◽  
Antipsychotic Drugs ◽  
Controlled Trial ◽  
Clinical Effectiveness ◽  
Cochrane Systematic Review ◽  
Cholinergic Drugs ◽  
Randomised Controlled

SUMMARYAntipsychotic drugs are associated with movement disorders, especially with long-term use. Tardive dyskinesia, a condition characterised by repetitive involuntary muscle activity, is considered to be the most chronic, distressing and disabling of antipsychotic-associated movement disorders. There is theoretical justification for the use of cholinergic drugs in tardive dyskinesia, and they are used in clinical practice. A Cochrane systematic review synthesised randomised controlled trial data evaluating the effectiveness of cholinergic drugs for tardive dyskinesia, and for a range of secondary outcomes, including quality of life. In line with the authors of the review, this Commentary concludes that much higher-quality evidence on the use of cholinergic drugs in tardive dyskinesia is necessary, and that a patient with tardive dyskinesia should be offered the opportunity to try a newer cholinergic drug, ideally in the context of a well-conducted and reported clinical trial. At the same time, given uncertainty regarding clinical effectiveness, and in view of their accepted adverse effects, it would be understandable if a person with tardive dyskinesia decided to avoid cholinergic drugs.DECLARATION OF INTERESTNone.

Antipsychotic-induced tardive dyskinesia: The role of glutamatergic system

2016 ◽  
Vol 33 (S1) ◽  
pp. S97-S97
Author(s):  
A. Boiko ◽  
S. Ivanova ◽  
A. Semke
Keyword(s):  
Tardive Dyskinesia ◽  
Glutamate Transporter ◽  
Antipsychotic Treatment ◽  
Nucleotide Polymorphisms ◽  
Antipsychotic Therapy ◽  
Drug Induced ◽  
Schizophrenic Patients ◽  
Competing Interest

Tardive dyskinesia (TD) occurs in 20–25% of patients with long-term antipsychotic therapy. Abnormalities in glutamatergic transmission are considered one of the key components of the pathogenesis of drug-induced side effects. Glutamate acts as excitotoxin under certain conditions and in excessive concentrations.Aim is to study the concentration of glutamate and analysis of single nucleotide polymorphisms (SNP) in genes coding the glutamate transporter and NMDA-receptors in schizophrenic patients with TD and without it.The study group included 156 patients with schizophrenia receiving long-term antipsychotic treatment. Patients were divided into two groups: 63 patients with TD and 93 patients without it. Glutamate was determined in serum by spectrophotometric method. Determination of allelic variants of gene SLC1A2 (rs4354668) and GRIN2A (rs2650427, rs1969060) was performed by polymerase chain reaction in real-time.We found a significant (P < 0.05) increase of the concentration of glutamate in patients with TD. Significant (P < 0.05) reduction in frequency of genotype GG of GRIN2A (rs1969060) and TT of SLC1A2 (rs4354668) were found in patients with TD in comparison to group without TD. In the study of glutamate concentration depending on the genotype GRIN2A (rs1969060) and genotype SLC1A2 (rs4354668) we observed a statistically significant change: elevated levels of glutamic acid identified with the heterozygous genotype in patients.It is possible to suggest that reduction in frequency of these genotypes increases the risk of movement disorders due to the protective effect of these genotypes.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Sign in / Sign up

Export Citation Format

Share Document