Serum immunoglobulins in tardive dyskinesia — implication for pathogenesis of the syndrome

AbstractLevels of immunoglobulins were measured in 32 schizophrenic patients with tardive dyskinesia and 34 schizophrenic patients without tardive dyskinesia. The duration of neuroleptic treatment in years was similar in the two groups. The serum immunoglobulin concentrations (mg%) were found to be significantly different in the two groups; IGA and IGM levels were higher in patients with tardive dyskinesia. The present results may be explained on the basis of dysfunction of the immunological system in tardive dyskinesia.

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The Current Status of Tardive Dyskinesia

Australian & New Zealand Journal of Psychiatry ◽

10.1080/j.1440-1614.2000.00737.x ◽

2000 ◽

Vol 34 (3) ◽

pp. 355-369 ◽

Cited By ~ 83

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.

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Immune modulation in resistant schizophrenic patients during long-term neuroleptic treatment

Biological Psychiatry ◽

10.1016/s0006-3223(97)87337-4 ◽

1997 ◽

Vol 42 (1) ◽

pp. 108S

Author(s):

S. Bignotti ◽

G.B. Tura ◽

G. Rossi ◽

R. Pioli ◽

M. Maes ◽

...

Keyword(s):

Immune Modulation ◽

Neuroleptic Treatment ◽

Schizophrenic Patients

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Treatment of tardive dyskinesia

Drug and Therapeutics Bulletin ◽

10.1136/dtb.16.14.55 ◽

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.

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The management of tardive dyskinesia

Drug and Therapeutics Bulletin ◽

10.1136/dtb.24.7.27 ◽

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

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