Polymorphic Drug Metabolism in Schizophrenic Patients With Tardive Dyskinesia

1995 ◽  
Vol 15 (3) ◽  
pp. 211-216 ◽  
Author(s):  
Holger Arthur ◽  
Marja-Liisa Dahl ◽  
Bo Siwers ◽  
Folke Sjoqvist
1990 ◽  
Vol 7 (2) ◽  
pp. 145-146 ◽  
Author(s):  
Hanafy Youssef

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.


1978 ◽  
Vol 16 (14) ◽  
pp. 55-56

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.


1986 ◽  
Vol 24 (7) ◽  
pp. 27-28

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


2007 ◽  
Vol 68 (07) ◽  
pp. 1031-1037 ◽  
Author(s):  
Igor Libov ◽  
Chanoch Miodownik ◽  
Yuly Bersudsky ◽  
Tzvi Dwolatzky ◽  
Vladimir Lerner

1978 ◽  
Vol 133 (1) ◽  
pp. 82-82 ◽  
Author(s):  
Alan C. Gibson

SummaryTwenty-five schizophrenic patients with tardive dyskinesia were given 600 mgs sodium valproate daily with their neuroleptic medication. After one month there was no change in their signs, as judged by a panel of nine viewing films of them taken before and at the end of this treatment.


1994 ◽  
Vol 54 (1) ◽  
pp. 71-86 ◽  
Author(s):  
P.Bart Vrtunski ◽  
Larry D. Alphs ◽  
Herbert Y. Meltzer

2012 ◽  
Vol 22 ◽  
pp. S56
Author(s):  
V.A. Gavrilova ◽  
O.Y. Fedorenko ◽  
E.V. Rudikov ◽  
E.G. Boyarko ◽  
A.V. Semke ◽  
...  

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