Benzodiazepines tardive dyskinesia

But later, in Phase II, after two years of continuous use, the SSRIs may contribute to a more ominous motor syndrome, the REM sleep behavior disorder described in chapter 8 as the enactment of dreamed movement. Eor reasons still not well understood, the drugs interfere with our normal ability to inhibit motor outputs. As with tardive dyskinesia victims, patients who develop SSRI-induced RBD may find that their sleep disorder does not abate when they discontinue the drug. The RBD can itself be treated with benzodiazepines—Clonazepam, for example. But that may be throwing good drug money after bad. And a more disturbing possibility, not yet observed, is that the SSRI-induced RBD will evolve in the same way that spontaneous RBD does to full-blown Parkinson s disease. 

Treatment of tardive dyskinesia is often unsatisfactory, especially in severe cases. A large number of treatments have been proposed (SEDA-20,40), including antiparkinsonian drugs, benzodiazepines, baclofen, hormones, calcium channel blockers, valproate, propranolol, opiates, cyproheptadine, tryptophan, lithium, manganese, niacin, botulinum toxin, ECT, dietary control, and biofeedback training. In an open study, 20 patients (mean age 65 years) with severe unresponsive tardive dyskinesia (mean duration 44 months, mean exposure 52 months) were treated with tetrabenazine (mean dose 58 mg/day) (310). The mean score on the AIMS motor subset, determined from videotapes, improved by 54%. Sedation was the only subjective complaint. 

Tiapride appears to be useful in alcohol withdrawal as an alternative to the benzodiazepines (2). It facilitates the management of ethanol withdrawal, but its use in patients at risk of severe reactions in acute withdrawal should be accompanied by adjunctive therapy for hallucinosis and seizures. Since it may prove difficult to identify such patients and since there is also a small risk of the neuroleptic malignant syndrome (particularly with parenteral administration), the usefulness of tiapride in this setting is likely to be limited. The potential risk of tardive dyskinesia at the dosage used in alcoholic patients following detoxification (300 mg/day) requires evaluation and necessitates medical supervision. It is unlikely to produce problems of dependence or abuse. 

Atypical drugs, particularly at high doses, can yet cause extrapyramidal effects and this strategy is not always helpful. If the classical antipsychotic is simply continued, tardive dyskinesia reiiiits spontaneously in aroimd 30% of patients within a year but since the condition is difficult to tolerate, patients may be keen to try other medications, even where evidence suggests that the success rates for remission are limited. These include vitamin E, benzodiazepines, 3-blockers, bromocriptine and... 

Umbrich P, Soares KV. Benzodiazepines for neuroleptic-induced tardive dyskinesia. Cochrane Database Syst Rev 2003 2 CD000205. 

Exhibiting fine, wormlike movements of the tongne is a symptom of tardive dyskinesia, which is an adverse effect that may develop after months or years of continnons therapy with a conventional antipsychotic medication. The medication should be discontinued, and a benzodiazepine should be administered. 

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