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Tardive dyskinesia , movement disorders

Tardive dyskinesia A chronic disorder of the nervous system characterized by involuntary jerky or writhing movements of the face, tongue, jaws, trunk, and limbs, usually developing as a late side effect of prolonged treatment with antipsychotic drugs. [Pg.1577]

Patients who have received neuroleptics for long periods of time may develop a hyperkinetic disorder of the extrapyramidal system characterized by involuntary, purposeless movements affecting many parts of the body. This is known as tardive dyskinesia. Most commonly, these are manifested in a syndrome involving abnormal movements of the tongue, mouth and masticatory muscles. There are also choreoathetoid movements of the extremities. The mechanism by which these symptoms develop remains unknown. [Pg.777]

The major adverse effects of first-generation drugs for schizophrenia are involuntary movement disorders. Symptoms include tremor, rigidity, restlessness, and slowness of movement, strongly reminiscent of the movement disorders in parkinsonism, about which more follows later. The worst of these movement disorders is tardive dyskinesia, an irreversible movement disorder. [Pg.305]

Antipsychotics also have a troublesome side effect burden that includes an often-irreversible movement disorder known as tardive dyskinesia (TD). Other side effects include so-called parkinsonism, dystonic reactions (i.e., abrupt onset of muscle spasms), akathisia (an uncomfortable sense of motoric restlessness), sedation, weight gain, dizziness, dry mouth, and constipation among others. These side effects, in particular the risk for TD, limit the usefulness of antipsychotics in the treatment of ADHD, and at this time the typical antipsychotics cannot be considered a reasonable monotherapy in uncomplicated ADHD. [Pg.249]

There are, of course, risks with long-term use of conventional antipsychotics. The most concerning is an irreversible movement disorder known as tardive dyskinesia. Nevertheless, some particularly fragile patients with BPD may require long-term antipsychotic treatment. If so, atypical antipsychotics are recommended. [Pg.329]

Q80 Tardive dyskinesia is a chronic movement disorder characterised by uncontrolled facial movements. Tardive dyskinesia is associated with the use of trifluoperazine. [Pg.278]

Tardive dyskinesia is a potentially irreversible movement disorder characterized by choreoathetoid movements. The possibility of a primary neurological disorder should be considered when a patient being treated with an antipsychotic develops involuntary movements. It should also be noted that patients might develop transient withdrawal dyskinesias as the dosage of neuroleptics is lowered or discontinued (Campbell et ah, 1999). It appears that withdrawal dyskinesias are more common in children than adults. [Pg.334]

Tardive dyskinesia is a disorder characterized by involuntary choreo-athetoid movements of the face, trunk, or extremities. The syn-... [Pg.99]

But the most insidious effects are in the third wave of long-delayed changes of the sort that we see with the antipsychotic drugs that have been taken for long periods of time. These changes often affect the motor system and may even outlast discontinuation of the drug. The best known of these is called tardive dyskinesia (delayed movement disorder). Tardive... [Pg.209]

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. [Pg.210]

Worse yet, if these D2 receptors in the nigrostriatal DA pathway are blocked chronically (Fig. 11—5), they can produce a hyperkinetic movement disorder known as tardive dyskinesia. This movement disorder causes facial and tongue movements such as constant chewing, tongue protrusions, and facial grimacing, as well as limb movements, which can be quick, jerky or choreiform (dancing). Tardive dyskinesia is thus caused by long-term administration of conventional antipsychotics and is... [Pg.404]

FIGURE 11-5. Long-term blockade of dopamine 2 receptors by dopamine 2 antagonists in the nigrostriatal dopamine pathway may cause these receptors to up-regulate. A clinical consequence of this may be the hyperkinetic movement disorder known as tardive dyskinesia. This up regulation may be the consequence of the neuron s futile attempt to overcome drug-induced blockade of its dopamine receptors. [Pg.406]

Tardive dyskinesia A movement disorder characterized by involuntary, fragmented movements of the mouth, face, and jaw (i.e., chewing, sucking, tongue protrusion, and the like). This disorder may occur during the prolonged administration of antipsychotic drugs. [Pg.631]

Chlorpromazine, the first modern drug to be used in the treatment of schizophrenia and other psychotic disorders, was introduced into psychiatry in 1952 [61]. It was followed by a number of other drugs for the treatment of these conditions (e.g., haloperidol, thioridazine). These were also called neuroleptics because of their neurological side effects, such as parkinsonian syndrome and tardive dyskinesia. Tardive dyskinesia is a movement disorder characterized by involuntary movements of the face and limbs. The antipsychotic properties of these drugs were inseparable from the extrapyramidal effects. [Pg.307]

In his review of the literature published in 1996, Leo already found 42 articles reporting 71 cases of motor symptoms that appeared for the first time during SSRI use. Akathisia was reported in 32 cases, dystonia in 20, parkinsonism in 10, tardive dyskinesia-like movements in 8, and tremors in 7. Several patients had combined disorders. [Pg.175]

Gerber and Lund (1998) reviewed the literature and located 127 case reports of SSRI-induced abnormal movements. These included akathisia (agitation with hyperactivity), tardive dyskinesia, parkinsonism, dystonia (muscle spasms), bruxism (tooth grinding), and related disorders. They found many additional case reports from the drug manufacturers, including 516 cases of parkinsonism and 76 cases of tardive dyskinesia. The term tardive dyskinesia is usually reserved for cases that are irreversible. [Pg.175]

Jeste, D., lager, A., 6c Wyatt, R. (1986). The biology and experimental treatment of tardive dyskinesia and other related movement disorders. In P. A. Berger 6c H. K. Brodie (Eds.), Biological psychiatry (pp. 535-580). New York Basic Books. [Pg.494]

Meyer-Lindenberg, A., Krausmck, B. (1997). Tardive dyskinesia in a neuroleptic-naive patient with bipolar-I disorder Persistent exacerbation after lithium intoxication. Movement Disorders, 12, 1108. [Pg.505]

Tarsy, D., 6c Baldessanm, R. (2006). Epidemiology of tardive dyskinesia Is risk declining with modern antipsycho tics Movement Disorders 21, 589-598. [Pg.520]


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See also in sourсe #XX -- [ Pg.440 , Pg.447 ]




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