Facial dyskinesia

Burke, R., 6c Kang, U. J. (1988). Tardive dystonia Clinical aspects and treatment. In J. Jankovic 6c E. Tolosa (Eds.), Facial dyskinesias Advances in neurology (Vol. 49,... 

Lee CH, Cheung RT, Chan TM. Ciprofloxacin-induced oral facial dyskinesia in a patient with normal liver and renal function. Hosp Med 2000 61(2) 142-3. 

Barone DA, Raniolo J. Facial dyskinesia from overdose of an antihistamine. N Engl J Med 1980 303(2) 107. 

An 8-year-old boy complained of abnormal facial movements and hallucinations. One day before these symptoms, he had been given his sister s Cordec DM droplets (carbinoxamine maleate 2 mg, pseudoephe-drine hydrochloride 25 mg, and dextromethorphan 4 mg) for a cold. He had facial dyskinesia, dilated pupils, pyrexia, tachycardia, and reduced bowel sounds and responded to a benzodiazepine. 

Tardive dyskinesia Oral-facial dyskinesia widespread After months or years of Excess function of Prevention crucial treatment... 

Thach BT, Chase TN, Bosma JF (1975) Oral facial dyskinesia associated with prolonged use of antihistaminic decongestant. N Engl J Med 293 486-490 Van Hecke E (1975) Ethylenediamine sensitivity from exposure to epoxy resin hardeners and mycolog cream. Contact Dermatitis 1 344-348 Vickers CFH (1961) Dermatitis medicamentosa. Br Med J 1 1366-1368... 

Phenothiazines and butyrophenones may cause various movement disturbances in man. Dystonia in children and young adults and parkinsonism or restlessness in older subjects may occur during treatment and are reversible. The facial dyskinesia which may occur in elderly subjects, especially those with evidence of brain damage, is often irreversible (see ref. 225 for review). Unlike reserpine, these substances have little effect on brain amine levels in animals. They behave as if they block amine receptors so that there is a compensatory activation of monoaminergic neurones with increased but functionally ineffective release of amines into the synaptic cleft. Thus,... 

Oral and facial dyskinesia have been described during acute treatment with L-dopa and dopamine receptor agonists and after therapy with anti-psychotic drugs, especially phenothiazine and butyrophenone derivatives (see Chapter 5). 

In 1973 Worz described a case of a 60-year-old woman in whom oral dyskinesia developed after prolonged use of a non-phenothiazine antihistamine mehydro-lin(25 ). Thach et al. 9 ) described 2 cases of oral facial dyskinesia associated with prolonged use of antihistamine decongestants, which must be briefly discussed here, since the drugs involved are very widely used, often for trivial indications. 

Tardive dyskinesia refers to uncontrollable facial movements. It is more likely to occur in the elderly. Tardive dyskinesia is commonly associated with the use of antipsychotic drugs, such as haloperidol. The atypical antipsychotics, such as clozapine, olanzapine, risperidone and quetiapine are less likely to cause tardive dyskinesia. 

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

Tachycardia heart rate more than 100 beats/min Tardive dyskinesia uncontrollable facial movements Thrombocytopenia a reduction in platelet count Tics repetitive involuntary movements Tinea corporis ringworm infection Tinea pedis athlete s foot... 

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... 

Tardive dystonia can make an individual appear unsympathetic or bizarre, especially to the uninformed observer, who equates the facial grimaces or neck distortions with being crazy. As in all the drug-induced dyskinesias, the individual may try to cover up the disorder with additional movements that make the disorder seem voluntary and therefore not a product of mental illness. The result can be very confusing and even distressing to the observer. I have read several medical records in which... 

Because TD often makes the sufferers look odd or even bizarre, they experience shame and humiliation, typically leading to lowered selfesteem and social withdrawal. Even a seemingly mild dyskinesia that affects facial expression can be sufficiently humiliating to cause a person to want to stay at home and away from people. Similarly, a speech abnormality that makes a person talk funny can lead to the avoidance of communicating. 

A type of automatic behavior, which can continue for hours, has been observed in addicts who inject large doses of central nervous system stimulants. Dyskinesias can occur, with strange facial and tongue movements or jerky motions of the arms and legs and a never-ending repetition of certain actions. Such stereotyped activity is induced in laboratory animals with high doses of amfetamine. 

Two cases of gabapentin-related dyskinesia have been reported (19). The patients were 60 and 41 years old and took gabapentin 900-1200 mg/day for generalized anxiety. Generalized dyskinetic movements and facial tics appeared after 3 days and disappeared after 2 days of withdrawal. 

Monitor for evidence of dyskinesia (difficulty with movement). Assess for clinical reversal of symptoms (improvement of tremor of head/hands at rest, masklike facial expression, shuffling gait, muscular rigidity). 

Most patients who returned to society were able to function moderately well, but if they stopped their medication their condition deteriorated. Also, CPZ and compounds related to this phenothiazine series produced motoric side effects, including extrapyramidal side effects (EPS) that resemble Parkinson s disease. These symptoms could be severe and developed in up to 90% of patients on typical antipsychotic drugs. This condition often progressed to irreversible tardive dyskinesias, involuntary movements of the limbs and facial muscles that resemble the symptoms of Huntington s disease. In addition, such typical antipsychotics, although they were effective in treating the positive or florid symptoms of schizophrenia, did not ameliorate the negative symptoms of the disease. 

Tardive Dyskinesia and Dopamine Receptor Supersensitivity - Tardive dyskinesia is a major complication of long term treatment with neuroleptic drugs 24,25,26,27 it is characterized by abnormal movement of facial muscles and extremities which frequently worsen when the neuroleptic dose is lowered or terminated. Increasing the dose, however, may temporarily alleviate the symptoms. The chronic treatment of rats and mice with neuroleptics leads to an increased motor activity and enhanced sensitivity to the motor stimulant effects of apomorphine, a direct dopamine receptor agonist28 ... 

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