Involuntary movements caused by phenytoin intoxication in epileptic patients.

Abstract

(Glaser, 1972). Although choreoathetosis has been described (Peters, 1962;Logan and Freeman, 1969;Kooiker and Sumi, 1974;McLellan and Swash, 1974), only a few cases have been documented adequately. During the last two years we have seen involuntary movements in four patients, two of whom presented with severe choreoathetosis. These patients are described in the following case reports. (Accepted 5 September 1974.) 225 signs. A left carotid arteriogram showed a shift to the right of the anterior cerebral artery, and a pneumoencephalogram (AEG) showed displacement of the ventricles to the right without significant alteration of ventricular size or shape. A gross unilateral abnormality over the left hemisphere posteriorly was seen on EEG. The pathological significance of these findings was uncertain. His fits were bizarre in pattern and were asymmetrical, being more marked on the right, and being accompanied by transient aphasia. A three day course of corticotrophin (ACTH) was without effect, but when pheneturide 400 mg daily was started the fits appeared to decrease in frequency and severity. However, four days after starting this drug, he developed marked choreoathetoid movements involving head, neck, and upper limbs. Although it was felt at the time that this was due to the same process as that causing the fits, the movements disappeared when pheneturide was withdrawn.

Anticonvulsant-induced dyskinesias: a comparison with dyskinesias induced by neuroleptics.

“…Apart from the proven association of such dyskinesias with anticonvulsant intoxication, it has been suggested that they appear more readily in epileptics with known cerebral pathology (Logan and Freeman, 1969;Shuttleworth et al, 1974;Ahmad et al, 1975). While many of the cases reported indeed had neurological deficits in addition to their epilepsy, some have been otherwise normal people.…”

Psychiatric symptomatology, scholastics, and phenytoin

“…The estimation of the serum phenytoin concentration is invaluable in such a situation. [4–6] It has a long mean half life of 40 h[7] and is very cheap compared to its competitors making it highly acceptable. However, the fact that phenytoin might be more deleterious to higher cognitive functions than carbamazepine or sodium valproate[28] is still commonly ignored and the drug widely used without exercising the necessary precautions entailed in its administration as this case depicts with serum phenytoin levels never having been estimated before hospitalization.…”

Electroencephalography and phenytoin toxicity in mentally retarded epileptic patients.

“…Of his patients, 80 to 83% showed the characteristic EEG pattern of such toxicity (slowing of the background rhythms and impaired reactivity to eye opening, which improved after drug withdrawal). Ahmad et al (1975) have also attributed involuntary movements and EEG changes to phenytoin intoxication. The findings of these authors support the view of Logan and Freeman (1969) that drug toxicity seems to interact with underlying cerebral disease, an observation that agrees well with our experience (Viukari, 1970;Iivanainen et al, 1977).…”

“…Because some patients are extremely susceptible to phenytoin toxicity, monitoring only serum concentrations of the drug is not enough. Severe signs of intoxication have been reported in patients whose serum phenytoin concentration was only S ,umol/l (1 ,ug/ ml) (Levy and Fenichel, 1965;Ahmad et al, 1975). Furthermore, in toxic combinations of anticonvulsant drugs, even though the serum concentrations of the individual drugs may be within their therapeutic range, EEG examination may reveal encephalopathy.…”