P.N. Suresh Kumar, S. Kishor Kumar widespread erythematous rashes. There were multiple target lesions involving the trunk and limbs with blister formation that lacerated easily. There was mucosal involvement with hemorrhagic areas on the oral mucosa, conjunctiva, and external genitalia. Sodium valproate was discontinued on 8th day after seeing the skin reaction, however haloperidol with trihexyphenidyl was allowed to continue, as he was psychiatrically symptomatic. The skin reaction was treated with oral prednisolone (60 mg/day in tapering dosage), oral antihistamine (cetrizine 20 mg/day) and topical calamine lotion. Within a week, severe ulceration of oral mucosa was seen. Hemorrhagic crusting and grayish white membrane were visible on the lips, palms and sole. The skin lesions showed typical “target lesions” with nercotized red area and grayish red swollen margins spread all over the body. After 4 weeks, the mucosal and skin lesions started subsiding; the eyes were the first to clear and no sequelae was evident. By continuing haloperidol and trihexiphenidyl in tapering dosage he became euthymic within 4 weeks. Discussion SJS is a severe and extensive type of erythema multiforme characterised by a severe necrotising cutaneous reaction and involvement of several mucosal sites (oral, conjuctival, and anogenital). Late complications include pigmentation, scarring, and skin contracture. The mortality rate of SJS is 5% to 15%. Treatment of SJS should be individually tailored according to the cause and complications of the syndrome. The most severe cases should be considered for the intensive treatment in a burns unit. Systemic corticosteroids should not be used routinely, but may be justified in the early stages of drug induced SJS. Treatment should also focus on early detection and prevention of common fatal complications such as infection. Prophylactic antibiotic therapy should be started before signs of infection manifest. Topical treatment may include hydrocolloid or gauze dressings. The clinical condition may require 3 to 6 weeks to resolve, depending upon the extent and severity of the lesions. Alternative systemic treatments are still experimental and include haemodialysis, plasmapheresis, and cyclosporin therapy (Poon & Ho, 2001). After millions of prescriptions of sodium valproate, mostly as an anti epileptic and recently as antimanic, there are only a few reported cases of SJS due to this drug (Platin et al, 1995; Tsai & Chen, 1998; Rzany et al, 1999 & Mishra et al, 2002). In the index case, the diagnosis of SJS was 270 consistent with the clinical description given in standard dermatology textbooks. The algorithms for the implication of a drug in causing an adverse skin reaction is as follows- a) alternative causes, especially infections should be excluded; b) the interval between the introduction of a drug and the onset of reaction should be examined (for drug- induced SJS it is 1-3 weeks); c) any improvement after drug withdrawal should be noted; d) the physician should determine whether similar reactions have been associated with the same compound; e) any reaction with readministration of the compound should be noted (Roujeau & Stern, 1994). In the absence of any systemic or local infection or exposure to any other drug except haloperidol and trihexyphenidyl (SJS is highly uncommon with these two drugs), the onset of SJS within the second week of starting treatment and with the fact that condition was improved with the discontinuation of sodium valproate, suggests that the condition was perhaps caused by sodium valproate. 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