2.7. Treatment

AQ Abdul Qavi
RG Ravindra Kumar Garg
HM Hardeep Singh Malhotra
AJ Amita Jain
NK Neeraj Kumar
KM Kiran Preet Malhotra
PS Pradeep Kumar Srivastava
RV Rajesh Verma
PS Praveen Kumar Sharma
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All patients having seizures were treated with oxcarbazepine (10–15 mg/kg body weight). If seizure control was not achieved, clobazam was added. Patients with cysticercal encephalitis were treated with corticosteroids (intravenous dexamethasone, 4 mg every 6 hours).

Patients, who gave consent and did not have any contraindication, for example, involvement inside-of orbital muscle cone (without excision), cardiac conduction pathway involvement, sensitivity to albendazole, or comorbid ailment preventing corticosteroid therapy, were subjected to antiparasitic treatment. Patients with lesion/s abutting the ventricular outflow tract (deemed to cause obstruction and life-threatening increase in intracranial pressure on degeneration) and those with cysticercal encephalitis were also considered ineligible for albendazole therapy. It may be noted that cysticercal encephalitis represents a patient in an altered state of consciousness with a heavy first-contact lesion load and generalized cerebral edema; any type of antiparasitic therapy may prove lethal in such a situation. Albendazole (15 mg/kg/day in two divided doses) was given for 28 days. Three days before starting albendazole, oral corticosteroids (methylprednisolone 0.75–1 mg/kg) were started and continued throughout albendazole therapy; these were subsequently tapered off (0.25 mg/kg/wk) in the next 3 to 4 weeks. A close watch for any untoward event, like raised intracranial pressure, altered sensorium, visual disturbances, cardiac conduction defect, or occurrence of myelitis, was kept. In case of any complication, albendazole was stopped, corticosteroids were continued and re-imaging was performed.

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