Focal Seizures With Single Small Ring-Enhancing Lesion Pratibha Singhi and Munni Ray An 8-year-old girl presented with simple partial seizures. The differential diagnosis and evaluation point out the fact that in most of the world, conditions considered rare in the United States are important diagnostic considerations. Copyright 9 1999 by W.B. Saunders Company CASE An 8-year-old girl who previously had been well presented with a focal sensory motor seizure involving the left upper limb, lasting for about 5 minutes. She first complained of pain in the affected limb, which was followed by abnormal tonic posturing of hand and subsequently clonic movements. There was no abnormal eye deviation or loss of consciousness. The event was followed by post ictal weakness of the left upper limb, which lasted for 1 to 2 hours. There was no history of headache or early morning vomiting suggesting raised intracranial pressure. There was no history of meningitis or encephalitis, head injury, mental retardation, or any other neurological illness. There was no history of epilepsy in the family, or contact with a case of tuberculosis. The child was born of a middle class, nonconsan- guinous marriage. She was not a vegetarian but did not eat pork. On examination the child had normal anthropometric param- eters. General physical examination was uuremarkable. There were no neurocutaneous markers or subcutaneous nodules. Neurological examination was essentially normal. There was no papilloedema, cranial nerve palsy or motor or sensory abnormal- ity. Comment Acute-onset partial seizures in an otherwise asymptomatic child may be idiopathic or symptomatic. In developing countries like India, more than 60% of partial seizures are symptomatic. The causes of symptomatic partial seizures in children in India have been found to be somewhat different from those reported from the West. Although common reported causes from developed countries (after exclusion of perinatal insults) are gliomas, cortical dysplasias, calcifications, and infarcts, ~-3those reported from Indian studies are predominantly infections (neurocysticercosis and tuberculomas) (Table 1).46 Investigations and Clinical Course A contrast computed tomography (CT) scan of the head was done, which revealed a single ring-enhancing lesion measuring 11.7 X 8.9 ram. There was significant edema, 42.5 • 40 mm, surrounding the lesion. There was no mass effect or calcifica- tion. Her EEG showed a good background rhythm of 8 to 9 seconds 30 to 40 gv. High-voltage (100 to 180 laV) slow waves were seen from the right temperoparietal region (Fig 1) indicat- From the Pediatric Neurology and Neurodevelopment Unit, Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Address reprint requests to Pratibha Singhi, MD, Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh 160 012, India. Copyright 91999 by W.B. Saunders Company 1071-9091/99/0603-0013510. 00/0 ing the presence of an underlying structural focal abnormality. Investigations to find the cause of this single, small ring- enhancing CT lesion (SSECTL) were undertaken. Her hemoglo- bin was 12:1 g%, and total and differential counts were normal. Work-up for tuberculosis revealed a negative mantoux test, normal chest radiograph, and erythrocyte sedimentation rate of 25 mm in the first hour. Neurocysticercosis serology was negative. To confirm the suspicion of neurocysticercosis, mag- netic resonance imaging (MRI) of the head was undertaken, which revealed a cystic lesion showing the scolex (Fig 2). The diagnosis of neurocysticercosis was confirmed and the child was started on 15 mg/kg/day of albendazole for 28 days along with prednisolone 2 mg/kg/d for 5 days. Carbamazepine 10 mg/kg/day was started for control of seizures. She had a seizure recurrence within 1 month following onset of therapy, the dose of anticonvulsant was increased to 15 mg/kg/day. Thereafter no further recurrence of seizures was noticed. A repeat scan done at the end of 1 month showed a decrease in size of the lesion to 7.1 X 4.3 mm and of the surrounding edema to 18.6 • 10.0 mm. The child was continued on carbamazepine therapy. MRI scan done after 3 months revealed total disappear- ance of lesion with no edema. The child remained seizure-free for 2 years. Carbamazepine was tapered off, and she has had no recurrence of seizures since then. DISCUSSION SSECTLs with perifocal hypodensity suggestive of edema are the commonest neuroimaging finding in children with partial epilepsy from India. 4,5 Controversy surrounded their etiology for quite some time. They were earlier considered to repre- sent post-ictal phenomenon, localized encephalitis, or tuberculomas. 6-8 A recent biopsy study has shown that most of these are neurocysticercosis.9,1~ Neurocysticercosis is a growing problem in tropical countries and is increasingly being recog- nized as the leading cause of epilepsy. In fact, it has become an important cause of neurological disease worldwide. 1H3 Cysticercosis is caused by the en- cysted larval stage of the tapeworm Taenia solium. Humans become the intermediate host in the life cycle of the cestode by ingesting its eggs from contaminated food or water, or througfi autoinfec- fion (anus to mouth) in individuals who harbor the adult parasite in their small intestine. Cysticercosis is a disease caused by poor sanita- tion: lack of proper water and sewage systems, poor personal habits, and coexistence of humans and animals, particularly pigs. Earlier, it was wrongly 196 Seminars in Pediatric Neurology, Vol 6, No 3 (September), 1999: pp 196-201