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| CASE REPORT |
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| Year : 2003 | Volume
: 51
| Issue : 4 | Page : 551-552 |
Neurocysticercosis presenting as Weber’s syndrome: As short report
Singh NN, Verma R, Pankaj BK, Misra S
Department of Neurology, BHU, Varanasi
Correspondence Address:
Department of Neurology, BHU, Varanas
This case report describes a rare, non-epileptic manifestation of neurocysticercosis where a 22-year-old male presented with acute onset right 3rd nerve palsy with left hemiplegia (Weber syndrome). Computerized tomography and magnetic resonance imaging revealed cysticercus granuloma. The patient improved and became asymptomatic with steroid treatment. Recognizing this clinical entity would avoid unnecessary antituberculous treatment and surgical intervention.
How to cite this article:
Singh N N, Verma R, Pankaj B K, Misra S. Neurocysticercosis presenting as Weber’s syndrome: As short report. Neurol India 2003;51:551-2 |
Weber's syndrome is a distinctive brainstem syndrome characterized by ipsilateral 3rd nerve palsy with contralateral hemiplegia and is due to an intrinsic or extrinsic lesion in the ventral midbrain. The first case was described by Sir Herman David Weber, a London-based physician in the 19th century, and the eponym of the syndrome goes in his name.[1] Since then many cases of non-vascular causes including aneurysm, tumor and demyelination have been reported. We report a rare cause of Weber's syndrome, cysticercus granuloma.
A 25-year-old male presented with acute onset left side weakness. The following day he noticed diplopia while looking forward and drooping of the right eyelid. Drooping of the right eyelid was complete in the next two days. By then the patient had marked difficulty in walking and had to take the support of a stick. He had no features of raised intracranial tension. He was not hypertensive or diabetic and was a non-smoker. Neurological examination revealed a conscious individual with normal higher functions. Cranial examination revealed complete right 3rd nerve palsy and normal ocular fundi. Motor system showed left side spastic weakness with grade 4/5 power. Deep tendon reflexes were brisk on the left side with up-going plantar response. Sensory system examination was essentially normal. There were no cerebellar signs.
Contrast enhanced Computerized tomography (CT) scan revealed a small enhancing ring lesion on the right side of the midbrain. Contrast enhanced magnetic resonance imaging (MRI) revealed a small ring enhancing granuloma in the ventral midbrain over the right side with eccentric nidus (isointense) [Figure:1]. Enzyme-linked immunosorbant assay using purified fraction from taenia solium cysticerci (PCF-ELISA) in cerebrospinal fluid (CSF) showed a strong positive result.
The patient was treated with steroids for two weeks. The patient showed rapid clinical improvement in his hemiparesis, ptosis and ocular movements. Neurological examination at 2 months follow-up showed that he was symptom-free with no neurological deficit. Follow-up MRI revealed no abnormality.
The most common cause of Weber's syndrome is vascular and is due to the occlusion of the peduncular and interpeduncular branches of the posterior cerebral artery, often due to embolic occlusion.[2] Cysticercus granuloma as the cause of Weber's syndrome has not been recorded earlier. In our case contrast MRI and CT scan revealed characteristic granuloma with eccentric nidus suggestive of neurocysticercosis.[3] The other evidence was PCF-ELISA positivity in CSF. The remarkable clinical and radiological improvement with steroids also supports the diagnosis of a cysticercus.[4]
Vascular events are common manifestations of neurocysticercosis and neurocysticercosis is considered to be a risk factor for stroke in the young in endemic areas. Strokes are caused by the inflammatory occlusion of the arteries at the base of the brain, secondary to cysticercus arachnoiditis. Small vessels of the circle of Willis are usually involved presenting as lacunar stroke.
The granulomatous stage represents cysticercal cyst in the degenerative phase. The role of anticysticercal treatment in this stage is controversial.[5] Steroids may be effective in containing the inflammatory response in such a situation.
| 1. | Liu CT, Cremer CW, Logigian EL, et al. Midbrain syndrome of Benedict, Claude, Nothnagel-setting record straight. Neurology 1992;42:1820-2.  |
| 2. | Koroshetz WJ, Ropper AH. Artery to artery embolism causing stroke in posterior circulation. Neurology 1987;37:292-6. |
| 3. | Rajshekhar V, Chandy MJ. Validation of diagnostic criteria for solitary cerebral cysticercus granuloma in patient presenting with seizures. Acta Neuro Scand 1997;96:76-81. [PUBMED] |
| 4. | DeSalva AD, Quagliato EM, Rossi CL. A quantitative enzyme linked immunosorbent assay (ELISA) for the immunodiagnosis of neurocysticercosis using purified fraction from taenia solium cysticerci. Diag Microbiol Inf Dis 2000;37:87-92. |
| 5. | Kramer LD. Medical treatment of cysticercosis - ineffective. Arch Neurol 1995;52:101-2. |
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