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Year : 2000  |  Volume : 48  |  Issue : 4  |  Page : 391--4

Neurocysticercosis presenting as stroke.

S Jha, V Kumar 
 Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India., India

Correspondence Address:
S Jha
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.
India

Abstract

Stroke is a common but under recognized complication of neurocysticercosis (NCC). We report six patients having NCC who presented with stroke. All patients were young with no vascular risk factors. The arteritis which resulted in ischaemic infarct in these patients was related to the presence and severity of arachnoiditis. All patients responded well to steroids and albendazole therapy with minimal residual deficit.



How to cite this article:
Jha S, Kumar V. Neurocysticercosis presenting as stroke. Neurol India 2000;48:391-4


How to cite this URL:
Jha S, Kumar V. Neurocysticercosis presenting as stroke. Neurol India [serial online] 2000 [cited 2020 Apr 1 ];48:391-4
Available from: http://www.neurologyindia.com/text.asp?2000/48/4/391/1491


Full Text




  ::   IntroductionTop


Neurocysticercosis (NCC) is the most common parasitic disease of the central nervous system. NCC is an endemic problem of India, China, sub-Saharan Africa and Latin America.[1] The clinical manifestation of NCC are nonspecific and varied depending on the number and topography of lesions. The clinical presentation includes seizures, progressive intellectual deterioration and symptoms of increased intracranial pressure. Several clinical reports have described cerebrovascular complications of NCC. The approximate incidence of cerebral infarct is 3%[2],[3],[4] and 2.5% of patients with cerebral infarcts have NCC. However, the incidence of stroke varies according to the underlying prevalence of cysticercosis in a given population.5 Nevertheless stroke is an under recognized complication of NCC. We report six patients of NCC presenting as stroke.






  ::   Material and methodsTop


Six patients of cerebrovascular complications of neurocysticercosis were admitted under neurology at Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow between July 97 to April 99. The age of these patients varied between 7 to 30 years, five out of six being males. The diagnosis of neurocysticercosis was based on clinical profile, neuroimaging and serological test of serum and CSF. The clinical and radiological picture of these patients and the outcome following treatment is given in the [Table I].

Illustrative Case : A 10 year right handed child presented with recurrent episodes of right focal motor seizures for 10 months and acute onset left hemiparesis with abnormal behaviour since 15 days prior to hospitalisation. On examination, patient had moderate dementia (mini-mental score 18) and left hemiparesis with power of grade 3/5 without any sensory deficit. Cardiovascular examination including echocardiography was normal and so was the haemogram, biochemistry and chest X-ray. Cerebro spinal fluid (CSF) examination revealed glucose -70mg/dl, protein - 190mg/dl, and cells - 10/mm3 (predominantly lymphocytes). CSF culture for mycobacterium and fungus was negative. CSF and serum for cysticercosis IgM antibodies by ELISA was positive. Cranial contrast enhanced CT revealed multiple ring enhancing lesions in frontal, parietal and periventricular regions of both cerebral hemispheres with perifocal oedema. [Right] middle cerebral artery territory and right posterior cerebral artery territory infarcts were seen. MRI revealed similar findings with MR angiography showing occlusion of M1 segment of right middle cerebral artery and right posterior cerebral artery.

Patient was treated with phenytoin sodium, albendazole (15mg/kg) and prednisolone (1mg/kg). He showed improvement in motor weakness and cognitive score increased to 20, in followup after 3 months




  ::   DiscussionTop


The association of neurocysticercosis and stroke has been widely accepted.[7],[8] Various mechanisms are involved in genesis of stroke in patients with NCC. Stroke in these patients may be related to thrombosis of superficial cortical vessels owing to chronic meningitis.[8],[9],[10] It may be due to fusiform aneurysms produced by weakening of wall of the vessels[2] or due to occlusion of small perforating vessels affected by endarteritis.[5],[6] Patients may present with lacunar infarct, large artery infarction, progressive mid brain syndrome and recurrent TIAs.[2],[8],[11] All the cases reported here met the inclusion criteria for cysticercosis induced cerebral infarct[8] which include : patients younger than 40 years having no risk factors for cerebral vascular disease, CT evidence of meningial cyst adjacent to infarct and CSF findings compatible with active arachnoiditis.

The severity of cerebrovascular complication of NCC is related to distribution of cysticercal disease and the severity of accompanying arachnoiditis.[7],[12] Hence, when cysts are confined to a focal area and associated with mild arachnoiditis, they involve small penetrating vessels manifesting as lacunar syndrome. The second case in this series had a single ring lesion in right parafalx area and mild arachnoiditis presenting with lacunar infarct in right anterior cerebral artery territory.

When the cysts are widespread and accompanied by significant arachnoiditis, the associated vasculitis involves the main vessels of the Circle of Willis with segmental narrowing of major intracranial arteries that produce large cerebral infarcts.[7] Case 1 and case 6 of this series had involvement of major intracranial arteries with widespread parenchymal neurocysticercosis. Ischaemic cerebrovascular disease has also been associated with tuberculous meningitis and tuberculomas. Presence of fever, neck stiffness, extracranial forms of tuberculosis and decreased CSF glucose favour tubercular aetiology. None of our cases had history of fever or evidence of decreased CSF glucose. Five out of six patients had high antibody titre of cysticercosis in serum and CSF by ELISA method. It is important to diagnose the cysticercotic angitis as these patients require immediate steroid therapy to reduce subarachnoid inflammatory reaction which may cause recurrent cerebral infarcts.[8] Stroke is thus a common but under recognized complication of neuro cysticercosis. The diagnosis of NCC should be included in the list of causes of stroke in the young, particularly in endemic areas.



References

1Centre for disease control and prevention : Neurocysticercosis Update : International task force for
2disease eradication. MMWR1992; 41 : 697-698.
3Mc Cormick GF , Gicannota S, Zee CS et al : Carotid occlusion in cysticercosis. Neurology1983; 33 : 1078- 1080.
4Scharf D : Neurocysticercosis: two hundred and thirtyfive cases from a California hospital. Arch Neurol 1988; 45 : 777-780.
5Sotelo J : Neurocysticercosis. In : Infections of the nervous system. Kenedy PGE, Johmon RT; eds . Butter Worth London. 1987; 145-155.
6Barinagarrementeria F, Del Brutto OH: Neurocysticercosis and pure motor hemiparesis . Stroke1988; 19 : 1156-1158
7Barinagarrementeria F, Cantu C : Frequency of cerebral arteritis in subarachnoid cysticercosis : an angiographic study. Stroke 1998; 29 : 123-125.
8Carlos Cantu, Fernando Barinagarrementaria : Cerebrovascular complications of neurocysticercosis, clinical and neuroimaging, spectrum. Arch Neurol 1996; 53 : 233-239.
9Del Brutto OH : Cysticercosis and cerebrovascular disease : a review. J Neurol Neurosurg Psychiatry 1992; 55 : 252-254 .
10Grisolia JS, Wiederholt WC : CNS cysticercosis. Arch Neurol 1982; 39 : 540-544.
11Cardenasy Cardenas J : Cysticercosis of the nervous system Pathologic and radiologic findings. J Neurosurg 1962; 635-640.
12Escobar A : The pathology of neurocysticercosis. In Cysticercosis of the nervous system. Palacios E, Rodrigues-Carbajal J,Taveras J (eds). III. Charles C Thomas Publishing. Sring Field. 1983; 27-54.
13Fer Penning B, Litchman CD, Heier L : Bilateral middle cerebral artery occlusion in neurocysticercosis. Stroke1992; 23 : 280-283.