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25222ournal of , Neurosurgery, and Psychiatry 1992;55:252-254

REVIEW J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.4.252 on 1 April 1992. Downloaded from Cysticercosis and cerebrovascular : a review

Oscar H Del Brutto

Abstract consider this parasitic disease in the differential Ischaemic cerebrovascular disease is a diagnosis of cerebral infarcts. This paper pre- relatively common but under-recognised sents a review of the literature on this subject, complication of neurocysticercosis. It is and discusses the pathophysiology of cysti- usually caused by inflammatory occlusion cercosis induced cerebrovascular disease. of the at the base of the secondary to cysticercotic arachnoiditis. Lacunar infarction In most cases, the involved vessels are of This is the most common cerebrovascular small diameter and the neurological pic- complication ofNCC. 5 Cysticercosis-induced ture is limited to a lacunar syndrome lacunar infarcts are usually located in the secondary to a small cerebral infarct. territory of the lenticulostriate branches of the However, large infarcts related to the anterior or middle cerebral ,20 and result occlusion ofthe middle cerebral artery or from occlusive endarteritis secondary to the even the internal carotid artery have also intense inflammatory reaction within the sub- been reported in this setting. CT and CSF arachnoid space that is triggered by meningeal examination usually support the cause- cysticerci. Such inflammatory reaction is com- and-effect relationship between neurocys- posed ofhyalinised parasitic membranes, colla- ticercosis and the cerebral infarct by gen fibres, lymphocytes, plasma cells, eosino- showing abnormalities compatible with phils, and multinucleated giant cells."9 These cysticercotic arachnoiditis. An accurate changes cause abnormal thickening of the diagnosis of this condition is important leptomeninges at the base of the skull with since early treatment with steroids is subsequent entrapment and occlusion ofblood advised to ameliorate the subarachnoid vessels around the circle ofWillis. inflammatory reaction which may cause Small cerebral infarcts due to NCC have recurrent cerebral infarcts. been associated with lacunar syndromes which are indistinguishable from those caused by Cysticercosis is the most frequent parasitic .5'7 These patients may present disease of the CNS, and one of the most with an ataxic , pure motor hemi- pleomorphic of neurological disorders.'5 Clin- paresis, or sensorimotor , due to a lacune ical manifestations of neurocysticercosis that is usually located in the posterior limb of http://jnnp.bmj.com/ (NCC) are nonspecific and largely depend on the internal capsule or the corona radiata. CT the number and topography of lesions and the provides clues to the aetiology of the infarct as host immune response to the parasite.'43039 it shows associated abnormalities in most NCC is usually manifested by , pro- cases. In a series of seven patients with a gressive intellectual deterioration, and signs lacunar syndrome due to NCC, we found CT and symptoms of increased intracranial pres- evidence ofNCC in six cases: four patients had

sure.4' In addition, a variety of focal neuro- a suprasellar cysticercus ipsilateral to the on September 30, 2021 by guest. Protected copyright. logical signs occur in many patients. While infarct, one had a large meningeal cyst in the such deficits are usually related to parenchymal vicinity ofthe infarct, and the other patient had brain cysticerci, in an important number of due to diffuse arachnoiditis.6 patients they occur as the result of a cere- CSF analysis is of paramount importance in brovascular event. 2738 45 the evaluation of patients with suspected cysti- Cerebrovascular complications of NCC cercotic angiitis, as it shows a mild pleocytosis were first described in the nineteenth century and elevated protein contents in most cases. In in a patient with cysticercotic who addition, immunological reactions (ELISA had angiitis of small intracranial vessels.29 and complement fixation test) for the detection Since then, several authors have recognised the of anticysticercal antibodies are almost always association between NCC and cerebrovascular positive in CSF due to active meningeal disease.2 11 2028 3348 Most of these reports have disease.35 may be com- Neurologic Service, Hospital Regional del focused on the histopathological and angio- pletely normal because the involved vessels are Instituto Ecuatoriano graphic aspects of cysticercotic angiitis, but too small to be imaged, or may show segmental de Seguridad Social, little emphasis has been placed on the clinical narrowing of major intracranial vessels when Guayaquil, Ecuador OH Del Brutto manifestations of this condition or in the the process of angiitis is more extensive.6 therapeutic approach. In recent years, several Correspondence to: Dr Del Brutto, PO Box patients with brain infarcts due to NCC have Large infarctions 09-01-3734, Guayaquil, 26 34 an Ecuador, South America been reported,5-7 nevertheless, stroke is Cerebral infarcts involving the deep and super- Received 5 March 1991. under-recognised complication of NCC, and ficial territory of a major intracranial artery Accepted 2 May 1991 authoritative textbooks ofneurology' 38 do not have occasionally been reported in patients Cysticercosis and cerebrovascular disease: a review 253

with cysticercotic angiitis. A search of the supine position. This patient had a large J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.4.252 on 1 April 1992. Downloaded from literature reveals only five well-documented cysticercus around the internal carotid artery cases.26 3447 These patients presented with that occluded its lumen and caused positional profound neurological deficits secondary to an cerebral ischaemia. On the other hand, we infarct that involved the basal ganglia, the have recently described a patient with transient cerebral cortex, or both. They had a protracted episodes of hemiparesis due to a large par- course and most of them died as the result of enchymal brain cysticercus.'6 Data from these either the cerebral infarct or the associated reports suggest that NCC may cause transient arachnoiditis. CT was available in three of neurological dysfunction resembling transient these patients and showed a large meningeal ischaemic attacks. The pathogenesis of this cysticercus adjacent to the brain infarct in condition, however, is not uniform. It may be every case. Angiography showed occlusion of of vascular origin or may be related to par- the supraclinoid segment of the internal car- enchymal brain cysts in a similar way to that otid artery in two patients, and occlusion ofthe described in patients with cerebral tumours.36 middle cerebral artery in the remaining three. Postmortem examination of the brain of patients dying with this disorder showed inter- Discussion esting findings. Besides occlusive endarteritis, As shown in this review, several clinical reports some blood vessels of large diameter showed have implied a link between NCC and isch- occlusion of their lumens by atheroma-like aemic cerebrovascular disease. This association deposits that resulted from disruption of the has been confirmed from data of large series endothelium secondary to the invasion of the showing that approximately 3% of patients vessel wall by a severe inflammatory reaction with NCC develop a cerebral infarct,273 45 induced by meningeal cysticerci.3 and that 2-5% ofpatients with cerebral infarcts have NCC.4 The proportion of patients with cerebral infarcts due to NCC, however, varies Progressive syndrome according to the underlying prevalence of This is one of the most devastating complica- cysticercosis in a given population. In Mexico, tions of NCC and has been associated with a cysticercosis is the second most frequent cause mortality rate of 85%.50 Those patients usually of non-atherosclerotic cerebral infarct.4 Such have a history ofshunted hydrocephalus due to incidence could be representative of several diffuse cysticercotic arachnoiditis. In a typical other developing countries and industrialised case, the patient is readmitted a few months nations with a high immigrant population after the shunt was placed because of pro- from areas where this parasitic disease is gressive neurological deterioration character- endemic.'0 18 21 23 31 ised by somnolence, paraparesis, impaired In endemic areas for cysticercosis, a patient vertical gaze, fixed and dilated pupils, and may have NCC and a cerebral infarct from urinary incontinence. CT shows normal-sized unrelated reasons. The diagnosis therefore of lateral ventricles and an ill-defined hypodense cysticercosis-induced cerebral infarct should zone in the midbrain tegmentum and medial be established only in patients who meet rigid thalamus. CSF analysis shows marked pleocy- inclusion criteria. These patients usually are http://jnnp.bmj.com/ tosis and increased protein contents, with younger than 40 years of age and have no risk positive immunological reactions to cysticerco- factors for cerebrovascular disease. The cause- sis. With the aid ofMRI, it has been possible to and-effect relationship between NCC and a visualise multiple areas of ischaemia in the cerebral infarct must be supported by CT midbrain and thalamus which are the result of evidence of a meningeal cyst adjacent to the the occlusion of paramedian thalamopedun- infarct or by CSF findings compatible with cular branches of the mesencephalic artery. active arachnoiditis. Such branches are prone to develop inflamma- Many infectious of the CNS have on September 30, 2021 by guest. Protected copyright. tory occlusion as the interpeduncular and been associated with cerebrovascular dis- 22 24 37 40 49 prepontine cisterns are where the gelatinous ease, 25 such as, the parallelism exudate associated with cysticercotic arachnoi- between the inflammatory arteriopathy caused ditis is more intense."9 The prognosis of these by NCC and that caused by tuberculous patients is bad, and they usually die after a meningitis. In both conditions, the arteries at protracted course.46 the base ofthe brain are surrounded by a dense exudate that causes inflammatory changes in the entire wall of perforating blood vessels. Transient ischaemic attacks Neither CT nor cerebral angiography permit There have been scarce reports ofpatients with the differential diagnosis between tuberculous NCC who complain of brief episodes of and cysticercotic meningitis as they show neurological deficit resembling transient similar changes in both conditions. Even nec- ischaemic attacks. The first description of this ropsy examination of the brain may cause association was made by Bickerstaff9 under misdiagnosis if an inexpert pathologist does the heading of "Transient loss of function". not recognise the scarce parasitic membranes While lacking pathological or angiographic within the leptomeningeal exudate. Corner- correlation, the author considered that such stones for an accurate differential diagnosis episodes were vascular in nature. McCormick between tuberculous and cysticercotic menin- et al26 reported a patient who experienced gitis are the of the transient episodes ofhemiparesis related to the patient and the result from CSF analysis. upright posture which was resolved in the Patients with NCC rarely, if ever, have fever or 254 Del Brutto

spective study of 556 tases. Eur Neurol 1988;28:70-72. J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.4.252 on 1 April 1992. Downloaded from neck stiffness; likewise, the levels of CSF 14 Del Brutto OH, Garcia E. Talamas 0, Sotelo J. Sex- related glucose are almost always normal in such severity of in parenchymal brain cysti- cercosis. Arch Intern Med 1988;145:544-6. patients.44 In contrast, patients with tubercu- 15 Del Brutto OH, Sotelo J. Neurocysticercosis: an update. lous meningitis usually have fever, neck stiff- Rev Infect Dis 1988;10:1075-87. 16 Del Brutto OH, Sotelo J. Another disturbing ring. Clini ness, and decreased CSF glucose levels.'2 Pearls 1988;11(1);7-8. The diagnosis of cysticercotic angiitis has 17 Del Brutto OH, Sotelo J. Albendazole therapy for sub- arachnoid and ventricular cysticercosis. Case report. J important therapeutic implications. Those Neurosurg 1990;72:816-8. patients should be started on steroid therapy as 18 Earnest MP, Reller LB, Filley CM, Grek AJ. Cysticercosis in the United States: 35 cases and a review. Rev Infect Dis soon as the diagnosis is established to amelior- 1987;9:961-79. ate the subarachnoid inflammatory reaction 19 EscobarA.The pathology ofneurocysticercosis. In: Palacios E, Rodriguez-Carbajal J, Taveras JM, eds. Cysticercosis of which may cause recurrent cerebral infarcts. the central nerwus system. Springfield: Charles C Thomas, Further follow up with serial CSF analysis will 1983:27-54. 20 Escobar A, Nieto D. Parasitic diseases. In: Minckler J, ed. permit, on individual basis, the tapering of Pathology ofthe , vol 3. NewYork: McGraw- steroids if the severity of inflammation has Hill, 1972:2503-21. 21 Garcia-Albea E. Cisticercosis en Espania: algunos datos subsided. This approach is in contrast with that epidemiol6gicos. Rev Clin Esp 1989;184:3-6. used in patients with atherosclerotic ischaemic 22 Leiguarda R, Berthier M, Starkstein S, Nogues M, Lylyk P. Ischemic infarction in 25 children with tuberculous stroke, where steroids have proved to be meningitis. Stroke 1988;19:200-4. harmful.'3 The diagnosis of NCC should be 23 Loo L, Braude A. Cerebral cysticercosis in San Diego: a report of 23 cases and a review of the literature. included in the list of causes of stroke in the 1982;61:341-59. - young, particularly in endemic areas, and this 24 Lyons EL, Leeds NE. The angiographic demonstration of arterial in purulent meningitis. Radiology condition must be ruled out by proper integra- 1967;88:935-8. tion ofdata from the neurological examination, 25 MacKenzie RA, Forbes GS, Karnes WE. Angiographic findings in herpes zoster arteritis. Ann Neurol 1981; CT findings, and CSF analysis before other 10:458-64. therapeutic measures are attempted. 26 McCormick GF, Giannotta S, Zee C-S, Fisher M. 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