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BRIEF COMMUNICATIONS: Gregory Youngnam Chang and James R. Keane Visual loss in cysticercosis: Analysis of 23 patients Neurology 2001; 57: 545-548 [Abstract] [Full text] [PDF]

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Reply to Dr. Garg

James R. Keane, Gregory Y. Chang   (6 May 2002)

Visual loss in cysticercosis

Ravindra Kumar Garg   (17 September 2001)

Reply to Dr. Garg 6 May 2002
James R. Keane LAC/USC Medical Center, Gregory Y. Chang Send Correspondence to journal: Re: Reply to Dr. Garg keane{at}dnamail.com James R. Keane, et al.	We appreciate Dr. Garg's interest in our article and hope that we can allay his concerns. As mentioned in the article, all of our cases fulfilled the proposed criteria for definite cysticercosis [l]. While we are perhaps less sanguine than Dr. Garg concerning the efficacy of anticysticercal therapy, nearly all of our patients are treated, some with multiple courses. Dr. Garg mirrors the enthusiasm of Del Brutto and colleagues [1] for a therapeutic trial of albendazole as a diagnostic aid. There are two sides to such a trial. Firstly, given the generally favorable but highly variable natural history of cysticercosis and the less than dramatic effects of treatment, a therapeutic trial in a single case has limited value. The obverse side, the "nontreatment trial" is much more valuable in retrospect: A benign course, in the absence of specific therapy, eliminates most of the ominous choices in the differential, such as intracranial tuberculosis. As an example, patient #21 queried by Dr. Garg, was admitted with severe headache, had pupillary light reactions of limited amplitude, and rapidly went into coma. CT scan showed definite hydrocephalus and prompt ventriculostomy revealed fluid under high pressure. He awoke during the next week, asymptomatic aside from blindness. Followup CT scan showed infarction in the territories of both posterior cerebral arteries. He has remained blind but otherwise well during many years of followup. (The CT pictured in our article shows no hydrocephalus because it was taken 14 years after his admission. ) His course, and those of our patients with posterior cerebral cysts and multiple suprasellar cysts, had no specific treatment for the other conditions raised by Dr. Garg, thus eliminating those diagnoses from consideration. Occipital infarction due to carotid artery occlusion is usually associated with a carotid origin of the posterior cerebral artery. In our case #20, infarction was produced by occlusion of the occipito-temporal branch of the middle cerebral artery [2]. Our occipital label was somewhat misleading, however, as the functionally significant portion of the infarct was probably anterior to the occipital lobe. In patients from endemic areas, cysticercosis has assumed the ancient mantle of syphilis as "the great imitator." At the Los Angeles County/University of Southern California Medical Center, a large part of our neurology working day is spent huddled with expert neuroradiologists balancing the probablities of cysticercosis. We fully agree with Dr. Garg that such diagnoses can be difficult and the possibility of other, more serious, conditions must always be considered. References 1. Del Brutto OH, Rajshekhar V, White ACJr et al. Proposed diagnostic criteria for neurocysticercosis. Neurology 2001 ;51: 177-183. 2, Caplan LR, Kelly M, Case CS et al. Infarcts of the inferior division of the right middle cerebral artery: mirror image of Wernicke's aphasia. Neurology 1986;36:1015-1020.
Visual loss in cysticercosis 17 September 2001
Ravindra Kumar Garg, Assistant professor Department of Neurology, King George's Medical College, Lucknow, India Send Correspondence to journal: Re: Visual loss in cysticercosis garg50{at}yahoo.com Ravindra Kumar Garg	I read with great interest the article by Chang and Keane [1] about visual loss in patients of neurocysticercosis. I do not agree with the authors’ explanations given for retrochiasmal causes of vision loss. Patients No 18,19, 22 and 23 reported to have parenchymal cysts. Authors, themselves, mentioned that viable cysticercal cysts are not likely to produce focal deficits until the cyst is inflamed and associated with perilesional edema so I presume that patient No. 19, 22, and 23 might be having a ring or disk enhancing CT/MRI lesions (no photograph is available in the article). Authors also speculated these lesions as inflamed cysticercal cysts. Infact, ring or disk enhancing CT lesions (if they are) are not specific for neurocysticercosis only, several other infective diseases like CNS tuberculoma, fungal infections, cerebral abscesses, and other parasitic infections like toxoplasmosis can produce similar images, and frequently it is difficult to differentiate. [2] As all patients are immigrants from Mexico and Central America, other infective possibilities are also equally likely. Patient No 20 had infarct of right occipital lobe and occlusion of right internal carotid artery due to a cysticercal cyst in the right sylvian fissure. The infarction of occipital region is unexplainable on the basis of occlusion of internal carotid artery. Patient No 21 had symmetrical infarctions of both the occipital regions. Authors think that bilateral posterior cerebral artery occlusions were because of transtentorial herniations due to obstructive hydrocephalus. It is not apparent from the CT picture (figure in center) that patient had definite hydrocephalus or raised intracranial pressure, instead, it seems that there is some amount of cerebral atrophy with ex vacuo dilatation of ventricles. CT picture is consistent with occlusion of top of basilar artery (top of basilar syndrome) presenting with cortical blindness. This study included 4 patients with suprasellar pathologies. Only in two patients (patient 14,15) histopathological confirmation is available. There can be several diseases producing similar cystic lesions in suprasellar regions like epidermoid cysts, subarachnoid cyst and craniopharyngioma. It is not possible to differentiate these diseases only on the basis of imaging and clinical features. In none of the patient anticysticercal therapy has been used. It is now very well documented that albendazole is effective for all form of neurocysticercosis including subarachnoidal [3] and intraventricular forms. Even partial resolution of these cystic lesions following albendazole therapy would have been a major point in favor of neurocysticercosis. [4] References 1. Chang GY, Keane JR. Visual loss in cysticercosis: analysis of 23 patients. Neurology 2001; 57: 545-548 2. Shah GV. Central nervous system tuberculosis. Neuroimaging Clin North Am 2000:10:355-374 3. Del Brutto OH, Rajshekhar V, White Jr. AC et al. Proposed diagnostic criteria for neurocysticercosis. Neurology 2001; 57: 177-183. 4. Del Brutto OH. Albendazole therapy for Subarachnoid cysticerci: clinical and neuroimaging analysis of 17 patients. J Neurol Neurosurg Psychiatry 1997; 62: 659-661