Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 52, Num. 2, 2004, pp. 265-267

Neurology India, Vol. 52, No. 2, April-June, 2004, pp. 265-267

Short Reports

New solitary cysticercus granulomas causing recurrent symptoms in patients with resolved solitary granulomas

Sujit Kumar GSamson , Rajshekhar Vedantam

Department of Neurological Sciences, Christian Medical College and Hospital, Vellore

Correspondence Address:Department of Neurological Sciences, Christian Medical College and Hospital, Vellore - 632004

Code Number: ni04083

Abstract

Keywords: Neurocysticercosis, epilepsy, computed tomography

Introduction

Solitary cerebral cysticercus granuloma (SCCG) is a common cause of seizures in endemic areas like India.[1] These granulomas usually resolve spontaneously with either complete disappearance or with a calcific residue. Nearly 70 % of SCCGs show some degree of resolution within six months of presentation.[2] Recurrence of seizures can occur in some patients with SCCG even after complete resolution of the granuloma. Recurrent symptoms are usually attributed to a calcific residue[3] or an epileptogenic scar. We report two patients with recurrent seizures and one with severe headache, all of whom had a resolved SCCG. A fresh SCCG at a location different from the initial site in all the three patients was demonstrated as the cause of the recurrent symptoms.

Case Reports

Patient 2
A 10-year-old boy presented with left facial focal motor seizures in February 1993. CT of the brain at that time showed a right frontal SCCG with perilesional edema. He was treated with AEDs for two years after which they were tapered off. He was asymptomatic till September 2000 when he reported one episode of severe headache. CT showed a right frontal 10 mm SCCG with perilesional edema [Figure - 2]a. The old lesion was seen as a calcific dot [Figure - 2]b. He was advised symptomatic therapy with regular follow-up monitoring.

Patient 3
This case has been reported earlier.[4] A 4-year-old boy was diagnosed to have SCCG in April 1994. CT of the brain at that time showed a 10 mm ring-enhancing lesion in the left parietal region with perilesional edema. He was treated with AEDs and a repeat CT in November 1994 revealed a tiny residue of the granuloma. The AEDs were tapered over the next six months. He was asymptomatic till February 1998 when he developed right focal seizures with secondary generalization. CT showed a 10 mm contrast-enhancing lesion in the left parietal region anterior to the location of the initial SCCG, which was seen as a calcific residue.

Discussion

In our second and third patients a new lesion was seen distinct from the initial lesions and the old lesions were seen as calcific dots. In the first patient, the comparison of the initial scan and the scan done during recurrence of symptoms showed that the granulomas were located at different sites. In our patients, the new lesions and not the residue of the first granulomas, were clearly the causes of the recurrent symptoms as they were associated with perilesional edema indicating that they were immunologically active.

Interestingly, the new lesions in all our patients were again solitary lesions. This suggests that in a patient who previously had a SCCG, neurocysticercosis is likely to manifest with a solitary lesion rather than with multiple lesions. This could be due to a unique host-parasite interaction based on the individual′s immunity and parasite-dependent factors or it could be related to the parasite load. In all three patients the new lesion occurred on the same side as the initial granuloma. The cause for this is unclear but as the parasite reaches the brain hematogenously, it is possible that cerebral hemodynamic factors unique to each of these patients ensured that the parasitic emboli were preferentially carried to one cerebral hemisphere. We postulate that all the new granulomas in our patients resulted from reinfection. It is possible that the new granuloma was the result of the initial infection. A live cyst from the initial infection might not have been visualized in the first scan as it was small and non-enhancing. Subsequent degeneration of the live cyst could have led to inflammation and enhancement with visualization on a CT scan. But this is a less likely explanation as there was an interval of 2.5, 4 and 7.5 years between the presentation of the two granulomas. One would expect that the degeneration of cysts from the same infection would not be temporally separated by such long intervals of time.

Reappearance of a SCCG at the same site after documented "resolution" was previously described by other authors.[5],[6],[7] The reappearance of the granuloma in these patients almost always coincided with recurrence of symptoms which prompted a repeat imaging of the brain. We postulated that lack of adequate contrast injection or thick CT slices (>5 mm) in the follow-up CT scan could have led to a false positive diagnosis of "disappearance" of the granuloma.[8]
The treatment for patients with recurrent seizures and a new SCCG is the same as that for the initial lesion. Therefore these patients were managed conservatively and the AEDs were stopped after the resolution of the new lesion. We decided to follow up the second patient and did not restart him on AEDs. In a previous study, we found that 14/15 patients who presented with severe episodic headache due to SCCG, did not develop seizures on follow-up.[9]

In conclusion, we recommend a repeat imaging in a patient with a resolved SCCG who presents with recurrent or new symptoms, even if the recurrent symptoms are similar to the initial symptomatology and can be explained by the location of the initial granuloma. A new lesion should be actively sought in these patients′ images. We postulate that when new lesions occur in patients with a SCCG they tend to be solitary rather than multiple and recommend that the management strategy for the new SCCG be the same as that used for the initial granuloma.

References

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