Correspondence Address:
Mahmood Dhahir Al-Mendalawi
P. O. Box 55302, Baghdad Post Office, Baghdad
Iraq

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Sir,

I have three comments on the interesting case report by Aulakh on hippocampal sclerosis (HS) in a 7-year-old Indian child with multiple neurocysticercosis (NCC).[1]

First, the author mentioned that magnetic resonance imaging showed that “the anterior head part of the right hippocampus appeared smaller as compared to the left side suggestive of HS.”[1] I presume that such a suggestion on HS needs to be confirmed by quantitative analysis of the hippocampus using volumetry. To my knowledge, normative volumetric data of the hippocampi for the Indian pediatric population between 6 and 12 years of age were constructed more than a decade ago. The mean right hippocampal volume (HV) was estimated to be 2.75cm3 and mean left HV to be 2.49cm3. The mean HV was measured to be 2.67cm3 (SD = 0.42). The upper and lower limits for HV were 3.51 and 1.83cm3, respectively, based on 95% (± 2SD) limits on either side of the mean. There was no effect of age or gender on the HV.[2] From a practical viewpoint, HV ≤ 1.83cm3 (≤2SD) was considered to be abnormal in the clinical setting.[2] I wonder why the author did not refer to the above-mentioned Indian normative data to firmly diagnose HS.

Second, the author mentioned that the child had continued to remain seizure-free during the follow-up period of 1.5 years despite evident right HS.[1] This point is really interesting as it contradicts with the antecedent observation reported by a set of Indian researchers pointing out that NCC patients with HS had more frequent clustering of seizures and extratemporal/bitemporal interictal epileptiform discharges as compared to patients with HS alone.[3]

Third, the author mentioned that “follow-up neuroimaging studies have revealed the development of HS 2 years after the diagnosis of NCC lends support to the hypothesis that NCC can be a causative factor in the development of HS and potential mechanism seems to be inflammation-mediated and not recurrent seizures.”[1] Actually, four plausible mechanisms underlying the pathophysiology combining NCC and HS have been suggested from studying a series of Indian patients with NCC-associated HS. These include the following: seizures due to NCC might constitute the initial precipitating illness for the HS development; the hippocampus might be involved in host brain inflammation and gliosis in response to a nearby degenerating cysticercus; the seizure focus formed by the degenerating cysticercus engenders epileptogenic changes in the hippocampus through kindling; and, finally, the two conditions might coexist purely by chance.[4]

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