Mahmood Dhahir Al-Mendalawi1. 1. Paediatrics and Child Health, Consultant Paediatrician, Department of Paediatrics, Al-Kindy College of Medicine, University of Baghdad, Baghdad, Iraq.
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 2.75 cm3 and mean left HV to be 2.49 cm3. The mean HV was measured to be 2.67 cm3 (SD = 0.42). The upper and lower limits for HV were 3.51 and 1.83 cm3, 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 ≤ 1.83 cm3 (≤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]