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LETTER TO THE EDITOR
Year : 2017  |  Volume : 12  |  Issue : 1  |  Page : 112
 

Hippocampal sclerosis in a child with multiple neurocysticercosis


Department of Pediatrics, Government Medical College and Hospital, Chandigarh, India

Date of Web Publication4-May-2017

Correspondence Address:
Roosy Aulakh
Department of Pediatrics, Government Medical College and Hospital, Sector 32, Chandigarh - 160 030
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpn.JPN_159_16

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How to cite this article:
Aulakh R. Hippocampal sclerosis in a child with multiple neurocysticercosis. J Pediatr Neurosci 2017;12:112

How to cite this URL:
Aulakh R. Hippocampal sclerosis in a child with multiple neurocysticercosis. J Pediatr Neurosci [serial online] 2017 [cited 2022 Jan 23];12:112. Available from: https://www.pediatricneurosciences.com/text.asp?2017/12/1/112/205638




Dear Sir,

A 7-year-old female child presented with the complaints of three episodes of the left focal seizures over a span of 16 months. Contrast-enhanced magnetic resonance imaging (MRI) brain with coronal (Panels A and D) and sagittal (Panels B and C) cuts depicted multiple peripheral ring-enhancing lesions seen in bilateral cerebral hemispheres, basal ganglia, thalami, midbrain, and cerebellar hemispheres suggestive of neurocysticercosis (NCC). She was given cysticidal therapy (albendazole for 28 days) under steroid cover and was started on eptoin (6.5 mg/kg/day). She remained seizure free for the next 2 years when a repeat plain MRI brain with axial (Panel E), sagittal (Panels F), and coronal (Panel G) cuts depicted single disc-shaped lesion measuring 7.5 mm in the left temporoparietal region with calcification. Anterior head part of the right hippocampus appeared smaller as compared to the left side suggestive of hippocampal sclerosis (HS). This child has continued to remain seizure free during a follow-up period of 1.5 years despite evident right HS.

Recent observations suggest that NCC might act as an initial precipitating injury causing mesial temporal lobe epilepsy associated with HS through two main pathophysiological mechanisms: inflammation-mediated and electrogenic-mediated.[1],[2] This case wherein 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. Another unusual finding, in this case, has been nondevelopment of refractory epilepsy despite the presence of HS. This observation needs confirmation through future studies as it suggests that damage to hippocampus in NCC patients might not render it epileptogenic leading to refractory epilepsy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Del Brutto OH, Engel J Jr., Eliashiv DS, García HH. Update on cysticercosis epileptogenesis: The role of the hippocampus. Curr Neurol Neurosci Rep 2016;16:1.  Back to cited text no. 1
    
2.
Bianchin MM, Velasco TR, Wichert-Ana L, Alexandre V Jr., Araujo D Jr., dos Santos AC, et al. Characteristics of mesial temporal lobe epilepsy associated with hippocampal sclerosis plus neurocysticercosis. Epilepsy Res 2014;108:1889-95.  Back to cited text no. 2
    



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