Dual/double pathology in neurocysticercosis causing drug resistant epilepsy – Chance association or causal?

• Published in: Epilepsy research 2020-12, Vol.168, p.106472-106472, Article 106472
• Main Authors: Mhatre, Radhika, Poyuran, Rajalakshmi, Arimappamagan, Arivazhagan, Sinha, Sanjib, Kulanthaivelu, Karthik, Kenchaiah, Raghavendra, Ajay, Asranna, Chowdary, Ravindranadh M, Saini, Jitender, Bharath, Rose Dawn, Zanzmera, Paresh, Seetharam, Raghavendra, Sadashiva, Nishanth, Jamuna, Rajan, Satishchandra, Parthasarathy, Malla, Bhaskara Rao, SK, Shankar, Anita, Mahadevan
• Format: Article
• Language: English
• Subjects: Cysticercosis; Drug resistant epilepsy; Epileptogenesis; Focal cortical dysplasia; Hippocampal sclerosis
• ISSN: 0920-1211; 1872-6844
• DOI: 10.1016/j.eplepsyres.2020.106472

•Drug resistant epilepsy secondary to neurocysticercosis is often associated with dual/ double pathology.•High frequency of neurocysticercosis with hippocampal sclerosis suggests it to be causal rather than chance association.•Perilesional changes leading to drug resistance include gliosis, dystrophic synaptic and axonal pathology.•Extended lesionectomy of perilesional zone gives the best surgical outcome. Neurocysticercosis (NCC) as cause of drug resistant epilepsy (DRE) is commonly reported from India. We reviewed the neuropathological findings in patients undergoing resective surgery for DRE due to NCC, to determine the pathomechanism of epileptogenesis. Clinical, demographic and neuropathological findings of histologically confirmed cases of NCC causing DRE between 2005–2019 were reviewed. NeuN, GFAP, phosphorylated neurofilament, vimentin, CD34 for glial/ neuronal alterations, and Masson trichrome, Luxol Fast blue for evidence of fibrosis/ demyelination was used to determine cause of epileptogenesis. There were 12 cases of NCC associated with dual/ double pathology, which constituted 3.02 % (12/398) of all the operated DRE. [Age range: 17–37y, Male:Female = 1.4:1]. Seizure duration ranged from 3–32y, with seizure onset between 4–27y. On MRI, lesions were of variable signal intensity on T1 and isointense on T2 with blooming on GRE/ SWI, and CT revealed calcification. Majority (11/12) had associated hippocampal sclerosis (HS) type 1 (dual pathology), localised to the same side as cysticercal cyst, suggesting it may be involved in the pathogenesis of HS. Ten had single cysticercal lesion involving ipsilateral hippocampus in 6, parahippocampal gyrus in 2, amygdala and temporal lobe in 1 case each. One had multiple NCC located in bilateral frontal, parietal and ipsilateral hippocampus. Adjacent cortex around the NCC evaluated in 6 cases, revealed inflammation, gliosis, axonal disruption/ beading, and variable synaptic/ neuronal dystrophic changes. There was a single case of NCC with Focal cortical dysplasia (FCD) type IIb (double pathology). In 11/12 cases Engel’s post-surgery outcome was available with all having class I outcome. HS was most common pathology associated with cysticercosis (Dual pathology), localised ipsilateral to the cysticercal cyst, suggesting that HS is a secondary/ epiphenomenon. Perilesional changes such as inflammation, gliosis, dystrophic synaptic and axonal pathology play a role in inducing or perpetuating the epileptiform activit