Abstract：OBJECTIVE: To investigate pathological changes in the epileptogenic foci of children with intractable epilepsy and their clinical significance. METHODS: Thirty children with intractable epilepsy were included in the study. The epileptogenic foci were surgically resected and pathological changes in the obtained specimens were observed under a light microscope (LM) and a transmission electron microscope (TEM). RESULTS: Under the LM, cortical dysplasia was found in 14 cases (47%), hippocampal sclerosis in 11 cases (37%), dysembryoplastic neuroepithelial tumor in 1 case (3%), ganglioglioma in 1 case (3%), and encephalomalacia in 3 cases (10%). The TEM observation revealed pathological changes in the ultrastructure of the hippocampus and extra-hippocampal cortex, such as changes in the number of synapses and synaptic structure, decrease in neurons and karyopyknosis, swelling and degeneration of astrocytes, and changes in mitochondrial structures. CONCLUSIONS: Pathological changes in the hippocampus and extra-hippocampal cortex, especially synaptic remodeling, may be the morphological basis for spontaneous recurrent seizures in children with intractable epilepsy. The pathological changes and epileptiform activity are related to an imbalance between excitatory and inhibitory neurotransmission.
FENG Li-Mei,XIA Gui-Zhi,REN Rong-Na et al. Pathological changes in the epileptogenic foci of children with intractable epilepsy[J]. CJCP, 2013, 15(5): 335-339.
［1］Gorter JA, van Vliet EA, Aronica E, Lopes da Silva FH. Progression of spontaneous seizures after status epilepticus is associated with mossy fibre sprouting and extensive bilateral loss of hilar parvalbumin and somatostatin-immunoreactive neurons［J］. Eur J Neurosci, 2001, 13(4): 657-669.
［2］Jankowsky JL, Patterson PH. The role of cytokines and growth factors in seizures and their sequelae［J］. Prog Neurobiol, 2001, 63(2): 125-149.
［3］Pitkanen A, Sutula TP. Is epilepsy a progressive disorder? Prospects for new therapeutic approaches in temporal-lobe epilepsy［J］. Lancet Neurol, 2002, 1(3): 173-181.
［4］Sharma AK, Reams RY, Jordan WH, Miller MA, Thacker HL, Snyder PW. Mesial temporal lobe epilepsy: pathogenesis, induced rodent models and lesions［J］. Toxicol Pathol, 2007, 35(7): 984-999.
［5］Bae EK, Jung KH, Chu K, Lee ST, Kim JH, Park KI, et al. Neuropathologic and clinical features of human medial temporal lobe epilepsy［J］. Clin Neurol, 2010, 6(2): 73-80.
［6］Yang T, Zhou D, Stefan H. Why mesial temporal lobe epilepsy with hippocampal sclerosis is progressive: uncontrolled inflammation drives disease progression?［J］. J Neurol Sci, 2010, 296(1-2):1-6.
［7］Berg AT, Berkovic SF, Brodie MJ, Buchhalter J, Cross JH, van Emde Boas W, et al. Revised terminology and concepts for organization of seizures and epilepsies: Report of the ILAE Commission on Classification and Terminology, 2005-2009［J］. Epilepsia, 2010, 51(4): 676-685.
［8］Kwan P, Arzimanoglou A, Berg AT, Brodie MJ, Hauser WA, Mathern G, et al. Definition of drug resistant epilepsy. Consensus proposal by the ad hoc Task Force of the ILAE Commission on therapeutic strategies［J］. Epilepsia, 2010, 51(6): 1069-1077.
［9］Engel J Jr, Van Ness PC, Rasmussen TB, Ojemann LM. Outcome with respect to epileptic seizures. Surgical Treatment of the Epilepsies［M］. 2nd ed. New York: Raven Press, 1993: 609-623.
［10］Spencer SS. Neural networks in human epilepsy: evidence of and implications for treatment［J］. Epilepsia, 2002, 43(3): 219-227.
［11］Hogan RE, Bucholz RD, Joshi S. Hippocampal deformation based shape analysis in epilepsy and unilateral mesial temporal sclerosis［J］. Epilepsia, 2003, 44(6): 800-806.
［13］Ben-Ari Y, Dudek FE. Primary and secondary mechanisms of epileptogenesis in the temporal lobe: there is a before and an after［J］. Epilepsy Curr, 2010, 10(5): 118-125.
［14］Baram TZ, Jensen FE. Does Acquired Epileptogenesis in the Immature Brain Require Neuronal Death?［J］. Epilepsy Currents, 2011, 11(1): 21-26.
［15］Tian GF, Azmi H, Takano T, Xu Q, Peng W, Lin J, et al. An astrocytic basis of epilepsy［J］. Nat Med, 2005, 11(9): 973-981.
［16］Takahashi DK, Vargas JR, Wilcox KS. Increased coupling and altered glutamate transport currents in astrocytes following kainic-acid-induced status epilepticus［J］. Neurobiol Dis, 2010, 40(3): 573-585.
［20］de Tisi J, Bell GS, Peacock JL, McEvoy AW, Harkness WF, Sander JW, et al. The long-term outcome of adult epilepsy surgery, patterns of seizure remission, and relapse: a cohort study［J］. Lancet, 2011, 378(9800): 1388-1395.
［21］Spencer S, Huh L. Outcomes of epilepsy surgery in adults and children［J］. Lancet Neurol, 2008, 7(6): 525-537.
［22］Dunkley C, Kung J, Scott RC, Nicolaides P, Neville B, Aylett SE, et al. Epilepsy surgery in children under 3 years［J］. Epilepsy Res, 2011, 93(2-3): 96-106.
