PURPOSE: Medically intractable temporal lobe epilepsy (TLE) due to hippocampal sclerosis (HS), with or without cortical dysplasia (CD), is associated with atrophy of the hippocampal formation and regional fluorodeoxyglucose positron-emission tomography (FDG-PET) hypometabolism. The relation between areas of functional and structural abnormalities is not well understood. We investigate the relation between FDG-PET metabolism and temporal lobe (TL) and hippocampal atrophy in patients with histologically proven isolated HS and HS associated with CD. METHODS: Twenty-three patients underwent en bloc resection of the mesial and anterolateral neocortical structures. Ten patients were diagnosed with isolated HS; 13 patients had associated microscopic CD. Temporal lobe volumes (TLVs) and hippocampal volumes were measured. Magnetic resonance imaging (MRI) and PET were co-registered, and regions of interest (ROIs) determined as gray matter of the mesial, lateral, and anterior temporal lobe. RESULTS: All patients (HS with or without CD) had significant ipsilateral PET hypometabolism in all three regions studied (p < 0.0001). In patients with isolated HS, the most prominent hypometabolism was in the anterior and mesial temporal lobe, whereas in dual pathology, it was in the lateral temporal lobe. TLVs and hippocampal volumes were significantly smaller on the epileptogenic side (p < 0.05). The PET asymmetries ipsilateral/contralateral to the epileptogenic zone and TLV asymmetries correlated significantly for the anterior and lateral temporal lobes (p < 0.05) in the HS+CD group, but not in the isolated HS group. Mesial temporal hypometabolism was not significantly different between the two groups. CONCLUSIONS: Temporal neocortical microscopic CD with concurrent HS is associated with more prominent lateral temporal metabolic dysfunction compared with isolated HS in TL atrophy. Further studies are needed to confirm these findings and correlate the PET hypometabolic patterns with outcome data in patients operated on for HS with or without CD.
PURPOSE: Medically intractable temporal lobe epilepsy (TLE) due to hippocampal sclerosis (HS), with or without cortical dysplasia (CD), is associated with atrophy of the hippocampal formation and regional fluorodeoxyglucose positron-emission tomography (FDG-PET) hypometabolism. The relation between areas of functional and structural abnormalities is not well understood. We investigate the relation between FDG-PET metabolism and temporal lobe (TL) and hippocampal atrophy in patients with histologically proven isolated HS and HS associated with CD. METHODS: Twenty-three patients underwent en bloc resection of the mesial and anterolateral neocortical structures. Ten patients were diagnosed with isolated HS; 13 patients had associated microscopic CD. Temporal lobe volumes (TLVs) and hippocampal volumes were measured. Magnetic resonance imaging (MRI) and PET were co-registered, and regions of interest (ROIs) determined as gray matter of the mesial, lateral, and anterior temporal lobe. RESULTS: All patients (HS with or without CD) had significant ipsilateral PET hypometabolism in all three regions studied (p < 0.0001). In patients with isolated HS, the most prominent hypometabolism was in the anterior and mesial temporal lobe, whereas in dual pathology, it was in the lateral temporal lobe. TLVs and hippocampal volumes were significantly smaller on the epileptogenic side (p < 0.05). The PET asymmetries ipsilateral/contralateral to the epileptogenic zone and TLV asymmetries correlated significantly for the anterior and lateral temporal lobes (p < 0.05) in the HS+CD group, but not in the isolated HS group. Mesial temporal hypometabolism was not significantly different between the two groups. CONCLUSIONS: Temporal neocortical microscopic CD with concurrent HS is associated with more prominent lateral temporal metabolic dysfunction compared with isolated HS in TL atrophy. Further studies are needed to confirm these findings and correlate the PET hypometabolic patterns with outcome data in patients operated on for HS with or without CD.
Authors: Dario J Englot; Pierre-Francois D'Haese; Peter E Konrad; Monica L Jacobs; John C Gore; Bassel W Abou-Khalil; Victoria L Morgan Journal: J Neurol Neurosurg Psychiatry Date: 2017-06-19 Impact factor: 10.154
Authors: W D Gaillard; M M Berl; E S Duke; E Ritzl; S Miranda; C Liew; A Finegersh; A Martinez; I Dustin; S Sato; W H Theodore Journal: Neurology Date: 2011-03-02 Impact factor: 9.910
Authors: Dario J Englot; Li Yang; Hamada Hamid; Nathan Danielson; Xiaoxiao Bai; Anthony Marfeo; Lissa Yu; Aliza Gordon; Michael J Purcaro; Joshua E Motelow; Ravi Agarwal; Damien J Ellens; Julie D Golomb; Michel C F Shamy; Heping Zhang; Chad Carlson; Werner Doyle; Orrin Devinsky; Kenneth Vives; Dennis D Spencer; Susan S Spencer; Catherine Schevon; Hitten P Zaveri; Hal Blumenfeld Journal: Brain Date: 2010-11-16 Impact factor: 13.501
Authors: Dario J Englot; Asht M Mishra; Peter K Mansuripur; Peter Herman; Fahmeed Hyder; Hal Blumenfeld Journal: J Neurosci Date: 2008-09-03 Impact factor: 6.167
Authors: Martine M Mirrione; Wynne K Schiffer; Joanna S Fowler; Dave L Alexoff; Stephen L Dewey; Stella E Tsirka Journal: Neuroimage Date: 2007-07-18 Impact factor: 6.556