Hippocampal Sclerosis in Temporal Lobe Epilepsy: Findings at 7 T 1

NEURORADIOLOGY: Hippocampal Sclerosis in Temporal Lobe EpilepsyHenry et al26 years. The mean age of the remainingeight patients with TLE was 28 years.The clinical characteristics of the patientsare summarized in Table 1 .Qualitative Visual AssessmentIn control subjects, the internal structurewas visible in all sections of the head,body, and tail of the hippocampus ( Fig 3 ).In each patient ( Table 2 ), the abnormalhippocampus had at least one ofthe following signs: atrophy ( n = 7), T2-weighted hyperintense signal ( n = 6),and flattening of the head ( n = 6). Ineach subject, hippocampal striation andadditional detailed anatomic featureswere clearly apparent. In each controlsubject, it was possible to delineate continuoushippocampal striation. This whitematter band appeared to be less distinguishedfrom surrounding gray matterin all sclerotic hippocampi. Thus, the partialloss of hippocampal striation wasobserved in the hippocampus on the sideof ictal onset in all but two patients(patients 1 and 7) and in none of thecontrol subjects. Definite hippocampalmalrotations were observed in three patients;they were seen twice in patientswith ipsilateral onset and once in a patientwith contralateral to ictal onset( Fig 4 ). Malrotations were observed infour control subjects: They were observedbilaterally in subject 1 and on theleft side in subjects 6, 10, and 11. Thedetermination of malrotation showed novariation between the first and secondobservations in 18 of 19 subjects; however,one healthy control subject (subject4) was rated as having bilateralhippocampal malrotation at the secondviewing but not at the first. Ratingsof hippocampal size, signal, shape, andstriation did not vary between the firstand second viewings.Each patient had either no or onehippocampal digitation on the side ofictal onset ( Table 2 ). Three patients alsohad either no or one contralateral hippocampaldigitation. Several patientshad definite hippocampal atrophy. Interestingly,one patient (patient 1) hadbilateral nondigitated hippocampalheads but only mild hippocampal atrophyon the epileptogenic side and contralateralnormal hippocampal volumeFigure 2Figure 2: Manual segmentation of two subregions of body of hippocampus on T2-weighted 7-T MRimages in subject 2 (24-year-old man). (a, b) Most posterior coronal section in (a) head and (b) bodyof hippocampus, as the image on the left of these pairs. Red cross marks the same point on the pairedcoronal and sagittal images, and on sagittal section (as the image on the right of these pairs) indicates levelof coronal section (front is on left side of sagittal image). (c) Limits of CA1–CA3 (dark blue) and CA4 anddentate gyrus (light blue) regions on coronal section in middle of body (with no colored subregions on leftimage and colored subregions on middle image, both showing the same image plane), as indicated on thesagittal section (right image). (d) Three-dimensional rendering of two subregions in body of hippocampus,displayed separately (left, with CA1–CA3 in dark blue, and middle, with CA4 and dentate gyrus in light blue)and together (right).( Fig 4, A ). All healthy subjects had twoor three bilateral digitations of the hippocampalhead; however, one of these22 hippocampal heads had one digitation,consistent with reports of postmortemstud ies in cadavers withoutRadiology: Volume 261: Number 1—October 2011 n radiology.rsna.org 203