25-27 Introduction Mesial temporal sclerosis is the commonest cause of partial complex seizures. The aetiology of this condi- tion is controversial, but it is postulat- ed that both acquired and develop- mental processes may be involved. Familial cases have also been reported. Magnetic resonance imaging (MRI) is the imaging investigation of choice for the diagnosis and has been shown to be highly sensitive and spe- cific. Once diagnosed, medical treat- ment is successful in 25% of cases, whilst anterior temporal lobectomy is effective in 70 - 95% of patients.1 Case report The case under discussion involved a 42-year-old woman. She had had numerous previous admis- sions related to her alcoholism, but presented on this occasion with new onset partial complex seizures and secondary generalisation. On clinical examination she had impaired short- term memory, however, no focal neu- rology was present. An EEG was per- formed and was assessed as normal. A MRI scan was done which revealed abnormal high signal in the right hip- pocampus on the T2-weighted and FLAIR sequences. The head, body and tail of the hippocampus were involved, with associated poor grey- white matter differentiation. In addi- tion, there was atrophy of the hip- pocampus and fornix, with dilatation of the temporal horn (Figs 1 - 4). Discussion Mesial temporal sclerosis (MTS) is the commonest cause of temporal lobe epilepsy. Pathologically, there is neuronal loss, atrophy and hippocam- pal gliosis. These findings are charac- teristic of this disorder and are thought to serve as an epileptogenic substrate. The histologic substrates can be divided into four other major catergories: (i) tumours; (ii) disorders of neuronal migration and cortical organisation; (iii) vascular malforma- tions; and (iv) neocortical sclerosis attributable to brain injury (trauma, infection, inflammation, or infarc- tion).1,2 In MTS, dual pathology occurs in 15% of cases, with cortical dysplasia being the commonest.1 MRI has the ability to detect subtle alterations in cortical architecture and changes in signal intensity and is therefore the most sensitive and spe- cific imaging technique for non-inva- sive identification of these epilepto- genic foci.2 In order to achieve accurate MRI interpretation, it is essential to know the regional anatomy of the inferome- dial temporal lobe and its related structures (Fig. 5). The hippocampus comprises the head (pes), body and tail. The hippocampal/dentate com- CASE REPORT 25 SA JOURNAL OF RADIOLOGY • July 2005 Mesial temporal sclerosis D H Jogi MB BCh, FCRad (Diag) (SA), FRCR (Lond) N17 East Rand Private Community Hospital Springs M Patel MB ChB, FCRad (Diag) (SA) Department of Radiology Chris Hani Baragwanath Hospital Johannesburg Fig. 1. Coronal FLAIR demonstrating atrophy of the right hippocampal head with dilatation of the temporal horn. Fig. 2. Coronal T1WI displaying loss of grey- white matter differentiation in the region of the right hippocampal head. Figs 3 and 4. Coronal FLAIR sequences exhibiting atrophy of the right hippocampal body and tail as well as the right fornix. 25-27 7/29/05 3:26 PM Page 25 CASE REPORT 26 SA JOURNAL OF RADIOLOGY • July 2005 plex is located in the medial aspect of the temporal lobe, posterior to the amygdala. It is separated from the amygdala by the uncal recess of the temporal horn and the alveus and its long axis is parallel to temporal gyri. Two interlocking ‘C’-shaped sheets of cortex form the hippocampal /dentate complex: (i) cornis ammonis (CA1, CA2, CA3 and CA4); and (ii) dentate gyrus (Figs 5 and 6). On MRI, the hippocampal head is seen in the same coronal plane as the interpeduncular cistern (Fig. 6). The body of the hippocampus is seen at the level of the midbrain (Fig. 7). It is ovoid in shape and is the most uni- form portion. It lies inferior to the choroidal fissure and is separated from the parahippocampal gyrus by the hippocampal fissure. The tail of the hippocampus is located at or behind the midbrain where it is seen adjacent to the crura of the fornices (Fig. 8). Various MRI sequences are rec- ommended for evaluation of the tem- poral lobe. These include T1WI sagit- tal images for the localisation of the hippocampus and thin-section high- resolution T2WI and FLAIR acquisi- tions angled perpendicular to the long axis of the hippocampus (Table I). Contrast is unnecessary unless there is a focal lesion.1 A spoiled gradient recalled (SPGR) echo sequence using 1.5 mm cuts in the oblique coronal plane can also be done. This provides a high-resolution T1-weighted vol- ume data set which can be reformat- ted in any plane, and can also be used to measure hippocampal volumes and co-register functional data.4,5 Primary findings in MTS are hip- pocampal atrophy (recognised by asymmetry in the case of unilateral atrophy) and increased signal intensi- ty of the hippocampus on T2WI. This is best appreciated on the coronal FLAIR sequence, which suppresses out the cerebrospinal fluid (CSF) sig- nal from the uncal recess and the choroidal fissure thus avoiding false positive high signal changes. Recent studies have shown that visual MRI interpretation of these features has sensitivities of 87 - 100%. 1,4 There are numerous secondary MR features that support the diagno- sis of MTS (Table II). These include temporal horn dilatation, loss of hip- pocampal internal architecture, decreased hippocampal signal on T1WI and poor parahippocampal grey-white matter definition. Other findings include ipsilateral atrophy of the temporal lobe, thalamus, fornix and mamillary body. These secondary features are present in 40 - 60% of Table I. MRI imaging protcols • High-resolution MR of the temporal lobes • T1 WI sagittal for localising the hippocampus • Coronal high-resolution T2 WI and FLAIR perpendicular to hippocampal axis (3 - 4 mm) • Coronal SPGR T1 perpendicular to hippocampal axis (1.5 mm) Fig. 5. 1. Temporal horn; 2. Cornu ammonis (Ammon’s horn, hippocampus proper); 3. Fornix; 4. Subarachnoid space; 5. Hippocampal sulcus; 6. Dentate gyrus; 7. Parahippocampal gyrus (containing entorhinal cortex); 8. Subiculum; 9. Choroid plexus.3 Fig. 6. Coronal T2 at the level of the interpe- duncular cistern showing the amygdala (large square), uncal fissure (large dot), hippocam- pal head (small dot) Fig. 7. Coronal T2 WI at the level of the mid- brain, demonstrating the ovoid hippocampal body (small sqaure) under the choroidal fis- sure (circle). Fig. 8. Coronal T2 WI just posterior to the midbrain illustrating the fornix (line) and hippocampal tail (square). 25-27 7/29/05 3:27 PM Page 26 CASE REPORT 27 SA JOURNAL OF RADIOLOGY • July 2005 patients with MTS. On their own, the above signs are unreliable, but in con- junction with the primary findings the diagnostic accuracy is improved.4 Decreased apparent diffusion coefficient (ADC) levels may be seen on diffusion-weighted imaging. MR spectroscopy would show reduced N- acetylaspartate levels in the ipsilateral mesial temporal lobe assisting in the lateralisation of temporal lobe epilep- sy (TLE), even in cases with negative MR images.1,4,5 There is bilateral involvement in 20% of cases and in these cases MRI-based hippocampal volumetry has been shown to quanti- tatively indicate the presence of hip- pocampal volume loss.1,6 MRI also provides information on the predictive value concerning neu- rologic outcome in patients undergo- ing temporal lobe surgery. MRI can identify hippocampal volume loss and coexisting extrahippocampal lesions which predict an unfavourable post- operative neurocognitive outcome.1,4 The MRI findings of the patient discussed in this case report are com- patible with MTS. She is currently on medical treatment and is being fol- lowed up monthly. Conclusion MRI is the radiological investiga- tion of choice for diagnosing MTS. Familiarity with the regional medial temporal lobe anatomy is important for correct MRI interpretation. Coronal high-resolution FLAIR is the best sequence to diagnose MTS, where hyperintensity and atrophy of the hippocampus are the most sensi- tive signs. References 1. Osborn AG, Cooper JA, Castillo M, et al. Diagnostic Imaging – Brain. St Louis: WB Saunders, 2004. 2. Jack CR jun. Magnetic resonance imaging in epilepsy. Mayo Clin Proc 1996; 71: 695-711. 3. Hippocampus. www.laxtha.com/bhbae/hip- pocampus/hippocampus.htm. (Last accessed 4 April 2005). 4. Connor EJ, Jarosz JM. Magnetic resonance imaging of patients with epilepsy. Clin Radiol 2001; 56: 787-801. 5. Cascino G. Clinical correlations with hip- pocampal atrophy. Magn Reson Imaging 1995; 13:1133-1136. 6. Arı´stides A. Capizzano, Kenneth DL, et al. Temporal lobe epilepsy: Qualitative reading of 1H MR spectroscopic images for presurgical evaluation. Radiology 2001; 218:144-151. Table II. Imaging findings Primary signs Secondary signs Hyperintense signal on T2 Enlarged temporal horn of lateral ventricle and FLAIR sequences Loss of internal architecture Decreased signal on T1WI Atrophy of hippocampus Poor grey-white matter definition Fornix, mamillary body, temporal lobe and thalamic atrophy 25-27 7/29/05 3:27 PM Page 27