Dragan Bajic

Incomplete hippocampal inversion-is there a relation to epilepsy?

Incomplete hippocampal inversion (IHI) has been described in patients with epilepsy or severe midline malformations but also in nonepileptic subjects without obvious developmental anomalies. We studied the frequency of IHI in different epilepsy syndromes to evaluate their relationship. Three hundred patients were drawn from the regional epilepsy register. Of these, 99 were excluded because of a disease or condition affecting the temporal lobes or incomplete data. Controls were 150 subjects without epilepsy or obvious intracranial developmental anomalies. The coronal MR images were analysed without knowledge of the clinical data. Among epilepsy patients, 30% had IHI (40 left-sided, 4 right-sided, 16 bilateral). Of controls, 18% had IHI (20 left-sided, 8 bilateral). The difference was statistically significant (P < 0.05). Of temporal lobe epilepsy (TLE) patients, 25% had IHI, which was not a significantly higher frequency than in controls (P = 0.34). There was no correlation between EEG and IHI laterality. A total of 44% of Rolandic epilepsy patients and 57% of cryptogenic generalised epilepsy patients had IHI. The IHI frequency was very high in some epileptic syndromes, but not significantly higher in TLE compared to controls. No causality between TLE and IHI could be found. IHI can be a sign of disturbed cerebral development affecting other parts of the brain, maybe leading to epilepsy.

Incomplete inversion of the hippocampus— a common developmental anomaly

Incomplete inversion of the hippocampus, an imperfect fetal development, has been described in patients with epilepsy or severe midline malformations. We studied this condition in a nonepileptic population without obvious developmental anomalies. We analyzed the coronal MR images of 50 women and 50 men who did not have epilepsy. Twenty of them were healthy volunteers and 80 were patients without obvious intracranial developmental anomalies, intracranial masses, hydrocephalus or any condition affecting the temporal lobes. If the entire hippocampus (the head could not be evaluated) were affected, the incomplete inversion was classified as total, otherwise as partial. Incomplete inversion of the hippocampus was found in 19/100 subjects (9 women, 10 men). It was unilateral, always on the left side, in 13 subjects (4 women, 9 men): 9 were of the total type, 4 were partial. It was bilateral in six subjects (five women, one man): four subjects had total types bilaterally, two had a combination of total and partial types. The collateral sulcus was vertically oriented in all subjects with a deviating hippocampal shape. We conclude that incomplete inversion of the hippocampus is not an unusual morphologic variety in a nonepileptic population without other obvious intracranial developmental anomalies.

Hippocampal Malrotation: No Real Malrotation and Not Rare

We read with great interest the article relating to hippocampal malrotation (HIMAL) by Gamss et al.[1][1] We did, however, find some of the terminology questionable. In particular, we thought that “incomplete hippocampal inversion” (IHI) would be a better descriptive term because the hippocampus

Asymmetric Development of the Hippocampal Region Is Common: A Fetal MR Imaging Study

BACKGROUND AND PURPOSE: Hippocampal development is poorly understood. This study evaluated the normal development of the hippocampal region during the fetal period by using MR imaging. MATERIALS AND METHODS: MR images of 63 fetuses without intracranial pathology were reviewed independently by 2 radiologists with no knowledge of the fetal GA. Three MR images were performed postmortem and 60 in vivo. The progress of hippocampal inversion was analyzed in coronal sections, and the left and right sides of the hippocampal region were compared in every case. RESULTS: The fetuses in the postmortem examinations were at GWs 17–18 and in the in vivo examinations, at GWs 19–36. The hippocampal sulcus was open, bi- or unilaterally, in 39 fetuses. The oldest was at GW 32. The sulcus was closed at GW 21 at the earliest, unilaterally. In 26/63 fetuses (41%), the deepening or closure of the hippocampal sulcus or hippocampal inversion was asymmetric; in 23 fetuses, the right side developed faster. A shallow collateral sulcus was found earliest at GW 17. A deep collateral sulcus was visible earliest at GW 26 unilaterally, but in all fetuses from GW 31 onward, it was seen bilaterally. The orientation of the collateral sulcus was not related to the GA. CONCLUSIONS: There are wide individual temporal variations in the development and the inversion process of the hippocampal sulcus as well as in the formation of the collateral sulcus. Asymmetric development is common, and in most of the asymmetric cases, the right hippocampus develops faster.

Development of the hippocampal region demonstrated by fetal MRI. A preliminary report.

Coronal slices of three fetal MRIs performed post mortem and 37 performed in utero, all without intracranial pathology, was assessed. Progress of the hippocampal inversion was analyzed, the left and right sides were compared and occurrence of the collateral sulcus was revealed. The fetuses in the post mortem examinations were at gestation weeks (GW) 17–18 and in the in utero examinations at GW 19–35. The symmetric development of the hippocampal sulcus was revealed in 26 subjects and asymmetric in 14. The non-ovoid hippocampal formation could be evaluated at GW 24 at earliest and an ovoid hippocampus at GW 29. The collateral sulcus could be recognized at GW 17 in post mortem and at GW 22 in in utero examinations. From GW 29 onwards it was seen in all fetuses and it was symmetric in all but one case. Evaluation of the hippocampi is difficult on fetal MRI, especially in in utero examinations. The hippocampal development is not fulfilled at GW 21 as presumed. There is a wide temporal variation in the development of the hippocampal region, and the developmental process does not progress simultaneously in the right and left side of the same individual.