Observing Hippocampai Sclerosis Development

Acute Changes in Patients with Epilepsy Progressing to Hippocampai Sclerosis

The presence of short-term, seizure-associated changes is an important issue. There is debate about whether seizures cause damage to the brain or whether all or a portion of the abnormalities seen in the brains of patients with epilepsy are due to pre-existing factors. A change in T2 relaxometry after a seizure would favor the idea that seizure-associated damage can occur. An early study suggested that recent seizures do not influence T2 values (289). In this study of 63 patients with chronic epilepsy, four patients were scanned a second time after a recent complex partial or secondary generalized seizure. There was no change of the T2 values after the seizure.

However, several other reports have shown an acute increase in T2-signal after a brain injury such as status epilepticus, together with an increase in hippocampai volume (Fig. 4.32) (290-293). Experimental models provide evidence that T2-time acutely increases after kainate injection, reflecting cytotoxic edema (294). A gradual resolution of the high T2 signal may occur, reflecting resolution of the edema. If there is no evolution into HS, and acute electro-encephalographic abnormalities resolve, T2-signal may normalize, as has been shown in some case reports (295, 296). However, several other cases have demonstrated the evolution into HS, with the typical MR features of hippocampai volume loss and T2 signal increase visible weeks to months after the acute insult (291, 297). Some examples of progression of the hippocampai changes are shown in Figures 4.33^1.35.

Information on pathologic changes is not always available and is therefore very important if given. Two reports show histopathologic results on patients who had acute T2-relaxometry changes within the region that was later microscopically assessed. One report describes a child who died 44 days after a refractory status epilepticus. Histopathology showed neuronal necrosis and gliosis in CA1, CA3, and dentate gyrus. Another child underwent a temporal lobectomy for seizure control 38 months after a prolonged febrile convulsion. Histopathology again showed the typical HS features of focal neuron loss and gliosis.

FIG. 4.32. Progression of hippocampal sclerosis after a prolonged seizure. (With permission from Nohria et al. 1994 (358).)

FIG. 4.32. Progression of hippocampal sclerosis after a prolonged seizure. (With permission from Nohria et al. 1994 (358).)

Whereas the studies reported above consist of case reports or small series, one recent report assessed a series of 35 children (298). All had MR investigations within 5 days of a generalized status epilepticus. Quantitative assessments included T2 relaxometry and hippocampal volumetry. T2 relaxation time was elevated in patients with prolonged febrile convulsions compared with control subjects when they were scanned within 2 days of the acute event, whereas no difference in the T2-values were found in patients examined 3-5 days after the event. These findings are consistent with another series in children, scanned within 14 days of the event (299). In this series, T2 relaxometry findings showed no abnormalities.

The development of HS, although most frequently observed in young children, has also been described in adults. It has been observed after severe seizures in adulthood (297), after a series of brief seizures (see Fig. 4.33) (300), in the context of other focal pathology such as cavernous angioma and neurocysticercosis (301), and also after domoic acid intoxication (302). The last report suggests that the human hippocampus is vulnerable to kainate receptor excitotoxicity and provides strong evidence for a supporting role of excitotoxic injury in epileptogenesis. These observations suggest that T2-signal increase occurring shortly after a seizure, associated with increased volume, reflects cell edema. This abnormality can evolve into HS, in which T2-signal increase is again increased but now associated with reduced volumes. This chronic change in T2-value increase may reflect gliosis, as outlined below.

Retrospective quantitative MRI studies have addressed the issue of progression of HS due to seizures, and suggested that seizure activity may (303, 304) or may not (305, 306) be associated with progressive hippocampal volume loss. Wieshmann et al. (291) and O'Brien et al. (307) described two patients with HS and progressive hippocampal volume loss on repeat MR imaging associated with frequent secondary generalized seizures. In a prospective study of patients with newly diagnosed partial epilepsy and a repeat MRI scan 1 year after the first MRI, one patient was observed with bilateral hippocampal atrophy and normal hippocampal T2s, who had significantly increased hippocampal T2s with no measurable further hippocampal volume loss on follow-up 7 months later. These hippocampal changes were associated with daily seizures and frequent secondary generalization (308).

Chronic Changes in the Hippocampus in Patients with Epilepsy

The original observation of increased hippocampal T2 relaxometry was made in patients with refractory temporal lobe epilepsy (241). This report recorded that the side of the seizure origin was ipsilateral to the hippocampal T2 abnormality when the abnormality was unilateral. When there were bilateral abnormalities with one side more abnormal than the other, the side of seizure origin also always correlated with the more abnormal hippocampal T2 signal.

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