Cytotoxic Edema in Status Epilepticus

Cytotoxic edema following status epilepticus can be at least partially reversible [22], as compared to cerebral ischemia, where these changes are usually irreversible. In cerebral ischemia, a significant compromise of blood supply leads to irreversible failure of energy metabolism. In sustained seizures, there is an increased cerebral metabolism with an increase in cerebral blood flow. This will maintain the energy state of the neuron provided there is sufficient oxygen supply.

The parts of the human brain that are most vulnerable include parts of the hippocampus (the CA1and CA3 segments, and the hilus), amygdala, pyriform cortex, thalamus, cerebellum, and cerebral cortex. NMDA receptors are predominantly located in the CA1 of the hippocampus and layers 3 and 4 in the cerebral cortex [32,33]. The Purkinje cell loss of the cerebellum, seen in severe epilepsy, may be explained by an increased demand for inhibition, re-suiting in GABA depletion and subsequent influx of calcium into neurons [34]. Unilateral hemispheric involvement is occasionally seen in status epilepticus.

Transient and reversible MR signal changes have been reported in patients following status epilepticus [16,19-23]. On the other hand, other lesions have been proven irreversible, resulting in selective neuronal necrosis, gliosis and delayed neuronal death with subsequent atrophy [24-26] (Figs. 8.6 and 8.7). Following

Cytotoxic EdemaStatus EpilepticusCytotoxic Edema
Figure 8.7 a-e

Hemiplegic hemiconvulsion epilepsy syndrome in a 2-year-old girl with partial status epilepticus involving the right face and hand. a T2-weighted image 24 h after seizure shows diffuse cortical hyperintense lesions in the entire left cerebral hemisphere,including the basal ganglia,and thalamus. b DW image shows diffuse left-sided cortical and subcortical hyperintense lesions with decreased ADC (c),representing cytotoxic edema.d MR angiography reveals dilatation of the left middle cerebral and posterior cerebral artery branches (arrows),representing hyperperfusion. e Diffuse atrophy with ventricular dilatation and hyperintense lesions in the left hemisphere seen on 5 months follow-up T2-weighted image.

status epilepticus, there has also been reported acute neuronal loss in the hippocampus accompanied by intense astrocytic reactions, called mesial temporal gliosis. This is pathologically different from mesial temporal sclerosis [16, 35, 36] (Fig. 8.6). However, these lesions may be the first step in the development of mesial temporal sclerosis [19,21]. Increased apparent diffusion coefficient (ADC) in the hippocampus has been reported in mesial temporal sclerosis [27].

Diffusion-weighted imaging and ADC maps are more sensitive than conventional MR imaging to show both gray and white matter involvement, and discriminate between cytotoxic and vasogenic edema following status epilepticus [22]. In experimental status epilepticus models,ADC decrease was first seen at about 3 hours and lasted until 48 hours after the onset of seizures, after which time it normalized or even increased [37-42]. The definite time course of DW

imaging changes in humans is unknown, but areas of signal abnormalities on DW imaging and ADC are seen in cytotoxic edema following status epilepticus, although they are sometimes reversible, as mentioned above [22].

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    Does status epilepticus cause cerebral edema?
    11 months ago
  • thorsten
    Can cytotoxic edema be caused by severe ischemia?
    6 months ago

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