During ictus there is an increase in metabolism (oxygen and glucose) in the seizure focus. This hyperme-tabolic state results in consumptive hypoxia, hyper-carbia and lactic acidosis, which impair vascular autoregulation in the affected areas of cortex,leading to vasogenic edema and disruption of the blood-brain barrier . If the seizures are not too prolonged, the
Hippocampal lesion following generalized tonic-clonic seizure in a 2-year-old female with febrile seizure leading to generalized tonic-clonic seizure. a T2-weight-ed and b FLAIR images 3 days after seizure show hyperintensity in the left hippocampus (arrows). c DW image shows increased signal in the left hippocampus (arrows) associated with normal or slightly decreased ADC (d), suggesting a subacute phase of the postictal hippocampal lesion periictal brain lesions will only show transient T2 hy-perintensity, mainly representing vasogenic edema. However, if the seizures are severe or prolonged, cy-totoxic edema can develop. This is often seen in patients with generalized tonic-clonic seizure or status epilepticus (Figs. 8.4,8.5,8.6 and 8.7). Whether these lesions show enhancement or not depends on the degree of blood-brain barrier disruption (Figs. 8.2 and 8.3).
Vasogenic edema in periictal brain lesions has variable signal intensity on DW imaging, which is associated with an increase in ADC (Figs. 8.1, 8.2 and 8.3). As mentioned above, DW imaging is useful in detecting and differentiating cytotoxic from vaso-genic edema.
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