Unilateral cerebral hemisphere oedema as a peri-ictal phenomenon

Focal peri-ictal abnormalities on cerebral imaging are well described [1], most commonly mimicking tumours [2, 5]. More extensive abnormalities resembling cerebral ischaemia are more rarely described. Here we describe a case of extensive peri-ictal cerebral oedema. A 37 year-old man with a known craniopharyngioma and secondary epilepsy presented following a cluster of tonic-clonic seizures occurring over the course of a day. At the time of admission he was experiencing generalised tonic-clonic seizures every 10 min. He was apyrexial and normotensive. Neurological examination showed rightsided hemiparesis, right hemianopia and dysphasia. His white blood cell count and C reactive protein were normal. Treatment with phenytoin and lorazepam resulted in resolution of his seizures. He had been diagnosed with craniopharyngioma at the age of 20 when he presented with a 4-year history of partial seizures manifesting as vacant episodes or right arm focal motor jerks. MRI scan at the time revealed the tumour to be compressing the left temporal and frontal lobes, and engulfing but not compromising the left middle cerebral artery (MCA). It was thought that the tumour was not resectable and his epilepsy was treated with sodium valproate and topiramate. He continued to experience monthly tonic-clonic seizures with partial seizures occurring at least weekly. On admission following his seizure cluster, CT scan of the head showed low attenuation of grey and white matter in the left hemisphere with the craniopharyngioma unchanged from previous scans (Fig. 1a–c). The appearances were suggestive of oedema and there was concern that it might have been of ischaemic etiology caused by tumour invasion into the left MCA. However, CT angiogram of the intracranial vessels demonstrated patent arteries in both hemispheres. An MRI scan on day 4 demonstrated oedema in the posterior frontal, parietal and occipital lobes, mainly affecting the cortical grey matter (Fig. 1d,e). Diffusion weighted imaging (DWI) revealed increased signal intensity in the same distribution; there was no evidence of acute restricted diffusion abnormality (Fig. 1f). The patient’s neurological deficit gradually resolved over the following 2 weeks. An MRI scan performed 5 months later showed complete resolution of oedema (Fig. 2), and his seizure frequency improved such that he only experienced very occasional complex partial seizures. Brain oedema is well described following prolonged epileptic seizures, including partial status [6, 8, 9], nonconvulsive status [3] and convulsive status [1, 7, 8]. The focal changes on imaging can imitate a tumour [5, 9] or ischaemic lesion [9]. Indeed, the focality of the changes has been suggested to be a useful marker for seizure focus [7]. Our case is unusual in having extensive oedematous involvement of one hemisphere. The changes evident on imaging are thought to be due to a combination of vasogenic and cytotoxic oedema due C. Carroll (&) C. O. Hanemann Department of Clinical Neurobiology, Peninsula Medical School, The John Bull Building, Tamar Science Park, Plymouth PL6 8BU, UK e-mail: camille.carroll@pms.ac.uk