Abstracts

Rationale: It is well documented that imaging changes can be seen as a result of seizures: These can range from transient increased T2/FLAIR/DWI changes in partial seizures to irreversible residual gliosis, atrophy, or laminar necrosis after multiple seizures or status epilepticus(Cartagena 2014; Cianfoni 2013; Milligan 2009). Milligan (2009) found MRI changes attributable to status epilepticus in 11.6% of patients. It is less clear whether or not interictal phenomenon, such as PLEDs, also result in imaging changes. This can be challenging to delineate, as PLEDs are often seen in association with acute brain lesions, most commonly ischemic stroke or focal encephalitis (Gurer 2004). There are multiple reported cases of patients with PLEDs on scalp EEG and associated functional SPECT or PET (Ergun 2006; Bozkurt 2002; Assal 2001; Lee 1988; Aye 2013). All but one reported increased cerebral blood flow in the concordant seizure focus during PLEDs and subsequent hypoperfusion in the same region once the PLEDs ceased. Methods: Case report Results: We present the case of a 66 year-old woman with a history of CNS lymphoma s/p Rituxan, Fentomustine, intrathecal Methotrexate, XRT and subsequent epilepsy who presented on 12/27/13 after waking up with right-sided weakness. Her exam on presentation: mental status was somnolent, decreased verbal output, 0/5 right-sided strength, and NIHSS=16. She was deemed not to be an iv-tPA candidate given the unclear time of onset (last seen normal >4.5 hours). CTH was without acute intracranial abnormality. MRI brain (12/27/2013) was compared to her prior MRI brain (9/17/13) and showed no acute findings: unchanged bilateral frontal white matter hyperintensity without evidence of abnormal enhancement. She was placed on continuous EEG monitoring which revealed diffuse background slowing and continuous 1-2Hz left posterior quadrant PLEDs. Over the ensuing few hours, she developed increased confusion as well as aphasia. There was no change or evolution in her EEG to suggest an ictal correlate to these clinical symptoms. Repeat MRI brain (12/28/2013) later that day revealed an interval development of T2 FLAIR sulcal/cortical hyperintensity in the posterior temporal and parietal regions without corresponding restricted diffusion. The patient clinically improved back to baseline with increased doses of AEDs. Follow-up imaging 2 months later (2/3/2014) showed resolution of the cortical swelling and sulcal T2 hyperintensity in the left temporoparietal region. Conclusions: The sequential MRIs in our case show T2/FLAIR changes in the same region as her PLEDs on scalp EEG, similar to the radiologic findings that may be seen after a seizure. The acute onset of the MRI hyperintensity and its reversibility suggest that these findings are a consequence of the PLEDs as opposed to the cause. These imaging findings, as well as our patient's clinical symptomatology and subsequent improvement with increased doses of AEDs suggest that our patient's continuous PLEDs may represent an ictal phenomenon.