Posterior Reversible Encephalopathy Syndrome, Seizures, and the EEG
Posterior Reversible Encephalopathy Syndrome, Seizures, and the EEG
Abstract & Commentary
By Steven Karceski, MD, Director of Clinical Trials, Cornell Comprehensive Epilepsy Center, Weill Cornell Medical College. Dr. Karceski reports he is on the speakers bureau for GlaxoSmithKline, Cyberonics, and Pfizer; and receives research support from Novartis and Cyberonics.
This article originally appeared in the February 2012 issue of Neurology Alert. It was edited by Matthew Fink, MD, and peer reviewed by M. Flint Beal, MD. Dr. Fink is Interim Chair and Neurologist-in-Chief, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York Presbyterian Hospital, and Dr. Beal is Anne Parrish Titzel Professor, Department of Neurology and Neuroscience, Weill Cornell Medical Center. Dr. Fink is a retained consultant for MAQUET, and Dr. Beal reports no financial relationships relevant to this field of study.
Synopsis: This clinical study evaluated patients with posterior reversible encephalopathy syndrome to determine the kind of seizures they experienced, abnormalities on EEG, and to correlate this with findings on neuroimaging (MRI).
Source: Kastrup O, et al. Posterior reversible encephalopathy syndrome (PRES): Electroencephalographic findings and seizure patterns. J Neurol 2011 DOI 10.1007/s00415-011-6362-9.
Posterior reversible encephalopathy syndrome (PRES) is a clinical and radiological diagnosis characterized by changes in mental status, headaches, visual obscurations, and seizures. Radiographically, there are characteristic changes on MRI, consisting of both white and gray matter hyperintensities. As the name of the syndrome suggests, MRI changes usually occur in the posterior quadrants of the brain and are usually symmetric. PRES is most often associated with hypertension (usually quite high), eclampsia, neurotoxins (such as chemotherapeutics), and immunosuppressants. The connection between these causes and the radiologic findings is unclear, though one hypothesis is that there is vasogenic leakage through the blood-brain barrier, accounting for the clinical and imaging findings.
In the medical literature, there is scant information about PRES and associated EEG findings. Kastrup and colleagues carefully reviewed the EEGs in 49 adults (ages 18-66) who were treated for PRES at the University of Duisburg-Essen, between 2004 and 2011. They performed a retrospective chart review of 49 patients who had radiologically confirmed PRES and 38 of these patients also had seizures. Of the 38 who had seizures, 17 had one or more EEGs during the course of their illness. Of the 17, one (5%) had focal visual seizures, and one (5%) had focal motor seizures. Two (12%) had serial grand mal seizures, defined as seizures that recurred within the first hour of the initial seizure. Three (17.6%) had recurrent grand mal seizures, defined as seizures that recurred within the first 3 hours of the initial seizure. None of the patients had status epilepticus nor seizures for more than 1 day after the initial seizure. About one-half (53%) were treated for their seizures.
EEGs were abnormal in all 17 patients. Diffuse slowing to the theta range was the most common finding, occurring in 13 of the 17 patients (76.5%). Diffuse delta was the next most common finding in 23.5%. Epileptiform discharges occurred in one patient, consisting of occipital sharp-slow wave discharges. One patient had periodic lateralized epileptiform discharges in the left hemisphere.
Kastrup et al noted that a single "grand mal" seizure was the most common type of seizure to occur in PRES. Serial or recurrent grand mal seizures occurred less often. Though described in the medical literature, status epilepticus and chronic epilepsy did not occur in this case series. No correlation was found between the occurrence of seizures and the pattern of abnormalities on MRI. The most common finding on EEG was diffuse slowing (theta and delta); infrequently, epileptiform discharges were recorded.
Commentary
PRES is known to cause seizures. This makes sense given the cortical involvement in most people who develop this syndrome. In the medical literature, most descriptions of the seizures that occur in PRES come from case series or case reports. Convulsions, focal seizures, and status epilepticus all have been reported. In most people, the seizures are self-limited, acute, and usually do not become chronic epilepsy.
Although very helpful, Kastrup's study is limited. Of the 49 patients, EEG results were available in only one-third (34%). Of the 38 who had seizures, an EEG was performed in fewer than one-half (44%). This is a limitation of a retrospective chart review; not all patients will have undergone the testing that the authors were interested in studying. A prospective study of PRES would eliminate this problem. Although such a study would take many years to complete, it would be helpful to perform an EEG in all patients who are diagnosed with PRES, providing EEG information for all patients with PRES, including the ones in whom seizures did not occur. It might be interesting to know if there are differences in the EEG of people who had seizures and those who did not. For instance, if there is a difference, the EEG information might identify people with PRES who are at greater risk for having seizures. Further study of this syndrome is needed.
This clinical study evaluated patients with posterior reversible encephalopathy syndrome to determine the kind of seizures they experienced, abnormalities on EEG, and to correlate this with findings on neuroimaging (MRI).Subscribe Now for Access
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