A 45–year–old man presented with encephalopathy after experiencing multiple seizures. The patient’s fiancée observed the patient’s body stiffen, then he had full–body jerking for 10 min. He lost bladder function, and afterwards was confused and tired. He had similar episodes 1 h later and then again in the ED. He was admitted and remained confused for 24 h, but experienced no further seizures. On exam, his vitals were normal and he did not have any focal neurologic deficits. Laboratory studies revealed an anion–gap metabolic acidosis, elevated SGOT and SGPT, and severe hypokalemia, all of which quickly resolved with conservative treatment. CSF cultures and Herpes Simplex Virus CSF PCR were negative. A head CT without contrast showed multiple focal areas of hypoattenuation bilaterally suggesting RPLS. A head MRI with contrast exhibited T2 hyperintensities of the posterior circulation including the cerebellum suggestive of RPLS. While initially not hypertensive, the patient developed hypertensive urgency on hospital day two, which required treatment with three anti–hypertensive medications to control his blood pressure.
Recurrent seizure is a diagnosis for which patients are frequently hospitalized. While treatment is typically benzodiazepines and anti–epileptic medications, the challenge for hospitalists is determining a cause for the condition. History may elucidate the etiology, but it is important to perform a complete laboratory and radiographic workup to ensure there is not a reversible or treatable reason for the seizures. Reversible Posterior Leukoencephalopathy Syndrome (RPLS) is a phenomenon that was first described in 1996 in patients with sudden headache, altered consciousness, visual changes or seizures associated with specific radiographic changes in the posterior cerebral white matter. The posterior regions are hypothesized to be the primary areas involved due to a higher concentration of adrenergic nerves in the anterior circulation to provide great autoregulation to the anterior brain tissue. RPLS may occur in normotensive patients as it is caused by both the percent elevation over baseline blood pressure and the severity of the hypertension. Seizures in RPLS are generally tonic–clonic, often recur, and may even result in status epilepticus. The typical CT radiologic finding is bilateral white matter edema in the posterior hemispheres which resolves in days to weeks. MRI may show increased signal in T2–weighted images. Initial treatment should focus on lowering diastolic blood pressure to 100 mmHg, then careful titration downward in 10–25% increments. Seizures may be treated with phenytoin or other antiepileptic drugs depending on the patient’s medical conditions and medications. RPLS has a favorable prognosis and low rate of recurrence.
The purpose of reporting this case is to inform hospital doctors that RPLS may be the cause of seizure in patients with normal blood pressures.
Figure 1Hyperattenuation in posterior brain regions on MRI in a patient with RPLS.