Recurrent posterior reversible encephalopathy syndrome of the brainstem in a hypertensive patient with end-stage renal disease.

A 59-year-old man with end-stage renal disease was brought to our emergency department with complaints of headache, nausea, dysarthria, tic, and weakness involving the bilateral arms and legs. He had the similar episode 4 month before, when he was treated elsewhere. The patient had received hemodialysis three times per week. His medications included for hypertension. On examination at his arrival, he was alert with reduced concentration and incoherent thoughts. The blood pressure was 181/87 mmHg and other vital signs were normal. Neurological findings showed slight dysarthria and slow movements but no other abnormalities. Laboratory data showed increased serum creatinine and potassium presumably for a session of periodical hemodialysis but normal sodium concentration. His cerebrospinal fluid examination was normal. We treated him by hemodialysis. Diagnosis of PRES was most likely because of the clinical features and the MRI findings. His symptoms had disappeared immediately and completely after we controlled high blood pressure. MRI on 13 days after admission showed the improvement of the abnormal findings. Although the pathophysiology of PRES is incompletely understood, renal failure was known as one of the risk factors. A relative lack of sympathetic innervation of posterior circulation could not protect the area when severe hypertension makes auto-regulatory control collapsed. However, PRES of the brainstem is uncommon although the posterior circulation involves it. Because control of his hypertension was not appropriate in the outpatient settings before this event, it could have contributed to the recurrence in this patient.

A 59-year-old man with end-stage renal disease was brought to our emergency department with the complaints of headache, nausea, dysarthria, tic and weakness involving the bilateral arms and legs. He had the similar episode 4 month before, when he was treated elsewhere. Patient had received hemodialysis 3 times/week. His medications included for hypertension.

On examination at his arrival, he was alert with reduced concentration and incoherent thoughts. The blood pressure was 181/87 mmHg and other vital signs were normal. Neurological findings showed slight dysarthria and slow movements, but no other abnormalities.

Laboratory data showed increased serum creatinine and potassium presumably for a session of periodical hemodialysis, but normal sodium concentration. His cerebrospinal fluid examination was normal. We treated him by hemodialysis after he received plain brain computed tomography [Figure 1] and magnetic resonance imaging (MRI) T2-weighted fluid attenuated inversion recovery [Figure 2a]. Diagnosis of posterior reversible encephalopathy syndrome (PRES) was most likely because of the clinical features and the MRI findings. His symptoms had disappeared immediately and completely after we controlled high blood pressure. Diagnosis of central pontine myelinolysis was unlikely due to the rapid disappearance of his symptoms only by controlling the blood pressure on the day of admission. MRI on 13 days after admission showed the improvement of the abnormal findings [Figure 2b].

Figure 1

Brain computed tomography on arrival revealed hypodense lesions with surrounding vasogenic edema in the brain stem

Figure 2a

Magnetic resonance imaging T2-weighted fluid attenuated inversion recovery on arrival showed high signal intensity of brain stem involving a ventral part of cerebellum

Figure 2b

MRI T2-weighted fluid attenuated inversion recovery 13 days after admission

Although the pathophysiology of PRES is incompletely understood, hypertension-induced vasogenic edema[12] is widely believed. Thus, it is overwhelming of cerebral autoregulation. Other mechanism is forced dilation of arterioles with leakage of serum through capillary walls into cerebral interstitium. Furthermore, unchecked vasogenic edema may lead to interstitial edema[3] Renal failure was also known as one of the risk factors related to them.[2] A relative lack of sympathetic innervation of posterior circulation could not protect the area when severe hypertension makes auto-regulatory control collapsed.[4] However, PRES of the brainstem is uncommon although the posterior circulation involves it.[5] Because control of his hypertension was not appropriate in the out-patient settings before this event, it could have contributed to the recurrence in this patient.