Abstract
Posterior reversible encephalopathy syndrome (PRES) is characterized by global encephalopathy, seizures, headache, or visual symptoms. Neuroimaging of PRES is typically associated with vasogenic edema in the occipital lobes and other posterior structures [1]. However, involvement of PRES in only pons is rare. The present study report a patient with isolated pons variant of PRES complicated with ischemic stroke which has not been previously reported in the literature. A 36-year-old right-handed woman was admitted to the emergency department with right-sided weakness, nausea and vomiting. She had no symptoms of headache, seizures, blurred vision or fever. She denied the history of hypertension. In admission, she was conscious with blood pressure 260/140 mmHg. Examination showed right hemiparesis (medical research council power grade 4 in the upper and the lower extremity) with extensor plantar response. The hemoglobin level was 11 g/dL and the platelet level was 145,000/mm. Her serum BUN and creatinine level were 6.15 mmol/L and 215 lmol/L, respectively. The results of serum electrolyte showed normal. The result of dynamic electrocardiogram (ECG) monitoring was normal too. The echocardiography revealed left ventricular hypertrophy. The kidney ultrasonography study exhibited a clear increase in renal parenchymal echogenicity with a poor corticomedullary differentiation. The signal in the pons and left periventricular white matter was increased in T2-weighted MRI test (Fig. 1a, b). Diffusion-weighted imaging (DWI) was normal and apparent diffusion coefficient (ADC) map showed high intensity signal in the pons (Fig. 1c, e). DWI showed hyperintense lesion corresponding to that on T2weighted images in the left periventricular white matter (Fig. 1d). The ADC map of the lesion demonstrated restricted diffusion in keeping with ischemia (Fig. 1f). Lumbar puncture and analysis of the cerebrospinal fluid were refused by her family members. She was treated with nicardipine and citicoline. Blood pressure was normalized and the patient’s weakness gradually improved within 15 days. An MRI at 18 days revealed that the pons changes were completely reversed and the lesion in the left periventricular white matter still exists (Fig. 1g, h). A diagnosis of isolated pons variant of PRES complicated with acute ischemic stroke was made and she was transferred to nephrology department. The renal biopsy revealed IgA nephropathy with proliferative sclerosing glomerulonephritis. PRES can be triggered by eclampsia, hypertensive emergency, or exposure to immunosuppression (most notably the calcineurin inhibitors) [2]. Hypertension from a renal origin has been reported to be a significant cause of PRES in one study of both pediatric and adult patients [1]. The vertebrobasilar system is relatively devoid of adrenergic sympathetic innervations, making the posterior brain regions more susceptible to overwhelm autoregulatory mechanism by acute upsurge of blood pressure [2]. Pons edema in the PRES had been reported uncommonly which H. Liang and D. Li contributed equally to this article.
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