Neuroradiology Case of the Month

February 2002

Christopher Bang, DO, Manoj Ketkar, MD, Ryan Lee, MD,
and Per-Lennart Westesson, MD, PhD, DDS

Clinical Presentation: A 56-year-old female with severe hypertension, renal insufficiency, acute mental status changes and new onset of seizures.

Radiological Findings: Symmetrical low attenuation lesions in the bilateral posterior parietal-occipital subcortical white matter (Fig. 1). These findings were not demonstrated on a previous CT scan one month prior (Fig. 2).

Differential Diagnosis:

• Acute hypoxic ischemia/Posterior cerebral artery territory infarction
  
• Posterior reversible encephalopathy syndrome (PRES)
  
• Cerebral edema from trauma
  
• Transient cerebral hyperemia/hyperperfusion postictal or postoperative
  
• Progressive multifocal leukoencephalopathy

Diagnosis: PRES secondary to severe hypertension (hypertensive encephalopathy).

Figure 1: Symmetrical low attenuation lesions in the bilateral posterior parietal-occipital subcortical white matter

Figure 2: Focal linear area of low attenuation in the right centrum ovale represents gliosis from old infarct and was noted on previous exam

Figure 3: Follow up CT scan one month later demonstrates resolution of the posterior low-attenuation changes.

Discussion: Posterior reversible encephalopathy syndrome (PRES) (or reversible posterior leukoencephalopathy syndrome) is an acute episode of vasogenic edema in the cerebral white matter, with a predeliction for the posterior temporal, parietal and occipital regions. The extracellular edema is likely due to autoregulatory dysfunction in the posterior circulation, and ensuing transudation of fluid because of blood-brain barrier breakdown.

It is a progressive disorder, but transient and reversible if the underlying condition is promptly and adequately addressed (i.e. hypertension, uremia, toxemia). In this case, the patient’s severe hypertension was treated. This can also be seen in patients on certain cytotoxic and immunosuppressive therapy (ie: cisplatin, cyclosporin, tacrolimus, etc.) and lesions usually resolve with discontinuance of the offending agent.

Radiologic distinction from PCA-territory infarction with cytotoxic edema is evident by the sparing of the cortical and paramedian occipital structures, as well as resolution of the lesions on follow-up imaging. Diagnosis can be easily recognized with magnetic resonance imaging. Acute infarction usually demonstrates hyperintensity on DWI and T2WI, with decreased ADC levels. As opposed to hypo- or isointensity on DWI, hyperintensity on FLAIR and T2WI, and markedly elevated ADC levels with PRES.

References:

1. Hinchey et al.: A reversible posterior encephalopathy syndrome. NEJM 334:494-500, 1996.
2. Ay et al.: Posterior leukoencephalopathy without severe hypertension: Utility of diffusion-weighted MRI. Neurology 51:1369-76, 1998
3. Jarosz et al.: Cyclosporine-related reversible posterior leukoencephalopathy: MRI. Neuroradiology 39:711-715, 1997.
4. Osborn A: Diagnostic Radiology. Mosby, 1994:176-179