Posterior Leukoencephalopathy Studied with Diffusion-Weighted MRI
abstract & commentary
Source: Ay H, et al. Posterior leukoencephalopathy without severe hypertension. Utility of diffusion-weighted MRI. Neurology 1998;51:1369-1376.
Posterior leukoencephalopathy syndrome (PLES) is an acute, progressive neurological condition characterized clinically by headache, nausea and vomiting, visual disturbances, altered mental status, seizures, and variable focal neurological deficits. Standard T2-weighted MR imaging demonstrates white matter hyperintensity spreading out from posterior brain regions. Although the most common cause of PLES is an abrupt and severe increase in blood pressure, the term comprises more than the hyperintensive encephalopathy syndrome: PLES also has been reported in normotensive patients taking immunosuppressive drugs1 or erythropoietin2 and in subjects with high-altitude cerebral edema.3,4
Ay and associates describe three women with the clinical syndrome of PLES who had only mild elevations in blood pressure. All had severe metabolic abnormalities such as sepsis, hyponatremia, urinary protein loss, and fever. One was taking corticosteroids and another had received a dose of taxol and carboplatin. In all three patients, the initial clinical diagnoses were bilateral posterior cerebral artery distribution strokes or watershed infarcts.
Serial imaging studies included CT, standard MRI, diffusion-weighted imaging (DWI), and apparent diffusion coefficient (ADC) maps. MRI showed T2 hyperintense regions in the posterior cerebrum with corresponding hyperintensity on ADC maps, signal characteristics consistent with vasogenic edema. (See Table.) One patient showed smaller patches of cortex with decreased ADC and bright DWI consistent with infarctions. Another, who died, converted a large posterior region to an ischemic pattern. The two survivors recovered clinically and convalescent MRIs showed resolution of lesions except in regions that had been hyperintense on DWI. Ay et al conclude that ADC maps and DWI can differentiate reversible PLES from early cerebral infarction in patients with an identical clinical presentation.
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| MRI Signal Intensities___________________________________________ | ||||
| MRI Sequence |
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| T2 |
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| FLAIR |
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| DWI* |
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| ADC* |
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| *See Text.
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Commentary
In PLES, neither the clinical presentation nor the appearance of lesions on T2-weighted MRI can distinguish acute bilateral occipital infarction from reversible, extracellular edema of white matter. For example, in another study of nine men with acute mountain sickness,3 Hackett and associates observed intense T2 signals in white matter areas, especially in the splenium of the corpus callosum. They concluded later that the abnormalities were due to vasogenic edema because they had resolved on MRIs performed after the subjects recovered.
In the present study, Ay et al used DWI, a technique that makes MR images sensitive to the motion of water molecules. In the early phase of cerebral infarction, the diffusion of water molecules decreases. Water becomes trapped intracellularly by the depletion of high-energy phosphates and the failure of ion pumps. Intracellular or cytotoxic edema due to ischemia is characterized by marked hyperintensity on DWI and hypointensity on ADC maps. (See Table.) Conversely, vasogenic or extracellular edema due to blood brain barrier leakage is characterized by an increase in the diffusion of water molecules and appears hypo- or iso-intense on DWI and hyperintense on ADC maps.
DWI and ADC mapping provides an essential method to distinguish between ischemia and vasogenic edema in PLES. In cases of acute ischemic stroke, neurologists may tolerate moderate hypertension, fearing that overtreatment could lead to hypotension and more extensive brain ischemia. In contrast, in patients with PLES secondary to acute hypertension or other causes of extracellular edema, treatment of hypertension can reverse the edema-causing process before permanent brain injury occurs.
References
1. Hinchey J, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334: 494-500. (Neurol Alert 1996;14:73-74).
2. Delanty N, et al. Erythropoietin-associated hypertensive posterior leukoencephalopathy. Neurology 1997; 49:686-689.
3. Hackett PH, et al. High-Altitude cerebral edema evaluated with magnetic resonance imaging. Clinical correlation and pathophysiology. JAMA 1998;280: 1920-1925.
4. Plum F. Cyclosporin, tacrolimus, and cerebral leukoencephalopathy. Neurol Alert 1996;14:73-74.
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