PERIVENTRICULAR WHITE MATTER LESIONS

Last edited: 7/1/2002 by Timothy C. Hain, MD, Chicago IL.

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periventricular white matter lesionsBetween a third and 80% of MRI scans done in persons over the age of 65 have changes in their cerebral white matter (Wong et al, 2002). MRI studies of older persons with disequilibrium and gait disturbances of unknown cause often show frontal atrophy and subcortical white matter T2 hyperintense foci. (Kerber et al, 1998). Pathological studies, though scanty, suggest frontal atrophy, ventriculomegaly, reactive astrocytes in the frontal periventricular white matter, and increased arteriolar wall thickness (Whitman et al, 1999).

Previous associations for periventriicular white matter (PWM) lesions have included normal senescent changes (called UBO's, for "unidentified bright objects), multi-infarct demetia (Binswanger's disease), as an accompaniment of migraine, and a familial variant, CADASIL. Of these, the most common association is that of simply growing older. Periventricular location seems to cause more serious consequences. Individuals with PVM lesions perform nearly 1 SD below average on tasks involving psychomotor speed. White matter (WM) abnormalities, not necessarily periventricular, as well as decreased white matter volume was found to be both independent factors in predicting decreased mobility in older persons (Guttman et al, 2000).

Pathologically, PWM correspond to areas of myelin thinning and gliosis, and are often accompanied by lacunar (small holes) infarctions and small vessel atherosclerotic disease. PVM relate to vascular disease and vascular risk factors. A long period of hypertension is the most common cause. Clinical studies also show association with diabetes, but not consistently with atherosclerosis.

WM lesions are associated with retinal microvascular abnormalities. Persons with both WM lesions and retinopathy have a much higher risk of clinical stroke (20% vs 1.4%), (Wong et al, 2002).

Treatment:

Practically, this is a statistical association. PVM cannot be clearly shown to cause any particular symptom complex. In other words, one can never be entirely certain that the patients gait disorder, or other neurological symptoms is caused by PWM vs. another cause. We advocate attention to reducing vascular risk factors, especially hypertension and diabetes. With respect to the gait ataxia symptom, empirical treatment including physical therapy, and in some cases, trials of medications such as antidepressants or anti-parkinsonian drugs should be considered.

 

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