Deep White Matter Ischemia

      Pathophysiology

      As the brain ages, structural, chemical, and metabolic changes occur that are reflected on the MR images. Most important for MR interpretation are the changes related to deep white matter ischemia. The deep white matter of the cerebral hemispheres receives its blood supply from long, small-caliber arteries and arterioles that penetrate the cerebral cortex and traverse the superficial white matter fiber tracts. The white matter does not have as generous a blood supply as the gray matter and is more susceptible to ischemia. As the nutrient arteries become narrowed by arteriosclerosis and lipohyaline deposits within the vessel walls, the white matter becomes ischemic on a chronic basis. Pathologically, one of the first changes in the aging brain is an increase in the perivascular interstitial fluid, predominantly at the arteriolar level of the vascular tree. With continued progressive ischemia of the white matter, additional histologic changes are observed, including atrophy of axons and myelin and tortuous, sclerotic, and thickened vessels. Maintenance of the myelin becomes deficient, resulting in "myelin pallor" on microscopic sections. Mild gliosis and increased interstitial fluid accompany the changes in the myelin. Necrosis is not seen until severe ischemia leads to frank infarction of brain tissue.

      As mentioned previously, the observed changes are secondary to chronic ischemia of the deep white matter and are found more often in patients with ischemic cerebrovascular disease, hypertension, and aging. A combination of arteriolar disease and episodic brain hypoperfusion probably leads to the histopathologic changes. Hypoperfusion can be caused by episodes of hypotension, hypoxia secondary to cardiac or carotid artery disease, hypertension, and/or aging.

      The most common locations for the hyperintensities are the subcortical and periventricular white matter, optic radiations, basal ganglia and brain stem, in decreasing order of frequency. The lesions are hyperintense on T2, proton density, and FLAIR images and have well defined but irregular margins. They are mildly hypointense on T1 weighted images, but the contrast between the lesions and the normal brain is much less than that on T2 weighted images. The white matter changes do not exhibit restriction diffusion, are not associated with breakdown of the blood brain barrier and do not enhance. The process tends to be multifocal, but as the lesions enlarge, a more confluent pattern may develop.

      Another pattern of white matter abnormality associated with deep white matter ischemia is a more or less continuous band of abnormal signal bordering the lateral ventricles. Normally, interstitial fluid does not accumulate around the ventricles except for small "CSF caps" around the frontal and occipital horns. White matter ischemia results in mild interstitial edema that exceeds the capacity of the ependymal transport system. The chronic accumulation of water around the ventricles adversely affects myelin maintenance and over time induces partial but irreversible loss of myelin that is reflected as myelin pallor of the periventricular white matter on pathologic examination. On T₂-weighted MR images this white matter abnormality appears as a hyperintense band of variable thickness located along the dorsolateral angles of the ventricles, closely apposed to the ependymal surface. A slightly heterogeneous texture and irregular outer margins distinguish it from the phenomenon of transependymal CSF flow or "periventricular halo" of obstructive hydrocephalus (see "Differential Diagnosis" further on). On T₁- weighted images the periventricular lesions are lower signal than the subcortical white matter lesions, probably due to increased water content.  

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