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Background
Focal white matter T2 hyperintensities are common, however, the differential diagnosis is wide with overlapping clinical and radiological features. Reaching a definitive diagnosis can be challenging. We aim to present a practical analytical approach to assist radiologists in reading such cases.

Educational Goals / Teaching Points
Understanding cerebral microvascular anatomy facilitates the comprehension of focal white matter lesions’ pathophysiology and how they appear on MRI. Deep white matter, especially border zone regions, is more susceptible to vascular compromise than the cortex and juxtacortical white matter due to fewer arterial anastomoses. Knowledge of normal and clinically insignificant findings including perivascular spaces, ependymitis granularis, and age-related hyperintensities is essential. Based on predominant lesion’s characteristics focal white matter lesions can be classified into three categories : vascular pattern, perivascular pattern, and nonspecific findings. Differential diagnosis of each category could be narrowed down according to clinical, laboratory and other radiological findings.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Vascular pattern is generally due to small vessel disease with age-related and vascular risk-factor-related small vessel disease being the most common type followed by cerebral amyloid angiopathy. Lesions are primarily at subcortical, deep border zone and periventricular white matter. Predominant supratentorial distribution, microhemorrhages and basal ganglia involvement are supportive features. The classic example of perivascular pattern is multiple sclerosis. Other causes include atypical demyelination, acute disseminated encephalomyelitis, inflammatory and autoimmune vasculitis, and some infections. Characteristic findings include juxtacortical and periventricular oval lesions with concomitant supra and infratentorial (mainly peripheral) distribution. Incomplete ring enhancement and absence of microhemorrhages are supportive features. Nonspecific findings include amorphous and round shape, deep nonborder zone white matter location, cortical involvement, and all patterns of enhancement except incomplete ring. These findings should be interpreted in the light of clinical findings and other radiological findings. If no predominate pattern could be identified, age-related and vascular risk-factor-related small vessel disease may be considered first. Otherwise, variable causes of microvascular ischemia and perivascular inflammation should be considered, particularly atypical and uncommon causes.

Conclusion
Analyzing focal white matter lesions characteristics and identifying the distinct patterns can significantly narrow down the differential diagnosis and assist the radiologist in reaching a definitive diagnosis.