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Among many conditions causing small vessel diseases, lipohyalinosis is the leading pathology next to microatheroma. Lipohyalinosis affects penetrating arteries distally than microatheroma. Proliferation of smooth muscle cells may occlude the lumen, reducing the blood flow and inducing lacunar infarction. In contrast, fibrinoid necrosis of smooth muscle cells in the media may weaken the vascular constriction, increasing the perfusion pressure in the capillary and damaging the blood brain barrier which can induce white matter lesion. Neurovascular unit (NVU) is a concept that neurons, astrocytes, and vessels function as a unit to support neuronal activity. NVU is involved in the maintenance of synapse, transmitter, energy metabolism, blood-brain barrier, and blood flow. Change in neuronal activity is transmitted to capillaries through NVU, where the information is collected along vessels proximally and regulates blood flow (proximal integration model). CARASIL and CADASIL both affect vascular smooth muscle cells, resulting in vascular dilatation, damaging NVU, and inducing white matter lesion. Occlusion of the affected vessels, causing cerebral ischemia, under these diseases is relatively infrequent. Similarity in pathophysiology between hypertensive arteriolar disease and the familial angiopathy may indicate that injury to NVU may indicate the common pathophysiology of white matter lesions.

Disturbance in neurovascular unit plays a pivotal role in pathophysiology of small vessel disease in the brain