Leukoaraiosis is the therm that designates diffuse, coalescing white mater abnormalities that are visible as hypointense foci on CT and hyperintense lesions on T2-weighted MRI and FLAIR, often with irregular margins. Leukoaraiosis is common in the elderly, in conjunction with vascular risk factors such as hypertension, or in the context of cognitive disorders.

The term leukoaraiosis was introduced in 1987 by Vladimir Hachinsky and colleagues with purely descriptive purpose to avoid the attribution of those diffuse white matter changes observed on CT to some specific diseases, later on providing a rational explanation for these lesions. The term comes from the Greek root "leuko-" = white, meaning white matter, and the adjective «araios" meaning "thin."

Leukoaraiosis typically occurs in the following cases:

  • In patients with ischemic stroke, especially lacunar stroke subtype. Approximately 7% of patients with ischemic stroke has leukoaraiosis on CT or MRI.
  • Patients with dementia of both vascular and non-vascular etiologies (degenerative, in Alzheimer's disease). However, leukoaraiosis is more common in vascular dementia, 2/3 of patients with this pathology presenting leukoaraiosis. Also, leukoaraiosis occurs in 30% of patients with Alzheimer's dementia.
  • Leukoaraiosis may be a phenomenon accompanying the physiological process of aging, confluent lesions corresponding to leukoaraiosis being viewed on 10% of asymptomatic individuals aged 50-75 years. The prevalence of leukoaraiosis increases with age in this group.


The main morphological changes observed in the regions of leukoaraiosis affect the white matter and the brain vessels of small caliber. Among the changes in the white matter can be noted myelin pallor, increased perivascular spaces, gliosis and axonal loss. Vascular lesions in regions of leukoaraiosis ranges from hyaline thickening and arteriosclerosis (occasionally the changes are identified as the simple pathology of small vessels) to lipohyalinosis - a term that refers to a more disorganized vascular wall with foamy macrophages (complex pathology of small vessels) and fibrinoid necrosis. In the case of leukoaraiosis of Alzheimer's disease, its most obvious cause appears to be cerebral amyloid angiopathy, although recent evidences confirm an increasing role of non-amiloid fibrohyalinosis.

Causes of leukoaraiosis

The causes of leukoaraiosis are divided into 3 groups:

  • Ischemic leukoaraiosis: lacunar stroke / transient ischemic attack (TIA). The risk factors in this case are age, hypertension and homocysteine
  • Sporadic cerebral amyloid angiopathy: The diagnosis is made according to the criteria of Boston.
  • CADASIL: clinical associations will be lacunar stroke / TIA, migraine and depressive symptoms.

Clinical manifestations

Leukoaraiosis is manifested by cognitive and executive troubles that constitutes the clinical picture of dementia. The presence of leukoaraiosis also changes the cognitive profile in Alzheimer's disease. Another characteristic of leukoaraiosis is abnormal gait and falls. Up to 80% patients with leukoaraiosis have gait disturbance. The mechanism these alteration is not well established, although atrophy of the frontal lobe with damage to circuits involved in the control of gait can play a role in this regard. Other manifestations of leukoaraiosis include bladder instability and depression.