Hyperintensitiesrefer to areas of high intensity on types of magnetic resonance imaging scans of the human brain or that of other mammals that reflect lesions produced largely by demyelination and axonal loss. These small regions of high intensity are observed on T2 weighted MRI images within cerebral white matter or subcortical gray matter. They are usually seen in normal aging but also in a number of neurological disorders and psychiatric illnesses. For example, deep white matter hyperintensites are 2.5 to 3 times more likely to occur in bipolar disorder and major depressive disorder than control subjects. WMH volume, calculated as a potential diagnostic measure, has been shown to correlate to certain cognitive factors. Hyperintensities appear as "bright signals" on an MRI image and the term "bright signal" is occasionally used as a synonym for a hyperintensity. Hyperintensities are commonly divided into 3 types depending on the region of the brain where they are found. Deep white matter hyperintensites occur deep within white matter, periventricular white matter hyperintensities occur adjacent to the lateral ventricles and subcortical hyperintensities occur in the basal ganglia. Hyperintensities are often seen in auto immune diseases that have effects on the brain. Postmortem studies combined with MRI suggest that hyperintensities are dilated perivascular spaces, or demyelination caused by reduced local blood flow.
In most elderly people, presence of severe WMH and medial temporal lobe atrophy MTA was linked with an increase in frequency of mild cognitive deficits. Studies suggest that a combination of MTA and severe WMH showed more than a fourfold increase in the frequency of mild cognitive deficits. It's also been consistently shown that severe WMH is known to be associated with gait disorders, impaired balance and cognitive disturbances. Certain features of gait pattern associated with WMH are: slight widening of the base, slowing and shortening of stride length and turning en bloc. Speed of cognitive processes and frontal skills may also be impaired in people with WMH. Pathological signs of oligodendritic apoptosis and damage to axonal projections have been evident. Sufficient damage to the axons that course through WMH can cause adequate interference with normal neuronal functions. It is also thought that WMH patients have a negative impact on cognition in Alzheimer's disease population. In Alzheimer's patients, higher WMH are associated with higher amyloid beta deposits, possibly associated with small vessel disease and reduced amyloid beta clearance.
