Hyperintensity

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MRI scans showing hyperintensities CADASIL.jpg
MRI scans showing hyperintensities

A hyperintensity or T2 hyperintensity is an area of high intensity on types of magnetic resonance imaging (MRI) scans of the brain of a human or of another mammal that reflect lesions produced largely by demyelination and axonal loss. These small regions of high intensity are observed on T2 weighted MRI images (typically created using 3D FLAIR) within cerebral white matter (white matter lesions, white matter hyperintensities or WMH) [1] [2] or subcortical gray matter (gray matter hyperintensities or GMH). The volume and frequency is strongly associated with increasing age. [2] They are also seen in a number of neurological disorders and psychiatric illnesses. For example, deep white matter hyperintensities are 2.5 to 3 times more likely to occur in bipolar disorder and major depressive disorder than control subjects. [3] [4] WMH volume, calculated as a potential diagnostic measure, has been shown to correlate to certain cognitive factors. [5] Hyperintensities appear as "bright signals" (bright areas) on an MRI image and the term "bright signal" is occasionally used as a synonym for a hyperintensity.

Contents

Hyperintensities are commonly divided into 3 types depending on the region of the brain where they are found. Deep white matter hyperintensities occur deep within white matter, periventricular white matter hyperintensities occur adjacent to the lateral ventricles and subcortical hyperintensities occur in the basal ganglia.[ citation needed ]

Hyperintensities are often seen in auto immune diseases that have effects on the brain. [6]

Postmortem studies combined with MRI suggest that hyperintensities are dilated perivascular spaces, or demyelination caused by reduced local blood flow. [7]

Causes

White matter hyperintensities can be caused by a variety of factors including ischemia, micro-hemorrhages, gliosis, damage to small blood vessel walls, breaches of the barrier between the cerebrospinal fluid and the brain, or loss and deformation of the myelin sheath. [8]

Cognitive effects

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. [9] Severe WMH is consistently shown 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. [10] [11] 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. [12]

It is also thought that WMH have a negative impact on cognition in people with Alzheimer's disease. In people with Alzheimer's, higher WMH are associated with higher amyloid beta deposits, possibly associated with small vessel disease and reduced amyloid beta clearance. [11]

See also

Related Research Articles

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Acute disseminated encephalomyelitis (ADEM), or acute demyelinating encephalomyelitis, is a rare autoimmune disease marked by a sudden, widespread attack of inflammation in the brain and spinal cord. As well as causing the brain and spinal cord to become inflamed, ADEM also attacks the nerves of the central nervous system and damages their myelin insulation, which, as a result, destroys the white matter. The cause is often a trigger such as from viral infection or vaccinations.

<span class="mw-page-title-main">Central pontine myelinolysis</span> Medical condition

Central pontine myelinolysis is a neurological condition involving severe damage to the myelin sheath of nerve cells in the pons. It is predominately iatrogenic (treatment-induced), and is characterized by acute paralysis, dysphagia, dysarthria, and other neurological symptoms.

<span class="mw-page-title-main">White matter</span> Areas of myelinated axons in the brain

White matter refers to areas of the central nervous system (CNS) that are mainly made up of myelinated axons, also called tracts. Long thought to be passive tissue, white matter affects learning and brain functions, modulating the distribution of action potentials, acting as a relay and coordinating communication between different brain regions.

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<span class="mw-page-title-main">Binswanger's disease</span> Medical condition

Binswanger's disease, also known as subcortical leukoencephalopathy and subcortical arteriosclerotic encephalopathy, is a form of small-vessel vascular dementia caused by damage to the white brain matter. White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. It usually presents between 54 and 66 years of age, and the first symptoms are usually mental deterioration or stroke.

<span class="mw-page-title-main">Caudate nucleus</span> Structure of the striatum in the basal ganglia of the brain

The caudate nucleus is one of the structures that make up the corpus striatum, which is a component of the basal ganglia in the human brain. While the caudate nucleus has long been associated with motor processes due to its role in Parkinson's disease, it plays important roles in various other nonmotor functions as well, including procedural learning, associative learning and inhibitory control of action, among other functions. The caudate is also one of the brain structures which compose the reward system and functions as part of the cortico–basal ganglia–thalamic loop.

<span class="mw-page-title-main">Cognitive disorder</span> Mental health condition affecting cognitive functions

Cognitive disorders (CDs), also known as neurocognitive disorders (NCDs), are a category of mental health disorders that primarily affect cognitive abilities including learning, memory, perception, and problem-solving. Neurocognitive disorders include delirium, mild neurocognitive disorders, and major neurocognitive disorder (previously known as dementia). They are defined by deficits in cognitive ability that are acquired (as opposed to developmental), typically represent decline, and may have an underlying brain pathology. The DSM-5 defines six key domains of cognitive function: executive function, learning and memory, perceptual-motor function, language, complex attention, and social cognition.

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<span class="mw-page-title-main">Perivascular space</span>

A perivascular space, also known as a Virchow–Robin space, is a fluid-filled space surrounding certain blood vessels in several organs, including the brain, potentially having an immunological function, but more broadly a dispersive role for neural and blood-derived messengers. The brain pia mater is reflected from the surface of the brain onto the surface of blood vessels in the subarachnoid space. In the brain, perivascular cuffs are regions of leukocyte aggregation in the perivascular spaces, usually found in patients with viral encephalitis.

<span class="mw-page-title-main">Neurological examination</span> Assessment to determine if the nervous system is impaired

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Pseudobulbar palsy is a medical condition characterized by the inability to control facial movements and caused by a variety of neurological disorders. Patients experience difficulty chewing and swallowing, have increased reflexes and spasticity in tongue and the bulbar region, and demonstrate slurred speech, sometimes also demonstrating uncontrolled emotional outbursts.

<span class="mw-page-title-main">Marchiafava–Bignami disease</span> Medical condition

Marchiafava–Bignami disease is a progressive neurological disease of alcohol use disorder, characterized by corpus callosum demyelination and necrosis and subsequent atrophy. The disease was first described in 1903 by the Italian pathologists Amico Bignami and Ettore Marchiafava in an Italian Chianti drinker. In this autopsy, Marchiafava and Bignami noticed that the middle two-thirds of the corpus callosum were necrotic. It is very difficult to diagnose and there is no specific treatment. Until 2008 only around 300 cases had been reported. If caught early enough, most patients survive.

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<span class="mw-page-title-main">Leukoaraiosis</span> Type of white matter abnormality near the lateral ventricles

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<span class="mw-page-title-main">Harding ataxia</span> Medical condition

Harding ataxia is an autosomal recessive cerebellar ataxia originally described by Harding in 1981. This form of cerebellar ataxia is similar to Friedreich ataxia including that it results in poor reflexes and balance, but differs in several ways, including the absence of diabetes mellitus, optic atrophy, cardiomyopathy, skeletal abnormalities, and the fact that tendon reflexes in the arms and knees remain intact. This form of ataxia is characterized by onset in the first 20 years, and is less severe than Friedreich ataxia. Additional cases were diagnosed in 1989, 1990, 1991, and 1998.

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neuGRID

neuGRID is a web portal aimed to (i) help neuroscientists do high-throughput imaging research, and (ii) provide clinical neurologists automated diagnostic imaging markers of neurodegenerative diseases for individual patient diagnosis. neuGRID's user-friendly environment is customised to a range of users from students to senior neuroscientists working in the fields of Alzheimer's disease, psychiatric diseases, and white matter diseases. neuGRID aims to become a widespread resource for brain imaging analyses.

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