Multiple Brain Hyperintensities (T2/FLAIR), Common

Gary M. Nesbit, MD

DIFFERENTIAL DIAGNOSIS

Common

Aging Brain, Normal
Normal Myelination
Reactive Astrocytosis (Gliosis) & Encephalomalacia
Atherosclerosis, Intracranial
Neurofibromatosis Type 1
- Myelin Vacuolization
Enlarged Perivascular Spaces
- Mucopolysaccharidoses
Lacunar Infarction
Chronic Hypertensive Encephalopathy
Acute Hypertensive Encephalopathy, PRES
Cerebral Infarct, Subacute
Cerebral Infarct, Chronic
Hypotensive Cerebral Infarct
Cerebral Edema, Traumatic
Cerebral Contusion
Diffuse Axonal Injury (DAI)
Multiple Sclerosis
Metastases, Parenchymal
Lymphoma, Primary CNS
Radiation and Chemotherapy
Periventricular Leukomalacia

ESSENTIAL INFORMATION

Helpful Clues for Common Diagnoses

Aging Brain, Normal
- White matter (WM) hyperintensities are normally seen
  - Rule of thumb: 1 per decade to age 50
- Increase in number & size is exponential from age 50 to 100 years
- Due to gliosis, leukoariosis, & enlarged perivascular spaces (PVS)
Normal Myelination
- T2 hyperintense myelin at birth, except posterior fossa, optic radiations, & corticospinal tracts
- Corpus callosum (CC) myelinates from 4 to 9 months, splenium to genu
- Parietal & frontal myelination from center to periphery until around 2 years of age
Reactive Astrocytosis (Gliosis) & Encephalomalacia
- Brain’s only response to insults: Infectious, stroke, trauma
- Gliosis is T2 hyperintense without mass effect, encephalomalacia often associated
- Encephalomalacia is a “hole” that follows CSF signal, often surrounded by gliosis
Atherosclerosis, Intracranial
- Results in distal emboli or hypoperfusion infarcts
- Variable infarct location, depends upon vessel involved
Neurofibromatosis Type 1
- Nonenhancing T2 hyperintensities in basal ganglia (BG) & deep cerebellum most commonly (myelin vacuolization)
- No mass effect, unlike astrocytoma, the main differential in NF1
- Develops in early childhood, peaks around age 8, & usually regresses by late teens
Enlarged Perivascular Spaces
- Commonly symmetric & peripheral in WM, but can be unilateral focal & deep
- Inferior BG, near anterior commissure common location
- Sharp margins & lentiform, follows CSF on T2/FLAIR in young patients
- Often associated with gliosis in the elderly (FLAIR hyperintense)
- Mucopolysaccharidoses
  - Dilated PVS usually with surrounding gliosis presenting in infancy
  - CC & periatrial WM most common
Lacunar Infarction
- Usually in lenticular & caudate nuclei, thalamus, internal capsules, periventricular WM
- Acute: T2 hyperintense, diffusion positive
- Chronic: Focal encephalomalacia with surrounding gliosis
Chronic Hyperintensive Encephalopathy
- Usually deep & periventricular WM confluent hyperintensities
- Often associated with T2 hypointensities from microhemorrhage on GRE images
Acute Hypertensive Encephalopathy, PRES
- Peripheral subcortical confluent hyperintensities, mild mass effect
- Bilateral occipital parietal is common, but many variations including hemorrhage
Cerebral Infarct, Subacute
- Embolic infarcts usually cortical, wedge-shaped with mass effect
- Microembolic infarcts are usually peripheral centrum semiovale or BG
- Enhancement typical
Cerebral Infarct, Chronic
- Results in focal encephalomalacia & gliosis
- Typically in a major vascular distribution
Hypotensive Cerebral Infarct
- Watershed infarcts
  - Parasaggital linear “string of pearls” in the centrum semiovale
  - Wedge-shaped regions in the border zone between vascular distributions
- Diffuse or multifocal cortical infarcts & BG
- Diffusion positive acutely
Cerebral Edema, Traumatic
- Cerebral swelling without T2 change early, may develop hyperintensities
- Contusion & DAI commonly with hemorrhage
Cerebral Contusion
- Cortical, subcortical hyperintensities with developing hemorrhage
- Regions of injury: Temporal, frontal lobe, superficial brain with direct trauma
Diffuse Axonal Injury (DAI)
- Shear stress deceleration injury: Gray-white, midbrain hemorrhage; diffusion positive early
- Typically in older children to young adults, as there is minimal subarachnoid space & brain movement
Multiple Sclerosis
- CC & peri 4th ventricular involvement characteristic
- Radiating periventricular location, “Dawson fingers”
- Acute tumefactive lesion: Large with T2 hypointense ring that enhances, usually little mass effect
Metastases, Parenchymal
- Hyperintensities may be punctate to massive, with variable surrounding edema, mass effect
- Hyperintensity, edema, & mass effect less prominent in posterior fossa, but risks higher
Lymphoma, Primary CNS
- Central region nearly T2 isointense due to high nuclear to cytoplasmic ratio
- Surrounding edema variable, usually crossing or around CC in immunocompetent
- Immunocompromised PCNSL will have multifocal ring-like “glioblastoma” look
Radiation and Chemotherapy
- Radiation leukomalacia: Confluent poorly marginated regions in the radiation field without enhancement
- Radiation necrosis: Irregular ring-enhancing lesions with variable mass effect, may grow, CBV/choline low
Periventricular Leukomalacia
- WM volume loss, gliosis, & focal cystic lesion in the periatrial WM
- Associated with prematurity

Image Gallery

Axial FLAIR MR shows minimal deep white matter hyperintensities

& minimal gyral atrophy in this healthy 76 year old patient. These hyperintensities may be seen as part of the aging process.

Axial FLAIR MR shows more extensive & confluent regions of hyperintensity including perivascular “leukoariosis”

in this 96 year old healthy individual. Note the minimal atrophy.

(Left) Axial T2WI MR shows a normal myelin pattern at 5 months of age. There is hyperintensity throughout the frontal & parietal white matter & hypointensity of normal myelination within the centrum semiovale

emanating from the internal capsules. (Right) Axial T2WI MR at 12 months of age shows normal residual hyperintense signal in the juxtacortical white matter of the frontal lobe & insula

and in the peripheral white matter of the parietal lobes

(Left) Axial FLAIR MR shows profound asymmetric periventricular white matter volume loss & hyperintensity indicative of gliosis

, along with generalized left greater than right atrophy in this microcephalic 14 year old. (Right) Axial T2WI MR shows volume loss with enlarged subarachnoid, sylvian, & ventricular CSF spaces