PRES (Posterior Reversible Encephalopathy Syndrome):

Seen with hypertension or chemotherapy. Features include asymmetric cortical and subcortical white matter edema (usually in parietal and occipital regions). PRES does NOT restrict on diffusion (helps tell you it’s not a stroke).

PRES – T2/FLAIR High Signal

Radiation-Induced Demyelination:

Seen as T2 bright areas and atrophy corresponding to the radiation portal. Can be seen with hemosiderin deposition, and mineralizing microangiopathy (calcifications involving the basal ganglia and subcortical white matter)

Osmotic Demyelination Syndrome (CPM):

Seen with rapid correction of sodium (usually in a drunk). Usually T2 bright in the central pons (spares the periphery). Can also have an extra-pontine presentation involving the basal ganglia, external capsule, amygdala, and cerebellum.  

CPM-T2 Bright Central Pons

Wernickc Encephalopathy:

Caused by thiamine deficiency. Just think contrast enhancement of the mammillary bodies (seen more in alcoholics). Additionally, think increased T2/ FLAIR signal in the bilateral medial thalamus and periaqueductal gray.

Wernicke High Signal in Medial Thalamus and Periaqueductal Gray

CNS Findings Secondary to Drugs or Toxins:

Carbon Monoxide: CT Hypodensity I T2 Bright Globus Pallidus (carbon monoxide causes “globus” warming).

Alcohol: Brain atrophy , especially the cerebellar vermis.

Marchiafava-Bignami: Seen in drunks. Swelling and T2 bright signal affecting the corpus callosum (typically beginning in the body, then genu, and lastly splenium). Will involve the central fibers and spare the dorsal and ventrals fibers (called a “sandwich sign” on sagittal imaging).

Marchiafava-Bignami -High T2/FLAIR in the Corpus Callosum

• Methanol: Optic nerve atrophy, hemorrhagic putaminal and subcortical white matter necrosis

Post-Radiation:

There is a latent period, so imaging findings don’t typically show up for about two months post therapy.

• Whole Brain Radiation changes are typically T2 bright in the periventricular white matter, sparing the subcortical regions early on. Peripheral extension to the subcortical regions occurs later.

• Localized Radiation: Usually we are talking about severe focal edema with mass effect and enhancement. Differentiation from residual tumor can be a sneaky sneaky thing, and MR perfusion may be useful in differentiating.

Post Chemotherapy:

You will have T2 effects acutely in the white matter, that can progress to atrophy. Enhancement or mass effect is rare unless it is very severe. Children receiving both radiation and chemotherapy can sometimes develop calcifications – “mineralizing microangiopathy.”

Disseminated necrotizing leukoencephalopathy: Severe white matter changes, which demonstrate ring enhancement , classically seen with leukemia patients undergoing radiation and chemotherapy. This is bad news and can. be fatal.

Neurodegenerative Disorders:

You can do dementia imaging with a variety of imaging modalities, including CT and MRJ for structure, and FDG PET and SPECT for function. Pearl: On FDG PET the motor strip is always preserved in dementia.  

Alzheimer Disease:

Most common cause of dementia. Most likely question is hippocampal atrophy (which is first), and out of proportion to the rest of the brain atrophy. They could ask temporal horn atrophy> 3mm , which is seen in more than 65% of cases.

Multi-infarct Dementia:

This is the second most common cause of dementia. Cortical infarcts and lacunar infarcts are seen on MRI. Most likely to be shown as a PET-FOG case, demonstrating multiple scattered areas of decreased activity

Crossed Cerebellar Diaschisis (CCD):

Depressed blood flow and metabolism affecting the cerebellar hemisphere after a contralateral supratentorial insult (infarct, tumor resection, radiation). Creates anAunt Minnie Appearance:

Crossed Cerebellar Diaschisis

Dementia with Lewy Bodies:

Thls is the third most common cause of dementia (second most common neurodegenerative), with a very similar clinical picture to the dementia seen with Parkinsons, with the major difference being that in DLB, the dementia comes fust. The hippocampi remain normal in size and you have some decreased FDG uptake in the lateral occipital cortex, with sparing of the mid posterior cingulate gyrus (Cingulate Island Sign).

Binswanger Disease:

This is a subcortical leukoencephalopathy that affects older people (55 and up), strongly associated with HTN. It’s basically a form of small vessel vascular demenlia. It classically spares the subcortical U fibers

FOG PET Brain

Alzheimer

Low posterior temporoparietal cortical activity

Identical to Parkinson Dementia

Multi Infarct

Scattered areas of decreased activity

Lyme, HIV, and Vasculitis are
mimics

Dementia with Lewy
Bodies

Low in lateral occipital cortex

Preservation of the midposterior cingulate gyrus (Cingulate Island Sign)

Picks/Frontotemporal/

Depression

Low frontal lobe

Depression is a mimic

Huntington

Low activity in caudate nucleus and putamen