White Matter Dz, Cerebral Infection, Toxic/Metabolic Flashcards
1
Q
Whit Matter Imaging Overview
What is the typical appearance of white matter injury?
What does tumefactive demyelination look like?
What is the key imaging finding of demyelinating disease?
What is a frequent pattern of white matter disease?
What would this pattern indicate in an older patient? How about in a younger patient?
A
- The typical MRI appearance of white matter injury is T2 prolongation of the affected white matter. Less commonly, tumefactive demyelination may be mass-like, enhance, and look very similar to a tumor.
- The key imaging finding of demyelinating disease is minimal mass effect relative to the lesion size. A frequent pattern of white matter disease consisting of scattered foci of T2 prolongation in the subcortical, deep, and periventricular white matter is seen very commonly, especially in older adults. In older patients, this pattern is most likely due to chronic microvascular ischemia. In younger patients, a similar pattern can be seen in chronic migraine headaches, as sequelae of prior infectious or inflammatory disease, and with demyelination.
2
Q
Normal structures may mimic white matter disease on T2 images
What are they?
First mimicker + J-shaped sella can be seen in what entity?
A
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Virchow-Robin spaces are tiny perivascular spaces that follow deep penetrating vessels into the subarachnoid space. Virchow-Robin spaces follow CSF signal on all sequences, including FLAIR.
- Enlarged Virchow-Robin spaces and a J-shaped sella can be seen in the mucopolysaccharidoses.
- Ependymitis granularis represents frontal horn periventricular hyperintensity on T2-weighted images due to interstitial CSF backup. despite the name (“-itis”), ependymitis granularis is not associated with inflammation.
3
Q
Multiple Sclerosis (MS)
What is it? Prevalence? In what population is it seen in most?
What are the two main clinical presentations? Which is most common?
What may represent the first sign of MS? In this case, what is the purpose of brain MRI?
What is happening histopathologically?
What are is the pathognomonic finding for MS? How do you make the dx of MS?
What are the suggestive imaging findings of MS?
What do enhancing lesions suggest?
What are “black holes”?
A
- Multiple Sclerosis - MS is idiopathic inflammatory destruction of CNS axons in the brain and spinal cord. MS is likely autoimmune in etiology and may be associated with other autoimmune diseases such as Graves disease and myasthenia gravis.
- MS is the most common chronic demyelinating disease. It often leads to severe disability.
- MS is more common in middle-aged Caucasian females from northern latitudes.
- There are two main clinical presentations of multiple sclerosis:
- Relapsing-remittng (most common): Partial or complete resolution of each acute attack.
-
Progressive: No resolution or incomplete resolution between acute attacks.
- Primary progressive: Slow onset without discrete exacerbations.
- Secondary progressive: Similar to relapsing-remittng but with less complete resolution between attacks, leading to progressive disability.
- Optic neuritis may represent the first sign of MS. The purpose of a brain MRI after optic neuritis is to look for other lesions, which may be clinically silent.
- Histopathologically, destruction of myelin is caused by lymphocytes attacking oligodendrocytes (which make CNS myelin).
- Although MRI imaging is highly sensitive, there are no pathognomonic imaging findings. The McDonald criteria describe strict imaging findings to diagnose MS. The McDonald criteria are most useful for clinically ambiguous cases.
- In order to make the diagnosis of MS, there must be lesions separated in space (different areas of the CNS) and in time (new lesions across scans).
- Suggestive imaging findings include periventricular ovoid foci of T2 prolongation that “point” towards the ventricles, called Dawson Fingers. The corpus callosum is often affected, best seen on sagittal FLAIR.
- In general, an enhancing lesion is suggestive of active demyelination, as enhancement is thought to be due to inflammatory blood brain barrier breakdown.
- Lesions that are dark on T1-weighted images are called “black holes” and are associated with more severe demyelination and axonal loss.
4
Q
Spinal MS involvement usually exhibits what pattern?
Is there such a thing as isolated spinal cord MS?
A
- MS involves the spinal cord in a substantial minority of patients and the spine is routinely evaluated in patients with MS. Spinal MS involvement is usually short-segment and unilateral. Isolated spinal cord involvement is seen in up to 20% of cases of MS.
5
Q
What does tumefactive MS describe?
How do you tell the difference between this and a brain tumor?
A
- Tumefactive MS describes the occasionally seen ring enhancement and mass-like appearance of an active MS plaque. In contrast to a brain tumor, the demyelinating lesion will not have any significant mass effect, and the ring of enhancement is usually incomplete.
6
Q
What does chronic MS lead to?
A
- Chronic MS leads to cortical atrophy, thinning of the corpus callosum, and changes in MRI spectroscopy, with decreased NAA, and an increase in choline, lipids, and lactate.
7
Q
What is Concentric (Balo) scerosis?
A
- Concentric (Balo) sclerosis is a very rare variant of MS with pathognomonic alternating concentric bands of normal and abnormal myelin. It is seen more often in younger patients.
8
Q
What is the Marburg variant of MS?
Imaging appearance?
A
- Marburg variant of MS (ie acute MS) is a fulminant manifestation of MS, leading to death within months.
- Extensive confluent areas tumefactive demyelination are seen with mass effect and defined rings and incomplete ring enhancement.
9
Q
Devic Disease (Neuromyelitis Optica)
What is it? Prognosis?
What is a highly specific blood test for this disorder?
Imaging appearance? Appearance in spinal cord involvement?
Brain lesions, if present, tend to be where?
A
- Devic disease is a demyelinating disease, distinct from MS, which involves both the optic nerves and spinal cord. Devic disease confers a worse prognosis compared to MS.
- NMO-IgG, an antibody to aquaporin 4, is highly specific for Devic disease. NMO-IgG activates the complement cascade and induces demyelination.
- Imaging shows MS-type lesions with involvement of the optic tracts and spinal cord.
- Spinal cord involvement is extensive, with high T2 signal spanning at least three vertebral segments, often many more (known as a longitudinally extensive spinal cord lesion)
- Brain lesions, if present, tend to be periventricular.
10
Q
Osmotic Demyelination
What is this caused by? What happens physiologically?
Which patients are most susceptible to this?
In what area of the brain does it typically occur? Where else could you see it?
MR appearance?
A
- Osmotic demyelination is caused by a rapid change in extracellular osmolality, typically occurring after aggressive correction of hyponatremia. The quick osmotic gradient change causes endothelial damage, blood-brain barrier breakdown, and release of extracellular toxins, which damage myelin.
- Patients with poor nutritional status, including alcoholics, chronic lung disease patients, and liver transplant recipients, are the most susceptible to osmotic demyelination.
- Osmotic demyelination is typically seen in the pons, but may occur elsewhere in the brainstem and deep gray nuclei.
- MRI features bilateral central T2 prolongation in the affected region. Signal abnormalities in the thalami and basal ganglia may also be present.
11
Q
What is Marchiafava-Bignami disease?
In what population is it seen?
A
- Marchiafava-Bignami is a fulminant demyelinating disease of the corpus callosum seen in male alcoholics.
12
Q
Wernicke Encephalopathy
What is it?
What is it caused by?
Imaging appearance?
A
- Wernicke encephalopathy is an acute syndrome of ataxia, confusion, and oculomotor dysfunction, which may be caused either by alcoholism or generalized metabolic disturbances, such as bariatric surgery.
- On imaging, there is T2 prolongation and possible enhancement within the mammillary bodies and medial thalamus. The non-alcoholic form may also affect the cortex.
13
Q
What is Posterior Reversible Encephalopathy Syndrome (PRES)?
What is it most commonly caused by?
What else may it be associated with?
Contrast this to infarction.
Imaging characteristics
A
- Posterior reversible encephalopathy syndrome (PRES) is a disorder of vasogenic edema with a posterior circulation predominance triggered by failed autoregulation and resultant hyperperfusion, most commonly caused by acute hypertension. In addition to hypertension, PRES is also associated with eclampsia, sepsis, autoimmune disorders, multidrug chemotherapy, and solid or stem cell transplantation.
- In contrast to infarction, the edema is vasogenic in etiology, not cytotoxic. Diffusion may be normal, increased, or restricted.
- Imaging shows symmetric regions of subcortical white matter abnormality hypoattenuation on CT and T2 prolongation on MRI, especially in the posterior circulation (occipital and parietal lobes and posterior fossa). Mild mass effect and enhancement can be seen.
14
Q
Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL)
What is this? What is it due to?
The clinical hallmark of CADASIL?
Where are the findings nearly always located? What is a possible association? What does CADASIL lead to?
Imaging appearance? What is a highly sensitive and specific finding for CADASIL?
Contrast to PRES.
A
- Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited disease characterized by recurrent stroke, migraine, subcortical dementia, and pseudobulbar palsy, due to small vessel arteriopathy.
- The clinical hallmark of CADASIL is recurrent episodes of stroke or transient ischemic attacks, which are nearly always found to be subcortical in the white matter or basal ganglia on imaging. There is often associated migraine. It may eventually lead to dementia.
- MRI shows symmetric foci of T2 prolongation in the subcortical white matter, which may become confluent as the disease progresses. Anterior temporal lobe or paramedian frontal lobe foci of T2 prolongation are highly sensitive and specific for CADASIL, especially with the clinical history of migraines. Although the symmetric subcortical pattern is similar to PRES, the distribution in CADASIL is anterior circulation.
15
Q
CNS Vasculitis
What is this?
Included etiologies?
MR appearance? The appearance may be similar to what entity? What is one way to tell the difference?
Vascular imaging appearance?
A
- CNS vasculitis is a group of vascular inflammatory disorders that primarily affects the small vessels, in particular the leptomeningeal and small parenchymal vessels.
- Etiologies include lupus, polyarteritis nodosa, giant cell arteritis, and Sjögren syndrome.
- MRI shows numerous small focal areas of T2 prolongation in subcortical and deep white matter. Although the appearance may be similar to MS, foci of hemorrhage (best seen on GRE or SWI) may be present in vasculitis, which would not be seen in multiple sclerosis.
- Vascular imaging (CT angiography and catheter angiography are more sensitive than MR angiography) shows a beaded, irregular appearance to the cerebral vessels.
16
Q
Microangiopathy
What does this describe?
In what percent of elderly patients have this?
Does this entitiy involve the corpus callosum? If it normally doesn’t what should be considered?
What is Binswanger disease?
A
- Microangiopathy describes age-related chronic axonal loss, gliosis, and ischemic changes seen in up to 80% of elderly individuals. Microangiopathy never involves the corpus callosum: If involvement of the corpus callosum is present, an alternative diagnosis should be considered, such as multiple sclerosis or neoplasm.
- Binswanger disease represents the combination of dementia and severe microangiopathy (basically a non-genetic form of CADASIL).
17
Q
What is Binswanger disease?
A
- Binswanger disease (subcortical arteriosclerotic encephalopathy) represents the combination of dementia and severe microangiopathy (basically a non-genetic form of CADASIL).
18
Q
Progressive Multifocal Leukoencephalopathy
What is this entity? Caused by what? What don’t you see in this disorder?
PML most commonly affects which patients? Who else can get it?
What is the drug associated with this disorder and what is it treating? How do you tell between PML and this disease?
In an AIDS patient, what is the primary DDx for white matter lesions?
Compare and contrast this DDx.
A
- Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of immunocompromised patients caused by reactivation of JC virus. There is progressive demyelination with lack of inflammatory response.
- PML occurs most commonly in AIDS patients (PML is an AIDS-defining illness), but can also be seen in patients with malignancy, status post organ transplant, or with autoimmune disorders.
- Approximately 1 in 1,000 patients with MS treated with natalizumab (Tysabri) may have superimposed PML and it may be difficult to distinguish between MS and PML. Diagnosis is made by PCR for JC virus DNA in CSF.
- MR imaging of PML shows asymmetric multifocal white matter lesions that may become confluent. There is rarely mass effect or enhancement. The arcuate (subcortical U) fibers are typically involved. Arcuate fibers are myelinated tracts at the gray-white junction that connects cortex to cortex.
- In an AIDS patient, the primary differential for white matter lesions is PML and HIV encephalitis. In contrast to PML, HIV encephalitis is usually bilateral and symmetric, spares the subcortical white matter, and is associated with cerebral atrophy:
- Diffuse bilateral involvement, sparing of subcortical white matter, and cerebral atrophy = HIV encephalitis.
- Asymmetric involvement, the involvement of subcortical white matter, and lack of atrophy = PML.
19
Q
What is subacute sclerosing panencephalitis?
What is it caused by?
Imaging appearance? What finding is found in distinction to other white matter entities?
A
- Subacute sclerosing panencephalitis - SSPE is a demyelinating disease caused by reactivation of measles virus, usually after a long latent period.
- Imaging shows periventricular white matter lesions, but in distinction to the other white matter entities, SSPE lesions tend to have surrounding edema and mass effect.
20
Q
Acute disseminated encephalomyelitis (ADEM)
What is this? What is it associated with?
Prognosis?
Imaging appearance?
Other areas of involvement?
What is the rapidly fulminant form of ADEM called?
A
- Acute disseminated encephalomyelitis (ADEM) is a monophasic demyelinating disorder seen primarily in children that typically occurs after a viral infection or vaccination.
- The majority of patients will make a full recovery, but a minority will have permanent neurologic sequelae.
- Imaging findings can be identical to MS, and occasionally cases of presumed ADEM will be reclassified as MS due to polyphasic clinical course. Similar to MS, ADEM may involve the brain, brainstem, or spinal cord.
- Optic neuritis and spinal cord involvement can be seen in ADEM, as with MS.
- The Hurst variant (acute hemorrhagic leukoencephalitis) is a rapidly fulminant form of ADEM that leads to death within days. Imaging of the Hurst variant shows multifocal T2 prolongation and associated white matter hemorrhage, which may appear as confluent hematomas.
21
Q
What is Hurst Disease?
Imaging appearance?
A
- The Hurst variant (acute hemorrhagic leukoencephalitis) is a rapidly fulminant form of ADEM that leads to death within days. Imaging of the Hurst variant shows multifocal T2 prolongation and associated white matter hemorrhage, which may appear as confluent hematomas.
22
Q
Radiation Injury
What does this cause?
Describe the acute, early delayed, and late delayed phases.
Include each of their imaging appearance.
What are other complications of brain radiation?
A
- Radiation injury causes small vessel arteritis and secondary ischemia. The acute phase occurs during radiation therapy, thought to reflect edema due to endothelial injury, and is of little clinical significance.
- The early delayed phase occurs between several weeks and up to six months after treatment, and is thought to be due to demyelination. MRI shows diffuse white matter T2 prolongation.
- The late delayed phase occurs months to years after radiation. It can present as white matter injury or a focal radiation necrosis.
- Mass effect, edema, and enhancement are common, and radiation necrosis should be considered in the differential of a ring-enhancing mass in a patient with history of prior radiation.
- Other complications of brain radiation include the development of meningioma, capillary telangiectasias, cavernous malformations, and/or moyamoya.
23
Q
What can chemotherapy do to white matter?
This happens especially in the setting of what?
A
- Chemotherapy may cause focal, multifocal, or diffuse white matter disease, especially in combination with radiation treatment.
24
Q
Pyogenic Abscess
What are the ways of getting a cerebral pyogenic abscess?
What are the stages of evolution of an abscess?
What is the imaging appearance of early stage of infection?
What is the classical imaging appearance of an abscess? The rim is ________ on T2WI.
Contrast the rim of an abscess to the rim of a glioma or metastasis.
When periventricular in location, what does an abscess classically show?
Rupture of a periventricular abscess may lead to what? Prognosis?
DWI appearance?
A
- A cerebral pyogenic abscess may be due to hematogenous dissemination, direct spread from paranasal sinusitis or mastoiditis, or a complication of bacterial meningitis.
- An abscess evolves over four stages (early cerebritis -> late cerebritis -> early abscess -> late abscess) and takes about two weeks to fully develop. In the early stage of infection, there is nonspecific T2 prolongation in the affected region, with heterogeneous enhancement
- After the abscess becomes discrete, the classic imaging appearance is a ring-enhancing mass. The rim is hypointense on T2-weighted images. Unlike the rim of a glioma or metastasis, an abscess rim is thin and smooth.
- When periventricular in location, an abscess classically tends to feature a thinner capsule oriented towards the ventricles. Disruption of the ventricular margin may herald impending rupture. Rupture may result in ventriculitis, with very high mortality.
- A pyogenic brain abscess almost always demonstrates restricted diffusion, appearing very bright on DWI due to restricted diffusion superimposed on inherent hyperintensity on T2-weighted images.
25
What is a cerebral tuberculoma?
What's one way to tell between a tuberculoma with a pyogenic abscess?
How would a tuberculoma mimic a pyogenic abscess?
What is an imaging characteristic that is shared with pyogenic abscesses?
* A tuberculoma is **a localized tuberculosis granuloma**. _It is not always possible to differentiate a tuberculoma from a pyogenic abscess._
* A tuberculoma **tends to have central hypointensity on** **T2-weighted** **image** (in contrast to a pyogenic abscess, which is hyperintense). **A cystic tuberculoma, however, may mimic a pyogenic abscess.**
* Similar to pyogenic abscess, **tuberculomas tend to show restricted diffusion.**
26
Lyme disease
Etiology?
Imaging appearance?
What associated findings may suggest this dx?
* Lyme disease, c**aused by the spirochete Borrelia burgdorferi**, can cause **white matter disease with a nonspecific imaging appearance of T2 prolongation predominantly in the _frontal subcortical white matter._**
* **Associated enhancement of multiple cranial nerves or meningeal enhancement** may suggest the diagnosis.
27
Neurocysticercosis
What kind of infection is this? Etiology? How does it clinically present?
What are the four described stages of neurocysticercosis?
How often does intraventricular neurocysticercosis occur? Where do they typically occur? Presentation? The cyst is most apparent on what sequence?
Treatment?
* Neurocysticercosis is the **most common parasitic CNS infection of immunocompetent patients**. It is **caused by the tapeworm Taenia** **solium** **and clinically presents with seizures.**
* Four stages of neurocysticercosis have been described:
* **Viable/vesicular**: Imaging shows several CSF-intensity cysts, without enhancement. many of these cystic lesions may demonstrate an eccentric “dot” representing the scolex.
* **Colloidal**: The colloidal stage has the least specific imaging findings, presenting as ring-enhancing lesions. In contrast to a pyogenic abscess, the lesions feature increased diffusivity.
* **Nodular/granular**: Edema decreases as the cyst involutes and the cyst wall thickens.
* **Calcified**: Imaging shows small parenchymal calcifications (on CT) and small foci of susceptibility (GRE).
* Intraventricular neurocysticercosis **can occur in up to 20% of cases, typically in the aqueduct of Sylvius or the fourth ventricle**. **Hydrocephalus may be the initial presentation**, with **the obstructing cyst most apparent on FLAIR images** _because the protein-rich intracystic fluid will not be nulled on FLAIR._
* The racemose form of neurocysticercosis is an older term describing a variant without a visible scolex, now thought to represent degeneration of the scolex.
* Treatment is with **antiparasitic medications including albendazole, supplemented with steroids for edema and antiseizure medications as needed.**
28
Toxoplasmosis
What is this? Etiology? Who is susceptible to it and when?
What is the 2 most common CNS infection in AIDS patients?
Typical appearance of toxo?
What is the asymmetric target sign?
What is the primary DDx consideration of a basal ganglia mass in an immunocompromised patient? How do you tell the difference between toxo and this entity?
* Toxoplasmosis is **the most common mass lesion in AIDS patients and is caused by the parasite *Toxoplasma*** ***gondii***. AIDS patients become susceptible to the parasite with a CD4 count less than 100 cells/microL. Toxoplasmosis is the **second most common CNS infection in AIDS patients, with HIV encephalitis being the most common****.**
* The **typical appearance of toxoplasmosis is single or multiple ring-enhancing lesions in the basal ganglia.**
* The **asymmetric target sign** is not frequently seen but is relatively specific and describes an _eccentric nodule of enhancement along the enhancing wall of the toxoplasmosis lesion__._
* The primary differential consideration of a basal ganglia mass in an immunocompromised patient is **CNS lymphoma**. In contrast to CNS lymphoma, **toxoplasmosis does not demonstrate reduced diffusivity and does not demonstrate increased relative cerebral blood volume on perfusion imaging**. Additional studies typically demonstrate _toxoplasmosis to be hypometabolic on FDG-PET, and not avid on thallium scintigraphy._
29
Herpes Encephalitis
What is this?
Clinical presentation?
When would herpes be the first consideration?
What should be obtained before MRI? Should one delay the treatment?
What does herpes encephalitis cause and in what areas?
CT appearance? MR appearance? Enhancement?
What else should be considered in an immunocompromised patient with above imaging appearance?
DDx of medial temporal lobe lesions? One way to clue you in herpes encephalitis?
Treatment?
* Herpes encephalitis is a **devastating (if untreated), necrotizing encephalitis caused by reactivation of latent HSV-1 within the trigeminal ganglion**. Clinical symptoms are nonspecific, with _fever and headache often being prominent complaints. Mental status may be altered._
* *Herpes should be the first consideration in **any patient with fever, mesial temporal lobe signal abnormality, and acute altered mental status.***
* Although **lumbar puncture** should be obtained before MRI and treatment should never be delayed for MRI, it is important to note that herpes encephalitis may be present when not clinically suspected and **PCR of HSV in cerebrospinal fluid is not 100% sensitive.**
* Herpes encephalitis causes **edema, hemorrhage, and necrosis, typically in the medial temporal lobes and the inferior frontal lobes.**
* CT is **often normal but can show ill-defined hypoattenuation in the affected regions.**
* MRI is much more sensitive and typically **shows bilateral (but usually asymmetric) T2 prolongation in the medial temporal lobe, insular cortex, cingulate gyrus, and inferior frontal lobe**. Once _the infection becomes hemorrhagic, MRI will show foci of T1 shortening and gradient susceptibility_. The affected areas typically **demonstrate reduced diffusion**.
* **Enhancement may develop later in the infection, and is typically gyral in morphology.**
* In an immunocompromised patient, **HSV-6 infection should be considered** with the above findings, _although enhancement and diffusion abnormalities may be absent._
* The differential diagnosis of medial temporal lobe lesions includes **MCA infarction, infiltrating glioma, limbic encephalitis, and seizure-related changes**. _Fever is typically absent in infarction and glioma._
* Treatment is **urgent antiviral therapy.**
30
HIV Encephalopathy
What is it? What is it caused by?
Imaging manifestation?
Contrast this entity with PML
* HIV encephalopathy is **the most common CNS infection in AIDS patients. It is a progressive neurodegenerative disease caused by direct infection of CNS lymphocytes and microglial cells (CNS macrophages) by the HIV virus**.
* On imaging, HIV encephalitis manifests as **diffuse cerebral atrophy and symmetric T2 prolongation in the periventricular and deep white matter.**
* In contrast to progressive multifocal leukoencephalopathy (PML), **HIV encephalitis _spares the subcortical U-fibers and tends to be symmetric._**
31
CMV Encephalitis
What patient population is affected by this and when?
What is the most common CNS manifestation of CMV infection?
Imaging appearance?
What about in neonates?
* Cytomegalovirus - CMV encephalitis **only affects the immunosuppressed, typically when the Cd4 cell count is less than 50 cells/microL.**
* The most common CNS manifestation of CMV infection is **ventriculitis or meningoencephalitis.**
* The characteristic imaging features of CMV ventriculitis include **subependymal FLAIR hyperintensity and enhancement throughout the ventricular system.**
* In _neonates_, CMV is **one of the most common TORCH infections and causes atrophy, encephalomalacia, ventricular enlargement, and periventricular calcification.**
32
Creutzfeldt-Jakob Disease (CJD)
What is this?
MR appearance?
What is the *pulvinar* sign?
What is the *hockey stick* sign?
* Creutzfeldt-Jakob disease (CJD) is a **rare neurodegenerative disease caused by a** **prion****.**
* The typical MRI appearance of CJD is **cortical ribboning, which describes ribbonlike FLAIR hyperintensity and restricted diffusion of the cerebral cortex.** _The basal ganglia and thalami are also involved_. _There is often sparing of the motor cortex__._
* The *pulvinar* sign describes **bright DWI and FLAIR signal within the pulvinar nucleus of the thalamus**.
* The *hockey stick* sign describes bright **DWI and FLAIR signal within the dorsomedial thalamus.**
33
How can liver disease manifest in the CNS?
* The classic brain MRI finding in liver disease is **hyperintense** **signal on T1-weighted images in the globus pallidus and substantia nigra**, thought to be due to manganese deposition.
34
How can hypoglycemia manifest in the CNS?
What else has a similar distribution?
* Severe hypoglycemia can show **bilateral T2 prolongation in the gray matter, including the cerebral cortex, hippocampi, and basal ganglia.**
* Hypoxemic-ischemic encephalopathy has a similar distribution.
35
Hypoxic-Ischemic Encephalopathy
What is this caused by and what does it lead to? What portends a worse prognosis?
Severe HIE affects what parts of brain? What is this distribution similar to?
MR and CT appearance?
What is the *white cerebellum* sign?
* Hypoxic-ischemic encephalopathy (HIE) in adults is **caused by circulatory or respiratory failure, leading to global hypoxia/anoxia.**
* Severe HIE **typically affects the gray matter, including the cerebral cortex, hippocampi, and basal ganglia**. This distribution is _similar to that of severe hypoglycemia_. Involvement of the _basal ganglia portends a worse prognosis._
* MR imaging shows **FLAIR and/or DWI hyperintensity of the affected regions.**
* On CT, there is **loss of gray-white differentiation, diffuse cerebral hypoattenuation, and sulcal effacement.** The *white cerebellum* sign describes the _typical sparing of the cerebellum, which appears relatively hyperattenuating compared to the affected supratentorial brain._
36
How can methanol poisoning manifest in the CNS?
What can be the initial presentation?
* Methanol poisoning **can present with optic neuritis** as the first symptom.
* **Hemorrhagic necrosis of the putamen and white matter edema** may follow.
37
How can CO poisoning manifest in the CNS?
* Carbon monoxide poisoning typically causes **symmetric T2 prolongation and restricted diffusion of the globus pallidus.**
38
CO vs Methanol poisoning
C**O** affest the gl**O**bus pallidus (medial basal ganglia).
Methanol affects the putamen (lateral basal ganglia).
