Tectal Glioma

Low Grade Neoplasm

High Grade Neoplasm

Progressive Multifocal Leukoencephalopathy (PML)

Abscess, Encephalitis

Acute onset of clinical symptoms, often hemiparesis (corticospinal tracts), cranial neuropathy (nuclei of III, IV; a nucleus of V), &/or ataxia (red nucleus)

Presence of reduced diffusion: High SI on DWI, low SI on ADC map

Often accompanied by lesion of basilar artery, so consider MRA or CTA

Appropriate clinical history; FLAIR, DWI particularly helpful to assess for edema (cytotoxic &/or vasogenic); GRE to assess for hemorrhage

Brainstem DAI typically dorsolateral, usually seen with hemispheric & callosal involvement; check for additional sites of injury

T2 bright lesions typically without reduced diffusion or GRE abnormality, often enhance post-gadolinium

Assess rest of brain for additional white matter (WM) lesions

Consider MR of optic nerves, spinal cord

Typically enhance, associated with vasogenic edema; additional lesions often present in brain, meninges, or bone

May be hemorrhagic

Often bright on T1 & T2WI; “mulberry-like” morphology; SI on GRE

Associated developmental venous anomaly (DVA) may be present

Usually seen at base of cerebral peduncles

Follow CSF on all MR sequences

Acute: Variable ↓ diffusion and ↑ SI on T2

Chronic: Volume loss; variable T2 SI

Cause of “congenital” hydrocephalus: May be due to a web or adhesion; often post-inflammatory or post-intraventricular hemorrhage

Assess tectum carefully on axial T2 & FLAIR to exclude subtle nonenhancing tectal glioma

Multiple histologies can affect midbrain & other parts of brainstem

Imaging varies with tumor histology

“Tectal gliomas”: Typically confined to tectum, nonenhancing, present with chronic hydrocephalus

Thiamine deficiency; most commonly seen in alcoholics; also malnutrition, malabsorption, HIV/AIDS

Classic clinical triad: Ataxia, encephalopathy, oculomotor dysfunction

Symmetrical ↑ T2 SI variably involves periaqueductal gray matter, dorsomedial thalami, mamillary bodies

↓ Diffusion, post-gad enhancement variably present acutely

Typically affects deep gray nuclei of cerebrum &/or gray matter structures of brainstem in symmetrical fashion

↓ Diffusion, ↑ T2 SI typically present with acute flare of disease

↑ Lactate peak may be seen with MR spectroscopy

Progressive multifocal leukoencephalopathy (PML)

Pyogenic abscess: Central ↓ diffusion; also ring enhancement, vasogenic edema

Nonspecific ↑ SI on T2WI; often ↓ diffusion

Downward displacement of midbrain, loss of cisterns; “folding” if severe

Atypical Parkinsonian syndrome: Supranuclear ophthalmoplegia, pseudobulbar palsy, dysarthria, postural instability, frontotemporal dementia

Neuropathological hallmark: Midbrain atrophy; tau + aggregates

MR: Midbrain atrophy; variable midbrain T2 hyperintensity

Imaging findings typically subtle; possible ↓ volume of substantia nigra, ↓ hypointensity of lateral margin of substantia nigra

Degenerative disease of upper and lower motor neurons in the motor cortex, brainstem, and spinal cord

Imaging hallmark: ↑ T2 SI of corticospinal tracts; no mass effect, enhancement