RITE imaging

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Last updated 10:10 AM on 2/4/26
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92 Terms

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MSA

  • hot cross bun sign

  • hyperintensities of cerebellar peduncles

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eye of the tiger sign

  • globus pallidus T2 hypointensity with central hyperintensity

  • PKAN

  • iron deposition disorder

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PSP imaging findings

  • micky mouse & hummingbird signs from midbrain atrophy

  • cerebellar atrophy, particularly in vermis

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panda sign

  • symmetric hyperintensities of putamen > caudate, thalamus, brainstem; red nuclei are eyes

  • wilson’s disease

  • from copper deposition

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bilateral MCP sign

  • fragile X-associated tremor/ataxia syndrome (FXTAS)

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developmental venous anomaly

  • network of dilated veins

  • caput medusae sign

  • typically asymptomatic, rarely cause hemorrhage

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capillary telangiectasia

  • dilated capillaries

  • most common in pons

  • typically asymptomatic, rarely cause hemorrhage

  • slightly bright on T2, subtle enhancement

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cavernoma

  • dilated vascular cavity lined by vascular endothelium

  • typically supratentorial

  • popcorn appearance on MRI, core can be hyperintense, dark rim on T2

  • can cause seizures, can bleed

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cerebral AVM

  • tangle of connected arteries & veins

  • can cause bleed, seizures, headaches, ischemic stroke (steal phenomenon)

  • bag of worms appearance on MRI

  • requires angiography for diagnosis

  • resection can be curative

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fibromuscular dysplasia

  • string of beads

  • commonly affects ICAs and verts

  • more common in females

  • slight incr risk TIA/stroke and dissection but often asymptomatic

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moyamoya

  • stenosis & occlusion of distal ICA and proximal MCA with prominent collateralization over time

  • treated with antiplatelets, EC-IC bypass

  • “puff of smoke” appearance on angio due to collateralization

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CADASIL/CARASIL

  • cerebral autosomal dominant/recessive arteriopathy with subcortical infarcts and leukoencephalopathy

  • NOTCH3 mutations

  • causes progressive cognitive decline, recurrent ischemic strokes (often lacunar), migraines

    • MRI features symmetric WM hyperintensities, including in anterior temporal poles

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… are bright on CT

  • acute blood (hyperacute can be isodense, old is hypodense)

  • bone

  • choroid plexus

  • minerals

  • calcification

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… are dark on CT

  • old blood

  • CSF

  • air

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what structures are dark & bright on T1 MRI

bright: fat (lipoma), mineral deposition, cortical necrosis, melanin, proteinacous stuff

  • My Best Friend is Pretty Cool (melanin, blood - subacute, fat, protein, cholesterol/calcium)

dark: CSF, edema, bone, most pathology (incr water content)

white matter brighter than grey matter

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what structures are dark & bright on T2 MRI

bright: fat, CSF, edema, most pathology

dark: fat, bone

gray matter brighter than white matter

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how to age blood on MRI

T1 generally goes from iso > bright > dark

T2 more complicated

hyperacute: isodense on both

acute: isodense on T1, dark on T2

early subacute (1 week): bright on T1, dark on T2

late subacute (>1w, <1mo): bright on both

chronic: dark on both

FLAIR same as T2

alternative way to remember: I Be IdDy BiDy BaBy Doo Doo

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differential for FLAIR non-suppression

CSF spaces still bright

  • hyperoxygenation

  • SAH

  • meningitis

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differential for diffusion restriction

  • acute-subacute infarct (arterial or venous)

  • abscess (core)

  • tumors (rim)

  • PRES

  • CJD (cortical)

  • diffuse anoxic injury

  • lymphoma

  • ODS

  • carbon monoxide toxicity

  • acute demyelination

  • hypoglycemia (cortical)

<ul><li><p>acute-subacute infarct (arterial or venous)</p></li><li><p>abscess (core)</p></li><li><p>tumors (rim)</p></li><li><p>PRES</p></li><li><p>CJD (cortical)</p></li><li><p>diffuse anoxic injury</p></li><li><p>lymphoma</p></li><li><p>ODS</p></li><li><p>carbon monoxide toxicity</p></li><li><p>acute demyelination</p></li><li><p>hypoglycemia (cortical)</p></li></ul><p></p>
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what structures enhance on T1-post contrast MRI

  • blood vessels

  • venous sinuses

  • choroid plexus

  • pineal gland

  • sinuses (the nose knows)

  • tumors, abscess, infections, subacute stroke, active demyelination, inflammation

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… are dark on GRE

  • blood

  • iron, calcium, manganese

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possibilities for bright lesion on DWI

dark on ADC > restricted diffusion

iso on ADC > T2 shine through

bright on ADC > facilitated diffusion

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imaging findings in intracranial hypotension

  • sagging brainstem

  • downward displacement of cerebellar tonsils

  • slit ventricles

  • diffuse pachymeningeal (dural) enhancement

  • subdurals, can be bilateral

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imaging findings in IIH

  • partially empty sella

  • optic nerve tortuosity, dilated optic nerve sheaths, visible protrusion of optic head into eyeballs

  • stenosis of transverse sinus

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differential for pituitary mass

  • pituitary adenoma: homogeneously enhancing

  • craniopharyngiomas: cystic/calcified

  • rathke cleft cyst: non-enhancing

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craniopharyngioma

  • suprasellar

  • cystic/calcified

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pituitary apoplexy

  • ischemia/hemorrhage of pituitary gland

  • higher risk if existing macroadenoma

  • often postpartum

  • p/w HA, CN deficits, panhypopituitarism

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colloid cyst

benign but can cause acute hydrocephalus

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EOM enlargement

can be caused by thyroid eye disease, ocular myositis, orbital pseudotumor

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ODS

  • central pons

  • hypodense on CT

  • can be diffusion restricting

  • hyperintense on T2/FLAIR

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pulvinar sign - bilateral FLAIR hyperintensities of pulvinar thalamic nuclei

can be seen in CJD, Fabry, status, ADEM

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hockey stick sign

bilateral hyperintensity of pulvinar nuclei and medial thalamus

can be seen in CJD or Wernicke’s

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Dandy Walker malformation

  • agenesis/hypoplasia of cerebellar vermis resulting in cystic enlargement of 4th ventricle

  • can exist with or without hydrocephalus

  • can be hypotonic & ataxic

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methanol toxicity

  • bilateral putaminal hemorrhages/necrosis

  • can also see damage to optic nerves

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lissencephaly

  • pachy or agyria (smooth brain)

  • enlarged ventricles

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porencephaly

“pore” lined with white matter, not communicating with ventricles

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schizencephaly

  • fluid-filled cleft that communicates with lateral ventricles

  • lined with gray matter

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arachnoid cyst

  • often congenital

  • extra-axial

  • same as CSF signal

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aqueductal stenosis

  • can be congenital or acquired

  • narrowing/obstruction of cerebral aqueduct between 3rd & 4th ventricles

  • marked enlargement of 3rd and lateral

  • effacement of cortical sulci

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gray matter heterotopia

  • disorder of neuronal migration

  • nodules/bands of gray matter in abnormal locations, can be periventricular, subcortical or lobar

  • isodense on T1/T2/FLAIR

  • cause seizures

  • includes subependymal nodules (seen in tuberous sclerosis)

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temporal lobe encephalocele

outpouching through skull defect

associated with epilepsy

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septo-optic dysplasia

  • hypoplastic or absent septum pellucidum

  • hypoplastic corpus callosum

  • hypoplastic optic nerves

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molar tooth sign

associated with Joubert syndrome (cerebellar vermis hypoplasia)

superior cerebellar peduncles horizontal & thick

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Alexander disease, type of genetic demyelinating leukodystrophy with bifrontal predominance

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imaging findings in CJD

  • pulvinar & hockey stick signs (bilateral FLAIR hyperintensities in pulvinar & medial thalamus)

  • cortical diffusion restriction

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imaging findings in Alzheimer’s

atrophy, particularly of temporal lobes

PET hypometabolism in parietal & temporal lobes

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Huntington’s disease

  • atrophy of caudate head causes enlargement of frontal horns

Neuroacanthocytosis

  • also cause BG degeneration

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Fahr disease

disorder of calcium deposition and cell loss

primarily in BG and cortex

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DESH (disproportionally enlarged subarachnoid space hydrocephalus)

associated with NPH

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abscess with double rim sign

  • outer rim hypointense

  • inner rim hyperintense

  • can diffusion restrict in core

  • can have surrounding vasogenic edema

differentiate from glioma which also has hypodense rim but more heterogenous enhancement and peripheral diffusion restriction

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glioblastoma

  • multicystic

  • heterogeneously enhancing

  • vasogenic edema

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ventriculitis

enhancement lining ventricles

can occur with EVD, bacterial meningitis, ruptured brain abscess, skull infection

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neurocysticercosis

  • hyperdense/calcified on CTH

  • hypointense core on MRI with edema, can rim-enhance

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toxoplasmosis

  • tend to be in BG but can be anywhere

  • rim or nodular enhancement

  • often with surrounding edema

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HSV encephalitis

  • affects temporal lobes & limbic structures

  • swollen, hyperintense, can be diffusion restricting or hemorrhagic

  • can see leptomeningeal enhancement

differential includes autoimmune (NMDAr) and paraneoplastic (LGI1) encephalitis which also favor temporal lobes

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congenital CMV

  • ventriculomegaly/hydrocephalus

  • periventricular calcifications

  • microcephaly

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rhombencephalitis

infection/inflammation of brainstem & cerebellum

most common infectious cause is listeria, also enterovirus 71 and HSV. can also be autoimmune (Behcet’s, SLE) or paraneoplastic

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bickerstaff brainstem encephalitis

  • AMS, ataxia, ophthalmoplegia

  • post-infectious

  • +GQ1b antibodies

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progressive multifocal leukencephalopathy (PML)

hypointense on T1, hyperintense on T2, can see peripheral patchy diffusion restriction, typically non-enhancing

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ADEM

  • large multifocal demyelinating lesions, can have tumefactive appearance

  • often involving cortex, subcortical grey matter, thalamus, brainstem

  • presents acutely in child with viral illness, typically monophasic

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bilateral thalamic infarct

artery of percheron stroke or straight sinus thrombosis

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core vs penumbra on perfusion imaging

rCBG < 30% = core = infarcted tissue

Tmax >6s = penumbra = tissue at risk

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subarachnoid hemorrhage

best seen on CTH

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anoxic brain injury post-arrest

  • loss of gray-white differentiation

  • swollen sulci, small ventricles

  • pseudo-SAH from proteinacous leakage into subarach space

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air embolism

  • punctate or curvilinear hypodensities

  • air darker than CSF

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vein of Galen malformation

presents in babies with high output heart failure

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hypothalamic hamartoma

benign malformation/tumor

p/w refractory gelastic seizures, precocious puberty

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spinal imaging

T1: CSF dark, pathology often dark

T2: CSF bright, pathology often bright

STIR (short tau inversion recovery): T2 with suppression of fat

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diffuse idiopathic skeletal hyperostosis

  • calcification and ossification of anterior longitudinal ligament

  • can accelerate spondylosis

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klippel fiel syndrome

  • incomplete segmentation of C-spine

  • congenital

  • limited mobility of neck and upper spine

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epidural lipomatosis

  • accumulation of excess fat in spinal epidural space resulting in spinal cord compression

  • associated with long-term steroid use

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chordoma

  • slow growing

  • thought to arise from cellular remnants of notocord

  • can cause cord compression

  • can grow along cord or in brain adjacent to sphenoid bone

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rheumatoid pannus

inflammatory synovial tissue commonly growing in cervical spine around C1-2, can cause neck pain/instability and cord compression

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spinal epidural abscess

  • non-enhancing core w rim of enhancement

  • can be diffusion restricting in core

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spinal epidural hematoma

  • heterogeneous appearance but mostly hyperintense on T1/2

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multiple myeloma vertebral lesions

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spinal meningioma

  • well circumscribed

  • dural attachment (dural tail sign)

  • homogeneous enhancement

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spinal schwannoma

  • arise from spinal nerve roots

  • homogeneous enhancement

  • differentiated from spinal meningioma by lack of dural tail

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spinal arachnoid cyst

  • CSF-filled cyst within arachnoid space

  • can be congenital or from trauma (most commonly T spine)

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arachnoid web

  • scalpel sign

  • thickened band of arachnoid over dorsal cord

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spinal ependymoma

  • central cord (arise from central canal)

  • enhancing

  • often cystic looking

  • often associated syrinx

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spinal astrocytoma

  • intramedullary

  • often eccentric (arise from cord parenchyma)

  • poorly defined margins

  • most enhance

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spinal hemangioblastoma

  • intramedullary

  • nodular appearance

  • may see vascular flow voids

  • vividly enhancing

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features of different causes of LETM

NMO - central often involving gray & white matter, bright & spotty, patchy enhancement, can see prominent swelling

MOG - central, sometimes restricted to gray (H sign), often non-enhancing, can involve conus

sarcoid - central, “trident” sign

paraneoplastic - tract-specific (often dorsal/lateral columns)

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H sign of grey matter restricted myelitis

associated with MOGAD

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trident sign

associated with neurosarcoid

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spinal dural AVF

  • present with gradual but progressive pain, leg weakness/numbness, bladder/bowel changes

  • flow voids on T2

  • can see intramedullary hyperintensity due to edema, often involving conus

  • confirmed with DSA

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owl eye sign

  • spinal cord infarct

  • anterior horn cells

  • can also be seen in ALS, polio

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subacute combined degeneration

  • demyelination of dorsal columns

  • B12 deficiency, syphilis, copper deficiency, methotrexate toxicity

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syringomyelia

  • collection of CSF in central cord around central canal

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chiari malformation

I: downward displacement of cerebellar tonsils, often associated with syringomyelia

II: downward displacement of medulla, 4th ventricle and cerebellum through foramen magnum, often associated with myelomeningocele

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tethered cord

  • progressive stretching from lengthening of spinal column

  • conus terminates at low position

  • can see other imaging findings of spinal dysraphism

  • can be associated with terminal lipoma (lipmeningocele)