Miscellaneous Flashcards
Which 3 organ systems does TS affect?
Cortical and subependymal tubers
AMLs
Cardiac rhabdomyomas
List key neurologic findings in TS
Cortical/subcortical tubers
Subependymal hamartomas - may enhance but this does not help distinguish from SEGA
White matter change (i.e. radial bands)
Causes of T1 shortening (hyperintense)
Fat Proteinaceous substance Gad Blood (both intra and extracellular methemoglobin, and slowly flowing blood) Melanin Minerals (copper, iron, Mg)
Causes of T2 shortening (hypointense)
Most blood (except hyper acute and extracellular methemoglobin)
Calcification
Fibrous lesion
Highly cellular tumours (i.e. lymphoma, medulloblastoma)
Vascular flow void
Mucin (unlike in the pelvis where these lesions are T2 bright)
DDx periventricular enhancement
- Primary CNS lymphoma
- Infectious ependymitis (usu CMV) - thin linear enhancement along margins of ventricles
- Primary glial tumour
- MS
DDx gyriform enhancement
- Herpes encephalitis (medial temp lobes and cingulate gyrus) or cerebritis
- Subacute infarct - luxury reperfusion or cortical laminar necrosis, occurs 1week-months after (can also see enhancement after thrombolysis or thrombectomy)
- Seizures, migraines
- PRES
- Neoplastic
- Drugs toxicity (chemo or immunosuppressants)
DDx dural/pachymeningeal enhancement
- Intracranial hypotension (thick/ linear enhancement, sagging of tonsils)
- Post-op
- Post LP
- Meningeal neoplasm (i.e. meningioma), mets from breast and prostate ca
- Granulomatous disease (sarcoid, TB, fungal disease) - typically in basal meninges
DDx leptomeningeal enhancement
- Meningitis (viral, bacterial, fungal)
- Leptomeningeal carcinomatosis (see below list)
- CNS neoplasms - MOCLEGG (medullo, oligo, choroid plexus tumor, lymphoma, ependymoma, GBM, germinoma)
- Mets - lymphoma, breast cancer
- Viral encephalitis - CN enhancement
- Slow vascular flow (i.e. Moya moya)
Which CN does not traverse the cavernous sinus?
V3 (mandibular) - exits inferiorly from Meckels cave through foramen ovale
Which CN does not exit via the superior orbital fissure?
V2 (maxillary) - exits via foramen rotundum
Where does CN6 travel?
Enters petrous portion of temp bone and travels via Dorello’s canal and along medial venous sinusoids
Clinical and imaging findings pseudo tumour cerebri
Headache, visual changes, increased ICP
Empty sella, expansion Meckel’s cave, optic disc edema and stenosis of the sigmoid and transverse sinuses
List the segments of the ICA
Key branches of C4 (2)
Key branches of C6 (2)
Key branches of C7 (4)
Cervical
Petrous
Lacerum
Cavernous - meningohypophyseal trunk (pituitary, tent, and dura of clivus) and inferolateral trunk (CNs 3-6)
Clinoid
Supraclinoid - ophthalmic artery (significance of aneurysms above versus below this point), superior hypophyseal artery
Communicating - P-comm, ACA, MCA, ant choroidal
What does recurrent artery of Heubner supply?
Caudate head, anterior limb internal capsule
Branch off ACA
What do medial lenticulostriate arteries supply?
Medial basal ganglia (from ACA)
What do lateral lenticulostriate arteries supply?
Lateral BG, including lateral putamen, external capsule, and posterior limb internal capsule (from MCA)
What does artery of Percheron supply? where does this originate?
Dom thalamic perforator supplying ventromedial thalami bilaterally and rostral midbrain (bil thalamic infarcts)
Arises from P1
What does anterior choroidal artery supply?
Last branch of ICA; supplies hippocampus, optic chasm, posterior limb of internal capsule
Most common persistent carotid-basilar connection
Persistent Trigeminal artery
Courses adjacent to trigeminal nerve
Trident or tau sign on angiography
Can connect to basilar artery (type I) or superior cerebellar artery (type 2)
Presentation, RF and imaging findings RCVS
Thunderclap headache, usu occipital, recurrent
Middle aged women
RFs: pregnancy/eclampsia, drugs, other
Imaging: vascular spasm, convexity subarachnoid hemorrhage, lobar hemorrhage, watershed infarct, vasogenic edema
DSA: smooth tapered narrowing of larger vessels, dilated segments (beading)
CT done to rule out aneurysmal cause of bleed (bc CT can be normal in RCVS too)
Most common location of hypertensive hemorrhage
BG, thalami, cerebellum (can also see microhemorrhages in the brainstem)
Most common location of cerebral amyloid angiopathy
Lobar and cortical, involving parietal and occipital lobes
Microhemorrhages also in cortex
Imaging findings moya moya
- ICA (supraclinoid) +/- PCA stenosis
- Concentric narrowing, no enhancement (differentiates this from other causes of vasculitis)
- Extensive pial collaterals (Ivy sign)
- Watershed infarcts
- ‘Puff of smoke’ sign on angiography
Imaging findings hepatic encephalopathy
Mg deposition - T1 hyperintense signal in globus pallidus and substantia nigra
DDx T1 shortening in BG = Lonely Wilson’s Trip to Hawaii (Liver disease, Wilson’s, TPN, Hyperglycemia)
Imaging findings severe hypoglycemia
Bilateral, asymmetric T2 prolongation and diffusion restriction in gray matter (cortex, hippocampus, BG)
Ddx: HIE
HH-NKT (non-ketotic hyperglycemia hemichorea) - involves one side of BG, produces hemichoria and hemiballimus on contralateral side
Imaging findings severe HIE
Affect grey matter (cortex, hippocampus, BG)
Diffuse edema with effacement of CSF spaces
Reversal sign
White cerebellum sign
ddx: severe hypoglycemia
Earliest findings on DWI
Imaging findings methanol poisoning
Optic neuritis
Increased T2 signal/restricted diffusion in PUTAMEN (may have bright T2 signal if hemorrhage ensues)
Imaging findings CO poisoning
Increased T2 signal/restricted diffusion in GLOBUS PALLIDUS
Imaging findings Wilson’s disease
Increased T2 signal in BG and thalamus
Panda sign in midbrain
DDx: disease involving putamen or BG
- mitochondrial disease (leigh)
- toxic encephalopathies (CO, methanol, CN)
- metabolic (Wilson’s, hypoglycemia)
- HIE
- infection (CJD)
Name the segments of the facial nerve
Intracranial/cisternal segment
Meatal/Cannicular (within IAC)
Labyrinthine (IAC to geniculate ganglion)
Tympanic (geniculate ganglion to pyramidal eminence)
Mastoid (pyramidal eminence to stylomastoid foramen)
Extratemporal
Most common tumour associated with NF2
Vestibular schwanommas
Imaging findings neurosarcoidosis
- Leptomeningeal enhancement (including hypothalamus/pituitary and cranial nerves, usu basal skull)
- Pachymeningeal enhancement
- Parenchymal involvement (extending along perivascular spaces, periventricular lesions)
Scimitar shaped sacrum
Anterior sacral meningocele
Rare, present later in life
Associated with sacral agenesis
Risk of rupture - bacterial meningitis
What things cause increased signal in CSF spaces on FLAIR?
- Poor CSF suppression/artifact
- Supplemental oxygen
- Blood
- Pus
- Tumour (leptomeningeal disease)
- Slow blood flow cortical arteries (stroke)
- Meningeal collateral (moya moya)
- Ruptured dermoid
Neurosarcoid findings
“Great mimicker”
- Basal cistern leptomeningeal enhancement
- Parenchymal enhancing lesions
- Cranial nerve involvement
- Optic nerve enhancement
- Suprasellar/pituitary involvement
History is key! (can look like TB, leptomeningeal carcinoma, meningitis etc)
Holoprosencephaly subtypes and findings
Lobar - partial fusion frontal horns ventricles (absent SP, CC +/- azygous ACA)
Semi-lobar - complete fusion frontal lobes (posterior brain is cleaved)
Alobar - pancake brain, monoventricle (other midline facial anomalies
Variants of holoprosencephaly
Arhinencephaly - absent olfactory bulbs (Kallman syndrome), minor HPE expression
Meckel-Gruber - encephalocele, renal cysts, polydactyly
Septo-optic dysplasia - absent SP, optic nerve hypoplasia, pituitary abnormalities, azygous ACA
50% have schizencephaly!
Most common cause of temporal lobe epilepsy
Mesial temporal sclerosis
#2 tumours in temporal lobe - most commonly ganglioglioma, #3 cortical dysplasia
Most significant RF for development of CNS neoplasm
Radiation
-most commonly meningioma
