Neuro Flashcards
HELPFUL VIDEOS
STROKE
https://www.youtube.com/watch?v=rruRwWIthbw
ISCHAEMIC STROKE
https://www.youtube.com/watch?v=2IgFri0B85Q
GBM
https://www.youtube.com/watch?v=GiV_XyyvNz8
TBI
https://www.youtube.com/watch?v=hssdJu-81g4
MYASTHENIA GRAVIS
https://www.youtube.com/watch?v=bYGxGdu9MsQ
PROGRESSIVE NEUROCOGNITIVE DISEASE
https://www.youtube.com/watch?v=KdcjyHvaAuQ
ACQUIRED DEMYELINATING DISEASES
https://www.youtube.com/watch?v=0jdT0OBZq90
LEUKODYSTROPHIES
https://www.youtube.com/watch?v=7eO8kQOW7GY
CNS TUMOURS
https://www.youtube.com/watch?v=ykrBO6F39zU
HUNTINGTINS
https://www.youtube.com/watch?v=wJAerjsZyZE
MUSCULAR DYSTROPHY
https://www.youtube.com/watch?v=DGOmN6rnsNk
MENINGITIS
https://www.youtube.com/watch?v=gIHUJs2eTHA
MS
https://www.youtube.com/watch?v=yzH8ul5PSZ8
Learning Neuroradiology youtube channel
https://www.youtube.com/channel/UC6RICkCkDRjxar5rdsVJStA
Virchow Robbins spaces (dilated perivascular spaces)
Fluid filled spaces that accompany perforating vessels.
Normal variant, very common. Can be associated with mucopollysaccharoidosis, cryptococcal meningitis, age. Have interstitial fluid, not CSF
Cavum variants
CAVUM SEPTUM PELLCIDUM
100% preterm infants, 15% adults. Rarely cause hydro. Anterior to foramen of Munroe between frontal horns
CAVUM VERGAE
Posterior continuation of cavum septum pellucidum, posterior to foramen of Munroe between bodies of lat ventricles
CAVUM VELUM INTERPOSITUM
Extension of quadrigeminal plate cistern to foramen of Munro. Seen above 3rd ventricle and below fornices.
Carotid canal anatomy
Split into 2 components by jugular spine.
PARS NERVOSA
anteromedial. CN9 and its tympanic branch Jacobsens nerve
PARS VASCULARIS
jugular bulb, CN10 and branch Arnolds nerve, CN11
Cavernous sinus
Carotid artery and CN6 medially (hence lateral rectus palsy in cavernous sinus pathology)
CN 3, 4, V1 and V2 in lateral wall
IAC
7UP COKE DOWN on heavy T2 weighted
CN7 and superior vestibular nerve are superior
CN8 and inferior vestibular nerve are inferior
Skull foraminae contents
OVALE
CNV3, accessroy meningeal a
ROTUNDUM
CNV2 (remember R2V2)
SOF
CN3, CN4, CNV1, CN6
IOF
CNV2
SPINOSUM
middle meningeal a
JUGULAR FORAMEN
Nervosa CN 9
Vascularis CN10, CN11
HYPOGLOSSAL CANAL
CN12
OPTIC CANAL
CN1, opthalmic a
CAVERNOUS SINUS
CN3, CN4, CNV1, CNV2, CN6, carotid a
IAC
7up coke down and sup/inf vestibular nerves
MECKEL CAVE
Trigeminal ganglion
DORELLOS CANAL
CN6, inferior petrosal sinus
Branches of external carotid
“some admin love fucking over poor medical students:
Superior thyroid Ascending pharyngeal Lingual Facial Occipital Posterior aricular Maxillary Superficial temporal
Segments of carotid artery
“cummon please learn clinical carotid organising classification”
Cervical Petrous Lacerum Cavernous Clinoid Opthalmic/supraclinoid Communicating
Acute CN3 palsy
PCOM aneurysm.
Anerysm at basilar artery or junction with superior cerebellar/posterior cerebral arteries can also cause this.
Vascular variants round COW
FETAL ORIGIN PCA
30% gen pop. posterior communicating is larger than P1 so occipital lobe is fed by ICA
PERSISTENT TRIGEMINAL ARTERY
Fetal connection between cavernous ICA and basilar. Tau sign on sag MRI. Increased risk of aneurysm
Anastomotic superficial veins
VEIN OF TROLARD (TOP)
Connects superficial middle cerebral vein and superior sagittal sinus. Small.
VEIN OF LABBE (LOW)
Connects superficial middle cerebral vein and transverse sinus. Large
EXTRA - NOTE ANASTOMOTIC
BASAL VEIN OF ROSENTHAL
Deep vein that passes lateral to midbrain through ambient cistern and drains into vein of Galen. SImilar course to PCA.
VEIN OF GALEN
Formed by union of two internal cerebral veins
Superficial vs Deep cerebral veins
SUPERFICIAL Superior cerebral veins Superior vein of Trolard Inf vein of Labbe Supperficial middle cerebral veins
DEEP
Basal vein of Rosenthal
Vein of Galen
Inferior Petrosal sinus
Brain myelination appearance
Infant brain has opposite signal characteristics on MRI due to myelin changes
Immature myelin has higher water content so is brighter on T2 and darker on T1. DUring maturation, water decrease and fat increase and signal characteristics change.
T1 changes precede T2 (adult T1 pattern age 1, adult T2 pattern age 2.
Immature myelin high water, low fat, T1 dark, T2 bright (adult opposite)
Brain myelination pattern
brainstem, posteior limb internal capsule myelinated at birth
ORDER OF PROGRESSION inferior to superior posterior to anterior central to peripheral sensory fibres prior to motor fibres subcortical white matter last to myelinate
Sinus development
Develop in following order:
Maxillary - present at birth, see on CT 5month
Ethmoid - present at birth, see on CT 1year
Sphenoid - NOT present at birth, see on CT 4year
Frontal - NOT present at birth, see on CT 6year
Corpus callosum agenesis (failure to form)
Forms front to back therefore agenesis often at back (splenium)
Colpocephaly (asymmetric dilatation of occipital horns) often shown which can be pericallosal lipoma or corpus callosum agenesis of splenium
“slit ventricles” in agenesis as Probst bundles are densely packed white matter tracts which would have otherwise crossed CC but now run parallel to interhemispheric fissure making ventricles look widely spaced and slit like. Steer Horn appearance on coronal.
Intracranial lipoma
Most classic association with CC agenesis. 50% at interhemispheric fissure, 2nd most common quadrigeminal cistern. Non fat sat T1 most helpful sequence. Asymptomatic.
Anencephaly (failure to form)
Neural tube defect at top of head. Top of head is absent above the eyes.
Reduced/absent cerebrum and cerebellum. Hindbrain will be present. Not compatible with life
Frog Eye appearance on conronal due to abent cranial bone/brain wit bulging orbits.
Antenatal USS with polyhydramnios (cant swallow). AFP elevated.
Iniencephaly (failure to form)
Neural tube defect at level of cervical spine. Deficient occipital bone with defect in cervical region (inion = back of head)
Extreme retroflexion of head. Enlarged foramen magnum. Usually not compatible with life.
Star Gazing Fetus. Makes face turn upward with hyperextend cervical spine, short neck. AFP elevated
Encephalocoele (aka meningoencephalocoele) failure to form
Brain and meninges herniate through a defect in cranium. Most midline and occipital. Most classic with Chiari 3
Cerebellar Vermis abnormality (failure to form)
RHOMBOENCEPHALOSYNAPSIS
Vermis absent. Trasnversely oriented single lobed cerebellum. Absence of vermis means abnormal fusion of cerebellum. SMall 4th ventricle. Absent primary fissure. Associated with holoprosencephaly.
JOUBERT SYNDROME
Absent or small vermis. Molar Tooth appearance of superior cerebellar peduncles. Small cerebellum, absence of pyramidal decussation. Large 4th ventricle. Associated with retinal dysplasia, MCDK, liver fibrosis (COACH syndrome)
Dandy Walker (failure to form)
3 KEY FINDINGS
Hypoplasia of vermis (usually inferior part).
Hypoplastic vermis is elevated and rotated.
Dilated cystic 4th ventricle.
cerebellar vehemispheres will be displaced forward and lateral but overall volume and morphology are preserved.
Torcula-lambdoid inversion. Normally the lambdoid is above torcula, in DW, torcula is elevated above lambdoid
Often identified on obstetric USS
Presents with symptoms of raised ICP
Most common macrocephaly in 1st month
Associated with hydrocephalus and can have CC agenesis, encephalocoeles, heterotopia, polymicrogyria
variants not quite meeting DW include mega cisterna magna and blake pouch (cystic protrusion through foramen of magendie into retrocerebellar region)
Holoprosencephaly (failure to cleave)
Occurs along spectrum. Failure of midline cleaving. Cleavage occurs back to front (opposite of CC)
LOBAR
Mild fusion frontal horns, incomplete septum. Normal thalamus. Absent septum pellucidum +/- CC.
SEMILOBAR
Fused frontal lobes >50%. Body of lateral ventricles are single chamber. Absent septum pellucidum, CC, anterior interhemispheric fissure, falx cerebri anteriorly. Cleft lip/palate. Thalamus fused
ALOBAR
Monoventricle with rim of cortical mantle. Cerebral hemisphere fused with single midline ventricle. Thalamus fused. Absent septum pellucidum, CC, interhemispheric fissure, falx cerebri. Cyclops face. Still born.
Buzz words for HPE. Monstor cyclops eye, cleft lip/palate, pyriform aperture stenosis, solitary median maxillary incisor (mega incisor)
Two random conditions
ARHINCEPHALY
Minor HPE expression. Midline olfactory bulbs/tracts absent. Cant smell. Can be part of Kallmann Syndrome (also has hypogonadismand mental retardation)
MECKELL-GRUBER
Occipital encephalocoele, multiple renal cysts and polydactyly. Strongly associated with HPE.
Septo-optic Dysplasia (de Morsier syndrome)
Absent septum pellucidum.
Hypoplastic optic structures such as optic chiasm and optic nerves.
Associated with scizencephaly. Also can have azygod anterior cerebral artery which is common trunk of anterior cerebral arteries.
Neuronal cortex formation
Brain forms from inside out. Neurons are all in slurry surrounding fetal ventricles (germinal matrix) then climb to cortex.
PROLIFERATION
Neuronal-glial cells in periventricular pit where they divide into additional cells symmetrically. Stay until they get signal to undergo apoptosis. Number of neurons in cortex determined by frequency and number of divisions by stem cells. Disturbance here will result in too few/too many/improper neurons
MIGRATION
Cells make climb to cortex guided by structural cells, chemical signals. Climb in 6 waves with preplate then cortical plate.Therefore, organised in inside-out pattern. Disturbance here results in undermigration/overmigration/ectopic neurons
ORGANIZATION
Cortical folding required once at destintion. Depends heavily on 1st 2 steps. Differential speed of cortex expansion is key to mechanism for brain folding. Need right number of cells migrating in right order. Continued differentation into structural cell types which organize into horizontal/vertical columns creating underlying cytoarchitecture for sturcture and function. DIsturbance here results in absence or excessive number of folds.
Unilateral dilated ventricle (failure to proliferate)
Failure to proliferate
HEMIMEGALENCEPHALY
Big side with big ventricle. Hamartomatous overgrowthof all or part of a cerebral hemisphere, secondary to differentiation/migration failure
RASMUSSENS ENCEPHALITIS
Small side with big ventricle. Shrunken half is atrophic resulting in ex-vacuo dilatation.
Lissencephaly Classic type 1
Undermigration.
Smooth surface, thick cortex. Colpocephaly figure 8 shape.
Failure to migrate both in amount and in order with a reverse outside in pattern. Large numbers neurons dont reach cortical plate depositing between ventricular and pial surfaces. 4 layers instead of 6. Cortical folding doesnt take place. Shallow sylvian fissures. Association with CMV
Double cortex band heterotopia
Undermigration.
Mildest form of classic Lissencephaly.
disorganized migration results in second layer of cortical neurons deep to superficial cortex. creates double cortex appearance. associated with seizure disorders.
gyral pattern is normal with subcortical band of heterotopic gray matter.
Cobblestone Lissencephaly type 2
Overmigration.
Overmigration of neurons to cortex reults in an additional layer of cortex composed of gray matter nodules.
Nodules in varying shapes/sizes. Most commonly located adjacent to sylvian fissures.
Cobblestone cortex. associated with congenital muscular dystrophy and retinal detachment.
Periventricular nodular heterotopia
Failed migration.
Neurons in periventricular/subependymal region did not migrate resulting in gray matter deposition along ventricle borders.
Most common spot for gray matter heterotopia. associated with seizures.
Polymicrogyria (failure to organize)
During normal migration, layer 5 can get affected by toxins/infection etc and cause more superficial layers to overfold and fuse resulting in excessive folding seen in polymicrogyria
Fine undulating bumpy cortex. Variety of shapes and sizes. Most common adjacent to sylvian fissure.
Scizencephaly (failure to organize)
Vascular insult proposed. 30% with scizencephaly also have non CNS vascular stigmata.
Cleft connecting CSF spaces with ventricular system. Can be unilateral or bilateral.
CLOSED LIP 20%
Less common, less severe. Lip is closed without a CSF cleft. Gray matter running accross norml corona radiata. Sometimes see nodule of gray matter at ventricular surface.
OPEN LIP 80%
More common, more severe. CSF filled cleft ventricle to pial surface. Lined with gray matter.
Associations: absent septum pellucidum, focally thinned CC, optic nerve hypoplasia, epilepsy.
Developmental failure mimics
PORENCEPHALIC CYST.
Brain celft/hole from prior insult resulting in encephalomalacia. Can communicate with subarrachnoid space externally or ventricle internally. NOT lined with gray matter
HYDRANENCEPHALY
bilateral ICA occlusion results in massive destruction both cerebral hemispheres. Only midbrain, cerebellum and falx remain. Herpes most classic but in utero infection with toxo or CMV also described.
Cephalocoeles
Herniation of contents through a defect in the skull
MENINGOCOELE
CSF and meninges, no brain
MENINGOENCEPHALOCOELE aka ENCEPHALOCOELE
CSF, meninges and brain
CYSTOCOELE
CSF, brain, meninges and ventricle
MYELOCOELE
Spinal cord
Chiari Malformations
TYPE 1
Herniation of cerebellar tonsils more than 5mm. Association with syrinx. Congenital underdevelopment of posterior fossa leading to overcrowding and downward displacement. Can get occipital hadache worse with sneezing. Weakness, spasticity, loss of proprioception. Can be associated with Klippel Feil syndrome - congenital c spine fusion. Not associated with neural tube defect
TYPE 2
Less tonsillar herniation, more cerebellar vermian displacement. Classic features low lying torcula, tectal beaking, hydrocephalus, clival hypoplasia. Can have interdigitated cerebral gyri. Lumbar myelomeningocoele/SPina Bifida. NTD sucks cerebellum downward prior to development of cerebellar tonsils.
TYPE 3
Features of 2. Also have occipital encephalocoele containing cerebellum and/or brainstem, occipital lobe and sometimes 4th ventricle. Associated with syrinx, tethered cord, hydrocephalus, agenesis CC.
TYPE 4.
Severe cerebellar hypoplasia.. Has fallen out of favor.
Mesial temporal sclerosis
Hipocampal volume loss + gliosis/scar resulting in intractable seizures. Likely developmental. Most common cause of partial complex epilepsy.
Reduced hippocampal volume, increased T2 signal from scar, loss of normal morphology/interdigitations. Can also get atrophy ipsilateral fornix and mammillary body. COntralateral amygdala enlargement.
Monro-Kellie Hypothesis
Head is closed shell. 3 major components: brain, blood and CSF are in state of dynamic equilibrium. As volume of one goes up, another goes down.
Intracranial Hypotension
Leaking CSF decreases overall fixed volume. As a result volume of venous blood increases to compensate. Causes meningeal engorgement (enhancement) and distension of dural venous sinuses, prominence to intracranial vessels and engorgement of pituitary. Development of SDH and hygromas is classic look
Idiopathic intracranial hypertension (pseudotumour cerebri)
Overweight middle aged woman with headache is classic.
Making too much CSF or not absorbing properly. Ventricles become slit like, pituitary shrinks, venous sinuses compress. vertical tortuosity of optic nerves and flattening of posterior sclera.
Can get downward displacement of brainstem stretching 6th nerve resulting in 6th nerve paresis.
Hydrocephalus
COMMUNICATING
All ventricles are big. Obstructin between basal cisterns and arachnoid granulation. CSF can exit all ventricles.
causes blood/pus/cancer clogging villi SAH, meningitis, carcinomatosis
causes brain atrophy, NPH, CSF secreting tumour
NON-COMMUNICATING
upstream ventricles big, obstruction within ventricular system, CSF cannot exit all ventricles.
causes FoM colloid cyst, aqueductal stenosis or tectal glioma,posterior fossa tumour, cerebellar edema/bleed
Normal Pressure Hydrocephalus
Idiopathic
Wet, wacky, wobbly (urinary incontinence, confusion, ataxia). Elderly patients, ataxia comes first.
ventricular size out of proportion to atrophy. Frontal and temporal horns most affected. Upward bowing of CC. Transependymal flow in acute hydro.
SHYMA is similar but in middle age (syndrome of hydrocephalus in young and middle-aged adult)
Congenital hydrocephalus
Typically diagnosed prior to birth via USS
Aqueductal stenosis
Neural tube defect - usually Chiari 2
Arachnoid cysts
Dandy Walker
Aqueductal Stenosis
Most common cause of congenital obstrctive hydrocephalus
Classicaly from web ofr diaphragm a the aqueduct. Non-communicating with dilatation of lateral ventricles and 3rd ventricle with normal 4th ventricle. Can have macrocephaly with thinning of cortical mantle.
Treatment shunting or ventriculostomy. Sunset eyes or upward gaze paralysis.
Arachnoid cysts
Cysts in subarachnoid space. CSF density without solid component or restricted diffusion. Can block CSF pathway and have mass effect on brain.
CSF shunt malfunction
Normal is proximal shunt in frontal horn lateral ventricle by FoM, valve to control flow and distal tip usually in peritoneum but can be right atrium or pleural space.
UNDERSHUNTING
Most common cause is ingrowth of choroid pexus and particulate debris/blood products. Can also be from catheter migration. ALso distally can be from pseudocyst (loculated fluid at distal tip)
OVERSHUNTING
Slit like ventricles can mean too much shunting. Concern is for SDH or hygroma formation
INFECTION
Usually within 6 months of placement. Blood cultures negative, need to cultre shunt fluid. Debris within ventricles. Need DWI for ventriculitis. Ventricular loculations
HYDROTHORAX
Catheter can be deliberately in pleural space or migrate there. A little fluid is fine but if patient symptomatic may need revision.
ASCITES
Little fluid is fine but large amounts can cause herniae or hydrocoeles
Edema
CYTOTOXIC
Intracellular swelling secondary to malfunction of Na/K pump. Favours gray matter, loss of GW differentiation. Seen in stroke or trauma. BBB intact
VASOGENIC
Extracellular, secondary to disruption of the BBB. Edema tracking through white matter. Seen with tumour and infection. Response to steroids is classic of vasogenic edema
Types of herniation
SUBFALCINE
Same as midline shift, can get ACA compression
DESCENDING TRANSTENTORIAL (UNCAL) Uncus and hippocampus herniate through tentorial incisura. Perforatingbasilar artery branches get compressed resulting in DUrets haemorrhages in midline at pontomesencephalic junction. CN3 gets compressed between PCA and SCA causing pupil dilatation and ptosis
ASCENDING TRANSTENTORIAL
Posterior fossa mass causing vermis to herniate upwards through tentorial incisura. Can cause severe obstructive hydrocaphalus.
CEREBELLAR TONSIL HERNIATION
Severe herniation after downwards transtentorial herniation. Or Chiari
Central Pontine Myelinolysis
T2 bright pons which spares the periphery. Restricted diffusion lower pons. Can have extra-pontine presentation involvng basal ganglia, external capsule, amygdala and cerebellum.
Low sodium corrected too quickly. Can become encephalopathic with spastic quadriparesis. SLurred speech, sensitive gag reflex and labile emotional response.
Wernicke Encephalopathy
High T2/Flair signal in medial thalamas and periaqueductal gray matter, mamillary bodies andtectal plate. MR spect shows lactate, treatment is thiamine replacement.
Clinical triad of acute confusion, ataxia and opthalmoplegia. Thiamine (vitamin B1) deficiency is cause. Can progress to chronic memory loss and confabulation (Korsakoff psychosis)
Marchiafava-Bignami
High T2/Flair in CC representing acute demyelination. Progresses, beginning in body then genu then splenium. Sanwhich sign on sagittal describes pattern of preference for central fivers with relative sparing of dorsal and ventral fibers. Thinned CC and cystic cavities favoring genu and splenium
Associated with alcohol. Presents with confusion and alterd gait. Seizure and muscle rigidity
Random metabolic findings
ALCOHOLIC INJURY
Most common is brain atrophy, particularly cerebellum esp vermis
COPPER AND MANGANESE DEPOSITION
T1 bright basal ganglia. Non specific and related to liver disease. Can be seen without hepatic encephalopathy. Also seen in TPN, Wilsons.
METHANOL TOXICITY
Optic nerve atrophy, haemorrhagic putaminal and subcortical white matter necrosis.
Carbon Monoxide vs Methanol
Carbon Monoxide has CT hypodensity/T2 bright in globus pallidus (carbon causes globus warming)
Methanol T2 bright putaminal which may be haemorrhagic and thus CT hyperdense
Posterior Reversible Encephalopathy Syndrome (PRES)
Asymmetric cortical and subcortical white matter edema, usually in parietal and occipital regions. Does NOT restrict diffusion (rule out stroke).
Poorly understood but issue with autoregulation. History of acute HTN or chemotherapy.
Post chemotherapy
PRES
Chemo is classic cause but tends to have non classic look relative to HTN cause, sparing occipital lobes and targeting basal ganglia, brainstem and cerebellum
LEUKOENCEPHALOPATHY
Treatment induced. Classic look would be centered in periventricular white matter. Bilateral, symmetrical confluent T2/Flair bright changes. Disseminated necrotizinf variant has severe changes including ring enhancement in leukaemia patients undergoing radio/chemo
Post radiotherapy
T2 bright areas and atrophy corresponding to the radiation portal. Also see haemosiderin deposition and mineralizing microangiopathy (calcs in basal ganglia and subcortical white matter). Latent period so findings not seen for up to 2 months post radiotherapy.
Heroin Inhalation Leukoencephalopathy
‘chasing the dragon’
High T2/Flair in centrum semiovale symmetrically. High signal in posterior limb of internal capsule, deep cerebellar white matter which spares dentate nucleus.
Multiple Sclerosis
Perivascular pattern involving juxtacortical and periventricular regions with lesions having ovoid/fusiform morphology.
Lesions disseminated in space (periventricular, juxtacortical, infratentorial, spinal cord) with more than 1 in at least 2 of these locations. Lesions disseminated in time. T2 bright lesion that does enhance (active) and one that doesnt enhance (non active).
Targets women 20-40.
Multiple subtypes with relapsing/remitting most common 85%.
Separated by time and space is critical.
Multiple Sclerosis Trivia
T2/Flair oval and periventricular perpendicularly oriented lesions (Dawsons fingers)
Involvement of calloso-septal interface is 98% specific for MS
Posterior fossa more commonly invovled in children
Brain atrophy accelerated in MS
Solitary spinal cord involvement can occur but usually in addition to brain lesions
Cervical spine most commonly spinal portion effected 65%
SPinal cord lesions peripherally located
MR spectroscopy shows reduced NAA peaks within plaques
Acute demyelinating plaques should enhance and restrict diffusion.
Big plaque will have INCOMPLETE ring enhancement - tumefactive demyelination
Multiple Sclerosis variants
ACUTE DEMYELINATING ENCEPHALOMYELITIS (ADEM)
Presents in childhood or adolescents after viral illness. Multiple large T2 bright lesions enhancing in nodular or open ring pattern. does NOT involve calloso-septal interface
ACUTE HAEMORRHAGIC LEUKOENCEPHALITIS (HURST DISEASE)
Fulminant form of ADEM with massive brain swelling and death. Haemorrhage seen at autopsy
DEVICS (NEUROMYELITIS OPTICA)
Transverse myelitis and optic neuritis. Lesions in cord and optic nerve
MARBURG VARIANT
Childhood variant that is fulminant reading to rapid death. Febrile prodrome.
Subcortical Arteriosclerotic Encephalopathy (SAE)
Binswanger disease. Multi infarct dementia.
Favours white matter of centrum semiovale. Spares subcortical U fibres. Strong association with hypertension. Seen in older people, 55 and up.
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)
SAE in younger person with migraines. Classic might say 40yo with migraines then strokes then eventual dementia.
CADASIL is most common hereditary stroke disorder.
Severe white matter disease high T2/Flair involving multiple vascular territories in the frontal and temporal lobes. Occipital lobes often spared. Temporal lobe classic
Alzheimers Dementia
Most common cause.
Tauopathy, neurofibrillary tangles, amyloid cascade.
Risk factors: Age. Downs syndrome get this early.
See hippocampal atrophy. Temporal horn atrophy >3mm in 65% cases.
FDG shows low posterior temporoparietal uptake (earmuff). Posterior cingulate first affected.
Multi-infarct Dementia (Vascular Dementia)
2nd most common and aka Vascular Dementia
Risk factors: HTN, smoking, poor diet. CADASIL
See cortical infarcts and lacunar infarcts. Brain atrophy advanced for age
FDG multiple scattered areas of decreased activity. No specific lobar predominance.
Can knock out motor strip (others dont).
Dementia with Lewy Bodies
3rd most common
Alpha synuclein and synucleinopathy buzzwords
Visual hallucinations, spontaneous Parkinsonisn, fluctuating ability to concentrate/stay alert. Clinical picture similar to Parkinsons but major difference is dementia comes BEFORE Parkinsonism.
See mild generalized atrophy without lobar predominance. Hippocampi normal in size.
FDG decreased uptake in lateral occipital cortex with sparing of mid cingulate gyrus.
Picks Dementia (Frontotemporal Dementia)
Onset is earlier, 40s.
Classic presentaiton is compulsive or innapropriate behaviours. Think being a PrICK (PICKs)
Severe symmetric atrophy frontal lobes, milder in temporal lobes.
FDG low uptake in frontal and temporal lobes
Nerodegeneration disorders
FAHR DISEASE
Extensive calcification basal ganglia and thalamus. Mostly asymptomatic.
HALLERVORDEN SPATZ
Iron in globus pallidus. Also called PKAN. T2 dark globus pallidus with central bright area of necrosis “eye of the tiger”. No enhancement or restricted diffusion.
AMYOTROPHIS LATERAL SCLEROSIS
Upper motor neuron loss in brain and spine. Most die within 5 years. No gross volumeloss. T2/Flair normal. Motor band sign on gradient
CORTICOBASAL DEGENERATION
Tauopathy. Alien limb phenomenon. Symmetric frontoparietal atrophy
HUNTINGTON DISEASE
AD repeat sequence 38 CAG. Caudate atrophy and reduced FDG uptake. Frontal horns become enlarged and outwardly convex
LEIGH DISEASE
Mitochondrial disorder. ELevated lactate peak. T2/Flair bright in brainstem, basal ganglia and cerebral peduncles. Do not enhance.
Neurodegeneration disorders cont
MELAS syndrome
Mitochondrial disorder. Lactic Acidosis Seizures and Strokes. Elevated lactate. Atypical strokes in cotical gray matter with nonvascular distribution. Underlying WM is normal
HURLER SYNDROME
Mucopolysaccharidoses/lysosomal storage disease. Macrocephaly with metopic beak. Enlarged perivascular spaces. Beaked inferior L1 vertebral body
Parkinsons Disease
Resting tremor, rigid/slow movements (shuffling gait). Reduced dopaminergic input into striatum.
Cant diagnose on CT/MRI alone but possibly mild midbrain volume loss with butterfly pattern.
Nuke scan DAT ioflupane 123. Sparing of midbrain and superior cerebellar peduncles
Multiple System Atrophy (MSA) - a Parkinson Plus Syndrome
Complex entity, 3 subtypes
Cerebellar subtype shows cerebellar hemisphere/peduncle atrophy with a shrunken flat pons and enlarged 4th ventricle. Hot cross bun sign on axial imaging with loss of transverse fibres.
I-123 MIBG can differentiate PD from MSA by looking at cardiac/mediastinal ratio, normal in MSA, abnormal in PD
Progressive SUpranuclear Palsy (PSP) - a Parkinson plus syndrome
Most common Parkinson plus. A tauopathy.
Micky Mouse sign - tegmentum atrophy with sparing of tectum and peduncles.
Hummingbird sign - midbrain volume loss with concave upper surface and relative sparing of pons
Wilsons Disease
AR copper metabolism malfunction. Once liver fills with copper it spills over into brain. Kayser Fleisher rings seen 95%.
CT shows cortical atrophy. MRI shows T1 and T2 bright basal ganglia with T2 bright dorsal medial thalamus
Panda sign has T2 bright tegmentum with normal dark red nuclei and substantia nigra
Deep Brain Stimulators
Treatment of Parkinsons, essential tremor and chronic ain
For PD, electrodes are in subthalamic nucleus with tips located 9mm from midline, just inside upper most margin of cerebral peduncle
MRI spectroscopy
Various metabolites exist in different concentrations depending on pathology.
NAA (N acetyl aspartate) is a neuronal marker so things that destroy neurons will lower NAA. Lower NAA = higher grade tumour.
Choline is marker of cell membrane turnover. High value means high grade tumour, demyelination, inflammation.
Creatinine is marker of energy metabolism. Decreased in tumour necrosis.
Lactate product of anaerobic metabolism. Elevated in abscess or if tumour has outgrown blood supply.
PPM is parts per million. Each metabolite has a value for this.
Hunters Angle. on graph with intensity on y and ppm on x. Hunters angle should go from low to high in normal setting. Choline then creatanine then NAA.
DEmyelinating vs DYsmyelinating
DEMYELINATING
Example MS. Destroys myelin
DYSMYELINATING
Example metachromatic leukodystrophy. Disrupts normal formation and turnover of myelin.
Leukodystrophy - classic
Deficiencies in lysosomal storage disease, peroxisomal function or mitochondrial dysfunction. Target white matter, more symmetric and extensive. Untreatable and fatal.
ADRENOLEUKODYSTROPHY (ALD)
Normal head size. Parieto-occipital. Extends accross splenium. Enhance and restrict. Male predominant
METACHROMATIC
Normal head size. Frontal predominant. Periventricular and deep white matter. Tigroid (stripes) appearance. Most common. U fibres spared.
ALEXANDER DISEASE
Big head. Frontal predominant.Can enhance.
CANAVAN DISEASE
Big head. Bilateral subcortical U fibres. Elevated NAA
KRABBE
Small head. Centrum semiovale parieto-occipital predominant. Spares subcortical U fibres
PELIZAEUS MERZBACHER
Normal head size. Diffuse total lack of normal myelination with extension to U fibres. No enhance, no restrict.
Leukodystrophy - mitochondrial disease
Asymmetric, favours gray matter. Gray matter needs more oxygen than white matter and mitochondrial disorders are inability to process oxygen.
MELAS (Mitochondrial Encephalomyopathy, Lactic Acidosis and Stroke like symptoms)
Parieto-occipital distribution. ‘migrating infarcts’
LEIGH DISEASE
Subacute necrotizing encephalomyopathy. Basal ganglia and periaqueductal gray matter. Normal head size.
Enhancement
ENHANCE
If extra axial or if blood brain barrier compromised.
Menigiomas or high grade tumour/infection.
Exceptions are low grade tumours Ganglioglioma and Pylocytic Astrocytoma
Intra vs Extra Axial
EXTRA-AXIAL CSF cleft. Displaced subarrachnoid vessels Cortical gray matter between mass and white matter Displaced/expanded subarrachnoid spaces Broad dural tail Bony reaction
Cerebral Metastases trivia
Most common CNS met in kid is neuroblastoma (bones/dura/orbit not brain)
Most common location is supratentorial GW matter junction - lots of blood flow and abrupt change in vessel calibre
Most common morphology round/spherical
50% solitary masses are mets
MRCT is bleeding mets (melanoma, renal, choriocarcinoma/carcinoid/thyroid)
Mets have more edema than a primary of same size normally
Multiple tumours
MULTIFOCAL Metastases Lymphoma Multicentric GBM Gliomatosis Cerebri
MULTIFOCAL FROM SEEDING Medulloblastoma Ependymoma GBM Oligodendroglioma
Syndromes
NF1
Optic Gliomas and Astrocytoma
NF2
Schwannomas, Meningiomas, Ependymomas
TUBEROUS SCLEROSIS
Subependymal Tubers
Intraventricular Giant Cell Astrocytoma (SEGAs)
Also AMLs
VON HIPPEL LINDAU
Hemangioblastomas
Cortically based tumours (PDOG)
PLEOMORPHIC XANTHOASTROCYTOMA
Usually temporal lobe and superficial. Seen in paeds 10-20yo. Enhance, have cyst wth nodule and dural tail. Can invade leptomeninges
DYSEMBRYOPLASTIC NEUROEPITHELIAL TUMOUR
Paeds <20yo. No enhancement, bubbly. Temporal lobe, High T2 with bright Flair rim. Drug resistant seizures. Hypodense on CT, little edema.
OLIGODENDROGLIOMA
Adult 40-50yo. Can enhance. Calcification common 90%. Expands cortex. Frontal lobe. 1p/19q deletion.
GANGLIOGLIOMA
Any age. Can enhance. Can look like anything. Temporal lobe. Classic would be 13yo with seizures and temporal lobe mass that is cystic/solid with calcification with possible overlying bony remodelling.
Intraventricular masses ddx
VENTRICULAR WALL AND SEPTUM Ependymoma (paeds) Medulloblastoma (paeds) SEGA (paeds) Subependymoma (adult) Central Neurocytoma (young adult)
CHOROID PLEXUS
Choroid plexus papilloma (paeds trigone adult 4th vent)
Choroid plexus carcinoma (paeds)
Xanthogranuloma (adults)
MISCELLANEOUS
Metastases
Meningioma
Colloid cyst
Ependymoma VENT WALL/SEPT
Bimodal distribution but think as paeds tumour. Can calcify 50%
in 4th ventricle 70% time. Seen inferiorly and squeezes out foramen of magendie and luschka “toothpaste tumour”
parenchymal supratentorial 30% time, usually big at presentation >4cm
IMAGE REMAINING NEURAL AXIS
Medulloblastoma VENT WALL/SEPT
Paediatric tumour, most before age 10
Arise from roof of 4th ventricle in the vermis. Much more common than ependymoma (ddx).
Dense mass on CT, heterogenous T1/T2 and enhances homogenously. Hypercellular, may restrict. Calcify 20% time
Dop met Zuckerguss (sugar coat) leptomeningeal enhancement. Met via CSF pathways.
Associated with basal cell nevus syndrome and turcots syndrome
IMAGE REMAINING NEURAL AXIS
Medulloblastoma vs Ependymoma
MEDULLOBLASTOMA More common Roof of 4th vent Project into 4th vent but not out (less plastic) ENhance homogenously Calcify less 20% Drop mets Zuckerguss
EPENDYMOMA Less common Floor of 4th vent Toothpaste squeeze out into basal cisterns Enhance heterogenously Calcify more 50%
Subependyal Giant Cell Astrocytoma SEGA VENT WALL/SEPT
Shown in setting of Tuberous Sclerosis (may mention AMLs or give history seizures/developmental delay
Seen in kids, average age 11
Arise lateral wall ventricle near foramen of Munro. Enhancing partially calcified lesion at foramen of Munro bigger than 5mm
Subependymoma VENT WALL/SEPT
Adult tumour.
Well circumscribed mass most commonly at foramen of Munro. Can cause hydrocephalus. T2 bright, dont enhance
Central Neurocytoma VENT WALL/SEPT
Most common intraventricular mass in adult 20-40
Swiss cheese - numerous cystic spaces on T2. Calcify a lot
Choroid plexus papilloma/carcinoma CHOROID
Paeds (85% <5yo) and adults.
15% brain tumours <1yo
Often making CSF so causes hydrocephalus.
Carinoma type only seen in kids and is supratentorial lateral ventricle/trigone. Associated with Le Fraumeni (bad p53). Angiography shows enlarged choroidal arteries which shunt blood to tumour. Typically solitary
Seen in 4th ventricle in adults
Xanthogranuloma CHOROID
Benign choroid plexus mass. Common, usually dont notice them.
Restrict on diffusion imaging so can be put in to trick you into working them up.
Metastases MISC
Most common spot is trigone lateral ventricles due to vascular supply of choroid. Most common primary lung or renal
Colloid cyst MISC
Almost exclusively i anterior part of 3rd venticle.
If cholesterol, high T1, dark T2. If not T2 bright. Dense on CT
Can cause sudden death via acute hydrocephalus. Will see transependymal oedema, best seen in Flair
Meningioma MISC
Most commonly at trigone lateral ventricle.
Mass in trigone lateral ventricle in patient over 40 is mets/lymphoma/meningioma
Mass in trigone lateral ventricle patient <10 is choroid plexus papilloma (think NF)
Vestibular schwannoma CPA MASS
75% CPA masses
If bilateral, think NF2.
Enhances strongly, but more heterogenous than meningioma.
May widen porus acousticus resulting in icecram cone IAC
Meningioma CPA MASS
10% CPA masses More common in women. Can calcify and have dural tail. Enhance strongly and homogeneously. Can be cuased by radiation Take p octreotide and TcMDP in nuc med Most common over cerebral convexity
Epidermoid CPA MASS
5% CPA masses Can be congenital or acquired (after trauma, LP etc) Usually off midline. Follow CSF density on CT and MRI Bright on Flair Restrict diffusion
Dermoid Cyst
4x less common than epidermoid
More common in kids/young adults. Usually midline.
Contain lipoid material and hypodense on CT, bright on T1, associated with NF2.
Usually in suprasellar cistern.
Can explode causing headache and seizure - chemical meningitis
Fat droplets floating in ventricles and/or subarrachnoid space
IAC lipoma
Can happen.
T1 fat signal and will fat sat out. Association with sensorineural hearing loss as vestibulocochlear nerve goes through it.
Arachnoid cyst
Common benign lesion that is located within subarachnoid space and contains CSF. Increased in mucopolysaccharidoses. Do NOT restrict.
Atypical Teratoma/Rhabdoid Tumour ATRT (INFRATENTORIAL
Highly malignant tumour WHO4 rarely occur in patients over 6yo.
Supra and infratentorial, most common in cerebellum.
Large angry looking tumours with necrosis and heterogenous enhancement.
Buzzword is increased head circumference
When vs Medulloblastoma Both are WHO4 in kids posterior fossa Both subtyoes of medulloblastoma. ATRT 2yo, medulloblastoma 6yo ATRT calcifications, medulloblastoma doesnt
Juvenile Pilocytic astrocytoma INFRATENTORIAL
Cyst with a nodule posterior fossa kid
WHO1 but enhance
Wall can enhance (hemangioma wall wont)
Hemangiblastoma INFRATENTORIAL
Cyst with a nodule in adult.
Seen in VHL multiple
Slow growing, indolent vascular tumours which can cause hydrocephalus from mass effect. 90% time in cerebellum
Association with polycythaemia
Medulloblastoma, Ependymoma and Ganglioglioma INFRATENTORIAL
All discussed prior in IV lesions and cortical lesions
Diffuse pontine glioma DPG INFRATENTORIAL
Kids 3-10
Most common location in pons, usually high grade fibrillary glioma. T2 bright with subtle or no enhancement. 4th ventricle flattened.
Astrocytoma SUPRATENTORIAL
Most common primary brain tumour in adults.
Astrocyte and oligocytes share same common origin (glial cells)
Trend toward genetically classifying tumours
Preoperative calcification associated with 1p19q deletion = oligodendroglioma
T2/Flair mismatchNOT seen with 1p19q = astrocytoma
ASTROCYTOMA Can be low grade Grade 2 diffuse Grade 3 anaplastic Grade 4 GBM in older patients worst prognosis
IDH MUTATION
Absent in 90% primary GBM.
10% will have it and these tend to be younger patients with better prognosis, probably secondary GBM from pregression of lower grade tumour
GBM
WHO4
Grows rapidly, can necrose giving ring enhancement.
Can cross midline. Restricts diffusion
Turcot syndrome and NF1 associated with GBM
Astrocytoma grade 1
SUBEPENDYAL GIANT CELL ASTROCYTOMA
IV mass near foramen of Munro in young patients with TS. Can cause obstructive hydrocephalus
PILOCYTIC ASTROCYTOMA
Cyst with nodule in posterior fossa of kid
Both break rule and enhance despite low grade
Astrocytoma grade 2
DIFFUSE
White matter preferred
No enhancement
T2 bright, Flair iso - MISMATCH
Astrocytoma grade 3
ANAPLASTIC
White matter preferred
Mild enhancement
T2 bright, Flair iso - MISMATCH
Astrocytoma grade 4
GBM
White matter preferred, can cross midline
Ring enhancement or can be heterogenous
T2 and Flair bright
Central locations like thalamus are worse than normal
NF1, Turcot, Li Fraumeni all associated
Glioamatosis Cerebri
Diffuse glioma with extensive infiltration. At least 3 lobes and is often bilateral. Usually see mild blurring of GW junction on CT with extensive T2 hyperintensity and little mass effect. No enhancement
Metastases
Most common supratentorial mass
Cerebrum favoured over cerebellum - blood supply thing.
Often multiple but can be solitary.
CTMR for mets that bleed
Carcinoic/Choriocarcinoma/Thyroid/Melanoma/Renal
CNS Lymphoma
End stage AIDS and post transplant patients. EBV plays a role. Most commonly Non Hodgkins B cell
Intensely enhancing solid mass in periventricular region with restricted diffusion
Thallium positive, toxoplasmosis is NOT (think thalliumphoma)
Paeds supratentorial
PLEOMORPHIC XANTHOASTROCYTOMA
Usually temporal lobe and superficial. Seen in paeds 10-20yo. Enhance, have cyst wth nodule and dural tail. Can invade leptomeninges
DYSEMBRYOPLASTIC NEUROEPITHELIAL TUMOUR
Paeds <20yo. No enhancement, bubbly. Temporal lobe, High T2 with bright Flair rim. Drug resistant seizures. Hypodense on CT, little edema.
DESMOPLASTIC INFANTILE GANGLIOGLIOMA/ASTROCYTOMA (DIG)
Large cystic tumours involving superficial cerebral cortex and leptomeninges.
WHO1.
ALways arise in supratentorial region.
Rapidly increasing head circumference
Skull base
CHORDOMA
Locally aggressive tumour that originates from notochord.
Always midline. Most common sacrum then clivus. T2 bright
CHONDROSARCOMA
Main differential of chordoma in clivus. Nearly always lateral to midline. T2 bright with arcs and rings matrix of chondrosarcoma.
Dural tumours
MENINGIOMA
Common and enhances homogenously. Most common over cerebral convexity. Can have adjacent hyperostosis.
HEMANGIOPERICYTOMA
Soft tissue sarcoma that can mimic an aggressive meningioma. Enhances homogenously. Dont calcify or cause hyperostosis but can invade skull.
METS
Most common to met to dura is breast cancer. More oedema than primary tumour of similar size.
Pituitary Adenoma SELLA ADULT
Most common tumour of sella. 97% of time are in adults. If >1cm, macroadenoma, if under microadenoma. When functional, most secrete prolactin
Prolactinoma women have menstrual irregularity and galactorrhoea. Prolactinoma men have decreased libido
T1 dark and T2 bright with slow enhancement
Microadenomas typically form in adenohypophysis. Prolactinoma most common functional type
Pituitary apoplexy SELLA ADULT
Haemorrhage or infarction of pituitary, usually into enlarged gland
Can be when taking bromocriptine or other prolactin drugs
Sheehan syndrome in postpartum women
T1 bright (diff to adenoma)
Lack of hormones can cause hypotension
Rathke cleft cyst SELLA ADULT
Usually incidental finding, rarely symptomatic.
Cleft between ant and post pituitary. Do not enhance, brght on T2
Epidermoid SELLA ADULT
5% CPA masses Can be congenital or acquired (after trauma, LP etc) Usually off midline. Follow CSF density on CT and MRI Bright on Flair Restrict diffusion
Cranioparyngioma SELLA ADULT
Papillary 10% and adamantinomatous 90%
Papillary type is adult, solid with no calcification and recur less frequently (has capsule) than adamantinomatous, strongly enhance, occur along infundibulum
Craniopharyngioma SELLA PAED
Adamantinomatous type is kids. Calcified and recur. Buzzword machinary oil. T1 and T2 bright CT/GRE show calcs Enhance strongly
Hypothalamic Hamartoma SELLA PAED
Hamartoma of tuber cinereum (between mammillary bodies and optic chiasm.
Classic history is gelastic seizures
Pineal region tumours
Vertical gaze palsy
GERMINOMA
Most common, almost exclusively in boys. precocious puberty may occur due to hCG secretion. Mass containing fat and calcification with variable contrast enhancement.Calcification on inside.
PINEOBLASTOMA
Occurs in childhood. Highly invasive. Associatedwith retinoblastoma. Heterogenous and enhance vividly. Calcification at periphery “blast”
PINEOCYTOMA
Rare in childhood. Well circumscribed and non invasive. More solid.
PINEAL CYST
Incidental finding. Calcifications 25%
Restricted diffusion
Supratentorial - abscess or lymphoma (or infarct)
Any hypercellular tumour can restrict, including GBM and medulloblastoma but will typically be lymphoma
CP angle will be epidermoid
Herpes encephalitis can restrict seen in temporal lobes
Crossing midline
Most likely GBM or lymphoma.
Can be radiation necrosis, a bigMS plaque or a falx meningioma
Calcification
Probably oligodendroglioma which calcify 90% time
However, astrocytoma calcify 20% but is a common tumour overall so keep this in mind
T1 bright
Most tumours are T1 dark, unless it has bleed or is MRCT met. Tumours with fat will be T1 bright or with melanin or cholesterol
FAT: dermoid, lipoma.
MELANIN: melanoma
BLOOD: bleeding met or tumour
CHOLESTEROL: colloid cyst
Syndromes
NF1 (CAFESPOT)
Cafe au lait spots, Axillary/groin frecking, fibromas, eye hamartomas, skeletal dysplasia, positive family history, Optic Nerve Gliomas
NF2 (MISME)
multiple inherited schwannomas, meningiomas and ependymomas
TS
SEGA, ependymal tubers, AML
GORLIN
Medulloblastoma, OKC, BCCs
TURCOT
GBMs, medulloblastoma, intestinal polyposis
COWDENs Lhermitte Duclos (dysplastic cerebellar gangliocytoma)
Lhermitte Duclos (Dysplastic Cerebellar Gangliocytoma)
Tiger stripe mass in one cerebellar hemisphere. Not a cancer but actually a hamartoma.
Seen in Cowdens syndrome - next step mammogram
MRS tumour pearls
HIGH GRADE TUMOUR Less NAA Less creatine More lactate More choline More lipids
RECURRENT TUMOUR
Rising choline = cell walls being turned over
RADIATION NECROSIS
Elevated lipids
Elevated lactate
NAA/Creatine/Choline low
GBM
Elevated choline
Neonatal Infection
CMV
Most common TORCH. Targets germinal matrix resulting in periventricular tissue necrosis. Periventricular calcifications. Highest association with polymicrogyria.
TOXOPLASMOSIS
Second most common TORCH. Random calcification pattern, targets basal ganglia. Increased in 3rd trimester. Hydrocephalus
RUBELLA
Less common due to vaccine. Calcification less common. High T2 signal in white matter related to vasculopathy and ischaemic injury
HSV
HSV 2 in 90% cases. Prefers endothelial cells resulting in thrombus and haemorrhagic infarction with encephalomalacia and atrophy
HIV
Not TORCH but occurs in pregnancy, at delivery or via breast feeding. Faint basal ganglia enhancement on CT an MRI preceding basal ganglia calcification. Brain atrophy favours frontal lobe.
Immunosuppressed Infections
Most common is toxoplasmosis. Most common fungal infection in cryptococcus. JC virus and CMV also important.
HIV ENCEPHALITIS
Affects 50% AIDS patients. CD4<200
Symmetric increased T2/Flair signal in deep white matter. Normal T1, no enhancement. May be brain atrophy. Spares subcortical U’s
PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY PML
Caused by JC virus. CD4<50
CT shows single or scattered hypodensities with corresponding T1 hypointensity.
Involves subcortical U’s
T2/Flair abnormality out of proportion to mass effect
Immunosuppressed Infections
CMV
Brain atrophy, periventricular hypodensities and thin ependymal enhancement (ependymal cells line ventricles and central portion spinal cord.
CRYPTOCOCCUS
Most common fungal infection in AIDS. Presents usually with meningitis with leptomeningeal enhancement involving base of brain. Dilated perivascular spaces filled with mucoid gelatinous material which doesnt enhance.. Could also be cryptococcomas in basal ganglia which are T1 dark, T2 bright and ring enhance
TOXOPLASMOSIS
Most common opportunistic infection in AIDS. T1 dark, T2 bright, ring enhancing. No restricted diffusion. Lots of edema.
Toxo vs lymphoma
TOXO Ring enhancing Haemorrhage more common after treatment Thallium cold PET cold Decreased CBV on perfusion
LYMPHOMA Ring enhancing Haemorrhage less common after treatment Thallium hot PET hot Increased CBV on perfusion
Immunosuppressed summary
ENCEPHALITIS
Symmetric T2 bright, spares U’s
PML
Asymmetric T2 bright, T1 dark, involves U’s
CMV
Periventricular T2 bright, thin ependymal enhancement
TOXO
RIng enhance, edema ++, no restricted diffusion, thaliium cold
CRYPTOCOCCUS
Dilated perivascular spaces, basilar meningitis
TB Meningitis
Enhancement of basilar meninges with minimal nodularity. May have dystrophic calcification. Can get vasculitis with infarct as well as hydrocephalus
Sarcoid can have similar look
HSV
HSV1 in adults, HSV2 in neonates.
Swollen T2 bright medial temporal lobe, uni or bilateral. Spares basal ganglia
Resitricted diffusion. Blooming on gradient indicates bleeding which is common in adults and rare in neonate.
Limbic encephalitis
Not an infection but commonly tested mimic. Paraneoplastic syndrome usually from small cell lung cancer looks similar to HSV.
Could show image looking like HSV then say HSV titer is negative. Raise this then recommend screening for lung cancer.
Creutzfeldt Jakob disease
Variable imaging and can be unialteral/bilateral/asymmetric/symmetric.
Sporadic 80-90%, mad cow rare or familiar 10%
DWI cortical gyriform restricted diffusion. Basal ganglia may also be involved.
Hockey stick sign of bilateral Flair bright dorsal medial thalamus
Pulvinar sign bilateral Flair bright posterior thalamus
Neurocysticercosis
Caused by eating undercooked pork. Bug is tinea solium (pork tapeworm).
Involvement of basal cisterns carries worse outcome. Most common locations subarrachnoid over cerebral hemispheres then basal cisterns then brain parenchyma then ventricles
STAGES
1: Vesicular: cyst + solex no enhancement
2: Colloidal: CT hyperdense cyst, MR edema and enhancement
3: Granular: CT early calcification, MR smaller cysts, less edema, less enhancement
4: Calcified/involutional: CT calfication, MR blooming on SWI
Meningitis and abscess
4 Types
Bacterial (acute pyogenic)
Viral (lymphocytic)
Chronic (TB or fungal)
Non-infectious (sarcoid)
Thick leptomeningeal enhancement in bacterial or carcinomatous meningitis
Complications venous thrombosis, vasospasm, empyema, ventriculitis, hydrocephalus, abscess
Fungal and carcinomatous meningitis lumpy/thick
ABSCESS
DWI restricts, MRS lactate high, PET increased
Meningeal enhancement
LEPTOMENINGEAL
Fills subarrachnoid spaces and extends into sulci and cisterns
PACHYMENINGEAL
Enhancement does not extend into sulci
Seen in intracranial hypotension, dural attachment of meningioma, sarcoid, TB, Wegeners, fungal.
Breast and prostate can met to dura
Secondary CNS lymphoma can be extra-axial and duralbased.
Empyema
Can be dural or epidural (like blood)
Subdural more common and have more complications.
Usually sequale of frontal sinusitis.
Enhancing contrast rim and restricted diffusion
Intra-axial abscess
Cavity that contains pus, debris and necrotic tissue.
Secondary to bacterial, fungal or parasitic infection usually via haematogenous spread.
Remember right to left shunts and pulmonary AVMs. Direct spread from sinus possible but less common.
Smooth ring enhancement, multiple lesions. Will restrict however atypicals (toxo) may not
Differential
Lymphoma but this will be hyperdense not low density
Tumour - irregular ring enhancement, bumpy/shaggy
Tumefactive demyelination incomplete ring
Cerebritis and ventricultis
CEREBRITIS
Early form of intra-axial infection can lead to abscess. Vasogenic edema without well defined central enhancing lesion. May be spotty restricted diffusion
VENTRICULITIS
Usually result of shunt placement or intrathecal chemo. Ventricle will enhance and can see fluid fluid levels. If septa develop can get hydrocephalus. Intraventricular extension of abscess is preterminal
MRI enhancement patterns
HETEROGENOUS
Most likely high grade tumour
COMPLETE RING
Abscesses and tumours are high suspects
INCOMPLETE RING
Tumefactive demyelination
GYRIFORM
Subacute stroke, PRES, encephalopathy/encephalitis
Parenchymal contusion
Rough part of skull can scrape brain as it slides in trauma. Typical locations are anterior temporal lobes and inferior frontal lobes. Coup and contre coup injuries.
Diffuse axonal injury
Initial head CT often normal
Favourite sites are posterior corpus callosum and GW junction in frontal and temporal lobes.
Multiple small T2 bright foci
GRADING
1: GW junction
2: Corpus callosum
3: brainstem
Extradural vs subdural
EXTRADURAL Trauma with skull fracture Biconvex or lentiform Can cross midline, cannot cross suture Usually arterial Can rapidly expand
SUBDURAL
Eldery, atrophic brain with falls tears cortical bridging veins
Biconcave, crescenteric
Does not cross midline, can cross sutures
Usually venous
More mass effect than expected for size
CT blood aging
Hyperacute (< 1hour) - hypodense
Acute (1 hour - 3 days) - hyperdense
Subacute (1 hour - 3 days) - progressively less dense, eventually becoming isodense to brain. Periheral rim enhancement may occur with contrast
Chronic (> 3 weeks) - hypodense
MRI blood aging
Hyperacute <24 hours oxyhaemoglobin/intracellular T1 iso T2 bright
Acute 1-3 days deoxyhaemoglobin/intracellular T1 iso T2 dark
Early subacute >3 days methaemoglobin/intracellular T1 bright, T2 dark
Late sbacute >7 days metheamoglobin/extracellular T1 bright T2 bright
Chronic > 14 days ferritin/haemosiderin/extracelular T1/T2 dark peripherally, center may be T2 bright
Subarrachnoid Haemorrhage
SEQUALE
Hydrocephalus early, vasospasm 7-10 days, superficial siderosis late
Trauma most common cause. FLAIR most sensitive sequence however note that supplemental oxygen can give a SAH appearance on FLAIR
ATRAUMATIC
Ruptured aneurysm
Benign perimesencephalic haemorrhage which is non aneurysmal venous bleed anterior to brainstem
Superficial siderosis is side effect of repeated SAH. Haemosiderin staining on surface of brain. Low signal GRE. Sensorineural hearing loss and ataxia
PSEUDOSUBARRACHNOID
Diffuse cerebral oedema, most commonly anoxic brain injury from near drowning or suicide attempt via hanging
Diffuse edema lowers attenuation of brain. Compression/collapse subarrachnoid spaces gives them hyperdense appearance.
Intraparenchymal hamorrhage
HTN
Basal ganglia, pons, cerebellum. Often have intraventricular extension
AMYLOID ANGIOPATHY
Old dialysis patient. Multiple lobes at diff ages with scattered microbleeds on GRE
SEPTIC EMBOLI
IVDU, transplant, cyanotic heart disease, AIDS, lung AVMs.
Numerous small foci of restricted diffusion. Septic emboli t brain result in abscess and mycotic aneurysm distal MCAs. GW jucntion and basal ganglia. Surrounding oedema and tiny abscess
OTHER
AVMs, vasculitis, tumours and mets
Intraventricular haemorrhage
Trauma, tumour HTN, AVMs and aneurysm
Epidural/subdural
Post traumatic.
Dural AVFs, high flow AVMs can bleed.
Stroke - watershed ischaemia
Watershed ischaemia favours border zones of different vascular territories.
Classic example would be severe hypotension, severe carotid stenosis.
Watershed infarcts in kid would be MoyaMoya (idiopathic supraclinoid vaso-occlusive disease)
Stroke CT signs
Subacute infarct enhances with no mass effect
Dense MCA
Insular Ribbon (loss normal high density insular cortex from cytotoxic oedema)
Loss of GW interface
Mass effect peaks 3-5 days
Enhancement - starts in 3 days, peaks in 3 weeks, gone by 3 months
FOGGING
Phase in stroke evolution when infarctedbrain looks like normal tissue. 2-3 weeks post infarct. Classically on noncon CT but T2 MRI sequences have similar effect.
Specific strokes
ARTERY OF PERCHERON
V shaped bilateral infarct medial thalamus. Artery of Percheron vascular variant where there is a solitary trunk originating from one of the two PCAs to feed rostral midbrain and both thalami
RECURRENT ARTERY HEUBNER
Caudate infarct. Artery of Heubner is deep branch off proximal ACA. Can get bagged during clipping of ACOM aneurysm
CARDIOEMBOLIC STROKE
Multiple foci of restricted diffusion in multiple vascular territories. AFib or endocarditis
FETAL PCOM
Infarcts in both ant and post circulation same hemisphere
Restricted diffusion
Bacterial abscess CJD Herpes encephalitis Epidermoids Hypercellular brain tumours (classic lymphoma) Acute MS Oxyhaemoglobin and post ictal Artefact
Restricted diffusion with bright FLAIR makes you think hyperacute stroke <6 hour
Haemorrhagic transformation
50% of infarcts with time period 6 hours -4 days
If getting TPA usually within 24 hours
90% tiny specs in grey matter - petechial
10% larger haematoma
At risk are people on antigoagulation, TPA, large embolic strokes, venous infarcts.
TPA patients predictors for HT
Multiple strokes, prox MXA occlusion, >1/3 MCA territory, >6 hours since delayed recanalization, absent collateral
Venous infarct
Secondary to venous occlusion (usually secondary to venus sinus thrombosis or deep cerebral vein thrombsis)
Higher risk for haemorrhagic transformation.
Babies - dehydration
kids - mastoiditis
adults - coagulopathies (protein C and S def) or COCP
Most common at superior sagittal sinus
Non con CT shows dense sinus or filling defect on contrast. Heterogeneous restircted diffusion. Vasogenic edema eventually resulting in stroke and cytotoxic oedema
Stigmata of chronic venous thrombosis include development of dAVF and/or increased CSF pressure from impaired drainage.
ASPECTS
Alberta Stroke Program Early CT Score
Guideline for giving TPA. Start with 10 points and subtract for findings
For MCA only
For acute ischaemia only
Sore of 8 or greater has a good outcome. 7 or less may contraindicate TPA
Aneurysm
Risk factors
Smokers, PCKD, connective tissue diseases, aortic coarctation, NF, FMD and AVMs
Occur at branch points. 90% in anterior circulation with ACom being most common site. Basilar is most common posterior circulation site.
Rupture risk increased with size, posterior location, prior SAH, smoking, history, female
Aneurysm types
SACCULAR
Most common and most common cause of non traumatic SAH. Congenital deficiency in internal elastic lamina and tunica media at branch points
FUSIFORM
Associated with PAN, connective tissue disorders or syphilis. Mostly posterior circulation
PSEUDOANEURYSM
Irregular outpouching in strange/atypical location. May see haematoma next to vessel. Traumatic after penetrating trauma or fracture. Mycotic with history of meningitis, endocarditis or thombophlebitis
BLISTER
broad based at non branching point. Supraclinoid ICA most common. angio often negative.
INFUNDIBULAR
Not true aneurysm, funnel shaped enlargement at origin of PCOM at junction with ICA. Not greater than 3mm
AVM ASSOCIATED
aneurysm on feeding artery to AVM. Higher risk of bleeding than the aneurysm
Aneurysm rupture
> 10mm have 1% risk rupture per year.
7mm rough threshold for treatment
Posterior circulation aneurysms higher rate of rupture per mm size
ACOM - interhemispheric fissure
PCOM - ipsilateral basal cistern
MCA trifurcation - Sylvian fissure
BASILAR TIP - interpeduncularcistern or intraventricular
PICA - posterior fossa or intraventricular
High flow AVM
Most common type of high flow
Congenital malformation
Supratentorial
Most common complication is bleeding 3% annually
Risk increased wit smaller AVM (under higher pressure) and smaller draining veins (cant reduce pressure), perinidal aneurysm, basal ganglia lication
Symptoms headache and seizure
Adjacent brain may be gliotic and atrophic
Has nidus
Dural AVF
Flow rate variable
Spinal AVFs most common - classic history gradual onset LE weakness
Risk of bleeding increased with direct cortical venous drainage
Not congenital -acquired usually from dural venous sinus thrombosis
Symptoms tinnitus if sigmoid sinus involved
No nids
Can be occult on MRI/MRA - need catheter angio if high suspicion
DVA
Variation in normal venous drainage.
Resection bad idea can get venous infarct
Associated with cavernous malformations
Almost never bleed in isolation, usually an associated cavernoma
Caput medusa collection of vessels converging toward large vein. Can have halo of gliosis
Cavernous malformation/Cavernoma
Low flow - WITHOUT intervening normal tissue
Can be induced from radiotherapy
Can ooze blood but not usually large bleed
Single or multiple
If see nearby DVA look for cavernoma
Popcorn like with peripheral rim of haemosiderin on gradient
Capillary telangiectasia
Low flow - WITH intervening normal tissue
Can be radiation induced
Usually dont bleed
Single lesion in pons with brushed or strippled pattern of enhancement
Best seen on gradient
Calcification
PINEAL GLAND
Common in adults, rare in kids. If calcified in kids think germinoma (inside cals) or pineoblastoma (blasted peripheral calcs)
HABENULAR
Curvilinear strucure few mm anterior to pineal body. 1/5 normal adults have calc here. Increased association with scizophrenia
CHOROID PLEXUS
Common in adults
DURAL
Common in adults. If bulky calcs and patient has OKCs think Gorlins
BASAL GANGLIA
Very common with age, favours globus pallidus. Extensive and symmetric = Fahrs disease
CAVERNOMA
Scattered dots or stippled popcorn calcs
AVMs
calcs in tortuous veins or nidus
Calcification in syndromes
TUBEROUS SCLEROSIS
Calcs in subependymal nodules at caudothalamic groove
STURGE WEBER
Tram track gyriform parallel to cerebral folds. Subcortical ischeamie secondary to pial angiomatosis
CONGENITAL CMV
Periventricular calcs. Can have brain atrophy
CONGENITAL TOXO
Basal ganglia calcs and hydrocephalus
NEUROCYSTICERCOSIS
Scattered quiescent calcified cystic remnants
Calcification in tumours
OEGAC
Oligodendroglioma Ependymoma Astrocytoma Glioblastoma Craniopharyngioma
Vasospasm
Vessels dont like to be bathed in blood. Classic timing is 4-14 days after SAH, not immediate. Smooth long segment stenosis. Can lead to stroke.
SAH - more volume more risk.
Also meningitis, PRES, migraine headache
Vascular dissection
Usually penetrating trauma or manipulation.
On MRI, T1 bright intramural blood
Vasculitis
Variety of causes. All look same with segmental areas
PRIMARY CNS
Primary angiitis of the CNS (PACNS)
SECONDARY CNS
Meningitis (bacerial, TB, fungal), septic emboli, sarcoid
SYSTEMIC WITH CNS INVOLVEMENT
PAN (polyarteritis nodosa), temporal arteritis, Wegeners, Takayasu
CNS VASCULITIS FROM SYSTEMIC DISEASE
Cocaine, RA, SLE, Lymes
Moyamoya
Poorly understood. Progressive non-atherosclerotic stenosis of supraclinoid ICA, eventually leading to occlusiin. Progressive enlargement leads to enlargement in basal perforating arteries.
Puff of smoke Watershed distribution In child think sickle cell Associated with NF, prior radiation, Downs Children stroke, adult bleeds
Crossed cerebellar daschisis
Depressed blood flow and metabolism affecting cerebellar hemisphere after a contralateral supratentorial insult (infarct, tumour resection, radiation)
Disruption of corticopontine-cerebellar-pathway
Spinal cord blood supply
ANTERIOR SPINAL ARTERY
Arises as 2 small arteries from termination of vertebrals. Joina round level of foramen magnum
ARTERY OF ADEMKIEWICZ
Most notable reinforcer of ant spin art. 75% comes off left aorta between T8-11. Supplies lower 2/3 cord. Gets covered with EVAR leading to spinal infarct.
POSTERIOR SPINAL ARTERY
Paired arteries either from vertebrals or PICA. Discontinuous and reinforced by multiple segmental or radiculopial branches
Conus
Terminates around L1. Below inferior endplate L2/3 shold think tethered cord
Epidural fat
Not evenly distributed. Epidural space predominantly filled with venous plexus. In lumbar spine there is fat pre and post cord.
EPidural lipomatosis is hypertrophy of this fat only occurs in patients on corticosteroids
Spinal stenosis
Can be congenital with shprt pedicles or acquired. Torg-Pavlov ration can be used to call it (<0.85).
Symptomatic stenosis more common in C spine
Degenerative change
SPONDYLOSIS DEFORMANS
Normal aging. Spine OA. Rim or margin centred characterised by osteophyte formation
INTERVERTEBRAL OSTEOCHONDROSIS
Pathologic but not necessarily symptomatic. Deteriorated disc. More centred in disc space as opposed to spondylosis. Favours nucleus pulposus and vertebral body endpates.
Osteophyte vs syndesmophyte
OSTEOPHYTE
More horizontal with claw like appearance. Seen in DJD/spondylosis
SYNDESMOPHYTE
More vertical and symmetrical. Ossification of anulus fibrosis. Seen in ank spond
Endplate MODIC changes
TYPE 1
Edema. T1 dark, T2 bright
TYPE 2
Fat. T1 bright, T2 bright
TYPE 3
Scar. T1 dark, T2 dark.
Annular Fissure
As disc ages it dries out and becomes friable and easily torn. Tears in annulus referred to as fissures as they are very common. Fissures can be asymptomatic and part of aging.
HIGH INTENSITY ZONE
Fluid signal gap in annuus
Annular fissures may be source of pain but are also incidental
Fissures in all degenerative discs but not all are visualized as HIZs
Random
SCHMORL NODE
Intravertebral herniation. Herniation of disc material through defect in vertebral body endplate. Common, 75 people. Favours inferior endplate, chronic may have sclerotic rim
SCHEURMANNS
Multiple levels of wedged vertebral bodies with schmorls nodes. Thoracic spine of teenager common resulting in kyphosis. 25% patients have scoliosis
LIMBUS VERTEBRA
Fracture mimic as result of herniated disc material between nonfused apophysis and adjacent vertebral body
Disc nomenclature
HERNIATION
Less than 25% of disc material beyond limits of disc space
BULGE
More than 25% of disc material beyond limits of disc space
PROTRUSION
Herniation base is wider than tall
EXTRUSION
Herniation taller than wide (small neck)
SEQUESTRATION
Free fragment
Can be central, subarticular, foraminal, extraforaminal (far lateral)
Conjoined nerve root
Asymmetry of anterolateral corner of dural sac on axial T1. Nerve root absent one level then duplicated above/below.
2 nerve roots arise from single dural sleeve. Most common developmental anomaly of the nerve root.
Surgical significane due to mobility of anomalous nerve roots and issues related to localization. Can be a source of FBSS (failed back surgery syndrome)
LP
CONTRAINDICATIONS
Increased intracranial pressure or obstructed CSF flow.
Bleeding diathesis (hypocoagulability)
Iodine contrast allergy if under fluro
overlying infection, haematoma or scarring
Blood patch and post dural puncture headache PDPH
Miniscule defect in thecal sac can cause CSF leak and intracranial hypotension and PDPH.
PDPH
Classic PDPH are bilateral, better laying down, worse when coughing or straining. start 24 hours after usually. Usually wait 72 hours before attempting patch
BLOOD PATCH
inject 3-20ml of patients own blood into epidural space near original puncture site in hope of sealing hole
Failed back surgery syndrome FBSS
Recurrent or residual lower back pain after disc surgery. Occurs about 40% time.
recurrent disc disease - will lack enhancement
epidural fibrosis - scar usually posterior will enhance
arachnoiditis - clumped nerve roots, empty thecal sac
Spinal AVF/AVMs
TYPE 1
By far most common 85%. DUral AVF. Fistula between radiculomedullary arteries and radiculomedullary vein/coronal sinus with dural nerve sleeve. Most common location thoracic spine. Gold standard angiography
TYPE 2
Intramedllary nidus from ant spin or post spin artery. Can have aneurysms and can bleed. Most common presentation is SAH. Associated with HHT and KTS and other vascular syndromes
TYPE 3
Juvenile, very rare and complex with bad prognosis
TYPE 4
Intradural perimedullary. Occur near conus
Foix Alajouanine syndrome
Congestive myelopathy associated with dural AVF. Classic is 45yo male with lower extremity weakness and sensory deficits.
Increased T2 signal with associated prominent vessels. Pathology is venous HTN secondary to vascular malformation.
Vascular malformation flow voids are punctate, serpentine and serpigenous.
Swollen high signal cord with serpentine flow voids along surface of cord.
Syrinx
aka hold in the cord
Syringomyelia not lined by ependyma, hydromyelia is lined by ependyma
90% congenital and associated with Chiari, Dandy Walker, Klippel Feil and myelomeningocoeles. Other 10% acquird by trauma, tumour or vascular insufficiency
If there is perfectly central mid cord high signal dilatation surrounded by normal appearing cord can call it central cord dilattion. If surrounding cord looks sick can use myelopathic change.
Spinal cord infarct
Most common idiopathic although in MCQ probably treating aneurysm with stent graft or embolizing bronchial artery.This will result in anterior spinal infarct
Owls eye appearance of anterior spinal cord
usually long segment more than 2 vertebral body levels
Demyelinating
MULTIPLE SCLEROSIS
Multiple lesions over space and time. Spine lesions short segment and affect part of cord. Cervical cord most common. Can enhance when acute
TRANSVERSE MYELITIS
Focal inflammation of cord. Multiple causes infectious/post vaccine/SLE/Sjogrens/AVMs. 2/3 cross sectional area involved
ADEM
Acute demyelinating encephalmomyelitis. After viral illness or infection in child/young adult. Favours dorsal white matter. Usually brain lesions
Demyelinating cont
NMO
Neuromyelitis Optica. Devics disease. monophasic or relapsing and favours optic nerves and cervical cord. Longer segment than MS and involves full transverse diameter of cord
SACD
Sbacute combined degeneration of the cord. Vitamin B12 deficiency. Bilaeral symmetric increased T2signal in dorsal columns without enhancement.
HIV VACUOLAR MYELOPATHY
Most common spinal cord dysfunction in untreated AIDS.. Late finding. Atrophy most common finding and in thoracic cord. Similar appearance to SACD
Arachnoiditis INFLAM/INFECT
Inflammation of subarrachnoid space. Infectious or post surgical. 10-15% time after spinal surgery and can be a cause of pain or FBSS.
Empty thecal sac sign - nerve roots adherent peripherally
Central nerve root clumping - range in severity from a few nerve roots to all fused in single central scarred band
Guillian Barre Syndrome INFLAM/INFECT
Acute inflammatory demyelinating polyeuropathy AIDP. Autoimmune disorder causing ascending flacid paralysis. Campylobacter but can also be after surgery or in patients with lymphoma or SLE Enhancement of nerve roots of cauda equina, anterior more than posterior
facial nerve most common cranial nerve affected
Chronic Inflammatory Demyelinating Polyneuropathy INFLAM/INFECT
Chronic counterpart to GBS. Gradual and protracted weakness. GBS improves in 8 weeks, this doesnt.
Thickened enhancing ‘onion bulb’ nerve roots.
Intramedullary
ASTROCYTOMA
Most common in paeds. Upper T spine. Fusiform dilatatio of cord over multiple levels. Eccentric, dark T1, bright T2 and enhance. Associated with syrinx
EPENDYMOMA
Most common tumour of lower cord and conus/filum. Most common intramedullary in adult. Myxopapillary form is in conus.Can be haemorrhagic and have dark cap on T2. Long segment. Can have tumoural cyst.
HEMANGIOBLASTOMA
VHL. T spine favoured. Wide cord with onsiderable oedema. May have adjacent meningeal varicosities
INTRAMEDULLARY METS
Rare but will probably be lung
VHL
Phaeochromocytomas CNS hemangioblastoma Endolymphatic sac tumour pancreatic Cyst Pancreatic islet cell tumours Clear cell RCC
Extramedullary Intradural
SCHWANNOMA
Most common extramedullary intradural. Benign solitary, usually from dorsal nerve roots. Multiple in NF2 and Carney complex. Dumbbell skinny handle intraforaminal component. T1 dark, T2 bright and ehance. May have central necrosis/haemorrhage
NEUROFIBROMA
Benign nerve tumour. 2 types solitary and plexiform. Plexiform is multilivel bulky enlargement that is pathognomonic for NF1. Lifetime risk for malignant degeneration is 5-10%. Rapid growth think malignant degeneration. Target sign with T2 bright rim and T2 dark centre.
MENINGIOMA
Adhere to but do not originate from dura. More common in women. Favour posterolateral thoracic spine and anterior cervical spine. Enhance. Can have calcs
DROP METS
Zuckerguss when coating nerve root. Medulloblastoma is most common to drop mets. Breast most common systemic followed by lung and melanoma.
EXTRADURAL
VERTEBRAL HEMANGIOMA
Very common. jail bar/cordouroy. T1 and T2 bright
OSTEOID OSTEOMA
Involve posterior elements, rare after 30. Nidus with surrounding sclerosis. Night pain improved with aspirin. Can radioablate. if over 2cm osteoblastoma
ANEURYSMAL BONE CYST
Posterior elements in kids. Expansile with fluid fluid levels. Can be big and look aggressive (can be confused with telangiectacic osteosarcoma)
GIANT CELL TUMOUR
Common in sacrum, nowhere else in spine. Lytic expansile lesion in sacrum with no rim of sclerosis
CHORDOMA
Most common in sacrum then clivus. If in vertebral bodies they are mroe aggressive and cover two levels with the intervening disc
LEUKAEMIA
Loss of normal fatty marrow. T1 dark
METS
Prostate, breast, lung, lymphoma and myeloma. Multiple lesions low T1
VERTEBRA PLANA
Pancake flat vertebral body. EG in kid, mets/myeloma in adult
