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1
Q

Solitary acute intracranial haemorrhage

A
  1. Intracerebral: hypertension (BG, Pons, cerebellum), cerebral amyloid angiopathy (lobar location, peripheral), haemorrhaging lesion (including infarct), traumatic
  2. Subarachnoid
  3. Subdural: elderly, also intracranial hypotension, dAVF
  4. Extradural: traumatic, arterial
  5. Intraventricular: extension from SAH or ICB. If isolated, may be due to subependymal vein rupture
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2
Q

Subarachnoid haemorrhage
-needs angiogram if no hx of trauma
Beware of pseudosubarachnoid and polycythaemia

A
  1. Trauma
  2. Intracranial aneurysm *blood in basal cistern
    - Posterior fossa: PICA aneurysm or spinal AVM
    - Sylvia’s fissure: MCA aneurysm
    - Interhemispheric fissure: ACOM aneurysm
  3. AV shunt: AVM or AVF
  4. Vasculopathy: RCVS, cerebral amyloid angiopathy, vasculitis
  5. Venous thrombosis: look for venous hyperdensity/expnsion
  6. Perimecencephalic: basal cistern around midbrain +/- pons
  7. Iatrogenic: post LP/surgery
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3
Q

Multifocal acute intracerebral haemorrhage

A
  1. Trauma: contusion, haemorrhaging shear injury (ie diffuse axonal injury located at GWM junction, corpus callosum, brainstem)
  2. Septic embolism
  3. Haemorrhaging neoplastic lesions eg: leukaemia
  4. Coagulopathy: horizontal blood-blood level suggestive
  5. Venous sinus thrombosis
  6. Vasculopathy: drugs, PRES, amyloid, RCVS
  7. Multiple cavernoma: young male, syndromic, rare
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4
Q

Microhaemorrhage on MRI
-<5mm foci of signal loss on blood sensitive MRI sequences (susceptibility-weighted imaging SWI/T2*) not due to calcification or flow voids)

A
  1. Acute trauma
  2. Hypertensive vasculopathy
  3. Cerebral amyloid angiopathy (cortical/subcortical, usually spares BG)
  4. Cavernoma
  5. Venous thrombosis/congestion
  6. Radiotherapy (Induced capillary telangiectasis)
  7. Cerebral vasculitis @ GWMJ
  8. Septic emboli
  9. Haemorrhaging met
  10. Sickle cell anaemia and beta thalassaemia (cerebral fat embolism from bone marrow infarct, seen in cerebral and cerebellum WM and corpus callosum)
  11. CADASIL: symmetrical multifocal WM hyperintensity in frontal and anterior temporal lobes + external capsule
  12. PRES: parietooccipital & superior frontal Gerald predominance
  13. Fat/air embolism
  14. Drugs eg: cocaine
  15. Critical illness-associated: hypoxaemia, high altitude, disseminated intramuscular coagulation
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5
Q

Superficial siderosis

-curvilinear low signal coating leptomeningeal on SWI/T2*

A

Classical: involves infratentorial region, spinal cord

  • Clinical triad of sensorineural hearing loss, ataxia, pyramidal weakness
  • Toxin effect of iron on neuron, from chronic recurrent low volume SAH
  1. Dural defect:
    - intracranial or spinal from previous trauma/surgery
    - seen as extra-arachnoid CSF collection or psuedomeningocoele
  2. Dural ectasia: Marfan
  3. CNS tumour
  4. Vascular malformation

Cortical: involves supratentorial compartment (may extend to infratentorial)

  1. Previous SAH
  2. Cerebral amyloid angiopathy: pt > 60yo, intracerebral microhaemorrhage may also be present
  3. RCVS: <60yo, associated with pregnancy and certain drugs
  4. Cerebral vasculitis
  5. Hyperperfusion syndrome: after revascularisation
  6. Infective endocarditis
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6
Q

Mimics of superficial siderosis

A
  1. Acute SAH
  2. Sequelae of cerebral infarction: petechial haemorrhage, laminar cortical necrosis (centred in cortex not subarachnoid space)
  3. Cortical vein thrombosis
  4. Cortical calcification eg: Sturge-Weber syndrome
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7
Q

Hydrocephalus
-commensurate enlargement of temporal horns, ventricles disproportionately enlarged compared to sulci, blunted third ventricle recesses, evidence of periventricular CSF transduction

A

(A) CSF overproduction
1. Choroid plexus tumour eg: papilloma, carcinoma

(B) Communicating

  1. Post-haemorrhagic
  2. Bacterial meningitis - may result in small cortical infarct
  3. Leptomeningeal carcinomatosis
  4. Idiopathic normal pressure hydrocephalus: narrowed callosal angle, crowding of gyro at vertex, widened Sylvian fissure (dementia, urinary incontinence, gait apraxia)
  5. Increased venous pressure from obstruction or vein of Galen malformation
  6. Vestibular schwannoma (due to increased CSF protein impairing CSF absorption)

(C)Obstructive:
(I) Any level:
1. haemorrhage
2. intraventricular tumour
3. ventriculitis: complication of meningitis, surgery, haemorrhage. Subtle ependymal enhancement and dependent sediment in lateral ventricles + restrict on DWI
4. neurocysticercosis: cyst best seen on steady state gradient echo sequences eg: FIESTA

(II) Foramen of Monro: dilated lateral ventricles, normal 3rd and 4th ventricle

  1. any cause of significant midline shift (compresses ipsilateral lateral ventricle and obstructs contralateral lateral ventricle)
  2. Colloid cyst: anterior roof of 3rd ventricle
  3. Subependymal giant cell astrocytoma: young pt with tuberous sclerosis, typically within lateral ventricle near foramen of Monro, avid enhancing, often calcified

(III) Cerebral aqueduct: dilated lateral & third ventricle, normal 4th ventricle

  1. Aqueduct stenosis: congenital, beak like appearance of aqueduct
  2. Textual plate glioma: typical in children or adolescent. Diffuse enlargement and T2 hyperintensity of textual plate. No enhancement as low grade
  3. Pineal region tumour

(IV) Fourth ventricle

  1. Any posterior fossa mass
  2. Chiari 1 malformation
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8
Q

Intracranial calcification

A

(A) Physiological: choroid plexus, basal ganglia, pineal, dural/falx

(B) Deep grey matter:

  1. Primary aka Fahr disease, familial, AD, symmetrical BG > thalami > cerebellum dentate nuclei > WM
  2. Endocrine: hyper- and hypoparathyroidism
  3. Inherited: Down’s mitochondrial disorder
  4. SLE: related to micro angiopathy b/g of volume loss and WM lesions
  5. Toxin: lead, carbon monoxide
  6. Posttherapeutic: eg: post chemoradiotherapy

(C) Ependymal/periventricular

  1. Tuberous sclerosis: calcified subependymal nodules (hamartoma), cortical tubers, transmantle WM dysplasia
  2. Perinatal TORCH infection: toxoplasma, rubella, CMV, HSV

(D) Gyriform

  • Sturge-Weber syndrome: unilateral associated with cerebral atrophy. Retinal enhancement, ipsilateral choroid plexus enlargement
    2. Post-infarct: due to cortical laminar necrosis
    3. CEC syndrome: rare, occipital calcification in pt with seizure & coeliac disease

(E) Focal lesions with calcification

  1. Tumour: meningioma, oligodendroglioma, craniopharyngioma (suprasellar), dermoid (contain fat), ependymoma (4th ventricle), central neurocytoma (septum pellucidum), pineal region tumour, metastasis
  2. Infection: neurocysticercosis, tuberculosis, perinatal TORCH infection
  3. Vascular: atherosclerosis, AVM, aneurysm, cavernoma
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9
Q

Solitary intracerebral mass

A

(A) Infiltrative, ill-defined

  1. Primary tumour:
    - diffuse glioma or gliomatosis cerebra if >3 lobe involved
  2. Celebrities/encephalitis
  3. Infarct (arterial or venous - greater oedema and risk of parenchyma haemorrhage)
  4. Demyelination: neuromyelitis optica (NMO), Behcet’s
  5. Contusion

(B) Discrete, well-defined

  1. Haematoma
  2. Metastasis: considerable oedema in WM, GWMJ
  3. Primary tumour: high grade glioma, discrete enhancement with central necrosis (glioblastoma), typically centred on WM (cf met), may infiltrate or cross corpus callosum. Versus lymphoma (often more homogenous enhancement, no central necrosis)
  4. Abscess: thin enhancement rim, thicker superficially and thinner at ventricular surface, may point towards ventricle/rupture into ventricle causing ventriculitis/hydrocephalus. Dual rim sign on SWI
  5. Carvenoma: complete haemosiderin rim and central mixed popcorn component on MRI
  6. Tumefactive demyelination: incomplete rim enhancement, younger group (aka monofocal acute inflammatory demyelination - MAID)
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10
Q

Solitary hyper dense intracranial lesion on unenhanced CT

A

Hypercellular mass: lymphoma (periventricular location), metastasis, medulloblastoma (cerebellum), germinoma (young, pineal/suprasellar)

Lesion containing blood/ protein: acute haematoma, haemorrhaging tumour (eg: met, melanoma, glioblastoma, pituitary adenoma with apoplexy), colloid cyst (anterior roof of 3rd ventricle), cavernoma, AVM

Lesion containing calcification

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11
Q

Intrinsic cortical mass

A
  1. Acute cortical infarction
  2. Acute celebrities/encephalitis
  3. Metastasis
  4. Neuronal-glial & glial tumour:
    - Oligodendroglioma: middle age, cortical/subcortical mass, well or ill-defined, often calcified. Heterogenous T2 signal/enhancement. No restricted diffusion
    - DNET Dysembroyoplastic Neuroepithelial Tumour: benign, slow growing, may scallop skull. Well defined T2 bright cortical mass (bubbly), partial FLAIR suppression & hyperintense rim. No oedema, diffusion restriction or enhancement). Associated with focal cortical dysplasia
  5. Focal cortical dysplasia: focal cortical thickening with blurring of GWMJ + T2 hyperintensity of the involved cortex, subcortical WM
    - Ganglioglioma: cystic mass with enhancing mural nodule. No oedema. Calcification common
    - Pleomorphic xanthoastrocytoma (PXA): similar to ganglioglioma but no calcification. Associated with reactive dural thickening mimicking a dural tail
  6. Cortical tubers: FLAIR and T2 bright cortical/juxtacortical lesion found in tuberous sclerosis
  7. Cavernoma
  8. Haematoma
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12
Q

Posterior fossa mass

A
  1. Met (most common infratentorial lesion)
  2. Haemangioblastoma (typically cerebellar hemisphere cystic tumour, avid enhancing solid mural nodule abutting the Pia mater with a nonenhancing cyst wall. Associated with vHL. No calcification
  3. Astrocytoma
    - Pilocytic: child/young adult. Cyst with mural nodule & enhancing cyst wall
    - Glioblastoma: older adults. Heterogenous ill-defined mass with irregular intrinsic enhancement
  4. Ependymoma: child/young adult, floor of 4th ventricle with plastic like extension through ventricular foramen a. Heterogenous calcified cystic. Associated w NF2
  5. Subependymoma: older. 4th > lateral ventricle. No enhancement
  6. Epidermoid: CT, T1, T2 indistinguishable from CSF, but hyperintense on DWI with incomplete suppression of signal on FLAIR
  7. Dermoid: well defined midline mass with fat and calcification. No enhancement
  8. Abscess
  9. Haematoma/cavernoma
  10. Diffuse midline glioma: child/young adult, pontine
  11. Hamartoma: Lhermitte-Duclos disease. Thickened, striated appearance of usually one cerebellar hemisphere with T2 hyperintensity. No enhancement. Associated with Cowden syndrome
  12. Rosette-forming glioneuronal tumour: young adult, typically midline at posterior aspect of 4th ventricle + local parenchyma invasion, mixed solid cystic
  13. Any cerebellopontine angle mass
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13
Q

Solitary ring enhancing lesion

A

(A) Infection

  1. Pyogenic abscess: thin regular enhancing capsule
  2. Tuberculoma: uniformly round with adjacent leptomeningeal enhancement and characteristic central low T2 signal. Look for associated basal leptomeningitis & hydrocephalus
  3. Toxoplasmosis: usually multiple
  4. Neurocysticercosis: usually multiple

(B) Neoplastic

  1. Met: central necrosis with thick, irregular, nodular rim enhancement, no intrinsic restricted diffusion
  2. Glioblastoma: centred on WM (indistinguishable from a single metastasis)
  3. Ganglioglioma/cytoma: child/young adult. Temporal lobe, calcified, slow growing +/- bone remodelling, no perilesional oedema (cf met, GBM)

(C) Inflammatory

  1. Demyelination: incomplete rim enhancement
  2. Radiation necrosis: month to year post radiotherapy. Heterogenous (linear, nodular, cortical) pattern of contrast enhancement in radiation field. Mimic recurrence but does not show increased CBV on perfusion
  3. Sarcoidosis: often coexist dural/cranial nerve disease
  4. PML-IRIS

(D) Vascular/trauma

  1. Subacute haematoma: signal drop out SWI/T2*
  2. Subacute infarct: rim or gyriform pattern of enhancement
  3. Thrombosed or inflammatory aneurysm
  4. Contusion
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14
Q

Multiple ring enhancing lesion

A

(A) Infection

  1. Abscess
  2. Septic emboli: check for arteritis, mycotic aneurysm
  3. Tuberculoma
  4. Toxoplasmosis: BG, GWMJ, concentric alternating low and high T2 signal, eccentric ‘target sign’ enhancement
  5. Neurocysticercosis: cyst in subarachnoid space/parenchyma

(B) Neoplastic:

  1. Met
  2. Multifocal glioma: lesions connected by abnormal T2 signal and conform to path of WM tracts
  3. Lymphoma: solid enhancement, may have atypical ring enhancement in immunocompromised or post-steroid tx pt. Tends to be fewer in number in subependymal distribution

(C) Inflammatory:

  1. Demyelination: open ring pattern incomplete to Gerald surface
  2. Radiation necrosis
  3. PML-IRIS

(D) Vascular/trauma: contusion/haematoma

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15
Q

Intracranial cyst with mural nodule

A

(A) Neoplastic

  1. Haemangioblastoma
  2. Pilocystic astrocytoma
  3. Cystic met (adenocarcinoma, SCC, thick irregular wall +/- haemorrhage)
  4. Pleomorphic xanthoastrocytoma (young, temporal lobe)
  5. Craniopharyngioma (multilocular cystic lesion, suprasellar region with variable calcification & high T1 signal)
  6. Ganglioglioma
  7. Rosette-forming glioneuronal tumour
  8. Pineocytoma

(B) Infection
1. Neurocysticercosis

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16
Q

Enhancing lesions in perivascular spaces

A
  1. Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroid (CLIPPERS): characteristic punctate & linear enhancement in pons with minimal oedema/mass effect.
  2. Neurosarcoid: abnormal thickening & enhancement of dura, cranial nerves, pituitary stalk
  3. Vasculitis: arteritis with stenoses, beading, infarct
  4. Lymphoma: elderly, fluctuating area of T2 & diffusion abnormality, surrounding mass-like enhancement
  5. Lymphomatoid granulomatosis: immunocompromised pt, multifocal periventricular linear T2 hyperintensity + enhancement
  6. Behcet’s : young, orogenital ulcer. Brainstem & deep ganglionic structure, oedema, mass effect
  7. Langerhans cell histocytosis: children, young adult, diabetes insipidus
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17
Q

Meningeal enhancement

-some degree of dural enhancement is normal seen at the falx, tentorium, carvenous sinus

A
  1. Dural enhancement seen on contiguous coronal slices
  2. Rim enhancement anteriorly capping the brainstem
  3. Abnormal cranial nerve enhancement or thickening
  4. Presence of coexistent FLAIR sulcal hyperintensity
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18
Q

Meningeal enhancement - Pachymeningeal (Dura-Arachnoid)

A
  1. Post-op (site of craniotomy, unilateral, thin, smooth)
  2. Intracranial hypotension (bilateral smooth thin. Associated with subdural effusion, convex dural venous sinuses, bulky pituitary from negative pressure pull)
  3. Infection (irregular thick) adjacent OM, sinusitis
  4. Neoplastic
    - Meningioma: reactive tapering dural thickening around lesion (dural tail)
    - Met: smooth or nodular enhancement
    - Secondary CNS lymphoma: meningeal > parenchyma involvement
    - Solitary fibrous tumour of dura: similar appearance to meningioma, lower T2 signal + internal flow void + higher propensity for skull invasion. No calcification or hyperostosis
  5. Granulomatous disease (multifocal nodular, thick enhancement) (TB, sarcoidosis, Wegner’s, rheumatoid, Sjogren, Behcet, Erdheim-Chester, syphilis, fungal)
  6. Extramedullary haematopoiesis (rare, seen in thalassemia, myelofibrosis) (associated with widened diploid space)
  7. Idiopathic hypertrophic cranial pachymeningitis (mass-like thickening of the dura, cranial nerve involvement, IgG2-related)
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19
Q

Meningeal enhancement - Leptomeningeal (Pia-Arachnoid)

-look for subtle cranial nerve enhancement

A
  1. Carcinomatosis (nodular)
  2. Meningoencephalitis (cerebral swelling)
  3. Granulomatous disease
  4. Vascular (collateral flow in ischaemia, increased flow eg: dural fistula, pail angioma)
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20
Q

Ependymal enhancement

A
  1. Infection (early sign of ventriculitis)
  2. Neoplastic (Nodular/linear: lymphoma, glioblastoma, ependymoma, germ cell tumour, met) (Mass-like: ependymoma, giant cell astrocytoma)
  3. Granulomatous: TB (basal meningitis), sarcoidosis (cranial nerves, dura)
  4. Intraventricular haemorrhage
  5. Subependymal venous congestion (mimic enhancement) (deep cerebral vein thrombosis, AVM/AVF, Sturge-Weber: cortical calcification, cerebral atrophy, enlarged ipsilateral choroid plexus)
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21
Q

Cranial nerve enhancement - Rules

A
  1. Cisternal and carvenous sinus CN enhancement always abnormal
  2. CN 7 enhancement is abnormal in cisternal, meatal, extracranial segment. (Venous plexus causes normal enhancement in labyrinthe, they panic, mastoid segments)
  3. CN 2: not a true nerve but CNS WM tract. Enhancement may indicate demyelination, glioma
  4. Multiple nerves: met, leukaemia, lymphoma, NF2, Lyme disease, chronic inflammatory demyelinating polyneuropathy
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22
Q

Cranial nerve enhancement

A

(A) Neoplastic
1. Schwannoma: CN 8, sporadic or NF2
2. Meningioma: ‘tram-track’ enhancement, CN 2
3. Neurofibroma: rarer to involve CN, T2 hyperintense rim with central low signal (target sign). NF1: plexiform neurofibromas of CN 8 and CN 5
4. Optic nerve glioma: pilocytic astrocytoma associated with NF1
5. Leptomeningeal dissemination: nodular
6. Perineural spread
(B) Infection
1. Meningitis: viral (CN 7), TB (surrounding exudate), cryptococcus neoformans (around optic react, nerve, chiasm)
2. Lyme disease: CN 3 - 7
3. Fungal: aspergillosis, mucormycosis, actinomycosis
(C) Inflammatory
1. Bell’s palsy: uniform enhancement of CN 7
2. Miler-Fisher syndrome: variant of Gillian-Barre multiple CN, linear enhancement
3. Chronic inflammatory demyelinating polyneuropathy: ‘onion-bulb’ thickening of multiple peripheral & cranial nerves with diffuse enhancement
4. Demyelinating: MS, NMO, optic neuritis
(D) Granulomatous
1. Sarcoidosis: any CN thickening, most commonly CN 2 centred around chiasm & pituitary stalk
2. Wegner’s granulomatosis: spread from sinuses, associated with dural thickening, vasculitis with infarct
3. Tolosa-Hunt: idiopathic inflammation of carvenous sinus & orbital apex (enlarged carvenous sinus with ICA narrowing & enhancement of CN within)
(E) Other
1. Post-radiation neuritis
2. Ischaemic: CN 2, 3, 6

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23
Q

Enlarged leptomeningeal perforator

A
  1. Collateralisation due to proximal progressive steno-occlusive disease
    - Moyamoya disease: idiopathic, progressive occlusion. ‘Puff of smoke’ & ‘Ivy sign’ pial collateral serpentine sulcal FLAIR hyperintensity & enhancement
    - Moyamoya-like syndrome: mimics eg: post radiation, NF1, Down’s syndrome, SCD, atherosclerosis
  2. Secondary to a distal ‘sump’ effect
    - AVM (multiple dilated vessel, no stenoses)
    - Tumour
  3. Sturge-Weber (facial cutaneous & leptomeningeal haemangioma, steal phenomenon causes atrophy of subject cortex & WM + tram-track calcification)
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24
Q

WM lesions with little mass effect - Punctate lesions

A
  1. Nonspecific & age-related: small peripheral lesion sparing subcortical U fibre (SUF). 1 lesion per decade
  2. Vascular:
    - Small vessel disease (SVD): punctate confluent. Periventricular WM lesions (>3mm from surface) & deep WM lesions. Spare corpus callosum & SUF
    - Hypertensive encephalopathy: ganglionic lacunar infarct & microhaemorrhage. Interrelated with SVD
    - Multi-infarct encephalopathy: SVD + additional emboli cortical & pontine infarct
    - Cerebral amyloid angiopathy
  3. Inflammatory:
    - MS: perivenous distribution, periventricular contacting surface, infratentorial, cortical/juxtacortical with involvement of SCUF. Involves corpus callosum at callososeptal interface. Incomplete ring enhancement. Short segment spinal cord lesions
    - NMO neuromyelitis optica: indistinct/fluffy lesions. Periaqueductal grey matter & area postrema (posterior medulla abutting 4th ventricle) + optic neuritis. Long segment spinal cord lesion
    - Vasculitis: multiple infarcts, bilateral, different vascular territory
    - Sarcoidosis
    - Connective tissue disease: can be indistinguishable from MS
  4. Military metastases: often @ GWMJ. greater mass effect and perilesional oedema. Rarely has callosal involvement
  5. Infection: granuloma, septic emboli +/- punctate restricted diffusion, microhaemorrhage, complete ring enhancement
  6. Diffuse axonal injury: shear-related injuries, microhaemorrhage, GWMJ, splenium, middle cerebellar peduncle
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25
Q

WM lesions with little mass effect - Confluent lesions (up to 20mm in size)

A

(A) Neoplastic
(B) Vascular
(C) Hypotensive cerebral infarct: deep & superficial watershed territories
(D) Infection:
1. Encephalitis: ill-defined, variable enhancement & restricted diffusion
-HSV = medial temporal lobes
-non-herpes = BG, thalamus, brainstem, cerebellum
2. Progressive multifocal leukoencephalopathy (PML)
-immunecompromised pt
-multifocal periventricular & subcortical lesions involving SCUF
-no contrast enhancement
-late cavitation/cystic change
3. PML-IRIS (immune reconstitution inflammatory syndrome) :
-mass effect, irregular enhancement
-paradoxical deterioration in PML due to exaggerated inflammatory reaction after reconstitution of immune system
-classically seen in HIV pt on therapy but recognised with MS immunotherapies
4. Lyme disease: resemble MS but greater abnormalities in BG, brainstem +/- CN involvement
(E) Inflammatory
1. MS, NMO, vasculitis, sarcoidosis
2. Tumefactive demyelination: often univocal, open ring enhancement, low CBV on perfusion, little to no mass effect/oedema. perivenous in distribution
3. Acute disseminated encephalomyelitis (ADEM): monophonic demyelination following infection/vaccination in children/adolescent. Bilateral asymmetrical subcortical lesions, spare calloseptal interface
(F) Osmotic myelinolysis
-Acute demyelination from rapid change in serum osmolality. Typically round or trident shaped lesion in central pons, but can be extrapontine (eg: symmetrical in BG +/- WM)
(G) Radiation necrosis

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26
Q

WM lesions with little mass effect - Diffuse WM lesions (spanning >2 lobes)

A

(A) Vascular
(B) Neoplastic
(C) Inflammatory: MS, NMO, vasculitis, sarcoidosis.
-Rasmussen encephalitis: child/young adult w intractable seizures, chronic encephalitis w patchy ipsilateral WM lesions & volume loss
(D) Leuokoencephalopathies: symmetrical, multifocal lesions. Childhood
1. Inherited:
-CADASIL: recurrent lacunar & subcortical infarct in anterior temporal & frontal lobes
-COL4A1: small vessel disease, dilated perivascular space, microhaemorrhage, intracerebral haemorrhages. SCUF spared
-X-linked adrenoleukodystrophy: adult onset, frontal lobe & genu of corpus callosum involvement predominates (vs child onset which has a predilection for occipitoparietal region)
-Krabbe disease: adult onset phenotype, slower progression. CT: hyperdense thalami, cerebellum & caudate nuclei. Periventricular abnormal WM signal
2. Toxic-metabolic: symmetrical involving splenium + corresponding restricted diffusion
3. HIV encephalopathy: symmetric periventricular & deep WM lesions + volume loss
(E) Degenerative: frontotemporal lobar degeneration & corticobasal degeneration, associated with volume loss
(F) Radiation leukoencephalopathy: diffuse confluent lesions with volume loss & evidence of indication for radiotherapy

27
Q

Corpus callosum lesions

A

(A) Atrophic/dysplastic callosum
1. Agenesis/dysgenesis: agenesis = early insult, dysgenesis = late insult & limited to rostrum or splenium
2. Atrophy: small vessel ischaemia, radiation therapy, leukodystrophy
(B) Multifocal lesions
1. Demyelination: MS, NMO. Lower border of CC at callososeptal interface
2. Vascular: asymmetric, adjacent to midline. Characteristic in Susac syndrome & typically spare the calloseptal interface +/- restricted diffusion & enhancement if acute. Young adult females w B/L sensorineuronal hearing loss & branch retinal artery occlusion
3. DAI: asymmetric involving both midline & borders of CC +/- microhaemorrhage on SWI
4. Marchiafava-Bignami syndrome: chronic alcohol w vitamin B deficiency. Body of CC > genu/splenium. Large lesion in central layer of CC
(C) Neoplasm
1. Butterfly glioma: high grade glioma, symmetrical midline crossing lesion most common in frontal lobes crossing and expanding genu. Heterogenous enhancement + central necrosis
2. Lymphoma: hypercellular, homogenous restricted diffusion & solid enhancement
(D) Transient lesions:
1. Cytotoxic lesions: transient cytotoxic oedema of splenium, well defined, oval, midline, T2 hyperintense + restricted diffusion. No enhancement.
(E) Hydrocephalus-related
1. Corpus callosum impingement syndrome: impingement against falx due to severe chronic hydrocephalus. Abnormal signal + atrophy in rostral CC
2. Post shunt decompression: diffuse oedema in CC occurring after shunt insertion

28
Q

Deep Grey Matter Abnormalities

-BG + thalamus

A

(A) Physiological
1. Age-related: GP calcification -> reduced T2 signal
2. Perivascular space (PVS): CSF signal on all sequences
(B) Vascular
1. Lacunar infarct: well-defined CSF density/intensity lesion + surrounding high signal rim evident on FLAIR
2. Hypertensive haemorrhage: enlarged perivascular space, microhaemorrhage
3. Global hypoxia ischaemic injury: B/L infarcts in region of high metabolic demand: GP, putamen, ventrolateral thalami, perirolandic regions, occipital cortex, hippocampal formation
4. Venous infarction: due to internal cerebral vein thrombosis, bithalamic involvement, marked swelling from venous congestion
5. Central variant PRES: can involve brainstem
(C) Neurodegenerative
1. Parkinson’s: loss of comma shaped taracer uptake in corpus striatum with full-stop shaped uptake only seen in caudate head
2. Multiple system atrophy-Parkinson’s type: reduced putamen volume w reduced T2 signal relative to globus pallidus. High T2 rim surrounding putamen (putamen rim sign)
3. Huntington’s disease: atrophy of caudate heads, ‘boxcar’ frontal horns
(D) Toxin
1. Chronic bilirubin encephalopathy: increased T1 & T2 signal in GP
2. Hypermanganesaemia: in total parenteral nutrition, haemodialysis, liver failure. High T1 signal in BG
3. Exogenous toxin: C.M. = GP, methanol = putamen, cyanide = corpus striatum & perirolandic cortex
(E) Acquired metabolic disease
1. Uraemia encephalopathy: ‘lentiform fork’ sign: T2 hyperintense internal & external capsule
2. Hyperammonaemic/hepatic encephalopathy: T2 hyperintense symmetric insular, thalami, posterior limb of IC
3. Hypoglycaemia: T2 hyperintense & restricted diffusion in BG, PLIC, splenium, parietooccipital cortex
(F) Inherited metabolic disease
1. Wilson’s disease: high T2 & volume loss in striatum & ventrolateral thalamus. ‘ Face of Giant panda’ sign in midbrain & ‘miniature panda’ sign in pons, ‘double panda sign’ if both present
2. Mitochondrial cytopathies: Kearns-Sayre syndrome (GP & cortical calcification) & Leigh syndrome (putamen, thalamus, periaqueductal grey mater)
3. Lipid storage disorder: Krabbe disease
4. Amino acid disorder: selective necrosis of GP
5. Neurodegeneration with bran iron accumulation (NBI)
6. Fahr disease: symmetrical calcification of BG, dentate nuclei, subcortical WM
(G) Infectious
1. Variant CJD: ‘hockey stick’ sign: T2 hyperintensity in pulvinar & dorsomedial thalamus (vs sporadic CJD which spares thalamus)

29
Q

Basal Ganglia Bright on T1

A

(A) Paramagnetic substances:
1. Methaemoglobin: haemorrhages, haemorrhaging necrosis in carbon monoxide or methanol poisoning
2. Copper
3. Manganese
4. Calcification
5. Chronic bilirubin encephalopathy
6. Prior administration of linear gadolinium chelates
(B) Unknown cause
1. Diabetic striatopathy: non-calcific hyperdensity caused by non-ketotic hyperglycaemia
2. Fabry disease: pulvinar T1 hyperintensity (vs CJD with T2 hyperintensity), Associated with posterior circulation infarct
3. NF1: focal areas of signal intensity (FASI), high on T1 and T2 in BG

30
Q

Symmetrical BG susceptibility changes

  • most commonly due to calcification or iron deposition (latter not appreciable on CT as much)
  • starts from GP -> putamina
A

Calcium

Iron: NBIA (nondegeneration with brain iron accumulation)< Huntungton’s disease

31
Q

Bilateral thalami lesions

A

(A) Vascular
1. Artery of Percheron infarct: arise from PCA supplying both paramedical thalami & rostral midbrain
2. Basilar tip thrombosis
3. Internal cerebral venous infarct: look for deep cerebral vein thrombus on CT & MRI loss of T2 flow void. Greater local swelling than arterial infarct. SWI may show serpiginous thrombosed deep medullary veins & associated microhaemorrhage
4. Hypertensive haemorrhage
5. Hypoxia ischaemic encephalopathy
(B) Infection
1. Encephalitis
2. Variant CJD
3. Acute necrotising encephalitis: immune related post viral
(C) Metabolic
1. Carbon monoxide poisoning
2. Wernicke encephalopathy: secondary to thiamine deficiency. Symmetric abnormal signal in thalami, mammillary bodies, textual plate, periaqueductal areas
3. Mitochondrial cytopathies
4. Fabry disease
5. Wilson disease
(D) Neoplastic
1. Bithalamic glioma: low grade astrocytoma in children and young adult. Expansile, often nonenhancing tumour +/- obstructive hydrocephalus

32
Q

Bilateral middle cerebellar peduncle (MCP) lesions

A

(A) Degenerative (40%)
1. MSA-cerebellar type (MSA-C):symmetrical high T2 signal & volume loss in MCP. ‘Hot cross bun’ sign in pons: cross of abnormal signal due to selective degeneration of pontocerebellar tracts
2. Fragile X: lesions in MCP & splenium
(B) Metabolic (20%): Wilson, cirrhotic liver, adrenoleukodystrophy, hypoglycaemia, solvent abuse, heroin inhalation (symmetrical involvement of PLIC & cerebellar WM)
(C) Cerebrovascular (15%)
1. PRES (central variant): typically precipitated by drugs or hypertension
2. Anterior inferior cerebellar artery infarct (AICA): restricted diffusion & signs of vertebral artery occlusion or dissection
(D) Infection/inflammatory (15%): MS, Behcet’s. ADEM, HIV, Japanese encephalitis, PML, PML-IRIS
(E) Neoplastic (10%)
1. Lymphoma
2. Brainstem glioma
3. Meningeal carcinomatosis

33
Q

Intrasellar mass - approach

A
  1. Lesion intrinsic or extrinsic to pituitary gland?
  2. Arising from sella or extending inferiorly from suprasellar?
  3. Slow or fast growing? (?bony remodelling or expansion of sella)
  4. Check for carvenous sinus involvement, optic nerve/chiasm compression or infiltration, obstructive hydrocephalus from compression of 3rd ventricle
  5. Correlate with pituitary function
34
Q

Intrasellar mass - intrinsic to gland

A
  1. Pituitary adenoma: mildly T2 hyperintense & T1 hypointense relative to normal gland
    -Microadenoma < 10mm, delayed enhancement (60s) relative to normal gland
    -Macroadenoma >10mm, suprasellar/carvenous sinus extension, +/- cystic degeneration & high T1 signal from internal haemorrhage or proteinaceous material. Sellar expansion from gradual remodelling
  2. Pituitary hyperplasia: enlarged but normal signal
    -Physiological: pregnancy, post-partum, lactation
    -Pathological: end-organ failure eg: hypothyroidism
  3. Pituitary haemorrhage/infarction
    -associated with macroadenoma
    -blood-fluid level
    -dense intrasellar mass on CT
    -variable signal & diffusion on MRI
    -Apoplexy when haemorrhage/infarct
  4. Intracranial hypotension
    -slightly swollen convex pituitary, often extends just above the sella
  5. Inflammatory hypophysitis: involves anterior and/or posterior pituitary and/or infundibulum. Causing enlargement, avid homogenous enhancement, without sellar remodelling (vs adenoma)
    If posterior pituitary is involved, the normal T1 bright spot is absent
    -Lymphocytic hypophysitis: late pregnancy or postpartum
    -Granulomatous hypophysitis: sarcoidosis, TB, Wegner
    -IgG4-related hypophysitis
  6. Metastasis
    -male = lung
    -female = breast
    -normal fossa size, bony destruction, dural thickening, irregular margin (vs adenoma)
  7. Pituitary abscess
    -rare, cystic lesion + peripheral enhancement
35
Q

Intrasellar mass - extrinsic to gland

A
  1. Meningioma
    - sphenoid, diaphragma sella, or carvenous sinus
    - projects into sella, displacing diaphragma sella inferiorly + enhancing dural tail +/- skull hyperostosis (whereas macroadenoma is sellar expansion/remodelling)
  2. Rathke’s cleft cyst (aka pars intermediate cyst)
    - lies btw anterior and posterior pituitray, <1cm usually, 50% has intracystic nodules. Claw sign of normal displaced pituitary
  3. Craniopharyngioma: purely intrasellar is rare. Usually suprasellar & sellar
36
Q

Pituitary infundibular lesion - Neoplastic

  • normal pituitary stalk = 2mm just above gland, 4mm at level of optic chiasm
  • associated with diabetes insipidus & panhypopituitarism
A
  1. Met
  2. Lymphoma (isolated stalk thickening or periventricular enhancing mass)
  3. Leukaemia (acute/chronic myeloid leukaemia, look for dural & optic nerve sheath deposit)
  4. Germ cell tumour (hyperdense on CT + homogenous solid enhancement & restricted diffusion) (child/young adult, germinoma most common, others: embryonic carcinoma, yolk sac tumour, choriocarcinoma, teratoma & mixed)
  5. Craniopharyngioma:
    - Adamantinomatous (90%): child > adult, 90% cystic, 90% calcified, 90% enhance. Multilocular, large with high T1 (oily) content
    - Papillary (10%): adult, solid enhancing mass. If small water-signal cysts, minimal enhancement. Calcification rare.
  6. Langerhans cell histocytosis: stalk thickening & enhancement +/- meningeal & choroid plexus involvement. Posterior pituitary bright spot absent. Look for lung, bone, skin disease. Child/young
  7. Pituicytoma: enhance homogenously. No sellar enlargement. Benign, men in 40-50s.
  8. Other primary tumours: gliomas, choristoma, tanycytomas (encase COW)
  9. Pituitary adenoma: occasionally arise in infundibular region (pars tuberalis)
37
Q

Pituitary infundibular lesion - Non-Neoplastic

A
  1. Neurosarcoid:
    - enhancing stalk granuloma, often involves adjacent optic pathways & floor of 3rd ventricle
    - check for dural, leptomeningeal, & CN involvement
  2. Lymphocytic infundibuloneurohypophysitis (LINH)
    - variant lymphocytic hypophysitis that predominantly affects infundibulum
  3. Other granulomatous hypophysitis: TB, Wegener’s, Erdheim-Chester, Whipple’s diseases.
  4. Ectopic posterior pituitary:
    - T1 bright spot located on median eminence of hypothalamus +/- pituitary stalk/gland hypoplasia.
    - Look for other midline abnormalities eg: deficient septum pellucidum
  5. Infundibular cyst
38
Q

Suprasellar mass

-overlaps with infundibular mass & pituitary mass with suprasellar extension

A

(A) Meningeal
1. Meningioma
2. Granulomatous
(B) Vascular
1. Saccular aneurysm: may erode into supra or para sellar region if giant (>25mm)
(C) Parenchyma
1. Pituitary
2. Infundibular masses
3. Hypothalamic harmatoma: arise from tuber cinereum. T2 iso/hyperintense to cerebral cortex, no enhancement
4. Germ cell tumour
5. Metastases/lymphoma
(D) Optic chiasm
1. Hypothalamic chiasmatic glioma: pilocytic astrocytoma typically arise from optic nerve/chiasm with variable involvement of hypothalamus. Variable enhancement. Associated with NF1
2. Chiasmal optic neuritis: NMO, MS. High T2 signal & swelling. Signs of demyelinating disease elsewhere
(E) Cisternal:
1. Epidermoid: paramidline cystic lesion, CSF density on CT, T1/T2 signal on MRI. Incomplete suppression on FLAIR & characteristic restricted diffusion enable differentiation from arachnoid cyst
2. Dermoid: midline cystic lesion with fat content & capsular calcification. Look for subarachnoid ‘fat droplets’ to indicate rupture which is associated with chemical meningitis & hydrocephalus
3. Teratoma: multiloculated, heterogenous mixed soft tissue, fat, calcification
4. Lipoma: fat density/signal lesion, calcification rate in suprasellar location
5. Arachnoid cyst: well defined cyst of variable size. Isointense to CSF, nonenhancing, noncalcified

39
Q

Cavenous sinus/parasellar mass

A
  1. Extrinsic from pituitary lesion: pituitary macroadenoma (tumour extension beyond intercarotid line suggestive of invasion) (ICA encased but not typically narrowed) (may invade skull base)
  2. Dural:
    - meningioma: associated with venous congestion, if ICA encased, it is narrowed
    - granulomatous/inflammatory infiltration: sarcoid (dural & nerve deposit), TB, idiopathic orbital inflammatory syndrome (orbital pseudotumour - most commonly involves extraocular muscles with rapid onset unilateral proptosis. Mass is ill-defined, T2 hypointense, due to fibrosis, narrows ICA & extend to superior orbital fissure) vs lymphoma which is more lobular w intermediate T2 signal. Links with IgG4-related disease, Wegner, Churg-Strauss. If involves orbital apex, carvenous sinus + painful ophthalmoplegia = Tolosa-Hunt syndrome
    - defect: meningocoele or encephalocoele. Due to raised ICP, partial empty sella from arachnoid herniation flatenning pituitary, enlarged Meckel’s caves
    - invasive fungal sinusitis: Aspergillus, immunocompromised & diabetic patients. Extends from paranasal sinuses. Hyperdense opacification of paranasal sinus on CT + susceptibility signal dropout on T2 weighted MRI
  3. Carvenous sinus met: haematogenous, direct extension, perineural spread (SCC, adenoid cystic carcinoma)
  4. Neurogenic: Schwannoma (involves CPA, Meckel’s cave, pterygomaxillary fissure, variably solid/cystic, ‘dumbbell’ shaped, avid enhancement w skull base remodelling)
  5. Vascular: carotino-carvenous fistula, aneurysm, carvenous sinus thrombosis, carvenous haemangioma (multilobular, well defined, very T2 bright heterogenous mass, may erode without hyperostosis, gradual filling)
  6. Skull base
    - Chordoma: older male, midline sphenooccipital synchondrosis, well-defined, very bright T2 + septa. Encases vessel without narrowing
    - Chondrosarcoma: osseous erosion with calcified chondroid matrix
    - Myeloma/met/lymphoma: lytic /sclerotic lesion with soft tissue component
40
Q

Optic nerve abnormal signal

-intraocular, intraorbital, intracanalicular (optic nerve sheath adhered to optic canal), prechiasmastic

A
  1. Optic neuritis: T2 hyperintense within optic nerve substance
  2. Optic perineuritis: thickening of optic nerve sheath ‘doughnut sign’ in intraorbital segment with surrounding fat stranding and less/no abnormal signal in optic nerve
  3. Ischaemic optic neuropathy: AION & PION (anterior & posterior)
    - Anterior: intraocular segment/optic nerve head. Associated with papilloedema suggested by flatening/bulging of optic nerve head on MRI. Arteritic (giant cell/temporal arteritis). Non-arteritic (vascular risk factors)
    - Posterior: all segments of optic nerve posterior to intraocular. No papilloedema. Watershed ischaemia due to hypoxia/hypovolaemia. Intracanalicular segment most severely affected due to optic nerve swelling and compartment syndrome within bony canal
  4. Traumatic: direct/indirect (intracanalicular segment most susceptible)
  5. Neoplastic:
    - Optic nerve glioma: rare, child, NF1. Intraorbital most common. Expanded with central isointense to WM signal + perineural high signal due to arachnoid gliomatosis. Variable enhancement, may extend to optic chiasm +/- hypothalamus
    - Optic nerve sheath meningioma: ‘tram-track’ sign, avid enhancing mass surrounding a nonenhancing optic nerve +/- calcification +/- adjacent bony hyperostosis. Adult > child. NF2
    - leukaemia/lymphoma
  6. Extrinsic compression
41
Q

Pineal region mass

A

(A) Pineal gland

  1. Pineal cyst: well defined CSF intensity unilocular cyst, often slightly T1 hyperintense w incomplete FLAIR suppression +/- slight rim enhancement. Rarely haemorrhagic
  2. Pineal germ cell tumour: all tend to engulf normal pineal calcification, associated with CSF seeding. Germinoma (homogenous hyperdense enhancing mass), mixed, teratoma etc all heterogenous enhancing
  3. Pineal parenchyma tumour: tend to disperse pineal calcification
    - Pineocytoma: adults, well defined noninvasive enhancing mass, any nodular enhancement
    - Pineoblastoma: children, large, aggressive, locally invasivem ass with CSF seeding. Hyperdense on CT, heterogenous signal w restricted diffusion. Associated with retinoblastoma

(B) Cystic
1. Pineal cyst: located below internal cerebral vein
2. Calum velum interpositum: enlarged CSF space behind foramen Monro, beneath column of cornices, above internal cerebral veins
3. Cyst of velum interpositum: when CVI > 1cm in axial dimension w convex bowed margins and mass effect
(C) Posterior brainstem
1. Tectal glioma: low grade astrocytoma in childhood, expands tectal plate, cause hydrocephalus
2. Infarct
3. Metastasis: heterogenous enhancement + vasogenic oedema
4. Demyelination

(D) Vascular lesions

  1. Vein of Galen malformation
  2. Internal cerebral vein thrombosis

(E) Other
1. Meningioma

42
Q

Intraventricular mass in adult

A

(A) Choroid plexus lesion

  1. Xanthogranuloma: degenerative cyst in elderly. Hyperintense on T1, FLAIR, DWI due to protein, lipid, blood product
  2. Cyst
  3. Papilloma: lobulated, frond-like avid enhancing intraventricular mass w hydrocephalus
  4. Carcinoma: child, heterogenous enhancement, ceros is, calcification, local parenchyma invasion
  5. Met

(B) Tumour of ventricular wall

  1. Central neurocytoma: young adult, arises from septum pellucidum near foramen Monro. Hyperdense, calcified, T2 bright bubbly mass w heterogenous enhancement
  2. Meningioma
  3. Ependymoma
  4. Subependymoma: elderly, 4th ventricle
  5. Subependymal giant cell astrocytoma: young w tuberous sclerosis
  6. CNS lymphoma: periventricular hypercellular mass w homogenous enhancement & restricted diffusion

(C) Nonchoroid cyst-like lesion

  1. Colloid cyst: more likely to be symptomatic if >1 cm
  2. Ependymal cyst
  3. Neurocysticercosis

(D) Others

  1. Intraventricular haemorrhage: from haematoma
  2. Epidermoid: CSF like signal intensity on MRI except for restricted diffusion & incomplete suppression on FLAIR
  3. Carvenous malformation: rare, T2 hyperintense, mildly T1 hyperintense globular lesion with blood degeneration products on SWI/T2* imaging
43
Q

Cerebellopontine angle mass

A
  1. Vestibular schwannoma:
    -Ovoid, intracanalicular, heterogenous T2 bright mass with avid enhancement. Small lesions solid, larger lesions may be cystic.haemorrhagic. Expands internal auditory meatus
  2. Meningioma
  3. Epidermoid: multilobular lesion, no enhancement
  4. Ependymoma
  5. Arachnoid cyst
  6. Vascular: aneurysm, ectasia
  7. Other schwannoma: Trigeminal, facial
  8. Lipoma
  9. Dural/leptomeningeal met
    10 Granuloma: dural sarcoid, TB, Wegner
  10. Neurenteric cyst: usually prep online, lobular mass, slightly denser than CSF, variable signal w proteinacecous material. No enhancement or restriction
  11. Paraganglioma: hypervascular mass extending from jugular foramen with erosive changes in skull base. Flow void & foci of blood degeneration products ‘salt & pepper’ appearance
44
Q

Cyst-like posterior fossa lesion

A
  1. Mega cisterna magna: communicate w 4th ventricle, basal CSF spaces
  2. Dandy-Walker spectrum: vermis hypoplasia, cystic dilatation of 4th ventricle +/- enlarged posterior fossa with torcula-labdoid inversion
  3. Blake’s pouch cyst: posterior diverticulum of 4th ventricle
  4. Arachnoid cyst
  5. Epidermoid cyst
  6. Pilocytic astrocytoma
  7. Cerebellar haemangioblastoma
  8. Trapped 4th ventricle
  9. Neuroglial/neurenteric cyst
  10. Neurocysticercosis
45
Q

Cerebral volume loss

A

(A) Generalised

  1. Normal ageing
  2. Cerebrovascular disease
  3. Drugs (alcohol - additional cerebellar vermis atrophy, steroid - transient)
  4. Postinflammatory: MS, variable cavitation
  5. Post traumatic eg: DAI
  6. Whole brain radiotherapy
  7. HIV encephalopathy: diffuse periventricular abnormal WM signal & volume loss

(B) Focal

  1. Post infarct: wedge-shaped cortical & subcortical V loss
  2. Post traumatic: typically orbitofrontal, anterior temporal
  3. Post infective

(C) Regional

  1. Alzheimer’s disease
    - classical: hippocampal & temporoparietal atrophy
    - posterior cortical atrophy: younger onset, visual agnosia, apraxia, occipitoparietal V loss
  2. Parkinson disease: generalised + atrophy of substantia nigra w sparing of hippocampi. Increased putaminal iron (reduced T2 signal). Loss of normal ‘swallowtail’ appearance of substantia nigra on SWI
  3. Frontotemporal lobar degeneration
  4. Progressive supranuclear palsy: reduced area of midbrain relative to pons, Mickey Mouse appearance on axial, hummingbird on Sagittarius
  5. Corticobasal degeneration: asymmetric atrophy of superior parietal lobules and para central gyri
  6. MSA-P: reduced putamen volume with reduced T2 signal relative to GP. High T2 rim surrounding putamen
  7. Huntington: atrophy of caudate nucleus
  8. Post encephalitis eg: media ltemporal lobe in HSV, autoimmune lambic encephalitis
46
Q

Cerebellar volume loss

A
  1. Normal aging
  2. Chronic alcohol
  3. Drugs: phenytoin, chemo, lithium, benzo
  4. Chronic vertebrobasilar ischaemia/insufficiency
  5. Chronic temporal epilepsy
  6. Cerebelliti
  7. MSA-C
  8. Olivopontocerebellar atrophy
  9. Superficial siderosis
  10. Post radiation therapy
  11. Inherited disease: Friedreich ataxia, ataxia telangiectasia, spinocerebellar ataxia syndromes
  12. Para Neoplastic cerebellar degeneration
  13. Gluten ataxia
  14. Crossed cerebellar diachisis
47
Q

Brainstem atrophy

A

(A) Diffuse

  1. Radiotherapy
  2. Inflammatory: MS (midbrain/pons > medulla), NMO (medulla > midbrain/pons), Behcet
  3. Wallerian degeneration
  4. Infectious rhombencephalitis: Listeria or enterovirus
  5. Infarction
  6. Spinocerebellar ataxia
  7. Inherited leukoencepjalopathies

(B) Regional

  1. Midbrain: progressive supranuclear palsy, Wilson’s disease
  2. Pons: MSA-C
  3. Medulla: hypertrophic olivari degeneration, adult onset Alexander disease
48
Q

Cortical hyperintensity on T2/FLAIR

A
  1. Cortical ischaemia/infarction
    - high T2 signal + restricted diffusion
  2. Encephalitis
    - HSV: mesial temporal lobe +/- insula & lateral temporal lobe. Haemorrhage common
    - Autoimmue: mesial temporal lobes + basal ganglia. Haemorrhage rare. Subacute to gradual onset
    - Paraneoplastic: indolent onset
  3. Encephalopathy: multifocal cortical T2 intensities +/- restricted diffusion
  4. Post-vital/status epilepticus: GM or subcortical WM signal change +/- restricted diffusion. Rapid onset, quick resolution
  5. Cortical contusion: blood degeneration products. Orbitofrontal & anterior temporal
  6. Cortical based tumour: look for mass effect
  7. Cortical malformation: focal cortical dysplasia, cortical tubers
  8. CJD: gyriform cortical T2 hyperintensity & persistent restricted diffusion, bithalamic abnormal signal (pulvinar & hockey stick sign)
49
Q

Sulcal FLAIR hyperintensity

-CSF or leptomeningeal pathology

A

(A) Changes to CSF content

  1. Subarachnoid haemorrhage: SWI signal drop out
  2. Ruptured dermoid

(B) Meningeal

  1. Bacterial meningitis: leptomeningeal enhancement, restricted diffusion (if purulent exudate)
  2. Aseptic meningitis: sarcoid, Wegner, RA
  3. Leptomeningeal carcinomatosis
    - Primary CNS: glioblastoma, medulloblastoma, ependymoma
    - Metastasis: including lymphoma, leukaemia
  4. Meningeal melanomatosis: rare primary melanocytes tumour of CNS, associated with cutaneous melanocytic lesion, hydrocephalus, hyperdense leptomeninges with high T1 signal

(C) Vascular

  1. Thrombosis of cortical vein
  2. Dilated leptomeningeal perforator eg: Moyamoya
  3. Slow flow in sulcal arteries

(D) Artefactual/Iatrogenic

  1. Hyperoxygenation
  2. CSF flow & pulsation artefact
  3. Recent gadolinium administration
50
Q

Cause of high T1 signal

A
  1. Fat eg: cortical laminar necrosis
  2. Methaemoglobin: subacute bleed, thrombus, cavernoma
  3. Proteinaceous material: colloid cyst, Rathke’s cleft cyst, craniopharyngioma, mutinous adenocarcinoma met
  4. Melanin
  5. Minerals: manganese, copper, iron
  6. Calcification
  7. Flow artefact
  8. Gadolinium enhancement
51
Q

Causes of low T2 signal

A
  1. Turbulent/rapid flow
  2. Air
  3. Cortical bone
  4. Metallic prosthesis
  5. Proteinaceous material: T2 signal reduces with increasing protein concentration
  6. Haemoglobin breakdown products
  7. High cellular lesion: lymphoma, high grade glioma, medulloblastoma
  8. Minerals
  9. Melanin
  10. Fungal hyphae
  11. Gadolinium
52
Q

MRI signal of haemorrhage

A 
Hyperacute (<1day) = oxyhaemoglobin = low/iso T1 + high T2
Acute (1-3 days) = deoxyhaemoglobin = low/iso T1 + low T2
Early subacute (3-7 days) = intracellular methaemoglobin = high T1 + low T2 
Late subacute (7-14 days) = extracellular methaemoglobin = high T1 + high T2
Chronic (>14days) = Haemosiderin = low T1 + low T2
53
Q

Causes of restricted diffusion

A

(A) Cortical

  1. Hypoxia-ischaemic
  2. Post-ictal: cortex & hippocampi
  3. PRES: parietooccipital & superior frontal gyri
  4. Encephalitis/cerebritis
  5. DAI: GWMJ, splenium, middle cerebellar peduncle + microhaemorrhage
  6. Hypoglycaemia: bioccipital & splenium
  7. CJD: insula & pulvinar
  8. M.R. artefact

(B) Focal lesion

  1. Infection: abscess (dual rim sign on SWI & T2 - hypointense outer rim + hyperintense inner rim)
  2. Hypercellular neoplasm: lymphoma (periventricular), medulloblastoma (4th ventricle/cerebellum), germinoma (midline), glioblastoma (high grade)
  3. Acute demyelination (incomplete ring enhancement)
  4. Epidermoid (lobular, insinuating cisternal lesion)
  5. Mucoid degeneration (choroid plexus cyst)
  6. Haemorrhage/haematoma
  7. Osmotic myelinolysis
54
Q

Fat-containing intracranial lesions

A
  1. Lipoma: interhemispheric fissure (+/- callosal dysgenesis) > suprasellar > pineal region > CPA
  2. Dermoid cyst: midline w chemical shift artefact +/- calcification
  3. Teratoma: midline multilobulated cystic mass
  4. Postsurgical fat plug eg: pituitary
  5. White epidermoid: rare variant containing triglycerides causing T1 hyperintensity
  6. Lipomatous degeneration of tumours: rare, seen in meningioma, small round blue cell tumour eg; medulloblastoma
55
Q

Skull lucency WITHOUT sclerotic edge

A

(A) Normal:
1. Parietal foramina (B/L symmetrical, anterior to lambdoid suture)
2. Normal ageing calvarium
3. Fontanelle:
-Anterior = closes < 18 months
-Posterior = closes <3 months
-Anterolateral x2, posterolateral x2
(B) Neoplastic (in adult)
1. Myeloma (pepper pot skull)
2. Metastases
3. Paget’s sarcoma (osteosarcoma, chondrosarcoma, fibrosarcoma)
-lytic, blastic, mixed lesion w cortical destruction & soft tissue component.
-usually little/no periosteal reaction
(C) Neoplastic (in child)
1. Met (neuroblastoma, leukaemia, sarcoma)
2. Langerhans cell histocytosis / eosinophilia granuloma (parietal bone, beveled edge, well defined lesion) or (multiple coalescing lesions with a geographic appearance).
-may contain central sequestrum of residual bone
-enhance avidly
(D) Traumatic
1. Fracture
2. Leptomeningeal cyst: skull fracture w trapped meninges. CSF pulsation causes progressive widening & scalloping.
3. Burr hole (+/- evidence of gliosis in subjaent brain parenchyma)
(E) Metabolic
1. Osteoporosis (vertebral insufficiency fracture common)
2. Hyperparathyroidism: salt & pepper skull +/- discrete brown tumour (expansile lytic lesion, causes cortical thinning, without cortical destruction or periosteal reaction +/- fluid-fluid level on MRI)
(F) Infective:
1. Acute pyogenic osteomyelitis (from sinusitis, mastoiditis).
-look for cortical breach of inner table
2. TB (punched out lesion with sequestrum + overlying soft tissue component
3. Hydrated cyst (expansile lobulated lesion centred in diploid space)
4. Syphillis (moth eaten appearance)
(G) Vascular
1. Haemangioma: expansile lesion with ‘sunburst’ pattern of radiating spicules, avid enhancement
2. Sinus pericranii (venous malformation, enlarged emissary vein, associated with soft tissue mass)
(H) Others
1. Osteoporosis circumscripta: lytic phase of Paget’s disease. Large, well defined @ inferior frontal, occipital bone, can cross suture
2. Neurofibroma: secondary to mesodermal dysplasia and skull erosion
3. Intradiploic arachnoid cyst

56
Q

Skull lucency with sclerotic edge

A

(A) Normal
1. Venous channel: serpiginous channel
2. Venous lakes: round or ovoid morphology, enhancement post contrast
3. Arachnoid granulation: round, well defined luciencies in region of venous sinuses with disruption of inner table.
-if multiple may consider chronically raised ICP
(B) Developmental
1. Epidermoid: rarely intradiploic, well defined, scalloped margin, similar to CSF on T1/2 but restricted diffusion & incomplete FLAIR suppression
2. Meningocoele / encephalocoele
-protrusion of meninges +/- brain through skull defect.

(C) Neoplastic

  1. Langerhans cell histocytosis (in healing phase)
  2. Treated lytic met

(D) Infective

  1. Chronic OM: greater association with soft tissue masses and dural thickening
  2. Frontal sinus mucocoele: completely opacified & expanded frontal sinus containing mucus with variable signal due to protein content. Thinning of sinus wall with variable resorption

(E) Others
1. Fibrous dysplasia: ground glass matrix, well defined, preserved overlying bone

57
Q

Generalised increase in skull vault density

A
  1. Paget’s disease:
    - elderly, multiple island of dense bone, loss of clarity of inner and outer tables, thickened skull vault, basilar impression
  2. Sclerotic met
  3. Fibrous dysplasia
  4. Myelofibrosis
    - diffuse sclerosis without architectural distortion
    - associate with extramedullary haematopoiesis
    - may have intracranial dural thickening
  5. Renal osteodystrophy:
    - 25% osteosclerosis, mimic Paget’s
  6. Acromegaly
    - enlarged frontal sinuses, prognathism, thickened skull vault, enlarged sella due to underlying pituitary adenoma
  7. Chronic haemolytic anaemia:
    - expansion of medullary spaces due to red marrow hyperplasia ‘hair-on-end’ appearance
    - variable sclerosis related to hyperplastic red marrow
  8. Sclerosing bone dysplasia
    - Osteopetrosis: diffuse sclerotic, thickened skeleton w fractures, narrowing of foramina compressing CN, orbital crowding, proptosis, poorly pneumatised sinuses
    - Pyknodysotosis: skull base, multiple worm Ian bone, wide sutures from delayed closure, frontoparietal bossing
    - Craniometaphyseal dysplasia: similar to osteopetrosis
  9. Prolonged phenytoin treatment: skull thickening + osteosclerosis + cerebellar volume loss
  10. Fluorosis (osteosclerosis, ossification of tendons/ligaments)
58
Q

Localised increased in skull vault density

A

WITHIN BONE

  1. Hyperostosis frontalis interna: symmetrical inner table growth
  2. Tumour (sclerotic met, osteoma, treated lytic met, treated brown tumour)
  3. Paget’s disease
  4. Fibrous dysplasia
  5. Depressed fracture

ADJACENT BONE

  1. Meningioma (reactive hyperostosis, can have invasion)
  2. Calcified cephalohaematoma (crecentic lesion overlying outer table of skull)
  3. Calcified epidermoid cyst
59
Q

Thickened skull

A

GENERALISED

  1. Normal variant
  2. Prolonged phenytoin treatment
  3. Acromegaly
  4. Chronic haemolytic anaemia
  5. Microcephaly
  6. Shunted hydrocephalus

FOCAL

  1. Normal variant
  2. Paget’s
  3. Fibrous dysplasia
  4. Meningioma
  5. Osteoma
  6. Sclerotic met
60
Q

Thin skull

A

GENERALISED

  1. Hyperparathyroidism
  2. Chronically raised ICP (empty sella, multiple arachnoid herniation, hydrocephalus, copper-beaten skull appearance)
  3. Osteogenesis imperfecta
  4. Rickets: frontal bossing, delayed fusion of cranial sutures, closure of fontanelles
  5. Hypophosphatasia: rare metabolic deficiency of alkaline phosphatase
  6. Lacunar skull: bone dysplasia of membranous skull associated with Chiari 2 malformation

FOCAL:

  1. Normal variant
  2. Osteoporosis circumscripta
  3. Large intracranial cyst
  4. Slow-growing tumour in cerebral cortex: DNET, ganglioglioma. Associated with gradual bony remodelling
61
Q

‘Hair on end’ skull - appearance of thickened trabeculae in expanded diploid space

A

(A) Haemolytic anaemia (red marrow hyperplasia)

  1. Thalassaemia
  2. Sickle cell anaemia
  3. Hereditary spherocytosis & elliptocytosis
  4. Pryucate kinase deficiency
  5. Glucose-6-phosphate dehydrogenase deficiency

(B) Other causes of red marrow hyperplasia

  1. Cyanosis heart disease
  2. Severe childhood iron deficiency anaemia

(C) Neoplastic (usually more focal)

  1. Haemagioma
  2. Meningioma
  3. Met
62
Q

Platybasia & basilar invagination/impression

A

(A) Congenital
1. Achondroplasia
2. Chiari malformation
Chiari 1: peg-shaped cerebellar tonsil extending > 5mm below FM +/- syrinx +/- hydrocephalus
Chiari 2: medulla, 4th ventricle, cerebellar vermis displaced through FM, small posterior fossa, beaked rectum. Associated with lumbar myelomeningocoele
Chiari 3: Chiari 2 with occipital encephalocoele
3. Osteogenesis imperfecta

(B) Acquired

  1. RA: erosion of dens/atlantoaxial subluxation
  2. Paget’s: bone softening
  3. Osteomalacia: bone softening
  4. Hyperparathyroidism: bone softening
  5. Localised bone destruction: lytic met & destructive infection
63
Q

J-shaped sella

-flattened tuberculoma sellar with prominent chiasmaticus

A
  1. Normal variant
  2. Optic chiasm glioma
  3. Neurofibromatosis
  4. Anchondroplasia
  5. Mucopolysaccharidoses
  6. Chronic hydrocephalus: caused by enlarged anterior aspect of 3rd ventricle
64
Q

Scalp mass

A

(A) Skin

  1. Epidermal inclusion cyst/sebaceous cyst
  2. Trichilemmal cyst/pillar cyst: from hair follicle. Calcifies more frequently than sebaceous
  3. Skin tag: pedunculated.
  4. Carcinoma
  5. Skin calcification: acne

(B) Subcutaneous tissue

  1. Lipoma
  2. Haemangioma

(C) Subgaleal plane

  1. Haematoma: not confined to cranial sutures
  2. Cephalohaematoma: confined to cranial sutures (subperiosteal haematoma)
  3. Dermoid - sinus tract
  4. Plexiform neurofibroma - NF1. High T2 signal with central low signal (target sign)
  5. Corsoid aneurysm: rare, fed by superficial temporal artery

(D) Bone lesion

  1. Osteoma: no effect on diploid space
  2. Malignancy
  3. Pott’s puffy tumour: subperiosteal abscess from sinusitis/trauma.
  4. Haemangioma: outer table involved, not inner
  5. Intraosseous meningioma
  6. Intraosseous epidermoid: fluid density with calcification
  7. Encephalocoele
  8. Sinus pericranii
  9. Paget’s

Skull And Brain (1 decks)

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