Neurologic Imaging (1)

Normal Brain
Brain MRI
• Calcification
• With aging, may start since birth
• Choroid plexus, pineal gland, globus pallidus, falx
• Cavum variants
• Cavum septum pellucidum: between frontal horns
• Cavum vergae: posterior continuation & never exists
without cavum septum pellucidum
• Cavum velum interpositum: extension of quadrigeminal
cistern to foramen of Monroe

• Myelinization
Myelination progresses from:
– central to peripheral
– caudal to rostral
– dorsal to ventral
Myelination milestones
– term birth : brainstem, cerebellum, posterior limb of the internal capsule
– 2 months : anterior limb of the internal capsule
– 3 months : splenium of the corpus callosum
– 6 months : genu of the corpus callosum
Radiographic features
– CT: Unmyelinated white matter is hypodense compared to normal white and grey
matter
– T1 WI is the most sensitive in children less than 1 year of age.
– T2 WI is the most sensitive in children between the age of 1 and 2 demonstrating
gradual shift from hyper- to hypo-intense relative to grey matter.
• Vascular territories
 Neural pathology
• Vascular disease
• Trauma
• Tumors
• Degenerative
• Hydrocephalus
• Infection
• Congenital
• Sellar & juxtasellar
• Spine
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Stroke
Infarction (CT)
Early CT Findings:
• Insular ribbon sign: loss of grey-white matter
interface at insular region
• Dense artery sign (arterial thrombosis)
• +ve Mass effect (edema): Sulcal effacement,
ventricular compression, midline shift
• Faint hypodensity (edema)
Late CT Findings:
• Deep hypodensity
• Hemorrhage in subacute stage (luxury perfusion /
haemorrhagic transformation)
• Chronic: CSF density (encephalomalacia), -ve mass
effect (widening of adjacent sulci & ventricles),
Porencephaly (cyst communicating with ventricle) ,
Wallerian degeneration (assymetrical brainstem
atrophy / T2 hyperintensity within ipsilateral
corticospinal tracts)
MRI Findings:
• Diffusion restriction (up to
subacute, not in chronic)
• FLAIR & T2 bright SI (acute
& subacute)
• T1 low SI (subacute)
• Chronic follows CSF SI in all
sequences
Grading of infarction:
• Hyperacute (0-6 hrs): bright DWI, Iso in T1, T2
& FLAIR
• Acute (6 hrs – 4 days): bright in DWI, T2 &
FLAIR, iso to hypo in T1
• Subacute (4-14 days): bright in T2 & FLAIR,
hyper  hypo in DWI, low in T1
• Chronic (>14 days): CSF SI (low in DWI,
FLAIR, T1….bright in T2)
N.B:
1. Always correlate DWI restriction with ADC map to
exclude T2 shine through effect (chronic lesions with
very long T2 relaxation times  DWI bright & ADC
bright)
2. Diffusion/perfusion mismatch: perfusion defect larger
than diffusion restriction denotes an area at risk
(penumbra)
3. Perfusion parameters: CBF= CBV/MTT
4. MTT: highly senstive early, increased
5. CBV: changes late, differentiate ischemia from
infarction
6. CBF = perfusion image
Small vessel disease
(deep white matter ishcemia)
Findings:
• Lacunar infarcts (<1cm), white
matter foci of signal alteration
• High SI on T2 & FLAIR WIs,
hypodense in CT
• Basal ganglia, periventricular,
centrum semiovale

Top of the Basilar $

Findings:
• Early: Dense basilar tip by CT, absent
flow void by MRI
• Late: infarctions in thalami, brainstem,
cerebellum, occipital lobes

Venous Infarcts (Sinus Thrombosis)

Findings:
• Haemorrhagic infarcts,
multifocal, Bilateral thalamic or
parasagittal, Infarcts not in
arterial territory
• Clot in sinus (dense by CT,
bright T1 & T2, no flow void),
requires phase contrast MRV
• Empty Delta sign (dural
enhancement of sinus margin on CECT)
• SSS > transverse > sigmoid
Amyloid angiopathy: CADASIL:
• Amyloid deposition in walls of blood • Cerebral Autosomal Dominant
vessels in edlerly normotensive Arteriopathy with Subcortical Infarcts
patients & Leukoencephalopathy
• Multiple foci of hemorrhage at • 40-50 years, migraines & TIAs
corticomedullary junction sparing the • Confluent T2 bright foci around
basal ganglia ventricles, pons, basal ganglia with
predilection to anterior temporal lobes
 Trauma
Intracranial Hemorrhage
Types:
• Extradural
• Subdural Extraaxial
• Subarachnoid
• Intraparenchymal (HTN, tumor, hgic infarct, DAI,
contusion)
Grading:
• CT (hyperdenseacute, isosubacute, hypochronic)
• MRI
Extradural vs Subdural

Subdural
NAI:
• Bilateral subdural hematomas, especially of different ages, in a child
are highly suggestive of non-accidental injury (NAI, child abuse,
Battered child, trauma X)
• Bilateral subdural hematomas can also occur in elderly patients with
recurrent falls
Hematocrit level:
• Fluid-fluid level with fresh blood (heavier due to more cellular
elements) appearing hyperdense, while old blood appears hypo
Subdural hygroma:
• CSF accumulation in subdural space following traumatic arachnoid
tear, DD: chronic subdural hematoma
Intraparenchymal hematoma
Causes:
• Cortical contusion  initially hypodense,
may bleed
• HTN hge  Basal ganglia (MCA), mass
effect
• Tumor hge  pituitary adenoma, others
Subarachnoid Hge (Aneurysm)
Findings:
• 1st  search for aneurysm (most
common cause)
• Hyperdense sulci & CSF spaces (CT),
bright SI on FLAIR
• Complications: 2ry vasospasm &
infarction, extension into ventricles
(intraventricular hemorrhage)2ry
hydrocephalus, leptomeningeal
siderosis (dark meninges on T2)

Intracranial Aneurysm
• Saccular: (Berry) aneurysm (most common)
• Associations: ADPKD, COA, FMD, collagen disorders (Marfan, Ehler-
Danlos $)
• Location: 90% in anterior circulation; ACA, ACOM, ICA, PCOM, MCA
• Giant aneurysm (>25mm): curvilinear peripheral calcification, mass effect, bone erosion
• Fusiform atherosclerotic aneurysm is seen with dolichoectasia (elongated, tortous & dilated
vertebro-basilar system)
Diffuse axonal injury
• Axonal disruption from shearing
forces of acc/deceleration
Findings:
• Petechial Hge at grey/white matter
interface, corpus callosum
• Hyperdense by CT (may be initially
normal)
• T2 / FLAIR bright SI, dark on T2*

Subfalcine herniation
• Cingulate gyrus slips under falx
Findings:
• Compression of ipsilateral ventricle, enlarged
contralateral ventricle, ACA territory
ischemia

Uncal herniation (descending transtentorial)

Findings:
• Effacement of ipsilateral suprasellar cistern, enlarged
ipsilateral CPA cistern, Duret Hge (compression of
anterior midbrain against contra-lateral tentorium),
Kernohan‟s notch (compression of cerebral peduncle
against contra-lateral tentorium), PCA territory ischemia

Carotid cavernous fistula

Clinical: traumatic or spontaneous;
ocular bruit
Findings:
• Enlarged ipsilateral superior
ophthalmic vein, cavernous
sinus
• Enlarged extraocular muscles
• Proptosis
 Neurologic Imaging (2)
Hypoxic-Ischemic Brain Injury Hypoxic-Ischemic Brain Injury
“Adult” “Neonate”

Hypoxic-Ischemic Brain Injury

Synonyms:
• Global hypoperfusion, Anoxic brain injury,
Hypoxic Ischemic encephalopathy (HIE)
• Clinical: seen in all age groups (from antenatal
to the elderly) as a result of numerous
etiologies:
• Neonates  perinatal asphyxia
• Older children  drowning and asphyxiation
• Adults  severe hypotension and/or impaired
oxygenation (cardiac arrest, hanging)
Findings:
• may be easily missed on CT or MRI due to symmetry, best detected
on DWI
• Neonates:
– Preterm  periventricular leukomalacia, germinal matrix Hge
– Term:
• severe (profound) asphyxia  multicystic
encephalomalacia
• mild  ulegyria, deep grey matter (basal ganglia) hypo on CT, restricted DWI
• Older children & adults:
– Predominantly grey matter affection & cerebellum (unlike neonates)
– “Reversal” & “white cerebellum” signs, pseudo-subarachnoid Hge, cortical laminar
necrosis, DWI  obvious grey-white matter differentiation, watershed infarcts
Carotid/ Vertebral artery Dissection
Clinical:
• young adult/child with stroke,
blunt trauma to neck or sudden
head turning, connective tissue
disease
Findings:
• U/S & CT  intimal flap, MRI
 expanded artery with high
signal hematoma surrounding
an eccentric signal void (true
lumen), DSA/CTA/MRA 
rat tail‟s / string appearance
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Vascular malformations
AVM
Findings:
• Solitary parenchymal or dural lesion, may calcify
• Serpiginous high & low SI, feeding artery &
draining vein by MRA / CTA
• No mass effect (replaces brain tissue), adjacent
parenchymal atrophy / ischemia due to a „vascular
steal‟ phenomenon
• Spetzler‟s criteria  higher score with higher
chance of hemorrhage
Cavernous malformation
Synonyms:
• cavernoma, cavernous hemangioma
Findings:
• Multiple, supratentorial heterogenous lesions
• Popcorn lesion (on T2): bright lobulated center, black hemosidrin rim
• Better detected by T2* or SWI (multiple blooming artifacts)
Venous anomaly
Findings:
• Multiple small veins
draining into large
transcortical vein
• Medusa head

Vein of Galen AVM

Clinical:
• high output CHF in infants,
hydrocephalus in children
Findings:
• Dilated midline venous structure
• Anechoic by U/S with Doppler flow

Moyamoya disease
Clinical:
• Japanese, idiopathic
progressive supraclinoid ICA
occlusion with multiple
collaterals
Findings:
• Puff of smoke on angiography
• FLAIR bright sulci (Ivy sign)
• Multiple tiny flow voids
 Brain Tumors
GBM (WHO grade 4 astrocytoma)
• Most common 1ry brain tumor, age > 50 yrs
Findings:
• Heterogeneous low density mass, cerebral
hemispheres
• Hge, necrosis common...No calcification or diffusion
restriction
• Intense enhancement, drop mets
• Butterfly glioma (crosses midline)
• MRS: elevated choline & Cho/Cr ratio, low NAA
(high grade malignancy)

Brain stem glioma

Clinical:
• 10 yrs child, late symptoms as tumor infiltrates rather than
destroys adjacent tissues, high grade, poor prognosis
Findings:
• Brainstem enlargement, pons>midbrain>medulla
• 4th ventricle displaced posteriorly
• Encasement of basilar artery
• Variable enhancement

Gliomatosis cerebri
Clinical:
• 30-40 yrs, poor prognosis
Findings:
• Diffuse T2 bright SI in white matter, may involve cortex, non-
enhancing
DD:
• lymphomatosis cerebri
• herpes encephalitis
• demyelinating disease (ADEM)
• radiation
Oligodendroglioma
Findings:
• Frontal lobe (commonly) large
cortical hypodense mass
• Cysts, large nodular clumpy
calcifications
• Variable enhancement
DD of posterior fossa cyst with mural nodule
Clinical:
• child / young adult
DD:
• Pilocytic astrocytoma
• hemangioblastoma (VHL)
Findings:
• Cyst with enhancing mural nodule in cerebellum

DD of temporal lobe mass

Clinical:
• child / young adult, epilepsy
DD:
• PXA (pleomorphic
xanthoastrocytoma)
• ganglioglioma /
ganglioneuroma
• DNET (dysembryoplastic
neuroepithelial tumor)
Findings:
• Cortically based Temporal lobe mass, +/- cystic element, +/- enhancement, +/- calcification
(more with ganglioglioma), +/- bone remodeling (scalloping)
DD of supratentorial mass
Clinical:
• young, middle age
DD:
• Astrocytoma
• Ependymoma
• PNET (neuroblastoma)
• mets, etc.
Findings:
• Aggressive malignancy:
More enhancement, more edema, MRS pattern of high grade malignancy
WHO grading of Astrocytoma
Low grade astrocytoma
• WHO grades 1 & 2
• 20-40 years; Mild or no enhancement
• Calcification (20%)
• Hemorrhage & edema rare
Anaplastic astrocytoma
• WHO grade 3
• 40-60 years
• Moderate enhancement
• Edema common; calcification rare
GBM
• WHO grade 4
• >50 years; strong enhancement
• Extensive vasogenic edema and hge common;
calcification rare
• Heterogenous low density mass (CT), no restricted DWI
• Butterfly glioma (bihemispheric spread), leptomeningeal drop metastasis
DD of intraventricular mass in adult
DD:
• central neurocytoma
• subependymoma
• Astrocytoma
• Meningioma
• Mets
• choroid plexus papilloma / carcinoma
Findings:
• Dilated ventricles (hydrocephalus) with
mass

DD of intraventricular mass in child

DD:
• choroid plexus papilloma
/ carcinoma
• Ependymoma
• PNET (medulloblastoma)
• central neurocytoma
• Astrocytoma
• meningioma
Findings:
• Dilated ventricles
(hydrocephalus) with mass
• Child, 4th ventricleependymoma vs medulloblastoma
Adult tumors
Subependymoma
• Elderly males, asymptomatic
• 4th ventricle > lateral ventricles
• May be multiple

Central Neurocytoma
• Lateral ventricle, attached to
septum pellucidum
• Mild to moderate enhancement, multiple cysts
• Calcification common
Pediatric tumors
Ependymoma
• 1-5 years
• 4th ventricle > lateral ventricles
• Tumor grows inside 4th ventricle & may extend through foramina
of Lushka & Magendie  Plastic ependymoma
• Hydrocephalus, fine calcifications (50%); Hemorrhage & cystic
areas
• Multiple or spinal ependymomas  associated with NF2
Choroid plexus papilloma / carcinoma
• < 5 years, cannot be differentiated radiologically
• Trigone of lateral ventricles (child) > 4th ventricle (adult)
• Intraventricular mass with intense contrast enhancement,
calcifications (25%)
• Complications: hydrocephalus, drop metastasis
PNET (primitive neuro-ectodermal tumor)
• Undifferentiated aggressive tumors in children
• Include:
• Medulloblastoma
• 1ry cerebral neuroblastoma
• Retinoblastoma
• Pinealoblastoma
• ependymoblastoma
• Intense contrast enhancement, dense cell packing, aggressive growth
Medulloblastoma
Clinical:
• child 2-8 yrs, Gorlin $ (basal cell nevi, odontogenic
keratocysts), Turcot $ (colonic polyposis)
Findings:
• Cerebellar midline mass (roof of 4th
ventricle)hydrocephalus
• Dense cell packinghyperdense on CT, restricted
diffusion
• Intense homogenous enhancement
• Drop mets
Meningioma
Clinical:
• female 40-60 yrs, typically benign [WHO grade I 
90%] (N.B: can be radiation induced)
Findings:
• A spherical well-circumscribed mass OR a flat,
infiltrating („en plaque‟) lesion
• Site: cerebral convexity (along falx), sphenoid ridge,
CPA
• Hyperdense on CT, Intense homogenous enhancement
• Round, lobulated mass with dural tail (better by MRI)
• T2 iso-intense, if bright  ?? malignant
• Hyperostosis at adjacent bone
• Angiography: spoke-wheel, dense persistent blush
DD of CPA mass
 Meningioma
 Schwannoma
 Epidermoid cyst

DD of pineal mass
 Germinoma
 Teratoma
 Pinealoblastoma
DD of fat containing mass
Findings: fat density, calcification,
midline
• Lipoma: pericallosal, avascular
• Dermoid: fat-fluid level, may
rupture  fat in CSF, headache
• Teratoma: pineal gland

Lymphoma
Findings:
• Hyperdense on CT, iso or hyperintense on T2
• Intense homogenous
enhancement, ring
enhancement (in AIDS)
• Solitary or multiple masses,
very radiosenstive (may
disappear with ttt)
• Periventricular WM, deep GM,
splenium of corpus callosum
(typical)
Metastasis
Findings:
• Marked vasogenic edema around
multiple T2 bright lesions with
enhancement
• Iso or hypointense T2 mets: Hge
(RCC, melanoma,
choriocarcinoma), mucin (GIT
adenocarcinomas), dense cell
packing (germ cell tumors)
• Leptomeningeal mets > dural: breast, lung,
melanoma
Pituitary Gland
Normal Findings (MRI sella):
• Anterior gland shows homogeneous SI
(which is isointense to white matter)
on T1WI and T2WI
• Posterior gland is bright on T1 (due to
stored neurosecretory material)
• Homogenous post-contrast
enhancement.

Pituitary Microadenoma
Clinical:
• functioning (prolactin, Growth
hormone, ACTH, FSH)
Findings (MRI sella only):
• Gland assymetry (confined),
small focal lesion (< 10 mm)
• Seen on 2 views (coronal &
sagittal)
• Convex superiorly, stalk deviation
• Dynamic contrast enhancement: slower than normal pituitary

Macroadenoma
Clinical:
• non-functioning, mass
effect (visual troubles,
hypopituitarism)
Findings:
• Ballooning of sella
• Extension to suprasellar
cistern (figure “8” shape, encasement of ICA, compression of optic chiasm, upward
displacement of 3rd ventricle)
• Heterogenous mass with solid & cystic components, no calcification
• Intense uniform or heterogenous enhancement
• Pituitary apoplexy  acute hemorrhage with rapid expansion and compression of optic
chiasm, headache
DD of suprasellar mass
• Macroadenoma
• Craniopharyngioma
• Hypothalamic hamartoma
• Eg of the stalk
• Germinoma
• Rathke‟s cleft cyst
• Chiasmatic glioma
• Thrombosed aneurysm
Craniopharyngioma
Clinical:
• 2 peaks of incidence (child
5-15 yrs, adult 50 yrs),
pressure manifestations
(bitemporal hemianopia,
growth retardation,
diabetes insipidus,
headache)
Findings:
• Heterogenous mass with cystic & solid elements
• Enhancement of solid component
• Calcification (90%)
• Obstruction of foramen of Monroe  hydrocephalus
Other suprasellar masses
Hypothalamic hamartoma
• Clinical: precocious puberty
• Nodule in floor of 3rd ventricle
• CT  isodense, T1 & T2  iso, no enhancement
Rathke’s cleft cyst
• Sellar or suprasellar, T1  bright
Chiasmatic (optic) glioma
• Thickening of chiasm, spread along optic pathway
Eosinophilic granuloma of the stalk
• Thickening and enhancement of the stalk; Clinical: diabetes insipidus
DD of benign cysts
• Arachnoid cyst (CSF SI, not
communicating with ventricles)
• Colloid cyst (at foramen of Monroe
anterior to 3rd ventricle, mostly
hyperdense on CT, T1 bright & T2
dark)
• Rathke‟s cleft cyst (intra & supra-
sellar, bright on T1, no calcification, may show rim enhancement)
• Pineal cyst
 Neurologic Imaging (3)
White Matter Disease
Multiple Sclerosis
Clinical:
• female, young adult, idiopathic demyelination,
mono-ocular visual loss, sensory deficit, gait
difficulties
Findings:
• Oval, Dawson‟s fingers (sagittal FLAIR)
• Multiple white matter plaques (at least 3 of > 5
mm), bright on T2 & FLAIR (McDonald‟s
criteria)
• Corpus callosum, periventricular, brainstem,
cord, optic nerve
• Devic disease: optic pathway & spinal cord
plaques, sparing brain
• Active plaques: enhancement (variable),
diffusion restriction
• Polyphasic, requires follow up
• Tumefactive MS resembles a tumor or infarct
DD:
• ADEM
• Vasculitis (e.g. lupus, anti-phospholipid
syndrome, Behcet‟s disease)

ADEM (Acute Disseminating Encephalo-Myelitis)

Clinical:
• immune response to viral illness or vaccination in children, monophasic
Findings:
• Bright T2 SI at subcortical white matter, variable enhancement
• Cerebrum, cerebellum,
brainstem
PRES (Posterior Rreversible Encephalopathy $)
Clinical:
• Blood pressure changes (HTN,
eclampsia), headache, visual
disturbances
Findings:
• Bright T2 SI at cortical &
subcortical regions, hypodense in
CT
• Occipito-parietal, brainstem
• Reversible
PML (Progressive Multifocal Leukoencephalopathy)
Clinical:
• AIDS, reactivation of a
latent viral infection by
JC polyomavirus,
gradual onset of limb
weakness, visual field
defects, speech
abnormalities, ataxia
and dementia
Findings:
• Bright T2 SI at white matter including subcortical regions
• Occipito-parietal
• Bilateral, asymmetrical
Osmotic myelinolysis
Clinical:
• alcoholic, malnourished
patient, rapid correction of
hyponatremia
Findings:
• Diffuse central pontine
bright T2 SI sparing
corticospinal tracts
• Can be extrapontine in cerebellum, subinsular regions, basal ganglia and thalami
• No mass effect, no enhancement
• Restricted diffusion
Metachromatic leukodystrophy
Clinical:
• most common, hereditary, < 2 yrs, death in
childhood, defecient
enzymeArysulfatase A
Findings:
• Tigeroid appearance of periventricular
white matter, butterfly distribution
• Sparing of subcortical „U‟ fibers, may
involve cerebellum
• T2 bright, hypodense by CT
Adrenoleukodystrophy
Clinical:
• preadolescent boys (X-linked
recessive), adrenal insufficiency
Findings:
• Disease starts occipital  spreads
anteriorly
• Symmetrical, hypodense by CT, T2 bright
• Leading edge enhancement
Leukodystrophies
Canavan disease
• N-acetylaspartylase defeciency  increased NAA on MRS
• Macrocephaly, white matter abnormal SI (high T2 & low T1)
Alexander disease
• Macrocephaly, normal NAA, frontal lobe & periventricular
• white matter abnormal SI, +/- large cystic cavities,
• +/- basal ganglia affection, contrast enhancement
Krabbe disease
• Galactocerebroside β-
Galactosidase defeciency
• White matter abnormal SI (more
posteriorly & centrally), basal
ganglia & thalamus hyperdense on
CT / low SI on T2
Leigh $:
• Inherited Mitochondrial disorder  Neurodegeneration
• T2 WI bright SI, bilateral symmetrical in BG, thalamus and brainstem
Leukodystrophies
• Mitochondrial disorders (MELAS $, MERRF $, Leigh $)
• Zellweger $
• Phenylketonuria
• Homocystinuria
• Cockayne $
• Pelzaeus-Merzbacher disease
MR spectroscopy (Normal)

MR spectroscopy
 Grey Matter Disease
Dementia
Senile Dementia, Alzheimer Type (SDAT)
• Most common; non-
specific findings
• Atrophy affecting anterior
temporal lobes, parietal,
latefrontal
• Decreased posterior
temporal & parietal perfusion on SPECT (HMPAO) & FDG-PET
Frontotemporal dysplasia (Pick disease)
• Presenile onset (<65 years)
• Frontotemporal atrophy with enlarged frontal horns
Vascular cortical dementia
• Multi-infarct dementia
• Subcortical dementia (Binswanger disease): periventricular
hyperintensities (small vessel disease)
Lewy body dementia
Prion diseases
• e.g: Creutzfeldt–Jakob disease (CJD)
Parkinsonism
Parkinson disease
• Clinically: cog-wheel rigidity, bradykinesia, tremors
• MRI: may be normal, T2WIblack basal ganglia
• Best for diagnosis is DaTSCAN using Ioflupane (I123)
(brain SPECT)
Parkinson plus syndromes
MSA (multisystem atrophy):
• volume loss of pons & cerebellum
• Midbrain is preserved
• “Hot cross bun” sign in pons on axial T2 &
FLAIR
PSP (progressive supranuclear palsy):
• volume loss of midbrain Humming bird sign
• Pons is preserved
DD of basal ganglia region bright T2 SI
Amyotrophic lateral sclerosis (ALS)
• Bright SI on FLAIR at middle & lower internal capsule
Huntington chorea
• Bright T2 SI in caudate, putamen
• Caudate atrophy, Frontal horn enlargement
Wilson disease
• Defective copper transport with resultant multi-organ copper deposition
• Low density basal ganglia on CT
• T2 bright SI in putamen & thalami, midbrain & pons
• Liver cirrhosis, Kayser-Fleischer ring (eye)
Creutzfeldt-Jakob disease (CJD) [cow madness]
• Bright T2, FLAIR, DWI SI in caudate, putamen, grey matter
DD of basal ganglia bright T2 SI
Carbon monoxide poisoning
• Bright T2, FLAIR, DWI SI in globus pallidus,
cortex, hippocampus
Hallervorden-Spatz disease
• Now known as “Pantothenate kinase-associated
neurodegeneration (PKAN)”
• Autosomal recessive disorder causing
involuntary spasticity and progressive
dementia; a subset of neurodegeneration with brain iron accumulation (NBIA)
• “Eye of the tiger” sign: bright globus pallidus with surrounding dark rim
Others:
• Lymphoma
• Venous infarctions
• Mitochondrial diseases
DD of basal ganglia calcifications
Causes:
• Aging (physiologic, mainly at globus pallidus)
• Hypoparathyroidism
• Toxoplasmosis
• CO, lead poisoning
• Radiation induced
• Fahr disease
• Mitochondrial disorders
Wernicke encephalopathy
Clinical:
• malnutrition, alcohol, vit B1 (thiamine) deficiency
Findings:
• Cerebellar volume loss
• T2 & FLAIR bright SI at periaqueductal GM,
tectal plate, mamillary bodies, medial thalami

Hydrocephalus
Findings:
• Dilated ventricles, ballooning of temporal horns
(Mickey Mouse ears)
• Periventricular CSF permeation, T2 bright SI
• Sulcal effacement due to mass effect
• Communicating vs non-communicating
 Brain Infections
Meningitis
Findings:
• Thickened, enhancing meninges
• Bacterial: convexity
• Granulomatous (TB, sarcoid, fungal):
basilar

Neurosarcoidosis
Clinical:
• pateints with pulmonary sarcoid
Findings:
• Plaque like dural thickening, T2 low
SI
• Homogenous enhancement of basal
meninges
• Rim enhancing small lesions, calcify
later

Intracranial hypotension
• Occurs when CSF volume is lowered by
leakage or withdrawal
Findings:
• Diffuse dural enhancement
• Downward displacement of tonsils &
midbrain

Empyema
Surgical emergency
Cause:
• sinusitis, otitis, postoperative
(craniotomy)
Findings:
• Commonly subdural with thickened
enhancing wall
• Restricted diffusion, hypodense by CT
Brain abscess
Clinical:
• IV drug abuse, Sepsis,
sinusitis, otitis, mastoiditis
Findings:
• Cavitary lesion with
surrounding edema &
mass effect
• Wall enhancement, restricted diffusion centrally
Neurocysticercosis
Cause:
• Taenia solium (pork tapeworm)
Clinical:
• seizures
Findings:
• Multiple cystic lesions of water
density
• Ring enhancement
• May calcify late
Other Fungal infections
Aspergillosis
• Hemorrhagic infarcts
• T2 iso / hypointense mass lesions
Cryptococcosis
• Cystic dilatation of Virchow Robin spaces (gelatinous pseudocysts)  T2 bright
• In HIV +ve patients
Perivascular spaces (Virchow Robin spaces)
 Virchow Robin spaces Virchow Robin spaces
(Normal) (Dilated)

Herpes encephalitis
Clinical:
• children & young adults, fever, DCL,
convulsions
Findings:
• EarlyNormal
• After 3 daystemporal lobe & insular patchy
gyral edema
• Restricted diffusion, gyral enhancement, +/- hge

Congenital infections
Cause:
• CMV, toxoplasmosis, Rubella, HSV
Findings:
• CMV: periventricular calcification,
polymicrogyria
• Toxoplasmosis: basal ganglia &
parenchymal calcification, hydrocephalus
• Rubella: Microcephaly, basal ganglia &
parenchymal calcification
 Neurologic Imaging (4)
Congenital Malformations
Chiari I malformation
Clinical:
• adult, 20 yrs
Findings:
• Tonsillar herniation (> 5 mm),
Normal position of 4th ventricle
• No brain anomalies, no
myelomeningocele  little or no
consequences
• Associations:
Syringohydromyelia, basilar invagination, Hydrocephalus, Klippel-Feil anomaly
Chiari II malformation
Clinical:
• newborn
Findings:
• Small posterior fossa: herniated vermis (peg),
towering cerebellum (upward herniation through
tentorium), heart shape wrap of cerebellum around
pons  “Banana sign” on obstetric U/S , Tectal beak
• Hypoplastic fenestrated falx (gyral interlocking), small crowded
gyri (stenogyria), biconcave 3rd ventricle, myelomeningocele
• Associations: Hydrocephalus, syringohydromyelia, corpus
callosum dysgenesis
• Chiari III = Chiari II + meningoencephalocele (high cervical or low
occipital)
Corpus callosum agenesis:
• Complete or partial (dysgenesis)
Findings:
• Absence of CC, poorly developed WM posteriorly (colpocephaly)
• Elevated 3rd ventricle, parallel lateral ventricles, small frontal horns (bull‟s horn), large
occipital horns
• Associations: Interhemispheric lipoma (50%), encephalocele, Dandy-Walker

Holoprosencephaly :
• Faliure of cleavage (absent septum pellucidum), associated with midline
facial anomalies (cyclopia, hypotelorism), 50% have Down $
Forms:
• Alobar (severe):
• cup-shaped brain (anterior cortical mantle), monoventricle, fused
thalami, absent falx & corpus callosum, dorsal cyst
• Semilobar (moderate):
• partial cleavage
• Lobar (mild):
• only fused rostral portion (DD: Septo-optic dysplasia: Absent
septum pellucidum & hypoplastic optic nerve/chiasm,
schizencephaly)
Cerebral hemiatrophy (Dyke-Davidoff-Masson $)
• Intrauterine or perinatal ICA
infarctionhemiatrophy
Findings:
• Hemiatrophy, midline shift
• Ipsilateral skull thickening, PNS enlargement

Migration/Sulcation abnormalities
1. Lissencephaly: lack of sulci, agyria or pachygyria (smooth brain surface)
2. Polymicrogyria: excessive convolutions, increased cortical thickness
3. Schizencephaly: GM-lined CSF cleft extending to ependyma, open or closed lip
4. Cortical heterotopia: normal GM in abnormal site, nodular (subependymal) or laminar
(band), periventricular, non-enhancing
Dandy-Walker malformation
Findings:
• Large posterior fossa, large cyst communicating with
4th ventricle, elevated tentorium
• Absent/abnormal inferior vermis, hypoplastic
cerebellum
• Associations: Hydrocephalus, agenesis of CC,
lipoma
• DW Variant: more common, less severe, posterior fossa not enlarged,
Key-hole deformity
• Mega Cisterna magna: mildest form of the disease spectrum, normal
cerebellum & 4th ventricle; D.D:- Posterior fossa Arachnoid cyst (no
communication with 4th ventricle)
 Phakomatoses
NF1:
Von-Recklinghausen disease, AD
Clinical:
• café au lait spots, Lisch nodules (pigmented iris nodules),
axillary/inguinal freckling, neurofibromas, optic nerve gliomas
Findings:
• CNS: low grade gliomas (optic pathway, brainstem), Moyamoya,
spinal neurofibromas, dural ectasiaposterior vertebral scalloping
& widened neural foramina, Unidentified Bright Objects (UBOs) or
(FASI: focal areas of signal intensity)  Basal ganglia, thalami,
brainstem; bright T2, iso to bright T1, no enhancement
• Plexiform neurofibromas (multinodular superficial tumor lesions
involving large nerves especially ophthalmic division of
Trigeminal; heterogenous, T1 hypo, T2 hyper with central low SI
target sign, mild enhancement)
• Skull: hypoplastic sphenoid wing  bare orbit sign
• Skeletal: pseudoarthroses, ribbon ribs, kyphoscoliosis
• Chest: progressive fibrosis
• Others: Renal artery stenosis / aneurysm, Pheochromocytoma
NF2
Findings:
• “MIS ME”: multiple inherited Schwannomas, meningiomas & ependymomas
• Bilateral acoustic neuromasdiagnostic

VHL disease
Findings:
• Hemangioblastomas
(multiplediagnostic)
• Renal carcinomas, cysts
(multiple, bilateral)
• Pheochromocytoma
• Other cysts: pancreas, liver,
spleen, epididymis
Tuberous sclerosis
Clinical (triad):
• adenoma sebaceum, seizures & mental retardation
Findings:
• CNS: cortical & subependymal tubers (hamartomas),
calcify, +/- enhancement, giant cell astrocytoma at foramen
of Monroe
• Renal: angiomyolipomas, cysts
• Cardiac: rhabdomyomas
• Pulmonary: LAM, chylothorax, pneumothorax

Sturge-Weber $
• Congenital capillary venous angiomas of the face (a port
wine naevus) with ipsilateral leptomeningeal cerebral
angiomas  abnormal venous drainage can cause chronic
ischaemia (leading to cortical atrophy and calcification)
Clinical:
• port-wine nevus, seizures, hemiparesis
Findings:
• Tramtrack cortical calcifications, primarily parieto-
occipital distribution
• Atrophic cortex with wide adjacent subarachnoid space
• Enlarged enhancing ipsilateral choroid plexus
• Ipsilateral skull thickening
• Venous angiomas (DVA)
Mesial temporal sclerosis
Clinical:
• children & young adults, seizures
Findings: (best by coronal FLAIR)
• Volume loss of hippocampus, bright T2
SI
• Dilated temporal horn
 Spinal disease
Spinal dysraphism
Incomplete closure of bone, neural & soft tissue
Types:
• open (aperta) & closed or occulta (skin covered)
Findings:
• Spina bifida: failure of fusion of the posterior spinal bony
elements (occulta occurs in 20% of general population
with no neurological deficit; aperta nervous tissue is
exposed and neurological defects are common, surgical
repair soon after birth)
• Tethererd cord: short thick filum terminale, low conus
medullaris (below L2)
• Dorsal dermal sinus: LSS > occipital, sinus tract from
skin to end in SC fat or meninges or cord or dermoid
cyst, overlying hair tuft
• Lipo-myelo-meningo-cele: protruding sac containing
nerve roots, CSF covered by meninges, with extradural lipoma
• Spinal lipoma
• Syrinx (syringohydromyelia)
• Diastemato-myelia: 2 hemicords split by fibrous or bony septum, Dorsolumbar
Meningocele
• Herniation of the spinal meninges through the
intervertebral foramina or a vertebral defect + varying
degrees of dural ectasia
• Usually accompany spinal dysraphisms
• Generalized or focal dural ectasia may also be seen in:
neurofibromatosis, Ehler–Danlos and Marfan‟s syndromes,
erosive arthropathies (e.g. ankylosing spondylitis)
Types:
• Anterior thoracic meningocele with ventral herniation
of the spinal cord: spinal cord is displaced anteriorly and is in
contact with a vertebral body near an intervertebral disc (commonly
T6)
• Lateral thoracic meningocele: commonly presents as a para-
vertebral mass (CXR); usually solitary and located on the right; there
is an angular kypho-scoliosis towards the side of the meningocele;
Neurofibromatosis is present in up to 85% of cases
• Anterior sacral meningocele: presacral and appear as a uni-locular,
complex lobular or multi-locular cystic mass; there is usually a large
eccentric anterior lower sacral defect (with a pathognomonic scimitar
appearance on XR) and an expanded sacral canal
• Posterior meningocele: mainly within the lumbosacral region

Spondylodiscitis
Cause:
• pyogenic (more disk destruction), TB
(more bone destruction)
Findings:
• Fragmentation and eventual loss of the
dark line of the vertebral end plates
above and below the affected disc
• Bright T2 SI in disk & adjacent
vertebrae
• Contrast enhancement
• Soft tissue mass
Pott’s disease (spinal TB)
Findings:
• Spondylodiscitis, several adjacent
levels, loss of disk height
• Gibbus deformity (anterior
vertebral bodies > posterior)
• Large paraspinous abscess, psoas
abscess

Degenerative spine disease

Findings:
• Disk degeneration (loss of water
contentloss of T2 bright SI)
• Disk herniation (posterior, anterior,
cephalocaudal)
• Vertebral end plate (VEP) marrow changes Modic: 1
(fluid), 2 (fat), 3 (fibrous)
• Osteophytes, facet hypertrophy, ligamentum flavum
hypertrophy
• Spondylolisthesis
Posterior disk herniation
Findings:
• Disk bulge: diffuse, > 50%
• Disk protrusion: focal, < 50%, wider than tall
• Disk extrusion: focal, < 50%, taller than wide (in any
plane)
• Site of focal: central, paracentral, posterolateral, lateral
• L4-L5, L5-S1 Lumbar, lower 4 dorsal, C5-C6, C6-C7
cervical
• 2ry spinal stenosis, foraminal stenosis
• Contrast is used in postoperative cases to differentiate scar from residual/recurrent disk (scar
enhances)
• Postoperative complication: Arachnoiditis  clumping of nerve roots within thecal sac,
myelographic block
Arachnoiditis

1ry spinal stenosis

Congenital
Findings:
• Short pedicles,
thick lamina, large
facets + arthropathy
• Morquio $,
Achondroplasia

Subacute combined degeneration

Clinical:
• myelopathy due to vit B 12 deficiency
Findings:
• Longitudinal T2 bright SI in dorsal columns
• Cervical & dorsal
DD:
• Syphilis (Tabes dorsalis)
 Spinal cord tumors
Classification:
• Intramedullary:
– within cord (Astrocytoma, ependymoma, hemangioblastoma, metastasis)
• Intradural extramedullary:
– Outside cord, within dural sac : Meningioma
Nerve sheath tumors:
• Schwannoma
• neurofibromaa
• Extradural:
– outside thecal sac

Scoliosis
• Lateral spine curvature with variable degree of
rotation of vertebrae
Findings:
• Determine side of convexity
• Scoliotic curve measurement (Cobb‟s angle)
• Rotation grading
Transcranial U/S
Indications:
• Screening & follow up of
hemorrhage, dilated
ventricles in premature
infants, ECMO
• Suspected cranial
anomalies (e.g. Down $)
Germinal matrix hemorrhage
Cause:
• birth trauma, prematurity &
coagulopathies
Grading:
1: subependymal hge (anterior
caudo-thalamic groove)
2: intraventricular hge without
dilatation
3: intraventricular hge with
dilatation
4: intraparenchymal hge (>50%
mortality, porencephaly)

Periventricular leukomalacia
Findings:
• Periventricular increased echogenicity
(early)
• Periventricular cystic areas (late)
• Adjacent to trigone, foramina of Monroe