SKULL & BRAIN

Question 1

SOLITARY ACUTE INTRACRANIAL

HAEMORRHAGE

Answer 1

1. Intracerebral.
   (a) Hypertension—basal ganglia, pons, cerebellum.
   (b) Cerebral amyloid angiopathy—lobar location, peripheral
   microhaemorrhages (often multifocal).
   (c) Haemorrhagic lesions—e.g. metastases, primary tumours,
   infarcts.
   (d) Traumatic—more commonly multifocal (see Section 13.3).
2. Subarachnoid—see Section 13.2. Extends into sulci ± basal
   cisterns.
3. Subdural—most common in elderly post trauma (which may be
   minor); also associated with intracranial hypotension or dural
   arteriovenous fistula (AVF). Crescentic shape, does not cross falx.
4. Extradural—traumatic; usually arterial bleed, rarely venous.
   Lentiform shape, does not cross cranial sutures.
5. Intraventricular—usually due to extension from subarachnoid or
   intracerebral bleed; isolated intraventricular haemorrhage is rare
   and due to subependymal vein rupture

Question 2

SUBARACHNOID HAEMORRHAGE (SAH)
Causes 7

Answer 2

1. Trauma—often localized to coup and contrecoup injuries, i.e. superficial.
2. Intracranial aneurysm—haemorrhage typically centred on the aneurysm (e.g. sylvian fissure = MCA aneurysm; interhemispheric fissure = anterior communicating artery aneurysm). Blood usually within basal cisterns, whereas nonaneurysmal causes are more often sulcal in location. An aneurysm may be seen as a filling defect within the acute haemorrhage.
3. Arteriovenous shunt—AVM (indirect shunt with nidus of vessels) or AVF (direct shunt between artery and vein). Prominent draining veins, may be partially calcified.
4. Vasculopathy—cerebral amyloid angiopathy, reversible cerebral
   vasoconstriction syndrome (RCVS; reversible arterial stenosis often
   associated with certain drugs) and vasculitis (multifocal arterial stenoses). Haemorrhage may be multifocal.
5. Venous thrombosis—look for venous hyperdensity/expansion.
6. Perimesencephalic—typically limited to the basal cisterns around the midbrain ± pons, especially interpeduncular cistern. Spontaneous, has a benign course. No cause is found on angiography; thought to be due to a venous bleed.
7. Iatrogenic—following lumbar puncture or surgery

Question 3

MULTIFOCAL ACUTE INTRACEREBRAL HAEMORRHAGE

7

Answer 3

1. Trauma—contusions (common, typically seen in the anteroinferior frontal lobes and temporal poles at sites of impact with the skull); haemorrhagic shear injury (i.e. diffuse axonal injury, located at grey-WM junction [GWMJ], corpus callosum and brainstem).
2. Septic embolism.
3. Haemorrhagic neoplastic lesions—metastasis, leukemia.
4. Coagulopathy—horizontal blood-blood levels are suggestive.
5. Venous sinus thrombosis.
6. Vasculopathy—drugs, cerebral amyloid angiopathy, vasculitis,
   posterior reversible encephalopathy syndrome (PRES) and RCVS ( reversible cerebral vasoconstriction Xd).
7. Multiple cavernomas—rare, syndromic, young males

Question 4

MICROHAEMORRHAGES ON MRI

15

Answer 4

1. Acute trauma—haemorrhagic shear injury.MRI is more sensitive than CT.
2. Hypertensive vasculopathy—central pattern involving the basal
   ganglia, thalami, brainstem and cerebellum.
3. Cerebral amyloid angiopathy—typically peripheral cortical/subcortical, usually spares the basal ganglia. Associated with lobar and subarachnoid haemorrhages.
4. Cavernomas—including familial syndromes.
5. Venous thrombosis/congestion.
6. Radiotherapy—radiation-induced capillary telangiectasia within the radiation field.
7. Cerebral vasculitis—usually at GWMJ.
8. Septic emboli—e.g. from infective endocarditis.
9. Haemorrhagic metastases—especially melanoma, RCC and
   intravascular lymphoma.
10. Sickle cell anaemia and beta thalassaemia*—associated with cerebral fat embolism from bone marrow infarcts. Seen in cerebral and cerebellar WM and corpus callosum.
11. CADASIL—symmetrical multifocal WM hyperintensity in frontal and anterior temporal lobes and external capsule, with noncharacteristic distribution of microhaemorrhages.
12. PRES—parietooccipital and superior frontal gyral predominance of microhaemorrhages.
13. Fat/air embolism—microbleeds may be associated with foci of restricted diffusion.
14. Critical illness–associated cerebral microbleeds—may be related to hypoxaemia, high altitude or disseminated intravascular coagulation.
15. Drugs—cocaine abuse

Question 5

SUPERFICIAL SIDEROSIS
Classical
6

Answer 5

1. Dural defect—either intracranial or spinal. Usually due to previous
   trauma or surgery. May see extraarachnoid CSF collection or
   pseudomeningocoele on MRI. Dural defect may be visible on CT
   myelography.
2. Dural ectasia—e.g. in Marfan.
3. CNS tumours.
4. Vascular malformations
5. Cerebral amyloid angiopathy (60% of patients)
6. Idiopathic ( 46%)

Question 6

SUPERFICIAL SIDEROSIS
Cortical
6

Answer 6

1. Previous SAH—of any cause (see Section 13.2), including
   subarachnoid extension of intracerebral haemorrhage and bleeding
   neoplasms.
2. Cerebral amyloid angiopathy—in older patients (>60 years).
   Intracerebral microhaemorrhages may also be seen.
3. RCVS—in younger adults (<60 years), associated with pregnancy
   and certain drugs.
4. Cerebral vasculitis.
5. Hyperperfusion syndrome—after revascularization, e.g. carotid
   stenting or endarterectomy.
6. Infective endocarditis.

Question 7

SUPERFICIAL SIDEROSIS

Mimics of superficial siderosis

Answer 7

1. Acute SAH—hyperattenuating on CT, increased signal in
   subarachnoid space on FLAIR/T1.
2. Sequelae of cerebral infarction—petechial haemorrhages and
   laminar cortical necrosis both cause susceptibility effects but are
   centred on the cortex rather than the subarachnoid space.
3. Cortical vein thrombosis—susceptibility effect follows the cortical
   veins.
4. Cortical calcification—e.g. in Sturge-Weber syndrome. Very dense
   on CT.

Question 8

HYDROCEPHALUS

CSF overproduction

Answer 8

1. Choroid plexus tumours—i.e. papilloma, carcinoma;

Question 9

HYDROCEPHALUS

Communicating 6

Answer 9

1. Posthaemorrhagic—especially SAH.
2. Bacterial meningitis—small cortical infarcts may be present as a
   complicating feature.
3. Leptomeningeal carcinomatosis—look for leptomeningeal
   enhancement.
4. Idiopathic normal pressure hydrocephalus—dilated ventricles
   with a narrowed callosal angle, crowding of gyri at the vertex and
   widened sylvian fissures. Classic clinical triad of dementia, urinary
   incontinence and gait apraxia.
5. Increased venous pressure—venous obstruction, vein of Galen
   malformation.
6. Vestibular schwannoma—rare, thought to be due to increased
   CSF protein impairing CSF absorption

Question 10

HYDROCEPHALUS

Obstructive

Answer 10

Any level
1. Haemorrhage.
2. Intraventricular tumours—see Section 13.33.
3. Ventriculitis—complication of meningitis, surgery or haemorrhage.
Look for subtle ependymal enhancement and dependent sediment
in lateral ventricles (restricts on DWI).
4. Neurocysticercosis—can cause obstruction either due to location
of cyst or by causing ventriculitis. Cysts are best seen on steadystate gradient echo sequences such as CISS/FIESTA-C.
Foramen of Monro
Dilated lateral ventricle(s), normal third and fourth ventricles.392 Aids to Radiological Differential Diagnosis
1. Any cause of significant midline shift—compresses the ipsilateral
lateral ventricle and obstructs the contralateral lateral ventricle.
2. Colloid cyst—characteristically located in the anterior roof of the
third ventricle. Well-defined, nonenhancing, hyperdense on CT due
to protein content.
3. Subependymal giant cell astrocytoma—in young patients with
tuberous sclerosis. Typically within a lateral ventricle near foramen
of Monro, avidly enhancing, often calcified.
Cerebral aqueduct
Dilated lateral and third ventricles, normal fourth ventricle.
1. Aqueduct stenosis—congenital, presents in childhood, ‘beak–like’
appearance of aqueduct, no obstructing mass lesion.
2. Tectal plate glioma—typically in children or adolescents. Diffuse
enlargement and T2 hyperintensity of tectal plate, usually with no
enhancement due to low grade nature of tumour.
3. Pineal region tumour—see Section 13.32.
Fourth ventricle
1. Any posterior fossa mass—e.g. in fourth ventricle (ependymoma,
medulloblastoma), within cerebellum or brainstem or extraaxial
tumours obstructing the foramina of Luschka and Magendie.
2. Chiari 1 malformation

Question 11

INTRACRANIAL CALCIFICATION

Deep grey matter

Answer 11

1. Primary—also known as Fahr disease. Familial, usually autosomal
   dominant, typically presents in middle age. Symmetrical involvement of basal ganglia > thalami > cerebellar dentate nuclei > WM. Other causes (following) must be excluded first.
2. Endocrine—hyper- and hypoparathyroidism, pseudo- and pseudopseudohypoparathyroidism. Appearance identical to Fahr
   disease.
3. Inherited—Down’s, mitochondrial disorders; rarely in Cockayne
   and Aicardi-Goutieres syndromes. Seen in children.
4. SLE—thought to be related to microangiopathy. Background of
   cerebral volume loss and WM lesions .
5. Toxins—lead, carbon monoxide.
6. Posttherapeutic—mineralizing microangiopathy following
   chemoradiotherapy in childhood.

Question 12

INTRACRANIAL CALCIFICATION

Ependymal/periventricular

Answer 12

1. Tuberous sclerosis*—calcified subependymal nodules
   (hamartomas); associated with cortical tubers (hallmark of the
   disease, often calcify) and transmantle WM dysplasia. If large or
   growing + intense enhancement, suggests subependymal giant cell
   astrocytoma.
2. Perinatal TORCH infections—toxoplasma, rubella, CMV (most
   common) and herpes simplex virus

Question 13

INTRACRANIAL CALCIFICATION

Gyriform

Answer 13

1. Sturge-Weber syndrome*—usually unilateral with associated
   cerebral atrophy. Look for retinal enhancement and ipsilateral
   choroid plexus enlargement.
2. Post infarction—due to cortical laminar necrosis.
3. CEC syndrome—rare disorder characterized by occipital
   calcifications in a patient with seizures and coeliac disease

Question 14

INTRACRANIAL CALCIFICATION

Focal lesions with calcification

Answer 14

1. Tumours.
   (a) Meningioma—may be partly or completely calcified.
   (b) Oligodendroglioma—most contain calcification. Other
   low-grade gliomas can also calcify.
   (c) Craniopharyngioma—suprasellar location. Calcification is
   common (in contrast to pituitary adenomas).
   (d) Dermoid—also contains fat.
   (e) Ependymoma—located in fourth ventricle.
   (f) Central neurocytoma—arises from septum pellucidum.
   (g) Pineal region tumours—either engulf or ‘explode’ the normal
   pineal calcification.
   (h) Metastasis—e.g. from breast, mucinous GI tumours, lung,
   osteosarcoma.
2. Infections.
   (a) Neurocysticercosis—multiple small calcifications in brain
   parenchyma and CSF spaces; reflects end–stage quiescent
   disease.
   (b) Tuberculosis*—foci of calcification are usually larger and fewer
   in number versus cysticercosis.
   (c) Perinatal TORCH infections.
3. Vascular.
   (a) Atherosclerosis.
   (b) AVM.
   (c) Aneurysm—rim calcification.
   (d) Cavernoma

Question 15

SOLITARY INTRACEREBRAL MASS

Infiltrative, ill–defined

Answer 15

. Primary tumour—diffuse glioma, or gliomatosis cerebri if
≥3 lobes involved. Ill-defined T2 hyperintensity with no or
minimal mass effect, enhancement or restricted diffusion.
Extensive despite minimal symptoms. Look for scalloping of
overlying calvarium (suggests longstanding slow-growing mass).
2. Cerebritis/encephalitis—acute clinical presentation (cf. diffuse
glioma).
3. Infarction—in both arterial and venous infarction vascular
occlusion suggested by hyperdense thrombus (CT), absent flow
voids and focal increased intravascular susceptibility on SWI (MRI).
Pattern of infarction is different:
(a) Arterial—follows vascular territory, typically shows restricted
diffusion.
(b) Venous—near to occluded vein, greater oedema and risk of
parenchymal haemorrhage (typically has a fragmented
appearance). DWI signal variable.
4. Demyelination—Neuromyelitis optica (NMO) spectrum disorders,
Behçet’s.
5. Contusion—in the context of trauma

Question 16

SOLITARY INTRACEREBRAL MASS

Discrete, well-defined

Answer 16

1. Haematoma—hypertensive haemorrhage classically ganglionic; cf.
   amyloid angiopathy where sulcal siderosis and peripheral
   microhaemorrhages are commonly seen.
2. Metastasis—e.g. from lung, breast, colorectal, melanoma, renal.
   Appearance varies depending on primary; often considerable
   oedema in surrounding WM (usually more than primary
   tumours). Typically located at GWMJ, may be solitary (20%)
   or multiple (80%).
3. Primary tumour—high-grade gliomas tend to have discrete
   enhancement with central necrosis (glioblastoma). Typically
   centred on WM (cf. metastasis). May infiltrate or cross corpus
   callosum—this can also be seen in lymphoma, but lymphoma
   typically shows homogeneous enhancement with no central
   necrosis (unless immunocompromised).
4. Abscess—central restricted diffusion and usually considerable
   associated oedema. Thin enhancing rim, thicker superficially and
   thinner at ventricular surface, may ‘point’ towards ventricle (more
   likely to rupture into the ventricles, causing ventriculitis and
   hydrocephalus). ‘Dual rim’ sign on SWI (cf. primary or metastatic
   tumour).
5. Cavernoma—characterized on MRI by complete haemosiderin rim
   and central mixed ‘popcorn’ components.Skull and brain 395
   13
6. Tumefactive demyelination—incomplete rim enhancement is
   characteristic. More likely in younger age group (20–40s) versus
   metastases.

Question 17

SOLITARY HYPERDENSE INTRACRANIAL
LESION ON UNENHANCED CT
Hypercellular mass

Answer 17

1. Lymphoma*—avid homogeneous enhancement and
   periventricular location are characteristic features.
2. Metastasis—e.g. from small-cell lung cancer.
3. Medulloblastoma—typically in children, located in the cerebellum.
4. Germinoma—young patients, located in the pineal or suprasellar
   region.

Question 18

SOLITARY HYPERDENSE INTRACRANIAL
LESION ON UNENHANCED CT
Lesion containing blood/protein

Answer 18

1. Acute haematoma—higher attenuation than adjacent brain
   parenchyma for up to 7–10 days.
2. Haemorrhagic tumours—especially metastases (e.g. from
   melanoma); less commonly glioblastoma, or pituitary adenoma
   with apoplexy.
3. Colloid cyst—homogeneously hyperdense due to protein content,
   nonenhancing, located in anterior roof of third ventricle.
4. Cavernoma—can mimic intracerebral haematoma on CT. On MRI,
   characteristically has complete haemosiderin rim with central
   mixed signal.
5. AVM.

Question 19

INTRINSIC CORTICAL MASS

Answer 19

1. Acute cortical infarction—results in cortical swelling/oedema with
   localized mass effect. Intense restricted diffusion on DWI.396 Aids to Radiological Differential Diagnosis
2. Acute cerebritis/encephalitis—can show restricted diffusion, but
   less intense and more patchy versus acute infarction.
3. Metastasis—centred on GWMJ (see Section 13.8).
4. Neuronal-glial and glial tumours—apart from (a), these typically
   present in children or young adults with intractable seizures.
   (a) Oligodendroglioma—middle-aged patients. Cortical/
   subcortical mass, well- or ill-defined, often calcified.
   Heterogeneous T2 signal and enhancement. No restricted
   diffusion.
   (b) Dysembryoplastic neuroepithelial tumour (DNET)—benign,
   slow-growing, may scallop overlying skull. Well-defined T2
   bright cortical mass (‘bubbly’), partial FLAIR suppression and
   characteristic hyperintense rim. No oedema. Variable
   calcification/microhaemorrhage. No restricted diffusion/
   enhancement. Associated with focal cortical dysplasia.
   (c) Ganglioglioma—classically cystic mass with an enhancing
   mural nodule, but can be purely solid. No surrounding
   oedema. Calcification is common.
   (d) Pleomorphic xanthoastrocytoma (PXA)—similar appearance
   to ganglioglioma, but calcification is rare. Often associated
   with reactive dural thickening mimicking a dural tail.
5. Focal cortical dysplasia (FCD)—focal cortical thickening with
   blurring of the GWMJ + T2 hyperintensity of the involved cortex
   and subcortical WM. Can mimic (or be associated with) a tumour.
   Potential epileptogenic lesion.
6. Cortical tubers—FLAIR and T2 bright cortical/juxtacortical lesions,
   found in tuberous sclerosis, <10% enhance.
7. Cavernoma—look for blood degradation products.
8. Haematoma—usually post trauma.

Question 20

POSTERIOR FOSSA MASS (ADULT)

13

Answer 20

1. Metastasis—most common infratentorial lesion
2. Haemangioblastoma—typically cerebellar hemisphere cystic
   tumour, avidly enhancing solid mural nodule abutting the
   pia mater with a nonenhancing cyst wall. Associated with
   vHL.
3. Astrocytoma.
   (a) Pilocytic—children and young adults, cyst with mural nodule
   and enhancing cyst wall (cf. haemangioblastoma).
   (b) Glioblastoma—older adults, heterogeneous ill-defined mass
   with irregular intrinsic enhancement.
4. Ependymoma—children and young adults, floor of fourth
   ventricle with ‘plastic-like’ extension through ventricular
   foramina. Heterogeneous, calcified and cystic. Associated
   with NF2.
5. Subependymoma—older adults, usually small, fourth > lateral
   ventricle. No enhancement.
6. Epidermoid—on CT, T1 and T2 indistinguishable from CSF but
   hyperintense on DWI and usually incomplete suppression of
   signal on FLAIR.
7. Dermoid—well-defined midline mass with fat and calcification.
   No enhancement.
8. Abscess—intrinsic restricted diffusion (see Section 13.8).
9. Haematoma/cavernoma—susceptibility effects from blood can
   cause variable DWI signal. Cavernoma often associated with
   nearby developmental venous anomaly.
10. Diffuse midline glioma—children and young adults, most
    commonly pontine, but can occur anywhere in the midline of
    the CNS.
11. Hamartoma—also known as Lhermitte-Duclos disease;
    characteristic thickened and striated appearance of usually one
    cerebellar hemisphere with T2 hyperintensity. No enhancement.
    Associated with Cowden syndrome.
12. Rosette-forming glioneuronal tumour—young adults, typically
    in the midline at the posterior aspect of the fourth ventricle +
    local parenchymal invasion; mixed solid-cystic.
13. Any cerebellopontine angle (CPA) mass

Question 21

SOLITARY RING-ENHANCING LESION

Infection 4

Answer 21

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 and hydrocephalus.
3. Toxoplasmosis—usually multiple
4. Neurocysticercosis—usually multiple;

Question 22

SOLITARY RING-ENHANCING LESION
Neoplastic
3

Answer 22

1. Metastasis—central necrosis with thick, irregular, nodular rim
   enhancement, no intrinsic restricted diffusion;
2. Glioblastoma—centred on WM but often indistinguishable from a
   single metastasis;
3. Ganglioglioma/cytoma—children and young adults. Temporal
   lobe, calcified, slow growing ± bony remodelling, no perilesional
   oedema (cf. glioblastoma, metastases).

Question 23

SOLITARY RING-ENHANCING LESION

Inflammatory

Answer 23

1. Demyelination—incomplete rim enhancement, typical locations;
   see Section 13.13.
2. Radiation necrosis—months to years after radiotherapy.
   Heterogeneous (linear, nodular and cortical) pattern of contrast
   enhancement in radiation field. May mimic tumour recurrence but
   does not show elevated cerebral blood volume (CBV) on perfusion
   and may regress over follow-up.
3. Sarcoidosis*—isolated granuloma very rare, often coexistent dural
   or cranial nerve disease.
4. PML-IRIS—prog multifocal leukoencephalopahty - immune recon inflamm syndrome , immunocompromised pt, activation of john cunningham virus, asymm multifocal perivent/subcortical T2 hyper WM, involves U fibres, no CE, IRIS in response to HAART

Question 24

SOLITARY RING-ENHANCING LESION

Vascular/trauma

Answer 24

1. Subacute haematoma—variable signal and diffusion dependent
   on age; signal drop out on SWI/T2*.
2. Subacute infarct—conforms to vascular territory, rim or gyriform
   pattern of enhancement.
3. Thrombosed or inflammatory aneurysm—arises from intracranial
   artery, appearance dependent on degree of thrombosis/flow and
   local inflammation.
4. Contusion

Question 25

MULTIPLE RING-ENHANCING LESIONS

Neoplastic

Answer 25

1. Metastases—at GWMJ, rarely involve corpus callosum (cf. glioma,
   lymphoma); see Section 13.8.
2. Multifocal glioma—often lesions are connected by abnormal T2
   signal (nonenhancing tumour) and conform to path of WM tracts
   (e.g. along genu of corpus callosum); see Section 13.8.
3. Lymphoma†*—typically solid enhancement but in the
   immunocompromised (or after steroid treatment) may show
   atypical ring enhancement. Important to differentiate from
   toxoplasmosis (see following); lymphoma tends to be fewer in
   number with a subependymal distribution.

Question 26

MULTIPLE RING-ENHANCING LESIONS
Infection
5

Answer 26

1. Abscesses†—may be localized due to direct spread from adjacent
   structures, e.g. sinusitis/mastoiditis; if haematogenous in origin S
   then can be scattered across all vascular territories;
2. Septic emboli†—multiple microabscesses and associated infarcts;
   check for arteritis (arterial irregularity and stenoses) and mycotic
   aneurysms. Risk factors: infective endocarditis, IV drug abuse,
   arteriovenous shunts and indwelling vascular lines.
3. Tuberculoma†
4. Toxoplasmosis†—basal ganglia and GWMJ, concentric alternating
   low and high T2 signal, eccentric ‘target sign’ enhancement.
5. Neurocysticercosis—endemic in South America, Asia and Africa.
   Cysts in subarachnoid space or parenchyma; appearance depends
   on stage

Question 27

MULTIPLE RING-ENHANCING LESIONS

Inflammatory 3

Answer 27

1. Demyelination—acute demyelinating plaques may enhance,
   usually with an ‘open ring’ pattern incomplete to the gyral surface.
   Characteristic locations: periventricular, juxtacortical, infratentorial
   and spinal cord;
2. Radiation necrosis
3. PML-IRIS†( Progressive multifocal leukoencephalopathy immune reconstitution inflammatory syndrome)

Question 28

MULTIPLE RING-ENHANCING LESIONS
Vascular/trauma
1

Answer 28

Contusion/haematoma—orbitofrontal and anterior temporal

regions;

Question 29

INTRACRANIAL CYST WITH
MURAL NODULE
Neoplastic

Answer 29

1. Haemangioblastoma—nonenhancing cyst wall, posterior fossa;
2. Pilocytic astrocytoma—enhancing cyst wall, posterior fossa; see
3. Cystic metastasis—adenocarcinoma, SCC. Thick irregular wall ±
   haemorrhage.
4. Pleomorphic xanthoastrocytoma—young adults, temporal lobe;
5. Craniopharyngioma—multilocular cystic lesion, often in
   suprasellar region with variable calcification and high T1 signal; see
6. Ganglioglioma
7. Rosette-forming glioneuronal tumour
8. Pineocytoma

Question 30

INTRACRANIAL CYST WITH
MURAL NODULE
Infection

Answer 30

1. Neurocysticercosis—vesicular and colloidal vesicular stages, central
   dot from scolex

Question 31

ENHANCING LESIONS IN
PERIVASCULAR SPACES
7

Answer 31

1. Chronic lymphocytic inflammation with pontine perivascular
   enhancement responsive to steroids (CLIPPERS)—characteristic
   punctate and linear enhancement in pons with minimal oedema/
   mass effect; normal intracranial arteries.
2. Neurosarcoid—associated with abnormal thickening and
   enhancement of dura, cranial nerves and pituitary stalk.
3. Vasculitis—evidence of arteritis with stenoses, beading and
   infarcts.
4. Lymphoma*—elderly, fluctuating areas of T2 and diffusion
   abnormality, surrounding mass-like enhancement.
5. Lymphomatoid granulomatosis—in the immunocompromised.
   Multifocal periventricular linear T2 hyperintensities + enhancement.
6. Behçet’s*—young adults, orogenital ulcers. Brainstem and deep
   ganglionic structures, oedema and mass effect (cf. CLIPPERS).
7. Langerhans cell histiocytosis*—children and young adults,
   commonly presents with diabetes insipidus;

Question 32

MENINGEAL ENHANCEMENT

Pachymeningeal (dura–arachnoid)

Answer 32

1. Postoperative—greatest at site of craniotomy, usually unilateral,
   smooth and thin dural enhancement.
2. Intracranial hypotension—due to a drop in CSF volume.
   Orthostatic headaches, brainstem ‘slumping’, subdural effusions
   and convex dural venous sinuses and bulky pituitary from
   pull of negative pressure. Bilateral smooth and thin dural
   enhancement. (subdural effusions, smooth diff pachymenin CE, eff suprasellar cist, reduced pontomesencephalic angle, reduced pontomamillary distance, cereb tonsillar descent, flattening of pons, convex of pituitary, rounding of transverse sinuses)
   (a) Following lumbar puncture—mild and transient.
   (b) Overshunting—slit-like ventricles.
   (c) Skull base leak—following surgery/trauma, presents with CSF
   rhinorrhoea or otorrhoea. Diagnosed with skull base CT
   looking for a fracture or defect.
   (d) Spinal leak—e.g. meningocoele, posttraumatic. Often subtle,
   may need a myelogram to localize.
3. Infection—localized to adjacent osteomyelitis or sinusitis. Irregular,
   thick enhancement.
4. Neoplastic.
   (a) Meningioma—reactive tapered dural thickening around lesion
   (‘dural tail’).
   (b) Metastasis—e.g. breast, prostate; smooth or nodular
   enhancement.
   (c) Secondary CNS lymphoma*—meningeal > parenchymal
   involvement.
   (d) Solitary fibrous tumour of the dura—similar appearance to
   meningioma, but tends to be of lower T2 signal, with internal
   flow voids and a higher propensity for skull invasion. No
   calcification or associated hyperostosis.
5. Granulomatous disease—TB, sarcoid, Wegener’s, rheumatoid,
   Sjögren’s, Behçet’s, Erdheim-Chester, syphilis, fungal disease.
   Multifocal nodular and thick enhancement. Basal distribution in TB
   meningitis.
6. Extramedullary haematopoiesis—dural involvement rare, seen
   in thalassemia and myelofibrosis. Widened diploic space in skull.
7. Idiopathic hypertrophic cranial pachymeningitis—mass-like
   thickening of the dura, often with cranial nerve involvement. Some
   cases are due to IgG4-related disease

Question 33

MENINGEAL ENHANCEMENT

Leptomeningeal (pia–arachnoid) 4

Answer 33

1. Carcinomatosis—typically nodular. Metastatic (breast, lung), lymphoma, ependymoma, germinoma, medulloblastoma, glioblastoma, pineoblastoma. Image whole neuraxis to assess extent of disease.
2. Meningoencephalitis—bacterial, viral, fungal, Lyme disease.
   Cerebral swelling.
3. Granulomatous disease—TB, sarcoid, Wegener’s, rheumatoid
   nodules, fungal disease.
4. Vascular—collateral flow (ischaemia) or increased flow, e.g. dural
   fistula, pial angioma of Sturge-Weber

Question 34

EPENDYMAL ENHANCEMENT

Answer 34

1. Infection—ventriculitis.
   (a) Bacterial—intraventricular pus restricts diffusion, and may be
   related to an adjacent cerebral abscess. Ependymal
   enhancement is an early sign of ventriculitis and warrants
   escalation of therapy and consideration of shunting for
   hydrocephalus.
   (b) Viral—CMV, VZV; immunocompromised patients.
2. Neoplastic—abutting ventricular surface or intraventricular.
   (a) Nodular/linear—lymphoma, glioblastoma, ependymoma,
   germ cell tumour, metastases.
   (b) Mass-like—ependymoma, giant cell astrocytoma.
3. Granulomatous—TB (basal meningitis), sarcoidosis (cranial nerves
   and dura).
4. Intraventricular haemorrhage—hyperdense blood within the
   ventricles.
5. Subependymal venous congestion—can mimic ependymal
   enhancement.
   (a) Deep cerebral vein thrombosis—hyperdense vein,
   oedema.
   (b) AVM or AVF—dilated abnormal vessels.
   (c) Sturge-Weber*—cortical calcification, cerebral atrophy and
   enlarged ipsilateral choroid plexus.

Question 35

CRANIAL NERVE (CN) ENHANCEMENT
Neoplastic
2

Answer 35

1. Primary.
   (a) Schwannoma—CN VIII; sporadic or NF2 (diagnostic if bilateral).
   (b) Meningioma—‘tram-track’ enhancement, CN II.
   (c) Neurofibroma—rarer to involve CN, T2 hyperintense rim with
   central low signal (target sign). NF1: plexiform neurofibromas
   of CN III and CN V.
   (d) Optic nerve glioma—pilocytic astrocytomas, associated with NF1
2. Secondary.
   (a) Leptomeningeal dissemination—nodular involvement,
   seeding from primary CNS (ependymoma, medulloblastoma,
   germinoma, lymphoma) or secondary metastatic (breast, lung,
   melanoma).
   (b) Perineural spread—from head and neck tumours, e.g.
   mucosal SCC and salivary gland adenoid cystic carcinoma (CN
   VII), lymphoma, melanoma.

Question 36

CRANIAL NERVE (CN) ENHANCEMENT
Infection
3

Answer 36

1. Meningitis.
   (a) Viral infections—HSV type 1, CMV, and VZV (Ramsay Hunt
   Syndrome—vesicular eruptions). CN VII.
   (b) TB*—cisternal segments of CN, surrounding exudate.
   (c) Cryptococcus neoformans—infiltration of meninges around
   optic tracts, nerves and chiasm.
2. Lyme disease—may involve CN III to VII.
3. Fungal—aspergillosis, mucormycosis, actinomycosis. Perineural
   spread from sinus disease. Elderly diabetic patients are most at risk

Question 37

CRANIAL NERVE (CN) ENHANCEMENT
Inflammatory
4

Answer 37

1. Bell’s palsy—uniform linear enhancement of CN VII.
2. Miller-Fisher syndrome—variant of Guillain-Barré, multiple CN,
   linear enhancement.
3. Chronic inflammatory demyelinating polyneuropathy—‘onion
   bulb’ thickening of multiple peripheral and cranial nerves, with
   diffuse enhancement.
4. Demyelinating—multiple sclerosis (MS) and NMO. CN II (optic
   neuritis

Question 38

CRANIAL NERVE (CN) ENHANCEMENT
Granulomatous

Answer 38

1. Sarcoidosis*—any CN with thickening, most commonly CN II
   centred around chiasm and pituitary stalk.
2. Wegener’s granulomatosis*—spread from sinuses, associated with
   dural thickening, vasculitis with infarcts.
3. Tolosa-Hunt—idiopathic inflammation of cavernous sinus and
   orbital apex. Painful ophthalmoplegia, enlarged cavernous sinus
   with internal carotid artery (ICA) narrowing and enhancement of
   CNs that pass through.

Question 39

CRANIAL NERVE (CN) ENHANCEMENT
Other

Answer 39

1. Post radiation neuritis—limited to radiation field.
2. Ischaemic—diabetics, vasculopaths; transient enhancement
   followed by gradual atrophy. CN II, III and VI.

Question 40

ENLARGED LEPTOMENINGEAL

PERFORATORS 3

Answer 40

1. Collateralization due to proximal progressive steno-occlusive disease.

(a) Moyamoya disease—idiopathic, progressive occlusion of the proximal intracranial arteries. ‘Puff of smoke’—angiographic appearance of small abnormal net-like collateral vessels. ‘Ivy sign’—pial collaterals have serpentine sulcal FLAIR hyperintensity and enhancement.
(b) Moyamoya-like syndromes—other proximal intracranial artery steno-occlusive diseases that mimic Moyamoya disease, e.g. post radiation, NF1, Down’s syndrome, SCD and atherosclerosis.

2. Secondary to a distal ‘sump’ effect.

(a) AVM—tangle of abnormal vessels with feeding arteries and draining veins. Often multiple dilated vessels, no stenoses (cf. Moyamoya).
(b) Tumour—vascular tumours recruit increased arterial flow to
both tumour and surrounding parenchyma/leptomeninges.

3. Sturge-Weber*—phakomatosis; facial cutaneous and leptomeningeal haemangiomas. Steal phenomenon causes atrophy of subjacent cortex and WM + ‘tram-track’ calcification

Question 41

WM LESIONS WITH LITTLE
MASS EFFECT
Punctate lesions
6

Answer 41

1. Nonspecific and age-related—small peripheral lesions in
   nontypical locations for an inflammatory cause (see following).
   Greater number reported in patients with migraine. Spare
   subcortical U-fibres (SCUF). Some authors arbitrarily say one lesion
   per decade is within normal limits.
2. Vascular.
   (a) Small-vessel disease (SVD)—periventricular WM lesions
   (>3 mm from surface, cf. MS) and deep WM lesions;
   tends to spare corpus callosum (cf. MS). Varies from
   punctate to confluent. Spares SCUF due to end-arterial
   distribution.
   (b) Hypertensive encephalopathy—ganglionic lacunar infarcts
   and microhaemorrhages. Interrelated with SVD.
   (c) Multi-infarct encephalopathy—SVD + additional embolic
   cortical and pontine infarcts.
   (d) Cerebral amyloid angiopathy—see Section 13.4.
3. Inflammatory.
   (a) Multiple sclerosis (MS)—perivenous distribution,
   periventricular (contacting surface, cf. SVD), infratentorial,
   cortical/juxtacortical with involvement of SCUF (cf. vascular
   aetiologies). Involves corpus callosum at callososeptal interface.
   Incomplete ring enhancement (cf. infection). Short segment
   spinal cord lesions.
   (b) Neuromyelitis optica (NMO)—often indistinct/fluffy lesions,
   classic locations: periaqueductal grey matter and area
   postrema (posterior medulla abutting fourth ventricle) + optic
   neuritis. Long segment spinal cord lesions (cf. MS).
   (c) Vasculitis—wide spectrum of vasculitides defined by
   size of vessel involvement and whether confined to CNS
   arteries or systemic. Multiple infarctions, usually bilateral
   in different vascular territories. Angiography demonstrates
   multifocal stenoses and occlusions. Black-blood contrast
   MRI may show enhancing inflammatory tissue cuffing
   arteries.
   (d) Sarcoidosis*—see Section 13.15.
   (e) Connective tissue disease (CTD)—can be indistinguishable
   from MS, e.g. SLE (associated with infarcts), Sjögren’s. Other
   signs of CTD.
4. Miliary metastases—e.g. lung, melanoma, breast. Often at GWMJ.
   Greater mass effect and perilesional oedema. Callosal involvement
   very rare (cf. MS).
5. Infection—granuloma, septic emboli; ± punctate restricted
   diffusion, microhaemorrhages, complete ring enhancement
6. Diffuse axonal injury (DAI)—shear-related injuries often with
   microhaemorrhage; common locations GWMJ, splenium and
   middle cerebellar peduncles.

Question 42

WM LESIONS WITH LITTLE
MASS EFFECT
Confluent WM lesions (up to 20 mm in size)

Answer 42

1. Neoplastic—e.g. glioma, lymphoma, metastases. Generally have
   more mass versus other differentials (see Section 13.8).
2. Vascular—same as above due to coalescence of multiple vascular
   insults.
3. Hypotensive cerebral infarction—deep and superficial watershed
   territories, typical signs of infarction if acute.
4. Infection.
   (a) Encephalitis—HSV predilection for medial temporal lobes;
   other non-herpes encephalitides can involve basal ganglia
   (BG), thalamus, brainstem and cerebellum. Ill-defined, variable
   enhancement and restricted diffusion. Acute presentation with
   fevers, seizures, reduced Glasgow Coma Scale (GCS) and
   nonspecific neurology.
   (b) Progressive multifocal leukoencephalopathy (PML)—JC
   polyomavirus opportunistic infection causing demyelination in
   immunocompromised patients (HIV, patients on
   immunotherapy). Multifocal periventricular and subcortical
   lesions involving SCUF. No contrast enhancement. Late
   cavitation/cystic change.
   (c) PML-immune reconstitution inflammatory syndrome
   (PML-IRIS)—paradoxical deterioration in PML due to
   exaggerated inflammatory reaction after reconstitution of
   immune system. Classically seen in HIV patients on therapy,
   but also recognized with MS immunotherapies. Associated
   with mass effect and irregular enhancement (cf. PML).
   (d) Lyme disease—resembles MS but greater abnormalities in BG
   and brainstem ± CN enhancement.
5. Inflammatory.
   (a) MS, NMO, vasculitis, sarcoidosis*—see earlier.
   (b) Tumefactive demyelination—large demyelinating lesion with
   relatively little mass effect or oedema, often unifocal.
   Open-ring enhancement, low CBV on perfusion (cf. tumour).
   Like MS often perivenous in distribution.
   (c) Acute disseminated encephalomyelitis (ADEM)—
   monophasic demyelination following infection/vaccination,
   usually in children or adolescents. Bilateral asymmetrical
   subcortical lesions, spare callososeptal interface (cf. MS).
6. Osmotic myelinolysis—acute demyelination from rapid change in
   serum osmolality (classically rapid correction of hyponatraemia).
   Typically a round or trident-shaped lesion in central pons, but can
   be extrapontine, e.g. symmetrical in BG and/or WM.
7. Radiation necrosis—s

Question 43

WM LESIONS WITH LITTLE MASS EFFECT
Diffuse WM lesions (spanning ≥2 cerebral lobes)
6

Answer 43

1. Vascular
2. Neoplastic—diffuse glioma.
3. Inflammatory.
   (a) MS, NMO, vasculitis, sarcoidosis
   (b) Rasmussen encephalitis—children and young adults with intractable seizures; chronic encephalitis of one hemisphere with ipsilateral patchy WM lesions and volume loss.
4. Leukoencephalopathies—all tend to cause symmetric, multifocal lesions. Most present in childhood.
   (a) Inherited—early adult onset.
   (i) CADASIL—recurrent lacunar and subcortical infarcts, especially in anterior temporal and frontal lobes (see
   (ii) COL4A1—small-vessel disease, dilated perivascular spaces, microhaemorrhages and intracerebral haemorrhages. SCUF spared.
   (iii) X-linked adrenoleukodystrophy—adult-onset phenotype, frontal lobe and genu of corpus callosum involvement predominates (cf. child onset, which has a predilection for occipitoparietal regions).
   (iv) Krabbe disease—adult-onset phenotype, slower progression. CT: hyperdense thalami, cerebellum and caudate nuclei. Periventricular abnormal WM signal.
   (b) Toxic–metabolic—dependent on cause, typically symmetrical
   and often involve splenium + corresponding restricted diffusion.
   (c) HIV encephalopathy—symmetric periventricular and deep WM lesions + volume loss.
5. Degenerative—e.g. frontotemporal lobar degeneration and corticobasal degeneration; associated volume loss
6. Radiation leukoencephalopathy—diffuse confluent lesions with volume loss and evidence of indications for radiotherapy, e.g. intracranial or head and neck tumour. U-fibre sparing

Question 44

CORPUS CALLOSUM (CC) LESIONS
Atrophic/dysplastic callosum

Answer 44

1. Agenesis/dysgenesis—CC develops from anterior to posterior;
   early embryonic insult = CC agenesis, late embryonic insult = CC
   dysgenesis limited to rostrum or splenium. Complete agenesis =
   parallel (‘racing car’) lateral ventricles, WM tracts paralleling the
   interhemispheric fissure (Probst bundles), high-riding third
   ventricle. Associated with pericallosal lipoma, dermoid and
   interhemispheric arachnoid cysts.
2. Atrophy—small-vessel ischaemia, radiation therapy,
   leukodystrophy. Extensive abnormal WM signal and volume loss
   beyond CC

Question 45

CORPUS CALLOSUM (CC) LESIONS
Multifocal lesions

Answer 45

1. Demyelination—MS, NMO. Lower border of CC at callososeptal
   interface (see Section 13.20).
2. Vascular—e.g. embolic infarcts, Susac syndrome. Asymmetric,
   adjacent to the midline. Callosal lesions are characteristic in Susac
   syndrome and typically spare the callososeptal interface, ±
   restricted diffusion and enhancement if acute; patients are typically
   young adult females presenting with a clinical triad of
   encephalopathy, bilateral sensorineural hearing loss and branch
   retinal artery occlusions.
3. DAI—asymmetric involving both midline and borders of CC +
   microhaemorrhage on SWI (see Section 13.20).
4. Marchiafava-Bignami syndrome—chronic alcoholics with vitamin
   B deficiency. Body of CC > genu/splenium. Large lesions in the
   central layer of CC

Question 46

CORPUS CALLOSUM (CC) LESIONS
Neoplasms

Answer 46

1. Butterfly glioma—high grade glioma, symmetric midline-crossing
   lesion most common in frontal lobes crossing and expanding
   genu, heterogeneous enhancement + central necrosis.
2. Lymphoma*—hypercellular (dense on CT), homogeneous
   restricted diffusion and solid enhancement (cf. butterfly glioma)

Question 47

CORPUS CALLOSUM (CC) LESIONS
Transient lesions

Answer 47

1. Cytotoxic lesions of the corpus callosum—transient cytotoxic
   oedema of the splenium; well-defined, oval, in the midline. T2
   hyperintense + restricted diffusion but no enhancement. Many
   causes: seizures, metabolic (hypoglycaemia, sodium imbalance),
   infections, drugs and toxins

Question 48

CORPUS CALLOSUM (CC) LESIONS
Hydrocephalus-related

Answer 48

1. Corpus callosum impingement syndrome—impingement of CC
   against falx due to severe chronic hydrocephalus; abnormal signal
   + atrophy in rostral CC.
2. Post shunt decompression—typically diffuse oedema in CC
   occurring after shunt insertion for chronic severe hydrocephalus

Question 49

DEEP GREY MATTER ABNORMALITIES

Physiological

Answer 49

1. Age-related—incidence of GP calcification increases with age.
   Increased iron deposition causes reduced T2 signal in GP and
   putamen (see Section 13.24).
2. Perivascular spaces (PVS)—CSF signal on all sequence

Question 50

DEEP GREY MATTER ABNORMALITIES

Vascular

Answer 50

1. Lacunar infarct—well-defined CSF density/intensity lesions +
   surrounding high signal rim evident on FLAIR.
2. Hypertensive haemorrhage—background of DGM lacunes,
   enlarged PVS and microhaemorrhages.
3. Global hypoxic ischaemic injury—bilateral infarcts in regions of
   high metabolic demand: GP, posterior putamen, ventrolateral
   thalami, perirolandic regions, occipital cortex and hippocampal
   formations.
4. Venous infarction—due to internal cerebral vein thrombosis;
   bithalamic involvement (see Section 13.25). Marked swelling from
   venous congestion.
5. Central variant PRES—can involve brainstem.

Question 51

DEEP GREY MATTER ABNORMALITIES

Neurodegenerative 3

Answer 51

1. Parkinson’s—18F-DOPA PET scan: loss of normal comma-shaped tracer uptake in the corpus striatum with full stop-shaped uptake only seen in the caudate head.
2. Multiple system atrophy-Parkinson’s type (MSA-P)—reduced putamen volume with reduced T2 signal relative to globus pallidus. High T2 rim surrounding putamen (‘putaminal rim’ sign) at 1.5T. (MSA-C- hot cross bun sign -pontocerebellar tracts)
3. Huntington’s disease—atrophy of caudate heads, ‘boxcar’ frontal horns.

Question 52

DEEP GREY MATTER ABNORMALITIES

Toxins

Answer 52

1. Chronic bilirubin encephalopathy (kernicterus)—increased T1
   and T2 signal in GP.
2. Hypermanganesaemia—e.g. total parenteral nutrition,
   haemodialysis, liver failure. High T1 signal in BG.
3. Exogenous toxins.
   (a) Carbon monoxide—GP.
   (b) Methanol—putamen.
   (c) Cyanide—corpus striatum and perirolandic cortex

Question 53

DEEP GREY MATTER ABNORMALITIES

Acquired metabolic disease

Answer 53

1. Uraemic encephalopathy—bilateral basal ganglia, thalamus and
   midbrain. ‘Lentiform fork’ sign—T2 hyperintense internal and
   external capsule.
2. Hyperammonaemic/hepatic encephalopathy—acute liver failure.
   Symmetric insular, thalamic and posterior limb of internal capsule
   (PLIC) T2 hyperintensity.
3. Hypoglycaemia—symmetric high T2 and restricted diffusion in
   basal ganglia, PLIC, splenium and parietooccipital cortex.

Question 54

DEEP GREY MATTER ABNORMALITIES

Inherited metabolic disease

Answer 54

1. Wilson’s disease—copper deposition disease. High T2 and volume
   loss in striatum and ventrolateral thalamus. ‘Face of giant panda’
   sign in midbrain and ‘miniature panda’ sign in pons—‘double
   panda’ sign if both are present.
2. Mitochondrial cytopathies.
   (a) Kearns-Sayre syndrome—GP and cortical calcification.
   (b) Leigh syndrome—putamen, thalamus and periaqueductal
   grey matter.
3. Lipid storage disorders—Krabbe disease (see Section 13.20).
4. Amino acid disorders—e.g. methylmalonic acidaemia; selective
   necrosis of GP.
5. Neurodegeneration with brain iron accumulation (NBIA)—see
   Section 13.24.
6. Fahr disease—symmetrical calcification of basal ganglia, dentate
   nuclei and subcortical WM

Question 55

DEEP GREY MATTER ABNORMALITIES

Infectious

Answer 55

1. Variant CJD (vCJD)—‘hockey stick’ sign: T2 hyperintensity in
   pulvinar and dorsomedial thalamus (cf. sporadic CJD which spares
   thalamus).

Question 56

BASAL GANGLIA: BRIGHT ON T1

Paramagnetic substances

Answer 56

1. Methaemoglobin—hypertensive haemorrhage, haemorrhagic
   infarction. Includes haemorrhagic necrosis, e.g. in carbon
   monoxide (GP) or methanol (putamina) poisoning.
2. Copper—Wilson’s disease.
3. Manganese—parenteral nutrition, haemodialysis, liver failure.
4. Calcification—some crystalline forms of calcium cause T1
   shortening (e.g. Fahr, hypoparathyroidism).
5. Chronic bilirubin encephalopathy (kernicterus)—increased T1
   and T2 signal in GP.
6. Prior administration of linear gadolinium chelates

Question 57

BASAL GANGLIA: BRIGHT ON T1

Unknown cause

Answer 57

1. Diabetic striatopathy—non-calcific hyperdensity is a characteristic
   feature; typically manifests with hemiballism-hemichorea caused by
   nonketotic hyperglycaemia. due to Zn or manganese deposition
2. Fabry disease—typically pulvinar T1 hyperintensity (cf. vCJD with
   T2 hyperintensity). Associated with posterior circulation infarcts.
3. NF1—focal areas of signal intensity (FASI), high on T1 and T2, in
   the basal ganglia; most common neuroimaging feature of NF1

Question 58

SYMMETRICAL BASAL GANGLIA
SUSCEPTIBILITY CHANGES
Iron
10–20 years—iron deposition starts in GP.
2. 20–40 years—iron deposition increases in GP + mildly visible in
putamina.
3. >40 years—iron deposition increases in GP and putamina to a
lesser extent. Calcification of the GP is also variably present

Answer 58

1. Neurodegeneration with brain iron accumulation (NBIA)—
   group of progressive neurological disorders that feature prominent
   extrapyramidal symptoms and iron deposition. Reduced signal in
   GP on T2/T2*/SWI sequences with central high signal: ‘eye of the
   tiger’ sign. Most common is pantothenate kinase-associated
   neurodegeneration (PKAN), which has abnormalities restricted to
   the GP and substantia nigra. Presence of pigmentary retinopathy is
   strongly suggestive of PKAN and is not seen in other forms of
   NBIA.
2. Huntington’s disease—atrophy of caudate heads.

Question 59

BILATERAL THALAMIC LESIONS

Vascular

Answer 59

1. Artery of percheron infarct—variant solitary arterial trunk that
   arises from one of the posterior cerebral arteries supplying both
   paramedian thalami and rostral midbrain.
2. Basilar tip thrombosis—hyperdense thrombus/loss of flow void in
   the basilar tip.
3. Internal cerebral venous infarct—look for deep cerebral vein
   thrombus on CT (hyperdense) and MRI (loss of T2 flow void).
   Greater local swelling than arterial infarcts. SWI may show
   serpiginous thrombosed deep medullary veins and associated
   microhaemorrhage.
4. Hypertensive haemorrhage.
5. Hypoxic ischaemic encephalopathy.

Question 60

BILATERAL THALAMIC LESIONS

Infection

Answer 60

1. Encephalitis—caused by arboviruses transmitted by mosquito or
   tick bites, e.g. Japanese encephalitis (Asia), West Nile encephalitis
   (Middle East), Murray Valley encephalitis (Australasia), St Louis
   encephalitis (USA). Bilateral thalamic involvement is typical ±
   extension into brainstem or basal ganglia; usually haemorrhagic.
   Fevers and fulminant course.
2. Variant CJD—see Section 13.22.Skull and brain 413
   13
3. Acute necrotizing encephalitis—haemorrhagic parainfectious
   syndrome in young children. Thought to be an immune
   overreaction to a mild antecedent viral infection.

Question 61

BILATERAL THALAMIC LESIONS
Metabolic
5

Answer 61

1. Carbon monoxide poisoning—bilateral GP and thalamus.
2. Wernicke’s encephalopathy—triad of mental status, gait and
   oculomotor dysfunction. Due to thiamine deficiency. Symmetric
   abnormal signal in thalami, mammillary bodies, tectal plate and
   periaqueductal areas.
3. Mitochondrial cytopathies—Leigh, Kearns-Sayre
4. Fabry disease (F-foam/febrile, A-angiokeratoma, B-Burning pain/Boys, R-renal failure, Y- Xlinked, C - CV disease/ceramide)
5. Wilson’s disease

Question 62

BILATERAL THALAMIC LESIONS

Neoplastic

Answer 62

1. Bithalamic glioma—low-grade astrocytoma in children and young
   adults; expansile and often nonenhancing tumour ± obstructive
   hydrocephalus

Question 63

BILATERAL MIDDLE CEREBELLAR
PEDUNCLE (MCP) LESIONS
Degenerative (~40%)
2

Answer 63

1. MSA-cerebellar type (MSA-C)—symmetrical high T2 signal and
   volume loss in MCPs, ‘hot cross bun’ sign in pons: cross of abnormal
   signal due to selective degeneration of pontocerebellar tracts.
2. Fragile X—lesions in MCPs and splenium

Question 64

BILATERAL MIDDLE CEREBELLAR
PEDUNCLE (MCP) LESIONS
Metabolic/toxic (~20%)
6

Answer 64

1. Wilson’s disease.
2. Cirrhotic liver disease.
3. Adrenoleukodystrophy—see Section 13.20.
4. Hypoglycemia.
5. Solvent abuse.
6. Heroin inhalation—symmetrical involvement of PLIC and
   cerebellar WM.

Question 65

BILATERAL MIDDLE CEREBELLAR
PEDUNCLE (MCP) LESIONS
Cerebrovascular (~15%)

Answer 65

1. PRES (central variant)—typically precipitated by drugs or hypertension.
2. Anterior inferior cerebellar artery (AICA) infarction—look for restricted diffusion and signs of vertebral artery occlusion or dissection

Question 66

BILATERAL MIDDLE CEREBELLAR
PEDUNCLE (MCP) LESIONS
Infection/Inflammatory (~15%

Answer 66

1. MS.
2. Behçet’s*—may involve bilateral basal ganglia, brainstem and
   thalamus.
3. ADEM.
4. HIV.
5. Japanese encephalitis—bilateral thalamic involvement.
6. PML and PML-IRIS.

Question 67

BILATERAL MIDDLE CEREBELLAR
PEDUNCLE (MCP) LESIONS
Neoplastic (~10%)

Answer 67

1. Lymphoma*.
2. Brain stem glioma.
3. Meningeal carcinomatosis—leptomeningeal enhancement and
   FLAIR sulcal hyperintensity

Question 68

INTRASELLAR MASS

Intrinsic to the gland

Answer 68

1. Pituitary adenoma—mildly T2 hyperintense and T1 hypointense
   relative to normal gland.
   (a) Microadenoma—<10 mm, shows slightly delayed (60 secs)
   enhancement relative to normal gland.Skull and brain 415
   13
   (b) Macroadenoma—>10 mm, often demonstrates suprasellar
   and/or cavernous sinus extension, ± cystic degeneration and
   high T1 signal from internal haemorrhage or proteinaceous
   material. Sellar expansion from gradual remodelling.
2. Pituitary hyperplasia—enlarged normal signal gland.
   (a) Physiological—pregnancy, postpartum, lactation and
   postpubertal females.
   (b) Pathological—end-organ failure, e.g. hypothyroidism.
3. Pituitary haemorrhage/infarction—associated with
   macroadenoma. Blood-fluid levels, dense intrasellar mass on CT
   and variable signal and diffusion on MRI. ‘Apoplexy’ when
   haemorrhage/infarction is associated with acute clinical
   symptoms—headache, sudden vision loss and oculomotor palsy.
4. Intracranial hypotension—slightly swollen convex pituitary often
   extending just above sella, due to negative intracranial pressure
   (see Section 13.16).
5. Inflammatory hypophysitis—these can involve anterior and/or
   posterior pituitary and/or infundibulum, typically causing
   enlargement and avid homogeneous enhancement, but without
   sellar remodelling (cf. adenoma). Pituitary dysfunction is common.
   If the posterior pituitary is involved the normal T1 ‘bright spot’ is
   absent.
   (a) Lymphocytic hypophysitis—typically in late pregnancy or
   postpartum.
   (b) Granulomatous hypophysitis—e.g. sarcoid, TB, Wegener’s.
   (c) IgG4-related hypophysitis—as part of systemic IgG4-related
   disease.
6. Metastasis—rare, males = lung, females = breast. Pituitary or
   infundibulum. Normal fossa size, bony destruction, dural
   thickening and irregular margins (cf. adenoma).
7. Pituitary abscess—rare, cystic lesion + peripheral enhancement,
   likely associated meningitis. Fever, meningism

Question 69

INTRASELLAR MASS

Extrinsic to the gland

Answer 69

1. Meningioma—sphenoid, diaphragma sellae or cavernous sinus.
   Typically projects into sella displacing diaphragma sellae inferiorly
   + enhancing dural tail ± skull hyperostosis (cf. macroadenoma).
2. Rathke’s cleft cyst—also known as pars intermedia cyst, typically
   lies between anterior and posterior pituitary. Usually <1 cm but
   can be large. 50% have intracystic nodule. ‘Claw sign’ of normal
   displaced pituitary.
3. Craniopharyngioma—purely intrasellar rare, usually suprasellar
   and sellar.

Question 70

PITUITARY INFUNDIBULAR LESION

Neoplastic

Answer 70

1. Metastases—e.g. from lung or breast
2. Lymphoma*—may present as isolated stalk thickening or periventricular enhancing masses. Seen in primary and secondary CNS involvement.
3. Leukaemia—acute/chronic myeloid leukemia. Diagnosis usually known prior to infundibular involvement. Look for dural and optic nerve sheath deposits.
4. Germ cell tumours—children/young adults. Germinoma most common, other types: embryonal carcinoma, yolk sac tumour, choriocarcinoma, teratoma and mixed. Hyperdense on CT, homogeneous solid enhancement and restricted diffusion.
5. Craniopharyngioma.
   (a) Adamantinomatous (90%)—children > adults, 90% cystic, 90% calcified and 90% enhance. Multilocular, large with high T1 (oily) contents.
   (b) Papillary (10%)—adults, typically a solid enhancing mass. Small water-signal cysts, minimal enhancement. Calcification is rare.
6. Langerhans cell histiocytosis (LCH)*—children/young adults, stalk
   thickening and enhancement ± meningeal and choroid plexus
   involvement. Posterior pituitary bright spot absent. Look for lung,
   bone and skin disease.
7. Pituicytoma—benign, men in 40–50s. Enhances homogeneously.
   No sellar enlargement. ( neurohypophysis cells)
8. Other primary tumours—gliomas, choristomas (normal tissue in abnormal location - benign) and tanycytomas ( new type of tumour-hypothal/suprasellar from tancyte) (encase circle of Willis).
9. Pituitary adenoma—may occasionally arise in the infundibular
   region (pars tuberalis)

Question 71

PITUITARY INFUNDIBULAR LESION
Nonneoplastic
5

Answer 71

1. Neurosarcoid—enhancing stalk granuloma, which often involves adjacent optic pathways and floor of third ventricle. Check for dural, leptomeningeal and CN involvement. Consider systemic involvement.
2. Lymphocytic infundibuloneurohypophysitis (LINH)—variant of lymphocytic hypophysitis that predominantly affects infundibulum;
3. Other granulomatous hypophysitis—TB, Wegener’s, Erdheim-Chester, Whipple’s disease. In isolation generally indistinguishable from sarcoidosis. TB associated with basal meningitis. Wegener’s associated with sinonasal disease
4. Ectopic posterior pituitary—T1 bright spot located on median eminence of hypothalamus ± pituitary stalk/gland hypoplasia. Look for other midline abnormalities, e.g. deficient septum pellucidum.
5. Infundibular cysts—pars intermedia cysts may rarely be confined to the stalk.

Question 72

SUPRASELLAR MASS
Meningeal
2

Answer 72

1. Meningioma—see Section 13.27.
2. Granulomatous—TB, sarcoid, LCH. Enhancing granulomas may be
   T2 hypointense

Question 73

SUPRASELLAR MASS

Vascular 1

Answer 73

1. Saccular aneurysm—giant aneurysms (>25 mm) may erode bone
   in the supra or parasellar region, appearances may be complicated
   by thrombus and flow void. Look for pulsation artefact in phase
   encoding direction. Angiographic imaging essentia

Question 74

SUPRASELLAR MASS

Parenchymal

Answer 74

1. Pituitary lesions—with suprasellar extension.
2. Infundibular masses—especially craniopharyngioma (often large,
   making it difficult to verify infundibular origin).
3. Hypothalamic hamartoma—arises from tuber cinereum; T2 iso/
   hyperintense to cerebral cortex, no enhancement. Gelastic seizures,
   precocious puberty and developmental delay.
4. Germ cell tumours.
5. Metastases/lymphoma*

Question 75

SUPRASELLAR MASS

Optic chiasm

Answer 75

1. Hypothalamic chiasmatic glioma—pilocytic astrocytoma typically
   arising from optic nerve/chiasm with variable involvement of
   hypothalamus. Variable enhancement. Associated with NF1.
2. Chiasmal optic neuritis—NMO, MS. High T2 signal and swelling.
   Signs of demyelinating disease elsewhere.

Question 76

SUPRASELLAR MASS

Cisternal 5

Answer 76

1. Epidermoid—paramidline cystic lesion, CSF density (CT) and T1/
   T2 signal (MRI). Incomplete signal suppression on FLAIR and
   characteristic restricted diffusion enable differentiation from
   arachnoid cyst.
2. Dermoid—midline cystic lesion with fat content and capsular
   calcification. Look for subarachnoid ‘fat droplets’ to indicate
   rupture which is associated with chemical meningitis and
   hydrocephalus.
3. Teratoma—multiloculated, heterogeneous mixed soft tissue, fat
   and calcification.
4. Lipoma—fat density/signal lesion, calcification rare in suprasellar
   location (cf. dermoid and interhemispheric lipomas).
5. Arachnoid cyst—well-defined cyst of variable size. Isointense
   to CSF, nonenhancing, noncalcified.

Question 77

CAVERNOUS SINUS (CS)/
PARASELLAR MASS
Extension from pituitary lesion

Answer 77

1. Pituitary macroadenoma—can invade the CS via lateral extension,
   causing bulging of the CS. Signal difference most appreciable on
   pre- and postcontrast T1. Tumour extension beyond the
   intercarotid line suggestive of invasion. ICA encased but not
   typically narrowed (cf. meningioma). May invade skull base,
   mimicking a primary bone lesion

Question 78

CAVERNOUS SINUS (CS)/PARASELLAR MASS
Dural

4

Answer 78

1. Meningioma—avidly enhancing mass with thickened dural tail;
   other meningiomas may be present. More often associated with
   venous congestion, and if ICA is encased it is often narrowed (cf.
   macroadenoma).
2. Granulomatous/inflammatory infiltration
   (a) Sarcoidosis—additional dural and nerve deposits, signs of
   systemic sarcoid in lungs.
   (b) TB—with basal meningitis ± tuberculomas.
   (c) Idiopathic orbital inflammatory syndrome—also known as
   orbital pseudotumour. Most commonly involves extraocular
   muscles with rapid onset unilateral proptosis. Mass is
   ill-defined and T2 hypointense due to fibrosis (cf. lymphoma,
   which is more lobular with intermediate T2 signal).
   Involvement of the orbital apex and cavernous sinus with
   painful ophthalmoplegia is termed Tolosa-Hunt syndrome;
   may also narrow the ICA and extend to superior orbital fissure.
   Linked to many autoimmune diseases, including:
   (i) IgG4-related disease—associated with pachymeningitis,
   hypophysitis and salivary/lacrimal gland enlargement.
   (ii) Wegener’s—look for sinonasal disease with abnormal
   soft tissue, osseous erosions and nasoseptal perforation.
   (iii) Churg-Strauss*—with lung involvement.
3. Defect—meningocoele/encephalocoele. Often due to raised
   intracranial pressure (ICP), clues include a partially empty sella
   (from arachnoid herniation flattening pituitary) and enlarged
   Meckel’s caves.
4. Invasive fungal sinusitis—Aspergillus; immunocompromised and
   diabetic patients. Extension from paranasal sinuses. Hyperdense
   opacification of paranasal sinus on CT, with susceptibility signal
   dropout on T2-weighted MRI.

Question 79

CAVERNOUS SINUS (CS)/
PARASELLAR MASS
Cavernous sinus metastases

Answer 79

1. Haematogenous.
   (a) Lymphoma*—homogeneous enhancement and restricted
   diffusion (more than pseudotumour).
   (b) Metastases—irregular, heterogeneous infiltrative enhancing
   tissue.
2. Direct extension—from malignant sphenoid sinus and
   nasopharyngeal tumours, with osseous erosion.
3. Perineural spread—squamous cell and adenoid cystic carcinomas;
   review skull base spaces, fissures and optic pathways. Abnormally
   thickened and enhancing nerve

Question 80

CAVERNOUS SINUS (CS)/
PARASELLAR MASS
Neurogenic

Answer 80

1. Schwannoma—may involve CPA, Meckel’s cave and
   pterygomaxillary fissure. Variably solid and cystic, ‘dumbbell’
   shaped, avidly enhancing with skull base remodelling.

Question 81

CAVERNOUS SINUS (CS)/PARASELLAR MASS
Vascular
4

Answer 81

1. Carotico-cavernous fistula—look for associated venous congestion
   in/around orbit (± proptosis, muscle swelling and chemosis clinically) and central skull base. May be direct, due to rupture of intracavernous ICA (e.g. traumatic or aneurysmal), or indirect, due to small AV shunts (associated with venous sinus thrombosis and subsequent revascularization).
2. Aneurysm—traumatic (pseudoaneurysm) and nontraumatic; prominent flow void and phase artefacts. May be partially thrombosed ± fistula.
3. Cavernous sinus thrombosis—nonenhancing thrombus in enlarged sinus ± adjacent dural enhancement and venous congestion. Often due to orbitofacial sepsis.
4. Cavernous haemangioma—multilobular, well-defined, very T2 bright heterogeneous mass, which can expand/erode into the adjacent sphenoid sinus without hyperostosis. May show gradual filling enhancement on dynamic contrast imaging (DDx - schwannoma, meningioma, chordoma, macroadenoma, chondrosarcoma)

Question 82

CAVERNOUS SINUS (CS)/
PARASELLAR MASS
Skull base

Answer 82

1. Chordoma—older males, in midline at sphenooccipital
   synchondrosis. Well-defined, very T2 bright + septa. Encases vessels
   without narrowing.
2. Chondrosarcoma—osseous erosion with calcified chondroid
   matrix. Greater risk of ophthalmoplegia (cf. chordoma).
3. Myeloma/metastases/lymphoma*—lytic/sclerotic lesion with
   variable soft-tissue component

Question 83

OPTIC NERVE ABNORMAL SIGNAL
• Intraocular—at the point it emerges through the scleral
opening.
• Intraorbital—longest segment, has a surrounding optic nerve
sheath (ONS) which contains CSF.
• Intracanalicular—segment in the bony optic canal along with
ophthalmic artery; ONS adherent to optic canal.
• Prechiasmatic—intracranial segment in suprasellar cistern

Answer 83

1. Optic neuritis—triad of visual impairment, pain and abnormal
   colour vision. T2 hyperintensity within optic nerve substance (cf.
   optic perineuritis).
   (a) Inflammatory.
   (i) MS—usually unilateral retrobulbar optic neuritis and
   papillitis with variable enhancement and classical WM
   lesions in the brain (see Section 13.20).
   (ii) NMO—usually bilateral with longer segment abnormal
   signal and enhancement and clinically more severe
   visual loss (cf. MS). Fewer intracranial WM lesions.
   (iii) SLE/sarcoid/Wegener’s*—optic perineuritis > neuritis
   (see later). SLE also associated with acute ischaemic
   optic neuropathy (abrupt severe visual loss).
   (b) Infective—herpes zoster, Lyme disease, syphilis and TB.
   (c) Post vaccination—ADEM (
   (d) Radiation-induced.
2. Optic perineuritis—idiopathic, SLE, sarcoid, Wegener’s, infective.
   Characterized by thickening of the ONS (‘doughnut’ sign) in the
   intraorbital segment with surrounding fat stranding and less/no
   abnormal signal in the optic nerve (cf. optic neuritis).
3. Ischaemic optic neuropathy.
   (a) Anterior (AION)—intraocular segment/optic nerve head;
   associated with papilloedema, suggested by flattening or
   bulging of the optic nerve head on MRI. Imaging generally
   not indicated.
   (i) Arteritic—due to giant cell/temporal arteritis. >70 years,
   history of jaw claudication and polymyalgia rheumatica.
   Greater risk of bilateral involvement. Temporal artery wall
   thickening + periarterial enhancing fat stranding.
   (ii) Non-arteritic—associated with vascular risk factors
   (hypertension, diabetes mellitus, smoking), >50 years, no
   optic nerve enhancement.
   (b) Posterior (PION)—all segments of optic nerve posterior to
   intraocular. No papilloedema. Watershed ischaemia due to
   hypoxia and/or hypovolaemia. Intracanalicular segment most
   severely affected due to optic nerve swelling and compartment
   syndrome within bony canal.
4. Traumatic.
   (a) Direct—direct nerve disruption, e.g. penetrating injury or
   fracture fragment (especially in the optic canal).
   (b) Indirect—transmitted forces cause shear stress on the nerve.
   The intracanalicular segment is most susceptible as the ONS at
   this point is tightly adherent to the periosteum of the optic
   canal.
5. Neoplastic.
   (a) Optic nerve glioma—rare, typically in children, often with
   NF1. Intraorbital segment most commonly involved and
   expanded with central isointense (to WM) signal + perineural
   high signal due to arachnoidal gliomatosis. Variable
   enhancement; may extend to optic chiasm ± hypothalamus.
   (b) Optic nerve sheath meningioma—‘tram-track’ sign: avidly
   enhancing mass surrounding a nonenhancing optic nerve, ±
   calcification ± adjacent bony hyperostosis. Adults > children,
   associated with NF2.
   (c) Leukaemia/lymphoma*—optic nerve and ONS are important
   review areas for potential CNS deposits.
6. Extrinsic compression—from adjacent lesion in the orbit, orbital
   apex, optic canal or suprasellar cistern

Question 84

PINEAL REGION MASS

Pineal gland

Answer 84

1. Pineal cyst—common incidental finding, well-defined CSF
   intensity unilocular cyst, often slightly T1 hyperintense with
   incomplete FLAIR suppression ± slight rim enhancement. Rarely
   haemorrhagic.
2. Pineal germ cell tumours—all tend to ‘engulf’ normal pineal
   calcification; associated with CSF seeding.
   (a) Germinoma (85%)—children and young adults;
   homogeneous hyperdense enhancing mass. Presence of pineal
   calcification in children is suspicious.
   (b) Others—e.g. mixed (commonest), teratoma (fat, calcification
   and cysts), embryonal carcinoma, choriocarcinoma and yolk
   sac tumour. All heterogeneously enhancing. Elevated αFP and/
   or ß-hCG, depending on type.
3. Pineal parenchymal tumours—tend to disperse (‘explode’) pineal
   calcification.
   (a) Pineocytoma—typically adults; well-defined noninvasive
   enhancing mass. May be entirely cystic mimicking a benign
   pineal cyst; any nodular enhancement is suggestive.
   (b) Pineoblastoma—typically children; large, aggressive, locally
   invasive mass with CSF seeding. Hyperdense on CT
   (hypercellular), heterogeneous signal with restricted diffusion
   on MRI. Associated with retinoblastoma.

Question 85

PINEAL REGION MASS

Cystic

Answer 85

1. Pineal cyst—see earlier. Located below internal cerebral veins.
2. Cavum velum interpositum (CVI)—enlarged CSF space behind
   the foramen of Monro, beneath the columns of the fornices and
   above the internal cerebral veins (cf. pineal cyst).
3. Cyst of the velum interpositum—when the CVI is >1 cm in axial
   dimensions with convex bowed margins and mass effect

Question 86

PINEAL REGION MASS
Posterior brainstem
4

Answer 86

1. Tectal glioma—low grade astrocytoma in childhood, expands tectal plate and causes hydrocephalus.
2. Infarct—prominent restricted diffusion.
3. Metastasis—heterogeneous enhancement + vasogenic oedema.
4. Demyelination—NMO

Question 87

PINEAL REGION MASS
Vascular lesions 2
Other 1

Answer 87

1. Vein of Galen malformation—presents in neonatal period with
   high output cardiac failure; dilated median prosencephalic vein,
   which appears as a large midline posterior vessel.
2. Internal cerebral vein thrombosis—hyperdense vein, loss of
   normal flow void on MRI, surrounding oedema/infarct ±
   haemorrhage.

Other
1. Meningioma—displaces pineal calcification rather than engulfing
or dispersing it. Homogeneous enhancement ± calcification.

Question 88

INTRAVENTRICULAR MASS IN ADULTS
Choroid plexus lesion
5

Answer 88

1. Xanthogranuloma—degenerative cyst common in elderly. May be
   hyperintense on T1, FLAIR and DWI due to protein, lipid and blood products.
2. Cyst—CSF signal.
3. Papilloma—lobulated, frond-like avidly enhancing intraventricular
   mass with hydrocephalus (either obstructive or due to CSF overproduction).
4. Carcinoma—young children; variable-appearing lesion with heterogeneous enhancement, necrosis, calcification and local parenchymal invasion.
5. Metastasis—renal, melanoma, breast, lymphoma. Local invasion ±additional parenchymal/dural metastases

Question 89

INTRAVENTRICULAR MASS IN ADULTS

Tumours of the ventricular wall

Answer 89

1. Central neurocytoma—young adults. In lateral ventricle, arises
   from septum pellucidum near foramen of Monro. Hyperdense,
   calcified and T2 bright bubbly mass with heterogeneous
   enhancement.
2. Meningioma—usually lateral ventricle. Avidly enhancing mass ±
   calcification.
3. Ependymoma—rare in adults; see Section 13.11.
4. Subependymoma—elderly, fourth ventricle; see Section 13.11.
5. Subependymal giant cell astrocytoma—young patient with
   tuberous sclerosis; see Section 13.6.
6. CNS lymphoma*—periventricular hypercellular mass with
   homogeneous enhancement and restricted diffusion.

Question 90

INTRAVENTRICULAR MASS IN ADULTS
Nonchoroid cyst-like lesions
3

Answer 90

1. Colloid cyst—anterior roof of third ventricle. Well-defined
   nonenhancing cyst, hyperdense on CT. More likely to be
   symptomatic if >1 cm.
2. Ependymal cyst—often CSF intensity with mass effect.
3. Neurocysticercosis—in ventricles or parenchyma; see Part 2

Question 91

INTRAVENTRICULAR MASS IN ADULTS

Others

Answer 91

1. Intraventricular haemorrhage—haematomas can form solid casts
   of the ventricles.
2. Epidermoid—CSF-like signal intensity on MRI except for restricted
   diffusion and incomplete suppression on FLAIR.
3. Cavernous malformation—rare; T2 hyperintense, mildly T1
   hyperintense globular lesion with blood degradation products on
   SWI/T2* imaging

Question 92

CEREBELLOPONTINE ANGLE MASS

Answer 92

1. Vestibular schwannoma—ovoid, intracanalicular, heterogeneous
   T2 bright mass with avid enhancement. Small lesions solid, larger
   lesions may be cystic and haemorrhagic. Expands internal
   auditory meatus. Bilateral schwannomas diagnostic for NF2.
2. Meningioma—solid uniformly enhancing mass ± calcification and
   dural tail.
3. Epidermoid—CSF signal on T1 and T2, incomplete suppression
   on FLAIR + restricted diffusion. Multilobular lesion, no
   enhancement.
4. Ependymoma—usually plastic-like extension from fourth
   ventricle, but can be purely in CPA; see Section 13.11.
5. Arachnoid cyst—isointense to CSF on all sequences.
6. Vascular.
   (a) Aneurysm—variable signal depending on degree of
   thrombosis.
   (b) Ectasia—tortuous, dilated vascular flow void.
7. Other schwannomas.
   (a) Trigeminal—enhancing lesion in Meckel’s cave extending
   into CPA.
   (b) Facial—same location as vestibular schwannoma, along the
   path of CN VII.
8. Lipoma—isointense to fat; may encase facial nerve.
9. Dural/leptomeningeal metastasis.Skull and brain 425
   13
10. Granuloma—dural sarcoid, TB, and Wegener’s.
11. Neurenteric cyst—usually prepontine, lobular mass. Slightly
    denser than CSF, variable signal (proteinaceous material). No
    enhancement or restricted diffusion.
12. Paraganglioma—hypervascular mass extending from jugular
    foramen with erosive changes in skull base on CT and MRI. Flow
    voids and foci of blood degradation products give ‘salt and
    pepper’ appearance on MRI

Question 93

CORTICAL HYPERINTENSITY ON

T2/FLAIR

Answer 93

1. Cortical ischaemia/infarction—cortical high T2 signal and
   restricted diffusion, caused by arterial occlusions or hypoxic/
   hypotensive episodes (watershed areas).
2. Encephalitis.
   (a) HSV—mesial temporal lobes ± insula and lateral temporal lobe
   involvement, haemorrhage common (cf. autoimmune). Fever
   and rapid course.
   (b) Autoimmune—mesial temporal lobes + basal ganglia
   involvement, haemorrhage rare (cf. HSV). Subacute to gradual
   onset.
   (c) Paraneoplastic—indolent onset, other features of malignancy.
3. Encephalopathy—drugs, toxic, metabolic and vasculopathic.
   Multifocal cortical T2 hyperintensities ± restricted diffusion.
   Includes hypoglycaemia, PRES and hypertensive encephalopathy.
4. Post ictal/status epilepticus—GM or subcortical WM signal
   change ± restricted diffusion. Rapid onset and quick resolution of
   imaging findings.
5. Cortical contusion—blood degradation products. Typically in
   orbitofrontal and anterior temporal regions.
6. Cortical-based tumour—look for mass effect; see Section 13.10.
7. Cortical malformations—e.g. focal cortical dysplasia, cortical
   tubers; see Section 13.10.
8. CJD—gyriform cortical T2 hyperintensity and persistent restricted
   diffusion. vCJD is also associated with bithalamic abnormal signal
   (‘pulvinar’ and ‘hockey stick’ sign).

Question 94

SULCAL FLAIR HYPERINTENSITIES

Changes to CSF content

Answer 94

1. Subarachnoid haemorrhage—hyperdense blood on CT, SWI
   signal dropout.
2. Ruptured dermoid—fat droplets, high T1 signal.

Question 95

SULCAL FLAIR HYPERINTENSITIES

Meningeal

Answer 95

1. Bacterial meningitis—leptomeningeal enhancement, purulent
   exudate also shows restricted diffusion; check for ventriculitis.
2. Aseptic meningitis—sarcoid, Wegener’s and rheumatoid arthritis.
3. Leptomeningeal carcinomatosis.
   (a) Primary CNS—glioblastoma, medulloblastoma, ependymoma.
   (b) Metastatic—breast, lung, melanoma, lymphoma, leukaemia.
4. Meningeal melanomatosis—rare primary melanocytic tumour of
   the CNS, associated with cutaneous melanocytic lesions and
   hydrocephalus; hyperdense leptomeninges with high T1 signal.

Question 96

SULCAL FLAIR HYPERINTENSITIES
Vascular
3

Answer 96

1. Thrombosis of cortical veins—hyperdense vein and loss of flow
   void + local cerebral swelling from venous congestion.
2. Dilated leptomeningeal perforators—Moyamoya
3. Slow flow in sulcal arteries—secondary to stenoses/occlusions

Question 97

SULCAL FLAIR HYPERINTENSITIES
Artefactual/Iatrogenic
3

Answer 97

1. Hyperoxygenation.
2. CSF flow and pulsation artefact.
3. Recent gadolinium administration—especially if there is adjacent
   pathology causing breakdown of the blood-brain barrier

Question 98

CAUSES OF HIGH T1 SIGNAL

8

Answer 98

1. Fat—e.g. lipid-laden macrophages in cortical laminar necrosis,
   fat-containing lesions .
2. Methaemoglobin—subacute haemorrhage, thrombus and cavernoma.
3. Proteinaceous material—colloid cyst, posterior pituitary (normal),
   mucinous adenocarcinoma metastases, Rathke’s cleft cyst and
   craniopharyngioma.
4. Gadolinium enhancement—look for normal mucosal and vascular
   enhancement.
5. Melanin—melanoma metastases, meningeal melanomatosis.
6. Minerals—manganese (hepatic encephalopathy), copper
   (Wilson’s), iron (NBIA).
7. Calcification—only with diamagnetic calcium salts especially in Fahr disease.
8. Flow artefact—CSF or slow vascular flow.

Question 99

CAUSES OF LOW T2 SIGNAL

Answer 99

1. Turbulent/rapid flow—vessels, aneurysms, CSF flow. Absent
   normal vascular flow voids may reflect thrombosis or stenosis.
2. Air—paranasal sinuses, mastoid air cells and pneumocephalus.
3. Cortical bone.
4. Metallic prosthesis.
5. Haemoglobin breakdown products—see following table.
6. Proteinaceous material—colloid cyst, Rathke’s cleft cyst, sinus
   secretions. T2 signal reduces with increasing protein
   concentration.
7. Highly cellular lesions—medulloblastoma, lymphoma, high
   grade gliomas.
8. Minerals—calcium, copper and iron deposition.
9. Melanin—melanoma metastases, meningeal melanomatosis.
10. Fungal hyphae—invasive fungal sinusitis.
11. Gadolinium—causes T2 relaxation. Applied in dynamic
    susceptibility contrast enhanced perfusion imaging.

Question 100

CAUSES OF RESTRICTED DIFFUSION
Cortical/subcortical
8

Answer 100

1. Hypoxic-ischaemic
   (a) Acute cerebral infarction—variable distribution: vascular territorial, watershed and lacunar patterns. Causes: thrombotic, embolic or vasculitic.
   (b) Hypoxic ischaemic injury—due to global hypoperfusion or hypoxia, e.g. cardiac arrest and drowning. Watershed and DGM infarcts.
2. Post ictal—cortex and hippocampi.
3. PRES—parietooccipital and superior frontal gyri.
4. Encephalitis/cerebritis
5. DAI—GWMJ, splenium and middle cerebellar peduncles + microhaemorrhages.
6. Hypoglycaemia—bioccipital and splenium.
7. CJD—insula and pulvinar (largest nucleus of thalamus - pulvinar sign - Fabry)
8. MR artefact—due to susceptibility artefact; affects cortex close to
   skull, paranasal sinuses and mastoid air cells.

Question 101

CAUSES OF RESTRICTED DIFFUSION

Focal lesion

Answer 101

1. Infection.
   (a) Abscess—ring-enhancing, ‘dual rim’ sign on SWI and T2
   (hypointense outer rim and hyperintense inner rim).
   (b) Empyema—extraaxial collection + rim enhancement.
   (c) Ventriculitis—pus dependent in ventricles (occipital horns).
2. Hypercellular neoplasms.
   (a) Lymphoma*—periventricular, homogeneous enhancement.
   (b) Medulloblastoma—fourth ventricle/cerebellum, in children.
   (c) Germinoma—children/young adults. Avid enhancement,
   midline.
   (d) Glioblastoma—high grade components show restricted
   diffusion.
3. Acute demyelination—active lesions only; restricted diffusion
   typically conforms to the incomplete ring enhancement.
4. Epidermoid—lobular, insinuating cisternal lesion. Restricted
   diffusion is the main feature differentiating this from arachnoid
   cyst.
5. Mucoid degeneration—e.g. choroid plexus cyst, Rathke’s cleft
   cyst.
6. Haemorrhage/haematoma—blood degradation products induce
   signal changes on DWI due to susceptibility effect.
7. Osmotic myelinolysis—central pons.

Question 102

FAT-CONTAINING

INTRACRANIAL LESIONS

Answer 102

1. Lipoma—interhemispheric fissure (± callosal dysgenesis) >
   suprasellar > pineal region > CPA.
2. Dermoid cyst—midline fatty mass with chemical shift artefact ±
   calcification. Can rupture causing chemical meningitis.
3. Teratoma—midline multiloculated cystic mass with fat, soft-tissue
   and calcified components.
4. Postsurgical fat plugs—e.g. following pituitary surgery.
5. White epidermoids—rare variant containing triglycerides causing
   T1 hyperintensity (normally CSF signal). Restricts diffusion (cf.
   dermoid).
6. Lipomatous degeneration of tumours—rare, has been reported
   in meningiomas and small round blue cell tumours, e.g.
   medulloblastoma

Question 103

CYST-LIKE POSTERIOR FOSSA LESIONS

Answer 103

1. Mega cisterna magna—enlarged retrocerebellar CSF space
   communicating with fourth ventricle and basal CSF spaces.
   Normal vermis, cerebellum and fourth ventricle.
2. Dandy-Walker spectrum—variable hypoplasia of vermis, cystic
   dilatation of fourth ventricle (displacing cerebellar hemispheres
   anterolaterally) ± enlarged posterior fossa with torcula-lambdoid
   inversion (torcula above lambdoid suture). If all features are
   present, it is termed a Dandy-Walker malformation.
3. Blake’s pouch cyst—posterior diverticulum of the fourth ventricle
   due to failed opening of the foramen of Magendie in utero,
   resulting in hydrocephalus of all four ventricles. Cyst
   communicates with fourth ventricle but not with cisterna magna.
   Vermis is of normal size but is displaced superiorly.
4. Arachnoid cyst—CSF signal + mass effect on vermis, which is of
   normal size. Hydrocephalus is rare.
5. Epidermoid cyst—restricted diffusion and incomplete
   suppression on FLAIR.
6. Pilocytic astrocytoma—in children; cystic cerebellar mass +
   enhancing mural nodule and walls.
7. Cerebellar hemangioblastoma—in adults; cystic cerebellar mass
   + enhancing mural nodule, but no wall enhancement.
   Surrounding abnormal vessels.
8. Trapped fourth ventricle—secondary to haemorrhage or
   ventriculitis. Typically noted after persistent fourth ventricular
   dilatation despite successful shunting of lateral ventricles.
   Associated with diplopia and ataxia
9. Neuroglial/neurenteric cyst—CSF signal parenchymal cyst. No
   enhancement or restricted diffusion.
10. Neurocysticercosis—most commonly in fourth ventricle; can
    cause obstructive hydrocephalus (see Part 2).

Question 104

CEREBRAL VOLUME LOSS

Generalized

Answer 104

1. Normal ageing—0.5% total brain volume loss per year is normal, >1.0% is likely abnormal.
2. Cerebrovascular disease—background of small-vessel disease
3. Drugs.
   (a) Alcohol—additional cerebellar vermian atrophy.
   (b) Steroids—short use: transient reduced volume, which
   recovers. Chronic use: irreversible volume loss.
4. Postinflammatory—MS and other inflammatory WM diseases;
   lesions with WM volume loss and variable cavitation related to
   chronic lesions.
5. Posttraumatic—if severe and especially if widespread DAI.
6. Whole brain radiotherapy—can also be regional if radiotherapy is
   confined; ± coexistent radiotherapy-induced meningiomas and
   cavernomas
7. HIV encephalopathy—diffuse symmetric periventricular abnormal
   WM signal and volume loss.

Question 105

CEREBRAL VOLUME LOSS

Focal

Answer 105

1. Postinfarction—wedge-shaped cortical and subcortical volume
   loss, limited to vascular territory.
2. Posttraumatic—contusion or haematom in typical locations
   (orbitofrontal and anterior temporal regions).
3. Postinfective—encephalitis and meningitis

Question 106

CEREBRAL VOLUME LOSS
Regional pattern
8

Answer 106

1. Alzheimer’s disease.
   (a) Classical—old age onset (70–80s), memory impairment with
   hippocampal and temporoparietal atrophy.
   (b) Posterior cortical atrophy—usually younger age onset
   (50–60s). Visual agnosia and apraxia with occipitoparietal
   volume loss.
2. Parkinson disease—tremor, rigidity, bradykinesia ± dementia. NB:
   in dementia with Lewy bodies, cognitive decline and visual
   hallucinations precede parkinsonism. Generalized cerebral atrophy
   and atrophy of substantia nigra with relative sparing of
   hippocampi. Increased putaminal iron (reduced T2 signal).
   Loss of normal ‘swallowtail’ appearance of substantia nigra
   on SWI.
3. Frontotemporal lobar degeneration—inappropriate behaviour
   and apathy with frontotemporal atrophy.
4. Progressive supranuclear palsy—reduced cognition, supranuclear
   vertical gaze palsy. Reduced area of midbrain relative to pons in
   sagittal plane. Midbrain has ‘mickey mouse’ appearance on axial
   and ‘hummingbird’ sign on sagittal imaging (the latter is
   subjective and of limited utility).
5. Corticobasal degeneration—apraxia and dystonia. Asymmetric
   atrophy of superior parietal lobules and paracentral gyri.
6. MSA-P—reduced putamen volume with reduced T2 signal relative
   to GP. High T2 rim surrounding putamen (‘putaminal rim sign’).
7. Huntington’s disease—autosomal dominant, progressive
   choreoathetoid movements with atrophy of caudate heads.
8. Post encephalitis—chronic volume loss in regions affected, e.g.
   mesial temporal lobes in both HSV and autoimmune limbic
   encephalitis.

Question 107

CEREBELLAR VOLUME LOSS

Answer 107

. Normal ageing.
2. Chronic alcoholism.
3. Drugs—phenytoin, chemotherapy, lithium, benzodiazepines.
4. Chronic vertebrobasilar ischaemia/insufficiency—posterior
circulation steno-occlusive disease with multiple infarcts.
5. Chronic temporal lobe epilepsy—independent of antiseizure
medication.
6. Cerebellitis—in children, post infection/vaccination. Acute:
generalized cerebellar swelling with cortical T2 hyperintensity +
obstructive hydrocephalus. Chronic: generalized cerebellar
volume loss.
7. MSA-C—‘hot cross bun’ sign in pons; see Section 13.26.
8. Olivopontocerebellar atrophy—atrophy of olivary nuclei and
cerebellar peduncles, associated with MSA-C.
9. Superficial siderosis—recurrent SAH with haemosiderin
depositions associated with deafness and ataxia. Susceptibilityrelated signal dropout lining cerebellar folia, best seen on
SWI.
10. Post radiation therapy.432 Aids to Radiological Differential Diagnosis
11. Inherited ataxias.
(a) Friedreich ataxia—AR, adolescent onset. Dorsal cervical cord
volume loss + hypertrophic cardiomyopathy.
(b) Ataxia telangiectasia—AR; multiple telangiectasia, ataxia
and lung infections. Vermian volume loss and cerebral WM
T2 hyperintensities.
(c) Spinocerebellar ataxia syndromes—wide range of inherited
syndromes characterized by atrophy of the spinal cord and
cerebellum.
12. Paraneoplastic cerebellar degeneration—lung, breast and
ovarian cancer.
13. Gluten ataxia—gluten sensitivity, improves with gluten-free diet.
14. Crossed cerebellar diaschisis—unilateral, due to contralateral
supratentorial gliosis

Question 108

BRAINSTEM ATROPHY

Diffuse

Answer 108

1. Radiotherapy.
2. Inflammatory.
   (a) MS—midbrain/pons > medulla.
   (b) NMO—medulla > midbrain/pons.
   (c) Behçet’s*—oedematous lesions + perivascular enhancement.
3. Wallerian degeneration—atrophy and signal change downstream
   of a supratentorial lesion (e.g. infarct, haemorrhage,
   demyelination). Diffuse or focal depending on extent of insult.
4. Infectious rhombencephalitis—encephalitis of the hindbrain
   (brainstem and cerebellum), e.g. by Listeria or enterovirus. Acute:
   swollen with enhancing WM lesions and cranial nerve
   enhancement. Chronic: generalized volume loss.
5. Infarction.
6. Spinocerebellar ataxia—see Section 13.43.
7. Inherited leukoencephalopathies—rare, child/young adult onset

Question 109

BRAINSTEM ATROPHY

Regional

Answer 109

1. Midbrain—progressive supranuclear palsy, Wilson’s disease.
2. Pons—MSA-C.
3. Medulla—hypertrophic olivary degeneration (late feature), adult
   onset Alexander’s disease

Question 110

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Normal

Answer 110

1. Parietal foramina—usually bilateral and symmetrical, anterior to
   lambdoid suture. If enlarged (>5 mm) then may be linked to
   genetic syndromes and other intracranial anomalies.
2. Normal ageing calvarium.
3. Fontanelle—anterior (closes <18 months), posterior (closes <3
   months), anterolateral ×2, posterolateral ×2

Question 111

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Neoplastic (adults)

Answer 111

1. Myeloma—multiple lytic lesions (pepper pot skull); can involve
   mandible (where metastases are very rare).
2. Metastases—e.g. lung, breast, renal, thyroid and leukaemia.
3. Paget’s sarcoma—osteosarcoma, chondrosarcoma, fibrosarcoma.
   Lytic, blastic or mixed lesion with cortical destruction and
   soft-tissue component on a background of Paget’s disease. Usually
   little/no periosteal reaction; suspect in an area of Paget’s that has
   undergone rapid change on serial imaging

Question 112

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Neoplastic (children)

Answer 112

1. Metastases—neuroblastoma, leukaemia and sarcoma.
2. Langerhans cell histiocytosis*—especially parietal bone; may be
   an isolated well-defined lesion with a beveled edge due to unequal
   involvement of inner and outer tables (also known as eosinophilic
   granuloma), or multiple coalescent lesions with a geographic
   appearance (LCH). May contain central sequestrum of residual
   bone. Enhances avidly

Question 113

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Traumatic

Answer 113

1. Fracture—easy to mistake for normal suture. If involving suture,
   check for diastasis.
2. Leptomeningeal cyst—also known as growing fracture. Skull
   fracture with trapped meninges; CSF pulsation causes progressive
   widening and scalloping. Usually in young children.
3. Burr hole—typically a perfect circle, often frontal or parietal
   location, ± evidence of gliosis in the subjacent brain parenchyma.

Question 114

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Metabolic
2

Answer 114

1. Osteoporosis—generalized reduced bone density most appreciable
   on CT. Vertebral insufficiency fractures common.
2. Hyperparathyroidism*—multiple foci of lucency and sclerosis (‘salt
   and pepper’ skull) ± a discrete brown tumour: expansile lytic
   lesion, which causes cortical thinning without cortical destruction
   or periosteal reaction, ± fluid-fluid levels on MRI.

Question 115

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Infective

Answer 115

1. Acute pyogenic osteomyelitis—from sinusitis (frontal bones),
   mastoiditis (temporal bones), penetrating head trauma or
   postsurgical. Look for cortical breach of the inner table to suggest
   intracranial involvement. Complications: intracranial empyema,
   abscess, meningitis, cerebritis, venous thrombophlebitis (especially
   with mastoiditis extending into sigmoid sinus).
2. TB*—rare, punched-out lesion with sequestrum + an overlying
   soft-tissue component.
3. Hydatid cyst—expansile loculated lesion centered in the diploic
   space.
4. Syphilis*—moth-eaten appearance.

Question 116

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Vascular
2

Answer 116

1. Haemangioma—expansile lesion with ‘sunburst’ pattern of
   radiating spicules, avid enhancement.
2. Sinus pericranii—congenital, traumatic or spontaneous venous
   malformation of the scalp characterized by an abnormally enlarged
   skull emissary vein, which connects the dural venous sinuses and
   extracranial veins. Soft tissue mass + an underlying serpiginous
   vascular channel in the skull

Question 117

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Others

Answer 117

1. Osteoporosis circumscripta—lytic phase of Paget’s disease;
   usually a large, well-defined lytic lesion most commonly in the
   inferior frontal or occipital bones (rarer at vertex); can cross
   sutures, ± separate regions of sclerosis reflecting later stage of
   Paget’s.
2. Neurofibroma—can be secondary to both mesodermal dysplasia
   and skull erosion by an adjacent neurofibroma.
3. Intradiploic arachnoid cyst—very rare, CSF density/signal.

Question 118

SKULL VAULT LUCENCY WITH
SCLEROTIC EDGE
Normal

Answer 118

1. Venous channels—transcalvarial serpiginous channels containing
   emissary veins connecting venous sinuses to extracranial veins.
2. Venous lakes—enlarged veins with a round or ovoid morphology,
   avid enhancement post contrast. Often connect to venous
   channels.Skull and brain 435
   13
3. Arachnoid granulations—arachnoid projections into skull; round,
   well-defined lucencies often in region of venous sinuses with
   disruption of inner table. CSF signal on MRI. Generally a normal
   variant but if multiple consider chronically raised ICP

Question 119

SKULL VAULT LUCENCY WITH
SCLEROTIC EDGE
Developmental

Answer 119

1. Epidermoid—intradiploic rare; well-defined, scalloped margins,
   similar to CSF on T1/T2 but with restricted diffusion and
   incomplete FLAIR suppression.
2. Meningocoele/encephalocoele—protrusion of meninges ± brain
   through skull defect. Can be congenital, following trauma/surgery
   or related to chronically raised ICP.

Question 120

SKULL VAULT LUCENCY WITH
SCLEROTIC EDGE
Neoplastic
2

Answer 120

1. Langerhans cell histiocytosis*—in healing phase;

2. Treated lytic metastasis

Question 121

SKULL VAULT LUCENCY WITH
SCLEROTIC EDGE
Infective
Others

Answer 121

1. Chronic osteomyelitis—staphylococci, pseudomonas and fungal.
   Same locations and risks as acute osteomyelitis (see Section 13.45).
   Greater association with soft-tissue masses and dural thickening.
2. Frontal sinus mucocoele—completely opacified and expanded
   frontal sinus containing mucus with variable signal due to protein
   content. Thinning of sinus walls with variable resorption.
   Others
3. Fibrous dysplasia—variable appearance, commonly exhibits a
   ground-glass matrix but can be an entirely lytic, expanded,
   well-defined lesion with preserved overlying bone. Monostotic >
   polyostotic.

Question 122

GENERALIZED INCREASE IN SKULL

VAULT DENSITY

Answer 122

1. Paget’s disease*—in the elderly. Multiple islands of dense bone,
   loss of clarity of inner and outer tables, thickened skull vault, ±
   basilar impression.
2. Sclerotic metastases—breast (especially post treatment), prostate.
3. Fibrous dysplasia—younger age group than Paget’s; see Section
   13.46.
4. Myelofibrosis—diffuse sclerosis without architectural distortion.
   Associated with extramedullary haematopoiesis, intracranially this
   may be indicated by dural thickening.
5. Renal osteodystrophy*—osteosclerosis in 25%; mimics Paget’s.436 Aids to Radiological Differential Diagnosis
6. Acromegaly*—enlarged frontal sinuses, prognathism and
   thickened skull vault, ± an enlarged sella due to the underlying
   pituitary adenoma.
7. Chronic haemolytic anaemias—expansion of medullary spaces
   due to red marrow hyperplasia causing ‘hair-on-end’ appearance
   (see Section 13.51); variable sclerosis also related to hyperplastic
   red marrow (as opposed to bone infarcts).
8. Sclerosing bone dysplasia.
   (a) Osteopetrosis—infantile (AR) and adult (AD) forms.
   Infantile form more severe with life expectancy <10 years.
   Diffusely sclerotic and thickened skeleton with fractures.
   Associated with narrowing of skull foramina with
   compression of traversing CNs and vessels. Orbital
   crowding + proptosis. Poorly pneumatized paranasal
   sinuses.
   (b) Pyknodysostosis—especially skull base; multiple wormian
   bones, wide sutures from delayed closure, frontoparietal
   bossing.
   (c) Craniometaphyseal dysplasia—diffusely thickened skull with
   compromise of foramina (like osteopetrosis), flared
   metaphyses in long bones.
9. Prolonged phenytoin treatment—skull thickening and
   osteosclerosis + cerebellar volume loss (see Section 13.43).
10. Fluorosis—due to excessive fluoride ingestion. Osteosclerosis and
    ossification of tendons/ligaments

Question 123

LOCALIZED INCREASE IN SKULL
VAULT DENSITY
Within bone

Answer 123

1. Hyperostosis frontalis interna—older females; benign symmetrical
   overgrowth of the inner table of the frontal bone, often lobulated.
   Can involve other skull bones and be diffuse.
2. Tumour.
   (a) Sclerotic metastasis—prostate (men), breast (women) and
   neuroblastoma (children).
   (b) Osteoma—benign well-defined bone lesion. Two main types:
   ivory (homogeneously very dense) and mature (has central
   marrow). Also commonly seen in paranasal sinuses (associated
   with Gardner syndrome).
   (c) Treated lytic metastasis.
   (d) Treated brown tumour of hyperparathyroidism*.
3. Paget’s disease*—see Section 13.45.
4. Fibrous dysplasia—see Section 13.46.
5. Depressed fracture—abrupt cortical irregularity and depression

Question 124

LOCALIZED INCREASE IN SKULL
VAULT DENSITY
Adjacent to bone

Answer 124

1. Meningioma—hyperostosis of adjacent bone is common and
   usually reactive, though occasionally associated with osseous
   invasion (look for abnormal enhancement extending into the
   skull).
2. Calcified cephalohaematoma—infants with history of traumatic
   birth. Well-defined peripherally calcified crescentic lesion overlying
   outer table of skull.
3. Calcified epidermoid cyst—usually still contains more typical
   cystic components (

Question 125

THICKENED SKULL

Generalized

Answer 125

1. Normal variant.
2. Prolonged phenytoin treatment.
3. Acromegaly*.
4. Chronic haemolytic anaemia—see Section 13.51.
5. Microcephaly.
6. Shunted hydrocephalus—secondary to chronic low ICP

Question 126

THICKENED SKULL

Focal

Answer 126

1. Normal variant—including hyperostosis frontalis interna.
2. Paget’s disease*.
3. Fibrous dysplasia.
4. Meningioma—due to reactive hyperostosis or osseous invasion.
5. Osteoma.
6. Sclerotic metastasis—prostate

Question 127

THIN SKULL
Generalized
6

Answer 127

1. Hyperparathyroidism*—see Section 13.45.
2. Chronically raised intracranial pressure—other signs of raised
   ICP, e.g. ‘empty sella’, multiple arachnoid herniations,
   hydrocephalus. May produce a ‘copper-beaten skull’ appearance.
3. Osteogenesis imperfecta—associated with wormian bones.
   Characteristic features: osteoporosis, fractures, blue sclera, dental
   fragility and hearing impairment.
4. Rickets*—frontal bossing, delayed fusion of cranial sutures and
   closure of fontanelles.
5. Hypophosphatasia—rare metabolic deficiency of alkaline
   phosphatase, variable severity and age of presentation. Generalized
   osteoporosis and premature fusion of cranial sutures.
6. Lacunar skull—bone dysplasia of membranous skull, associated with
   Chiari 2 malformation. Indentations or pits in frontal and parietal
   regions that may be full-thickness; defects separated by thin rims of
   bone; usually resolves by 6 months. Not associated with raised ICP

Question 128

THIN SKULL

Focal

Answer 128

1. Normal variant.
2. Osteoporosis circumscripta—see Section 13.45.
3. Large intracranial cyst—arachnoid, porencephalic. Causes bony
   remodelling with smooth, scalloped thinning of the adjacent skull.
4. Slow-growing tumour in cerebral cortex—DNET, ganglioglioma.
   Also associated with gradual bony remodelling

Question 129

‘HAIR-ON-END’ SKULL VAULT

Haemolytic anaemias

Answer 129

1. Thalassaemia*—marrow hyperplasia more marked in this than
   other anaemias.
2. Sickle cell anaemia—initially in frontal region but can involve the
   whole skull where diploic space (marrow cavity) is present, i.e.
   above level of internal occipital protuberance.
3. Hereditary spherocytosis and elliptocytosis.
4. Pyruvate kinase deficiency.
5. Glucose-6-phosphate dehydrogenase deficiency

Question 130

‘HAIR-ON-END’ SKULL VAULT
Other causes of red marrow hyperplasia
2

Answer 130

1. Cyanotic heart disease.

2. Severe childhood iron deficiency anaemia

Question 131

‘HAIR-ON-END’ SKULL VAULT

Neoplastic

Answer 131

1. Haemangioma*—‘sunburst’ spicules; see Section 13.45.
2. Meningioma—more suggestive of skull invasion rather than
   reactive thickening; look for abnormal skull enhancement to
   support this. Also seen in primary intraosseous meningioma (see
   Section 13.54).
3. Metastases.

Question 132

PLATYBASIA AND BASILAR
INVAGINATION/IMPRESSION
Congenital
Platybasia: abnormal asymptomatic flattening of skull base, basal
angle >143 degrees.
Basilar invagination: dens telescopes through normal FM.
Basilar impression: dens telescopes through abnormal FM due
to bone softening or destruction.
Both basilar invagination and impression are associated with
symptoms of spinal cord/brainstem compression ± hydrocephalus.

Answer 132

1. Achondroplasia*—rhizomelic dwarfism.
2. Chiari malformations.
   (a) Chiari 1—peg-shaped cerebellar tonsils extending >5 mm
   below FM (excluding those caused by raised ICP) ± syrinx ±
   hydrocephalus.
   (b) Chiari 2—medulla, fourth ventricle and cerebellar vermis
   displaced through FM; small posterior fossa, beaked tectum.
   Nearly always associated with a lumbar myelomeningocoele.
   (c) Chiari 3—like Chiari 2 but with occipital encephalocoele.
3. Osteogenesis imperfecta—wormian bones

Question 133

PLATYBASIA AND BASILAR
INVAGINATION/IMPRESSION
Acquired

Answer 133

1. Rheumatoid arthritis*—ligamentous softening, erosion of dens
   and atlantoaxial subluxation.
2. Paget’s—bone softening (see Section 13.45).
3. Osteomalacia—bone softening.
4. Hyperparathyroidism*—bone softening.
5. Localized bone destruction—lytic metastases and destructive
   infection (e

Question 134

J-SHAPED SELLA

Answer 134

1. Normal variant.
2. Optic chiasm glioma—if chiasmatic sulcus very depressed (W- or
   omega-shaped sella), glioma may be bilateral.
3. Neurofibromatosis*.
4. Achondroplasia*.
5. Mucopolysaccharidoses*.
6. Chronic hydrocephalus—enlarged anterior aspect of third
   ventricle causes remodelling of sella.

Question 135

SCALP MASS

Skin

Answer 135

1. Epidermal inclusion cyst—also known as ‘sebaceous’ cyst
   (misnomer as they do not arise from sebaceous glands).
   Well-defined, usually of homogeneous fluid density on CT ±
   calcification. Commonly seen on the scalp, face and neck. If
   multiple, consider Gardner syndrome.
2. Trichilemmal cyst—also known as pilar cyst, originates from hair
   follicle so common on the scalp. Similar in appearance to
   epidermal inclusion cyst but calcifies more frequently.
3. Skin tags—pedunculated mass arising from skin; normal
   subcutaneous layer.
4. Carcinoma—squamous and basal cell, melanoma. Infiltrating,
   ulcerating soft-tissue mass with variable enhancement. Gorlin-Goltz
   syndrome: multiple BCCs and odontogenic keratocysts.
5. Skin calcification—associated with acne

Question 136

SCALP MASS

Subcutaneous tissue

Answer 136

1. Lipoma—encapsulated fatty mass, often does not contact skin. If
   internal soft-tissue component, multiple septations or large
   (>5 cm) then consider liposarcoma.
2. Haemangioma—early infancy, rapidly grow then involute before
   adolescence. High T2 signal, avid enhancement and intrinsic flow
   voids.

Question 137

SCALP MASS

Subgaleal plane

Answer 137

1. Subgaleal haematoma—post trauma in adults or children;
   crescentic haematoma beneath galeal aponeurosis but superficial
   to periosteum, not confined by cranial sutures.
2. Cephalohaematoma—following birth trauma; subperiosteal
   lentiform haematoma confined by cranial sutures. Parietal region
   most common.
3. Dermoid—most commonly midline, associated with sinus tracts.
   Fat density mass ± remodelling of underlying skull.
4. Plexiform neurofibroma—diagnostic of NF1. Thickening of the
   nerve sheath across multiple fascicles. Diffuse soft-tissue mass with
   a branching appearance. High T2 signal with central low signal
   (‘target’ sign). 10% undergo sarcomatous degeneration.
5. Cirsoid aneurysm—rare AVM of scalp usually fed by the superficial
   temporal artery

Question 138

SCALP MASS

Bone lesions

Answer 138

1. Osteoma—dense bone lesion projecting out from skull with no
   effect on diploic space.Skull and brain 441
   13
2. Malignancy—metastasis (lytic or sclerotic), plasmacytoma
   (expansile and lytic), lymphoma (soft-tissue mass often on both
   sides of skull with relatively little bone destruction), sarcoma.
3. Pott’s puffy tumour—subperiosteal abscess from frontal bone
   osteomyelitis secondary to frontal sinusitis or trauma. Opacified
   frontal sinus with overlying subperiosteal collection and
   inflammatory stranding.
4. Haemangioma—frontal and parietal bones, outer table involved
   with sparing of inner table, high T1 and T2 signal + flow voids.
5. Intraosseous meningioma—expands inner and outer tables of
   skull, dural component not always present.
6. Intraosseous epidermoid—fluid density with variable calcification
   on CT, high T2 signal and characteristic restricted diffusion.
7. Encephalocoele—defect in the skull and dura with extracranial
   herniation of intracranial structures. Directly related to trauma/
   surgery or secondary to chronic raised ICP.
8. Sinus pericranii—see Section 13.45.
9. Paget’s disease*—skull thickening with expansion of the diploic
   space and variable sclerosis and lysis