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Flashcards in SKULL & BRAIN Deck (138)
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1
Q

SOLITARY ACUTE INTRACRANIAL

HAEMORRHAGE

A
  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
2
Q
SUBARACHNOID HAEMORRHAGE (SAH)
Causes 7
A
  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
3
Q

MULTIFOCAL ACUTE INTRACEREBRAL HAEMORRHAGE

7

A
  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
4
Q

MICROHAEMORRHAGES ON MRI

15

A
  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
5
Q

SUPERFICIAL SIDEROSIS
Classical
6

A
  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%)
6
Q

SUPERFICIAL SIDEROSIS
Cortical
6

A
  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.
7
Q

SUPERFICIAL SIDEROSIS

Mimics of superficial siderosis

A
  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.
8
Q

HYDROCEPHALUS

CSF overproduction

A
  1. Choroid plexus tumours—i.e. papilloma, carcinoma;
9
Q

HYDROCEPHALUS

Communicating 6

A
  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
10
Q

HYDROCEPHALUS

Obstructive

A

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

11
Q

INTRACRANIAL CALCIFICATION

Deep grey matter

A
  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.
12
Q

INTRACRANIAL CALCIFICATION

Ependymal/periventricular

A
  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
13
Q

INTRACRANIAL CALCIFICATION

Gyriform

A
  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
14
Q

INTRACRANIAL CALCIFICATION

Focal lesions with calcification

A
  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
15
Q

SOLITARY INTRACEREBRAL MASS

Infiltrative, ill–defined

A

. 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

16
Q

SOLITARY INTRACEREBRAL MASS

Discrete, well-defined

A
  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.
17
Q

SOLITARY HYPERDENSE INTRACRANIAL
LESION ON UNENHANCED CT
Hypercellular mass

A
  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.
18
Q

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

A
  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.
19
Q

INTRINSIC CORTICAL MASS

A
  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.
20
Q

POSTERIOR FOSSA MASS (ADULT)

13

A
  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
21
Q

SOLITARY RING-ENHANCING LESION

Infection 4

A
  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;
22
Q

SOLITARY RING-ENHANCING LESION
Neoplastic
3

A
  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).
23
Q

SOLITARY RING-ENHANCING LESION

Inflammatory

A
  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
24
Q

SOLITARY RING-ENHANCING LESION

Vascular/trauma

A
  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
25
Q

MULTIPLE RING-ENHANCING LESIONS

Neoplastic

A
  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.
26
Q

MULTIPLE RING-ENHANCING LESIONS
Infection
5

A
  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
27
Q

MULTIPLE RING-ENHANCING LESIONS

Inflammatory 3

A
  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)
28
Q

MULTIPLE RING-ENHANCING LESIONS
Vascular/trauma
1

A

Contusion/haematoma—orbitofrontal and anterior temporal

regions;

29
Q

INTRACRANIAL CYST WITH
MURAL NODULE
Neoplastic

A
  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
30
Q

INTRACRANIAL CYST WITH
MURAL NODULE
Infection

A
  1. Neurocysticercosis—vesicular and colloidal vesicular stages, central
    dot from scolex
31
Q

ENHANCING LESIONS IN
PERIVASCULAR SPACES
7

A
  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;
32
Q

MENINGEAL ENHANCEMENT

Pachymeningeal (dura–arachnoid)

A
  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
33
Q

MENINGEAL ENHANCEMENT

Leptomeningeal (pia–arachnoid) 4

A
  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
34
Q

EPENDYMAL ENHANCEMENT

A
  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.
35
Q

CRANIAL NERVE (CN) ENHANCEMENT
Neoplastic
2

A
  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.
36
Q

CRANIAL NERVE (CN) ENHANCEMENT
Infection
3

A
  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
37
Q

CRANIAL NERVE (CN) ENHANCEMENT
Inflammatory
4

A
  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
38
Q
CRANIAL NERVE (CN) ENHANCEMENT
Granulomatous
A
  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.
39
Q
CRANIAL NERVE (CN) ENHANCEMENT
Other
A
  1. Post radiation neuritis—limited to radiation field.
  2. Ischaemic—diabetics, vasculopaths; transient enhancement
    followed by gradual atrophy. CN II, III and VI.
40
Q

ENLARGED LEPTOMENINGEAL

PERFORATORS 3

A
  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.

  1. 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.

  1. Sturge-Weber*—phakomatosis; facial cutaneous and leptomeningeal haemangiomas. Steal phenomenon causes atrophy of subjacent cortex and WM + ‘tram-track’ calcification
41
Q

WM LESIONS WITH LITTLE
MASS EFFECT
Punctate lesions
6

A
  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.
42
Q

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

A
  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
43
Q

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

A
  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
44
Q
CORPUS CALLOSUM (CC) LESIONS
Atrophic/dysplastic callosum
A
  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
45
Q
CORPUS CALLOSUM (CC) LESIONS
Multifocal lesions
A
  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
46
Q
CORPUS CALLOSUM (CC) LESIONS
Neoplasms
A
  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)
47
Q
CORPUS CALLOSUM (CC) LESIONS
Transient lesions
A
  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
48
Q
CORPUS CALLOSUM (CC) LESIONS
Hydrocephalus-related
A
  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
49
Q

DEEP GREY MATTER ABNORMALITIES

Physiological

A
  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
50
Q

DEEP GREY MATTER ABNORMALITIES

Vascular

A
  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.
51
Q

DEEP GREY MATTER ABNORMALITIES

Neurodegenerative 3

A
  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.
52
Q

DEEP GREY MATTER ABNORMALITIES

Toxins

A
  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
53
Q

DEEP GREY MATTER ABNORMALITIES

Acquired metabolic disease

A
  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.
54
Q

DEEP GREY MATTER ABNORMALITIES

Inherited metabolic disease

A
  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
55
Q

DEEP GREY MATTER ABNORMALITIES

Infectious

A
  1. Variant CJD (vCJD)—‘hockey stick’ sign: T2 hyperintensity in
    pulvinar and dorsomedial thalamus (cf. sporadic CJD which spares
    thalamus).
56
Q

BASAL GANGLIA: BRIGHT ON T1

Paramagnetic substances

A
  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
57
Q

BASAL GANGLIA: BRIGHT ON T1

Unknown cause

A
  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
58
Q

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

A
  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.
59
Q

BILATERAL THALAMIC LESIONS

Vascular

A
  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.
60
Q

BILATERAL THALAMIC LESIONS

Infection

A
  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.
61
Q

BILATERAL THALAMIC LESIONS
Metabolic
5

A
  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
62
Q

BILATERAL THALAMIC LESIONS

Neoplastic

A
  1. Bithalamic glioma—low-grade astrocytoma in children and young
    adults; expansile and often nonenhancing tumour ± obstructive
    hydrocephalus
63
Q

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

A
  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
64
Q

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

A
  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.
65
Q

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

A
  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
66
Q

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

A
  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.
67
Q

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

A
  1. Lymphoma*.
  2. Brain stem glioma.
  3. Meningeal carcinomatosis—leptomeningeal enhancement and
    FLAIR sulcal hyperintensity
68
Q

INTRASELLAR MASS

Intrinsic to the gland

A
  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
69
Q

INTRASELLAR MASS

Extrinsic to the gland

A
  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.
70
Q

PITUITARY INFUNDIBULAR LESION

Neoplastic

A
  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)
71
Q

PITUITARY INFUNDIBULAR LESION
Nonneoplastic
5

A
  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.
72
Q

SUPRASELLAR MASS
Meningeal
2

A
  1. Meningioma—see Section 13.27.
  2. Granulomatous—TB, sarcoid, LCH. Enhancing granulomas may be
    T2 hypointense
73
Q

SUPRASELLAR MASS

Vascular 1

A
  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
74
Q

SUPRASELLAR MASS

Parenchymal

A
  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*
75
Q

SUPRASELLAR MASS

Optic chiasm

A
  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.
76
Q

SUPRASELLAR MASS

Cisternal 5

A
  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.
77
Q

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

A
  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
78
Q
CAVERNOUS SINUS (CS)/PARASELLAR MASS
Dural

4

A
  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.
79
Q

CAVERNOUS SINUS (CS)/
PARASELLAR MASS
Cavernous sinus metastases

A
  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
80
Q

CAVERNOUS SINUS (CS)/
PARASELLAR MASS
Neurogenic

A
  1. Schwannoma—may involve CPA, Meckel’s cave and
    pterygomaxillary fissure. Variably solid and cystic, ‘dumbbell’
    shaped, avidly enhancing with skull base remodelling.
81
Q

CAVERNOUS SINUS (CS)/PARASELLAR MASS
Vascular
4

A
  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)
82
Q

CAVERNOUS SINUS (CS)/
PARASELLAR MASS
Skull base

A
  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
83
Q

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

A
  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
84
Q

PINEAL REGION MASS

Pineal gland

A
  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.
85
Q

PINEAL REGION MASS

Cystic

A
  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
86
Q

PINEAL REGION MASS
Posterior brainstem
4

A
  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
87
Q

PINEAL REGION MASS
Vascular lesions 2
Other 1

A
  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.

88
Q

INTRAVENTRICULAR MASS IN ADULTS
Choroid plexus lesion
5

A
  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
89
Q

INTRAVENTRICULAR MASS IN ADULTS

Tumours of the ventricular wall

A
  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.
90
Q

INTRAVENTRICULAR MASS IN ADULTS
Nonchoroid cyst-like lesions
3

A
  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
91
Q

INTRAVENTRICULAR MASS IN ADULTS

Others

A
  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
92
Q

CEREBELLOPONTINE ANGLE MASS

A
  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
93
Q

CORTICAL HYPERINTENSITY ON

T2/FLAIR

A
  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).
94
Q

SULCAL FLAIR HYPERINTENSITIES

Changes to CSF content

A
  1. Subarachnoid haemorrhage—hyperdense blood on CT, SWI
    signal dropout.
  2. Ruptured dermoid—fat droplets, high T1 signal.
95
Q

SULCAL FLAIR HYPERINTENSITIES

Meningeal

A
  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.
96
Q

SULCAL FLAIR HYPERINTENSITIES
Vascular
3

A
  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
97
Q

SULCAL FLAIR HYPERINTENSITIES
Artefactual/Iatrogenic
3

A
  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
98
Q

CAUSES OF HIGH T1 SIGNAL

8

A
  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.
99
Q

CAUSES OF LOW T2 SIGNAL

A
  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.
100
Q

CAUSES OF RESTRICTED DIFFUSION
Cortical/subcortical
8

A
  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.
101
Q

CAUSES OF RESTRICTED DIFFUSION

Focal lesion

A
  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.
102
Q

FAT-CONTAINING

INTRACRANIAL LESIONS

A
  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
103
Q

CYST-LIKE POSTERIOR FOSSA LESIONS

A
  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).
104
Q

CEREBRAL VOLUME LOSS

Generalized

A
  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.
105
Q

CEREBRAL VOLUME LOSS

Focal

A
  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
106
Q

CEREBRAL VOLUME LOSS
Regional pattern
8

A
  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.
107
Q

CEREBELLAR VOLUME LOSS

A

. 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

108
Q

BRAINSTEM ATROPHY

Diffuse

A
  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
109
Q

BRAINSTEM ATROPHY

Regional

A
  1. Midbrain—progressive supranuclear palsy, Wilson’s disease.
  2. Pons—MSA-C.
  3. Medulla—hypertrophic olivary degeneration (late feature), adult
    onset Alexander’s disease
110
Q

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Normal

A
  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
111
Q

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Neoplastic (adults)

A
  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
112
Q

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Neoplastic (children)

A
  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
113
Q

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Traumatic

A
  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.
114
Q

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Metabolic
2

A
  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.
115
Q

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Infective

A
  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.
116
Q

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Vascular
2

A
  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
117
Q

SKULL VAULT LUCENCY WITHOUT
SCLEROTIC EDGE
Others

A
  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.
118
Q

SKULL VAULT LUCENCY WITH
SCLEROTIC EDGE
Normal

A
  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
119
Q

SKULL VAULT LUCENCY WITH
SCLEROTIC EDGE
Developmental

A
  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.
120
Q

SKULL VAULT LUCENCY WITH
SCLEROTIC EDGE
Neoplastic
2

A
  1. Langerhans cell histiocytosis*—in healing phase;

2. Treated lytic metastasis

121
Q

SKULL VAULT LUCENCY WITH
SCLEROTIC EDGE
Infective
Others

A
  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.
122
Q

GENERALIZED INCREASE IN SKULL

VAULT DENSITY

A
  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
123
Q

LOCALIZED INCREASE IN SKULL
VAULT DENSITY
Within bone

A
  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
124
Q

LOCALIZED INCREASE IN SKULL
VAULT DENSITY
Adjacent to bone

A
  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 (
125
Q

THICKENED SKULL

Generalized

A
  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
126
Q

THICKENED SKULL

Focal

A
  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
127
Q

THIN SKULL
Generalized
6

A
  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
128
Q

THIN SKULL

Focal

A
  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
129
Q

‘HAIR-ON-END’ SKULL VAULT

Haemolytic anaemias

A
  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
130
Q

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

A
  1. Cyanotic heart disease.

2. Severe childhood iron deficiency anaemia

131
Q

‘HAIR-ON-END’ SKULL VAULT

Neoplastic

A
  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.
132
Q

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.

A
  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
133
Q

PLATYBASIA AND BASILAR
INVAGINATION/IMPRESSION
Acquired

A
  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
134
Q

J-SHAPED SELLA

A
  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.
135
Q

SCALP MASS

Skin

A
  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
136
Q

SCALP MASS

Subcutaneous tissue

A
  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.
137
Q

SCALP MASS

Subgaleal plane

A
  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
138
Q

SCALP MASS

Bone lesions

A
  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