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Intracerebral .
Hypertension —basal ganglia, pons, cerebellum.
Cerebral amyloid angiopathy —lobar location, peripheral microhaemorrhages (often multifocal).
Haemorrhagic lesions —e.g. metastases, primary tumours, infarcts.
Traumatic —more commonly multifocal (see Section 13.3 ).
Subarachnoid —see Section 13.2 . Extends into sulci ± basal cisterns.
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.
Extradural —traumatic; usually arterial bleed, rarely venous. Lentiform shape, does not cross cranial sutures.
Intraventricular —usually due to extension from subarachnoid or intracerebral bleed; isolated intraventricular haemorrhage is rare and due to subependymal vein rupture.
Unless there is a clear history of trauma (with typical SAH distribution) most cases will require angiography to look for the underlying cause. If the blood load is centred on the posterior fossa or foramen magnum (FM), consider a posterior inferior cerebellar artery aneurysm or spinal AVM, which may require imaging of the spine. Beware of ‘pseudosubarachnoid’ sign in hypoxic brain injury (look for loss of grey–white matter [WM] differentiation). Polycythaemia may also cause hyperdensity mimicking SAH on plain CT.
Trauma —often localized to coup and contrecoup injuries, i.e. superficial.
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.
Arteriovenous shunt —AVM (indirect shunt with nidus of vessels) or AVF (direct shunt between artery and vein). Prominent draining veins, may be partially calcified.
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.
Venous thrombosis —look for venous hyperdensity/expansion.
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.
Iatrogenic —following lumbar puncture or surgery.
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).
Septic embolism .
Haemorrhagic neoplastic lesions —metastasis, leukemia.
Coagulopathy —horizontal blood-blood levels are suggestive.
Venous sinus thrombosis .
Vasculopathy —drugs, cerebral amyloid angiopathy, vasculitis, posterior reversible encephalopathy syndrome (PRES) and RCVS.
Multiple cavernomas —rare, syndromic, young males.
Definition: <5 mm foci of signal loss on blood sensitive MRI sequences (susceptibility-weighted imaging [SWI]/T2*) not due to calcifications or flow voids.
Acute trauma —haemorrhagic shear injury (see Section 13.3 ). MRI is more sensitive than CT.
Hypertensive vasculopathy —central pattern involving the basal ganglia, thalami, brainstem and cerebellum.
Cerebral amyloid angiopathy —typically peripheral cortical/subcortical, usually spares the basal ganglia. Associated with lobar and subarachnoid haemorrhages.
Cavernomas —including familial syndromes.
Venous thrombosis/congestion.
Radiotherapy —radiation-induced capillary telangiectasia within the radiation field.
Cerebral vasculitis —usually at GWMJ.
Septic emboli —e.g. from infective endocarditis.
Haemorrhagic metastases —especially melanoma, RCC and intravascular lymphoma.
Sickle cell anaemia and beta thalassaemia *—associated with cerebral fat embolism from bone marrow infarcts. Seen in cerebral and cerebellar WM and corpus callosum.
CADASIL —symmetrical multifocal WM hyperintensity in frontal and anterior temporal lobes and external capsule, with noncharacteristic distribution of microhaemorrhages.
PRES —parietooccipital and superior frontal gyral predominance of microhaemorrhages.
Fat/air embolism —microbleeds may be associated with foci of restricted diffusion.
Critical illness – associated cerebral microbleeds —may be related to hypoxaemia, high altitude or disseminated intravascular coagulation.
Drugs —cocaine abuse.
Best seen on SWI/T2* as curvilinear low signal coating the leptomeninges. Two different patterns:
Involves the infratentorial regions and spinal cord. Clinical triad of sensorineural hearing loss, ataxia and pyramidal weakness, related to toxic effects of iron on neurons. Due to chronic recurrent low-volume SAH, which is clinically silent. Causes include:
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.
Dural ectasia —e.g. in Marfan.
CNS tumours .
Vascular malformations .
Involves the supratentorial compartment (especially cerebral convexities) but may also extend to the infratentorial region. Causes include:
Previous SAH —of any cause (see Section 13.2 ), including subarachnoid extension of intracerebral haemorrhage and bleeding neoplasms.
Cerebral amyloid angiopathy —in older patients (>60 years). Intracerebral microhaemorrhages may also be seen.
RCVS —in younger adults (<60 years), associated with pregnancy and certain drugs.
Cerebral vasculitis.
Hyperperfusion syndrome —after revascularization, e.g. carotid stenting or endarterectomy.
Infective endocarditis.
Acute SAH —hyperattenuating on CT, increased signal in subarachnoid space on FLAIR/T1.
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.
Cortical vein thrombosis —susceptibility effect follows the cortical veins.
Cortical calcification —e.g. in Sturge-Weber syndrome. Very dense on CT.
Large ventricles do not always equate to hydrocephalus: cerebral atrophy can lead to relative enlargement of ventricles. Hydrocephalus is more likely if:
Commensurate enlargement of temporal horns.
Ventricles disproportionately enlarged compared to sulci.
Blunted third ventricular recesses.
Evidence of periventricular CSF transudation.
Hydrocephalus can be caused by increased CSF production, reduced CSF absorption through arachnoid granulations (communicating) or obstruction to CSF flow (obstructive). A ‘compensated’ hydrocephalus cannot be readily determined on imaging from a single time point but is likely if the appearances are static and asymptomatic.
Choroid plexus tumours —i.e. papilloma, carcinoma; see Section 13.33 .
Posthaemorrhagic —especially SAH.
Bacterial meningitis —small cortical infarcts may be present as a complicating feature.
Leptomeningeal carcinomatosis —look for leptomeningeal enhancement.
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.
Increased venous pressure —venous obstruction, vein of Galen malformation.
Vestibular schwannoma —rare, thought to be due to increased CSF protein impairing CSF absorption.
Pattern of ventricular enlargement depends on level of obstruction:
Haemorrhage .
Intraventricular tumours —see Section 13.33 .
Ventriculitis —complication of meningitis, surgery or haemorrhage. Look for subtle ependymal enhancement and dependent sediment in lateral ventricles (restricts on DWI).
Neurocysticercosis —can cause obstruction either due to location of cyst or by causing ventriculitis. Cysts are best seen on steady-state gradient echo sequences such as CISS/FIESTA-C.
Dilated lateral ventricle(s), normal third and fourth ventricles.
Any cause of significant midline shift —compresses the ipsilateral lateral ventricle and obstructs the contralateral lateral ventricle.
Colloid cyst —characteristically located in the anterior roof of the third ventricle. Well-defined, nonenhancing, hyperdense on CT due to protein content.
Subependymal giant cell astrocytoma —in young patients with tuberous sclerosis. Typically within a lateral ventricle near foramen of Monro, avidly enhancing, often calcified.
Dilated lateral and third ventricles, normal fourth ventricle.
Aqueduct stenosis —congenital, presents in childhood, ‘beak–like’ appearance of aqueduct, no obstructing mass lesion.
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.
Pineal region tumour —see Section 13.32 .
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.
Chiari 1 malformation .
Choroid plexus, basal ganglia, pineal, dural (e.g. falx).
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.
Endocrine —hyper- and hypoparathyroidism, pseudo- and pseudopseudohypoparathyroidism. Appearance identical to Fahr disease.
Inherited —Down's, mitochondrial disorders; rarely in Cockayne and Aicardi-Goutieres syndromes. Seen in children.
SLE —thought to be related to microangiopathy. Background of cerebral volume loss and WM lesions (see Section 13.20 ).
Toxins —lead, carbon monoxide.
Posttherapeutic —mineralizing microangiopathy following chemoradiotherapy in childhood.
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.
Perinatal TORCH infections —toxoplasma, rubella, CMV (most common) and herpes simplex virus.
Sturge-Weber syndrome *—usually unilateral with associated cerebral atrophy. Look for retinal enhancement and ipsilateral choroid plexus enlargement.
Post infarction —due to cortical laminar necrosis.
CEC syndrome —rare disorder characterized by occipital calcifications in a patient with seizures and coeliac disease.
Tumours .
Meningioma —may be partly or completely calcified.
Oligodendroglioma —most contain calcification. Other low-grade gliomas can also calcify.
Craniopharyngioma —suprasellar location. Calcification is common (in contrast to pituitary adenomas).
Dermoid —also contains fat.
Ependymoma —located in fourth ventricle.
Central neurocytoma —arises from septum pellucidum.
Pineal region tumours —either engulf or ‘explode’ the normal pineal calcification.
Metastasis —e.g. from breast, mucinous GI tumours, lung, osteosarcoma.
Infections .
Neurocysticercosis —multiple small calcifications in brain parenchyma and CSF spaces; reflects end–stage quiescent disease.
Tuberculosis *—foci of calcification are usually larger and fewer in number versus cysticercosis.
Perinatal TORCH infections .
Vascular .
Atherosclerosis .
AVM.
Aneurysm —rim calcification.
Cavernoma.
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).
Cerebritis/encephalitis —acute clinical presentation (cf. diffuse glioma).
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:
Arterial —follows vascular territory, typically shows restricted diffusion.
Venous —near to occluded vein, greater oedema and risk of parenchymal haemorrhage (typically has a fragmented appearance). DWI signal variable.
Demyelination —Neuromyelitis optica (NMO) spectrum disorders, Behçet's.
Contusion —in the context of trauma.
Haematoma —hypertensive haemorrhage classically ganglionic; cf. amyloid angiopathy where sulcal siderosis and peripheral microhaemorrhages are commonly seen.
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%).
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).
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).
Cavernoma —characterized on MRI by complete haemosiderin rim and central mixed ‘popcorn’ components.
Tumefactive demyelination —incomplete rim enhancement is characteristic. More likely in younger age group (20–40s) versus metastases.
Lymphoma *—avid homogeneous enhancement and periventricular location are characteristic features.
Metastasis —e.g. from small-cell lung cancer.
Medulloblastoma —typically in children, located in the cerebellum.
Germinoma —young patients, located in the pineal or suprasellar region.
Acute haematoma —higher attenuation than adjacent brain parenchyma for up to 7–10 days.
Haemorrhagic tumours —especially metastases (e.g. from melanoma); less commonly glioblastoma, or pituitary adenoma with apoplexy.
Colloid cyst —homogeneously hyperdense due to protein content, nonenhancing, located in anterior roof of third ventricle.
Cavernoma —can mimic intracerebral haematoma on CT. On MRI, characteristically has complete haemosiderin rim with central mixed signal.
AVM .
See Section 13.7 .
Acute cortical infarction —results in cortical swelling/oedema with localized mass effect. Intense restricted diffusion on DWI.
Acute cerebritis/encephalitis —can show restricted diffusion, but less intense and more patchy versus acute infarction.
Metastasis —centred on GWMJ (see Section 13.8 ).
Neuronal-glial and glial tumours —apart from (a), these typically present in children or young adults with intractable seizures.
Oligodendroglioma —middle-aged patients. Cortical/subcortical mass, well- or ill-defined, often calcified. Heterogeneous T2 signal and enhancement. No restricted diffusion.
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.
Ganglioglioma —classically cystic mass with an enhancing mural nodule, but can be purely solid. No surrounding oedema. Calcification is common.
Pleomorphic xanthoastrocytoma (PXA) —similar appearance to ganglioglioma, but calcification is rare. Often associated with reactive dural thickening mimicking a dural tail.
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.
Cortical tubers —FLAIR and T2 bright cortical/juxtacortical lesions, found in tuberous sclerosis, <10% enhance.
Cavernoma —look for blood degradation products.
Haematoma —usually post trauma.
Metastasis —most common infratentorial lesion (see Section 13.8 ).
Haemangioblastoma —typically cerebellar hemisphere cystic tumour, avidly enhancing solid mural nodule abutting the pia mater with a nonenhancing cyst wall. Associated with vHL.
Astrocytoma .
Pilocytic —children and young adults, cyst with mural nodule and enhancing cyst wall (cf. haemangioblastoma).
Glioblastoma —older adults, heterogeneous ill-defined mass with irregular intrinsic enhancement.
Ependymoma —children and young adults, floor of fourth ventricle with ‘plastic-like’ extension through ventricular foramina. Heterogeneous, calcified and cystic. Associated with NF2.
Subependymoma —older adults, usually small, fourth > lateral ventricle. No enhancement.
Epidermoid —on CT, T1 and T2 indistinguishable from CSF but hyperintense on DWI and usually incomplete suppression of signal on FLAIR.
Dermoid —well-defined midline mass with fat and calcification. No enhancement.
Abscess —intrinsic restricted diffusion (see Section 13.8 ).
Haematoma/cavernoma —susceptibility effects from blood can cause variable DWI signal. Cavernoma often associated with nearby developmental venous anomaly.
Diffuse midline glioma —children and young adults, most commonly pontine, but can occur anywhere in the midline of the CNS.
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.
Rosette-forming glioneuronal tumour —young adults, typically in the midline at the posterior aspect of the fourth ventricle + local parenchymal invasion; mixed solid-cystic.
Any cerebellopontine angle (CPA) mass —see Section 13.34 .
Pyogenic abscess —thin regular enhancing capsule; see Section 13.8 .
Tuberculoma —uniformly round with adjacent leptomeningeal enhancement and characteristic central low T2 signal. Look for associated basal leptomeningitis and hydrocephalus.
Toxoplasmosis —usually multiple; see Section 13.13 .
Neurocysticercosis —usually multiple; see Section 13.13 .
Metastasis —central necrosis with thick, irregular, nodular rim enhancement, no intrinsic restricted diffusion; see Section 13.8 .
Glioblastoma —centred on WM but often indistinguishable from a single metastasis; see Section 13.8 .
Ganglioglioma/cytoma —children and young adults. Temporal lobe, calcified, slow growing ± bony remodelling, no perilesional oedema (cf. glioblastoma, metastases).
Demyelination —incomplete rim enhancement, typical locations; see Section 13.13 .
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.
Sarcoidosis *—isolated granuloma very rare, often coexistent dural or cranial nerve disease.
PML-IRIS —see Section 13.20 .
Subacute haematoma —variable signal and diffusion dependent on age; signal drop out on SWI/T2*.
Subacute infarct — conforms to vascular territory, rim or gyriform pattern of enhancement.
Thrombosed or inflammatory aneurysm —arises from intracranial artery, appearance dependent on degree of thrombosis/flow and local inflammation.
Contusion —see Section 13.3 .
Knowledge of the patient's immune status is essential. Conditions associated with immunocompromised state (HIV, immunosuppression etc.) are labelled with †.
Metastases —at GWMJ, rarely involve corpus callosum (cf. glioma, lymphoma); see Section 13.8 .
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 .
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.
Abscesses †—may be localized due to direct spread from adjacent structures, e.g. sinusitis/mastoiditis; if haematogenous in origin then can be scattered across all vascular territories; see Section 13.8 and septic emboli, below.
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.
Tuberculoma †—see Section 13.12 .
Toxoplasmosis †—basal ganglia and GWMJ, concentric alternating low and high T2 signal, eccentric ‘target sign’ enhancement.
Neurocysticercosis —endemic in South America, Asia and Africa. Cysts in subarachnoid space or parenchyma; appearance depends on stage (see Part 2).
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; see Section 13.20 .
Radiation necrosis —see Section 13.12 .
PML-IRIS †—see Section 13.20 .
Contusion/haematoma —orbitofrontal and anterior temporal regions; see Section 13.3 .
Haemangioblastoma —nonenhancing cyst wall, posterior fossa; see Section 13.11 .
Pilocytic astrocytoma —enhancing cyst wall, posterior fossa; see Section 13.11 .
Cystic metastasis —adenocarcinoma, SCC. Thick irregular wall ± haemorrhage.
Pleomorphic xanthoastrocytoma —young adults, temporal lobe; see Section 13.10 .
Craniopharyngioma —multilocular cystic lesion, often in suprasellar region with variable calcification and high T1 signal; see Section 13.28 .
Ganglioglioma —see Section 13.10 .
Rosette-forming glioneuronal tumour —see Section 13.11 .
Pineocytoma —see Section 13.32 .
Neurocysticercosis —vesicular and colloidal vesicular stages, central dot from scolex; see Part 2.
Normal vascular enhancement is regular and linear. Pathological enhancement is more prominent and can be ill-defined/irregular.
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.
Neurosarcoid —associated with abnormal thickening and enhancement of dura, cranial nerves and pituitary stalk.
Vasculitis —evidence of arteritis with stenoses, beading and infarcts.
Lymphoma *—elderly, fluctuating areas of T2 and diffusion abnormality, surrounding mass-like enhancement.
Lymphomatoid granulomatosis —in the immunocompromised. Multifocal periventricular linear T2 hyperintensities + enhancement.
Behçet's *—young adults, orogenital ulcers. Brainstem and deep ganglionic structures, oedema and mass effect (cf. CLIPPERS).
Langerhans cell histiocytosis *—children and young adults, commonly presents with diabetes insipidus; see Section 13.28 .
Some degree of dural enhancement is normally seen at the falx, tentorium and cavernous sinus. Hints to pathological enhancement/meningeal disease include:
Dural enhancement seen on contiguous coronal slices.
Rim enhancement anteriorly capping the brainstem.
Abnormal cranial nerve enhancement or thickening.
Presence of coexistent FLAIR sulcal hyperintensity (see Section 13.36 ).
Postoperative —greatest at site of craniotomy, usually unilateral, smooth and thin dural enhancement.
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.
Following lumbar puncture —mild and transient.
Overshunting —slit-like ventricles.
Skull base leak —following surgery/trauma, presents with CSF rhinorrhoea or otorrhoea. Diagnosed with skull base CT looking for a fracture or defect.
Spinal leak —e.g. meningocoele, posttraumatic. Often subtle, may need a myelogram to localize.
Infection —localized to adjacent osteomyelitis or sinusitis. Irregular, thick enhancement.
Neoplastic .
Meningioma —reactive tapered dural thickening around lesion (‘dural tail’).
Metastasis —e.g. breast, prostate; smooth or nodular enhancement.
Secondary CNS lymphoma *—meningeal > parenchymal involvement.
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.
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.
Extramedullary haematopoiesis —dural involvement rare, seen in thalassemia and myelofibrosis. Widened diploic space in skull.
Idiopathic hypertrophic cranial pachymeningitis —mass-like thickening of the dura, often with cranial nerve involvement. Some cases are due to IgG4-related disease.
Look for subtle cranial nerve enhancement indicating leptomeningeal pathology.
Carcinomatosis —typically nodular. Metastatic (breast, lung), lymphoma, ependymoma, germinoma, medulloblastoma, glioblastoma, pineoblastoma. Image whole neuraxis to assess extent of disease.
Meningoencephalitis —bacterial, viral, fungal, Lyme disease. Cerebral swelling.
Granulomatous disease —TB, sarcoid, Wegener's, rheumatoid nodules, fungal disease.
Vascular —collateral flow (ischaemia) or increased flow, e.g. dural fistula, pial angioma of Sturge-Weber (see Section 13.19 ).
Look specifically for hydrocephalus and radiological contraindications to lumbar puncture.
Infection —ventriculitis.
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.
Viral —CMV, VZV; immunocompromised patients.
Neoplastic —abutting ventricular surface or intraventricular.
Nodular/linear —lymphoma, glioblastoma, ependymoma, germ cell tumour, metastases.
Mass-like —ependymoma, giant cell astrocytoma.
Granulomatous —TB (basal meningitis), sarcoidosis (cranial nerves and dura).
Intraventricular haemorrhage —hyperdense blood within the ventricles.
Subependymal venous congestion —can mimic ependymal enhancement.
Deep cerebral vein thrombosis —hyperdense vein, oedema.
AVM or AVF —dilated abnormal vessels.
Sturge-Weber *—cortical calcification, cerebral atrophy and enlarged ipsilateral choroid plexus.
Enhancement of cisternal and cavernous sinus CN segments always abnormal.
CN VII enhancement—abnormal in the cisternal, meatal and extracranial segments. Venous plexus causes normal enhancement of the labyrinthine, tympanic and mastoid segments.
Multiple nerves—metastases, leukaemia, lymphoma, NF2, Lyme disease, chronic inflammatory demyelinating polyneuropathy.
Optic nerve (CN II)—different pathologies as not a true nerve but CNS WM tract: demyelination, gliomas.
Primary.
Schwannoma —CN VIII; sporadic or NF2 (diagnostic if bilateral).
Meningioma —‘tram-track’ enhancement, CN II.
Neurofibroma —rarer to involve CN, T2 hyperintense rim with central low signal (target sign). NF1: plexiform neurofibromas of CN III and CN V.
Optic nerve glioma —pilocytic astrocytomas, associated with NF1 (see Section 13.31 ).
Secondary.
Leptomeningeal dissemination —nodular involvement, seeding from primary CNS (ependymoma, medulloblastoma, germinoma, lymphoma) or secondary metastatic (breast, lung, melanoma).
Perineural spread —from head and neck tumours, e.g. mucosal SCC and salivary gland adenoid cystic carcinoma (CN VII), lymphoma, melanoma.
Meningitis.
Viral infections —HSV type 1, CMV, and VZV (Ramsay Hunt Syndrome—vesicular eruptions). CN VII.
TB *—cisternal segments of CN, surrounding exudate.
Cryptococcus neoformans —infiltration of meninges around optic tracts, nerves and chiasm.
Lyme disease —may involve CN III to VII.
Fungal— aspergillosis, mucormycosis, actinomycosis. Perineural spread from sinus disease. Elderly diabetic patients are most at risk.
Bell's palsy —uniform linear enhancement of CN VII.
Miller-Fisher syndrome —variant of Guillain-Barré, multiple CN, linear enhancement.
Chronic inflammatory demyelinating polyneuropathy —‘onion bulb’ thickening of multiple peripheral and cranial nerves, with diffuse enhancement.
Demyelinating —multiple sclerosis (MS) and NMO. CN II (optic neuritis).
Sarcoidosis *—any CN with thickening, most commonly CN II centred around chiasm and pituitary stalk.
Wegener's granulomatosis *—spread from sinuses, associated with dural thickening, vasculitis with infarcts.
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.
Post radiation neuritis —limited to radiation field.
Ischaemic —diabetics, vasculopaths; transient enhancement followed by gradual atrophy. CN II, III and VI.
Collateralization due to proximal progressive steno-occlusive disease.
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.
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.
Secondary to a distal ‘sump’ effect.
AVM —tangle of abnormal vessels with feeding arteries and draining veins. Often multiple dilated vessels, no stenoses (cf. Moyamoya).
Tumour —vascular tumours recruit increased arterial flow to both tumour and surrounding parenchyma/leptomeninges.
Sturge-Weber *—phakomatosis; facial cutaneous and leptomeningeal haemangiomas. Steal phenomenon causes atrophy of subjacent cortex and WM + ‘tram-track’ calcification.
WM lesions are common, of varied aetiologies and frequently an incidental finding, which creates management and follow-up challenges. They may be classified based on pattern into punctate, confluent and diffuse lesions.
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