Skull and brain

Published on 12/06/2015 by admin

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Last modified 12/06/2015

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Skull and brain


Acute arterial infarct: CT

1. Initial appearances often normal in first few hours. Larger infarcts more conspicuous.

2. Initial signs:

3. Later signs:

4. Contrast enhancement usually unhelpful and often confusing; simply reflects breakdown of blood–brain barrier. Any enhancement pattern possible.

5. CT perfusion study may demonstrate decreased perfusion in wider area of brain (ischaemic penumbra) suggesting further tissue at risk.

6. CT angiography can demonstrate dissection/stenosis/occlusion (embolic or thrombotic).


Acute arterial infarct: MRI

1. More sensitive than CT but signs similar (reduced attenuation on CT = increased T2 signal on MRI). Wedge shaped; grey and white matter involvement; often initially cortical change). Signal change usually (but not always) evident within 3–6 hours (within minutes on DWI). Increased T2 signal due to cytotoxic oedema (cell swelling; restricted diffusion).

2. Acute infarcts show increased DWI signal and low ADC. Low ADC signal ‘pseudonormalizes’, i.e. becomes bright from around 5–10 days postinfarct.

3. Mass effect – local and/or general as on CT.

4. Absent flow voids in affected major vessels; increased signal on T2 and FLAIR; most often seen in MCA (check carotid canal at skull base) or basilar.

5. Contrast enhancement may be confusing as on CT; prolonged transit time of contrast through distal or collateral vessels may be seen on postgadolinium T1 sequences.

6. Perfusion-weighted imaging may show poor perfusion in wider territory than changes on standard sequences: diffusion/perfusion mismatch may demonstrate ischaemic penumbra representing potentially salvageable brain tissue.

7. MR angiography may show vessel stenosis/occlusion in extracranial or intracranial vessels.


Venous infarcts

1. Usually secondary to venous sinus thrombosis:

2. If an area of infarction is seen which is not in arterial distribution, consider sinus thrombosis.

3. Venous infarction often haemorrhagic (but this is not a contraindication to anticoagulation; aim of anticoagulation is to stop propagation of thrombus).

4. Beware symmetrical low attenuation in deep grey matter structures (especially thalami); suggests involvement of deep cerebral veins which may not otherwise be seen on scans.


Indications for CT and MRI in acute stroke


Appearances of blood on scans


Subarachnoid haemorrhage


Intracranial aneurysms


Vascular malformations

Two main types: those with arteriovenous shunts and those without shunts.

Malformations with AV shunts

1. Arteriovenous malformations – present in young to middle-aged adults with one or combination of haemorrhage (40%), seizures (30%), neurological deficit or headache (20%). Annual cumulative rupture risk ~3% per year. Consist of one or more arterial pedicles draining directly to enlarged draining veins through nidus. Multiple lesions in various syndromes: e.g. Osler–Weber–Rendu and Wyburn–Mason.

2. Dural arteriovenous fistulae – acquired lesions presenting in older population (50–70 years) compared to AVMs (20–40 years). Occur following damage to venous structures (post-thrombosis, surgery, trauma). Symptoms and signs secondary to arterialization of venous system: bruit, venous hypertension, pulsatile tinnitus (if primary involvement is sinuses); haemorrhage, focal neurology, seizures (if primary or major secondary involvement of cortical veins). Caroticocavernous fistula may give rise to proptosis and chemosis.

Malformations without AV shunts

1. Cavernous angioma (cavernoma) – sinusoidal spaces lined with endothelium; occur anywhere in CNS, commonest pons. Present with small haemorrhages (usually not associated with large haemorrhages) or seizures; often incidental findings. Multiple cavernomas may be familial.

2. Developmental venous anomaly (venous angioma) – probably due to persistent embryonic veins which drain normal brain. Not thought to have increased haemorrhage risk.


CNS infection


Diagnosis made by lumbar puncture, not imaging. Indications for neuroimaging in possible meningitis are to assess complications: ischaemia/infarction, hydrocephalus, venous thrombosis, subdural empyema, ventriculitis and cerebral abscess.

1. Bacterial meningitis – CT usually normal. May see generalized brain swelling and/or focal or generalized ischaemia. Scanning only postcontrast may mask pathology. If contrast to be used, precontrast and postcontrast scans should be obtained. Lack of enhancement does not exclude meningitis. Hydrocephalus may be communicating and/or obstructive.

2. Subdural effusion or empyema – low attenuation extra-axial collection ± rim enhancement.

    May be very subtle, especially if parafalcine. Parafalcine empyemas rapidly lead to sinus thrombosis. If frontal, look at frontal sinuses carefully.

3. Cerebritis – diffuse area of parenchymal low attenuation which may develop into abscess.

4. Abscess – thin-walled rim-enhancing lesion; may be very little systemic disturbance.

5. Viral meningitis – neuroimaging usually entirely normal.


HIV and the brain

HIV is a neurotropic virus that can affect the brain directly or can predispose to opportunistic infection (commonest toxoplasma, Cryptococcus, progressive multifocal leukoencephalopathy). Increased incidence of intracerebral lymphoma.



Head injury

Primary effects

1. Fracture – impact head injury; commonest = linear; complex fractures (diastatic, stellate, depressed) tend to occur with mechanisms involving greater degrees of force; skull base fractures may be occult (look for secondary clues such as fluid in sphenoid sinus or mastoid air cells; pneumocephalus); facial nerve palsy or ossicular disruption in temporal fractures.

2. Extradural haemorrhage – usually arterial bleed (middle meningeal); biconvex lentiform haematoma (limited by coronal and lambdoid sutures as inner layer of dura bound to sutures but may cross sagittal suture); mixed attenuation haematoma may mean ongoing bleeding.

3. Subdural haemorrhage – usually venous low-pressure bleed; crescentic biconcave collection over cerebral hemisphere (can cross coronal and lambdoid but not usually sagittal sutures).

4. Subarachnoid haemorrhage – post-traumatic SAH usually low-volume scattered bleeds; peripheral distribution.

5. Contusions – larger mixed attenuation (CT) or signal (MRI) intra-axial lesions; tend to occur in inferior frontal and anterior temporal lobes (impact against bony anterior walls of anterior and middle cranial fossae); usually surrounding oedema adding to mass effect.

6. Diffuse axonal injury – smaller lesions than contusions; shearing injury secondary to rotational or acceleration/deceleration forces; tend to be widespread occurring at grey–white junction, corpus callosum, internal capsule and brainstem.



Large ventricles not always due to increased CSF volume: cerebral atrophic processes can lead to relative enlargement of ventricles; ventricles may be congenitally large (probably secondary to reduced white matter volume).

Hydrocephalus more likely if:

Increased CSF volume may be due to:


CT attenuation of cerebral masses

Relative to normal brain (masses with variable appearances not included).


Differential diagnosis of a solitary intracerebral mass

1. Primary brain tumour – high-grade tumours tend to have most mass effect (tumour and surrounding oedema), heterogeneous with areas of necrosis (glioblastoma); may infiltrate and involve/cross corpus callosum; variable enhancement but tends to increase with increased grade.

2. Metastasis – appearance variable on scans depending on primary; often considerable associated oedema (vasogenic, white matter), multiple/solitary, often located grey–white junction.

3. Arterial infarct – developing low attenuation (CT), high T2 signal (MRI) wedge-shaped lesion with variable mass effect; various enhancement patterns if contrast given.

4. Venous infarct – area of low attenuation (CT), high signal (MRI) not in arterial distribution, often associated mass, often haemorrhagic.

5. Abscess – homogeneous, thin enhancing rim, usually considerable vasogenic oedema.

6. Acute demyelinating plaque – may be very large with minimal clinical signs; low attenuation (CT) and high T2 signal (MRI); variable enhancement.

7. Haematoma – subacute to chronic.

8. Cerebritis/encephalitis – poorly defined area of low attenuation (CT); HSV predilection for limbic system; variable enhancement.

9. Aneurysm – may give rise to mass effect by itself but also often associated oedema in surrounding brain; appearance varies according to whether patent or associated intramural thrombus ± calcification.


Intracranial calcification

Normal variant

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