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Radiology I: CT head 

In clinical practice the formal report of an emergency CT head is not always immediately available. 

As a result it is vitally important that neurocritical care clinicians can detect conditions in which urgent intervention is required.

Interpreting a CT head requires a good knowledge of neuroanatomy (see Anatomy I: the basics).

Taking time to develop a conceptual approach to reading a CT head improves clinical decision making.

Perron et al.

The CT interpretation method set out in this post is pragmatic.

It should not be viewed as a replacement for the reports provided by radiology specialists.

Always check that your opinion correlates with that of the formal report when starting out.

It would be remiss of the team not to direct also you to the best FOAMed radiology resources available online:

This is a good starting point aimed at medical students and non-radiology residents.

A neuroradiology site with a great database of interesting annotated cases.

Free to access with great content, but the website could do with a makeover. is worthy of a special mention, the most comprehensive online resource, set up (and constantly added to) by a multinational team of FOAMed radiologists.

The images used here on are courtesy of Dr Jeremy Jones, Dr Craig Hacking, Dr Andrew Dixon and A.Prof Frank Gaillard from

Their iOS app is also full of golden nuggets of knowledge and is largely accessible gratis.

The web-based (small fee paying) emergency and trauma courses are excellent.

Any profits enable free access to the teaching courses in the developing world.

" here.

Let's to learn how to read a CT head."

How to read a CT head in neurocritical care

  • Make sure it is the correct study and patientIs there any contrast present?

  • Select brain windowing

  • Start at the top slices of the axial imaging

  • Scan twice up and down through the image stack and look for anything big

  • Look specifically for signs of herniation

  • Use the aide memoire Blood Can Be Very Bad to look systematically at the Blood, Cisterns, Brain, Ventricles and Bone. Use appropriate windowing.

  • Scroll up and down looking for symmetry and the presence or absence of normal anatomy. Now look for the vascular anatomy.

  • If coronal images are available use them to visualise any pathology and try to think in 3 dimensions, pay particular attention to the falx and tentorium cerebelli.

  • Go back and look specifically at the soft tissues, sinsues, mastoid air cells and orbits 

Normal non-contrast head CT

Make sure it is the right study and patient. Is there any contrast present?
  • Always cross check the identity of the imaging with that of your patient.

  • Are the images from the date you are interested in?

  • For a CT head contrast is given intravenously. Any enhancing areas will appear brighter than in the plain slices. Depending on the timing it is possible to see the arterial or venous anatomy.

The importance of selecting the right windowing
  • The importance of windowing; Our eyes can only differentiate between a limited distribution of shades of grey.

  • PACS windowing can be changed to improve the contrast between subtle shades of grey and visualise any pathology better. 

  • Standard brain windowing may present both acute blood and bone as bright white. Without changing the windowing small extra-axial haematomas can be easily missed.

  • Remember not everything bright in the brain on CT is blood.

  • The choroid plexus, pineal gland, globus pallidus and dentate nucleus in the cerebellum may calcify with increasing patient age.

Starting at the top. Look for anything big.
  • Starting at the top of the axial images, look at the sulci and gyri.

  • The gyri should go all the way to the edges to meet the inner table of the skull.

  • If they don't an isodense subdural haemorrhage could be present.

  • Are there any large space occuping lesions or extra-axial bleeds?

Look specifically for signs of herniation:


  • Subfalcine herniation in practice is an interchangable term with midline shift.

  • It causes contralateral lateral ventricle hydrocephalus as the foramen of Munro is distorted or occluded by swelling.

  • As the ipsilateral frontal lobe is compressed under the firm dural falx the anterior cerebral artery circulation can be threatened.

  • This may lead to ACA territory infarction but may only be apparent on repeat imaging after 24hours.


  • Uncal herniation refers to the medial movement of the medial temporal lobe.

  • This will cause compression of the suprasellar cistern and clinically results in an ipsilateral 3rd nerve palsy with a dilated, down and out pupil.

  • Radiologically the uncus compresses the midbrain (one of Mickey mouse's ears) and the temporal horn of the lateral ventricle is displaced medially ad inferiorly.

  • As the degree of herniation worsens the patient may develop an ipsilateral hemiparesis as the contralateral cerebral peduncle (Mickey's other ear containing the descending pyramidal tract fibres) is compressed into Kernohan's notch (The edge of the tentorium cerebelli). This is known as a false localising sign.

  • If the uncal herniation continues unchecked then downward transtentorial herniation will occur occasionally leading to a central midbrain haemorhage known as a Duret haemorrhage. This is a poor prognostic sign.

  • The PCA circulation can be threatened by compression against the tentorium, again this may lead to infarction only apparent on later imaging.

  • Ascending transtentorial herniation effacing the quadrigeminal cistern (upwards through the tentorium) is possible in posterior fossa pathology. 


  • Tonsillar herniation compresses the brainstem leading to the Cushing response and death unless immediate decompression in acheived.

  • Loss of the normal CSF pattern in a circle around the medulla together with compression of the 4th ventricle as the cerebellar tonsils decend into the foramen magnum (crowding).


  • The term transalar herniation has been used to describe brain pushed up or down across the sphenoid wing. In descending transalar herniation the MCA circulation can be threatened.

  • Transcalvarial herniation is the precise term for an external herniation of the brain through a crainectomy wound or skull fracture.

Blood Can Be Very Bad: a systematic check of 
Blood; Cisterns; Brain; Ventricles; Bone
  • Scroll up and down through the images. Look in a circular fashion for: 

  • Blood appears differently on CT depending on it's age. 

  • Hyperacute blood may appear low density before clot occurs and is responsible for the swirl sign. 

  • Acute blood appears bright white. Isodense at 1 week. Hypodense at 2 weeks.

"Is there any blood present?"

"Is it extra-axial (outside the brain parenchyema) or intraparenchymal?"

  • Does not cause oedema in the underlying brain.

  • In a lens shape which does not cross the suture lines is an extradural haematoma.

  • Sickle-shaped blood which is not confined by the suture lines and follows the dural reflections is subdural haematoma.

  • The volume of subdural blood present is often underestimated, check for tentorial and falcine thickening.

  • Blood which follows the sulci or is pooled in the cisterns will be subarachnoid (in the CSF space), check in the interpeduncular cistern (inbetween Mickey's ears).

  • Intraventricular haemorrhage is subject to gravity (it will settle dependently). Check the occipital horn for traces.

  • Anterior to the temporal lobes is a blind spot for benign extraaxial blood, it is often venous.




  • Causes oedema in the brain surrounding the haematoma (hypodense irregularity).

  • Intraparencymal haemorrhages can be primary or secondary resulting from an underlying lesion

  • Primary hypertensive haemorrhage occurs in the deep basal ganglia, thalamus, pons or cerebellum. They may extend into the subdural, subarachnoid or ventricular space.

  • Primary lobar haemorrhages are located superficially within the lobes of the brain at the grey-white junction, they may follow the axonal tracts into the brain. In the elderly they are due to cerebral amyloid microangiopathy.

  • In younger patients the haemorrhage may be secondary to an underlying arteriovenous malformation.

  • A haemorrhage with a rounded outline or surrounded by a large quantity of vasogenic oedema may be secondary to a cerebral tumour.

  • Irregular finger-like peripheral haemorrhages or a heterogeneous gyriform pattern associated with cortical oedema may be due to venous hypertension.


"Are the cisterns present?

Are they effaced (compressed)?"

  • The cisterns are normal CSF collections present within the skull. 

  • There should be a clear perimesencephalic basal ring of cisterns around midbrain.

  • The suprasellar cistern is star-shaped and the site of the circle of Willis. The most common site for aneurysmal SAH to collect.

  • Quadrigeminal W-shaped

  • Sylvian fissure represents the frontotemporal interface and contains the M2 sections of the MCA vessels

  • There should clearly be CSF in the foramen magnum.


"Is the brain symmetrical?

Is there grey-white differentiation"

  • Locate the central sulcus (looks like a reverse omega), the tip of this corresponds to the motor innervation of the hand and thumb. Remember the precentral gyrus has motor innervation, the postcentral gyrus sensory innervation.

  • Assess for sulcal effacement. The gyri should go all the way to the edges to touch the inner table of the skull.

  • Look for symmetry and presence of an space occupying lesion as you scroll up and down the imaging.

  • Change the windowing to stroke or brain and look clockwise around the grey-white matter junction checking for clear differentiation or microhaemorrhages (seen in diffuse axonal injury). There should not be any blurring or smudging. (See disease specific teaching: CVA).

  • Systematically check particular important areas: the deep grey structures like the caudate, putamen, globus pallidus, thalamus and the basal ganglia. Check white matter tracts of the internal capsule and external capsule up to the corona radiata.

  • Look again at the cerebellar tonsils, brainstem and medulla.

  • The midbrain should look like Mickey Mouse whose ears are the cerebral peduncles.

  • At the level of the pons axial anatomy looks like Darth Vader's face.

  • Check the vascular structures. Follow the carotids and vertebral arteries up to the circle. Trace the venous anatomy down from sagittal sinus to transverse sinus to sigmoid sinus then into the jugular system.


"Are the ventricles of normal size and shape?

Do they contain blood?"

  • Using the standard brain windowing.

  • Follow the CSF circulation from the 'Back-to-back comma' lateral ventricles through the foramen of Munro into the slit-like 3rd ventricle

  • Continue scrolling down looking through the cerebral aqueduct into 4th ventricle then follow the foramen of Luschka bilaterally and foramen of Megendie in the midline down into the spinal canal.

  • Check for effacement. Are the ventricles compressed? What has squashed them?

  • Have the ventricles been shifted from their normal position. Observe their shape, size and symmetry.

  • Temporal horn of the lateral ventricle dilates first in hydrocephalus. It moves in herniation syndromes.

  • Check for blood in dependent areas particularly the occipital horns of the lateral ventricles.


"Is there a fracture?

Is there soft tissue swelling?"

  • Set the windowing to Bone.

  • Look for widened suture lines or fractures. 

  • Evaluate the normal air filled spaces within the skull; Sinuses and mastoid air cells. Do they contain fluid? 

  • Go back to standard windowing and look specifically for soft tissue swelling, remember to look in the orbits and pharyngeal tissues. Fat pads in the neck should demonstrate symmetry.

  • Are there any foreign bodies? 

"Why not head over to the scrollable images on to practice"

Marshall Scoring

Many trials in neurocritical care report the Marshall score of a CT.

This scoring system roughly predicts mortality but should not be used in prognostication alone.

It is used in our unit to track changes in outcome from year to year.

  • Diffuse injury I  (no visible pathology)

    • no visible intracranial pathology

  • Diffuse injury II

    • midline shift of 0 to 5 mm

    • basal cisterns remain visible

    • no high or mixed density lesions >25 cm3

  • Diffuse injury III (swelling)

    • midline shift of 0 to 5 mm

    • basal cisterns compressed or completely effaced

    • no high or mixed density lesions >25 cm3

  • Diffuse injury IV (shift)

    • midline shift >  5mm

    • no high or mixed density lesions >25 cm3

  • Evacuated mass lesion V

    • any lesion evacuated surgically

  • Non-evacuated mass lesion VI

    • no high or mixed density lesions >25 cm3

    • ​not surgically evacuated

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