ct of acute intracranial pathology
TRANSCRIPT
CT of Acute Intracranial Pathology
Dr Anne CarrollDr Eric HeffernanDepartment of Radiology
St Vincent’s University HospitalDublin, Ireland
www.svuhradiology.ie
Introduction
• Head CT is one of the most frequent studies performed on-call by Radiologists
• The main indications for on-call head CT are for trauma and for suspected stroke
• This tutorial will illustrate the most common pathological appearances that we encounter in these conditions
Introduction
• Unlike most CT examinations performed on other parts of the body, head CT for trauma or stroke is performed without IV contrast, as the abnormalities we look for are readily visible on unenhanced CT
• In some circumstances, IV contrast will subsequently be injected:– To perform CT angiography in patients with acute stroke
who may be candidates for thrombectomy– When the initial non-contrast CT raises the possibility of
an underlying tumour or infection
What to look for on head CT
• Haemorrhage– Acute haemorrhage is bright on CT– When describing this we can call it ‘dense’, ‘high
attenuation’, or ‘hyperattenuating’• Oedema– This is less dense than normal brain and appears relatively
dark (‘decreased density’, ‘low attenuation’)– Oedema can be ‘cytotoxic’ (grey and white matter involved,
seen in strokes), or vasogenic (white matter only, seen around tumour, abscess and intraparenchymal haemorrhage)
What to look for on head CT
• Mass effect– Effacement of sulci (compare to opposite side)– Effacement of ventricles– Midline shift
• Hydrocephalus– Can develop acutely in the setting of subarachnoid
haemorrhage
What to look for on head CT
• Skull fracture– Frequently associated with intracranial
haemorrhage and occasionally pneumocephaly (intracranial air – most commonly seen when a fracture extends through the frontal sinus)
– Skull fractures are often difficult to see when reviewing a CT on regular soft tissue windows so we need to switch to a bone window to pick them up*
*’Windows’ are explained in the CT section of our website
Trauma
• Pathology to look for in patients with a history of head injury:– Extradural haematoma– Subdural haematoma– Subarachnoid haemorrhage– Intraparenchymal haemorrhage– Skull fracture– Combinations of the above
Extradural haematoma
• Young patients• Often associated with a skull fracture– Injury to middle meningeal vessels
• Characteristic biconvex (‘lens’) shape• Extension is limited by dural attachments at
skull sutures• Mass effect including midline shift are usually
present
Two different patients with extradural haematomas – these often look exactly like this and tend not to present much of a diagnostic challenge. Note the scalp haematoma in the patient on the left (arrow), indicating the site of injury. A skull fracture was alsopresent in this case (seen on bone windows). Note the mass effect on the left-hand image – the right lateral ventricle is effaced (compressed) and there is mild midline shift.
Mid
line
Midline shift
Subdural haematoma
• Older patients/alcoholics• Due to tearing of bridging veins in subdural space• Not limited by sutures so can extend all the way
along the cerebral hemisphere– Typically crescentic in shape
• Underlying brain is usually atrophic therefore haematoma needs to be larger before it will cause midline shift
Acute subdural haemorrhage. Note how this crescent shaped haematoma is not limited by the sutures and in fact has extended along the cerebellum (arrowhead). Note the midline shift (dotted line = midline).
Subdural haematoma
• Unlike extradural haematomas, subdural haemorrhages often don’t present in acute phase
• This is important as subacute or chronic subdural haemorrhage appears different to acute– Subacute – lower attenuation than acute blood, may be
very similar density to normal brain making it hard to spot– Chronic – similar attenuation to CSF, which can also make
this hard to spot• A mixed picture (e.g. acute on chronic subdural) is
frequently present
Chronic subdural haematoma • The haematoma is less
dense than the adjacent brain parenchyma
• Note the effaced left lateral ventricle (*)
*
Chronic subdural haemorrhage is often bilateral as in this example
Bilateral subacute subdural haemorrhage
The haematomas in this case are almost the same density as the adjacent grey matter, which can make them difficult to spot
Traumatic subarachnoid haemorrhage
• This is usually confined to a small number of sulci and can be quite subtle
• It looks very different to the classic picture of non-traumatic subarachnoid haemorrhage (see later)
• Look for linear high density between gyri
Acute traumatic subarachnoid haemorrhage
Note the scalp haematoma at the site of injury (*). The linear high density extending along several sulci represents subarachnoid blood (arrows). There is also some subdural haemorrhage extending between the occipital lobe and the cerebellum (arrowhead).
*
Intracerebral haemorrhage
• Following head injury, one or more areas of intraparenchymal haemorrhage may be visible on CT
• The typical sites for these ‘contusions’ is in the inferior aspects of the frontal lobes and the anterior aspects of the temporal lobes
• They frequently occur directly opposite the side of the traumatic force to the head (‘contre-coup injuries’)
• When large, they may rupture into the subarachnoid space or ventricles
Multiple intraparenchymal haemorrhagic contusions of varying sizes in the inferior aspects of both frontal lobes.
Skull fracture on bone windows
Depressed skull fracture
Pneumocephaly
Head injury with multiple findings:
Depressed skull fractureExtradural haematoma (yellow)Intraparenchymal haemorrhage (*)
**
Acute ischaemic stroke
• Non-contrast CT brain is the initial imaging modality of choice in suspected CVA
• CT is often normal in the first few hours after onset of symptoms– Main role of CT is to exclude haemorrhage, in
order to guide treatment• Majority of strokes will be visible on CT after
24 hours
Acute ischaemic stroke
• CT signs– Low attenuation in infarcted parenchyma– Loss of grey-white matter differentiation– Obscuration of basal ganglia– Loss of visualization of insula (‘insular ribbon’ sign)– Dense MCA sign or dot sign– Mass effect (sulcal +/- ventricular effacement)– Haemorrhagic transformation may occur
Acute left-sided CVA
• Low density parenchyma• Loss of grey-white matter
differentiation• Sulcal effacement
Subacute (>24 hours) MCA infarct
• Loss of grey-white matter differentiation
• Obscured basal ganglia (normal outlined on left side)
• Midline shift• Effaced right lateral
ventricle
More examples of subacute infarcts
Subtle early left MCA infarct – slightly reduced parenchymal density. Note how the usually bright grey matter of the insula (the ‘insular ribbon’) has become indistinguishable on the left (normal right insular ribbon indicated by arrows). This patient has had previous infarcts – these are the very low density areas in the occipital lobes (*).
Right Left
**
MCA dot sign (due to thrombus) Acute MCA infarct (same patient)
Dense MCA sign
Dense MCA sign with corresponding occlusion on CT angiogram
Occipital infarct (left) with subsequent haemorrhagic transformation (right, arrows)
How to tell that an infarct is old:
• This patient has an old right frontal infarct (yellow arrows)
• Very low density (similar to CSF)
• No mass effect• Instead, nearby sulci become
widened and ventricle enlarges (white arrows)
Haemorrhagic stroke
• Hypertensive patients• Typically centred in basal ganglia
Haemorrhagic stroke
• Centred in left basal ganglia and extending into temporal lobe
• Note mass effect – effaced sulci and left lateral ventricle
• Also has small haemorrhage on right side (arrow)
Atraumatic subarachnoid haemorrhage
• Usually due to ruptured aneurysm• Dense blood accumulates around
circle of Willis• Classical appearance is a 5-pointed
star, with blood extending along left and right posterior cerebral arteries, left and right middle cerebral arteries and anterior cerebral arteries (these run alongside each other)
Left ACA
Righ
t ACA
Left MCARight MCA
Left PCARight
PCA
Atraumatic subarachnoid haemorrhage
• Haemorrhage may extend into ventricles and can cause acute hydrocephalus
• CT can be normal with small bleeds, hence need for lumbar puncture when clinically suspected
• When a subarachnoid haemorrhage is detected on CT, a CT angiogram is performed to search for a treatable aneurysm
Classic 5-pointed star appearance of acute subarachnoid haemorrhageThis patient also has acute hydrocephalus (dilated ventricles - *)
* *
*
Often, there will be uneven distribution of blood which can be a clue to the location of the causative aneurysm, as in this case where it was located at the tip of the left middle cerebral artery
Subarachnoid haemorrhage with intraventricular extension (orange arrows) and acute hydrocephalus (yellow arrows)
Massive subarachnoid haemorrhage with causative aneurysm on CT angiography
ACA – anterior cerebral artery, MCA – middle cerebral artery, large arrow - aneurysm
The last few examples have shown dramatic subarachnoid haemorrhage, however they are often much more subtle, as in this case
• Linear high density in a small number of sulci (yellow arrows)
• Small amount of blood in right lateral ventricle (orange)
• Remember, cytotoxic oedema causes low attenuation in both grey and white matter– strokes
• Vasogenic oedema only affects the white matter, sparing the grey matter– Suggests more sinister pathology• Primary brain tumour• Metastases• Abscess
Vasogenic oedema in right frontal lobe (*), sparing the grey matter (arrows)
*
(Same patient as previous slide)• MRI shows how extensive the vasogenic oedema is, and that it also involves white
matter of the left frontal lobe (arrows, left image - this is a FLAIR image, which is explained in the MRI section of the www.svuhradiology.ie website)
• Post-contrast image on the right shows that there is an enhancing underlying mass, which turned out to be a glioblastoma (arrows)
In this patient, the non-contrast CT image on the left shows extensive vasogenic oedema with mass effect and midline shift. IV contrast-enhanced CT on the right shows a huge underlying ring-enhancing mass (arrows) which turned out to be an abscess. The patient was an intravenous drug abuser.
