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Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Atrial Fibrillation |Atrial Myxoma |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Cardioembolic stroke |CT Basics for Stroke |Endocarditis and Stroke |Haemorrhagic Stroke |Stroke Thrombolysis |Hyperacute Stroke Care
Different Hounsfield units
Medium | Hounsfield Units | Appearance |
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Air | -1000 | Black |
Fat | -80 to -100 | Black |
Water | 0 | Black |
CSF | +5 | Black |
White matter | +30 | Dark Grey |
Grey matter | +40 | Light Grey |
Acute haemorrhage | +70 | White |
Bone | +400 to +3000 | Bright White |
Scan | Dose |
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Natural Background | 3.1 mSv/year |
Domestic pilots | 2.2 mSv/year |
Average US Exposure | 6.2 mSv/year |
CXR (AL and lateral) | 0.10 mSv/year |
Chest CT | 7.0 mSv/year |
Chest Abdomen Pelvis CT | 21.0 mSv/year |
Brain CT (standard) | 2.0 mSv/year |
CTA/CTP Head | 16.4 mSv/year |
Clinically there are no real contraindications for CT if clinically indicated. There are no concerns about pacemakers or defibrillators or metal clips or recent surgery. It is probably unwise if the patient is moribund and too unwell for any intervention and better served by palliation but that's a specialist call. Scans are incredibly quick nowadays and patients can be closely monitored. The only real difficulty is with agitated or confused patients in whom scan quality will be degraded with movement artefact. A doctor can be at the side of the patient during a CT with an appropriate lead apron or behind a screen for protection if needed. CT does not prevent monitoring equipment of infusions or drips. It may be occasionally necessary to intubated and ventilate a patient prior to scanning.
Non-contrast CT scan is the standard imaging modality for hyperacute stroke care. It is fast, cheap, accessible, and very sensitive for haemorrhage and there is no problem with pacemakers or monitoring equipment. Claustrophobic or monitored patients can be scanned relatively easy. Done early many scans will be normal despite significant clinical findings. Stroke is primarily a clinical diagnosis and not a radiological diagnosis.
Clinical Indications for urgent CT i.e. within 1 hour of arrival at hospital |
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This involves a mechanism by which one can select for different Hounsfield numbers. Used well it can help increase the contrast between various structures. For example, a window of 2000 will show most CT numbers. A wide window (W) 400-2000 HU is useful for showing low and higher density tissues. A narrow window 50-350 HU is better at showing soft tissue. Window Level (L) is the midpoint of the CT range. The brain is W80:L40, Stroke is W8:L32 or W40:L40.
Indication | Parameters |
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Brain window to best show white/grey matter differentiation | W=80 L=40 |
Bone windows for bone pathology | W=3500 L=700 |
Subdural windows for small or isodense subdurals | W=250 L=70 |
CT is incredibly useful but not infallible and its limitations should be respected. A normal CT scan is entirely compatible with a large ischaemic stroke when within 6 hours of onset. There may be some subtle early changes. CT is also very poor at picking up changes in tissue density in bony spaces such as temporal bones and posterior fossa due to what is called beam hardening as the x-ray beam is distorted by the dense bone traversed. Metallic objects such as aneurysm clips or piercings that weren't removed can cause a radiating streak pattern. Partial volume artefacts can cause streaks or bands of alternating dark and light stripes and beam hardening also affect the posterior fossa. CT scanning cannot differentiate between hypodensity due to infarction or haemorrhage after 1-2 weeks and MRI with GRE or T2* must be used. Subacute ischaemic stroke after several days can show haemorrhage and irregular patterns of density and haemorrhagic changes which can resemble tumour s. Follow up interval scanning will be needed.
Caution : What may be missed on a CT scan |
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Make sure you understand the terms axial, sagittal and coronal. Axial is simple horizontal slices from above down. Sagittal is in the same plane as cutting the brain in the midline or parallel to this (parasagittal). The falx cerebri that separates the brain hemispheres lies in the sagittal plane. Coronal is like a tiara or 'corona'. It is vital to have a good inner representation of the cerebral vessels as they enter the skull and join the circle of Willis and the circle of Willis as well and the position of the vessels. A few simple points will help greatly. The circle of Willis (COW) is at the level of the midbrain. Find the midbrain and then look for the vessels. This is a good place to start looking for the hyperdense MCA as the MCA leaves the COW laterally within the Sylvian fissure.
Axial | Coronal | Sagittal |
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Starting with imaging. It is important to take your time and go through each slice from top to bottom in every case. Don't be distracted by the most obvious "big" finding and make sure you take time to ensure that you don't miss things. This is even more important in thrombolysis cases where the main concern is "is there any blood" and great care must be taken in what is a time-pressured environment. In that situation, I look at the scan whilst it is being done in the CT and then as soon as the patient is out and before we give open the Alteplase I will go off to a monitor away from the team and distractions and quickly go through all the slices without interruption at least twice. As I have become more experienced and seen more and more cases I think this level of care is important. It's one of the reasons why I don't rush to give Alteplase in the CT scanner as the control room is not the best place to look at a scan with diagnostic quality. I feel that several minutes quickly reviewing the scan in a controlled way is important especially in patients where things may just not seem clinically right. In most cases, we do not get a radiology review before lysis. I will actively look for any suggestion of a thin layer of subdural blood or any hyperdensity that might reflect acute bleeding. Sometimes it is difficult if there is asymmetrical basal ganglia calcification that can mimic blood or it may actually be blood. I will take particular care to look for any subarachnoid blood within the ventricles and cisterns as well as convexity blood in the sulci. I have seen excellent colleagues caught out with very subtle basal ganglia blood that looked very much like calcification even when shared with the neuroradiologist and also subtle sulcal convexity blood probably due to cerebral amyloid. One possible clue is that often the NIHSS if the neurology is due to very subtle haemorrhage is usually in that low threshold to treatment range. The rest of the time scans can be looked at with time. It is very important whatever stage you are at the look at every scan. It may not mean much at the start but you are building up your own visual memory bank of imaging with which to compare every new scan and it quickly trains your visual skills.
Top down Axial Imaging
Image below:The top image two slices here are useful for just ensuring that there is no subdural blood or any other abnormality. It is on the top few slices that we may see a subtle anterior cerebral artery infarct that can have caused contralateral leg weakness and these slices must be looked at very carefully. It is important to recognise calcification of the choroid plexus which is within the ventricles and produces CSF. It is possible to get a focal haemorrhage up at this level. Each slice needs careful review.
Image below:A good view to look for any evidence of parenchymal abnormality in the cerebral hemispheres. Here we have brain supplied by ACA, MCA and PCA. Look for any asymmetry and look closely for any space between the parenchyma and the inner skull that could be subdural. Appreciate the contrast between the outer grey matter and the more central darker white matter.
Image below:A good view to look for any evidence of parenchymal abnormality in the cerebral hemispheres. You can also see the frontal and temporal horns of the lateral ventricle and the slit-like third ventricle. Any enlargement of these particularly the temporal horns can suggest hydrocephalus.
Image below:This is the level going through the Midbrain. Identify the V shape of the midbrain. This is formed by the cerebral peduncle which carries the descending motor fibres in the front of the "V". This is a good position or a slice above or below to see the branches of the circle of Willis and this is often the level at which one can see clot "the hyperdense artery sign" within the MCA or even PCA. You can also see the frontal and temporal horns of the lateral ventricle and the slit-like third ventricle. Any enlargement of these particularly the temporal horns can suggest hydrocephalus.
Image below:This is the level going through the Upper Pons. As you can see the pons is a slightly rounded structure with the cerebellum attached posteriorly separated by the fourth ventricle. This a common area to contain blood in those who have had bleeding into the ventricular system.
This is the level going through the lower Pons
This is the level going through the medulla
Some degree of basal ganglia calcification is normally seen and the main issue is to differentiate it from blood. There are extreme variants and the so-called Fahr syndrome. Normal calcification is seen in middle age and beyond. Unless extreme it is rarely associated with any problems.
It is important to develop your ability to study imaging and correlate it with brain structure and function. There is a standard anatomical vocabulary with terms such as axial, sagittal and coronal which are commonly used in both CT and MR to describe different cross-sectional images. Modern-day imaging actually allows the brain to be imaged and reconstructed in any plane but these are the standard and familiar views.
Look at as much brain imaging as possible, the ones that you request and more. The key is to see a wide variety of normality and to build up some pattern matching skills and experience in identifying important structures and lesions. You will have an advantage over the radiologist who has only the clinical details on the card whereas you have the patient.
Definitive distinctive changes may not occur until 6-8 hours. In the meantime, more subtle signs are seen. At about 6 hours and sometimes earlier there may be loss of grey-white matter differentiation - seen at the cortical surface due to localised changes such as cytotoxic oedema within the grey matter which has a higher metabolic requirement and so becomes oedematous quicker. These signs are subtle and can be missed by even the most experienced
This can be the earliest sign of a large vessel stroke is accompanied by a corresponding Left MCA stroke syndrome. There are no obvious tissue changes and the patient is within the window and NIHSS is raised and no contraindications should be considered for thrombolysis/thrombectomy if safe. Occasionally due to good collaterals, there may be minimal symptoms and in others, they can be profound. A dense artery may just be calcium in the vessel wall and scans must be interpreted within the clinical context.
The patient was comatose and sustained massive damage to the posterior circulation. This is an important sign in a deteriorating and comatose and quadriplegic patient needing consideration for thrombectomy. There are no parenchymal changes seen yet.
This shows an evolved subacute infarct as the edges are still indistinct and so there is ongoing liquefactive necrosis. This is about Day 2-4 or beyond. There is some mild midline shift due to some localised oedema.
Infarction involves both occipital lobes. The patient who survived is blind.
There is no bright white fresh blood so this is a subacute bleed and it can be surprising how well these are tolerated. The midline is shifted. This is not stroke. It needs urgent discussion with neurosurgeons. Any anticoagulants or antithrombotic therapy must be stopped. The decision on whether to operate will depend as well on the clinical state of the patient.
Later signs (6-24 hrs) of Acute Ischaemic Stroke | |
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Late signs ( > 24 hrs) of Acute Ischaemic Stroke | |
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Non-contrast CT false negatives (there is a stroke) usually in infarcts when done early or in those who present 7-10 days after stroke and there is a visible hypodensity but no blood and so aetiology of perhaps a small bleed may be missed. In these cases, a gradient echo will show haemosiderin deposition around the margins suggesting haemorrhage as he cause.
NCCT false positives are seen particular in older hypertensive patients where Lacunar infarcts are common and most often asymptomatic but appear on scans done for a myriad of reasons so unless there is corresponding new neurology do not diagnose acute stroke but do treat for "stroke disease".
The Alberta Stroke Program Early (non-contrast) CT score (ASPECT) is a scoring system used to assess the extent of early ischaemic changes in the middle cerebral artery territory on non-contrast computed tomography. The clinician/radiologist studies the appearance at two different axial slices corresponding with two different anatomical levels and subtracts 1 from the total maximum of 10 for each area affected. A score of 0 suggests extensive MCA infarction and correlates inversely with NIHSS. A score of 10 is normal. An ASPECTS score less than or equal to 7 predicts a worse functional outcome at 3 months as well as symptomatic haemorrhage. Online training and more information is available from link
Basically the higher the ASPECTs score the better the prognosis. High scores such as 10 are normal and low scores < 5 suggests evolved ischaemic changes. |
A normal CT scan has an ASPECTS of 10 points. One point is subtracted for ischaemic changes in each region of the MCA territory. | |
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Lentiform nucleus level / Subcortical Structures | |
M1 Anterior MCA cortex (Frontal operculum) | -1 |
M2 MCA cortex lateral to the insular ribbon (Anterior temporal lobe) | -1 |
M3 Posterior MCA cortex (Posterior temporal lobe) | -1 |
Lentiform (L) | -1 |
Caudate nucleus (C) | -1 |
Internal capsule any part (IC) | -1 |
Insular ribbon/cortex (I) | -1 |
Centrum semiovale level | |
M4 (Anterior)superior to M1 | -1 |
M5 (Lateral)superior to M2 | -1 |
M6 (Posterior) superior to M3 | -1 |
Total ASPECTS Score. | ?/10 |
The ASPECTS score has some clinical correlation. A normal brain has a score of 10 and as more areas are affected the score falls. A full MCA territory infarct with CT changes would have a score of 0. A sharp increase independence and death occurs with an ASPECTS of 7 or less. A common misunderstanding of ASPECTS scoring is to assess only two standardised cuts, i.e. one ganglionic cut through the thalamus and one supraganglionic cut above this. Be sure to include the assessment of all axial cuts of the brain NCCT scan. The ASPECT score is not needed prior to thrombolysis but it does give an element of quantitative rigor to assessing the CT analysis and may be mentioned in any discussion with a stroke physician so useful to have heard of it. The aspects does not incorporate ACA and PCA territories but adjacent infarcts may well have clinical implications.
The ASPECTs scoring system has been utilised in many ways. It has been used to prognosticate for example the score is a strong predictor of functional outcome. It has also been used to direct therapies. The effectiveness of intra-arterial thrombolysis in patients with middle cerebral artery occlusion shows effect modification by the Alberta Stroke Program Early CT Score. Those with a low ASPECTS score suggesting large MCA infarction can be excluded from futile intra-arterial treatments which are unlikely to result in patient functional independence and increases the risk of haemorrhage.
Definitive distinctive changes may not occur until 6-8 hours. In the meantime, more subtle signs are seen. At about 6 hours and sometimes earlier there may be loss of grey-white matter differentiation - seen at the cortical surface due to localised changes such as cytotoxic oedema within the grey matter which has a higher metabolic requirement and so becomes oedematous quicker. These signs are subtle and can be missed by even the most experienced
Findings | Explanation |
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Hyperdense Artery or more distal MCA "dot sign" | This may be a sign of large vessel occlusion but does not replace a CTA if needed. The hyperdense vessel sign is most specific but has low sensitivity. Always look at it in context. Some arteries are simply calcified. It may support the diagnosis of large vessel infarct in the clinical context. It is not just seen with the MCA but can also be seen with PCA and basilar arteries. |
Loss of Grey white differentiation | This is a very important and early sign of ischaemic stroke. The outer cortical surface of the brain has a different appearance to the subcortical grey matter usually. When ischaemic one of the early signs is that this difference begins to be lost. It is often accompanied by oedema |
Loss of insular ribbon or Obscuration of the Sylvian fissure or Lentiform nucleus | Both signs suggest a sign similar to loss of grey-white differentiation with localised cytotoxic oedema. Vascular supply here is more vulnerable due to poor collateralisation and so this may show first. loss of the normal attenuation difference of the globus pallidus and/or putamen with respect to contiguous white matter structures |
Hypoattenuation | Hypoattenuation seen on CT is highly specific for irreversible ischaemic brain damage and infarction if it is detected within first 6 hours. It suggests that the patient may not benefit from reperfusion therapies. |
Wedge shaped infarcts | Clearly delineated wedge shaped hypodense region involving cortex and adjacent white matter related to the occluded artery anatomy and collaterals at 12 hours. Can suggest large artery disease. Often embolic. |
Lacunes | Small round infacts often in basal ganglia and pons. Usually < 1.5 cm in diameter. Seen with age, diabetes and HTN. |
Haemorrhagic transformation | Bleeding into brain parenchyma. Many large strokes show some of this in the first fortnight. May be some haemorrhagic transformation. Estimated incidence of haemorrhagic transformation is up to 40% in the subacute period even when not thrombolysed. |
Watershed infarcts | These occur between vascular territories often bilateral strokes between ACA and MCA territory and MCA and PCA may suggest carotid disease or a systemic drop in BP |
Fogging | Fogging - density of ischaemic tissue reaches same intensity as normal brain tissue and so evidence of infarction not seen |
Encephalomalacia | Late changes over weeks and months shows continue as the infarcted zone has density of CSF and there is loss of volume. |
Non contrast CT false negatives (there is a stroke) usually in infarcts when done early or in those who present 7-10 days after stroke and there is a visible hypodensity but no blood and so aetiology of perhaps a small bleed may be missed. In these cases a gradient echo will show haemosiderin deposition around the margins suggesting haemorrhage as he cause.
NCCT false positives are seen particular in older hypertensive patients where Lacunar infarcts are common and most often asymptomatic but appear on scans done for a myriad of reasons so unless there is corresponding new neurology do not diagnose acute stroke but do treat for "stroke disease".