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CT Imaging for Stroke

Learning objectives

  • Role of CT Imaging in stroke
  • Limitations
  • Basic Interpretation

    Introduction

    Until the advent of cross sectional imaging the management of strokes was fraught with difficulties. The only way to correlate clinical signs and causality was with post mortem studies. The idea of looking after patients stroke with no access to any form of imaging seems slightly horrifying nowadays. Imaging has changed everything and access to the CT scanner has been transformational. The later addition of MRI and the new sequences that are being developed has also helped but still there is often uncertainty and new dilemmas are introduced.

    Basics of CT Imaging

    The first CT scanner was developed in 1972 by Sir Godfrey Hounsfield. It wasn't until the mid to late 80's that CT was available initially in teaching hospitals for assessing stroke patients. Prior to this there was no way to discern ischaemic and haemorrhagic strokes ante-mortem. The CT scanner consists of an X-ray tube and on the opposite side of the cylinder where the patient lies is a set of x-ray detectors. Through a process of data acquisition the X-ray tube and detectors rotate around the patient and acquires a vast amount of imaging information which then undergoes image reconstruction. Between the x-ray tube and the detectors there is a loss of attenuation as it travels through structures and this is known as the attenuation coefficient which reflects the degree to which the x-ray intensity is reduced by the material. These values are scaled to give values known as Hounsfield units seen in the table below. The overall appearance can be altered by varying Window level and window width. Different windows can be used to look at different structures as shown below. Helical scans mean that there is continuous movement of the patient through the gantry whilst imaging.

    Different Hounsfield units

    MediumHounsfield UnitsAppearance
    Air-1000Black
    Fat-80 to -100Black
    Water0Black
    CSF +5Black
    White matter +30Dark Grey
    Grey matter +40Light Grey
    Acute haemorrhage +70White
    Bone+400 to +3000Bright White

    CT is really 4000 shades of grey from -1000 for air to +3000 for bone

    Different Windows W=Width L=Length

    IndicationParameters
    Brain window to best show white/grey matter differentiationW=80 L=40
    Bone windows for bone pathologyW=3500 L=700
    Subdural windows for small or isodense subdurals W=250 L=70

    The modern CT scanner now takes 10 seconds to acquire 20-35 axial images from vertex to skull base. 20 years ago it took 10 minutes. Most CT time now is spent getting the patient on and off the table. Many of us push our own patients to CT in the desire to get door to needle times of less than 20 minutes and radiographers do appreciate a team that facilitates this process.

    Clinically there are no real contraindications for CT if clinically indicated to potentially alter management. The only real difficulty is with agitated or confused patients in whom scan quality will be degraded with movement artefact. It may be occasionally necessary to intubated and ventilate a patient prior to scanning. The main downside is radiation exposure to about 2 mSV of exposure which is about 8 months of background radiation exposure. In pregnancy the fetus can be shielded.

    Non contrast CT scan in Ischaemic stroke

    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. There is evidence that early CT can help reduce cost as diagnoses are made earlier and patients can be placed on the correct clinical pathways. 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.

    Indications for CT scanning

    Clinical Indications for urgent CT i.e. within 1 hour of arrival at hospital
    Anticoagulant treatment, a known bleeding tendency
    Depressed level of consciousness
    Unexplained progressive or fluctuating Symptoms
    Papilloedema
    Neck stiffness or fever
    Severe headache at onset

    Limitations of CT: What may be missed on a CT scan

    Caution : What may be missed on a CT scan
    Early infarcts
    Isodense Subdural haematoma
    >Brainstem or Posterior fossa pathology though more recent scanners are much improved
    Low attenuation lesions near skull missed 'beam hardening'
    Suspected Haemorrhage over 2 weeks ago (get GRE MRI)
    Multiple sclerosis plaques

    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.

    Anatomical Planes

    When discussing imaging ensure you understand or revise the terms axial, sagittal and coronal.

    Axial/Horizontal is simple horizontal slices from above down. It is the commonest way that we look at imaging from above down in horizontal slices.

    Sagittal is in the same plane as dividing the brain into left and right. The falx cerebri that separates the brain hemispheres lies into right and left hemispheres is in the mid-sagittal sometimes called parasagittal plane.

    Coronal is the plane that splits things into anterior and posterior or dorsal and ventral. It shows images from front to back.

    It is vital to have a good inner representation of the cerebral vessels as the 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 "V" shaped midbrain on axial imaging and then look in front for the basilar artery and the other vessels. This is a good place to start looking for the hyperdense MCA as the MCA leaves the COW laterally within the Sylvian fissure.

    CT Interpretation

    Definitive distinctive changes may not occur until 6-8 hrs. 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

    • Cortical Sulcal effacement - suggests some increased oedema
    • Loss of Grey/White differentiation in the basal ganglia
    • Loss of insular ribbon sign is 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.
    • Obscuration of the sylvian fissure: Similar to insular ribbon sign
    • Hypoattenuation seen on CT is highly specific for irreversible ischaemic brain damage and infarction if it is detected within first 6 hours.
    • Hyperdense MCA sign or more distal MCA "dot sign" it may be normal is a sign of clot (thrombotic or embolic) (not a contraindication to lysis) but shows extent of possible infarct which depends also on collateral flow.

      Dense MCA artery sign

    • Obscuration of the lentiform nucleus (loss of the normal attenuation difference of the globus pallidus and/or putamen with respect to contiguous white matter structures
    • Watershed infarcts between vascular territories often bilateral strokes between ACA and MCA territory and MCA and PCA
    • Clearly delineated wedge shaped hypodense region involving cortex and adjacent white matter related to the occluded artery anatomy and collaterals at 12 hours.
    • May be some haemorrhagic transformation. Estimated incidence of haemorrhagic transformation is up to 40% in the subacute period even when not thrombolysed. Lacunar infarcts may be seen deep within white matter and within the basal ganglia.
    • Occasionally due to collateralisation or perhaps reperfusion of the MCA the cortex remains unaffected but subcortical areas infarct and become hypodense and this is seen with a striato-capsular type of stroke.
    • Late changes over days and weeks is most marked Hypodensity due to cytotoxic oedema initially and Vasogenic oedema secondarily and best seen days 3-10.
    • Left MCA Infarct

    • Fogging - density of ischaemic tissue reaches same intensity as normal brain tissue and so evidence of infarction not seen
    • Late changes over weeks and months shows continue as the infarcted zone has density of CSF and there is loss of volume. A hypodense caudate suggests MCA occlusion proximally taking out lenticulostriate arteries. Depends on leptomeningeal anastomoses of ACA and PCA

    NCCT 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".

    CT of Left Posterior cerebral artery infarct

    Different types of Infarcts and possible causes

  • Large vessel: These may be embolic or thrombotic with large vessel occlusions which show a wedge shaped area of infarction from the arterial occlusion out to the cortex. Most commonly seen with MCA occlusions.
  • Small Vessel/Lacunar: Small vessel occlusion causing lacunar type infarcts in the basal ganglia, pons, cerebellum. Occlusion of lenticulostriate arteries or pontine perforators of the basilar artery. Usually less than 1.5 cm in diameter and rounded.
  • Striatocapsular: Usually seen in the subcortical MCA territory and resembles a large MCA infarct only that the overlying cortex is preserved. The underlyign process is unclear and it may be that collateral supply to the cortex is sufficient to prevent infarction. It is sometimes seen post thrombolysis and may suggest timely reperfusion or it may suggest occlusive thrombus on M1/M2 blocking perforating branches but with some MCA flow.
  • Watershed: the borders between arterial supplies require both arteries to maintain sufficient perfusion. If one is lost then an infarct usually linear occurs at this area. Can be seen at the border between ACA and MCA and MCA and PCA. The other borders are between small and large vessels within the corona radiata. The cause is low flow at a distance which may be an ipsilateral carotid or even a cardiac or other event causing hypotension to an area already being starved of sufficient perfusion.

    CT Angiography (CTA)

    Can be performed by giving a single IV bolus of contrast through good IV access. Helical CT scan can capture and follow contrast as it enters the brain thus imaging the great vessels. Scan acquisition is done such that vessels are imaged at the point of peak opacification. Can give good imaging of circle of willis and branches as well as extra cranial vessels. Three dimensional imaging can be reconstructed. Can be useful in determining diagnoses e.g. conforming a basilar artery stroke or in planning further intravascular procedures depending on whether clot is seen occluding major vessels. Post acquisition software analysis can reconstruct very useful 3D images of the vascular structure without other soft tissues known as a Maximum intensity projection. In terms of ability to detect aneurysms it is 94-98% sensitive the only difficulty being in aneurysm less than 3 mm in diameter where the pick up rate is about 70%. CTA may be undertaken in acute stroke to identify the ongoing presence of thrombus when there is consideration for either intra-arterial thrombolysis or mechanical management of the thrombus. CTA is also useful when looking for arterial evidence of arterial dissection or pseudoaneurysm formation. CTA can also identify the presence of vasospasm. However in almost all cases it is second best to CT angiography and there has to be a clinical assessment of risks and benefits. In many cases CTA is sufficient.

    CT Perfusion

    The brain volume can be mapped during perfusion in a CT slice following an injection of IV contrast. The first pass is measured as the contrast perfuses the brain and can be done along with CTA. Modern scanners can take 10 and more images per second. Multislice scanners allows different slices to be taken simultaneously. A time density curve for each pixel can be generated.

    Can calculate relative cerebral blood volume CBV (CBV) and the mean transit time (MTT) which can be displayed in a colour map. Cerebral blood flow can be calculated from CBF=CBV/MTT.

    The volume of blood per unit of brain 4-5 ml/100 g, Flow to grey matter is 50-60 ml/100 g/min. Transit time is from arterial inflow to venous outflow can be measured as can Time to peak enhancement - beginning of contrast injection to the maximum contrast in the area under study. CT Perfusion shows the volume of viable brain at risk due to reduced flow. This can help to demonstrate the penumbra.

    CT perfusion has been explored as useful tool in acute large vessel occlusive stroke disease and it may be used alongside MRI DWI to assess extent of stroke and possibly to direct therapies. It is still very much a research tool and not commonly used outside the teaching hospital. Its place in the hyperacute stroke protocol remains unclear.

    CT in Haemorrhagic Stroke

    Blood stands out well on a NCCT as 'hyperdense' as it absorbs and attenuates x-rays well compared with water and CSF and normal brain tissue. Within 24 hours of a haemorrhagic stroke the sensitivity is about 99% which then falls off as blood is reabsorbed and changes it characteristics. After 1-2 weeks it is quiet possible that there is no sign of blood but only an area of apparent reduced attenuation. AT this stage the only way to have any evidence of haemorrhage is to use MRI Gradient Echo which will be discussed later.

    Haemorrhage is almost always unilateral and asymmetrical. Several 'bright' structures may be seen on a CT scan including basal ganglia calcification and choroid plexus calcification. Bright lesions may be seen to be the tip of bony skull prominences by ascending and descending skull slices. Intraparenchymal blood should be easy to see and describe. Once spotted then the next things to look for are signs of midline shift. Changes in the midline and obvious bulging of pressure into ventricles can be significant. If there is bleeding into ventricles then hydrocephalus can happen so simple signs such as enlargement of the IIIrd ventricle all become important. Always make sure that the circumference of the brain is looked at - there can easily be a small subdural present and if chronic it becomes hypodense and the blood loses its brightness and it gradually has the consistency of brain and then CSF. Look for asymmetry and pressure effects.

    Subarachnoid haemorrhage is quite simple to spot - there is hazy blood through the folds on the surface of the brain and this also extends along the natural folds including the sylvian fissure and the interhemispheric fissure and in the prepontine spaces in front of the brainstem where free subarachnoid blood can gravitate as the patient is lying supine in the scanner. If the cause is a ruptured berry aneurysm then the site of most blood collection may give clue to the artery involved. Again look for developing hydrocephalus and if there is a haematoma then for pressure effects.

    Cerebral Digital Subtraction angiography (DSA)

    This is the gold standard test for studying cerebral vasculature. It is used mainly in tertiary centres to get the best possible image of cerebral vasculature. A catheter is inserted at the femoral artery and threaded up iliac and descending aorta to the aortic arch. From here it may be threaded up from the vertebral artery to the circle of Willis and either subclavian or carotids systems cannulated depending in the vasculature to be examined. Radio-opaque iodinated contrast is injected and X-rays are taken to show the passage of the contrast. It is useful post haemorrhage in diagnosing small aneurysms, arteriovenous malformations and vasculitis where it may show occlusion or narrowing or beading. There is a small approximately 1% risk of stroke. Other than that there is a small risk of vascular injury at insertion site, haemorrhage and infection. Care must be taken with contrast in those with renal impairment.


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