Ischemic stroke results from a sudden cessation of adequate amounts of blood reaching parts of the brain. Ischemic strokes can be divided according to territory affected or mechanism.
Stroke is the second most common cause of morbidity worldwide (after myocardial infarction) and is the leading cause of acquired disability 2.
Risk factors for ischemic stroke largely mirror the risk factors for atherosclerosis and include age, gender, family history, smoking, hypertension, hypercholesterolemia, and diabetes mellitus.
An ischemic stroke typically presents with rapid onset neurological deficit, which is determined by the area of the brain that is involved. The symptoms often evolve over hours, and may worsen or improve, depending on the fate of the ischemic penumbra.
The vascular territory affected will determine exact symptoms and clinical behavior of the lesion:
- anterior circulation infarct
- posterior circulation infarct
Interruption of blood flow through an intracranial artery leads to deprivation of oxygen and glucose in the supplied vascular territory. This initiates a cascade of events at a cellular level which, if circulation is not re-established in time, will lead to cell death, mostly through liquefactive necrosis.
The mechanism of vessel obstruction is important in addressing therapeutic maneuvers to both attempt to reverse or minimize the effects and to prevent future infarcts.
- perforator thrombosis: lacunar infarct
- acute plaque rupture with overlying thrombosis
- arterial dissection
Global cerebral hypoxia (as is seen in drowning or asphyxiation) is, usually, considered separately.
In many institutions with active stroke services which provide reperfusion therapies a so-called code stroke aimed at expediting diagnosis and treatment of patients will include a non-contrast CT brain, CT perfusion and CT angiography.
Aging ischemic strokes can be important in a number of clinical and medicolegal settings. Both CT and MRI can help in determining when a stroke occurred as imaging features evolve in a reasonably predictable fashion. There is substantial heterogeneity in the terminology denoting time from onset. For the purposes of this article the following definitions are used 10:
- early hyperacute: 0 to 6 hours
- late hyperacute: 6 to 24 hours
- acute: 24 hours to 1 week
- subacute: 1 to 3 weeks
- chronic: more 3 weeks
Non-contrast CT of the brain remains the mainstay of imaging in the setting of an acute stroke. It is fast, inexpensive and readily available. Its main limitation, however, is the limited sensitivity in the acute setting. Detection depends on the territory, the experience of the interpreting radiologist and of course the time of the scan from the onset of symptoms. Whether tissue is supplied by end arteries (e.g. lenticulostriate arteries) or has collateral supply (much of the cerebral cortex) will influence how quickly cytotoxic edema develops 6. For example detection of MCA territory infarct has been shown to be approximately 60-70% in the first 6 hours 3, although changes in the deep grey matter nuclei (especially lentiform nucleus) can be visible within 1 hour of occlusion in up to 60% of patients 6.
The goals of CT in the acute setting are:
- exclude intracranial hemorrhage, which would preclude thrombolysis
- look for any "early" features of ischemia
- exclude other intracranial pathologies that may mimic a stroke, such as tumor
The earliest CT sign visible is a hyperdense segment of a vessel, representing direct visualization of the intravascular thrombus / embolus and as such is visible immediately 7. Although this can be seen in any vessel, it is most often observed in the middle cerebral artery (see hyperdense middle cerebral artery sign and middle cerebral artery dot sign). It may be of therapeutic and prognostic value to differentiate this hyperdense 'regular' thromboembolus from a calcified cerebral embolus.
Within the first few hours, a number of signs are visible depending on the site of occlusion and the presence of collateral flow. Early features include:
- loss of grey-white matter differentiation, and hypoattenuation of deep nuclei:
- lentiform nucleus changes seen as early as 1 hour after occlusion, visible in 75% of patients at 3 hours 6
- cortical hypodensity with associated parenchymal swelling with resultant gyral effacement
- cortex which has poor collateral supply (e.g. insular ribbon) is more vulnerable 6
With time the hypoattenuation and swelling become more marked resulting in a significant mass effect. This is a major cause of secondary damage in large infarcts.
As time goes on the swelling starts to subside and small amounts of cortical petechial hemorrhages (not to be confused with hemorrhagic transformation) result in elevation of the attenuation of the cortex. This is known as the CT fogging phenomenon 5. Imaging a stroke at this time can be misleading as the affected cortex will appear near normal.
Later still the residual swelling passes, and gliosis sets in eventually appearing as a region of low density with negative mass effect. Cortical mineralisation can also sometimes be seen appearing hyperdense.
CT perfusion has emerged as a critical tool in selecting patients for reperfusion therapy as well as increasing the accurate diagnosis of ischemic stroke among non-expert readers four-fold compared to routine non-contrast CT 9.
It allows both the core of the infarct (that part destined to never recover regardless of reperfusion) to be identified as well as the surrounding penumbra (the region which although ischemic has yet to go on to infarct and can be potentially salvaged). CT perfusion may also demonstrate early evidence of associated crossed cerebellar diaschisis.
The key to interpretation is understanding a number of perfusion parameters:
Areas which demonstrate matched defects in CBV and MTT represent the unsalvageable infarct core, whereas areas which have prolonged MTT but preserved CBV are considered to be the ischemic penumbra 9.
These factors will be discussed further separately. See CT perfusion.
- may identify thrombus within an intracranial vessel, and may guide intra-arterial thrombolysis or clot retrieval.
- evaluation of the carotid and vertebral arteries in the neck
- may be necessary prior to thrombolysis in pediatric stroke
- some guidelines only advise that children with an arterial thrombus benefit from thrombolysis
Multiphase or delayed CT angiography
Multiphase or delayed CT angiography is showing benefit either replacing CT perfusion or as an additional 4th step in the stroke CT protocol as it guides patient selection for endovascular therapy by assessing collateral blood flow in the ischemic and infarct tissue.
MRI is more time consuming and less available than CT but has significantly higher sensitivity and specificity in the diagnosis of acute ischemic infarction in the first few hours after onset.
Within minutes of arterial occlusion, diffusion weighted imaging demonstrates increased DWI signal and reduced ADC values 4,10. This correlates well with infarct core (for a detailed discussion of DWI and ADC in stroke see diffusion-weighted MRI in acute stroke). At this stage, the affected parenchyma appears normal on other sequences, although changes in flow will be detected (occlusion on MRA) and the thromboembolism may be detected (e.g. on SWI). Slow or stagnant flow in vessels may also be detected as a loss of normal flow void and high signal on T2/FLAIR and T1 C+ (intravascular enhancement).
If infarction is incomplete then cortical contrast enhancement may be seen as early as 2 to 4 hours 10.
Generally, after 6 hours, high T2 signal will be detected, initially more easily seen on FLAIR than conventional fast spin echo T2 10. This change continues to increase over the next day or two.
T1 hypointensity is only seen after 16 hours 10, and persists.
During the first week, the infarcted parenchyma continues to demonstrate high DWI signal and low ADC signal, although by the end of the first week ADC values have started to increase. The infarct remains hyperintense on T2 and FLAIR, with T2 signal progressively increasing during the first 4 days. T1 signal remains low, although some cortical intrinsic high T1 signal may be seen as early as 3 days after infarction 10. After day 5 the cortex usually demonstrates contrast enhancement on T1 C+ 10. Less common patterns of enhancement include arterial enhancement, encountered in approximately half of strokes and becomes evident after 3 days, and meningeal enhancement which is uncommon and is usually seen between 2 and 6 days 10.
Hemorrhage, most easily seen on susceptibility weighted imaging (SWI), is not a good indicator of age. Although most commonly seen after 12 hours and within the first few days, it may occur earlier or as late as 5 days 10.
ADC demonstrates pseudonormalization typically occurring between 10-15 days 10. As ADC values continue to rise, infarcted tissue progressively gets brighter than normal parenchyma. In contrast, DWI remains elevated due to persistent high T2/FLAIR signal (T2 shine through), unless hemorrhage (T2 blackout) or cystic encephalomalacia 10. T2 fogging is also encountered typically between 1 and 5 weeks, most commonly around week 2 10,11.
T1 weighted sequences continue to show hypointensity with cortical intrinsic high T1 signal due to cortical laminar necrosis or pseudolaminar necrosis 10. Cortical enhancement is usually present throughout the subacute period.
T1 signal remains low with intrinsic high T1 in the cortex if cortical necrosis is present 10. T2 signal is high. Cortical contrast enhancement usually persists for 2 to 4 months 10. Importantly if parenchymal enhancement persists for more than 12 week the presence of an underlying lesion should be considered 10.
ADC values are high, resulting in high signal. DWI signal is variable, but as time goes on signal progressively decreases.
Transcranial Doppler ultrasound
Often described as an emerging application of point-of-care ultrasonography, the use of transcranial Doppler (TCD) sonography has been utilized for the diagnosis of intracranial vessel occlusion, as well as the differentiation between ischemic and hemorrhagic stroke 14.
In the context of a CT negative for intracerebral hemorrhage and a clinically suspicious patient presentation, diagnostic criteria for occlusion of an insonated vessel are as follows 12;
- complete absence of color flow Doppler signals
- absence of pulsed wave Doppler signals
- concurrent adequate visualization of surrounding parenchyma and vessels
- color flow and pulsed wave Doppler signals must be demonstrated adequately in the remainder of circle of Willis 16
Sonographic monitoring of the complications of ischemic stroke is also possible, including the detection of;
- hemorrhagic transformation 16
- midline shift 15
- elevated intracranial pressure (ICP)
- measurement of the optic nerve sheath diameter (ONSD) in common use as an intracranial pressure surrogate
Treatment and prognosis
In the past treatment for ischemic stroke was supportive, and the earliest improvements in patient outcome were in dedicated stroke unit care and attempts at preventing the numerous complications which are encountered by patients with neurological impairment (e.g. aspiration pneumonia, pressure ulcers, etc.).
Neurosurgical intervention can also allow patients to survive the period of maximal swelling by performing decompressive craniectomies (with or without duroplasty).
More recently various reperfusion therapies have been developed including:
- intravenous or intra-arterial thrombolysis (e.g. streptokinase, rtPA)
- mechanical thrombectomy - response graded with TICI
Regardless of the therapy, early presentation and triage are essential if any outcome gains are to be had.
- 1. Robbins SL, Kumar V, Abbas AK et-al. Robbins and Cotran Pathologic Basis of Disease. W.B. Saunders Company. (2010) ISBN:1416031219. Read it at Google Books - Find it at Amazon
- 2. Tomandl BF, Klotz E, Handschu R et-al. Comprehensive imaging of ischemic stroke with multisection CT. Radiographics. 23 (3): 565-92. Radiographics (citation) - Pubmed citation
- 3. Lev MH, Farkas J, Gemmete JJ et-al. Acute stroke: improved nonenhanced CT detection--benefits of soft-copy interpretation by using variable window width and center level settings. Radiology. 1999;213 (1): 150-5. Radiology (citation) - Pubmed citation
- 4. Srinivasan A, Goyal M, Al azri F et-al. State-of-the-art imaging of acute stroke. Radiographics. 2006;26 Suppl 1 : S75-95. doi:10.1148/rg.26si065501 - Pubmed citation
- 5. Becker H, Desch H, Hacker H et-al. CT fogging effect with ischemic cerebral infarcts. Neuroradiology. 1979;18 (4): 185-92. - Pubmed citation
- 6. Nakano S, Iseda T, Kawano H et-al. Correlation of early CT signs in the deep middle cerebral artery territories with angiographically confirmed site of arterial occlusion. AJNR Am J Neuroradiol. 2001;22 (4): 654-9. AJNR Am J Neuroradiol (citation) - Pubmed citation
- 7. Pressman BD, Tourje EJ, Thompson JR. An early CT sign of ischemic infarction: increased density in a cerebral artery. AJR Am J Roentgenol. 1987;149 (3): 583-6. AJR Am J Roentgenol (citation) - Pubmed citation
- 8. Allmendinger AM, Tang ER, Lui YW et-al. Imaging of stroke: Part 1, Perfusion CT--overview of imaging technique, interpretation pearls, and common pitfalls. AJR Am J Roentgenol. 2012;198 (1): 52-62. doi:10.2214/AJR.10.7255 - Pubmed citation
- 9. Hopyan J, Ciarallo A, Dowlatshahi D et-al. Certainty of stroke diagnosis: incremental benefit with CT perfusion over noncontrast CT and CT angiography. Radiology. 2010;255 (1): 142-53. doi:10.1148/radiol.09091021 - Pubmed citation
- 10. Allen LM, Hasso AN, Handwerker J et-al. Sequence-specific MR Imaging Findings That Are Useful in Dating Ischemic Stroke. Radiographics. 2012;32 (5): 1285-97. doi:10.1148/rg.325115760 - Pubmed citation
- 11. O'Brien P, Sellar RJ, Wardlaw JM. Fogging on T2-weighted MR after acute : how often might this occur and what are the implications?. Neuroradiology. 46 (8): 635-41. doi:10.1007/s00234-004-1230-2 - Pubmed
- 12. Nedelmann M, Stolz E, Gerriets T, Baumgartner RW, Malferrari G, Seidel G, Kaps M. Consensus recommendations for transcranial color-coded duplex sonography for the assessment of intracranial arteries in clinical trials on acute stroke. (2009) Stroke. 40 (10): 3238-44. doi:10.1161/STROKEAHA.109.555169 - Pubmed
- 13. Kaps M, Damian MS, Teschendorf U, Dorndorf W. Transcranial Doppler ultrasound findings in middle cerebral artery occlusion. (1990) Stroke. 21 (4): 532-7. Pubmed
- 14. Mäurer M, Shambal S, Berg D, Woydt M, Hofmann E, Georgiadis D, Lindner A, Becker G. Differentiation between intracerebral hemorrhage and ischemic stroke by transcranial color-coded duplex-sonography. (1998) Stroke. 29 (12): 2563-7. Pubmed
- 15. Lau VI, Arntfield RT. Point-of-care transcranial Doppler by intensivists. (2017) Critical ultrasound journal. 9 (1): 21. doi:10.1186/s13089-017-0077-9 - Pubmed
- 16. Blanco P, Blaivas M. Applications of Transcranial Color-Coded Sonography in the Emergency Department. (2017) Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine. 36 (6): 1251-1266. doi:10.7863/ultra.16.04050 - Pubmed
Related Radiopaedia articles
Stroke and intracranial haemorrhage
stroke and intracranial hemorrhage
- general discussions
- scoring and classification systems
- Alberta stroke program early CT score (ASPECTS)
- Canadian Neurological Scale
- NIH Stroke Scale
- Mathew Stroke Scale
- modified Rankin scale
- Orgogozo Stroke Scale
- Scandinavian Stroke Scale
- thrombolysis in cerebral infarction (TICI)
- TOAST classification
- by region
- hemispheric infarcts
- frontal lobe infarct
- parietal lobe infarct
- temporal lobe infarct
- occipital lobe infarct
- internal capsule infarct
- ataxic hemiparesis syndrome: MCA perforators or basilar artery perforators
- lacunar infarct
- thalamic infarct
- striatocapsular infarct
- cerebellar infarct
- midbrain infarct
- pontine infarct
- Brissaud-Sicard syndrome
- facial colliculus syndrome
- Gasperini syndrome: basilar artery or AICA
- inferior medial pontine syndrome (Foville syndrome): basilar artery
- lateral pontine syndrome (Marie-Foix syndrome): basilar artery or AICA
- locked-in syndrome: basilar artery
- Millard-Gubler syndrome: basilar artery
- Raymond syndrome: basilar artery
- medullary infarct
- acute spinal cord ischemia syndrome
- hemispheric infarcts
- by vascular territory
- anterior cerebral artery infarct
- anterior choroidal artery infarct
- anterior inferior cerebellar artery infarct
- basilar artery infarct
- middle cerebral artery infarct
- posterior cerebral artery infarct
- posterior inferior cerebellar artery infarct
- superior cerebellar artery infarct
- treatment options
- by region or type
- basal ganglia hemorrhage
- cerebellar hemorrhage
- cerebral contusions
- cerebral microhemorrhage
- hemorrhagic venous infarct
- hemorrhagic transformation of an ischemic infarct
- hypertensive intracranial hemorrhage
- intraventricular hemorrhage (IVH)
- lobar hemorrhage
- pontine hemorrhage
- jet hematoma
- extra-axial hemorrhage
- extradural versus subdural hemorrhage
- extradural hemorrhage (EDH)
- intralaminar dural hemorrhage
- subdural hemorrhage (SDH)
subarachnoid hemorrhage (SAH)
- vasospasm following SAH
- grading systems
- intra-axial hemorrhage
- ischemic stroke