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Imaging in stroke and vascular disease—part 1: ischaemic stroke Shelley Renowden A separate version of this paper which includes much more detail is available on the Practical Neurology website. To see this paper please visit the journal online (http://dx.doi.org/ 10.1136/practneurol-2013000802) Correspondence to Dr Shelley Renowden, Department of Neuroradiology, Frenchay Hospital, Bristol, UK; [email protected]
INTRODUCTION Stroke is the third leading cause of death in Europe, the USA, Canada and Japan, and is the primary cause of adult disability in these countries. Over 80% are ischaemic (cardiogenic, atherosclerotic, lacunar, haemodynamic and cryptogenic). The remainder are haemorrhagic (largely parenchymal and subarachnoid) and are considered in a separate article. Some
pathologies may cause infarction and haemorrhage, for example, hypertensive vascular disease, moyamoya, vasculitis, reversible vasoconstriction syndrome, arterial dissection and venous occlusive disease. Cranial CT is the most useful initial imaging modality to differentiate between ischaemia and haemorrhage, and to exclude stroke mimics.
Published Online First 5 February 2014
▸ http://dx.doi.org/10.1136/ practneurol-2013-000802
Figure 1 Axial non-contrasted CT head scans (A–E) and a coronal CT angiogram reconstruction (F) in a 60-year-old man with a hyperacute ischaemic stroke. Note dense thrombus in the left terminal internal carotid and middle cerebral artery (MCA) and an MCA branch in the Sylvian fissure. The hyperdense MCA is 100% specific, but only 5–50% sensitive for the diagnosis of MCA occlusion. There is loss of insular definition, obscuration of the lentiform nucleus and ill-defined low density in the left peri-Sylvian cortex reflecting early ischaemic change. CT angiogram confirms occlusion of the left terminal internal carotid artery, M1 and M2 branches with some distal MCA filling from collaterals (F).
To cite: Renowden S. Pract Neurol 2014;14:77–87.
Renowden S. Pract Neurol 2014;14:77–87. doi:10.1136/practneurol-2013-000801
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Figure 2 Hyperdense basilar artery sign: Axial non-contrasted CT head scans (A–D) in a 66-year-old man who had experienced an episode of dizziness and a few hours later became unconscious. Note the dense thrombus within the occluded basilar artery, compared with non-contrasted CT obtained 2 weeks before (E and F). The hyperdense basilar artery sign is 71% sensitive and 98% specific for basilar artery thrombosis. CT detects fewer infarctions in the posterior fossa because of beam-hardening artefact induced by the dense bony petrous ridges. Additionally, many brainstem infarctions are small, despite causing significant neurological deficit (see figure 15).
Figure 3 Axial non-contrasted CT scans: 65-year-old woman with sudden onset left-sided weakness and left homonymous hemianopia showing dense thrombus in the right posterior cerebral artery (A, arrow). Compare (A) with (B, 36 h later). The parenchyma appeared normal at this stage. There is subtle ischaemic change at 36 h (C and D) with low density in the cortex of the right occipital lobe and right anterior thalamus. The established infarct is clear at 5 days as a distinct, well-demarcated cortical low density in the occipital lobe (E).
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Figure 4 Axial cranial non-contrasted CT scans in an 81-year-old man, with hyperacute ischaemic stroke, 1.5 h post-ictus, National Institutes of Health Stroke Scale (NIHSS) 26, in atrial fibrillation, and with type 2 diabetes mellitus. There is dense thrombus in the terminal left internal carotid artery, low density in the insula, obscuration of the lentiform nucleus, ill-defined low density involving the cortex of more than one-third of the middle cerebral artery territory, and left cerebral hemisphere swelling with sulcal effacement. These imaging findings of extensive early ischaemic change with swelling would contraindicate lytic therapy or thrombus extraction because of the risk of haemorrhagic transformation and greater risk of iatrogenic damage.
Figure 5 Axial non-contrasted CT scans show a large right middle cerebral artery infarction, 2 days after intravenous thrombolysis, complicated by haemorrhagic transformation. There is mass effect with sulcal effacement, effacement of the Sylvian fissure and ventricular compression. Haemorrhagic transformation may follow reperfusion of severely ischaemic brain, often with embolic occlusions.
Renowden S. Pract Neurol 2014;14:77–87. doi:10.1136/practneurol-2013-000801
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Figure 6 Axial cranial CT scans: A 60-year-old man with a hyperacute ischaemic stroke (2 h post-ictus) with dense thrombus in his right M1 (A). There is subtle cortical low-density early ischaemic change involving more than one-third of the middle cerebral artery (MCA) territory (B). He was treated with intravenous thrombolysis but without benefit (only 20–30% of M1 occlusions respond and achieve a good outcome) and a scan 3 days later confirms established infarction of the right MCA territory (C). The infarct is now easily seen—more hypodense and more defined with sharp margins and mild mass effect (the Sylvian fissure is effaced). Mass effect is usually most marked between days 3 and 5, and rarely is considerable, but on occasion can be associated with subfalcine herniation (see figure 7) and uncal herniation. Brain swelling begins to decrease after the first week and usually resolves by 12–21 days.
Figure 7 Axial non-contrasted CT in a 65-year-old man with left cervical internal carotid artery occlusion and a right hemiparesis. Initial scans (A–C) show hyperdensity in the left middle cerebral artery. The parenchyma is normal. Scans 24 h later (D–F) show the defined infarction with mild swelling and scans a further 24 h (G–I) later demonstrate massive infarct swelling with uncal herniation, risking secondary infarction in the posterior cerebral artery territory; subfalcine herniation has resulted in anterior cerebral artery infarction. Decompressive craniectomy may help to avoid the effects of massive brain swelling (G–I) and secondary infarctions, but is controversial except in cerebellar hemisphere infarction.
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Figure 8 Hyperacute ischaemic stroke, 2 h post-ictus, National Institutes of Health Stroke Scale (NIHSS) 21, axial non-contrasted CT scans (A and B) show dense thrombus in the left middle cerebral artery and terminal internal carotid artery (A), loss of grey-white definition in basal ganglia with obscuration of the lentiform nucleus and loss of the insula. Coronal CT angiogram reconstructions (C and D) confirm occlusion of the terminal internal carotid artery and M1 on the left, with distal branches filling via collaterals, but also a critical stenosis involving the left carotid bulb and cervical internal carotid artery origin (D, arrow). This tight stenosis required angioplasty after clot extraction from the intracranial terminal internal carotid artery and M1. It is extremely unlikely that he would have responded well to intravenous thrombolysis.
Figure 9 A 68-year-old man with pins and needles in his left arm who has a tight short-segment stenosis involving the right M1 (A, frontal oblique right carotid angiogram, arrow). FLAIR coronal MRI (B and C) confirm a small right temporal cortical infarction (B) and hyperintense signal in the middle cerebral artery branches distal to the stenosis (C, arrow).
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Figure 10 Axial T2W MR (A–D) and a coronal FLAIR MRI (E) in a 30-year-old woman with sudden onset mild left hemiparesis and dysarthria, 10 h post-ictus. There is cortical T2 hyperintensity, due to embolic infarction, in the right insular cortex and inferior frontal gyrus. Note the absence of flow void from the right internal carotid artery, indicating occlusion (A, B and E arrows). Compare with the cranial CT scans performed earlier ( J–N). The MR axial apparent diffusion coefficient maps (F and G) and diffusion image (H) confirm the decreased diffusion in the acute infarction. Diffusion remains decreased for approximately 5–7 days post-ictus. Contrast-enhanced middle cerebral artery, coronal reconstruction (I) confirms occlusion of the right cervical internal carotid artery, probably due to dissection, with reconstitution of intracranial flow via the anterior communicating artery. Note extensive recanalisation several months later on the CT angiographic reconstructions (O and P).
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Figure 10 Continued.
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Figure 11 Axial apparent diffusion coefficient MRI (A) in a patient with a transient right hemiparesis demonstrates an area of decreased diffusion in the deep white matter adjacent to the left lateral ventricle. Contrast-enhanced MR angiogram (coronal, B) and localised oblique sagittal reconstruction of the left internal carotid artery bifurcation (C) demonstrates that the source of the embolus was almost certainly a severe, critically stenosed ulcerated plaque involving the carotid bulb (C arrow).
Figure 12 CT angiogram reconstructions (A, oblique coronal, B, sagittal, C, oblique sagittal) including the aortic arch, cervical and intracranial arteries in a 65-year-old man who has suffered a left hemisphere transient ischaemic attack. Note the critical irregular stenosis of the left carotid bulb and internal carotid artery origin.
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Figure 13 CT angiogram reconstructions (A, oblique sagittal; B, oblique coronal) of the left common carotid artery in a patient with left carotid artery territory transient ischaemic attacks showing tandem lesions. There is a densely calcified plaque creating a critical stenosis at the origin of the left internal carotid artery, and a second severe stenosis at the origin of the left common carotid artery (arrow). This second important lesion would not have been detected by Doppler ultrasound scanning. Such dense irregular plaque calcification at the internal carotid artery bifurcation can make it difficult to measure the precise luminal dimension.
Figure 14 T2W (A) and T1W (B) axial MRIs at the level of the foramen magnum demonstrate the typical findings of a left internal carotid artery dissection with hyperintense haematoma in the arterial wall (arrows). The patient presented with left-sided neck pain and a Horner’s syndrome. Contrast-enhanced MR angiogram (C) confirmed the full extent of the dissection, internal carotid artery narrowing, commencing just above the carotid bulb and finishing at the skull base. The bony confines of the carotid canal usually prevents the vessel wall haematoma from progressing intracranially.
Figure 15 Axial T2W MRIs (A–C) in a patient presenting with right-sided neck pain, dysarthria and swallowing difficulties, demonstrate a small right lateral medullary infarction and a small right-sided cerebellar infarction due to right vertebral artery dissection. Note the stenosis (arrows) at C1/2, the commonest site for a vertebral artery dissection on the contrast-enhanced MR angiogram images (D and E).
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Figure 16 Coronal (A) and sagittal (B) CT angiogram reconstructions in a 77-year-old woman presenting with subarachnoid haemorrhage secondary to rupture of a 3 mm basilar top aneurysm (C arrow). The CT angiogram shows typical features of medial fibromuscular dysplasia affecting the cervical internal carotid artery bilaterally (no internal carotid artery digital subtraction angiogram performed). Note the typical ruffled string of beads, or baggy stockings appearance so characteristic of this condition—areas of concentric narrowing and outpouchings. The vertebral artery digital subtraction angiogram ( performed at the time of aneurysm coiling) lateral projection also confirms involvement of the distal cervical left vertebral artery.
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Figure 17 T2W axial MRIs (A–D) in a 22-year-old man presenting with transient left-sided weakness. Note the ischaemic deep white matter changes in a watershed distribution, more extensive on the right. Wallerian degeneration is present in the right cerebral peduncle. Note the diminished abnormal flow voids of the terminal internal carotid artery’s, and proximal anterior and middle cerebral arteries. Digital subtraction angiogram (lateral projections of a right internal carotid artery angiogram, E and F) confirms distal internal carotid artery, proximal anterior and middle cerebral artery narrowing and hypertrophy of the lenticulostriates (the ‘puff of smoke’ typical of moyamoya). Note also the collateral circulation from the posterior cerebral artery supplying distal anterior and middle cerebral artery territory. These changes were similar on the left (not shown).
Extra reading Leiva-Salinas C, Wintermark M. Imaging of acute ischemic stroke. Neuroimaging Clin N Am 2010;20:455–68.
Competing interests None. Provenance and peer review Commissioned; externally peer reviewed. This paper was reviewed by Joanna Wardlaw, Edinburgh, UK.
De Lucas EM, Sanchez E, Gutierrez A, et al. CT protocol for acute stroke: tips and tricks for general radiologists. Radiographics 2008;28:1673–87. Barber PA, Demchuk AM, Zhang J, et al. Validity and reliability of a quantitative computed tomography score in predicting outcome of hyperacute stroke before thrombolytic therapy. ASPECTS Study Group. Alberta Stroke Programme Early CT Score. Lancet 2000;355:1670. Pavlovic AM, Barras CD, Hand PJ, et al. Brain Imaging in transient ischaemic attack- redefining TIA. J Clin Neurosci 2010;17:1105–10. Rodallec MH, Marteau V, Gerber S, et al. Craniocervical arterial dissection: spectrum of imaging findings and differential diagnosis. Radiographics 2008;28:1711–28. Touze E, Oppenheim C, Trystram D, et al. Fibromuscular dysplasia of cervical and intracranial arteries. Int J Stroke 2010;5:296–305. Renowden S. Pract Neurol 2014;14:77–87. doi:10.1136/practneurol-2013-000801
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Imaging in stroke and vascular disease—part 1: ischaemic stroke Shelley Renowden A separate version of this paper which includes much more detail is available on the Practical Neurology website. To see this paper please visit the journal online (http://dx.doi.org/ 10.1136/practneurol-2013000802) Correspondence to Dr Shelley Renowden, Department of Neuroradiology, Frenchay Hospital, Bristol, UK; [email protected]
INTRODUCTION Stroke is the third leading cause of death in Europe, the USA, Canada and Japan, and is the primary cause of adult disability in these countries. Over 80% are ischaemic (cardiogenic, atherosclerotic, lacunar, haemodynamic and cryptogenic). The remainder are haemorrhagic (largely parenchymal and subarachnoid) and are considered in a separate article. Some
pathologies may cause infarction and haemorrhage, for example, hypertensive vascular disease, moyamoya, vasculitis, reversible vasoconstriction syndrome, arterial dissection and venous occlusive disease. Cranial CT is the most useful initial imaging modality to differentiate between ischaemia and haemorrhage, and to exclude stroke mimics.
Published Online First 5 February 2014
▸ http://dx.doi.org/10.1136/ practneurol-2013-000802
Figure 1 Axial non-contrasted CT head scans (A–E) and a coronal CT angiogram reconstruction (F) in a 60-year-old man with a hyperacute ischaemic stroke. Note dense thrombus in the left terminal internal carotid and middle cerebral artery (MCA) and an MCA branch in the Sylvian fissure. The hyperdense MCA is 100% specific, but only 5–50% sensitive for the diagnosis of MCA occlusion. There is loss of insular definition, obscuration of the lentiform nucleus and ill-defined low density in the left peri-Sylvian cortex reflecting early ischaemic change. CT angiogram confirms occlusion of the left terminal internal carotid artery, M1 and M2 branches with some distal MCA filling from collaterals (F).
To cite: Renowden S. Pract Neurol 2014;14:77–87.
Renowden S. Pract Neurol 2014;14:77–87. doi:10.1136/practneurol-2013-000801
77
REVIEW
Figure 2 Hyperdense basilar artery sign: Axial non-contrasted CT head scans (A–D) in a 66-year-old man who had experienced an episode of dizziness and a few hours later became unconscious. Note the dense thrombus within the occluded basilar artery, compared with non-contrasted CT obtained 2 weeks before (E and F). The hyperdense basilar artery sign is 71% sensitive and 98% specific for basilar artery thrombosis. CT detects fewer infarctions in the posterior fossa because of beam-hardening artefact induced by the dense bony petrous ridges. Additionally, many brainstem infarctions are small, despite causing significant neurological deficit (see figure 15).
Figure 3 Axial non-contrasted CT scans: 65-year-old woman with sudden onset left-sided weakness and left homonymous hemianopia showing dense thrombus in the right posterior cerebral artery (A, arrow). Compare (A) with (B, 36 h later). The parenchyma appeared normal at this stage. There is subtle ischaemic change at 36 h (C and D) with low density in the cortex of the right occipital lobe and right anterior thalamus. The established infarct is clear at 5 days as a distinct, well-demarcated cortical low density in the occipital lobe (E).
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Figure 4 Axial cranial non-contrasted CT scans in an 81-year-old man, with hyperacute ischaemic stroke, 1.5 h post-ictus, National Institutes of Health Stroke Scale (NIHSS) 26, in atrial fibrillation, and with type 2 diabetes mellitus. There is dense thrombus in the terminal left internal carotid artery, low density in the insula, obscuration of the lentiform nucleus, ill-defined low density involving the cortex of more than one-third of the middle cerebral artery territory, and left cerebral hemisphere swelling with sulcal effacement. These imaging findings of extensive early ischaemic change with swelling would contraindicate lytic therapy or thrombus extraction because of the risk of haemorrhagic transformation and greater risk of iatrogenic damage.
Figure 5 Axial non-contrasted CT scans show a large right middle cerebral artery infarction, 2 days after intravenous thrombolysis, complicated by haemorrhagic transformation. There is mass effect with sulcal effacement, effacement of the Sylvian fissure and ventricular compression. Haemorrhagic transformation may follow reperfusion of severely ischaemic brain, often with embolic occlusions.
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Figure 6 Axial cranial CT scans: A 60-year-old man with a hyperacute ischaemic stroke (2 h post-ictus) with dense thrombus in his right M1 (A). There is subtle cortical low-density early ischaemic change involving more than one-third of the middle cerebral artery (MCA) territory (B). He was treated with intravenous thrombolysis but without benefit (only 20–30% of M1 occlusions respond and achieve a good outcome) and a scan 3 days later confirms established infarction of the right MCA territory (C). The infarct is now easily seen—more hypodense and more defined with sharp margins and mild mass effect (the Sylvian fissure is effaced). Mass effect is usually most marked between days 3 and 5, and rarely is considerable, but on occasion can be associated with subfalcine herniation (see figure 7) and uncal herniation. Brain swelling begins to decrease after the first week and usually resolves by 12–21 days.
Figure 7 Axial non-contrasted CT in a 65-year-old man with left cervical internal carotid artery occlusion and a right hemiparesis. Initial scans (A–C) show hyperdensity in the left middle cerebral artery. The parenchyma is normal. Scans 24 h later (D–F) show the defined infarction with mild swelling and scans a further 24 h (G–I) later demonstrate massive infarct swelling with uncal herniation, risking secondary infarction in the posterior cerebral artery territory; subfalcine herniation has resulted in anterior cerebral artery infarction. Decompressive craniectomy may help to avoid the effects of massive brain swelling (G–I) and secondary infarctions, but is controversial except in cerebellar hemisphere infarction.
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Figure 8 Hyperacute ischaemic stroke, 2 h post-ictus, National Institutes of Health Stroke Scale (NIHSS) 21, axial non-contrasted CT scans (A and B) show dense thrombus in the left middle cerebral artery and terminal internal carotid artery (A), loss of grey-white definition in basal ganglia with obscuration of the lentiform nucleus and loss of the insula. Coronal CT angiogram reconstructions (C and D) confirm occlusion of the terminal internal carotid artery and M1 on the left, with distal branches filling via collaterals, but also a critical stenosis involving the left carotid bulb and cervical internal carotid artery origin (D, arrow). This tight stenosis required angioplasty after clot extraction from the intracranial terminal internal carotid artery and M1. It is extremely unlikely that he would have responded well to intravenous thrombolysis.
Figure 9 A 68-year-old man with pins and needles in his left arm who has a tight short-segment stenosis involving the right M1 (A, frontal oblique right carotid angiogram, arrow). FLAIR coronal MRI (B and C) confirm a small right temporal cortical infarction (B) and hyperintense signal in the middle cerebral artery branches distal to the stenosis (C, arrow).
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Figure 10 Axial T2W MR (A–D) and a coronal FLAIR MRI (E) in a 30-year-old woman with sudden onset mild left hemiparesis and dysarthria, 10 h post-ictus. There is cortical T2 hyperintensity, due to embolic infarction, in the right insular cortex and inferior frontal gyrus. Note the absence of flow void from the right internal carotid artery, indicating occlusion (A, B and E arrows). Compare with the cranial CT scans performed earlier ( J–N). The MR axial apparent diffusion coefficient maps (F and G) and diffusion image (H) confirm the decreased diffusion in the acute infarction. Diffusion remains decreased for approximately 5–7 days post-ictus. Contrast-enhanced middle cerebral artery, coronal reconstruction (I) confirms occlusion of the right cervical internal carotid artery, probably due to dissection, with reconstitution of intracranial flow via the anterior communicating artery. Note extensive recanalisation several months later on the CT angiographic reconstructions (O and P).
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Figure 10 Continued.
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Figure 11 Axial apparent diffusion coefficient MRI (A) in a patient with a transient right hemiparesis demonstrates an area of decreased diffusion in the deep white matter adjacent to the left lateral ventricle. Contrast-enhanced MR angiogram (coronal, B) and localised oblique sagittal reconstruction of the left internal carotid artery bifurcation (C) demonstrates that the source of the embolus was almost certainly a severe, critically stenosed ulcerated plaque involving the carotid bulb (C arrow).
Figure 12 CT angiogram reconstructions (A, oblique coronal, B, sagittal, C, oblique sagittal) including the aortic arch, cervical and intracranial arteries in a 65-year-old man who has suffered a left hemisphere transient ischaemic attack. Note the critical irregular stenosis of the left carotid bulb and internal carotid artery origin.
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Figure 13 CT angiogram reconstructions (A, oblique sagittal; B, oblique coronal) of the left common carotid artery in a patient with left carotid artery territory transient ischaemic attacks showing tandem lesions. There is a densely calcified plaque creating a critical stenosis at the origin of the left internal carotid artery, and a second severe stenosis at the origin of the left common carotid artery (arrow). This second important lesion would not have been detected by Doppler ultrasound scanning. Such dense irregular plaque calcification at the internal carotid artery bifurcation can make it difficult to measure the precise luminal dimension.
Figure 14 T2W (A) and T1W (B) axial MRIs at the level of the foramen magnum demonstrate the typical findings of a left internal carotid artery dissection with hyperintense haematoma in the arterial wall (arrows). The patient presented with left-sided neck pain and a Horner’s syndrome. Contrast-enhanced MR angiogram (C) confirmed the full extent of the dissection, internal carotid artery narrowing, commencing just above the carotid bulb and finishing at the skull base. The bony confines of the carotid canal usually prevents the vessel wall haematoma from progressing intracranially.
Figure 15 Axial T2W MRIs (A–C) in a patient presenting with right-sided neck pain, dysarthria and swallowing difficulties, demonstrate a small right lateral medullary infarction and a small right-sided cerebellar infarction due to right vertebral artery dissection. Note the stenosis (arrows) at C1/2, the commonest site for a vertebral artery dissection on the contrast-enhanced MR angiogram images (D and E).
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Figure 16 Coronal (A) and sagittal (B) CT angiogram reconstructions in a 77-year-old woman presenting with subarachnoid haemorrhage secondary to rupture of a 3 mm basilar top aneurysm (C arrow). The CT angiogram shows typical features of medial fibromuscular dysplasia affecting the cervical internal carotid artery bilaterally (no internal carotid artery digital subtraction angiogram performed). Note the typical ruffled string of beads, or baggy stockings appearance so characteristic of this condition—areas of concentric narrowing and outpouchings. The vertebral artery digital subtraction angiogram ( performed at the time of aneurysm coiling) lateral projection also confirms involvement of the distal cervical left vertebral artery.
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Figure 17 T2W axial MRIs (A–D) in a 22-year-old man presenting with transient left-sided weakness. Note the ischaemic deep white matter changes in a watershed distribution, more extensive on the right. Wallerian degeneration is present in the right cerebral peduncle. Note the diminished abnormal flow voids of the terminal internal carotid artery’s, and proximal anterior and middle cerebral arteries. Digital subtraction angiogram (lateral projections of a right internal carotid artery angiogram, E and F) confirms distal internal carotid artery, proximal anterior and middle cerebral artery narrowing and hypertrophy of the lenticulostriates (the ‘puff of smoke’ typical of moyamoya). Note also the collateral circulation from the posterior cerebral artery supplying distal anterior and middle cerebral artery territory. These changes were similar on the left (not shown).
Extra reading Leiva-Salinas C, Wintermark M. Imaging of acute ischemic stroke. Neuroimaging Clin N Am 2010;20:455–68.
Competing interests None. Provenance and peer review Commissioned; externally peer reviewed. This paper was reviewed by Joanna Wardlaw, Edinburgh, UK.
De Lucas EM, Sanchez E, Gutierrez A, et al. CT protocol for acute stroke: tips and tricks for general radiologists. Radiographics 2008;28:1673–87. Barber PA, Demchuk AM, Zhang J, et al. Validity and reliability of a quantitative computed tomography score in predicting outcome of hyperacute stroke before thrombolytic therapy. ASPECTS Study Group. Alberta Stroke Programme Early CT Score. Lancet 2000;355:1670. Pavlovic AM, Barras CD, Hand PJ, et al. Brain Imaging in transient ischaemic attack- redefining TIA. J Clin Neurosci 2010;17:1105–10. Rodallec MH, Marteau V, Gerber S, et al. Craniocervical arterial dissection: spectrum of imaging findings and differential diagnosis. Radiographics 2008;28:1711–28. Touze E, Oppenheim C, Trystram D, et al. Fibromuscular dysplasia of cervical and intracranial arteries. Int J Stroke 2010;5:296–305. Renowden S. Pract Neurol 2014;14:77–87. doi:10.1136/practneurol-2013-000801
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