Imaging ischemic infarction.pptx

d/t types of ischemic strokes, imaging modalities, imaging features on different imaging modalities. differential diagnosis of different imaging findings.

1. Seminar Presentation Imaging Of CEREBROVASCULAR ACCIDENT AND ISCHEMIC STROKE By Dr. Irko worku (Radiology resident ) DEC 21 , 2023 1

2. OUTLINES Introduction Types of Ischemia Pathophysiology Principles of imaging Goals of imaging Cerebral venous infarction Acute cerebellar infarcts Vasculopathies

3. INTRODUCTION A  stroke  is a clinical diagnosis that refers to a sudden onset focal neurological deficit of presumed vascular origin. Stroke is generally divided into two broad categories  : ischaemic stroke  haemorrhagic stroke Stroke- clinical determination Infarction - pathologic term - based on imaging, pathology, and/or persistent neurologic symptoms, with other causes excluded. silent CNS infarction- If there is imaging or pathologic evidence of an infarct but no attributable clinical symptoms.

4. Clinical presentation An ischaemic 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 ischaemic penumbra . The vascular territory affected will determine the exact symptoms and clinical behaviour of the lesion:

5. Con’t brain tissue is sensitive to ischemia, because of the absence of neuronal energy stores. In the complete absence of blood flow, the available energy can maintain neuronal viability for approximately 2–3 minutes. However, in acute stroke, ischemia is more often incomplete- collateral blood supply from uninjured arterial and leptomeningeal territories.

6. PATHOPHYSIOLOGY

7. The vascular territory anterior circulation infarct anterior cerebral artery infarct middle cerebral artery infarct lacunar infarct striatocapsular infarct posterior circulation infarct posterior cerebral artery infarct cerebellar infarct brainstem infarct

8. Ageing ischaemic strokes radiopedia 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 than 3 weeks

9. Goals of Imaging

10. Stroke Imaging modalities In many institutions with active stroke services which provide reperfusion therapies, a so-called code stroke aimed at expediting diagnosis and treatment of patients multimodality imaging. Stroke protocol (CT ) non-contrast CT (brain) CT perfusion (brain) CT angiography (aortic arch to the vertex of the skull) Brain MRI For vascular evaluation MRA (TOF, phase contrast MRI , contrast enhanced angiography) Carotid Ultrasound/ Transcranial Doppler ultrasound

11. Non contrast CT imaging Non-contrast CT of the brain remains the mainstay of imaging in the setting of an acute stroke . limited sensitivity in the acute setting . Detection depends on : the territory, the experience of the interpreting radiologist and time of the scan from the onset of symptoms. Whether tissue is supplied by end arteries Pattern of collateral supply

12. Con’t The goals of CT in the acute setting are: exclude intracranial haemorrhage , which would preclude thrombolysis look for any "early" features of ischaemia exclude other intracranial pathologies that may mimic a stroke, such as a tumour

13. Immediate CT finding in ischemic stroke hyperdense segment of a vessel.   hyperdense MCA sign   MCA dot sign ) Basilar artery hyperdense sign DDX-  calcified cerebral embolus .

14. Hyperdense MCA sign focal hyperdensity of the  MCA(M1) on non-contrast brain CT. is the direct visualisation of t hromboemboli . earliest visible sign greater than 8 mm-no chance of recanalization by IVT. DDX: Polycythaemia calcified atherosclerotic disease HSV encephalitis

15. MCA dot sign, Sylvian fissure sign distal MCA branches seen in the Sylvian fissure (M2 segment ). The principally affected area of the brain is the  insula. better outcome than the hyperdense MCA sign. Ddx: Punctate vascular calcification along the M2 segment of the MCA within the Sylvian fissure

16. CON’T

17. Calcified cerebral embolus small in size , 2-3 mm. calcific   AS  (most common) mitral annular calcification calcified  Major vessels If multiple (   salted pretzel sign ) round or ovoid shape , higher attenuation (~160 HU) Ddx :   haemorrhage ,  vessel wall calcification , infection (e.g.  neurocysticercosis ),  cavernomas ,

18. Early hyperacute loss of grey-white matter differentiation , and hypoattenuation of deep nuclei. Use stroke window (8w/c32) cortical hypodensity with associated parenchymal swelling with resultant gyral effacement. The insular ribbon sign

19. Insular ribon sign and obscuration of the lentiform nucleus, which appears hypoattenuated because of cytotoxic edema

20. Con’t

21. Summary of evolution of infarction on CT Acute The hypoattenuation and swelling petechial haemorrhages significant mass effect secondary damage   . Subacute swelling starts to subside and elevation of the attenuation of the cortex. affected cortex will appear near normal .( CT fogging phenomenon )

22. Chronic residual swelling passes gliosis  sets in eventually appearing as a region of low density with a negative mass effect.

23. Quantitation of Ischemic Involvement the European Cooperative Acute Stroke Study trial, involvement of more than one-third of the MCA territory depicted at unenhanced CT was a criterion for the exclusion of patients from thrombolytic therapy because of a potential increase in the risk for hemorrhage. The Alberta Stroke Program Early CT Score (ASPECTS) was proposed in 2001 as a means of quantitatively assessing acute ischemia on CT images by using a 10-point topographic scoring system. the MCA territory is divided into 10 regions, each of which accounts for one point in the total score

24. ASPECT SCORE One point for each region. Score ---/10 M1 to M3 are at the level of the basal ganglia M4 to M6 are at the level of the ventricles immediately above the basal ganglia score less than or equal to 7 predicts a worse functional outcome at 3 months as well as symptomatic haemorrhage , with thrombolysis did not have a good clinical outcome

25. pc-ASPECTS thalami (1 point each ) occipital lobes (1 point each) midbrain (2 points) pons (2 points) cerebellar hemispheres (1 point each ) Score---/10

26. D ifferentiating between acute and chronic infarction  on a  CT acute   cytotoxic oedema Hypoattenuating area -more dense than  CSF Has positive mass effect sulcal / ventricular effacement, midline shift/   herniation. chronic:  encephalomalacia ;  Wallerian degeneration Hypoattenuating area has Negative mass effect like-widened sulci, ex vacuo dilatation of ipsilateral ventricle CSF density.

27. MRI more time consuming and less available  BUT higher sensitivity and specificity for early ischemic infarction. Early hyperacute DWI demonstrates increased signal and reduced ADC values. thromboembolism may be detected (e.g. on  SWI, GRE ). 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). 

28. Hyperacute infarct (0–6 hours) Diffusion is reduced in an acute infarct by two factors: 1) Shift from extracellular to intracellular water due to Na/K ATPase pump failure . 2) Increased viscosity of infarcted brain due to cell lysis and increased extracellular protein . C, Diffusion-weighted image reveals extensive ganglionic and cortical hyperintensity indicative of hyperacute infarction. D, Apparent diffusion coefficient map reveals diffuse hypointensity indicative of restricted diffusion.

29. CON’T… If infarction is incomplete then cortical contrast enhancement may be seen as early as 2 to 4 hours. In a minority of cases( 6.8 %), DWI may be normal -   DWI-negative acute ischaemic stroke

30. DWI-negative acute ischaemic stroke DWI is reported to fail in the detection of ischaemic strokes involving: posterior circulation infarction : 5x more likely to be DWI-negative than anterior circulation ischaemia , especially within the first 48 hours  small strokes , particularly small brainstem infarcts hyperacute ischaemia : within 3 hours of symptom onset.

31. Acute infarct (6 hours–72 hours) • The acute infarct phase is characterized by increase in vasogenic edema and mass effect. On imaging, there is increased sulcal effacement and mass effect . The mass effect peaks at 3–4 days, MRI shows hyperintensity of the infarct core on T2-weighted images, best seen on FLAIR. The FLAIR abnormality is usually confined to the gray matter. DWI continues to show restricted diffusion . due to increased collateral flow there may be some arterial enhancement . Perfusion images most commonly show increase in size of the infarct core with resultant decrease in size of the penumbra.

32. T2W FLAIR

33. Early subacute infarct • blood flow to the affected brain is re-established by leptomeningeal collaterals and ingrowth of new vessels into the region of infarction. The new vessels have an incomplete blood-brain barrier , causing a continued increase in vasogenic edema and mass effect , which peaks at 3–4 days. MR imaging shows m arked hyperintensity on T2-weighted images involving both gray and white matter ( vasogenic edema) (in contrast to the acute stage which usually involves just the gray matter, cytotoxic edema). • The ADC map becomes less dark or even resolves if there is extensive edema; the DWI images typically remain bright due to underlying T2 shine-through.

34. Late subacute infarct • resolution of vasogenic edema and reduction in mass effect. • A key imaging finding is gyriform enhancement , which may occasionally be confused for a neoplasm. Unlike a tumor, however, a subacute infarction will not have mass effect. The enhancement of a subacute infarct - “ 2-2-2” rule, which states that enhancement begins at 2 days, peaks at 2 weeks, and disappears by 2 months. DWI may remain bright due to T2 shine-through, although the ADC map will either return to normal or show increased diffusivity.

35. Chronic infarct In the chronic stage of infarction, cellular debris and dead brain tissue are removed by macrophages and replaced by cystic encephalomalacia and gliosis .

36. Wallerian degeneration

37. Evolution of infarction

38. Perfusion Imaging Characterize microscopic flow at the capillary level. The central volume principle : CBF=CBV/MTT The CBF of the normal brain ranges between 45 and 110 mL /min/100 g of tissue. Cerebral oligemia (about 20 to 40 mL /min/100 g) is defined as under perfused asymptomatic region of brain that will recover spontaneously.

39. Cont’d… Intravenous contrast is then administered and various parameters of  cerebral perfusion calculated. cerebral blood volume (CBV) cerebral blood flow (CBF) mean transit time (MTT) time-to-maximum ( Tmax ) or  time to peak (TTP ) In patients where volume of brain at risk is greater than the already infarcted brain by more than 20%, treatment may result in improved outcome.

40. cerebral perfusion

41. MRI DIFFUSION PERFUSION STUDY On the left we first have a diffusion image indicating the area with irreversible changes (dead tissue). In the middle there is a large area with hypoperfusion . On the right the diffusion-perfusion mismatch is indicated in blue. This is the tissue at risk. This is the brain tissue that maybe can be saved with therapy. Diffusion in yellow. Perfusion in red. Mismatch in blue is penumbra .

42. Con’t

43. Vascular evaluation Carotid Ultrasound/Transcranial Doppler Magnetic Resonance Angiography(There are three different techniques used to generate MRA: time-of-flight (TOF), phase contrast (PC), and contrast enhanced angiography ) Computed Tomographic Angiography Conventional Catheter Angiography

44. Carotid Ultrasound

45. Transcranial Doppler ultrasound is a noninvasive means used to evaluate the basal cerebral arteries through the infratemporal fossa. It evaluates the flow velocity spectrum of the cerebral vessels and can provide information regarding the direction of flow, the patency of vessels, focal narrowing It can determine adequacy of middle cerebral artery flow

46. contrast MRA FIGURE 3-9 Magnetic resonance angiography (MRA) 1.5 Tesla (1.5T) versus 3T. A, 1.5T and (B) 3T maximum intensity projection reconstructions from cranial MRA shows improved visualization of small and peripheral vessels at 3T. The aneurysm at the anterior communicating artery complex is more clearly defined on the 3T image

47. C ontrast enhanced CTA abrupt occlusion Of the internal carotid artery

48. Conventional Catheter Angiography I s the definitive imaging modality for vascular lesions of the brain and great vessels of the neck. In the hyperacute stroke setting, catheter angiography is primarily used in stroke treatment for planning and execution of thrombolysis and stenting. Catheter angiography is a safe (but not completely harmless) study and in many situations provides crucial information.

49. Conventional Catheter Angiography Indications if the MRA, CTA, or/and carotid ultrasound are equivocal; if MRA is contraindicated (e.g., in patients with pacemakers); if cardiac output is too low to produce a diagnostic CTA; to evaluate complex aneurysms or vascular malformations responsible for an intracranial hemorrhage; and for the evaluation of vasculitis.

50. Cerebral venous infarction most commonly secondary to cerebral venous thrombosis and frequently manifests with haemorrhage . Thrombosis of a cortical vein or a deep venous sinus is one of the more common causes. of stroke in younger patients. Risk factors for venous thrombosis include pregnancy, oral contraceptives, thrombophilia, malignancy, and infection . On non contrast CT is increased density within the thrombosed sinus or cortical vein ( the cord sign ). On contrast-enhanced CT, the empty delta sign signifies a filling defect in the superior sagittal sinus. MR venogram will show lack of flow in the thrombosed vein or dural venous sinus .

51. Cont’d… Venous thrombosis leads to venous hypertension, which may cause infarction and parenchymal hemorrhage. There are three characteristic patterns of venous infarction, dependent on the location of the thrombosed vein: Superior sagittal sinus thrombosis infarction of the parasagittal high convexity cortex. Deep venous system thrombosis infarction of the bilateral thalami. Transverse sinus thrombosis infarction of the posterior temporal lobe.

52. Transverse sinus is usualy assymetric -larger may be mistaken for thrombosis. newborns -normal polycythemia ->increased vascular density, the relative hypodensity of the brain, frequent occurrence of minimal perinatal paratentorial hemorrhage can mimic the appearance of sinus thrombosis.

53. Acute Cerebellar Infarcts < 5% , Male predominance and a mean age of 65 years. The abrupt onset of posteriorly located headaches , s evere vertigo , dysarthria,nausea and vomiting, nystagmus , ipsilateral dysmetria , and unsteadiness of gait . delayed alteration of consciousness seen in 90% of patients with mass effect due to cerebellar swelling. This can occur rapidly (within a few hours) or up to 10 days after the ictus . These infarcts are often difficult to identify on CT because beam-hardening artifact or partial volume averaging in the posterior fossa. visualize the fourth ventricle and quadrigeminal plate cistern because subtle asymmetry.

54. VASCULOPATHIES Traditional term “vasculitis” endothelial damage and thrombosis produced by circulating antigen-antibody complexes, mural edema, and/or spasm . Heterogeneous group of diseases with immunologic basis and similarity of the appearances of many of these diseases. Prolonged insults may result in fibrosis and fixed narrowing regardless of the initial insult. Catheter angiography remains the imaging “gold standard ” 3T MRA

55. Con’t … T he vasculopathies can be said to affect extracranial and extradural arteries; ( e.g FMD) arteries at the skull base at or near the circle of Willis; ( e.g Moya moya,TB meningitis ) secondary and tertiary branches of the carotid and/or basilar arteries (e.g., sylvian and convexity branches of the MCA); e.g wegner granulomatosis , polyartritis nodosa small perforating arteries (e.g., lenticulostriate arteries). e.g collagen vascular disease , Sjogren syndrome,migraine

56. Fibromuscular dysplasia

57. Reference

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