CT in CVA

Role of CT in CVA

1. CT-CVA (CEREBRO VASCULAR ACCIDENT) OSR Dr. Yash Kumar Achantani

2. Introduction CVA or Stroke is an acute CNS injury that results in neurologic deficits, brought on by a reduction or absence of perfusion to a territory of the brain. The disruption in flow is from either an occlusion (ischemic) or rupture (hemorrhagic) of the blood vessel. Ischaemic stroke  results from a sudden cessation of adequate amounts of blood reaching parts of the brain. Ischaemic strokes can be divided according to territory affected or mechanism.

3. Stroke Infarction 85% Cerebral atherothrombosis 30-40% Cardiogenic embolism 20-25% Penetrating artery disease ( lacune ) 20% Other unusual causes 5% Hemorrhage 15%

4. Epidemiology Stroke is the third most common cause of morbidity worldwide (after myocardial infarction and cancer) and is the leading cause of acquired disability. Risk factors for ischemic stroke are: age, gender family history smoking, alcohol hypertension hypercholesterolaemia diabetes

5. Clinical presentation An ischemic stroke typically presents with rapid onset neurological deficit , which is determined by the area of 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 behaviour of the lesion

6. Patho -physiology

7. Cerebral blood volume (CBV) : the volume of blood per unit of brain tissue(G/W:4/2 ml/100gm) Cerebral blood flow (CBF) : the volume of blood flow per unit of brain tissue per minute(G/W:60/25 ml/100gm/min) Mean transit time (MTT) : defined as the time difference between the arterial inflow and venous outflow(G/W:4/4.8sec)

8. Normal cerebral blood flow (CBF) is 50–60 mL/100 g brain tissue/min. Cerebral autoregulation responds to a fall in cerebral perfusion pressure (CPP) with vasodilatation and recruitment of collateral vessels, thus increasing cerebral blood volume (CBV) and reducing resistance, in order to maintain CBF The average time a blood cell remains with a particular volume of tissue rises due to vasodilatation and collateral flow, resulting in a prolonged mean transit time (MTT) and thereby allowing improved oxygen delivery.

9. After the vessels are fully dilated the autoregulatory system cannot properly respond to any further reduction in CPP and therefore CBF starts to decline. Oxygen extraction goes up to compensate, but once this is maximal any further fall in CBF causes cellular dysfunction The loss of normal neuronal electrical function occurs when CBF falls to 15–20 mL /100 g/min . This may be reversible , depending on the severity and duration of the ischemia, Irreversible infarction is likely to occur within minutes if the CBF <10 , but moderate ischemia (10–20) may be reversible for a few hours

10. At levels of CBF <10, hypoxaemia leads to failure of the ATP-driven cell integrity systems, resulting in cell depolarisation and influx of Na+ and water. Cellular swelling and cell death occurs ( cytotoxic oedema). In time, structural breakdown of the blood–brain barrier occurs due to ischemic damage to capillary endothelium. Leakage of intravascular fluid and protein into the extracellular space and later net influx of water to the infarcted area cause vasogenic oedema .

11. The Penumbra Model Following a thromboembolic cerebral arterial occlusion, the decline in regional CBF in the affected brain parenchyma is not uniform. It has a centred infarct core with very low CBF and cell depolarisation. A peripheral zone — the penumbra —has moderately diminished CBF, resulting in loss of electrical function but preserved cell integrity. The duration of ischemia in the penumbra is critical, and strategies to recanalise the vessel and restore normal CBF are likely to convey the greatest benefit.

12. Failure or, more crucially, a delay in achieving this, however, may lead to progression to infarction, especially as this tissue is poorly autoregulated and more vulnerable. Surrounding the penumbra is a zone of benign oligaemia . Here CBF is only mildly impaired and tissue is likely to survive.

13. Causes Large Vessel Thromboembolic Stroke (40%) Cardioembolic Stroke (15–30%) Small Vessel or Lacunar Stroke (15–30%)

14. Large Vessel Thromboembolic Stroke (40%) • Most commonly due to thrombus at the site of atherosclerotic plaque or embolisation more distally (artery-to-artery). • Sites: carotid bifurcation > intracranial internal carotid artery (ICA) > proximal MCA (> anterior cerebral artery (ACA)); vertebral artery origins > distal vertebral (VA) > basilar artery. • Also vasculopathy (e.g. large vessel vasculitis , dysplasia such as fibromuscular dysplasia (FMD)), dissection.

15. Cardioembolic Stroke (15–30%) Intracardiac thrombus: myocardial infarct, enlarged left atrial appendage, aneurysm, arrhythmia (especially paroxysmal atrial fibrillation (AF)); valvular disease— endocarditis , prosthetic valves, inadequate anticoagulation; right-to-left shunts. Cardiac tumours.

16. Small Vessel or Lacunar Stroke (15–30%) • Small infarcts (<1.5 cm) in deep perforator territories; typically • Lenticulostriate perforators from M1 segment of MCA with infarcts in the lentiform nuclei, internal capsules and corona radiate. • Thalamic branches from posterior choroidal perforators from basilar tip, proximal PCAs and posterior communicating arteries cause infarcts in the thalami and posterior internal capsules. • Perforators from the basilar artery and its major branches resulting in brainstem infarcts.

17. Borderzone Infarction Also known as watershed ischemia . This occurs at the boundaries of the major vessel territories—superficially between the leptomeningeal collaterals of the MCA and ACA which also extend into the corona radiata deep to the superior frontal sulcus , and those of the MCA and PCA. In the deep white matter of the inferior corona radiata and external capsules lies the deep borderzone between the cortical branches and deep M1 perforators of the MCA Postulated mechanisms include local (e.g. carotid stenosis ) and global (e.g. cardiac insufficiency) hypoperfusion , but embolic infarcts at these sites can also occur.

18. Borderzone ischaemia in the posterior fossa is uncommon but usually occurs between the superior cerebellar artery (SCA) and posterior inferior cerebellar artery (PICA) territories, and occasionally between the SCA, PICA and anterior inferior cerebellar artery (AICA) territories.

19. In addition to bilateral chronic small vessel ischaemic change, on the left there is patchy cortical infarction in a borderzone distribution.

20. Global Hypoxic– Ischaemic Injury Inadequate oxygen supply to the entire brain can be the consequence of severe hypotension or impaired blood oxygenation. Global hypoperfusion can result in watershed infarcts, but profound hypoxia can also cause symmetric ischaemia in the basal ganglia, thalami and hippocampal formations. Anoxia due to defective blood oxygenation such as in carbon monoxide poisoning tends to cause infarcts in sensitive regions.

21. Diffuse low attenuation is seen throughout the brain in keeping with severe cerebral ischaemia. 

22. Stroke Classification Deep white matter infarcts are typically small vessel in nature but can result from emboli originating from large vessel atheroma or from a cardiac source. Middle cerebral artery (MCA) territory infarcts can arise from emboli from the heart or carotid artery, or from in situ thrombosis in the middle cerebral artery. Small peripheral infarcts in a vascular territory are usually embolic but the source is not always clear (i.e. cardiac vs carotid vs MCA) Peripheral infarcts involving multiple vascular territories must be from a proximal source and most likely the heart.

23. Scoring and classification systems Alberta stroke program early CT score (ASPECTS) TOAST classification NIH Stroke Scale Orgogozo Stroke Scale Canadian Neurological Scale Mathew Stroke Scale Scandinavian Stroke Scale

24. TOAST classification in acute ischemic stroke The  TOAST (trial of ORG 10172 in acute stroke treatment) classification  denotes five sub types of  ischaemic stroke. large-artery atherosclerosis (embolus / thrombosis) cardioembolism (high-risk / medium-risk) small-vessel occlusion ( lacune ) stroke of other determined aetiology stroke of undetermined aetiology

25. Alberta stroke program early CT score The  Alberta stroke programe early CT score (ASPECTS)  is a 10-point quantitative topographic CT scan score used in patients with middle cerebral artery (MCA) stroke. caudate lentiform internal capsule insular cortex M1: "anterior MCA cortex," corresponding to frontal operculum M2: "MCA cortex lateral to insular ribbon" corresponding to anterior temporal lobe M3: "posterior MCA cortex" corresponding to posterior temporal lobe M4: "anterior MCA territory immediately superior to M1" M5: "lateral MCA territory immediately superior to M2" M6: "posterior MCA territory immediately superior to M3"

26. A = anterior circulation; P = posterior circulation; C = caudate; L = lentiform ; IC = internal capsule; I = insular ribbon; M1 = anterior middle cerebral artery (MCA) cortex; M2 = MCA cortex lateral to insular ribbon; M3 = posterior MCA cortex; M4, M5 and M6 are anterior, lateral and posterior MCA territories immediately superior to M1, M2 and M3, rostral to basal ganglia.

27. Two NECT axial slices are examined level of basal ganglia and internal capsule; bodies of the lateral ventricles Ten regions are identified (four deep and six cortical) Starting with a score of 10, 1 point is deducted for each of these areas that is involved. If the score is <7, the infarct is considered >1/3 of an MCA territory

28. Radiographic features 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:- Non-Contrast CT brain, CT perfusion CT angiography. 

29. Objectives of NECT in Acute Stroke To exclude haemorrhage and allow administration of aspirin therapy To exclude an alternative cause of the fixed neurological deficit. Around 30% of patients presenting with a stroke-like episode have a non-vascular cause To exclude infarcts > 1/3 MCA territory In cases of suspected posterior circulation stroke, to attempt to identify an obviously thrombosed basilar artery

30. Infarct Imaging Signs

31. Immediate The earliest CT sign visible is a hyperdense segment of a vessel , representing direct visualisation of the intravascular thrombus / embolus and as such is visible immediately. Although this can be seen in any vessel, it is most often observed in the middle cerebral artery ( hyperdense middle cerebral artery sign). 

32. Dense Artery sign

33. Early (1-3 hours) 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 hypo attenuation of deep nuclei : lentiform nucleus,  changes seen as early as 1 hour after occlusion,  visible in 75% of patients at 3 hours cortical hypodensity with associated parenchymal swelling with resultant gyral effacement cortex which has poor collateral supply (e.g. insular ribbon ) is more vulnerable. 

34. Lentiform nucleus sign

35. Insular ribbon sign

36. First week ( 3-7days) With time the hypo-attenuation and swelling become more marked resulting in significant mass effect . Maximum Edema This is a major cause of secondary damage in large infarcts. 

37. Second and third week (7-21 days) Petechial Hemorrhage- Hemorrhagic transformation Correlates with BBB breakdown and Gyral enhancement Fogging Effect CT in 2 nd week post infarction Decrease in edema and accumulation of protein from cell lysis balance each other out, hence can have a normal appearance on CT. Imaging a stroke at this time can be misleading as the affected cortex will appear near normal.   Rule of 3’s Peaks 3days to 3weeks and resolves by 3months

38. Left MCA territory infarct with hemorrhagic transformation

39. Hemorrhagic Transformation- The Spot sign

40. 30-90days BBB repair, loss of enhancement Months Post infarct CSF takes up the previously occupied brain Ex vacuo dilatation of adjacent ventricle Widening of adjacent Sulci Gliotic scar and encephalomalacia

41. Extensive area with attenuation of CSF replacing part of the brain parenchyma in the vascular territory of the right middle cerebral artery. Ex vacuo  dilatation of the ipsilateral lateral ventricules .

42. CT PERFUSION

43. CT Perfusion CT perfusion has emerged as a critical tool in selecting patients for reperfusion therapy as well as increasing the accurate diagnosis of ischaemic stroke among non-expert readers four fold compared to routine non-contrast CT. 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). 

44. The key to interpretation is understanding a number of perfusion parameters: cerebral blood volume (CBV) cerebral blood flow (CBF) mean transit time (MTT)  time to peak (TPP) 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 .

45. Objectives of Penumbral Imaging To more accurately delineate the size of the core infarct To establish whether a penumbra of salvageable tissue is present To evaluate the size and severity of ischemia of the penumbra

46. Large core infarcts have a poorer outcome , regardless of penumbra size or severity. Specifically, core volumes greater than 70 mL are associated with adverse outcomes regardless of recanalisation therapy. Core infarcts with small penumbra are described as ‘ matched ’ defects and carry reduced reperfusion benefit. However, some units proceed with thrombolysis in this situation because of the possibility of partial reversibility. Large areas of salvageable tissue, known as ‘ mismatch ,’ are likely to benefit most from recanalisation therapy. Areas of mildly ischemic penumbra may reperfuse spontaneously—known as ‘ benign oligaemia ’. Appropriate patient selection using penumbral imaging may extend the therapeutic time window beyond 4.5 hours.

47. Case of a 67 year old male patient who presented with hemiplegia No acute haemorrhage. Loss of grey-white differentiation at the caudate head and insula ribbon. Hyperdense left M1 segment. 

48. There is a large region of reduced CBV, CBF and time to peak perfusion affecting the whole left cerebral hemisphere. This is in keeping with a large left MCA infarct. A very small region of mismatch reduced time to peak perfusion is suggestive of only a tiny penumbra.

49. Expected evolution of known left MCA territory infarct with left cerebral hemisphere loss of grey-weight differentiation with oedema and positive mass effect. Hyperdense left MCA again demonstrated. No haemorrhagic transformation. 

50. CT Angiography 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  establishing stroke aetiology ( eg . atherosclerosis, dissection) access limitation for endovascular treatment (e.g. tortuosity , stenosis )

51. Case of right hemiparesis in a 84 year old female CT shows increased attenuation of the proximal portion of left the MCA, as well the onset of a ​​ill-defined hypoattenuation area involving the left capsular region (ischemia). 

52. CTA study confirms the occlusion of proximal left MCA and no involvement of the left ACA. 

53. Goals of Acute Stroke Imaging Parenchyma: Assess early signs of acute stroke and rule out hemorrhage Pipes: Assess extracranial and intracranial circulation for evidence of intravascular thrombus Perfusion : Assess cerebral blood volume, cerebral blood flow, and mean transit time Penumbra : Assess tissue at risk of dying if ischemia continues without recanalization of intravascular thrombus Rowley HA. AJNR 2001;22:599–601.

54. Venous infarct Causes of cerebral venous thrombosis include trauma, i nfection (particularly subdural empyema) and hypercoagulability disorders including those due to oral contraceptives. Venous infarcts do not conform to arterial territories and are often haemorrhagic and multifocal. The superior sagittal sinus is most commonly involved, which can lead to bilateral parasagittal infarcts . Isolated occlusion of the transverse sinus or the deep cerebral veins can occur. On unenhanced CT acute thrombosis will cause a venous sinus to appear expanded and hyperdense . IV contrast medium causes more intense enhancement of the walls of the sinuses than of their contents, the so-called ‘ delta sign’ .

55. Delta sign in superior sagittal sinus thrombosis. (A) Young man with a seizure after several days of headaches. An unenhanced CT shows a small right parietal acute haematoma. The superior sagittal sinus is occluded by acute thrombus. It appears expanded and the same density as the intraparenchymal clot (arrow). (B) Contrast-enhanced CT shows the dura around the sinus (long arrow) is higher density than the lumen (short arrow).

56. NONTRAUMATIC INTRACRANIAL HAEMORRHAGE

57. Spontaneous SAH is due to a ruptured arterial aneurysm in 70–80 per cent of patients and an arteriovenous malformation in about 10 per cent. In the remaining approximately 15 per cent, no underlying cause is found on angiography. CT is positive for SAH in 98 per cent within 12 h of onset but this falls to less than 75 per cent by the third day. Recent SAH causes increased density of the cerebrospinal fluid (CSF) spaces on CT . Most aneurysms are located on or close to the circle of Willis and blood is therefore seen in the basal cisterns, although the entire intracranial subarachnoid space may be opacified and intraventricular blood is common. SAH

58. Cerebral aneurysms may be saccular, fusiform, or dissecting. However majority are saccular aneurysms, which are usually round or lobulated and arise from arterial bifurcations. Giant aneurysms by definition measure over 25 mm in diameter and account for approximately 5 per cent of all cerebral aneurysms. Around 90 per cent of intracranial aneurysms arise from the carotid circulation, the remaining 10 per cent from vertebral or basilar arteries.

59. Anterior communicating artery aneurysm rupture. (A) CT shows diffuse subarachnoid haemorrhage (short arrows) and a small haematoma in the septum pellucidum indicating the likely source is an aneurysm of the anterior communicating artery (long arrow). The temporal horns of the lateral ventricles and anterior recesses of the third ventricle are enlarged (arrowheads) due to secondary communicating hydrocephalus, an extremely common finding in acute SAH. (B) A 3D angiogram shows a lobulated aneurysm in the predicted location (long arrow). The left proximal anterior cerebral artery (short arrow), middle cerebral artery (arrowhead) and internal carotid artery (open arrow) are clearly shown.

60. INTRACEREBRAL HAEMORRHAGE Nontraumatic intracerebral haemorrhage in older people is frequently from rupture of a small perforating vessel due to hypertension . The preferential sites of hypertensive haemorrhage are the basal ganglia, thalamus and pons . Larger hypertensive bleeds in the basal ganglia often extend into the ventricles or Sylvian fissure. Haemorrhage may also be due to vascular malformations and ‘recreational’ drugs such as cocaine. Other causes include coagulopathies , anticoagulation , vasculitis , venous infarcts and haemorrhagic transformation of arterial infarcts . Intracerebral haemorrhage is reliably detected on CT appearing as increased density.

61. Non-contrast CT of the brain demonstrates a large right temporo -parietal haemorrhage. It is associated with moderate midline shift.

62. AVM’S Intracranial vascular malformations can be classified according to the presence or otherwise of arteriovenous shunting. The former comprises cerebral (or subpial ) arteriovenous malformations (AVMs) and dural fistulae; the latter includes developmental venous anomalies (DVAs), cavernous angiomas (‘ cavernomas ’) and capillary telangiectasias . Cerebral ( subpial ) AVMs are probably congenital anomalies consisting of direct arteriovenous shunts without a normal intervening capillary bed. Cerebral haemorrhage is the commonest clinical presentation, others being epilepsy, headache or focal neurological deficit. They are usually detectable on CT as serpiginous areas of high density (with marked contrast enhancement). CT may show calcification . There may be haemorrhage at different stages of evolution . AVMs may be surrounded by areas of ischaemic damage that are low attenuation on CT. Dilated feeding arteries and early opacification of draining veins are the angiographic hallmarks of these lesions.

63. Noncontrast axial images demonstrating a serpiginous hyperdensity is in the left parietal region. Arteriovenous malformation is located superficially in the parieto -occipital region on the left It receives most of its supply from the left middle cerebral artery branches Venous drainage appears predominantly superficial, with vein coursing posteriorly to drain into the superior sagittal sinus. There is no evidence of haemorrhage or thrombosis or aneurysm formation.