12 b. ct brain

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12 b. ct brain

  1. 1. CT BRAIN / MR – An introduction to Normal Anatomy, Interpretation and Some Common Pathologies Anupama Chandrasekharan Associate Professor & Consultant Radiologist Dept of Radiology and Imaging Sciences Sri Ramachandra Medical College & Research Institute Chennai
  2. 2. Indications for CT / MR ……..  Stroke  Trauma  Altered sensorium  Neurological deficit  Seizures  Headache
  3. 3. How the CT study is usually planned… 15-20 degree angulation to canthomeatal line to decrease radiation to the lens.
  4. 4. Plain CT Contrast CT
  5. 5. Indications for a contrast CT….  Seizures  Infections  Venous thrombosis  Tumors  Atypical stroke findings on plain CT  Atypical hemorrhage on plain CT  Focal edema on plain CT
  6. 6. Brain Window Bone Window
  7. 7. Descriptive Terms …….  Hypodense / Hypointense  Isodense / Isointense  Hyperdense / Hyperintense
  8. 8. Lesions appearing Hypodense on Plain CT  Infarct (non hemorrhagic)  Edema
  9. 9. Lesions appearing Hyperdense on Plain CT  Hemorrhage  Calcifications
  10. 10. Normal Intracranial Calcifications
  11. 11. NINDS trial Thrombolysis CT criteria No hemorrhage CT criteria No hemorrhage Parenchymal hypodensity in  1/3 MCA ECASS
  12. 12. Purpose of imaging in stroke  Definite diagnosis of stroke.  To document the presence or absence of hemorrhage This information is critical since anticoagulation is a standard therapy for ischemic stroke  Identify ischemic penumbra  Assess location & extent of brain damage (e.g. impending herniation)  To exclude stroke mimics.
  13. 13. Ischemic Penumbra
  14. 14. Stroke Frequency Based on Aetiology : Harvard Stroke Series Ischaemic (82%) Atherosclerotic Thrombosis – 22% Embolism – 30 % Lacunar – 18 % Indeterminate Cerebral Venous Dissection  Haemorrhagic (18%) Primary Intracerebral Hematoma – 12% AVM + Aneurysm – 4% Others: Cavernoma, AVF, bleeding disorders -2 %
  15. 15. Stroke Based on Territory  Anterior circulation stroke Embolus : 70% Thrombosis : 30%  Posterior circulation stroke Thrombosis : 70% Embolus : 30%
  16. 16. Normal in 50% of ischemic strokes < 6 hrs
  17. 17. 2 hrs 24 hrs
  18. 18. CT in Hyperacute Stroke ( 0-6 hrs )  Not v.sensitive for infarction  Sensitive for a/c hemorrhage & gross lesions precluding thrombolytic therapy 20 % within 2 hrs 82 % within 6 hrs Neuroradiology.1996 Jan;38(1):31-33
  19. 19. Hyperacute Stroke On CT EARLY ISCHEMIC CHANGES  Hyperdense vessel sign  Attenuation of lentiform nucleus  Loss of insular ribbon  Effacement of sulci  Loss of corticomedullary differentiation
  20. 20. Significance of Early Ischemic Signs No contraindication to thrombolysis Patel et al JAMA 2001;286:2830–2838 Indicate more extensive ischemia AJNR 2004;25:933-938 Hyperdense vessel sign Obscuration of basal ganglia Loss of grey-white matter interface Effacement of sulci Strong association with later hemorrhagic transformation AJNR 1991;12:1115-1121
  21. 21. Subacute infarct (1-7 days )  Hemorrhagic transformation in 5-40 % of all ischemic stroke Neurology 2001; 57:1603-1610 Stroke 1999;30:761-764
  22. 22. Lacunar Infarcts
  23. 23. Diffusion Weighted Imaging Radiology 2000;217:331-345 Detects Infarct As Early As 15-30 minutes
  24. 24. AJNR 2003 ;24:878-885 • 46 patients with acute stroke • CT and DWI within 6 hours • Mean delay 24.5 min. (R 10–41 min.) • EIC on CT - 33/46 (Sn 73%) • DWI 42/45 - (Sn 93%) CT vs DWI
  25. 25. Hyperacute hemorrhage 2.5 hr 18 hr GRE T2* WI MRI as sensitive as CT for acute hemorrhage More sensitive than CT for chronic hemorrhage (JAMA 2004;292:1823-30)
  26. 26. CT sensitivity for SAH  Day of SAH – 98 %  After Day 1 – 90 %  After Day 5 – 80 %  After 1 wk – 50 % Neuroradiology 1982:23:153-156
  27. 27. Acute SAH - 100 % Chronic SAH – 63 % Chronic SAH ( CT ) – 46 % Radiology .1995;196(3):773-777 Radiology.1997;203(1):257-262
  28. 28. Acute hemorrhage  MRI – 96% sens. 99% accuracy  CT - 89% sens. 98% accuracy Chronic hemorrhage •MRI – 96% sens. 99% accuracy •CT - 40% sens. 78 accuracy HEME study
  29. 29. CT Angiography  Site of occlusion  Length of occluded segment  Arteries beyond occluded segment – collateral flow  Detection & exclusion of large vessel intracranial occlusion – sens – 98.4% and spec.-98.1% JCAT 2001; 25(4):520-8
  30. 30. CT Perfusion  If no penumbra…..increased risk of bleed with thrombolysis RCNA 44(2006)41-62
  31. 31. MTT rCBVrCBF DWI ADC
  32. 32. Can MR replace CT as first imaging modality in hyperacute stroke? Yes  MR immediately available  Protocol is optimized  Skilled personnel
  33. 33. Unlikely to replace CT ....... • Cost • Limited availability • Time • Lack of evidence that MR has a positive influence on prognosis
  34. 34. Delta Sign
  35. 35.  Extradural haematoma  Subdural haematoma  Subarachnoid haemorrhage  Intraventricular haemorrhage  Cerebral contusions  Intracerebral haemorrhage  Diffuse cerebral edema EXTRA-AXIAL LESIONS INTRA-AXIAL LESIONS Imaging in Craniocerebral Trauma
  36. 36. Extradural Hematoma Acute Subdural Hematoma
  37. 37. Diffuse Axonal Injury
  38. 38. 23 yr old male c/o fever and intense headache
  39. 39.  Ring enhancing lesions – granuloma / abscess  Calcifications  Cerebritis  Meningeal abnormalities  Complications
  40. 40. Differential Diagnosis of Ring Enhancing Lesions  Granulomas  Brain abscess  Tumors – metastasis, glioma  Resolving hematoma
  41. 41. Encephalitis  MRI – within 48 hrs  CT - at least 3-5 days
  42. 42.  Widely available  Cost  Quick  Hemorrhage  Trauma  Hyperacute infarcts  Posterior fossa  Diffuse axonal injuries  White matter diseases  Subtle abnormalities of neuroparenchyma
  43. 43. Contraindications for MRI  Metallic implants  Pacemakers  Prosthetic valves  Aneurysm clips  Claustrophobia
  44. 44. Thank U
  45. 45. Epidural Abscess Subdural Empyema  Notice the rim enhancing epdural fluid collection (arrowheads) ).
  46. 46. Encephalitis  Diffuse nonfocal brain parenchymal inflammatory process  Most common agents - viruses  Immunocompetent individuals - Herpes viruses  Immunocompromised individuals  Human immunodeficency virus (HIV)  Cytomegalovirus (CMV)  Papovavirus
  47. 47. Tuberculous meningitis
  48. 48. Cerebellar AtrophyCerebral Atrophy
  49. 49. ARTERIOVENOUS MALFORMATION
  50. 50. ARTERIOVENOUS MALFORMATION
  51. 51. SUBACUTE SDH
  52. 52. ACUTE ON CHRONIC SDH
  53. 53. CONTUSION SAH
  54. 54. Complications EARLY  ABSCESS  SUBDURAL/EPIDUR AL EMPYEMA  VENTRICULITIS  INFARCTION  VENOUS THROMBOSIS LATE  SUBDURAL/ EPIDURAL EFFUSION  ENCEPHALOMALACIA  HYDROCEPHALUS  ATROPHY
  55. 55. SUBDURAL EMPYEMA
  56. 56. EXTRA-AXIAL INTRA-AXIAL
  57. 57. Hypertensive Hemorrhage  Hypertensive hemorrhage accounts for approximately 70-90% of non-traumatic primary intracerebral hemorrhages. It is commonly due to vasculopathy involving deep penetrating arteries of the brain. Hypertensive hemorrhage has a predilection for deep structures including the thalamus, pons, cerebellum, and basal ganglia, particularly the putamen and external capsule. Thus, it often appears as a high-density hemorrhage in the region of the basal ganglia. Blood may extend into the ventricular system. Intraventricular extension of the hematoma is associated with a poor prognosis.
  58. 58. Haemorrhagic StrokeEtiology  Hypertension  Vascular malformation  Aneurysm  Trauma  Amyloid angiopathy  Tumor  Coagulopathy  Hemorrhages can occur in the intraparenchymal, subarachnoid, intraventricular, subdural and extradural spaces.  Location of hypertensive hemorrhage: Putamen, external capsule, thalamus, pons, cerebellum, subcortical white matter
  59. 59. Subarachnoid hemorrhage  In the absence of trauma, the most common cause of subarachnoid hemorrhage is a ruptured cerebral aneurysm. Cerebral aneurysms tend to occur at branch points of intracranial vessels and thus are frequently located around the Circle of Willis. Common aneurysm locations include the anterior and posterior communicating arteries, the middle cerebral artery bifurcation and the tip of the basilar artery. Subarachnoid hemorrhage typically presents as the "worst headache of life" for the patient. Detection of a subarachnoid hemorrhage is crucial because the rehemorrhage rate of ruptured aneurysms is high and rehemorrhage is often fatal.
  60. 60. Subarachnoid hemorrhage  CT is currently the imaging modality of choice because of its high sensitivity for the detection of subarachnoid hemorrhage. CT is most sensitive for acute subarachnoid hemorrhage. After a period of days to weeks CT becomes much less sensitive as blood is resorbed from the CSF. If there is a strong clinical indication, LP may be warranted despite a negative CT since small bleeds can be unapparent on imaging. On CT, a subarachnoid hemorrhage appears as high density within sulci and cisterns. The insular regions and basilar cisterns should be carefully scrutinized for subtle signs of subarachnoid hemorrhage. Subarachnoid hemorrhage may have associated intraventricular hemorrhage and hydrocephalus. 
  61. 61. MR Spectroscopy Normal Infarct
  62. 62. Venous Sinus Thrombosis with Venous Infarct  Clinical symptoms – head ache, seizures  Pathology is due to decrease in perfusion pressure as the venous pressures elevate due to occlusion.  Predisposing conditions are dehydration, infection, polycythemia, sickle cell disease, hypercoagulable states, peripartum, OCP poisoning. Imaging findings  Unilateral / bilateral parenchymal hypodensities  Not limited to an arterial territory  May be associated with hemorrhage  Signs: Delta sign, Enhancement of walls of sinus than their contents.
  63. 63. MR Spectroscopy  Dynamic study depicting intracellular metabolism of cerebral ischemia.  Within the region of infarct, lactate appears elevated whereas NAA and total creatinine are reduced.
  64. 64. Radionucleotide studies in acute stroke  PET is an accurate method of quantifying changes in cerebral hemodynamics.  As cerebral blood flow (CBF) falls, cerebral blood volume (CBV) and oxygen extraction factor (OEF) increase.  PET measures changes in CBF, CBV and OEF using O15  Plays a limited role due to limited availability .  SPECT with Tc 99m HMPAO or ECD will show a perfusion defect.
  65. 65. Radionucleotide Studies in Acute Stroke  SPECT – Tc99m HMPAO  PET – O15  Adv – Early detection  Limitation - Not widely available
  66. 66.  MRI has been increasingly utilized in early stroke since it is more sensitive than CT in the first twelve hours  Bright on Diffusion weighted images (detected as early as 15 to 30 min after vessel occlusion).
  67. 67. CT / MR Perfusion imaging  Concentrates on the assessment of mean transit time (MTT), relative cerebral blood volume (RCBV) and derived relative cerebral blood flow. RCBF = MTT / RCBV  Prolonged MTT is the earliest & most consistent sign of impaired perfusion.  In addition to this, there is a simultaneous drop in RCBV indicating tissue at risk for infarction.
  68. 68. Stroke in Children Constitutes 3% of cerebral infarcts  Most common cause is congenital heart disease. Other causes are vasospasm & vasculitis,  Echo, CT, MRI & catheter angiogram should be performed as and when required.
  69. 69.  There are several advantages to performing a CT scan instead of other imaging modalities. A CT scan: - Is readily available - Is rapid - Allows easy exclusion of hemorrhage - Allows the assessment of parenchymal damage The disadvantages of CT include the following: - Old versus new infarcts is not always clear - No functional information (yet) - Relatively limited evaluation of vertebrobasilar system A CT is 58% sensitive for infarction within the first 24 hours (Bryan et al, 1991). MRI is 82% sensitive. If the patient is imaged greater than 24 hours after the event, both CT and MR are greater than 90% sensitive.
  70. 70. Epidural Hematoma  An epidural hematoma is usually associated with a skull fracture. It often occurs when an impact fractures the calvarium. The fractured bone lacerates a dural artery or a venous sinus. The blood from the ruptured vessel collects between the skull and dura. On CT, the hematoma forms a hyperdense biconvex mass. It is usually uniformly high density but may contain hypodense foci due to active bleeding. Since an epidural hematoma is extradural it can cross the dural reflections unlike a subdural hematoma. However an epidural hematoma usually does not cross suture lines where the dura tightly adheres to the adjacent skull
  71. 71. Cerebral Contusion  Cerebral contusions are the most common primary intra-axial injury. They often occur when the brain impacts an osseous ridge or a dural fold. The foci of punctate hemorrhage or edema are located along gyral crests. The following are common locations: - Temporal lobe - anterior tip, inferior surface, sylvian region - Frontal lobe - anterior pole, inferior surface - Dorsolateral midbrain - Inferior cerebellum
  72. 72. Cerebral Contusion On CT, cerebral contusion appears as an ill-defined hypodense area mixed with foci of hemorrhage. Adjacent subarachnoid hemorrhage is common. After 24-48 hours, hemorrhagic transformation or coalescence of petechial hemorrhages into a rounded hematoma is common.
  73. 73. Diffuse Axonal Injury  Diffuse axonal injury is often referred to as "shear injury". It is the most common cause of significant morbidity in CNS trauma. Fifty percent of all primary intra-axial injuries are diffuse axonal injuries. Acceleration, deceleration and rotational forces cause portions of the brain with different densities to move relative to each other resulting in the deformation and tearing of axons. Immediate loss of consciousness is typical of these injuries. The CT of a patient with diffuse axonal injury may be normal despite the patient's presentation with a profound neurological deficit. With CT, diffuse axonal injury may appear as ill-defined areas of high density or hemorrhage in characteristic locations. The injury occurs in a sequential pattern of locations based on the severity of the trauma. The following list of diffuse axonal injury locations is ordered with the most likely location listed first followed by successively less likely locations: - Subcortical white matter - Posterior limb internal capsule - Corpus callosum - Dorsolateral midbrain
  74. 74. Encephalitis CT scan is often normal , especially early in the disease.  Ill defined hypodense lesions may be seen e.g. temporal lobe changes are predominant in Herpes Encephalitis.  MRI is far more sensitive in the evaluation of patients with encephalitis
  75. 75. Skull Fractures  Skull fractures are categorized as linear or depressed, depending on whether the fracture fragments are depressed below the surface of the skull. Linear fractures are more common. The bone windows must be examined carefully. A skull fracture is most clinically significant if the paranasal sinus or skull base is involved. Fractures must be distinguished from sutures that occur in anatomical locations (sagittal, coronal, lambdoidal) and venous channels. Sutures have undulating margins both sutures and venous channels have sclerotic margins. Venous channels have undulating sides. Depressed fractures are characterized by inward displacement of fracture fragments.
  76. 76. Ventriculitis / Ependymitis  Inflammation and enlargement of the ventricles characterizes ventriculitis. Ependymitis shows hydrocephalus with damage to the ependymal lining and proliferation of subependymal glia. A CT of patients with these conditions reveals the presence of periventricular edema and subependymal enhancement. Ventriculitis and Ependymitis affect approximately 30% of the adult patients and 90% of the pediatric patients with meningitis.
  77. 77. Cerebrovascular Complications of Meningitis  The development of cerebrovascular problems is the most common complication of meningitis. Arterial infarction can occur which often affects the basal ganglia due to the occlusion of small perforating vessels. Hemispheric infarction can also occur due to major vessel spasm. Venous infarctions are also common and can include cortical venous occlusion or the involvement of the superior sagittal sinus.
  78. 78. Subdural Empyema  Subdural empyema is usually due to meningitis, sinusitis, trauma or prior surgery. It is a neurosurgical emergency. Subdural empyema leads to rapid clinical deterioration, especially if it is due to sinusitis. On CT it appears as an isodense or hypodense extra- axial mass. It has a lentiform or crescentic shape. The margin of collection often enhances with contrast material administration due to the presence of granulation tissue or subjacent cortical inflammation.
  79. 79. Extra-axial CNS Infection  Extra-axial CNS infections can cause epidural abscess or subdural empyema. Extra-axial CNS infections account for 20-30% of CNS infections. Fifty percent of extra-axial infections are associated with sinusitis, usually frontal sinusitis. The infection occurs by direct extension or septic thrombophlebitis. Thirty percent of extra-axial infections occur post-craniotomy. Finally, 10-15% of extra-axial CNS infections are related to meningitis. CT findings include a focal fluid collection usually with an enhancing margin in a subdural or epidural location.
  80. 80. Pathophysiology Flow abnormalities - Perfusion Cellular dysfunction – DWI / CT/ MR Structural breakdown – CT / MRI
  81. 81. Ischemic Stroke  Occurs due to obstruction of cerebral arteries or cerebral veins.  The clinical spectrum of ischemia includes TIA (Transient ischemic attacks) RIND (Reversible ischemic neurological deficit) PRIND (partially reversible ischemic neurological deficit) Evolved stroke  Pathophysiology: Normal cerebral blood flow to the brain cortex is approximately 50 to 66 ml/100gm/min. When cerebral perfusion pressure falls below critical levels (<15ml/gm/min) ischemia results. Ischemia produces energy depletion in the affected cells. This results in accumulation of Ca++, Na+ and Cl-, along with osmotically obligated water. This secondary accumulation of water results in the imaging features of stroke such as edema and mass effect.
  82. 82. Hyperdense vessel sign  Seen in 25% of stroke patients.  In patients presenting with clinical deficit referable to the middle cerebral artery territory, the hyperdense vessel sign is present 35-50% of the time.  This sign
  83. 83. Lentiform Nucleus Obscuration  Due to cytotoxic edema in the basal ganglia  Indicates proximal middle cerebral artery occlusion, which results in limited flow to lenticulostriate arteries  Can be seen as early as one hour post onset of stroke.
  84. 84. Insular Ribbon Sign  Loss of the gray-white interface at the lateral margins of the insula.  Supplied by the insular segment of the middle cerebral artery  Particularly susceptible to ischemia because it is the most distal region from either anterior or posterior collaterals  May involve only the anterior or the posterior insula
  85. 85. Diffuse Hypodensity and Sulcal Effacement  Most consistent sign of infarction.  Extensive parenchymal hypodensity is associated with poor outcome.  If > 50% of MCA territory involvement ,there is, on average, an 85% mortality rate. Hypodensity in greater than one-third of the middle cerebral artery territory is generally considered to be a contra-indication to thrombolytic therapy.
  86. 86. Newer Imaging Techniques In Acute Stroke  MR Diffusion imaging:  CT / MR Perfusion imaging  Combined MR perfusion & Diffusion imaging  MR Spectroscopy  Radionucleotide studies
  87. 87. Ventriculitis / Ependymitis
  88. 88. Cerebral Blood flow for Survival Average blood flow : 55ml/ 100gm/ mt Ischemic threshold : 20 ml/ 100gm/ mt Tissue death : <10 ml/ 100gm/ mt Functional failure without cell death: 10-20ml/ 100gm/ mt.
  89. 89. Concept of Ischemic Penumbra Ischemic Insult  Focal core area of infarct (irreversible)  Surrounded by viable neuronal cell on the brink of cell death  “Ischemic Penumbra”   Geographic area of tissue surrounding a profoundly ischemic core. Identified on DWI / per MRI Saving this potential salvageable area leads to significant chance of improvement
  90. 90. Ischemic stroke  Thrombotic stroke  Embolic stroke  Lacunar infarct  Global cerebral hypoperfusion
  91. 91. • Ischemic Stroke (83-85%) • Hemorrhagic Stroke (15-17%)
  92. 92. MRI in Hyperacute Stroke  DWI – Infarct core  FLAIR - SAH , Parenchymal changes  T2* GRE – Intracranial hemorrhage  PWI – Perfusion deficit  MRA – Vessel occlusion
  93. 93. Diffusion Weighted Imaging  Sensitivity : 88 – 100 %  Specificity : 95 – 100 %  Initial diffusion lesion volume correlates well with final infarct volume & neurologic and functional outcome  Multiple a/c lesions in diff.vasc territories in pts. with 1 symptomatic insult …. embolic Neurology.1999 Jun 10;52(9):1784- 1792 Ann Neurol.1997 Aug;42(2):164-170
  94. 94. False Negative DWI Brainstem infarct Deep GM nucleus infarct Neuroradiology2000;42:444–447 Stroke2000;31:1965–1972 AJNR 1999;20:1871–1875 Neurology 1999;52:1784-52
  95. 95. 4 h 24 h Dept. Neurosciences Univ. of Rome La Sapienza
  96. 96. Reversibility of Ischemic lesions on DWI Occlusion of MCA 1 hour - DWI lesion  or resolution Occlusion of MCA 2 hour - Lesion size same or  Radiology 2000;217:331-345 Successful thrombolysis may revert DWI changes
  97. 97. Diffusion changes in TIAs • 29% to 67% will show restricted diffusion • May reverse or persist • Perfusion deficits  Stroke vs TIA DWI lesions of TIA are less intense Stroke 2004;35:1095 AJNR 2004;25:1645-52
  98. 98. Hyperacute Hemorrhage Wiesmann M, et al. Eur Radiol. 2001;11:849-53.
  99. 99. Stroke 2004;35:502-506
  100. 100. Nederkoorn PJ et al. Stroke 2003;34:1324-32
  101. 101. MR Spectroscopy in acute stroke Stroke 2003;34:e82-876 pts within 7 hrs of stroke onset Lactate alone – metabolic injury - Reversible Lactate +  NAA- more severe – Irreversible Lac/Cho ratio from acute lesions improves the prediction of stroke outcome Neurology 2000;55:498
  102. 102. CT Venography
  103. 103. 25 yr old lady c/o fever and altered sensorium x 1 wk. Had 1 episode of GTC seizures. Admitted elsewhere , LP done showed proteins-55 mg % and sugar –105 mg % .. ABG- pH – 7.55 HCO3 – 28.3 , PCO2-32.9, PO2 –322.9,SPO2-99.8 CT – Normal Discharged at request. H/o fever,headache and vomitting on and off x 5 mths -
  104. 104.  O/E – GCS – E1V1M5 BP – 140/100 , PR – 116 Pupils – 4mm dilated , sluggish light reaction Neck Rigidity + Kernig’s & Brudeski’s - ve  Hb-13.5  TC- 12,200  Platelets-4.2  MP/MF – negative  BUN, creatinine – normal  Urine R/E – proteins +++, pus cells 5-8  Coagulation Profile - WNL  134/3.4/26/102
  105. 105. Q qq
  106. 106. HIV Encephalopathy
  107. 107. Thank You
  108. 108. Hyperdense artery •SPECIFICTY 100% •SENSITIVITY 10% TO 50% Seen as early as 90 minutes AJNR 1996; 17:79-85
  109. 109. Hyperdense MCA / Vessel Sign  Persistent large vessel occlusion  Large clot burden  Not a contraindication for i.v. thrombolysis Neurology 2001:57:1603-1610
  110. 110. Infarct VS Tumor
  111. 111. CT Findings in Stroke Hyperacute infarct (<12 hrs)  Normal (50 to 60%)  Hyperdense MCA  Obscuration of lentiform nucleus Acute infarct (12 – 24hrs)  Loss of grey - white matter interface (insular ribbon sign)  Low density basal ganglia  Sulcal effacement.
  112. 112. Hyperdense vessel sign • Indicates poor outcome and poor response to iv - TPA therapy.
  113. 113. CT Findings in Stroke (Contd)… Subacute infarct (1- 7days)  Mass effect  Wedge shaped hypodensity involving grey & white matter  Hemorrhagic transformation.  Gyral enhancement. Chronic infarct ( 1 to 8 weeks)  Encephalomalacic changes  Reduced mass effect
  114. 114. Global Cerebral Hypoperfusion  Consequence of global hypoperfusion.  Common causes are hypotension, cardiac arrest with successful resuscitation, neonatal asphyxia and CO inhalation. Imaging patterns  1) Water shed infarct in the parieto- occipital region & basal ganglia infarcts.  2) Cortical laminar necrosis with hemorrhagic foci in basal ganglia & cerebral cortical gyri.  3) In severe cases “reversal sign” is noted.
  115. 115. Reversal sign
  116. 116. Infarct With Hemorrhagic Transformation
  117. 117. CT VS MRI in the setting of acute stroke  MRI is more sensitive  Diffusion weighted MR images has the highest sensitivity & specificity for acute cerebral infarction.  CT is more sensitive to detect hemorrhage.  CT is more widely available in many institutions.  CT is less expensive  CT is more rapid
  118. 118. CT Angiography  Useful in MCA embolic stroke & predictive of infarction volume in MCA territory  Less useful –deep grey matter & brainstem stroke (Taipei)1999:62:255-260
  119. 119. Subacute SAH  FLAIR + (GRE) T2*-weighted superior to either alone J Neurol Neurosurg Psychiatry.200170(2):205-211
  120. 120. Hypertensive Hemorrhage
  121. 121. Subarachnoid hemorrhage
  122. 122. Combined MR Perfusion & Diffusion Imaging  In hyperacute stage, larger abnormality is noted on the perfusion images than on diffusion weighted images. This diffusion perfusion mismatch is the ischemic penumbra. This is the tissue at risk which would benefit from thrombolysis.
  123. 123. Stroke Protocol Normal Infarct Haemorrhage Diffusion / Perfusion CT Perfusion Intraparenchymal SAH HT Atypical site Angiogr Angiogram Mismatch Matches Angiogr Thrombolysis
  124. 124. To Summarize the Role of CT in Stroke  Haemorrhagic or non-haemorrhagic  Arterial or venous  Territory involved  Acute,subacute or chronic  Assess the mass effect  Exclude Stroke mimics like subdural hematoma, tumors
  125. 125. How the CT study is usually planned…  Thinner sections are studied through the posterior fossa
  126. 126. Hounsfield Units AIR - - 1000 FAT - - 30 to -100 CSF - 0 GREY MATTER - 32 - 41 WHITE MATTER - 23 - 34 ACUTE BLOOD - 56 - 76 CALCIFICATION - 60 - 400 BONE - 1000

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