12 B. CT Brain.ppt
- 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. Indications for CT / MR …….. Stroke Trauma Altered sensorium Neurological deficit Seizures Headache
- 3. How the CT study is usually planned… 15-20 degree angulation to canthomeatal line to decrease radiation to the lens.
- 4. Plain CT Contrast CT
- 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. Brain Window Bone Window
- 18. Descriptive Terms ……. Hypodense / Hypointense Isodense / Isointense Hyperdense / Hyperintense
- 19. Lesions appearing Hypodense on Plain CT Infarct (non hemorrhagic) Edema
- 20. Lesions appearing Hyperdense on Plain CT Hemorrhage Calcifications
- 24. NINDS trial Thrombolysis CT criteria No hemorrhage CT criteria No hemorrhage Parenchymal hypodensity in 1/3 MCA ECASS
- 25. 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.
- 27. 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 %
- 28. Stroke Based on Territory Anterior circulation stroke Embolus : 70% Thrombosis : 30% Posterior circulation stroke Thrombosis : 70% Embolus : 30%
- 30. Normal in 50% of ischemic strokes < 6 hrs
- 31. 2 hrs 24 hrs
- 32. 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
- 33. 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
- 34. 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
- 36. Subacute infarct (1-7 days ) Hemorrhagic transformation in 5-40 % of all ischemic stroke Neurology 2001; 57:1603-1610 Stroke 1999;30:761-764
- 38. Lacunar Infarcts
- 39. Diffusion Weighted Imaging Radiology 2000;217:331-345 Detects Infarct As Early As 15-30 minutes
- 40. 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
- 41. 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)
- 42. 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
- 43. Acute SAH - 100 % Chronic SAH – 63 % Chronic SAH ( CT ) – 46 % Radiology .1995;196(3):773-777 Radiology.1997;203(1):257-262
- 44. 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
- 45. 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
- 46. CT Perfusion If no penumbra…..increased risk of bleed with thrombolysis RCNA 44(2006)41-62
- 50. Can MR replace CT as first imaging modality in hyperacute stroke? Yes MR immediately available Protocol is optimized Skilled personnel
- 51. Unlikely to replace CT ....... • Cost • Limited availability • Time • Lack of evidence that MR has a positive influence on prognosis
- 52. Delta Sign
- 55. 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
- 64. 23 yr old male c/o fever and intense headache
- 65. Ring enhancing lesions – granuloma / abscess Calcifications Cerebritis Meningeal abnormalities Complications
- 67. Differential Diagnosis of Ring Enhancing Lesions Granulomas Brain abscess Tumors – metastasis, glioma Resolving hematoma
- 75. Encephalitis MRI – within 48 hrs CT - at least 3-5 days
- 76. Widely available Cost Quick Hemorrhage Trauma Hyperacute infarcts Posterior fossa Diffuse axonal injuries White matter diseases Subtle abnormalities of neuroparenchyma
- 77. Contraindications for MRI Metallic implants Pacemakers Prosthetic valves Aneurysm clips Claustrophobia
- 78. Thank U
- 81. Epidural Abscess Subdural Empyema Notice the rim enhancing epdural fluid collection (arrowheads) ).
- 82. Encephalitis Diffuse nonfocal brain parenchymal inflammatory process Most common agents - viruses Immunocompetent individuals - Herpes viruses Immunocompromised individuals Human immunodeficency virus (HIV) Cytomegalovirus (CMV) Papovavirus
- 90. SUBACUTE SDH
- 91. ACUTE ON CHRONIC SDH
- 92. CONTUSION SAH
- 93. Complications EARLY ABSCESS SUBDURAL/EPIDUR AL EMPYEMA VENTRICULITIS INFARCTION VENOUS THROMBOSIS LATE SUBDURAL/ EPIDURAL EFFUSION ENCEPHALOMALACIA HYDROCEPHALUS ATROPHY
- 94. SUBDURAL EMPYEMA
- 99. 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.
- 100. Haemorrhagic Stroke Etiology 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
- 101. 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.
- 102. 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.
- 104. 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.
- 105. 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.
- 106. 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.
- 107. Radionucleotide Studies in Acute Stroke SPECT – Tc99m HMPAO PET – O15 Adv – Early detection Limitation - Not widely available
- 108. 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).
- 109. 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.
- 110. 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.
- 111. 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.
- 112. 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
- 113. 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
- 114. 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.
- 115. 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
- 116. 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
- 117. 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.
- 118. 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.
- 119. 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.
- 120. 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.
- 121. 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.
- 122. Pathophysiology Flow abnormalities - Perfusion Cellular dysfunction – DWI / CT/ MR Structural breakdown – CT / MRI
- 123. 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.
- 124. 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
- 125. 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.
- 126. 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
- 127. 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.
- 128. Newer Imaging Techniques In Acute Stroke MR Diffusion imaging: CT / MR Perfusion imaging Combined MR perfusion & Diffusion imaging MR Spectroscopy Radionucleotide studies
- 130. 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.
- 131. 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
- 132. Ischemic stroke Thrombotic stroke Embolic stroke Lacunar infarct Global cerebral hypoperfusion
- 133. • Ischemic Stroke (83-85%) • Hemorrhagic Stroke (15-17%)
- 134. MRI in Hyperacute Stroke DWI – Infarct core FLAIR - SAH , Parenchymal changes T2* GRE – Intracranial hemorrhage PWI – Perfusion deficit MRA – Vessel occlusion
- 135. 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
- 136. 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
- 137. 4 h 24 h Dept. Neurosciences Univ. of Rome La Sapienza
- 138. 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
- 139. 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
- 141. Hyperacute Hemorrhage Wiesmann M, et al. Eur Radiol. 2001;11:849-53.
- 147. Nederkoorn PJ et al. Stroke 2003;34:1324-32
- 148. MR Spectroscopy in acute stroke Stroke 2003;34:e82-87 6 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
- 151. CT Venography
- 154. 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 -
- 155. 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
- 157. Q qq
- 160. HIV Encephalopathy
- 162. Thank You
- 163. Hyperdense artery •SPECIFICTY 100% •SENSITIVITY 10% TO 50% Seen as early as 90 minutes AJNR 1996; 17:79-85
- 164. Hyperdense MCA / Vessel Sign Persistent large vessel occlusion Large clot burden Not a contraindication for i.v. thrombolysis Neurology 2001:57:1603-1610
- 165. Infarct VS Tumor
- 167. 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.
- 168. Hyperdense vessel sign • Indicates poor outcome and poor response to iv - TPA therapy.
- 169. 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
- 170. 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.
- 171. Reversal sign
- 172. Infarct With Hemorrhagic Transformation
- 174. 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
- 175. 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
- 176. Subacute SAH FLAIR + (GRE) T2*-weighted superior to either alone J Neurol Neurosurg Psychiatry.200170(2):205-211
- 184. 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.
- 185. Stroke Protocol Normal Infarct Haemorrhage Diffusion / Perfusion CT Perfusion Intraparenchymal SAH HT Atypical site Angiogr Angiogram Mismatch Matches Angiogr Thrombolysis
- 186. 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
- 189. How the CT study is usually planned… Thinner sections are studied through the posterior fossa
- 190. 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