Head ct scan general part one
- 1. Imaging Brain--CT Scan Head By: DR REKHA KHARE MD RADIOLOGY
- 2. When do you need CT scan Head? • Head injury • Stroke • Seizure/ Fit/ epilepsy • Pyrexia of unknown origin • Altered consciousness • Headache- unusual
- 3. How to perform CT? • In order to perform a head CT, the patient is placed on the CT table in a supine position and the tube rotates around the patient in the gantry • In order to prevent unnecessary irradiation of the orbits and especially the lenses, Head CTs are performed at an angle parallel to the base of the skull • Slice thickness may vary, but in general, it is between 5 and 10 mm for a routine Head CT.
- 4. How to read CT scan? • Cranial cross-sectional anatomy is very important to know prior to analyzing a head CT • Symmetry is an important concept in anatomy and is almost always present in a normal head CT unless the patient is incorrectly positioned • Intravenous contrast is not routinely used, but may be useful for evaluation of tumors, cerebral infections, and in some cases for the evaluation of stroke patients, it is Radiologist decision
- 5. Slice 1 A. Orbit B. Sphenoid Sinus C. Temporal Lobe D. External Auditory Canal E. Mastoid Air Cells F. Cerebellar Hemisphere
- 6. Slice 2 A. Frontal Lobe B. Frontal Bone (Superior Surface of Orbital Part) C. Dorsum Sellae D. Basilar Artery E. Temporal Lobe F. Mastoid Air Cells G. Cerebellar Hemisphere
- 7. Slice 3 A. Frontal Lobe B. Sylvian Fissure C. Temporal Lobe D. Suprasellar Cistern E. Midbrain F. Fourth Ventricle G. Cerebellar Hemisphere
- 8. Slice 4 A. Falx Cerebri B. Frontal Lobe C. Anterior Horn of Lateral Ventricle D. Third Ventricle E. Quadrigeminal Plate Cistern F. Cerebellum
- 9. Slice 5 A. Anterior Horn of the Lateral Ventricle B. Caudate Nucleus C. Anterior Limb of the Internal Capsule D. Putamen and Globus Pallidus E. Posterior Limb of the Internal Capsule F. Third Ventricle G. Quadrigeminal Plate Cistern H. Cerebellar Vermis I. Occipital Lobe
- 10. Slice 6 A. Genu of the Corpus Callosum B. Anterior Horn of the Lateral Ventricle C. Internal Capsule D. Thalamus E. Pineal Gland F. Choroid Plexus G. Straight Sinus
- 11. Slice 7 A. Falx Cerebri B. Frontal Lobe C. Body of the Lateral Ventricle D. Splenium of the Corpus Callosum E. Parietal Lobe F. Occipital Lobe G. Superior Sagittal Sinus
- 12. Slice 8 A. Falx Cerebri B. Sulcus C. Gyrus D. Superior Sagittal Sinus
- 13. TRAUMA---Head fracture Examine bone window carefully for linear # : more common depressed # : the fracture fragments are depressed below the surface of the skull. • 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. • Depressed fractures are characterized by inward displacement of fracture fragments
- 14. Skull fracture
- 15. Extra axial/ Intraaxial haemorrhage • Extradural haemorrhage • Subdural haemorrhage • Subarachnoid haemorrhage • Intraventricular haemorrhage • Intracerebral haemorrhage/ contusion
- 16. Subarachnoid haemorrhage • SAH occurs with injury of small arteries or veins on the surface of the brain. The ruptured vessel bleeds into the space between the pia and arachnoid matter • Traumatic cause of SAH occurs over the cerebral convexities or adjacent to cerebral contusion • Non traumatic cause of SAH is the rupture of a cerebral aneurysm particularly in basal cistern ,if so Cerebral Angiography is needed for further evaluation • On CT, subarachnoid hemorrhage appears as focal high density in sulci and fissures or linear hyperdensity in the cerebral sulci.
- 18. Acute subdural haematoma • Deceleration and acceleration or rotational forces that tear bridging veins can cause an acute subdural hematoma. • The blood collects in the space between the arachnoid matter and the dura matter • The hematoma on CT has the following characteristics: - Crescent shaped - Hyperdense, may contain hypodense foci due to serum, CSF or active bleeding - Does not cross dural reflections
- 19. ACUTE SDH
- 20. Sub acute subdural haematoma • Subacute SDH may be difficult to visualize by CT because as the hemorrhage is reabsorbed it becomes isodense to normal gray matter • A subacute SDH should be suspected when there is shift of midline structures without an obvious mass • Giving contrast may help in difficult cases because the interface between the hematoma and the adjacent brain usually becomes more obvious due to enhancement of the dura and adjacent vascular structures • Some of the notable characteristics of subacute SDH are:- Compressed lateral ventricle - Effaced sulci - White matter "buckling" - Thick cortical "mantle
- 21. CHRONIC SDH Chronic SDH becomes low density as the hemorrhage is further reabsorbed It is usually uniformly low density but may be loculated Rebleeding often occurs and causes mixed density and fluid levels.
- 23. Epi/extra dural haematoma • An epidural hematoma is usually associated with a skull fracture. 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.
- 25. Diffuse axonal injury ---Shear injury 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 -- Subcortical white matter ,Posterior limb internal capsule, Corpus callosum and Dorsolateral midbrain
- 27. 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. 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.
- 28. Iintraventricular haemorrhage Traumatic intraventricular hemorrhage is associated with diffuse axonal injury, deep gray matter injury, and brainstem contusion. An isolated intraventricular hemorrhage may be due to rupture of subependymal veins.
- 30. Cerebro-vascular accidents STROKE • Strokes are classified into two major types – • Hemorrhagic strokes are due to rupture of a cerebral blood vessel that causes bleeding into or around the brain. • Ischemic stroke is caused by blockage of blood flow in a major cerebral blood vessel, usually due to a blood clot. • Ischemic strokes are further subdivided based on their etiology into several different categories including thrombotic strokes, embolic strokes, lacunar strokes and hypoperfusion infarctions.
- 31. What is Stroke?
- 32. HAEMORRHAGIC STROKE There are two major categories Intracerebral hemorrhage is the most common, due to rupture of a cerebral aneurysm • Intracerebral Hemorrhage non traumatic cause is hypertensive hemorrhage. • Other causes include amyloid angiopathy, a ruptured vascular malformation, coagulopathy, hemorrhage into a tumor, venous infarction, and drug abuse
- 33. Hypertensive haemorrhage • It is commonly due to vasculopathy involving deep penetrating arteries of the brain. • It has a predilection for deep structures including the thalamus, pons, cerebellum, and basal ganglia, particularly the putamen and external capsule • It often appears as a high-density hemorrhage in the region of the basal ganglia.Blood may extend into the ventricular system
- 35. Coagulopathy related ICH • It can be due to drugs such as coumadin or a systemic abnormality such as thrombocytopenia • On imaging, this hemorrhage often has a heterogeneous appearance due to incompletely clotted blood. A fluid level within a hematoma suggest coagulopathy as an underlying mechanism
- 37. ICH due to arteiovenous malformation • An underlying arteriovenous malformation (AVM) may or may not be visible on a CT scan • However, prominent vessels adjacent to the hematoma suggest an underlyingAVM • In addition, some AVM contain dysplastic areas of calcification and may be visible as serpentine enhancing structures after contrast administration
- 39. Non traumatic SAH Ruptured Cerebral aneurysm Cerebral aneurysms 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
- 40. SAH due to cerebral aneurysm • On CT, subarachnoid hemorrhage appears as focal high density in sulci and fissures or linear hyperdensity in the cerebral sulci • Bleed may extend to ventricle may cause Hydrocephalus
- 41. Ischaemic stroke • Causes could be: Thrombosis, Embolism, Hypoperfusion Lacunar infarctions. • Thrombotic stroke occurs when a blood clot forms in situ within a cerebral artery and blocks or reduces the flow of blood through the artery. • This may be due to an underlying stenosis, rupture of an atherosclerotic plaque, hemorrhage within the wall of the blood vessel, or an underlying hypercoagulable state. • This may be preceded by a transient ischemic attack and often occurs at night or in the morning when blood pressure is low.
- 42. Ischaemic stroke Embolic stroke occurs when a detached clot flows into and blocks a cerebral artery. The detached clot often originates from the heart or from the walls of large vessels such as the carotid arteries. Atrial fibrillation is also a common cause Lacunar infarction occurs when the walls of small arteries thicken and cause the occlusion of the artery. These typically involve the small perforating vessels of the brain and result in lesions that are less than 1.5 cm in size Hypoperfusion infarctions occur under two circumstances. Global anoxia may occur from cardiac or respiratory failure and presents an ischemic challenge to the brain. Tissue downstream from a severe proximal stenosis of a cerebral artery may undergo a localized hypoperfusion infarction.
- 43. Role of Imaging in Stroke • Stroke" is a clinical diagnosis; however imaging is playing an increasingly important role in its diagnosis and management. The most important issue to determine when imaging a stroke patient is whether one is dealing with a hemorrhagic or ischemic event • This has crucial therapeutic and triage implications. • Decisions that must be made concerning therapy are dependent on the diagnosis and may include the following: - Is the patient a thrombolysis candidate and should thrombolytic therapy be used? - Intravenous or intrarterial therapy? - Neurosurgery or neurology patient? In addition about 2% of clinically definite "strokes" are found to be a result of some other pathology such as a tumor, a subdural hematoma or an infection
- 44. Why CT scan is preferred? • There are several advantages to performing a CT scan instead of other imaging modalitie • Advantages of CT scan : Is readily available Is rapid Allows easy exclusion of hemorrhage Allows the assessment of parenchymal damage Disadvantages of CT: - Old versus new infarcts is not always clear - No functional information (yet) - Limited evaluation of vertebrobasilar system
- 45. CT Pathophysiology • After a stroke, edema progresses, and brain density decreases proportionately. Severe ischemia results in a 3% increase in intraparenchymal water within 1 hour. This corresponds to 7-8 Hounsfield Unit decrease in brain density. There is also a 6% increase in water at 6 hours. The degree of edema is related to the severity of hypoperfusion and the adequacy of collateral vessels.
- 46. Common CT signs of ischaemia/ Infarction One of the first findings to look for is the presence or absence of hemorrhage.
- 48. Hyperdense Vessel Sign Dense MCA sign • A hyperdense vessel is defined as a vessel denser than its counterpart and denser than any non-calcified vessel of similar size • 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 indicates poor outcome and poor response to IV-TPA therapy.
- 49. Basilar thrombosis • Thrombosis of the basilar artery is a common finding in stroke patients. • CT findings include a dense basilar artery without contrast injection
- 50. Lentiform Nucleus Obscuration • Lentiform nucleus obscuration is due to cytotoxic edema in the basal ganglia. This sign indicates proximal middle cerebral artery occlusion, which results in limited flow to lenticulostriate arteries. • Lentiform nucleus obscuration can be seen as early as one hour post onset of stroke
- 51. Insular ribbon sign • Loss of the gray-white interface in the lateral margins of the insula. • This area is supplied by the insular segment of the middle cerebral artery and is particularly susceptible to ischemia because it is the most distal region from either anterior or posterior collaterals.
- 52. Obscured lentiform nucleus Insular ribbon sign
- 53. Diffuse Hypodensity and Sulcal Effacement • Diffuse hypodensity and sulcal effacement is the most consistent sign of infarction. • If this sign is present in greater than 50% of the middle cerebral artery territory 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.
- 54. Acute infarct on CT scan
- 55. CT scan in subacute infarction 1 -3 days: - Increasing mass effect - Wedge shaped low density - Hemorrhagic transformation After 4 - 7 days: - Gyral enhancement - Persistent mass effect In 1-8 weeks: - Mass effect resolves - Enhancement may persist
- 56. Enhancement in infarction • Ninety percent of infarcts enhance on CT examinations with intravenous contrast at 1 week after the infarct. • Faint enhancement begins near the pial surface or near the infarct margins. • The enhancement is initially smaller than the area of infarction. It subsequently becomes gyriform. • Enhancement is due to breakdown of the blood brain barrier, neovascularity, and reperfusion of damaged brain tissue
- 57. Hyperintensity on MRI = Irreversible changes
- 58. Stroke on CT & MRI Haemorrhage is seen better on CT but can be seen on gradiant scan
- 59. MRI Quick Basic sequences • T2 weighted: Plain axial ( T2 FSE) • FLAIR sequence: Axial • Diffusion-weighted imaging (DWI) : Axial • Susceptibility weighted imaging (SWI): Axial
- 60. MRI Sequence for stroke signal intensity
- 61. HAVE A NICE DAY THANK YOU