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Premium member Presentation Transcript Craniocerebral trauma: Craniocerebral trauma Major Dhanalakshmi B 18 Oct 10 1Slide 2: CNS injuries remain the leading cause of morbidity and mortality for young people throughout the world. 2Slide 3: Neuroimaging is fundamental to the diagnosis and management of patients with traumatic brain injury The choice of imaging depends on the specific pathology that we are dealing with 3CLASSIFICATIONS: CLASSIFICATIONS Based on the AREA of involvement -Focal -Diffuse Based on the TYPE of injury -Primary( Fractures, Extracerebral lesions and Intraaxial lesions) -Secondary(complications like hydrocephalus, infarction etc) 4Slide 5: Based on the type of TRAUMA -Blunt -Penetrating Based on the PATHOLOGY Most useful classification 5Slide 6: Fractures Intra cerebral Hematoma Epidural Hematoma Subdural Hematoma Subarachnoid Hematoma Contusions Diffuse Axonal (Shear) Injury Brain swelling and Edema Penetrating Injury Vascular Injury 6IMAGING MODALITIES: IMAGING MODALITIES Skull Radiography Computed Tomography Cerebral Angiography Magnetic Resonance Imaging Other Imaging Modalities 7CT SCANS: CT SCANS Primary modality for investigating Acute Head trauma Rapidly demonstrates surgically correctable lesions, fractures and sub arachinoid hemorrhages Delineates acute hemorrhage from brain edema Determines whether hematoma is intracerebral or extracerebral 8PROTOCOL: PROTOCOL 10 mm sections without inter slice gap taken at an angle of 15 to 20 degrees to the cantho meatal line and parallel to the skull base Posterior fossa – 5 mm slices to reduce beam hardening effects 9Slide 10: 3 different window setting for -Soft tissues( infarct and hemorrhage) -Extracerebral spaces( detect hematomas) -Bone for detection of fractures IV contrast usually not required except when there is considerable mass effect and normal plain study and to pick up small lesions and isodense SDHs. Skull base fractures need direct coronal scans or coronal reconstructions( slice thickness should be less than or equal to 3 mm) 10MRI: MRI Better for subacute and chronic cases. Better than CT for DAI, non hemorrhagic contusions and SDHs and equivalent to CT for hemorrhagic Contusions New non ferromagnetic ventilators compatible with MRIs Disadvantages include long scan time, inability to detect fractures, SAH and hyperacute hemorrhage 11TECHNIQUE: TECHNIQUE Conventional T1 and T2 weighted spin echo sequences used Proton density and T2 weighted sequences useful for non hemorrhagic lesions like contusions( sensitive to extracellular water) T2* Gradient recalled echo highly sensitive for small acute and chronic hemorrhagic lesions Fast spin echo helpful in saving time in acute trauma but not as sensitive as standard spin echo 12Slide 13: Advantages of MRI include multiplanar capability and superior contrast resolution Sagittal T1 weighted and axial T2 weighted sequences supplemented with T2* GRE sequence is the best combination 5 mm slice thickness with a 2.5 mm gap and a 256 x 192 matrix 13FRACTURES: FRACTURES TYPES SIMPLE FRACTURES ( Linear) linear, although they may be irregular, particularly if due to a sharp direct blow. When acute, they are typically well defined, and appear as fine lines of decreased density . They sometimes branch, and must be distinguished from vascular markings, including the groove in the squamous temporal bone caused by a deep temporal artery. 14Slide 15: DIFFERENCES FROM VASCULAR MARKINGS Acute fractures are usually straighter, more angulated, more radiolucent and do not have corticated margins. A fracture passing through a sinus or air cell is effectively compound, and of much greater potential significance than a simple fracture. Fractures may be associated with widening (diastasis) of one or more sutures, particularly the lambdoid 15Slide 16: Bilateral vault fracture, with fluid level in sphenoid sinus (open arrow). Two fracture lines are seen; the more anterior (upper on this film) is better defined and is therefore on the side nearer the film. Apparent islands of bone within (small arrows) are typical of an acute fracture. (Brow-up.) 16Slide 17: 17Slide 18: 18Slide 19: 19Depressed Fractures: Depressed Fractures A direct blow may depress a fragment of bone. On plain skull film, one border of the fragment appears dense where it overlaps the adjacent bone, and a projection at right angles shows a dense bony flake lying beneath the cranial vault. Unlike demonstration of simple linear fractures, this observation has important therapeutic consequences, and should not be overlooked. CT is particularly effective at demonstrating depressed fractures provided bone windows are used. Usually there is a focal contusion in the underlying cerebral cortex (a coup contusion). 20Slide 21: Stellate depressed fracture produced by a direct blow. Lateral (A) and half axial (B) projections: the former shows the typical appearance of a dense flake deep to the skull vault. Note fracture line running vertically from bottom of figure in both A and B. 21Slide 22: Majority of these injuries are managed conservatively Depressed fractures adjacent to venous sinuses are left intact due to fear of bleeding. 22Slide 23: The arrow points to the presence of a comminuted fracture involving the left frontal bone with a significant degree of depression. Note that the adjacent portion of the frontal sinus is also partially opacified indicating its involvement. 23Slide 24: 24Slide 25: Comminuted depressed fracture of the left parietal bone by more than the thickness of the calvarium itself. Associated with underlying haemorrhagic contusion and air. 25BASILAR FRACTURES: BASILAR FRACTURES Fractures of the skull base often are manifest on plain films only as fluid and fluid levels representing bleeding or leakage of cerebrospinal fluid, particularly in the sphenoid sinus and petromastoid air cells. Air may also be seen within the cranium. If sharply defined, lying superficially, adjacent to the midline or the expected position of the fractured sinus, it is usually extradural; it may be very extensive when subdural. 26Slide 27: Diffuse air, in bubbles, or outlining the brain, is more likely to be subarachnoid, in which case the leptomeninges have been torn. Purely intraventricular air is uncommon but can be severe, with acute hydrocephalus. CT can also be extremely helpful in assessment of fractures of the skull base, including the petrous bone, where it may also reveal ossicular dislocation, a treatable cause of traumatic hearing loss. Thin section CTs (1–3 mm) are recommended. 27Slide 28: Important clinical signs of skull base fracture include CSF rhinorrhea or otorrhea, battle's sign, raccoon eyes, hemotympanum or cranial nerve palsy (7th or 8th). The arrow in this image points to an occipital bone fracture. Additional air fluid levels are noted within the maxillary sinus on the left as well as air within the left infra-temporal fossa and subcutaneous air involving the left eyelid. 28Slide 29: On the first image, there is a fracture through the left occipital bone. On the second image, a haemorrhagic contusion is seen in the cerebellum. 29Petrous temporal bone : Petrous temporal bone Petrous temporal bone fractures can be divided into transverse and longitudinal. They may be associated with post traumatic deafness; the transverse fracture is the more severe in this respect. 30Slide 31: Note the longitudinal petrous bone fracture. The peripheral fracture margins are arrowed. Note also the blood in the sphenoid sinuses, consistent with a basal skull fracture. 31Slide 32: Unenhanced, axial scans: A fracture perpendicular to the longitudinal axis of the petrous bone is visualized in the bone window scan of the skull base The mastoid cells are obscured, which points to haemorrhage 32PARANASAL SINUS FRACTURES: PARANASAL SINUS FRACTURES Posterior wall of the frontal sinus require surgical closure due to disrupted dura to prevent CSF leak. Comminuted ones are treated surgically Fractures of cribriform plate associated with anosmia. 33Slide 34: The arrow points to the presence of a mildly depressed fracture involving the anterior wall of the left maxillary sinus with a small associated air fluid level. The complete opacification of the right maxillary sinus may be as the result of blood in the setting of trauma or may be due to extensive sinus mucosal disease. Air within the infero-temporal fossae bilaterally (arrow heads) is most likely the result of paranasal sinus fracture. However extension from any other focus of subcutaneous air is possible 34Pneumocephalus: Pneumocephalus Air locules usually indicàte traumatic air entry from fracture of paranasal sinus or mastoid air cells. Complications like meningitis, CSF leak and empyema are seen. 35Slide 36: Pneumocephalus (small arrow) with associated intraparenchymal fractured fragment (double arrow) 36Slide 37: Intracranial air over frontal lobes, in suprasellar region and over left temporal lobe. Left temporal haematoma and air in soft tissue over left temporal area. 37GROWING FRACTURES: GROWING FRACTURES Growing fractures (leptomeningeal cysts) usually occur after severe head injuries early in life. The dura mater underlying a linear fracture is torn, often with laceration of the underlying brain. Exposure of the remodelling bone to pulsation of the cerebrospinal fluid (CSF) results in progressive widening of the fracture line over weeks or months. CT is very satisfactory for the investigation of growing fractures, because it also shows the changes in the underlying brain, which is seen to herniate through the skull defect. A prominent porencephalic cyst or focal dilatation of the lateral ventricle usually underlies the fracture, and on rare occasions may even communicate through it with an extracranial fluid collection. 38Slide 39: 39INTRACEREBRAL HEMATOMA: INTRACEREBRAL HEMATOMA Distinguished from hemorrhagic contusions by -Homogenous hyperdensity -Sharply marginated -Surrounded by a rim of decreased density Common sites are frontal and temporal lobes Frequently associated with other lesions like SAH Appear within 48 hours following the injury 40Slide 41: Delayed appearance (more than 48 hours) due to: -Focal loss of autoregulation -Surgical evacuation of lesions like SDH with loss of tamponade effect 41Slide 42: Acute haemorrhage appears as increased radiographic density on CT and reaches around 100 HU. Its CT density depends on the initial haemoglobin level, dilution by extracellular fluid and partial volume effects. Very rarely haematomas can be isointense to the surrounding brain, in severely anaemic patients with a haematocrit of 20% or less. Calcified and highly proteinaceous material can reach a similar density to fresh blood clot, but the clinical context usually suggests the diagnosis. Contrast enhancement of tumours can also render them of similar density, so that CT is always performed without contrast medium if haemorrhage is possible 42Slide 43: An acute intracerebral clot is usually rounded and of homogeneous radiodensity. There is typically no oedema around a fresh clot and a fine rim of low density indicates clot retraction . In deep-seated or extensive intracranial haemorrhage, blood frequently leaks into the ventricles where it may adhere to the ependyma or to the choroid plexus; alternatively, it can sink to the most dependent part of the ventricular system, usually the occipital horns, forming a fluid level within the ventricular fluid. 43Slide 44: Over the course of several days, an untreated haematoma becomes less radiodense, from the periphery towards the centre, and therefore appears smaller. Vasogenic oedema may develop in the surrounding white matter, and should IV contrast medium be given at this stage, it usually produces a halo of enhancement. After several weeks, the CT density of the blood products can be similar to that of the brain or CSF. 44Slide 45: The single arrow points to the presence of an area of intraparenchymal hemorrhage. Note the associated frontal bone fracture. The arrow heads point to soft tissue densities within the scalp bilaterally representing the presence of scalp hematoma. 45Slide 46: 46Slide 47: CT examination: Unenhanced, axial scans: In the thalamic region on the right side, a small hyperdense lesion can be seen (arrow). In the picture on the right side, a large hyperdense lesion can be seen (arrows) in the left hemisphere, in the region of the basal ganglia. The space-occupying is obvious, the left lateral ventricle is compressed, and the midline structures are dislocated to the right (double arrow). 47Slide 48: The MRI appearance of intracerebral haemorrhage tends to follow a certain time-course, in which the presence of various haemoglobin degradation products and red cell lysis play important roles. As the haematoma ages, haemoglobin passes through a number of paramagnetic breakdown products, which include Deoxyhaemoglobin methaemoglobin haemosiderin; the latter is taken up by macrophages. 48 MR signal characteristics of intracerebral haemorrhage (according to Bradley) : MR signal characteristics of intracerebral haemorrhage (according to Bradley) Stage Form of haem iron T1-weighted MRI T2-weighted MRI Hyperacute (first few hours) Oxyhaemoglobin Iso- or hypointense Slightly hyperintense Acute (1–3 days) Deoxyhaemoglobin Slightly hypointense Hypointense Early subacute (3–7 days) Intracellular methaemoglobin Hyperintense Hypointense Late subacute (1–4 weeks) Extracellular methaemoglobin Hyperintense Hyperintense Chronic Haemosiderin Iso- or hypointense Markedly hypointenseSlide 50: (A) Red cells containing oxyhaemoglobin (O), which gives signal similar to brain on both T1- and T2-weighting, are extravasated. (B) The oxyhaemoglobin in some of the cells at the centre of the clot is converted to deoxyhaemoglobin (DE), giving lower signal on T1-weighted images. The clot is now surrounded by a variable amount of cerebral oedema (small circles). which gives nonspecific increased signal on T2-weighted images. (C) Most of the hemoglobin is now converted to methaemoglobin (M), which gives high signal on both T1- and T2-weighted images: however, lower signal due to the continued presence of deoxyhaemoglobin (DE) may still be evident centrally. Progressive lysis (interrupted outline) of the red cells is occurring. Surrounding oedema may become more extensive. (D) The red cells have now broken down, leaving a post-haemorrhagic cyst. This still contains methaemoglobin (M), and returns high signal on all the commonly used sequences. The oedema around the clot has resolved, but the macrophages (circles with 3 engulfed particles) which surround the cavity contain haemosiderin granules (H) which, because of susceptibility effects, give markedly reduced signal with T2-weighting and, to a lesser extent, on T1-weighted images. Persistence of high signal from methaemoglobin and low signal from haemosiderin is variable, but in some patients these effects can be seen for many months after documented bleeding. 50Slide 51: Gradient-echo, or T2*-weighted sequences are much more sensitive than conventional or fast spin-echo sequences to the magnetic field inhomogeneities induced by the presence of paramagnetic breakdown products of blood. These field inhomogeneities cause signal loss, which frequently appears larger than the extent of the actual haemorrhage. T2*-weighted gradient-echo sequences therefore have a greater sensitivity for detecting both acute and old haemorrhage (deoxyhaemoglobin and haemosiderin, respectively). Acute haematomas are still mainly investigated by CT. 51Slide 52: Extreme hypointensity in acute stage is due to Preferential T2 Proton Relaxation Enhancement of intracellular deoxyhemoglobin (PRT2PRE) Mechanism of relaxation for methhemoglobin is Proton-Electron Dipole-Dipole Relaxation Enhancement (PEDDRE). FSE not as sensitive as standard spin echo sequences. 52TRAUMATIC HAEMORRHAGE : TRAUMATIC HAEMORRHAGE Trauma may cause bleeding into the scalp, between the cranial vault and the dura mater (extra- or epidural), between the dura and arachnoid mater (subdural), or into the subarachnoid space, brain or ventricular system. The objective aim of imaging in the acute stage is to identify patients with intracranial bleeding requiring surgery; CT is the imaging procedure of choice, rather than MRI, as haematomas are about the most readily recognizable abnormality on plain CT. 53Slide 54: 54EXTRADURAL HAEMATOMAS : EXTRADURAL HAEMATOMAS Extradural haematomas are commonly due to bleeding from the middle meningeal artery, and plain skull films and CT scout views frequently show a fracture crossing the groove of that vessel in the temporoparietal region. The acute extra- or epidural haematoma is a relatively stereotyped lesion . Because the dura mater tends to adhere to the skull, the haematoma is seen on CT sections as a dense area immediately beneath the skull vault, convex towards both the brain and the vault. 55Slide 56: The temporoparietal convexity is the most common site(Axial images) Frontal, vertical and posterior cranial fossa collections (coronal images shallow extradural haematomas may be overlooked, especially when adjacent to contused or haemorrhagic brain. Wide window CT images may help distinguish the intermediate density of the clot from bone and underlying brain. 56Slide 57: Acute epidural haematoma; CT with intermediate window display. Large biconvex right temporal epidural collection. Note the effacement of the right temporal horn and lack of visualization of suprasellar cistern, compatible with tentorial herniation. 57Slide 58: ACUTE- Heterogeneous in attenuation with areas of hyperdense blood and isodense serum SUBACUTE- Homogeneously hyperdense with solid blood clot CHRONIC- Heterogeneous or decreased attenuation with an enhancing membrane Tend to regress spontaneously Criteria for conservative treatment Diameter less than 1.5 cms Midline shift less than 2 mm 58Slide 59: Note the biconvex hyperdense area (arrows). The blood collection is between the skull and dura. It crosses dural attachments, but not sutures. The etiology is secondary to a lacerated meningeal artery or dural sinus. The Subdural windows may help to discern extra-axial collections such as blood in this case 59Chronic Frontal epidural Hematoma: Chronic Frontal epidural Hematoma 60Slide 61: 61Slide 62: This example shows a more unusual, lower location. Note also the gas within the haematoma - this indicates a basal skull fracture or, as in this case, it is post surgical. Note also the dilated lateral ventricle on the opposite side. 62Slide 63: MRI allows distinction between EDH and SDH in tough cases Not recommended routinely Dura is seen as a band of decreased signal intensity between the hematoma and the brain parenchyma Can distinguish arterial and venous bleeds Good for Posterior fossa hematomas as no beam hardening artifacts 63Slide 64: Acute epidural haematoma; MRI in a neonate with traumatic delivery. (A) Axial T1-weighted image (750/16). Slightly hyperintense epidural collection (arrow) in the right temporal region. (B) Axial T2-weighted image (3000/120), epidural collection is hypointense and is invisible except for deformation of the underlying cortex. This is the MR signature of deoxyhaemoglobin. 64SUBDURAL HEMATOMA: SUBDURAL HEMATOMA Subdural bleeding often, but not always, is associated with damage to the brain, and arises from rupture of veins which cross the subdural space; vault fractures are less commonly present Acute subdural haematomas are also radiodense on CT and peripherally situated, being more or less crescentic, i.e. concave on their deep surface. This is because the blood within them, while under less pressure, is less restricted and tends to spread out over the surface of the brain very extensive subdural bleeding may extend over an entire cerebral hemisphere. 65Slide 66: The high morbidity of these lesions, particularly in the aged, is due in large part to the associated Swelling contusion laceration of the underlying brain. It is often evident that midline displacement is greater than would be accounted by the mass of the haematoma alone. Dilatation of the contralateral ventricle is a bad prognostic sign. 66Slide 67: Acute subdural haematoma, 85-year-old woman; CT. Heterogeneous density of irregular shape occupies extra-axial space overlying the left cerebral convexity. There is moderate mass effect exhibited by effacement of convexity sulci and midline shift with subfalcial herniation. This required surgical decompression 67Slide 68: 68Slide 69: Acute SDH need not always be classically homogeneously hyperdense. Other patterns may be: Marginal hypodensity Central irregular area of hypodensity Laminar area of hypodensity Low density is due to unclotted blood or CSF. 69Slide 70: CT examination: Unenhanced, axial scans: An inhomogenous, extremely hyperdense, sickle-shaped haematoma is visible (arrow) on the left side temporally, between the brain convexity and the inner surface of the skull bone (subdural haematoma). Beside this a right frontal (black arrow), frontotemporal linear fracture (double arrow) and small intracerebral haematoma caused by contusion are visible. ( => picture ) 70Slide 71: SDH s located adjacent to the tentorium may simulate an intra axial lesion Distinguishing points are (Supratentorial) -Well defined medial margin corresponding to the edge of the tentorium -Sheet like area of increased density that slopes laterally -Trigone of the lateral ventricle is rotated anteriorly and superiorly Coronal CT sections may be useful in distinguishing supra- and infratentorial bleeding. 71Slide 72: Trauma. CT. A biconvex density of blood over the left cerebellar hemisphere indicates an extradural haematoma (thick arrow). A crescent of fresh subdural blood spreads over the left temporal lobe and tracks along the tentorium (arrowhead); this feature differentiates it from an extradural. Typical sites of haemorrhagic contusions are seen; gyrus recti and temporal lobe. 72Slide 73: The interhemispheric subdural haematoma extends along the falx cerebri and may spread onto the tentorium, giving a characteristic comma shape on axial CT sections May be confused for a SAH which has a zigzag configuration confirming to the cortical sulci 73SUBDURAL HEMATOMA ALONG THE FALX CEREBRI : SUBDURAL HEMATOMA ALONG THE FALX CEREBRI The arrow head points to the presence of hyperdense blood interdigitating within the sulci. The arrow points to the presence of an acute subdural hematoma which has collected between the leaves of the falx. The double-stemmed arrow points to the presence of a symmetric scalp soft tissue density for a hematoma. 74Slide 75: Sub- or extradural collections low in the posterior cranial fossa, which may be life-threatening, may be overlooked, and the presence of unexplained hydrocephalus after acute head injury should prompt thorough examination of that region. The CT density of the blood in a subacute subdural haematoma slowly decreases: as a rule of thumb, it remains denser than the brain for 1 week, is less dense after 3 weeks. an interim period of up to 2 weeks when it may be ‘isodense’ with brain. Not all isodense haematomas are subacute an acute bleed can be isodense in a very anaemic patient if there is continued leakage of venous blood, a chronic haematoma may not be of low density.Slide 76: Indirect signs midline shift, with compression of the ipsilateral ventricle; contralateral ventricular enlargement effacement of cerebral sulci medial displacement of the junction between the white and grey matter (‘buckling’). (Some of these signs may be absent if there are bilateral collections; the frontal horns may then lie closer together than normal, giving a ‘rabbit’s ear’ configuration) Intravenous contrast medium, by highlighting the vessels on the surface of the brain, may remove any doubts about the extracerebral location of the lesion. 76Slide 77: Bilateral isodense subdural haematomas on contrast-enhanced CT. The ventricles (A) are slit-like and displaced medially, giving a ‘rabbit’s ears’ appearance. A higher section (B) indicates that the normal grey-white interface lies too near the midline; the cortex appears abnormally thick. On close inspection, both sections show cortical vessels (arrows) displaced away from the cranial vault. 77Slide 78: Subacute right subdural haematoma: CT. The lesion is less dense than brain but denser than CSF; it is denser posteriorly. Displacement of midline structures is greater than would be expected from the size of the lesion, suggesting extensive swelling of the underlying hemisphere. The contralateral (left) ventricle is dilated. 78CHRONIC SDH: CHRONIC SDH Chronic SDHs are usually caused by trauma but the episode is usually so trivial that it is forgotten Seen in the older age group and can present with change in personality 79Slide 80: On CT, chronic subdural collections assumed a biconvex form density is less than that of brain, approaching that of CSF Fluid/fluid levels may be seen between denser blood elements in the more dependent portions and serous fluid above, particularly if haemorrhage has been repeated membrane on their deep surface frequently shows contrast enhancement which is capillary rich and prone to repeated episodes of bleeding 80Slide 81: Chronic left subdural collection: CT. The extracerebral collection is of CSF density; underlying sulci are effaced. 81Slide 82: less useful in the acute stages of trauma but is the preferred imaging technique for assessing damage to the underlying brain Subdural haematomas display the temporal evolution of signal intensity as has been previously described in intracranial haemorrhage. They have a convex cerebral surface on coronal images. In the subacute and chronic phase, MRI is probably the most accurate imaging method to detect the smallest subdural haematomas, mainly due to its multiplanar capability. 82 MRISlide 83: 83Slide 84: Axial T1-weighted MRI image shows subacute subdural haematoma in left frontoparietal region and acute subdural haematoma in left anterior frontal (white arrows). Note large lateral ventricles and the shrunken right cerebral cortex. 84SUBARACHNOID HEMORRHAGE: SUBARACHNOID HEMORRHAGE Subarachnoid haemorrhage commonly follows severe head injury and, if diffuse, may render the basal cisterns isodense with brain, simulating cisternal compression Caused by damage to the blood vessels of the pia arachnoid CT is the modality of choice due to the hyperdensity of clotted blood Difficult to visualise on MRI due to high oxygen content CSF prevents degradation of oxyhemoglobin 85Slide 86: CT is positive in over 90% of cases if the scan is carried out within a few days of the haemorrhage. On CT, the hallmark of recent SAH is increased density of the cerebrospinal fluid spaces. As in all blood clots, haemoglobin is the main determinant of detectability : a few red cells in the subarachnoid space will not be detected, but once the haematocrit of the fluid increases by a few per cent, increased radiodensity is evident 86Slide 87: The blood can flow freely, and with profuse bleeding the entire intracranial subarachnoid space may be opacified, with reflux or breakthrough into the ventricular system. If the CT scan is negative and there is a strong clinical suspicion of SAH, a lumbar puncture has to be performed, which may show evidence of acute haemorrhage or xanthochromia and confirm the diagnosis. 87LEFT FRONTAL HEMORRHAGIC CONTUSION. RIGHT TRAUMATIC SUBARACHNOID HEMORRHAGE : LEFT FRONTAL HEMORRHAGIC CONTUSION. RIGHT TRAUMATIC SUBARACHNOID HEMORRHAGE The single arrow head points to an area of hemorrhagic frontal contusion. The arrow points to acute blood interdigitating within the sulci of the occipito-parietal region. This is traumatic subarachnoid hemorrhage. Nontraumatic subarachnoid hemorrhage should always be considered to be secondary to a ruptured aneurysm or hemorrhage from an A-V (arteriovenous) malformation and necessitates an angiogram for confirmation. 88 SAH: SAH 89Slide 90: This patient was semiconcious with subarachnoid bleeding. The filling in of the sulci over the cerebral hemispheres was subtle (not shown), but the clue is visible on this image; there is abnormal increased attenuation due to fresh blood in the 4th ventricle, which has settled posteriorly. The prepontine cistern is also indistinct and may contain blood. 90 MRI: MRI Conventional spin-echo MR sequences are much less reliable than CT in detecting acute SAH. The sensitivity of MRI for the presence of blood in the subarachnoid space can, however, be considerably increased by using a FLAIR sequence. On the FLAIR sequence the signal from cerebrospinal fluid is nulled and appears normally black but blood-stained fluid produces an area of high signal. 91Slide 92: Subarachnoid haemorrhage. (A) CT shows blood in the right Sylvian fissure and in the interhemispheric fissure. This appears of high signal intensity on the fluid-attenuated inversion recovery (FLAIR) MRI (B), as opposed to the normal CSF which appears dark. A 3D TOF MRA (C) shows a right middle cerebral artery aneurysm (double arrow), which has bled, and an incidental ophthalmic artery aneurysm (single arrow); both are confirmed with DSA. 92Slide 93: T2-weighted image shows slight swelling of the gyri in the corresponding region of subarachnoid hemorrhage. 93 FLAIR image is the most sensitive for subarachnoid hemorrhage and demonstrates the area of subarachnoid hemorrhage (arrow).CONTUSIONS: CONTUSIONS Traumatic intracerebral bleeding is usually haemorrhagic contusion . In general, a focal, well-defined, rounded area of abnormal CT density or MRI signal in the brain represents a blood clot, but usually there are multiple areas of altered density or signal indicating blood, surrounded by low density or signal change suggestive of oedema. These often seem to enlarge in the first few days 94Slide 95: The common sites of haemorrhagic contusion are the inferior frontal and anterior temporal lobes and the bleeding is often subcortical. Contrecoup injuries , with the haemorrhage diametrically opposite the point of impact, with or without a fracture, are classical. Less commonly, deeper haemorrhages occur. Occasionally they can be large and resemble spontaneous haemorrhage, though usually other signs of injury are present as well 95Slide 96: Depressed skull fracture with parenchymal contusion. (A,B) CT, ‘brain and bone windows’. Large depressed fragment of the right temporal bone, with underlying irregular hyperdensity representing temporal lobe contusion 96Slide 97: It may be difficult to pick contusions in the posterior fossa due to beam hardening artifacts Sometimes lesions are not visible and can be identified only by indirect signs MRI studies are equivalent to CT in picking hemorrhagic contusions but are more sensitive for non hemorrhagic contusions. Same pattern of evolution as ICH Also more sensitive for lesions in the posterior fossa and subacute and chronic lesions 97RIGHT FRONTAL HEMORRHAGIC CONTUSION : RIGHT FRONTAL HEMORRHAGIC CONTUSION The arrowhead points to a punctate area of intraparenchymal hemorrhage which does not demonstrate significant mass effect. Please note the symmetry of the frontal horns of the lateral ventricles as well as the midline position of the third ventricle. The Sylvian fissures are also well characterized bilaterally. 98Slide 99: There is a focal area of haemorrhagic contusion in the right frontal lobe, with surrounding low density due to infarction or oedema. This is a frequent location for a contre-coup injury following a blow to the back of the head. 99Slide 100: This T1-weighted coronal image shows a heterogeneous-appearing lesion in the left temporal lobe with mass effect, consistent with a cerebral contusion. The caudate nucleus also appears atrophic. 100DIFFUSE AXONAL INJURY: DIFFUSE AXONAL INJURY Diffuse axonal injury (DAI) involves predominantly the white matter, including the corpus callosum. poor prognosis Most of the damaged white matter appears normal on CT and MRI, though patchy changes in regional mean diffusivity have been reported in diffusion tensor MRI only in research settings at present. What may be seen on clinical images are smaller foci of accentuated damage, which are haemorrhagic pathologically but often appear nonhaemorrhagic on CT or MRI. They are due to a shearing injury with rupture of small intracerebral vessels, and in a comatose patient with no other obvious cause they imply a severe diffuse brain injury with a poor prognosis. 101Slide 102: In acceleration injury the head is put into motion from a stand still position, as a result of which the different layers of the brain travels at different velocities with shearing effects and rotation of the brain within the skull. The shearing stresses between different layers of the brain result in petechial haemorrhages as well as diffuse axonal injury involving the white matter and brain stem.Slide 103: They occur in juxtacortical white matter especially in the parasagittal regions posterior corpus callosum low centrum semiovale upper midbrain. 103Slide 104: Diffuse vascular injury is more severe, and there are usually multiple basal haemorrhages. These marker lesions of DAI are of low density on CT and high signal on T2 weighted MRI unless modified by haemorrhage. Gradient-echo MRI may help identify older lesions as being of traumatic origin by demonstrating persistent haemosiderinSlide 105: This image demonstrates a small petechial haemorrhage in a typical location at the grey-white matter interface (arrow). As is often the case, there were multiple such lesions on other slices 105Slide 106: Axial and sagittal T2-weighted MR images. Hyperintensities in the right tectal midbrain, corpus callosum, mainly posterior third, and splenium. 106BRAIN SWELLING AND EDEMA: BRAIN SWELLING AND EDEMA This is of several types in head injury. Probably the commonest is hyperaemic brain swelling, where the brain swells due to an increase in blood volume, not oedema. Grey-white matter contrast is preserved on both CT and MRI and it can be difficult to assess. Slit-like ventricles do not reliably indicate raised intracranial pressure, but effacement of the basal cisterns (especially the chiasmatic) is more reliable. 107Slide 108: Other types of brain swelling are accompanied by CT density or MRI signal changes: oedema due to cortical contusion secondary neuronal injury due to diffuse hypoxic-ischaemic damage or infarction in specific arterial territories. (The latter is often due to severe transtentorial and subfalcine herniation producing cortical infarcts in posterior and anterior cerebral arterial territories, respectively.) MRI especially T2 weighted images are very sensitive to extracellular water and can detect small regions of edema 108Slide 109: If there is an associated increase in density of white matter , it is due to transient hyperemia due to loss of autoregulation Serial CT scans show gradual resolution over 3 to 5 days Cerebral edema is evident as decreased density within and surrounding areas of contusion and hematoma Edema typically appears 24 hours after injury, then increases, becomes maximum at 3 to 5 days and then gradually resolve 109AREA OF DEEP WHITE MATTER EDEMA WITHIN RIGHT PARIETO-FRONTAL REGION : AREA OF DEEP WHITE MATTER EDEMA WITHIN RIGHT PARIETO-FRONTAL REGION 110PENETRATING INJURIES: PENETRATING INJURIES Gunshot wounds are common cause CT can evaluate the position of the missile and the extent of injury Prognosis best when limited to a single lobe Complications like CSF leak, osteomyelitis, abscesses and seizures possible Presence of metal projectiles are relative contraindication for MRI 111Slide 112: Gunshot wound with displaced bony fragments 112OTHER MODALITIES: OTHER MODALITIES Cerebral angiography This is rather unhelpful in assessment of intra-axial lesions. It may show active bleeding from a ruptured artery. Traumatic arterial dissection, or a penetrating injury, may cause aneurysms. 113Slide 114: When intracranial pressure is very high, contrast medium injected into any of the main cervical arteries may fail to enter the head: the usual picture is of a static column of contrast medium in a narrowed artery, from catheter tip to carotid siphon. The grave prognostic significance of such an ‘agonal’ angiogram will readily be appreciated; it has in some countries been accepted as evidence of brain death. This picture must not, therefore, be confused with similar patterns produced by arterial dissection, embolic or arteritic occlusion just beyond the ophthalmic artery, severe catheter-induced spasm or subintimal injection. 114Slide 115: Acute traumatic arterial aneurysm: carotid angiogram, lateral projection. Metallic fragments are seen posteriorly; the vessels around them are stretched and narrowed, and a rounded collection of contrast medium, representing the traumatic aneurysm, is seen (arrow), unrelated to an arterial bifurcation. 115Slide 116: A number of radiological techniques conventional, digital subtraction radionuclide or Doppler angiography CT with IV contrast medium (showing absence of enhancement) have been proposed for diagnosing brain death. In a number of countries, including Britain, the diagnosis of brain death is a clinical one and the role, if any, of imaging tests is to identify a cause of irreversible coma. In some countries, the ‘agonal’ angiogram is used as an indication for terminating life-support therapy. 116VASCULAR INJURIES: VASCULAR INJURIES Traumatic arteriovenous fistulas Whenever an artery and an adjacent vein are injured, the stage is set for an arteriovenous fistula. Recognized sites in the head and neck include: the temporoparietal region (middle meningeal artery) around the transverse venous sinus (dural arteries, including the middle meningeal and occipital) in the scalp (usually involving the superficial temporal artery) in the neck (internal carotid or, more frequently, the vertebral arteries); cavernous sinus, where the internal carotid artery actually lies within the venous system 117Slide 118: Such fistulas frequently cause hypertrophy of feeding arteries and/or draining veins, enlarging, for example, the foramen spinosum and meningeal vascular grooves. An extracranial soft-tissue mass may be present. Traumatic caroticocavernous fistulas most commonly drain to the superior ophthalmic vein, and can enlarge one or both superior orbital fissures. 118Slide 119: In cases of caroticocavernous fistula, CT or MRI may show proptosis, with a markedly dilated superior ophthalmic vein, and the ipsilateral cavernous sinus may also be enlarged. Swelling of the extraocular muscles, due to raised venous pressure, is inconstant, but is frequently the main cause of exophthalmos. 119Slide 120: 120 caroticocavernous fistulaSlide 121: Treatment of large direct communications such as carotico-cavernous or vertebrovertebral fistula is currently by means of detachable balloons introduced during angiography; there is no indication for surgical intervention. Particulate emboli are employed for the more diffuse dural or scalp lesions, and may be combined with surgery 121TRAUMATIC DISSECTIONS: TRAUMATIC DISSECTIONS Magnetic resonance angiogram after traumatic carotid artery dissection causing 50% vessel narrowing of the cervical vessels (arrow), with arterial dissection distal to the narrowing. 122COMPLICATIONS OF CNS TRAUMA: COMPLICATIONS OF CNS TRAUMA HYDROCEPHALUS Diffuse brain injury followed by resolution of edema will lead to dilatation of the ventricles Non communicating hydrocephalus is due to intraventicular hemorrhage leading to obstruction Communicating hydrocephalus is due to decreased absorption of CSF at the arachnoid villi 123Slide 124: 124 2.ATROPHY: 2.ATROPHY Contusions or intraparenchymal haematomas may show remarkable resolution, but more common end results are focal atrophy in more severe cases, extensive softening and cyst formation—encephalomalacia. MRI may show evidence of past haemorrhage. The inferior frontal lobes commonly show evidence of prolongation of T1 and T2 on MRI, or low density on CT. 125Slide 126: Traumatic hemiatrophy , the result of an injury early in life, can affect both the brain and the overlying skull; it may be due to associated vascular damage rather than to direct trauma 126Slide 127: Porencephalic cyst: CT. A CSF-containing cyst communicates with the ventricular system. Such cysts can exert mass effect. 127Slide 128: Cranial hemiatrophy. The left hemicranium is smaller than the right, (arrows indicate the groove for the superior sagittal sinus); the left petrous bone is elevated, and the paranasal sinuses are more extensive on the affected left side. These changes are secondary to impaired growth of the underlying cerebral hemisphere. 1283.INFARCTION: 3.INFARCTION Secondary to vasospasm, vascular occlusion or direct vessel damage On CT, hypodensity or isodense lesion with brain swelling noted MRI more sensitive Hyperintense signals can be picked up between 8 to 24 hours on T2 weighted images when CT may be normal 129Slide 130: Post-traumatic ischemic infarct of both posterior cerebral Aa. 130T2 weighted image: T2 weighted image Acute infarct of middle cerebral A due to traumatic thrombosis of left internal carotid A. 1314.POST TRAUMATIC LEAK: 4.POST TRAUMATIC LEAK Leakage of CSF from the ear (otorrhoea) or nose (rhinorrhoea) is evidence that a basal fracture communicates with the subarachnoid space. It may also occur with congenital anomalies, erosion by tumour or as a manifestation of chronically raised intracranial pressure. Whatever the aetiology, the leak indicates the presence of a pathway for infection from the exterior to the subarachnoid space, which must be located and repaired. The point of external leakage is, however, a poor guide to the site of the fistula: CSF may enter the ear, for example, but leave the nose via the Eustachian tube. 132Slide 133: Currently, only one imaging investigation is required: CT cisternography , carried out at a time when the patient is actively leaking fluid. The patient is placed prone in the CT scanner after subarachnoid injection of myelographic contrast medium, and fine CT sections are obtained covering at least the region from the frontal to sphenoid sinuses necessary to examine the ears. A positive result is indicated by contrast medium in the sinuses and nasal cavity. 133 CT cisternographySlide 134: CT cisternography showing a large defect in the superior and lateral walls of the sphenoid sinus. Please note the cisterns and the sphenoid sinus completely filled with the dye, and the dye leaking through the defect into the nose. 1345.INFECTION: 5.INFECTION Direct extension of microorganisms Meningitis, cerebritis, abscesses, subdural and epidural empyema Contrast enhanced MRI more sensitive than contrast enhanced Ct to pick up meningeal enhancement Hyperintense edema noted on T2 weighted images 135Slide 136: MRI, T2-weighted image. Marked hyperintensity of the left frontal cortex, due to cerebritis. A posterior interhemispheric collection along the falx is also seen, as well as posterior mesial frontoparietal involvement. 1366.TENSION PNEUMOCEPHALUS: 6.TENSION PNEUMOCEPHALUS Air enters the cranial cavity through a fistula in sufficient amounts to cause mass effect Mechanism poorly understood Complication of trauma to the skull base Infection with gas forming organisms 137Other Imaging Modalities: Other Imaging Modalities A few reports of selected head-injury subjects suggest a role for functional imaging techniques (SPECT, PET, xenon-enhanced CT, functional MRI) to assess cognitive and neuropsychologic disturbances as well as recovery following head trauma. SPECT studies may reveal focal areas of hypoperfusion that are discordant with findings of MRI or CT. On the basis of these results, some investigators suggest that these functional imaging techniques may explain or predict post injury neuropsychologic and cognitive deficits that are not explained by MRI or CT abnormalities. 138Slide 139: Furthermore, focal lesions demonstrated by SPECT offer objective evidence of organic injury in patients whose neuroimaging studies are otherwise normal. One study found that a pattern of global reduction of cerebral blood flow by SPECT predicted a poor likelihood of recovery in persistent vegetative state patients due to head injury. SPECT, PET, and xenon-enhanced CT do not provide the anatomic detail or image resolution of CT or MRI for demonstrating acute or neurosurgical lesions of closed head injury, so their use is generally limited to subacute or chronic patients. 139Slide 140: Transcranial Doppler (TCD) sonography offers a noninvasive bedside evaluation of cerebral blood flow velocity and resistance in the major proximal vessels of the circle of Willis. Several investigators have suggested that TCD can be used to monitor early changes in blood flow velocities that may relate to vasospasm, hypervolemia, low velocity state, or edema, especially in management of the acutely brain injured patient. 140SUMMARY: SUMMARY Craniocerebral injuries are a common cause of hospital admission following trauma, and are associated with significant long-term morbidity and mortality, particularly in the adolescent and young adult population. Neuroimaging plays an essential role in identification and characterization of traumatic brain injuries. CT remains essential for detecting lesions that require immediate neurosurgical intervention (i.e., acute subdural hematoma) as well as those that require in-hospital observation and medical management. 141Slide 142: Other imaging modalities, such as MRI, depict nonsurgical pathology not visible on CT. SPECT, PET, and transcranial Doppler (TCD) have a complementary role in the assessment of brain injury. Because cervical spine trauma may accompany a head injury, cervical spine imaging is indicated for patients with head injury who have signs, symptoms, or a mechanism of injury that might result in spinal injury, and in those who are neurologically impaired. 142Slide 143: THANK YOU 143 You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
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Premium member Presentation Transcript Craniocerebral trauma: Craniocerebral trauma Major Dhanalakshmi B 18 Oct 10 1Slide 2: CNS injuries remain the leading cause of morbidity and mortality for young people throughout the world. 2Slide 3: Neuroimaging is fundamental to the diagnosis and management of patients with traumatic brain injury The choice of imaging depends on the specific pathology that we are dealing with 3CLASSIFICATIONS: CLASSIFICATIONS Based on the AREA of involvement -Focal -Diffuse Based on the TYPE of injury -Primary( Fractures, Extracerebral lesions and Intraaxial lesions) -Secondary(complications like hydrocephalus, infarction etc) 4Slide 5: Based on the type of TRAUMA -Blunt -Penetrating Based on the PATHOLOGY Most useful classification 5Slide 6: Fractures Intra cerebral Hematoma Epidural Hematoma Subdural Hematoma Subarachnoid Hematoma Contusions Diffuse Axonal (Shear) Injury Brain swelling and Edema Penetrating Injury Vascular Injury 6IMAGING MODALITIES: IMAGING MODALITIES Skull Radiography Computed Tomography Cerebral Angiography Magnetic Resonance Imaging Other Imaging Modalities 7CT SCANS: CT SCANS Primary modality for investigating Acute Head trauma Rapidly demonstrates surgically correctable lesions, fractures and sub arachinoid hemorrhages Delineates acute hemorrhage from brain edema Determines whether hematoma is intracerebral or extracerebral 8PROTOCOL: PROTOCOL 10 mm sections without inter slice gap taken at an angle of 15 to 20 degrees to the cantho meatal line and parallel to the skull base Posterior fossa – 5 mm slices to reduce beam hardening effects 9Slide 10: 3 different window setting for -Soft tissues( infarct and hemorrhage) -Extracerebral spaces( detect hematomas) -Bone for detection of fractures IV contrast usually not required except when there is considerable mass effect and normal plain study and to pick up small lesions and isodense SDHs. Skull base fractures need direct coronal scans or coronal reconstructions( slice thickness should be less than or equal to 3 mm) 10MRI: MRI Better for subacute and chronic cases. Better than CT for DAI, non hemorrhagic contusions and SDHs and equivalent to CT for hemorrhagic Contusions New non ferromagnetic ventilators compatible with MRIs Disadvantages include long scan time, inability to detect fractures, SAH and hyperacute hemorrhage 11TECHNIQUE: TECHNIQUE Conventional T1 and T2 weighted spin echo sequences used Proton density and T2 weighted sequences useful for non hemorrhagic lesions like contusions( sensitive to extracellular water) T2* Gradient recalled echo highly sensitive for small acute and chronic hemorrhagic lesions Fast spin echo helpful in saving time in acute trauma but not as sensitive as standard spin echo 12Slide 13: Advantages of MRI include multiplanar capability and superior contrast resolution Sagittal T1 weighted and axial T2 weighted sequences supplemented with T2* GRE sequence is the best combination 5 mm slice thickness with a 2.5 mm gap and a 256 x 192 matrix 13FRACTURES: FRACTURES TYPES SIMPLE FRACTURES ( Linear) linear, although they may be irregular, particularly if due to a sharp direct blow. When acute, they are typically well defined, and appear as fine lines of decreased density . They sometimes branch, and must be distinguished from vascular markings, including the groove in the squamous temporal bone caused by a deep temporal artery. 14Slide 15: DIFFERENCES FROM VASCULAR MARKINGS Acute fractures are usually straighter, more angulated, more radiolucent and do not have corticated margins. A fracture passing through a sinus or air cell is effectively compound, and of much greater potential significance than a simple fracture. Fractures may be associated with widening (diastasis) of one or more sutures, particularly the lambdoid 15Slide 16: Bilateral vault fracture, with fluid level in sphenoid sinus (open arrow). Two fracture lines are seen; the more anterior (upper on this film) is better defined and is therefore on the side nearer the film. Apparent islands of bone within (small arrows) are typical of an acute fracture. (Brow-up.) 16Slide 17: 17Slide 18: 18Slide 19: 19Depressed Fractures: Depressed Fractures A direct blow may depress a fragment of bone. On plain skull film, one border of the fragment appears dense where it overlaps the adjacent bone, and a projection at right angles shows a dense bony flake lying beneath the cranial vault. Unlike demonstration of simple linear fractures, this observation has important therapeutic consequences, and should not be overlooked. CT is particularly effective at demonstrating depressed fractures provided bone windows are used. Usually there is a focal contusion in the underlying cerebral cortex (a coup contusion). 20Slide 21: Stellate depressed fracture produced by a direct blow. Lateral (A) and half axial (B) projections: the former shows the typical appearance of a dense flake deep to the skull vault. Note fracture line running vertically from bottom of figure in both A and B. 21Slide 22: Majority of these injuries are managed conservatively Depressed fractures adjacent to venous sinuses are left intact due to fear of bleeding. 22Slide 23: The arrow points to the presence of a comminuted fracture involving the left frontal bone with a significant degree of depression. Note that the adjacent portion of the frontal sinus is also partially opacified indicating its involvement. 23Slide 24: 24Slide 25: Comminuted depressed fracture of the left parietal bone by more than the thickness of the calvarium itself. Associated with underlying haemorrhagic contusion and air. 25BASILAR FRACTURES: BASILAR FRACTURES Fractures of the skull base often are manifest on plain films only as fluid and fluid levels representing bleeding or leakage of cerebrospinal fluid, particularly in the sphenoid sinus and petromastoid air cells. Air may also be seen within the cranium. If sharply defined, lying superficially, adjacent to the midline or the expected position of the fractured sinus, it is usually extradural; it may be very extensive when subdural. 26Slide 27: Diffuse air, in bubbles, or outlining the brain, is more likely to be subarachnoid, in which case the leptomeninges have been torn. Purely intraventricular air is uncommon but can be severe, with acute hydrocephalus. CT can also be extremely helpful in assessment of fractures of the skull base, including the petrous bone, where it may also reveal ossicular dislocation, a treatable cause of traumatic hearing loss. Thin section CTs (1–3 mm) are recommended. 27Slide 28: Important clinical signs of skull base fracture include CSF rhinorrhea or otorrhea, battle's sign, raccoon eyes, hemotympanum or cranial nerve palsy (7th or 8th). The arrow in this image points to an occipital bone fracture. Additional air fluid levels are noted within the maxillary sinus on the left as well as air within the left infra-temporal fossa and subcutaneous air involving the left eyelid. 28Slide 29: On the first image, there is a fracture through the left occipital bone. On the second image, a haemorrhagic contusion is seen in the cerebellum. 29Petrous temporal bone : Petrous temporal bone Petrous temporal bone fractures can be divided into transverse and longitudinal. They may be associated with post traumatic deafness; the transverse fracture is the more severe in this respect. 30Slide 31: Note the longitudinal petrous bone fracture. The peripheral fracture margins are arrowed. Note also the blood in the sphenoid sinuses, consistent with a basal skull fracture. 31Slide 32: Unenhanced, axial scans: A fracture perpendicular to the longitudinal axis of the petrous bone is visualized in the bone window scan of the skull base The mastoid cells are obscured, which points to haemorrhage 32PARANASAL SINUS FRACTURES: PARANASAL SINUS FRACTURES Posterior wall of the frontal sinus require surgical closure due to disrupted dura to prevent CSF leak. Comminuted ones are treated surgically Fractures of cribriform plate associated with anosmia. 33Slide 34: The arrow points to the presence of a mildly depressed fracture involving the anterior wall of the left maxillary sinus with a small associated air fluid level. The complete opacification of the right maxillary sinus may be as the result of blood in the setting of trauma or may be due to extensive sinus mucosal disease. Air within the infero-temporal fossae bilaterally (arrow heads) is most likely the result of paranasal sinus fracture. However extension from any other focus of subcutaneous air is possible 34Pneumocephalus: Pneumocephalus Air locules usually indicàte traumatic air entry from fracture of paranasal sinus or mastoid air cells. Complications like meningitis, CSF leak and empyema are seen. 35Slide 36: Pneumocephalus (small arrow) with associated intraparenchymal fractured fragment (double arrow) 36Slide 37: Intracranial air over frontal lobes, in suprasellar region and over left temporal lobe. Left temporal haematoma and air in soft tissue over left temporal area. 37GROWING FRACTURES: GROWING FRACTURES Growing fractures (leptomeningeal cysts) usually occur after severe head injuries early in life. The dura mater underlying a linear fracture is torn, often with laceration of the underlying brain. Exposure of the remodelling bone to pulsation of the cerebrospinal fluid (CSF) results in progressive widening of the fracture line over weeks or months. CT is very satisfactory for the investigation of growing fractures, because it also shows the changes in the underlying brain, which is seen to herniate through the skull defect. A prominent porencephalic cyst or focal dilatation of the lateral ventricle usually underlies the fracture, and on rare occasions may even communicate through it with an extracranial fluid collection. 38Slide 39: 39INTRACEREBRAL HEMATOMA: INTRACEREBRAL HEMATOMA Distinguished from hemorrhagic contusions by -Homogenous hyperdensity -Sharply marginated -Surrounded by a rim of decreased density Common sites are frontal and temporal lobes Frequently associated with other lesions like SAH Appear within 48 hours following the injury 40Slide 41: Delayed appearance (more than 48 hours) due to: -Focal loss of autoregulation -Surgical evacuation of lesions like SDH with loss of tamponade effect 41Slide 42: Acute haemorrhage appears as increased radiographic density on CT and reaches around 100 HU. Its CT density depends on the initial haemoglobin level, dilution by extracellular fluid and partial volume effects. Very rarely haematomas can be isointense to the surrounding brain, in severely anaemic patients with a haematocrit of 20% or less. Calcified and highly proteinaceous material can reach a similar density to fresh blood clot, but the clinical context usually suggests the diagnosis. Contrast enhancement of tumours can also render them of similar density, so that CT is always performed without contrast medium if haemorrhage is possible 42Slide 43: An acute intracerebral clot is usually rounded and of homogeneous radiodensity. There is typically no oedema around a fresh clot and a fine rim of low density indicates clot retraction . In deep-seated or extensive intracranial haemorrhage, blood frequently leaks into the ventricles where it may adhere to the ependyma or to the choroid plexus; alternatively, it can sink to the most dependent part of the ventricular system, usually the occipital horns, forming a fluid level within the ventricular fluid. 43Slide 44: Over the course of several days, an untreated haematoma becomes less radiodense, from the periphery towards the centre, and therefore appears smaller. Vasogenic oedema may develop in the surrounding white matter, and should IV contrast medium be given at this stage, it usually produces a halo of enhancement. After several weeks, the CT density of the blood products can be similar to that of the brain or CSF. 44Slide 45: The single arrow points to the presence of an area of intraparenchymal hemorrhage. Note the associated frontal bone fracture. The arrow heads point to soft tissue densities within the scalp bilaterally representing the presence of scalp hematoma. 45Slide 46: 46Slide 47: CT examination: Unenhanced, axial scans: In the thalamic region on the right side, a small hyperdense lesion can be seen (arrow). In the picture on the right side, a large hyperdense lesion can be seen (arrows) in the left hemisphere, in the region of the basal ganglia. The space-occupying is obvious, the left lateral ventricle is compressed, and the midline structures are dislocated to the right (double arrow). 47Slide 48: The MRI appearance of intracerebral haemorrhage tends to follow a certain time-course, in which the presence of various haemoglobin degradation products and red cell lysis play important roles. As the haematoma ages, haemoglobin passes through a number of paramagnetic breakdown products, which include Deoxyhaemoglobin methaemoglobin haemosiderin; the latter is taken up by macrophages. 48 MR signal characteristics of intracerebral haemorrhage (according to Bradley) : MR signal characteristics of intracerebral haemorrhage (according to Bradley) Stage Form of haem iron T1-weighted MRI T2-weighted MRI Hyperacute (first few hours) Oxyhaemoglobin Iso- or hypointense Slightly hyperintense Acute (1–3 days) Deoxyhaemoglobin Slightly hypointense Hypointense Early subacute (3–7 days) Intracellular methaemoglobin Hyperintense Hypointense Late subacute (1–4 weeks) Extracellular methaemoglobin Hyperintense Hyperintense Chronic Haemosiderin Iso- or hypointense Markedly hypointenseSlide 50: (A) Red cells containing oxyhaemoglobin (O), which gives signal similar to brain on both T1- and T2-weighting, are extravasated. (B) The oxyhaemoglobin in some of the cells at the centre of the clot is converted to deoxyhaemoglobin (DE), giving lower signal on T1-weighted images. The clot is now surrounded by a variable amount of cerebral oedema (small circles). which gives nonspecific increased signal on T2-weighted images. (C) Most of the hemoglobin is now converted to methaemoglobin (M), which gives high signal on both T1- and T2-weighted images: however, lower signal due to the continued presence of deoxyhaemoglobin (DE) may still be evident centrally. Progressive lysis (interrupted outline) of the red cells is occurring. Surrounding oedema may become more extensive. (D) The red cells have now broken down, leaving a post-haemorrhagic cyst. This still contains methaemoglobin (M), and returns high signal on all the commonly used sequences. The oedema around the clot has resolved, but the macrophages (circles with 3 engulfed particles) which surround the cavity contain haemosiderin granules (H) which, because of susceptibility effects, give markedly reduced signal with T2-weighting and, to a lesser extent, on T1-weighted images. Persistence of high signal from methaemoglobin and low signal from haemosiderin is variable, but in some patients these effects can be seen for many months after documented bleeding. 50Slide 51: Gradient-echo, or T2*-weighted sequences are much more sensitive than conventional or fast spin-echo sequences to the magnetic field inhomogeneities induced by the presence of paramagnetic breakdown products of blood. These field inhomogeneities cause signal loss, which frequently appears larger than the extent of the actual haemorrhage. T2*-weighted gradient-echo sequences therefore have a greater sensitivity for detecting both acute and old haemorrhage (deoxyhaemoglobin and haemosiderin, respectively). Acute haematomas are still mainly investigated by CT. 51Slide 52: Extreme hypointensity in acute stage is due to Preferential T2 Proton Relaxation Enhancement of intracellular deoxyhemoglobin (PRT2PRE) Mechanism of relaxation for methhemoglobin is Proton-Electron Dipole-Dipole Relaxation Enhancement (PEDDRE). FSE not as sensitive as standard spin echo sequences. 52TRAUMATIC HAEMORRHAGE : TRAUMATIC HAEMORRHAGE Trauma may cause bleeding into the scalp, between the cranial vault and the dura mater (extra- or epidural), between the dura and arachnoid mater (subdural), or into the subarachnoid space, brain or ventricular system. The objective aim of imaging in the acute stage is to identify patients with intracranial bleeding requiring surgery; CT is the imaging procedure of choice, rather than MRI, as haematomas are about the most readily recognizable abnormality on plain CT. 53Slide 54: 54EXTRADURAL HAEMATOMAS : EXTRADURAL HAEMATOMAS Extradural haematomas are commonly due to bleeding from the middle meningeal artery, and plain skull films and CT scout views frequently show a fracture crossing the groove of that vessel in the temporoparietal region. The acute extra- or epidural haematoma is a relatively stereotyped lesion . Because the dura mater tends to adhere to the skull, the haematoma is seen on CT sections as a dense area immediately beneath the skull vault, convex towards both the brain and the vault. 55Slide 56: The temporoparietal convexity is the most common site(Axial images) Frontal, vertical and posterior cranial fossa collections (coronal images shallow extradural haematomas may be overlooked, especially when adjacent to contused or haemorrhagic brain. Wide window CT images may help distinguish the intermediate density of the clot from bone and underlying brain. 56Slide 57: Acute epidural haematoma; CT with intermediate window display. Large biconvex right temporal epidural collection. Note the effacement of the right temporal horn and lack of visualization of suprasellar cistern, compatible with tentorial herniation. 57Slide 58: ACUTE- Heterogeneous in attenuation with areas of hyperdense blood and isodense serum SUBACUTE- Homogeneously hyperdense with solid blood clot CHRONIC- Heterogeneous or decreased attenuation with an enhancing membrane Tend to regress spontaneously Criteria for conservative treatment Diameter less than 1.5 cms Midline shift less than 2 mm 58Slide 59: Note the biconvex hyperdense area (arrows). The blood collection is between the skull and dura. It crosses dural attachments, but not sutures. The etiology is secondary to a lacerated meningeal artery or dural sinus. The Subdural windows may help to discern extra-axial collections such as blood in this case 59Chronic Frontal epidural Hematoma: Chronic Frontal epidural Hematoma 60Slide 61: 61Slide 62: This example shows a more unusual, lower location. Note also the gas within the haematoma - this indicates a basal skull fracture or, as in this case, it is post surgical. Note also the dilated lateral ventricle on the opposite side. 62Slide 63: MRI allows distinction between EDH and SDH in tough cases Not recommended routinely Dura is seen as a band of decreased signal intensity between the hematoma and the brain parenchyma Can distinguish arterial and venous bleeds Good for Posterior fossa hematomas as no beam hardening artifacts 63Slide 64: Acute epidural haematoma; MRI in a neonate with traumatic delivery. (A) Axial T1-weighted image (750/16). Slightly hyperintense epidural collection (arrow) in the right temporal region. (B) Axial T2-weighted image (3000/120), epidural collection is hypointense and is invisible except for deformation of the underlying cortex. This is the MR signature of deoxyhaemoglobin. 64SUBDURAL HEMATOMA: SUBDURAL HEMATOMA Subdural bleeding often, but not always, is associated with damage to the brain, and arises from rupture of veins which cross the subdural space; vault fractures are less commonly present Acute subdural haematomas are also radiodense on CT and peripherally situated, being more or less crescentic, i.e. concave on their deep surface. This is because the blood within them, while under less pressure, is less restricted and tends to spread out over the surface of the brain very extensive subdural bleeding may extend over an entire cerebral hemisphere. 65Slide 66: The high morbidity of these lesions, particularly in the aged, is due in large part to the associated Swelling contusion laceration of the underlying brain. It is often evident that midline displacement is greater than would be accounted by the mass of the haematoma alone. Dilatation of the contralateral ventricle is a bad prognostic sign. 66Slide 67: Acute subdural haematoma, 85-year-old woman; CT. Heterogeneous density of irregular shape occupies extra-axial space overlying the left cerebral convexity. There is moderate mass effect exhibited by effacement of convexity sulci and midline shift with subfalcial herniation. This required surgical decompression 67Slide 68: 68Slide 69: Acute SDH need not always be classically homogeneously hyperdense. Other patterns may be: Marginal hypodensity Central irregular area of hypodensity Laminar area of hypodensity Low density is due to unclotted blood or CSF. 69Slide 70: CT examination: Unenhanced, axial scans: An inhomogenous, extremely hyperdense, sickle-shaped haematoma is visible (arrow) on the left side temporally, between the brain convexity and the inner surface of the skull bone (subdural haematoma). Beside this a right frontal (black arrow), frontotemporal linear fracture (double arrow) and small intracerebral haematoma caused by contusion are visible. ( => picture ) 70Slide 71: SDH s located adjacent to the tentorium may simulate an intra axial lesion Distinguishing points are (Supratentorial) -Well defined medial margin corresponding to the edge of the tentorium -Sheet like area of increased density that slopes laterally -Trigone of the lateral ventricle is rotated anteriorly and superiorly Coronal CT sections may be useful in distinguishing supra- and infratentorial bleeding. 71Slide 72: Trauma. CT. A biconvex density of blood over the left cerebellar hemisphere indicates an extradural haematoma (thick arrow). A crescent of fresh subdural blood spreads over the left temporal lobe and tracks along the tentorium (arrowhead); this feature differentiates it from an extradural. Typical sites of haemorrhagic contusions are seen; gyrus recti and temporal lobe. 72Slide 73: The interhemispheric subdural haematoma extends along the falx cerebri and may spread onto the tentorium, giving a characteristic comma shape on axial CT sections May be confused for a SAH which has a zigzag configuration confirming to the cortical sulci 73SUBDURAL HEMATOMA ALONG THE FALX CEREBRI : SUBDURAL HEMATOMA ALONG THE FALX CEREBRI The arrow head points to the presence of hyperdense blood interdigitating within the sulci. The arrow points to the presence of an acute subdural hematoma which has collected between the leaves of the falx. The double-stemmed arrow points to the presence of a symmetric scalp soft tissue density for a hematoma. 74Slide 75: Sub- or extradural collections low in the posterior cranial fossa, which may be life-threatening, may be overlooked, and the presence of unexplained hydrocephalus after acute head injury should prompt thorough examination of that region. The CT density of the blood in a subacute subdural haematoma slowly decreases: as a rule of thumb, it remains denser than the brain for 1 week, is less dense after 3 weeks. an interim period of up to 2 weeks when it may be ‘isodense’ with brain. Not all isodense haematomas are subacute an acute bleed can be isodense in a very anaemic patient if there is continued leakage of venous blood, a chronic haematoma may not be of low density.Slide 76: Indirect signs midline shift, with compression of the ipsilateral ventricle; contralateral ventricular enlargement effacement of cerebral sulci medial displacement of the junction between the white and grey matter (‘buckling’). (Some of these signs may be absent if there are bilateral collections; the frontal horns may then lie closer together than normal, giving a ‘rabbit’s ear’ configuration) Intravenous contrast medium, by highlighting the vessels on the surface of the brain, may remove any doubts about the extracerebral location of the lesion. 76Slide 77: Bilateral isodense subdural haematomas on contrast-enhanced CT. The ventricles (A) are slit-like and displaced medially, giving a ‘rabbit’s ears’ appearance. A higher section (B) indicates that the normal grey-white interface lies too near the midline; the cortex appears abnormally thick. On close inspection, both sections show cortical vessels (arrows) displaced away from the cranial vault. 77Slide 78: Subacute right subdural haematoma: CT. The lesion is less dense than brain but denser than CSF; it is denser posteriorly. Displacement of midline structures is greater than would be expected from the size of the lesion, suggesting extensive swelling of the underlying hemisphere. The contralateral (left) ventricle is dilated. 78CHRONIC SDH: CHRONIC SDH Chronic SDHs are usually caused by trauma but the episode is usually so trivial that it is forgotten Seen in the older age group and can present with change in personality 79Slide 80: On CT, chronic subdural collections assumed a biconvex form density is less than that of brain, approaching that of CSF Fluid/fluid levels may be seen between denser blood elements in the more dependent portions and serous fluid above, particularly if haemorrhage has been repeated membrane on their deep surface frequently shows contrast enhancement which is capillary rich and prone to repeated episodes of bleeding 80Slide 81: Chronic left subdural collection: CT. The extracerebral collection is of CSF density; underlying sulci are effaced. 81Slide 82: less useful in the acute stages of trauma but is the preferred imaging technique for assessing damage to the underlying brain Subdural haematomas display the temporal evolution of signal intensity as has been previously described in intracranial haemorrhage. They have a convex cerebral surface on coronal images. In the subacute and chronic phase, MRI is probably the most accurate imaging method to detect the smallest subdural haematomas, mainly due to its multiplanar capability. 82 MRISlide 83: 83Slide 84: Axial T1-weighted MRI image shows subacute subdural haematoma in left frontoparietal region and acute subdural haematoma in left anterior frontal (white arrows). Note large lateral ventricles and the shrunken right cerebral cortex. 84SUBARACHNOID HEMORRHAGE: SUBARACHNOID HEMORRHAGE Subarachnoid haemorrhage commonly follows severe head injury and, if diffuse, may render the basal cisterns isodense with brain, simulating cisternal compression Caused by damage to the blood vessels of the pia arachnoid CT is the modality of choice due to the hyperdensity of clotted blood Difficult to visualise on MRI due to high oxygen content CSF prevents degradation of oxyhemoglobin 85Slide 86: CT is positive in over 90% of cases if the scan is carried out within a few days of the haemorrhage. On CT, the hallmark of recent SAH is increased density of the cerebrospinal fluid spaces. As in all blood clots, haemoglobin is the main determinant of detectability : a few red cells in the subarachnoid space will not be detected, but once the haematocrit of the fluid increases by a few per cent, increased radiodensity is evident 86Slide 87: The blood can flow freely, and with profuse bleeding the entire intracranial subarachnoid space may be opacified, with reflux or breakthrough into the ventricular system. If the CT scan is negative and there is a strong clinical suspicion of SAH, a lumbar puncture has to be performed, which may show evidence of acute haemorrhage or xanthochromia and confirm the diagnosis. 87LEFT FRONTAL HEMORRHAGIC CONTUSION. RIGHT TRAUMATIC SUBARACHNOID HEMORRHAGE : LEFT FRONTAL HEMORRHAGIC CONTUSION. RIGHT TRAUMATIC SUBARACHNOID HEMORRHAGE The single arrow head points to an area of hemorrhagic frontal contusion. The arrow points to acute blood interdigitating within the sulci of the occipito-parietal region. This is traumatic subarachnoid hemorrhage. Nontraumatic subarachnoid hemorrhage should always be considered to be secondary to a ruptured aneurysm or hemorrhage from an A-V (arteriovenous) malformation and necessitates an angiogram for confirmation. 88 SAH: SAH 89Slide 90: This patient was semiconcious with subarachnoid bleeding. The filling in of the sulci over the cerebral hemispheres was subtle (not shown), but the clue is visible on this image; there is abnormal increased attenuation due to fresh blood in the 4th ventricle, which has settled posteriorly. The prepontine cistern is also indistinct and may contain blood. 90 MRI: MRI Conventional spin-echo MR sequences are much less reliable than CT in detecting acute SAH. The sensitivity of MRI for the presence of blood in the subarachnoid space can, however, be considerably increased by using a FLAIR sequence. On the FLAIR sequence the signal from cerebrospinal fluid is nulled and appears normally black but blood-stained fluid produces an area of high signal. 91Slide 92: Subarachnoid haemorrhage. (A) CT shows blood in the right Sylvian fissure and in the interhemispheric fissure. This appears of high signal intensity on the fluid-attenuated inversion recovery (FLAIR) MRI (B), as opposed to the normal CSF which appears dark. A 3D TOF MRA (C) shows a right middle cerebral artery aneurysm (double arrow), which has bled, and an incidental ophthalmic artery aneurysm (single arrow); both are confirmed with DSA. 92Slide 93: T2-weighted image shows slight swelling of the gyri in the corresponding region of subarachnoid hemorrhage. 93 FLAIR image is the most sensitive for subarachnoid hemorrhage and demonstrates the area of subarachnoid hemorrhage (arrow).CONTUSIONS: CONTUSIONS Traumatic intracerebral bleeding is usually haemorrhagic contusion . In general, a focal, well-defined, rounded area of abnormal CT density or MRI signal in the brain represents a blood clot, but usually there are multiple areas of altered density or signal indicating blood, surrounded by low density or signal change suggestive of oedema. These often seem to enlarge in the first few days 94Slide 95: The common sites of haemorrhagic contusion are the inferior frontal and anterior temporal lobes and the bleeding is often subcortical. Contrecoup injuries , with the haemorrhage diametrically opposite the point of impact, with or without a fracture, are classical. Less commonly, deeper haemorrhages occur. Occasionally they can be large and resemble spontaneous haemorrhage, though usually other signs of injury are present as well 95Slide 96: Depressed skull fracture with parenchymal contusion. (A,B) CT, ‘brain and bone windows’. Large depressed fragment of the right temporal bone, with underlying irregular hyperdensity representing temporal lobe contusion 96Slide 97: It may be difficult to pick contusions in the posterior fossa due to beam hardening artifacts Sometimes lesions are not visible and can be identified only by indirect signs MRI studies are equivalent to CT in picking hemorrhagic contusions but are more sensitive for non hemorrhagic contusions. Same pattern of evolution as ICH Also more sensitive for lesions in the posterior fossa and subacute and chronic lesions 97RIGHT FRONTAL HEMORRHAGIC CONTUSION : RIGHT FRONTAL HEMORRHAGIC CONTUSION The arrowhead points to a punctate area of intraparenchymal hemorrhage which does not demonstrate significant mass effect. Please note the symmetry of the frontal horns of the lateral ventricles as well as the midline position of the third ventricle. The Sylvian fissures are also well characterized bilaterally. 98Slide 99: There is a focal area of haemorrhagic contusion in the right frontal lobe, with surrounding low density due to infarction or oedema. This is a frequent location for a contre-coup injury following a blow to the back of the head. 99Slide 100: This T1-weighted coronal image shows a heterogeneous-appearing lesion in the left temporal lobe with mass effect, consistent with a cerebral contusion. The caudate nucleus also appears atrophic. 100DIFFUSE AXONAL INJURY: DIFFUSE AXONAL INJURY Diffuse axonal injury (DAI) involves predominantly the white matter, including the corpus callosum. poor prognosis Most of the damaged white matter appears normal on CT and MRI, though patchy changes in regional mean diffusivity have been reported in diffusion tensor MRI only in research settings at present. What may be seen on clinical images are smaller foci of accentuated damage, which are haemorrhagic pathologically but often appear nonhaemorrhagic on CT or MRI. They are due to a shearing injury with rupture of small intracerebral vessels, and in a comatose patient with no other obvious cause they imply a severe diffuse brain injury with a poor prognosis. 101Slide 102: In acceleration injury the head is put into motion from a stand still position, as a result of which the different layers of the brain travels at different velocities with shearing effects and rotation of the brain within the skull. The shearing stresses between different layers of the brain result in petechial haemorrhages as well as diffuse axonal injury involving the white matter and brain stem.Slide 103: They occur in juxtacortical white matter especially in the parasagittal regions posterior corpus callosum low centrum semiovale upper midbrain. 103Slide 104: Diffuse vascular injury is more severe, and there are usually multiple basal haemorrhages. These marker lesions of DAI are of low density on CT and high signal on T2 weighted MRI unless modified by haemorrhage. Gradient-echo MRI may help identify older lesions as being of traumatic origin by demonstrating persistent haemosiderinSlide 105: This image demonstrates a small petechial haemorrhage in a typical location at the grey-white matter interface (arrow). As is often the case, there were multiple such lesions on other slices 105Slide 106: Axial and sagittal T2-weighted MR images. Hyperintensities in the right tectal midbrain, corpus callosum, mainly posterior third, and splenium. 106BRAIN SWELLING AND EDEMA: BRAIN SWELLING AND EDEMA This is of several types in head injury. Probably the commonest is hyperaemic brain swelling, where the brain swells due to an increase in blood volume, not oedema. Grey-white matter contrast is preserved on both CT and MRI and it can be difficult to assess. Slit-like ventricles do not reliably indicate raised intracranial pressure, but effacement of the basal cisterns (especially the chiasmatic) is more reliable. 107Slide 108: Other types of brain swelling are accompanied by CT density or MRI signal changes: oedema due to cortical contusion secondary neuronal injury due to diffuse hypoxic-ischaemic damage or infarction in specific arterial territories. (The latter is often due to severe transtentorial and subfalcine herniation producing cortical infarcts in posterior and anterior cerebral arterial territories, respectively.) MRI especially T2 weighted images are very sensitive to extracellular water and can detect small regions of edema 108Slide 109: If there is an associated increase in density of white matter , it is due to transient hyperemia due to loss of autoregulation Serial CT scans show gradual resolution over 3 to 5 days Cerebral edema is evident as decreased density within and surrounding areas of contusion and hematoma Edema typically appears 24 hours after injury, then increases, becomes maximum at 3 to 5 days and then gradually resolve 109AREA OF DEEP WHITE MATTER EDEMA WITHIN RIGHT PARIETO-FRONTAL REGION : AREA OF DEEP WHITE MATTER EDEMA WITHIN RIGHT PARIETO-FRONTAL REGION 110PENETRATING INJURIES: PENETRATING INJURIES Gunshot wounds are common cause CT can evaluate the position of the missile and the extent of injury Prognosis best when limited to a single lobe Complications like CSF leak, osteomyelitis, abscesses and seizures possible Presence of metal projectiles are relative contraindication for MRI 111Slide 112: Gunshot wound with displaced bony fragments 112OTHER MODALITIES: OTHER MODALITIES Cerebral angiography This is rather unhelpful in assessment of intra-axial lesions. It may show active bleeding from a ruptured artery. Traumatic arterial dissection, or a penetrating injury, may cause aneurysms. 113Slide 114: When intracranial pressure is very high, contrast medium injected into any of the main cervical arteries may fail to enter the head: the usual picture is of a static column of contrast medium in a narrowed artery, from catheter tip to carotid siphon. The grave prognostic significance of such an ‘agonal’ angiogram will readily be appreciated; it has in some countries been accepted as evidence of brain death. This picture must not, therefore, be confused with similar patterns produced by arterial dissection, embolic or arteritic occlusion just beyond the ophthalmic artery, severe catheter-induced spasm or subintimal injection. 114Slide 115: Acute traumatic arterial aneurysm: carotid angiogram, lateral projection. Metallic fragments are seen posteriorly; the vessels around them are stretched and narrowed, and a rounded collection of contrast medium, representing the traumatic aneurysm, is seen (arrow), unrelated to an arterial bifurcation. 115Slide 116: A number of radiological techniques conventional, digital subtraction radionuclide or Doppler angiography CT with IV contrast medium (showing absence of enhancement) have been proposed for diagnosing brain death. In a number of countries, including Britain, the diagnosis of brain death is a clinical one and the role, if any, of imaging tests is to identify a cause of irreversible coma. In some countries, the ‘agonal’ angiogram is used as an indication for terminating life-support therapy. 116VASCULAR INJURIES: VASCULAR INJURIES Traumatic arteriovenous fistulas Whenever an artery and an adjacent vein are injured, the stage is set for an arteriovenous fistula. Recognized sites in the head and neck include: the temporoparietal region (middle meningeal artery) around the transverse venous sinus (dural arteries, including the middle meningeal and occipital) in the scalp (usually involving the superficial temporal artery) in the neck (internal carotid or, more frequently, the vertebral arteries); cavernous sinus, where the internal carotid artery actually lies within the venous system 117Slide 118: Such fistulas frequently cause hypertrophy of feeding arteries and/or draining veins, enlarging, for example, the foramen spinosum and meningeal vascular grooves. An extracranial soft-tissue mass may be present. Traumatic caroticocavernous fistulas most commonly drain to the superior ophthalmic vein, and can enlarge one or both superior orbital fissures. 118Slide 119: In cases of caroticocavernous fistula, CT or MRI may show proptosis, with a markedly dilated superior ophthalmic vein, and the ipsilateral cavernous sinus may also be enlarged. Swelling of the extraocular muscles, due to raised venous pressure, is inconstant, but is frequently the main cause of exophthalmos. 119Slide 120: 120 caroticocavernous fistulaSlide 121: Treatment of large direct communications such as carotico-cavernous or vertebrovertebral fistula is currently by means of detachable balloons introduced during angiography; there is no indication for surgical intervention. Particulate emboli are employed for the more diffuse dural or scalp lesions, and may be combined with surgery 121TRAUMATIC DISSECTIONS: TRAUMATIC DISSECTIONS Magnetic resonance angiogram after traumatic carotid artery dissection causing 50% vessel narrowing of the cervical vessels (arrow), with arterial dissection distal to the narrowing. 122COMPLICATIONS OF CNS TRAUMA: COMPLICATIONS OF CNS TRAUMA HYDROCEPHALUS Diffuse brain injury followed by resolution of edema will lead to dilatation of the ventricles Non communicating hydrocephalus is due to intraventicular hemorrhage leading to obstruction Communicating hydrocephalus is due to decreased absorption of CSF at the arachnoid villi 123Slide 124: 124 2.ATROPHY: 2.ATROPHY Contusions or intraparenchymal haematomas may show remarkable resolution, but more common end results are focal atrophy in more severe cases, extensive softening and cyst formation—encephalomalacia. MRI may show evidence of past haemorrhage. The inferior frontal lobes commonly show evidence of prolongation of T1 and T2 on MRI, or low density on CT. 125Slide 126: Traumatic hemiatrophy , the result of an injury early in life, can affect both the brain and the overlying skull; it may be due to associated vascular damage rather than to direct trauma 126Slide 127: Porencephalic cyst: CT. A CSF-containing cyst communicates with the ventricular system. Such cysts can exert mass effect. 127Slide 128: Cranial hemiatrophy. The left hemicranium is smaller than the right, (arrows indicate the groove for the superior sagittal sinus); the left petrous bone is elevated, and the paranasal sinuses are more extensive on the affected left side. These changes are secondary to impaired growth of the underlying cerebral hemisphere. 1283.INFARCTION: 3.INFARCTION Secondary to vasospasm, vascular occlusion or direct vessel damage On CT, hypodensity or isodense lesion with brain swelling noted MRI more sensitive Hyperintense signals can be picked up between 8 to 24 hours on T2 weighted images when CT may be normal 129Slide 130: Post-traumatic ischemic infarct of both posterior cerebral Aa. 130T2 weighted image: T2 weighted image Acute infarct of middle cerebral A due to traumatic thrombosis of left internal carotid A. 1314.POST TRAUMATIC LEAK: 4.POST TRAUMATIC LEAK Leakage of CSF from the ear (otorrhoea) or nose (rhinorrhoea) is evidence that a basal fracture communicates with the subarachnoid space. It may also occur with congenital anomalies, erosion by tumour or as a manifestation of chronically raised intracranial pressure. Whatever the aetiology, the leak indicates the presence of a pathway for infection from the exterior to the subarachnoid space, which must be located and repaired. The point of external leakage is, however, a poor guide to the site of the fistula: CSF may enter the ear, for example, but leave the nose via the Eustachian tube. 132Slide 133: Currently, only one imaging investigation is required: CT cisternography , carried out at a time when the patient is actively leaking fluid. The patient is placed prone in the CT scanner after subarachnoid injection of myelographic contrast medium, and fine CT sections are obtained covering at least the region from the frontal to sphenoid sinuses necessary to examine the ears. A positive result is indicated by contrast medium in the sinuses and nasal cavity. 133 CT cisternographySlide 134: CT cisternography showing a large defect in the superior and lateral walls of the sphenoid sinus. Please note the cisterns and the sphenoid sinus completely filled with the dye, and the dye leaking through the defect into the nose. 1345.INFECTION: 5.INFECTION Direct extension of microorganisms Meningitis, cerebritis, abscesses, subdural and epidural empyema Contrast enhanced MRI more sensitive than contrast enhanced Ct to pick up meningeal enhancement Hyperintense edema noted on T2 weighted images 135Slide 136: MRI, T2-weighted image. Marked hyperintensity of the left frontal cortex, due to cerebritis. A posterior interhemispheric collection along the falx is also seen, as well as posterior mesial frontoparietal involvement. 1366.TENSION PNEUMOCEPHALUS: 6.TENSION PNEUMOCEPHALUS Air enters the cranial cavity through a fistula in sufficient amounts to cause mass effect Mechanism poorly understood Complication of trauma to the skull base Infection with gas forming organisms 137Other Imaging Modalities: Other Imaging Modalities A few reports of selected head-injury subjects suggest a role for functional imaging techniques (SPECT, PET, xenon-enhanced CT, functional MRI) to assess cognitive and neuropsychologic disturbances as well as recovery following head trauma. SPECT studies may reveal focal areas of hypoperfusion that are discordant with findings of MRI or CT. On the basis of these results, some investigators suggest that these functional imaging techniques may explain or predict post injury neuropsychologic and cognitive deficits that are not explained by MRI or CT abnormalities. 138Slide 139: Furthermore, focal lesions demonstrated by SPECT offer objective evidence of organic injury in patients whose neuroimaging studies are otherwise normal. One study found that a pattern of global reduction of cerebral blood flow by SPECT predicted a poor likelihood of recovery in persistent vegetative state patients due to head injury. SPECT, PET, and xenon-enhanced CT do not provide the anatomic detail or image resolution of CT or MRI for demonstrating acute or neurosurgical lesions of closed head injury, so their use is generally limited to subacute or chronic patients. 139Slide 140: Transcranial Doppler (TCD) sonography offers a noninvasive bedside evaluation of cerebral blood flow velocity and resistance in the major proximal vessels of the circle of Willis. Several investigators have suggested that TCD can be used to monitor early changes in blood flow velocities that may relate to vasospasm, hypervolemia, low velocity state, or edema, especially in management of the acutely brain injured patient. 140SUMMARY: SUMMARY Craniocerebral injuries are a common cause of hospital admission following trauma, and are associated with significant long-term morbidity and mortality, particularly in the adolescent and young adult population. Neuroimaging plays an essential role in identification and characterization of traumatic brain injuries. CT remains essential for detecting lesions that require immediate neurosurgical intervention (i.e., acute subdural hematoma) as well as those that require in-hospital observation and medical management. 141Slide 142: Other imaging modalities, such as MRI, depict nonsurgical pathology not visible on CT. SPECT, PET, and transcranial Doppler (TCD) have a complementary role in the assessment of brain injury. Because cervical spine trauma may accompany a head injury, cervical spine imaging is indicated for patients with head injury who have signs, symptoms, or a mechanism of injury that might result in spinal injury, and in those who are neurologically impaired. 142Slide 143: THANK YOU 143