Brain anatomy
Mechanism of injury in head trauma Direct trauma by compression or crushing. Acceleration-Deceleration Injuries Brain has inertia. For example, when a person falls backwards onto a hard floor, the back of the person’s head hits the floor and stops. The brain, however, is still moving until it strikes the inside of the skull. If the brain gets bruised, there is bleeding, also called a hemorrhage. This bleeding causes further damage to the brain. The skull does not need to strike an object in order for the brain to get injured. There are many situations in motor vehicle crashes where the forces are transmitted through the brain without the skull hitting the dashboard, windshield, steering wheel or window. Coup/Contrer-Coup Injuries: Related to acceleration-deceleration injuries (e.g injury to temporal lobe in contralateral temporal trauma)
Head Trauma 1-Skull fractures. 2-Extradural ,subdural & subarachinoid. 3-Cerebral contusion& intraventricular Hge. 4-Diffuse Axonal Injury (DAI). 5-Related Brain edema & herniation.
Skull Fracture A skull fracture is a break in the skull bone and generally occurs as a result of direct impact . Uncomplicated skull fractures themselves rarely produce neurologic deficit, but the associated intracranial injury may have serious neurologic sequelae.
Four major types of skull fractures may occur: (1) linear, (2) depressed, (3) diastatic, (4) basilar.
Linear skull fractures
Depressed skull fractures Cech Petr
Basilar skull fractures Most basilar fractures occur at 2 specific anatomic locations — namely, the temporal region and the occipital condylar region.
Other Types Ping-pong skull fractures . Birth fractures (Caput succedaneum or cephalohematoma ). Growing skull fractures (leptomeningeal cyst, traumatic meningocele, cerebrocranial erosion, cephalhydrocele, meningocele, and spuria.
Epidural Hematoma An epidural hematoma is usually associated with a skull fracture. It often occurs when adirect impact fractures the calvarium . The fractured bone lacerates a dural artery (middle meningeal artery) or a venous sinus. On CT, the hematoma forms a hyperdense biconvex mass. It is usually uniformly high density but may contain hypodense foci due to active bleeding. Comment on midline shift .
Natasha Richardson March 2009
Subdural Hematoma Acute, subacute & chronic Deceleration and acceleration or rotational forces that tear bridging veins can cause an acute subdural hematoma so it occurs in cases of wide subdural space(old age & children) Causes of subdural are:in minimal trauma in old age, child abuse and ventricular decompression, may occur in patients receiving anticoagulants or patients with a coagulopathy condition. The blood collects in the space between the arachnoid matter and the dura matter, Because the subdural space is not limited by the cranial sutures, blood can spread along the entire hemisphere and into the hemispheric fissure, limited only by the dural reflections . We have 3 major types : Acute, subacute & chronic
Acute Subdural Hematoma Crescent shaped; Hyperdense, may contain hypodense foci due to serum, CSF or active bleeding
In children, subdural hematomas occurring along the posterior interhemispheric fissure and the tentorium have been described as common findings following violent nonaccidental shaking (ie, shaken baby syndrome) .
Subacute Subdural Hematoma Subacute SDH may be difficult to visualize by CT because as the hemorrhage is reabsorbed it becomes isodense to normal gray matter. A subacute SDH should be suspected when you identify shift of midline structures without an obvious mass. Giving contrast may help in difficult cases because the interface between the hematoma and the adjacent brain usually becomes more obvious due to enhancement of the dura and adjacent vascular structures. Some of the notable characteristics of subacute SDH are: - Compressed lateral ventricle & or midline shift - Effaced sulci .
Chronic Subdural Hematoma Chronic SDH becomes low density as the hemorrhage is further reabsorbed. It is usually uniformly low density but may be loculated. Rebleeding often occurs and causes mixed density and fluid levels.
Subarachnoid Hemorrhage A subarachnoid hemorrhage occurs with injury of small arteries or veins on the surface of the brain. The ruptured vessel bleeds into the space between the pia and arachnoid matter. The most common cause of subarachnoid hemorrhage is trauma . In the absence of significant trauma, the most common cause of subarachnoid hemorrhage is the rupture of a cerebral aneurysm.
If there is a large amount of SAH particularly in the basilarcisterns,sulci&fissures the physician should consider whether a ruptured aneurysm led to the subsequent trauma. When traumatic, subarachnoid hemorrhage occurs most commonly over the cerebral convexities or adjacent to otherwise injured brain (i.e. adjacent to a cerebral contusion)
Cerebral Contusion Brain contusions commonly are identified in patients with traumatic brain injury (TBI) . The second mechanism is related to countercoup acceleration or deceleration ,which causes the brain to strike the skull. In an event in which the head is in motion, cortical injury occurs adjacent to the floor of the anterior or posterior cranial fossa, the sphenoid wing, the petrous ridge, the convexity of the skull, and the falx or tentorium. The inferior frontal and temporal lobes are particularly vulnerable Cerebral contusions are the most common primary intra-axial injury. They often occur when the brain impacts an osseous ridge or a dural fold. The foci of punctate hemorrhage or edema are located along gyral crests. The following are common locations: - Temporal lobe - anterior tip, inferior surface, sylvian region - Frontal lobe - anterior pole, inferior surface - Dorsolateral midbrain - Inferior cerebellum
On CT, cerebral contusion appears as an ill-defined hypodense area mixed with foci of hemorrhage. Adjacent subarachnoid hemorrhage is common. After 24-48 hours, hemorrhagic transformation or coalescence of petechial hemorrhages into a rounded hematoma is common CT scans often demonstrate progression over time in the size and number of contusions and the amount of hemorrhage within the contusions MRI findings typically demonstrate the lesions from the onset of injury, but many facilities cannot perform MRI on an emergent basis On MRI, contusions are isointense to hyperintense on T1-weighted and hyperintense on T2-weighted image& The signal intensity is increased in the affected region on DWIs .
Diffuse Axonal Injury Diffuse axonal injury is often referred to as "shear injury". It is the most common cause of significant morbidity in CNS trauma. Fifty percent of all primary intra-axial injuries are diffuse axonal injuries . When shearing forces occur in areas of greater density differential, the axons suffer trauma; this results in edema and in axoplasmic leakage (which is most severe during the first 2 weeks following injury). The exact location of the shear-strain injury depends on the plane of rotation Immediate loss of consciousness is typical of these injuries .
The true extent of axonal injury typically is worse than that visualized using current imaging techniques The CT of a patient with diffuse axonal injury may be normal despite the patient's presentation with a profound neurological deficit . With CT, diffuse axonal injury may appear as ill-defined areas of high density or hemorrhage in characteristic locations. One or more small intraparenchymal (petechial) hemorrhages less than 2 cm in diameter, located in the cerebral hemispheres at the grey white interface as well as corpus callosum &brainstem. One may also observe small focal areas of low density on CT scans; these correspond to areas of edema
Stage I - This involves the parasagittal regions of the frontal lobes, the periventricular temporal lobes, and, less likely, the parietal and occipital lobes, internal and external capsules, and cerebellum. Stage II - This involves the corpus callosum in addition to the white-matter areas of stage I. Most commonly, the posterior body and splenium are involved; however, the process is believed to advance anteriorly with increasing severity of disease. Both sides of the corpus callosum may be involved; however, involvement more frequently is unilateral and may be hemorrhagic. The involvement of the corpus callosum carries a poorer prognosis. Stage III - This involves the areas associated with stage II, with the addition of brainstem involvement. A predilection exists for the superior cerebellar peduncles, medial lemnisci, and corticospinal tracts .
Intraventricular Hemorrhage Traumatic intraventricular hemorrhage is associated with diffuse axonal injury, deep gray matter injury, and brainstem contusion. An isolated intraventricular hemorrhage may be due to rupture of subependymal veins .
Cerebral Edema Severe brain edema or a large intracranial hemorrhage may cause downward brain displacement and coning, which is usually fatal
Stroke Stroke is a clinical term for sudden, focal neurological deficit ischemic stroke caused by blockage of blood flow in a major cerebral blood vessel, usually due to a blood clot . account for about 84% of all strokes. Hemorrhagic strokes due to rupture of a cerebral blood vessel that causes bleeding into or around the brain . account for 16% of all strokes .
Hemorrhagic Stroke Hemorrhagic strokes account for 16% of all strokes Intracerebral hge is the most common, accounting for 10% of all strokes . Subarachnoid hge, due to rupture of a cerebral aneurysm, accounts for 6% of strokes overall.
Hypertensive hemorrhage . Now Dudes tell me what are the reasons of cerebral hemorrhage!??? Hypertensive hemorrhage . Amyloid angiopathy. Ruptured vascular malformation. Coagulopathy(A fluid level within the hematoma) . Hemorrhage into a tumor . Venous infarction. Drug abuse.
Subarachnoid Hemorrhage Common aneurysm locations include the anterior and posterior communicating arteries, the middle cerebral artery bifurcation and the tip of the basilar artery. Subarachnoid hemorrhage typically presents as the "worst headache of life" for the patient .
Ischemic stroke Ischemic strokes are caused by thrombosis, embolism of thrombosis, hypoperfusion and lacunar infarctions(1%) A thrombotic stroke (53%)occurs when a blood clot forms in situ within a cerebral artery and blocks or reduces the flow of blood through the artery An embolic stroke (30%) occurs when a detached clot flows into and blocks a cerebral artery
A CT is 58% sensitive for infarction within the first 24 hours (Bryan et al, 1991). MRI is 82% sensitive. If the patient is imaged greater than 24 hours after the event, both CT and MR are greater than 90% sensitive. After a stroke, edema progresses, and brain density decreases proportionately.
Diffuse Hypodensity and Sulcal Effacement Hypodensity in greater than one-third of the middle cerebral artery territory is generally considered to be a contra-indication to thrombolytic therapy.
Hyperdense Vessel Sign A hyperdense vessel is defined as a vessel denser than its counterpart and denser than any non-calcified vessel of similar size. This sign indicates poor outcome and poor response to IV-TPA therapy.
Basilar Thrombosis Thrombosis of the basilar artery is a common finding in stroke patients. CT findings include a dense basilar artery without contrast injection.
Lentiform Nucleus Obscuration
Subacute Infarction -Increasing mass effect - Wedge shaped low density - Hgic transformation After 4 - 7 days the CT - Gyral enhancement - Persistent mass effect In 1-8 weeks: - Mass effect resolves - Enhancement may persist
Chronic Infarction
Case 1
Gunshot injury leading to brain contusion,localized subarachnoid hemorrhage & skull fracture at the site of the bullet entry
Case 2
Depressed skull fracture,pneumocephaly
Case 3
Subacute subdural hematoma
Case 4
Chronic subdural hematoma with fluid fluid level secondary to new bleeding &mix of recent and old blood
Case 5
Intraventricular hemorrhage,extending from intracerebral hge
Case 6
Ischemic cerebral stroke Hyperdense vessel sign of MCA
Case 8
Chronic cerebral infarction
Case 9
Brain contusion(TBI)