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)
1-Skull fractures.
1-Skull fractures.
2-Extradural ,subdural & subarachinoid.
3-Cerebral contusion& intraventricular Hge.
4-Diffuse Axonal Injury (DAI).
5-Related Brain edema & herniation.
A skull fracture is a break in the skull bone and generally occurs as a result of direct impact .
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:
Four major types of skull fractures may occur:
(1) linear,
(2) depressed,
(3) diastatic,
(4) basilar.
Most basilar fractures occur at 2 specific anatomic locations — namely, the temporal region and the occipital condylar region.
Most basilar fractures occur at 2 specific anatomic locations — namely, the temporal region and the occipital condylar region.
An epidural hematoma is usually associated with a skull fracture. It often occurs when adirect impact fractures the calvarium .
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
Natasha Richardson
March 2009
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)
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
Crescent shaped; Hyperdense, may contain hypodense foci due to serum, CSF or active bleeding
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) .
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 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
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 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.
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.
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 .
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.
When traumatic, subarachnoid hemorrhage occurs most commonly over the cerebral convexities or adjacent to otherwise injured brain (i.e. adjacent to a cerebral contusion)
When traumatic, subarachnoid hemorrhage occurs most commonly over the cerebral convexities or adjacent to otherwise injured brain (i.e. adjacent to a cerebral contusion)
Brain contusions commonly are identified in patients with traumatic brain injury (TBI) .
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
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 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 .
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 .
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 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 .
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 .
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 .
Severe brain edema or a large intracranial hemorrhage may cause downward brain displacement and coning, which is usually fatal
Severe brain edema or a large intracranial hemorrhage may cause downward brain displacement and coning, which is usually fatal
due to rupture of a cerebral blood vessel that causes bleeding into or around the brain .
account for 16% of all strokes .
Intracerebral hge is the most common, accounting for 10% of all strokes .
Intracerebral hge is the most common, accounting for 10% of all strokes .
Now Dudes tell me what are the reasons of cerebral 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.
Common aneurysm locations include the anterior and posterior communicating arteries, the middle cerebral artery bifurcation and the tip of the basilar artery.
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 .
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
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
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.
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.
Hypodensity in greater than one-third of the middle cerebral artery territory is generally considered to be a contra-indication to thrombolytic therapy.
Hypodensity in greater than one-third of the middle cerebral artery territory is generally considered to be a contra-indication to thrombolytic therapy.
A hyperdense vessel is defined as a vessel denser than its counterpart and denser than any non-calcified vessel of similar size.
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.
Thrombosis of the basilar artery is a common finding in stroke patients. CT findings include a dense basilar artery without contrast injection.
Thrombosis of the basilar artery is a common finding in stroke patients. CT findings include a dense basilar artery without contrast injection.
-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
-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
