13. Central Nervous System Trauma

What are axial loading fractures?

Axial loading, also referred to as vertical compression, occurs when sufficient force is exerted vertically through the spinal column. The vertebral bodies may undergo compression fracture. Bone fragments and disk matter are sent in all directions, including into the spinal canal. Injury from this mechanism often occurs with shallow diving or head-first tackling and generally results in significant SCI.

What is seen on imaging of subdural hematomas and whaat is the treatment?

CT scanning is usually the first evaluation in patients with suspected acute subdural hematoma. Acute SDH is visualized on head CT as a superdense (white) crescent-shaped mass between the inner table of the skull and the surface of the cerebral hemisphere. SDHs are concave toward the brain and unlimited by suture lines. In contrast to SDH, epidural hematoma is convex toward the brain on CT because its collection is restricted by firm dural attachments at the cranial sutures. Principles of treatment. An acute SDH requires immediate medical attention. In most cases, emergency surgery must be done to drain the hematoma and to control bleeding. If surgical treatment is delayed mortality may be high.

What are cerebral contusions and lacerations?

Cerebral contusions and lacerations involve structural brain damage and thus are more serious than concussions. Cerebral contusions are bruises of the brain, usually caused by a direct, strong blow to the head. Cerebral lacerations are disruption of the pial-glial membrane with tearing of the underlying tissue. In a simple contusion, the overlying pial-glial membrane is intact. Disruption of this membrane with tearing of the underlying tissue constitutes a laceration. Contusions and lacerations form a continuum of tissue injury.

What causes a cerebral contusion?

Cerebral contusions result when mechanical forces damage the small blood vessels (capillaries, veins or arteries) and other tissue components (nerve and glial cells and their processes) of the neural parenchyma. Contusions are typically surface lesions of the brain. • If the force of impact is mild, cerebral contusion is limited to the outer layers of cortex and the crests of gyri. The bleeding from damaged blood vessels is the most obvious feature and pathologic findings are limited to superficial microhemorrhages visible only under the microscope. • Greater force destroys larger areas of cortex, causing confluent hemorrhagic necrotic lesions extending through the cortex into the subcortical white matter. • An even greater force may even lacerate the cortex, causing intraparenchymal hemorrhage. Bruised, necrotic tissue is phagocytosed by macrophages and eliminated in large part via the bloodstream. Astrocytosis then leads to local scar formation, which persists as telltale evidence of a prior contusion. Usually some residual hemosiderin imparts an orange-brown hue to the old contusion.

What is dementia pugilistica?

Chronic traumatic encephalopathy (CTE) was formerly believed to exist primarily among boxers and was referred to as dementia pugilistica. CTE is a progressive degenerative disease, which afflicts the brain of people who have suffered repeated concussions and traumatic brain injuries, such as athletes who take part in contact sports (American football, soccer, ice hockey and rugby), members of the military in training and combat.

What is the clinical presentation of diffuse axonal injury?

Coma is the most common immediate impairment that has been associated with the severity of DAI. The functional loss of axonal activity may immediately render the patient comatose in the absence of mass lesions, but imaging may show only small hemorrhages and focal edema along midline structures. Patients either remain comatose or go into a persistent vegetative state. Persistent vegetative state is absence of responsiveness and awareness due to overwhelming dysfunction of the cerebral hemispheres, with sufficient sparing of the diencephalon and brain stem to preserve autonomic and motor reflexes and sleep-wake cycles.

What is a concussion?

Concussion is the mildest form of diffuse injury. The term concussion is synonym for "mild traumatic brain injury" (TBI). Concussion is produced by a direct blow to the head that imparts a quick rotational acceleration to the brainstem causing a temporary paralysis of the brainstem reticular formation neurons which play a crucial role in maintaining behavioral arousal and consciousness. Approximately 2.5 million people sustain a TBI in the United States every year. The most common causes of TBI are motor vehicle accidents, falls, occupational accidents, recreational accidents, and assaults. Concussion also occurs in contact sports; American football, ice hockey, soccer, boxing, and rugby are associated with a particularly high incidence of concussions. Concussion is defined as a transient loss of consciousness of less than 30 minutes, amnesia surrounding the traumatic event and Glasgow Coma Scale (GCS) score of 13 to 15. Other signs and symptoms that occur often after a concussion include headache, confusion, dizziness, nausea and vomiting. Others symptoms may be delayed for hours or days after injury, such as concentration, irritability, deficit in attention and reaction time. The clinical symptoms largely reflect a functional disturbance rather than structural injury, and as such, no abnormality is seen on standard structural neuroimaging studies. The impairment of neurologic function is short-lived and resolves spontaneously. However, concussion is not as harmless as previously thought, and repeat concussions often result in some degree of permanent neurological impairment. There is increased experimental evidence that some permanent damage is present in the more severe grades. Experimental models of repetitive mild or "concussive" traumatic brain injury in mice have demonstrated axonal cytoskeletal disruption, intraaxonal organelle compaction and irregularities in axon caliber on ultrastructural examination of the brain. The activation of microglia and formation of microglial clusters (areas of microglia proliferation/macrophage infiltration) were also observed.

What causes linear skull fractures? What vessels may be injured?

A linear skull fracture is a single fracture that most often extends through the entire thickness of the calvarium. Linear skull fractures result from low-energy blunt trauma over a wide surface area of the skull. The great majority of linear skull fractures have minimal or no clinical significance. However, fractures that cross the middle meningeal groove in the temporal bone or venous dural sinuses may disturb these vascular structures causing epidural hematoma and venous sinus thrombosis, respectively.

What are the clinical presentations of patients with complete cord injuries, incomplete injuries, central cord syndrome, anterior cord syndrome, and transient paralysis and spinal shock?

1. Complete cord injury. In a complete cord injury, there will be a rostral zone of spared sensory levels (e.g., the C5 and higher dermatomes spared in a C5-6 fracture-dislocation), reduced sensation in the next caudal level, and no sensation in levels below. Similarly, there will be reduced muscle power in the level immediately below the injury, followed by complete paralysis in more caudal myotomes. In the acute stage, reflexes are absent, there is no response to plantar stimulation, and muscle tone is flaccid. 2. Incomplete injury. In incomplete injuries, there are various degrees of motor function in muscles controlled by levels of the spinal cord caudal to the injury. Sensation is also partially preserved in dermatomes below the area of injury. 3. Central cord syndrome. An acute central cord syndrome is characterized by motor deficits that are more pronounced in the upper extremities as compared to the lower extremities, as well as bladder dysfunction (retention) and a variable degree of sensory loss below the level of injury after relatively mild trauma. 4. Anterior cord syndrome. Lesions affecting the anterior or ventral two-thirds of the spinal cord, sparing the dorsal columns, usually reflect injury to the anterior spinal artery. It is believed that this more often represents a direct injury to the anterior spinal cord by retropulsed disc or bone fragments rather than primary disruption of the anterior spinal artery. 5. Transient paralysis and spinal shock. Immediately after a spinal cord injury, there may be a physiological loss of all spinal cord function caudal to the level of the injury, with flaccid paralysis, anesthesia, absent bowel and bladder control, and loss of reflex activity. This altered physiologic state may last several hours to several weeks and is sometimes referred to as spinal shock. Clinical manifestations may normalize or are replaced by a spastic paresis reflecting more severe morphologic injury to the spinal cord.

What are the two basic mechanisms of head injuries? What causes them and what are some complications that can arise from each?

1. Local contact injuries. Examples of injuries caused by local contact mechanism include most linear and depressed skull fractures, some basilar skull fractures, epidural hematomas, and coup contusions. A linear skull fracture occurs as a result of local skull bending at the impact site that exceeds the local strain limit for the bony tissue. Epidural hematoma is a complication of skull bending that is usually associated with skull fracture. In the limiting case, dural vessels are torn as the fracture propagates and travels past a vessel. Coup contusions occur beneath the site of impact under certain conditions. Coup contusions are not associated with skull fracture. These contusions are due to direct injury to the brain and its surface vessels that lie beneath the area of skull deformation. Local contact mechanism can produce remote injuries as a result of skull distortion. This mechanism contributes to vault fractures away from the impact site, to basilar skull fractures, and to contrecoup contusions. 2. Head inertial (acceleration/deceleration) injuries. Whiplash is the common term used to describe acceleration-deceleration injuries. Whiplash was so named because of the head's lashing motion during the accident. Acceleration-deceleration is a more accurate description of what is happening inside the skull. During a car accident, for example, the head and extremities continue moving forward, despite the fact the car has suddenly stopped. The head, arms and legs continue accelerating until something stops them, like reaching their limits. The same acceleration deceleration action happens inside the body as well, the brain continues moving forward until it is stopped by the skull. The brain literally slides back and forth within the skull, an action called shearing. High-speed motor-vehicle accidents and rear end collisions are the most common cause of acceleration- deceleration injuries. Contact sports and other activities may also cause this type of brain injury. Acceleration- deceleration injury may be caused by shaking a child violently, otherwise known as shaken baby syndrome.

Which bones are involved in basilar fractures? What clinical signs can signify a basilar fracture? What nerves may be damaged?

A basilar fracture is a linear fracture at the base of the skull. It is usually associated with a dural tear. Basilar skull fractures involve at least one of the five bones that comprise the base of the skull: cribriform plate of the ethmoid bone, orbital plate of the frontal bone, petrous and squamous portion of the temporal bone, and the sphenoid and occipital bones. Basilar skull fractures occur most commonly through the temporal bone; this is due to the temporal bone's relative weakness and the proximity of the middle meningeal artery and vein. The dural tear creates a communication between the subarachnoid space, the paranasal sinuses, and the middle ear. CSF leaks develop in up to 45% of basilar skull fractures. Clinical signs of basilar skull fractures include the following: (a) retroauricular or mastoid ecchymosis (i.e., Battle sign); (b) "raccoon eyes" (i.e., periorbital ecchymosis); Battle sign and raccoon eyes are typically NOT present during the examination immediately following the injury but appear one to three days later; (c) CSF leaks such as clear rhinorrhea or otorrhea; and (d) hemotympanum, i.e., blood behind the tympanic membrane. In addition, basilar fractures can damage oculomotor, trochlear, abducens, facial, and acoustic nerves giving rise to extraocular muscle paralysis, facial nerve palsies or hearing loss.

Where is brain damage most severe in diffuse axonal injury? What immunostain can be used to detect axonal lesions?

Brain damage is most severe along midline structures (corpus callosum, brainstem) where the shear forces are greatest, and at the cortex-white matter junction because of the change in the consistency of brain tissue. Axonal swellings can be detected with H&E and silver stains 15 hours after the injury. Immunostains with antibodies to beta-amyloid precursor protein (BAPP) can detect the axonal lesions in 2-3 hours after the injury. BAPP is produced by neurons as a reaction to injury. It flows down the axon and accumulates at points of axonal constriction or transection. Distal to the swellings, axons and myelin degenerate and gliosis develops over time. Severe DAI may cause decrease of white matter volume, atrophy of the corpus callosum, and dilatation of the lateral ventricles.

What is the clinical presentation of contusions and lacerations?

Contusions and lacerations may be very small, causing only minimal damage to the brain, with few symptoms or symptoms of minor head injury. However, with larger contusions people may have symptoms of severe head injury. For example, people often are unconscious for a few minutes or longer. When awake, people often are drowsy, confused, restless, or agitated. They may also have vomiting, seizures, or impaired balance or coordination. The ability to think, control emotions, move, feel, speak, see, hear, smell, and remember may be impaired. Severe anterior temporal lobe contusions are often associated with delirium; orbitofrontal contusions are associated with disinhibited behavior and impulsiveness; medial temporal lobe contusions may be associated with memory loss; convexity contusions may be associated with focal deficits such as aphasia or hemiparesis.

Where do contusions most often occur?

Contusions are most commonly located at superficial cortical regions at the impact point or where the moving brain rubs or comes to a stop along the inner surface of the skull. Contusions most frequently involve the inferior aspect of the frontal lobes, inferolateral part and poles of the temporal lobes and the cortex above and below the Sylvian fissures where brain comes into contact with the irregular bony surfaces and the anterior and middle cranial fossae due to the motion of the brain in relation to the skull at these sites. The occipital lobes and cerebellum are rarely contused as the posterior part of the skull is relatively smooth. Contusions are most severe in the frontal and temporal lobes, irrespective of the site of cranial impact, provided that the forces acting on the head are sufficient to impart movement of the brain over the irregular bony surfaces of the anterior and middle cranial fossa. Both frontal and occipital impacts result in contusions that are most severe in the frontal and temporal lobes. For example, a fall to the back with the occiput hitting the ground causes contusions in the inferior frontal and temporal lobes.

What are the different types of contusions?

Contusions can be classified as coup (from the French, "blow") or contrecoup injuries. Coup contusions occur at the location of impact, whereas contrecoup contusions occur on the opposite side or at a point distant from the impact. Contusions may be present in any part of the brain but are most common in the frontal, temporal and occipital lobes. Contrecoup lesions are often more severe and extensive than those at the impact site. This phenomenon is particularly common at the frontal and temporal poles in association with a blow to the back of the head. In the case of traumatic brain injury with midline occipital impact, the coup contusions are primarily in the cerebellum, while contrecoup contusions are localized in bilateral frontal and temporal lobes. In this case, these contrecoup lesions are more severe due to the rough edges of the sphenoid wings and the floor of the frontal anterior fossa, compared to occipital lobe injuries.

What causes depressed fractures? What region of the skull is most likely to be affected?

Depressed skull fractures result from a high-energy direct blow to a small surface area of the skull with a blunt object such as a baseball bat. It drives a segment of the skull below the level of the adjacent skull. Most of the depressed fractures are over the frontoparietal region because the bone is thin, and the specific location is prone to an assailant's attack. These fractures often involve injury to the brain parenchyma and place patients at significant risk for CNS infection, seizures, and death.

What causes diastatic fractures?

Diastatic skull fractures (DSFs) occur as a result of external trauma. The fracture line in DSF transverses one or more sutures of the skull causing a widening of the suture line. While this type of fracture is usually seen in infants and young children as the sutures are not yet fused it can also occur in adults. DSFs most commonly involved the occipito-mastoid and lambdoid sutures of the occipital area. DSF is observed on simple skull radiographs as a wider lucent line, with no interdigitation compared with normal sutures. DSF is complicated by epidural hemorrhage, subgaleal hematomas and growing skull fractures. Subgaleal hematoma is bleeding in the potential space between the skull periosteum and the scalp galea aponeurosis.

What is diffuse axonal injury?

Diffuse axonal injury (DAI) is a special traumatic lesion in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area. Over the past 70 years, DAI has emerged as one of the most common and important pathological features of traumatic brain injury. Subjects with DAI may develop coma and persistent vegetative state in absence of gross hematomas, contusions or lacerations. It occurs in about half of all cases of severe head trauma.

What are growing skull fractures?

Growing skull fracture (GSF) consists of progressive widening of a diastatic fracture, tear of the dura matter, formation of a cranial defect, herniation of the leptomeninges, and ultimately, herniation of the underlying brain parenchyma through the defect. The brain tissue and arachnoid membrane become entrapped within the fracture margins with or without the development of neurological deficits. GSF are more common in the parietal region, although they may occur anywhere. Patients present with a progressively enlarging pulsatile mass or an enlarging palpable cranial defect. It may enlarge over months after the initial skull fracture. Neurological complications include seizures, hemiparesis and psychomotor retardation. Skull radiographs demonstrate a diastatic fracture, with the edges separated by more than 3 mm.

What causes epidural hematoma?

Hematoma develops when the fracture transects blood vessels. Most of EDHs are of arterial origin as the result of tearing of meningeal arteries. A few of them are of venous origin as the result of tearing of venous dural sinuses. EDHs are most frequently found in the temporoparietal regions (73%), where the middle meningeal arteries and veins have been damaged usually by a fracture involving the squamous temporal bone. Eleven percent of EDHs occur in the anterior cranial fossa (anterior meningeal artery), 9% in the parasagittal regions (sagittal sinus), and 7% in the posterior fossa (occipital meningeal artery and transverse and sigmoid sinuses.

What causes hyperextension injuries?

Hyperextension injury is a consequence of falls, when the chin strikes and immovable object, or in a rear-end collision. Hyperextension injury produces a stretch or tear of the anterior longitudinal ligaments, possible fracture and subluxation of the vertebrae and rupture of the disks. If the integrity of the spinal canal is compromised, the spinal cord may be damaged. Injury also occurs when the hyperextended spinal cord is stretched excessively so that it is compressed by the ligamentum flavum, causing cord contusion and ischemia.

What are some types of hyperflexion injuries?

Hyperflexion injury occurs when a portion of the spine receives a force exerted toward the anterior surface of the vertebral body, causing flexion beyond the normal range of motion. This is often associated with head-on collisions. Hyperflexion injuries are associated with anterior vertebral compression (wedge) fracture and possible intervertebral disk herniation. Posterior ligaments are stretched and may tear, allowing the vertebrae to subluxate. Subluxation of the vertebral column disrupts the continuity of the spinal canal, stretching and impinging on the spinal cord and altering spinal cord blood flow. Disk matter can also extrude into the spinal canal toward the cord.

How are epidural hematomas identified and treated?

Plain radiography of the head (skull radiography) may reveal skull fractures, though CT scanning has largely replaced the use of skull radiography. The systematic use of CT scanning has resulted in the increased recognition of EDHs. EDH appears as a superdense (white) lens-shaped mass situated between the brain and the skull. Principles of treatment. Surgical evacuation constitutes definitive treatment of this condition. Craniotomy or laminectomy is followed by evacuation of the hematoma, and coagulation of bleeding sites.

What is a ring fracture?

Ring fractures encircle the foramen magnum and results from falls or jump from heights, usually > 5 stories, onto the feet or buttocks. The cervical spine is forced into the skull, breaking off a rim of occipital bone.

What are the three classifications of subdural hematomas?

SDH can be classified as acute, subacute, or chronic. An acute SDH becomes evident within 3 days of injury, subacute between 3 and 21 days, and chronic if more than 21 days pass between injury and clinical presentation. Pathologically, an acute SDH is composed of fresh and jelly-like clot, a subacute SDH represents a mixture of clotted blood and fluid, as a result of fibrinolysis occurring within the clot; and a chronic SDH is one that is in fluid phase.

What types of injuries cause subdural hematomas?

SDH usually occurs after head injuries from falls, assaults, vehicular accidents and sporting mishaps. Bridging veins are particularly prone to tearing along their course through the dural layers. In older individuals with brain atrophy, the bridging veins are stretched, hence the increased rate of subdural hematomas in these patients, even after relatively minor head trauma. Less often SDHs are unrelated to trauma and occur in patients with chronic alcohol abuse, hematological disorders, anticoagulant and thrombolytic therapy.

What is the clinical presentation of subdural hematomas?

SDHs have a wide clinical spectrum. Acute SDH is more common in younger patients with a history of trauma. Chronic SDH occurs more often in elderly and alcoholic patients as they are most prone to atrophy and/or coagulopathy. Severe head trauma may result in SDH with coma; up to 38% of patients have a transient "lucid interval" after the acute injury that is followed by a progressive neurologic decline to coma. A lesser injury may produce acute SDH with only momentary loss of consciousness. Subacute and chronic SDH may present insidiously, typically with altered mental state (confusion, apathy and somnolence) and less frequently with focal deficits (ipsilateral or contralateral hemiparesis).

What are some consequences of spinal cord injuries?

Spinal cord compression occurs due to the displacement of a vertebra, through herniation of an intervertebral disk, or from displacement of a vertebral bone fragment. The pressure caused by these mechanisms results in physical damage to the cord. A cord transection is an injury that partially or completely severs the spinal cord. In a complete transection, the cord is totally cut and the potential to send and receive nerve impulses below the site of injury is lost. With a spinal cord transection below the beginning of the thoracic spine, the signs and symptoms include incontinence and paraplegia. A transection in the cervical spine region can cause quadriplegia, incontinence and partial or complete respiratory paralysis

What are the symptoms of chronic traumatic encephalopathy?

Symptoms of CTE include difficulties with balance, motor features of parkinsonism, behavioral and mood changes, memory loss, cognitive impairment and dementia.

What generates the shearing forces associated with diffuse axonal injury?

The parasagittal cerebral hemispheres are anchored to arachnoid granulations, whereas the lateral aspects of the cerebrum move more freely. This anatomic feature, together with the differential density of gray and white matter, permits generation of shearing forces between different brain regions, leading to axonal shearing injuries. Shearing injuries can distort or stretch axons, leading to immediate loss of function. This sudden deformation causes changes in the axonal cytoskeleton (compaction of neurofilaments, loss of microtubules) that lead to an arrest of the fast axoplasmic flow. Components of this flow, including mitochondria and other organelles, accumulate proximal to the lesion and cause axonal swellings. Some axons with mild lesions probably recover but many eventually rupture. It takes several hours from trauma to axonal rupture. This cascade of reactions leads to the formation of axonal swellings located at nodes of Ranvier where the axolemma is more liable to deform because there is no myelin. The disruption of the axolemma causes influx of calcium into the cell and unleashing a variety of degrading processes. Possible routes of calcium entry include pores torn in the 12 membrane during stretch, and failure of ATP-dependent transporters due to mechanical blockage or lack of energy. High levels of intracellular calcium contribute to the degradation of cytoskeleton and mitochondria, generation of reactive oxygen species and activation of phospholipases and proteolytic enzymes that damage sodium channels. The presence of high concentrations of calcium in the cell cytoplasm initiates the caspase cascade that usually leads to apoptosis. These processes generally occur 1 to 6 hours into the process of post-stretch injury.

What can be seen on imaging of patients with diffuse axonal injury?

The predominant pathology of DAI—microscopic axonal swellings—has proven extremely difficult to illuminate with noninvasive methods despite its extensive nature. Accordingly, patients with little macroscopic injury after diffuse brain injury typically have normal appearing images of the brain. Clinically, DAI is often a "diagnosis of exclusion" based on the inability of conventional imaging techniques to detect brain pathology despite overt symptoms, such as prolonged unconsciousness or cognitive dysfunction after brain trauma.

What is a subdural hematoma and what veins are the primary cause?

The subdural hematoma (SDH) is formed when blood collects in the potential space between the dura and the arachnoid. Although the hematoma occupies the 'subdural space' there is normally no such anatomical compartment. Classically, SDHs are due to tearing of bridging veins that span the subdural space to drain cortical blood directly into dural sinuses. In contrast, epidural hematomas are usually caused by tears in arteries. SDHs are much more common than EDHs. SDHs have been classified on the basis of etiology (traumatic or nontraumatic), and chronology (acute, subacute, or chronic).

What is the clinical presentation of epidural hematomas?

The ultimate size of the EDH depends on the size and nature of the vessels lacerated and how tightly the dura is adherent to the inner table of the skull. When the hemorrhage is more than 1 cm deep or more than 25 mL in volume, the EDH is usually clinically significant and an indication for surgical evacuation; in fatal cases, the hemorrhage volume is ≥100 mL. The classic clinical course of a patient with EDH consists of an initial loss of consciousness after trauma, transient complete recovery ("lucid interval"), then rapid progression of neurological deterioration. This classic presentation occurs in only 20% of patients. Instead, patients with EDH may be unconscious from the time of initial injury, may regain consciousness after a brief coma, or may have no loss of consciousness whatsoever. Neurological deterioration from an expanding EDH typically results in altered level of consciousness (obtundation), nausea and vomiting, focal neurologic deficit [such as contralateral hemiparesis, ipsilateral papillary dilatation (due to uncal herniation)], bradycardia and arterial hypertension (indicative of elevated intracranial pressure and Cushing triad), and finally, apnea and death. Development of these symptoms depends on hematoma size.

What is a primary vs secondary injury?

Traumatic brain injuries may be divided into primary and secondary types of injury. Primary injury consists of the initial damage directly resulting from the mechanical forces affecting the cerebral tissues. Secondary injury refers to the cascade of cellular and molecular processes initiated by the primary injury. In addition, secondary injury consists of the cerebral damage due to hypotensive events, cerebral swelling, raised intracranial pressure and hydrocephalus. The concept of focal and diffuse brain injuries is based on the presence of focal (mass) lesions on the CT head scan. The main mechanism responsible for focal injury is local brain damage produced by collision forces acting on the skull and resulting in compression of the tissue underneath the cranium at the site of impact (coup) or of tissue oppositely to the impact (contrecoup). The location and severity of impact to the skull ultimately determine the cerebral pathology and neurological deficits. Focal injury constitutes subdural and epidural hematomas, intraparenchymal hematomas, and (hemorrhagic) contusions. Diffuse brain injury entails widely distributed damage to axons, diffuse vascular injury, hypoxic-ischemic injury, and brain swelling (edema). Pathological studies of comatose patients with CT evidence of diffuse injury showed widespread white matter axonal damage which is known as 'diffuse axonal injury'.

What is a traumatic intracerebral hematoma?

Traumatic intracerebral hematoma (TICH) is defined as the occurrence after cranial trauma of parenchymal brain hematoma two cm or greater in diameter, not in contact with the surface of the brain. TICHs are most commonly found in either the orbitofrontal or temporal lobes. They are located within the deep white matter, while contusions are more superficial cortical in location. TICHs are associated with severe trauma and clinically appear as expanding mass lesions with significant focal neurologic deficit. TICHs typically result from rupture of intrinsic cerebral vessels (a small parenchymal artery in most cases). Deeper TICHs, such as those occurring in the basal ganglia and internal capsule, are much less common.

What is the cause of diffuse axonal injury?

Unlike brain trauma that occurs due to direct impact and deformation of the brain, DAI is the not the result of a direct impact and deformation of the brain. DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated. DAI occurs most frequently in motor vehicle accidents and following blows to the unsupported head.