Brain Trauma (Gianani( Flashcards
Mechanisms of brain injury
Direct impact (cerebral contusion and laceration). Movement of the brain inside the skull (subdural hematoma and diffuse axonal injury).
Direct impact on the brain–>
can cause laceration or contusion in areas close to or remote from the impact (kinetic energy transmitted through the brain).
This motion stretches axons, tears blood vessels, and damages the surface of the brain as it bounces against bony ridges at the base of the skull.
Classification of traumatic brain injury
Skull fractures.
Parenchymal injury.
Traumatic vascular injury.
Skull fractures classification.
- Linear skull fracture (breaks in bone that transverse the full thickness of the bone from inner to outer table).
- Depressed skull fracture (a fracture displaced by a thickness equal or larger than the thickness of the bone).
- Diastatic skull fracture.
- Basilar skull fracture .
skull fracture in general
- does not necessarily indicate underlying brain damage.
- may create a communication between the intracranial compartment and septic areas such as air sinuses, nasal fossae, and middle and external ear, –> infection of the brain and meninges.
- Linear fracture - usually not clinically significant unless they transverse or parallel in close proximity a suture or involve a vascular structure. may –> suture diastasis, venous sinus thrombosis or epidural hematoma.
Depressed skull fracture usually result from
blunt force trauma.
usually a comminuted fracture in which small bone fragments are displaced inward.
Compound depressed fractures- usually soft tissue laceration above the fracture.
- Depressed skull fracture can be complicated by parenchymal hemorrhage or injury, esp. if associated with torn dura (Complex depressed fracture).
Parenchymal injury.
Concussion. (not actual tissue damage)
Direct parenchymal injury (transmission of kinetic energy to the brain).
1. Contusion (bruising of the brain). 2. Laceration (tearing of the tissue).
Diffuse axonal injury.
CEREBRAL CONTUSIONS
= hemorrhagic necrosis of brain tissue.*
When the head is abruptly brought to a stop against a solid object, such as the dashboard or the ground, the brain continues to move for an instant, hitting the inside the now stationary skull.
The soft brain is easily contused and lacerated by the hard bony ridges at the base of the skull or by the tentorium cerebelli and falx cerebri.
Contusions usually involve the surface of the brain, especially the crowns of gyri, and are ** more frequent in the orbital surfaces of the frontal lobes and the tips of the temporal lobes.
Contre -coup contusions
Contusions that develop opposite the impact.
DIFFUSE AXONAL INJURY
(TRAUMATIC AXONAL INJURY)
a special traumatic lesion, which occurs most frequently in motor vehicle accidents and following blows to the unsupported head.
In the course of such injuries, the cerebrum goes into a back and forth gliding motion, pivoting around the upper brainstem.
The brainstem, together with the cerebellum, is held firmly fixed by the tentorium, and the falx prevents side-to-side motion.
Axons are stretched but do not snap from this injury.
what is prone to diffuse axonal injury?
** Deep white matter is most prone to acceleration-deceleration injury.
Can be mild to severe (shearing injury)
Moderate to severe axonal injury results in Wallerian degeneration.
CNS myelin made by oligodendrocytes, not Schwann cells (PNS)…they don’t come back like Schwann cells.
Traumatic vascular injury (types)
Epidural hematoma.
Subdural hematoma.
Traumatic sub-arachnoid hemorrhage.
Vessels that bleed
(brain)
Middle meningeal artery (R or L) runs in the epidural space
Bridging veins that go across the dura (meningeal layer) to the skull and bleed in the subdural space between the arachnoid layer and meningeal layer of dura.. [cause subdural hematoma]
Cerebral arteries in subarachnoid space.
Key factors in an epidural hematoma
Usually impact injury with tear of middle meningeal artery
the MMA Is a branch of external carotid artery…supplies dura…does not go into brain parenchyma
Lens shaped
Biconvex on CT
Epidural hematoma- blathering
- Rapidly expanding hemorrhage under arterial pressure
- peels the dura away from the inner surface of the skull,–> lens-shaped biconvex hematoma
- no spread past the cranial sutures where the dura is tightly apposed to the skull
- Initially may have no symptoms (lucid interval).
- Within hours hematoma –> compress brain tissue, –> elevated intracranial pressure–> herniation and death unless treated surgically.
- no epidural space normally; dura is adherent to the skull.
- Fracture of the inner table of the skull can tear arteries and veins that run between the dura and the skull.
- blow to the head may cause instant deformation of the skull without a fracture–> vascular tears. Bleeding from these vessels lifts the dura off of the skull forming an epidural blood clot.
- Epidural hematomas develop most commonly with fractures of the squamous portions of the temporal and parietal bones that tear the middle meningeal vessels. Less commonly, they result form tears of diploic veins and dural sinuses.
Symptoms of increased intracranial pressure in epidural hematomas with arterial rupture usually develop within hours after the injury. With venous bleeding, they take longer. There is a natural epidural space around the spinal cord. Spinal epidural hematoma may occur as a result of trauma, but may also develop spontaneously in patients with bleeding disorders.
Subdural Hematoma- key facts
- Subdural space is not connected to arachnoid space where the CSF is.
- half moon shaped/ crescent shaped
Large subdural hematomas raise the intracranial pressure and compress the brain. With arterial bleeding, symptoms develop rapidly. In many instances, especially with venous subdurals of infants and old people, there is an interval between trauma and the onset of symptoms. Sometimes the preceding injury is insignificant, or no history of trauma can be elicited.
how do you know an epidural hematoma is there?
CT scan
Subdural Hematoma- Epidemiology and etiology
Head trauma is the most common cause of SDH, with the majority of cases related to motor vehicle accidents, falls, and assaults
subdural hematoma- common risk factors (blathering)
Patients with significant cerebral atrophy are at high risk for SDH.
- elderly
- history of chronic alcohol abuse
- previous traumatic brain injury.
In such patients, trivial head trauma or even pure whiplash injury in the absence of physical impact may –> SDH.
Thus, SDH, particularly chronic SDH, is seen in older adults more commonly than younger adults.
SDH may be more common than epidural hematoma.
The use of antithrombotic agents increases the risk of SDH,
acute subdural hematoma info
for acute- impact velocity must be quite high.
usually associated with other serious injuries, such as traumatic subarachnoid hemorrhage and brain contusion. –> worse prognosis than with chronic subdural hematoma or even epidural hematoma.
coma is present from the time of injury half the time.
Posterior fossa SDH, like most space-occupying lesions in this location, presents with symptoms of elevated intracranial pressure including headache, vomiting, anisocoria, dysphagia, cranial nerve palsies, nuchal rigidity, and ataxia.
In some instances of SDH, cerebral hypoperfusion due to increased intracranial pressure or mass effect may –> cerebral infarction, esp in the posterior fossa, where the posterior cerebral arteries are vulnerable to compression along the edge of the tentorium cerebelli.
Radiological appearance of subdural hematomas
crescent shaped, spread over a large area
Density depends on the age of the blood.
- acute blood is hyperdense, bright on CT scan.
- After 1 to 2 weeks, the clot begins to liquefy and may appear isodense.
- If no further bleeding, after 3 to 4 weeks the hematoma will be completely liquefied and will appear uniformly hypodense
- if continued occasional bleeding, there will be a mixed density appearance resulting from liquefied chronic blood mixed with clotted hyperdense blood.
Chronic subdural hematoma
insidious onset of headaches, light-headedness, cognitive impairment, apathy, somnolence, and occasionally seizures, may occur as a consequence of chronic SDH, and symptoms may not become evident until weeks after the initial injury. Global deficits such as disturbances of consciousness are more common than focal deficits after SDH.
Focal deficits may be either ipsilateral or contralateral to the side of the SDH. Contralateral hemiparesis can occur as a result of direct compression of cortex underlying the hematoma, whereas ipsilateral hemiparesis can occur with lateral displacement of the midbrain caused by the mass effect of the hematoma. Such midbrain displacement results in compression of the contralateral cerebral peduncle against the free edge of the tentorium. Symptoms due to chronic SDH may be transient or fluctuating.
Bitemporal chronic SDH may present with intermittent paraparesis that is proximal and painless.
where SDH comes from
Subdural haemorrhages occur more frequently than EDHs
less likely to be associated with skull fracture.
SDHs may be preceded by head injury, or no history of trauma
- Those at the extremes of life, chronic alcoholics–> greatest risk (anatomy of the subdural space, cerebral atrophy and an increased propensity for falls etc.)
SDHs may be ‘acute’, ‘sub-acute’ or ‘chronic’.
Bleeding - from torn bridging (‘communicating’) veins crossing the subdural space from the cerebral cortex to the dural sinuses,
- thought to be due to rotational and/or ‘shear’ strains which are often a result of impact.
- impact may not be necessary; frequently encountered in infants who have allegedly been ‘shaken’.
- usually 35- 100 mls blood–> ‘irritant’ or space occupying lesion.
Chronic SDHs- yellow/brown ‘membrane’ on the under-surface of the dura, may be an incidental finding in the elderly, the effects of which may have been confused clinically with dementia or a stroke.
the look of SDH on CT with continued occasional bleeding
there will be a mixed density appearance resulting from liquefied chronic blood mixed with clotted hyperdense blood. Sometimes, with mixed-density hematomas, the denser acute blood settles to the bottom, giving a characteristic hematocrit effect.
Chronic Subdural Hematoma –>
Hygroma
Development of chronic subdural hematoma — Initial meningeal trauma/ development of SDH–> dural collagen synthesis; fibroblasts spread over the inner surface of the dura to form a thick outer membrane –> thinner inner membrane develops–> encapsulation of the clot. approx 2 weeks.
chronic SDH may liquefy to form a hygroma, and the membranes may calcify
larger initial clot size appears to be related to a greater likelihood of subsequent expansion.
At any time, the hematoma may expand secondary to recurrent bleeding (“acute-on-chronic” SDH) or from osmotic draw of water into the hygroma, owing to its high protein content. Thalamic lesions and secondary brainstem injury may develop as a consequence of the mass effect produced by a large SDH.
Subdural hygroma
can come from SDH degeneration or passively as a consequence of traumatic brain injury followed by brain atrophy, dehydration, or decreased intracranial pressure.
mechanism: separation of the arachnoid layer from the dura, which can occur when a contracting brain pulls the arachnoid along with it while the dura remains adherent to the skull.
Most subdural hygromas will resolve with adequate reexpansion of the intracranial contents (ie, hydration).
some –> chronic.
related to the formation of pseudomembranes (as discussed above) that line the space created between the arachnoid and the dura during the acute phase. These subsequently become vascularized by abnormally permeable capillaries that allow for further accumulation of subdural fluid.
Traumatic Subarachnoid Hemorrhage
- most frequent traumatic brain lesion.
- results from rupture of corticomeningeal vessels and from hemorrhagic contusions of the brain.
- Usually diffuse; does not exert localized pressure.
- Blood is diluted by the CSF and does not clot unless massive.
- A large subarachnoid hemorrhage raises the intracranial pressure, impairs cerebral perfusion and causes HIE.
- Hemoglobin released form RBCs in the subarachnoid space triggers vascular spasm. also incites fibrosis of the arachnoid membrane and the subarachnoid space, which may impair CSF circulation leading to hydrocephalus.
The Shaken Baby Syndrome (SBS) is characterized by a triad of ***
1) encephalopathy
2) subdural hematomas
3) retinal hemorrhages
The subdural hematomas are located in the interhemispheric fissure or over the convexities and may be of varying ages.
They are usually small initially but may enlarge later or additional subdurals may appear when brain atrophy develops in infants who survive.
the brain atrophy of shaken baby is due to
HIE
low yield– response to SBS
Schwann cells -rapid.
activate ErbB2 receptors –> MAPK activity –> decreased synthesis of myelin lipids
myelin sheaths separate from the axons
Schwann clear up the myelin debris, attract macrophages (release of cytokines and chemokines)
Schwann cells mediate the initial stage of myelin debris clean up, macrophages come in to finish the job.
Macrophages - facilitated by opsonins, which label debris for removal.
Schwann cells emit growth factors that attract new axonal sprouts growing from the proximal stump after complete degeneration of the injured distal stump. This leads to possible reinnervation of the target cell or organ. However, the reinnervation is not necessarily perfect, as possible misleading occurs during reinnervation of the proximal axons to target cells.
In comparison to Schwann cells, oligodendrocytes require axon signals to survive. In their developmental stages, oligodendrocytes that failed to make contact to axon and receive any axon signals underwent apoptosis.
Experiments in Wallerian degeneration have shown that upon injury oligodendrocytes either undergo programmed cell death or enter a state of rest. Therefore, unlike Schwann cells, oligodendrocytes fail to clean up the myelin sheaths and their debris.
CNS rates of myelin sheath clearance are very slow and could possibly be the cause for hindrance in the regeneration capabilities of the CNS axons as no growth factors are available to attract the proximal axons. Another feature that results eventually is Glial scar formation. This further hinders chances for regeneration and reinnervation.
Oligodendrocytes fail to recruit macrophages for debris removal. Macrophage entry in general into CNS site of injury is very slow.
These findings have suggested that the delay in Wallerian degeneration in CNS in comparison to PNS is caused not due to a delay in axonal degeneration, but rather is due to the difference in clearance rates of myelin in CNS and PNS
Concept of Concussion
Loss of consciousness, in particular, may be due to dysfunction of the reticular activating substance of the upper brainstem. This is the part of the CNS that is subjected to the highest twisting force during sagittal rotation of the hemispheres. More important, it has become evident that repeated concussion, especially before symptoms from the previous one resolve, have a cumulative effect and can cause ** chronic traumatic encephalopathy.
Chronic traumatic encephalopathy
- pathology involves
pathology involves the cerebral cortex, white matter, deep nuclei, and the brainstem
Syndrome of CTE blathering
acute phase: concussion (esp. side-to-side hits to the head) –> DAI, release of tau and beta amyloid in the brain. + cerebral hypoxia, excitotoxicity and inflammatory mediators, –> neurodegeneration many years later.
syndrome of CTE begins insidiously
years after the patients have stopped playing sports,
-inattention, mood and behavior disturbances, confusion, and memory loss–> full blown dementia and parkinsonism.
brain atrophy, dilatation of the lateral and third ventricles, and thinning of the corpus callosum.
neuronal loss and tau deposition in neurons (neurofibrillary tangles-NFTs, neuropil neurites) and in astrocytes. T
- cerebral cortex, white matter, deep nuclei, and the brainstem.
In the cortex, the changes are patchy and affect the superficial cortex, perivascular areas, and deeper parts of cerebral sulci.
- tau deposition = key cellular change in CTE.
what do we see on brain section from a person with repeated traumatic brain injuries?
dense tau deposits, neurofibrillary tangles and abnormal neurites
The most common initial clinical symptom of Alzheimer’s is
impaired memory, although a wide range of other higher functions, such as personality and judgment, are also affected. Yet in very early, asymptomatic Alzheimer’s, pre-tangle Tau aggregates (oligomers) and Tau protein tangles are already present in the entorhinal cortex and hippocampal regions of the brain (see image below). These are the same regions where neuronal degeneration and loss of neuronal cells eventually occurs. With time, Tau tangles also form in the parieto-temporal and frontal region of the cortex, resulting in neuronal dysfunction (see image below). These processes are correlated with the worsening of clinical symptoms.
the final result of contusions/ bleeds/ edema/ increased CSF/ tumor
Contusion/bleed/edema/increased CSF/tumor….parenchymal damage-increased intracranial pressure…..herniation***
Pathophysiology of delayed brain injury
Angiographic vasospasm
Cortical spreading ischemia
delayed neurological complications (seizures, infection, etc.)
Delayed systemic complications (infection, fever, pulmonary edema, etc.)
Subfalcine herniation
Usually no clinical
- May compress anterior cerebral artery…infarction
central herniation
- VI cranial nerve(s) compromised…lateral rectus palsy
- bilateral uncal herniation…hemiparesis or full paresis…coma
uncal transtentorial herniation
hemiplagia, coma
3rd cranial nerve compromised…blown pupil
May compress posterior cerebral artery…primary visual cortex
tonsillar herniation
Brain stem compromise with
respiratory and cardiac effects…death
Common symptoms and signs of elevated intracranial pressure
headache
altered mental satus– esp. irritability and depressed level of alertness and attention
nausea and vomiting
papilledema
visual loss
diplopia
cushing’s triad: HTN, bradycardia, irregular respirations
Transtentorial Herniation
herniation of the medial temporal lobe, especially the uncus (uncal herniation), inferiorly through the tentorial notch.
Uncal herniation is heralded by the clinical triad of a “blown” pupil, hemiplegia, and coma. Compression of the oculomotor nerve (CN III), usually ipsilateral to the lesion, produces first a dilated, unresponsive pupil (a blown pupil), and, later, impairment of eye movements. In uncal herniation, the dilated pupil is ipsilateral to the lesion in 85% of cases.
Compression of the cerebral peduncles can cause hemiplegia (paralysis of half of the body).
Compression of the cerebral peduncles can cause
hemiplegia (paralysis of half of the body).
The relationship of the hemiplegia to the side of the lesion is more complicated than the pupil findings. Recall that the corticospinal tract crosses to the opposite side as it descends through the medulla into the spinal cord at the pyramidal decussation. Thus, often the hemiplegia is contralateral to the lesion either because of uncal herniation compressing the ipsilateral corticospinal tract in the midbrain, or because of a direct effect of the lesion on the ipsilateral motor cortex, or because of both. However, sometimes in uncal herniation, the midbrain is pushed all the way over until it is compressed by the opposite side of the tentorial notch. In these cases the contralateral corticospinal tract is compressed, producing hemiplegia that is ipsilateral to the lesion. This is called Kernohan’s phenomenon.
