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CNSLF Path - Traumatic Brain + Spinal Injury (ii) (Chronic traumatic…
CNSLF Path - Traumatic Brain + Spinal Injury (ii)
Extra-axial intracranial haemorrhage
traumatic SAH
most common sequelae of TBI
typically a/w contusions + lacerations due to damaged cortical vessels
a/w higher ICP + a worse clinical outcome
trauma to neck can result in vertebral art dissection/rupture (even in absence of fracture), with devastating outcomes
a late consequence is the development of communicating hydrocephalus
EDH
biconvex (like a lemon) - haetoma forms between skull + dura (doesn't cross suture lines)
90% a/w skull fracture
most common in temporal + parietal areas
commonly a/w art lacerations (middle meningeal art)
"talked + died" - lucid interval, then sudden death due too accumulating blood
risk of tonsillar or subfalcine herniation
SDH
can be acute or chronic
collection of blood between dura + arachnoid
most commonly venous in origin, but occasionally art
bleeding can spread (flow freely) unlike EDH
acute
most commonly seen after falls + assaults
5% of all hosp admissions for head injuries
typically due to rupture of bridging veins
mortality = 30-50%
key factor in determining outcome is extent of associated parenchymal pathology, esp contusions + brain swelling
can resolve spontaneously (clot reabsorbed)
chronic
seems to be a separate entity, possible related to subclinical subdural bleeds (not an evolution of acute)
often follows an episode of relatively trivial head injury (may evolve over several wks
therapeutic anticoagulation = biggest risk factor
granulation tissue forms a membrane around area of haemorrhage
can often see rebleeding or enlargement due to friable blood vessels in granulation tissue _ osmotic effect of blood breakdown products
Chronic traumatic encephalopathy (CTE)
clinical features continue to be debated + formal dx limited to autopsy
neuropsych features often with movement disorder (usually parkinsonism), but in some cases predominantly ataxia
unclear if varying degrees of severity are related to degree of trauma or represent a progressive neurodegenerative disorder
evolving concept, although current evidence suggests a novel tauopathy (neurodegenerative)
P-tau aggregates = pathognomonic (pathological hallmark) - tend to aggregate most in depths of sulci
causality between repetitive TBI currently remains unproven, associated epidemiological risk factors have not been assessed
research: imaging + serum biomarkers
causes brain atrophy (ventricles enlarge) + neuronal loss
Diffuse brain injuries
diffuse traumatic axonal injury
axonal damage secondary to trauma
a/w angular or rotational acceleration (not trauma)
can be focal or diffuse
typically unconscious from moment of impact, no lucid interval - remain unconscious, vegatative, or @ least severely disabled until death
macroscopically brain often looks normal - sometimes petechial haemorrhages (black dots on gradient ECHO) @ corpus callous + dorsal brainstem (restricted diffusion)
trauma disrupts normal axonal flow - axonal swelling, varicosities (beading), 'retraction' bulbs
axonal loss - areas of glial scarring + patchy areas of demyelination
primary axonal injury = physical tear
secondary axonal injury = biochem changes
diffuse vasc injury
in a small prop of patients who die mins after head injury, the only discernible structural abnormalities are petechial haemorrhages
mostly in frontal (watershed area) + temporal white matter, diencephalon + brainstem
this diffuse vasc damage probably results from acute deformation, stretching + tearing of small blood vessels
ischaemia
infarct + widespread hypoxic-ischaemic brain damage are common after head trauma
likely in patients with...
clinically evident hypoxia
hypotension with sys BP<80mmHg for @ least 15 mins
episodes of raised ICP (i.e. >30 mmHg)
earliest sign = @ hippocampus, deep grey structures, watershed areas in cortex, Purkinje cells in cerebellum
infarct may be secondary to raised ICP + herniation
Diffuse brain swelling + raised ICP
brain swelling + herniation are common forms of secondary brain damage after head injury
brain swelling occurs in about 75% of patients + is a major factor (along with haemorrhages) contributing to an increase in ICP
it is thought to result from...
cerebral vasodilation - increased cerebral blood vol (i.e. congestive brain swelling)
damage to blood vessels + extravasation of fluid through defective BBB (i.e. vasogenic oedema)
increase in water content of neurons + glia (i.e. cytotoxic cerebral oedema)