Traumatic Brain Injury Flashcards
Major cause of disability and death
Traumatic Brain Injury (TBI)
Major causes of TBI
MVA and falls in elderly
Violence cause closed head injury
7-10% of the cases
TBI other cases
Violence
Penetrating injury
Blast injury
TBI
Occur in all ages but peak in
Young adults
TBI
Leading cause of death in
<25, M>F
Violent shaking or jarring of the brain and resultant transient functional impairment
Concussion
Mild TBI defined by
Transient appearance of neurologic signs
Symptoms ff a direct or rapid movement in the brain causing extreme rotational or translational brain acceleration or deceleration injury
Concussion core features
immediately after trauma and largely reversible
T / F
Concussion
• Loss of consciousness at impact is not required for diagnosis
True
T / F
Concussion
• There is evidence of structural brain injury using conventional neuroimaging
• Physiologic injury to brain
False
Concussion MOI
Transient functional
disruption of ARAS caused by rotational forces to the upper brainstem
Transient functional
disruption of ARAS caused by rotational forces to the upper brainstem
Concussion
Concussion Clinical manifestation
Concussive convulsions
Retrograde amnesia
Anterograde amnesia
Immediate loss of
consciousness, suppression of supporting reflexes, transient respiratory arrest, brief bradycardia and fall in BP following a momentary rise
Appears normal
Brief period of
disorientation, staggering or amnesia
may occur immediately after LOC and confer an increased risk of later seizures
Conclusive convulsions
T or F
Athletes who have had a concussion are more likely than others to have another concussion in the same playing season
True
There is a decreased in reaction time and in other neuropsychologic tests atter concussion, which do no return to baseline over several days or weeks
T/F
False
- do return
The number of recollected concussions is proportional to the degree of impairment on neuropsychological tests
T/F
True
Who to image based from the New Orleans Criteria
Headache
Vomiting
Age > 60
Drug / Alcohol intoxication
Persistent anterograde amnesia
Evidence of injury above clavicle
Seizure
% of persons with single uncomplicated concussions fully recover within 2 weeks
80-90
Recurrent concussion outcome
more prolonged recovery with decreasing threshold to injury
Likely to express migraine headaches, mood disorders, BPPV
increased risk of developing major neuropsychiatric disorder associated with aging, including depression, dementia, PD, ALS and erratic psychosocial behavior
Types of skull fx
Linear
Depressed
Comminuted
Open
Closed
Most common type of skull fx
Linear (80%)
Most common location of Linear skull fx
Temporaparietal region
one or more bony fragments are displaced inward, compressing the underlying brain, 85% are open and prone to infection and CSF leakage
Depressed
multiple, shattered bony fragments
Comminuted
scalp over fracture is lacerated
Open or compound
scalp over fracture is lacerated
Open
Basal skull fx is best identified by
NCCT bone window
May be missed by skull X-ray
• Best identified by NCCT bone window
• May have cranial nerve injury or dural tear
• Delayed meningitis
Basal skull fx
hemotympanum or tympanic perforation, hearing loss, CSF otorrhea, PFP, Battle sign
• Petrous portion of temporal bone
anosmia, bilateral periorbital ecchymosis,
CSF rhinorrhea
• Sphenoid, frontal or ethmoid bones
Periorbital eccymosis
Bruising around the eyes
Basal skull fx
Racoon eyes
bruising behind the ear
Basal skull fx
Battle sign
presence of blood in the middle ear cavity
Basal skull fx
Hemotympanum
• Traumatic coma lasting >6 hrs caused by multiple small lesions in the white matter tracts
• Widespread micro-and macroscopic axonal-shearing injury
• Diffuse degeneration of white matter
Diffuse axonal injury
Duration of mild diffuse axonal injury
6-24 hrs
Duration of moderate / severe diffuse axonal injury
> 24 hours
Brainstem and hypothalamic injury (autonomic dysfunction, brainstem signs and extensor posturing)
Single most important cause of persistent disability after traumatic brain damage
Diffuse axonal injury
Cajal 1928
• Swollen, beaded and varicose upon release
• If axon was to rupture, the proximal stub would become a mass of axoplasm called retraction balls
Diffuse axonal injury
Course of diffuse axonal injury
Initial axonal stretch causes temporary ondulation and cytoskeletal isalignment associated with mechanical injury of the Na channels, causing massive Na influx
• Depolarization of the axonal openings for voltage gated Ca channels causing massive Ca influx
• Activation of various metabolic pathways and cytoskeletal changes, including activation of calpain, a protease that degrades microtubule proteins
DAI
Axon shearing injury is most severe at regions that are
anatomically predisposed to maximal stress from rotational forces
DAI
Macroscopic tears occur in
midline structures (dorsolateral midbrain and pons, posterior corpus callosum, parasagittal white matter, periventricular regions and internal capsule)
If axon was to rupture, the proximal stub would become a mass of axoplasm called
Retraction balls
DAI
Diffuse microscopic damage occurs as manifested by
stearic conformational changes of proteins
leakage of ion channels,
axonal etraction bulbs throughout the white matter of the cerebrum following microporation of membranes,
Cerebral swelling mechanisms
• Mass (ie hematoma)
• Cerebral edema
• Increase cerebral blood volume due to abnormal vasodilation
• Hyperperfusion, increased vascular permeability causing plasma leakage and vasogenic edema
• Delayed inflammatory response or dysfunction of cerebral vasomotor regulatory centers in the brainstem
• During first 24 hrs, there is cerebral hypoperfusion followed by hyperemia in 1-3 days after severe head injury, followed by arterial vasospasm in day 4-7
Course of cerebral swelling
During first 24 hrs, there is cerebral hypoperfusion followed by hyperemia in 1-3 days after severe head injury, followed by arterial vasospasm in day 4-7
T/F
Cerebral Swelling
The magnitude of swelling does always correlate with the severity of injury
False
Cerebral swelling Imaging
NCCT
T/F
Cerebral Swelling
The magnitude of swelling does always correlate with the severity of injury
False
Diffuse Axonal Injury Imaging
GRE/T2 FLAIR
Focal parenchymal hemorrhages that result form
“scraping” and “bruising” of the brain as it moves across the inner surface of the skull
Cerebral Contusion
Cerebral contusion most common loc
inferior frontal and temporal lobes
• Irregular protuberances at skull base
Cerebral confusions description
Small and multiple and cortical in location
• Bruised and bloodied brain
Cerebral contusion course of appearance
• May appear in delayed fashion >1day after trauma
• Frequently enlarge over 12-24 hrs
Cerebral contusion type
Coup
Countercoup
On the surface of the brain beneath the point of impact
Coup
• Opposite pole as brain impacts on the inner table of the skull
Countercoup
Cerebral confusions
causes it to be flung against the side of the skull that is struck, pulled away from contralateral side and to be impaled against bony promontories within the cranial cavity
The inertia of the malleable brain
Cerebral contusion imaging
NCCT
• Tearing of small or medium sized vessels within the brain parenchyma
• Focal blood collection that displace brain structures
Intracerebral Hematoma
Intracerebral Hematoma Imaging
NCCT
Source of subdural hematoma
Venous
Location of subdural hematoma
Potential space between dura and arachnoid
Subdural Hematoma MOI
Movements of the brain within the skull that leads to stretching and tearing of bridging veins that drain the surface of brain to dural sinuses
Subdural Hematoma neuroimaging
Crescent shaped density on CT
Subdural hematoma
Population @ risk
Elderly, alcoholic patients with cerebral atrophy
Coagulopathy
• Symptomatic within 72 hrs after injury
• More common after falls or assaults
• May lose consciousness as SDH enlarges
• Ipsilateral pupillary dilation with contralateral hemiparesis
Acute SDH
Acute SDH
Symptomatic within
72 hrs after injury
Acute SDH
More common after
Falls or assaults
Acute SDH
• — pupillary dilation with —-hemiparesis
Ipsilat
Contralat
Chronic SDH
Symptomatic after
21 days
Chronic SDH
More common in
> 50 y/o
Chronic SDH
% does not recall injury
25-50%
Chronic SDH
After 2 weeks, there is encapsulation of the clot and eventually liquefies into a
Hygroma
Subdural Hematoma
Treatment
evacuation of hematoma
Rare complication of head injury
Epidural Hematoma
Epidural Hematoma
Occurs in —% of all cases but is found in ||% of autopsies
<1%
5-15% of autopsies
Epidural Hematoma
Source
Arterial
Epidural Hematoma
Location
Bleeding into the epidural space
Mechanism of epidural hematoma
Tear in one of the meningeal arteries, usually middle meningeal artery (15%, bleeding from dural sinus)
(75% with skull fracture)
Dura is separated from the skull by blood, and the clot enlarges until the ruptured vessel is compressed or occluded by the hematoma
Neuroimaging epidural hematoma
Convex shaped on NCCT
Epidural Hematoma
Population @ risk
Young adults
Dura in elderly is very adherent to skull
Epidural Hematoma
Course
5 Fixed and dilated pupil with uncal herniation
Ipsilateral nonreactive pupil
Coma with hemiplegia
Lucid interval
1 Immediate loss of consciousness
Epidural Hematoma
Mortality Rate
100% in untreated, 5-30% in treated
Treatment of epidural hematoma
Surgical evacuation (craniotomy, drainage and ligation of bleeding vessel)
• No or short period of LOC
• “talk and die”
• Late deterioration because of expansion of subdural or epidural hematoma, worsening edema around a contusion or delayed appearance of epidural clot
Serious Cerebral Damage Following a Lucid
Interval
Blood is distributed over the convexities
• Vs SAH secondary to aneurysmal rupture - over the basal cisterns
Traumatic Subarachnoid Hemorrhage
Penetrating injury
Mortality from GSW to head is
> 95%
Penetrating injury
Amount of tissue damage is dependent on
kinetic energy and velocity of the missile, angle of entrance, number of bony fragments, affected structures and configuration of secondary bullet tracts due to ricochet
• Explosive missiles initiate overpressure waves that translate mechanical, thermal and electromagnetic energy to the brain by spallation, implosion and inertia directly through the cranium and indirectly through oscillating pressure in the fluid-containing large vessels
Blast Injury
• Damage to BBB and to gray-white matter junction with deafferentations of the cortical columnar structure
• Loss of consciousness and altered mental status
Blast Injury
Blast Injury
% have long term neurologic deficits
30
Blast Injury
% PTSD
Blast Injury
• Secondary blast injury due to debris resulting in
Penetrating/blunt trauma
• Violent shaking of the body or head of an infant, resulting in rapid acceleration and deceleration of the cranium
• Combination of subdural and retinal hemorrhages
• High risk of slowing of cognitive development, acquired microcephaly (brain atrophy)
Shaken Baby Syndrome
Shaken baby syndrome
Combination of — & — hemorrhages
Subdural & retinal
Immediate Clinical Evaluation
• Assessment and stabilization of airway, breathing and circulation
• Resuscitation, history taking and examination
• Spine immobilization
• Imaging studies
• Management of coagulopathies
• Management of increased ICP
emergency imaging of choice for head and cervical spine injury
CT
CT application
• Bone
• Hematoma or hemorrhages
• Cerebral edema
• Pneumocephalus
• Mass effect and brain tissue displacement
• Compression or obliteration of the mesencephalic cisterns or midline shifts
focal lesions related to DAl but not for emergency evaluations
MRI
Acute DAI
MRI
hyperintense on DWI and hypointense on ADC
Early Complications of TBI
• CSF fistula
• Pneumocephalus
• Carotid-cavernous fistula
• CN injury
• Vascular injury and thrombosis
• Infection
Late complications of TBI
• Postconcussion syndrome
• Seizure and post traumatic epilepsy
• Cognitive impairment
• Post traumatic movement disorder
Tearing of dura and arachnoid membranes
CSF fistula
CSF Fistula usually associated to
fractures of ethmoid, sphenoid or orbital plate of the frontal bone
CSF Fistula CT
pneumocephalus
Sx CSF fistula
CSF lead from scalp laceration, nose (CSF rhinorrhea), ear (CSF otorrhea)
• Test for glucose or tau (+) CSF, (-) mucus
• Mucus will leave the material stiff
Treatment of CSF Fistula
head elevation (85%); lumbar drain; if >2 weeks, surgical repair
Risk CSF Fistula
Meningitis
collection of air in the cranial cavity
Aerocrole
Aerocele
Type
Pneumatocoele or pneumocephalus
Pocket of air in the epidural or subdural space over the convexities, between hemispheres
Aerocele
Aerocele
Small collection of air is absorbed without incident but large volume may produce
mass effect (tension pneumocranium) and may need surgical aspiration
• Result from traumatic laceration of the ICA
within the cavernous sinus
• Pulsating exophthalmos, ocular chemosis, orbital bruit
• Carotid-cavernous fistula
Course of Carotid-cavernous fistula
• Blood enters the sinus and distends the superior and inferior ophthalmic veins
• Tight and painful
• Partial or completely immobile
What pulsates in carotid cavernous fistula
exophthalmos, ocular chemosis, orbital bruit
Carotid-cavernous fistula
• Distended orbital and periorbital veins and paralysis of the — as they pass through or within the walls of the cavernous sinus
CN Ill, IV, V, VI
Carotid-cavernous fistula
•Risk: permanent visual loss caused by
venous retinal infarction
Carotid cavernous fistula dx
Angiography
Carotid cavernous fistula tx
endovascular ballon placement through the defect in arterial wall into the venous side of the fistula
Acute Complications of Head Injury
Traumatic arterial dissection and vascular injuries (thrombosis and thromboembolism)
• Secondary subfalcine herniation with ACA infarction or PCA pressed against the tentorium
• Cranial nerve injuries
• Infections - extradural (osteomyelitis), subdural (empyema), subarachnoid (meningitis) or intracerebral (abscess)
-CCF
40%
• Cranial pain, dizziness, fatigue, insomnia, irritability, restlessness and inability
to concentrate
• Overlap with depression and anxiety
• May persist for years
• Duration of symptoms is not related to severity of injury
• Tx: psychotherapy, antidepressants or anxiolytics
Post concussion Syndrome
Rare
• Action tremor
• Cerebellar ataxia, rubral tremor, palatal myoclonus - shearing of the SCP, midbrain, dentatorubro-olivary triangle, respectively
• Parkinsonism and other basal ganglia syndromes
Post Traumatic Movement Disorder
Dementia pugilistica or punch drunk syndrome
• Delayed neurodegenerative cerebral disease that follows mild traumatic brain injury after many years
• Development year after exposure to head injury a state of forgetfulness, slowness in thinking and other signs of dementia with prominent behavioral changes
Chronic Traumatic Encephalopathy
Chronic Traumatic Encephalopathy other name
• Dementia pugilistica or punch drunk syndrome
• Enlargement of the lateral ventricles, thinning of the corpus callosum, glial scarring over the inferior cerebellar cortex
Chronic Traumatic Encephalopathy
Loss of pigmented cells of the substantia nigra and locus cereulus, presence of Alzheimer neurofibrillary changes
Chronic Traumatic Encephalopathy
Chronic Traumatic Encephalopathy autopsy
Deposition of tau in depths of sulci of the frontal and temporal lobes and other areas of the brain
treatment of choice for massive acute and chronic subdural, epidural or parenchymal hematoma with mass effect
• With ligation or clipping of bleeding vessel
Craniotomy
liquified chronic subdural hematomas
• Burr hole or twist drill
cerebral edema and intracranial hypertension
Decompressive hemicraniectomy
