1- Injury Mechanism & Recovery Flashcards
Open vs Closed TBI
- An open, or penetrating TBI , when head is hit by an object that breaks the skull and enters the brain.
- A closed TBI occurs when the brain is injured but the skull remains intact.
The single most common cause of death and injury in automobile accidents?🔑
Ejection of the occupant from the vehicle
Cuccurollo 4th Editio Chapter 2 TBI pg55
Types and causes of traumatic ABI (TBI)?
Intentional
- Violence (Adult)
- Child Abuse
- Blast Injuries (Military)
Non-Intentional
- Falls (Too young, too old)
- MVA (Teenagers)
- Sport Injuries (Adult)
Causes of Non-Traumatic ABI? 🔑🔑
- Tumours (benign/meningioma only)
- Anoxia
- Subarachnoid hemorrhage (non-focal)
- Meningitis
- Encephalitis/encephalopathy (viral, bacterial, drug, hepatic)
- Subdural Hematoma
ERABI Module 1 pg4
List 4 causes of TBI. 🔑🔑
Adult
- MVA: 53%
- Falls: 24%
- Violence: 13%
Pediatric
- Falls (72.8%)
- Transportation related (28%)
- Sports and recreational activities (17%)
- Assault (7%)
Cuccurollo 4th Editio Chapter 2 TBI pg56-57
Demographics/Risk Factors for TBI.
Who is at risk for TBI?
- Too young <5 years or too old >65 years
- Male > Female
- African American
- Violence/assault
- Ethyl alcohol (ETOH) use
- Substances abuse
- Psychosocial stress
- Prior psychiatric history (history of anxiety, depression)
- Lower socioeconomic status
increased exposure to high risk occupations, personal violence, older vehicles, and substandard housing
Braddom 6th Edition Chapter 43 TBI pg917-918
Two primary categories of injury mechanisms 🔑
Primary Injury. Definition, Location & Mechanism of Injury. 🔑🔑
💡 Direct disruption of the brain tissue from impact which occurs immediately (minutes to hours after the impact) and is not amenable to medical intervention.
1. CONTUSIONS
Coup Injury: Contusions under the impact site and result from a rapid change in skull distortion during impact.
Counter Coup Injury: Contusions in the opposite to the impact occur due to negative pressure generated
Location
- Inferior frontal lobe
- Anterior paretial lobe
- Inferior occipital lobes
2. DIFFUSE AXONAL INJURY(DAI)
Result from acceleration–deceleration and rotational forces
Lead to loss of consciousness and coma
MRI: White matter punctate petechial hemorrhages
3. IMPACT DEPOLARIZATION
Increase in extracellular potassium and glutamate release (excitatory) → excitotoxicity (secondary injury).
Cuccurollo 4th Edition Chapter 2 TBI pg57
ERABI Module 1 pg14
List 4 Signs of basal skull fracture 🔑🔑
Anterior fossa fracture:
- CSF rhinorrhea
- Raccon eye (Bilateral periorbital heamatoma)
- Subconjuntival hemorrhage
Petrous bone fracture
- Ear bleeding
- Otorrhea
- Battle’s sign (bruising over the mastoid)
Primary vs Secondary Injury 🔑🔑 6 primary neuropathologic changes in TBI
PRIMARY INJURY
💡 Direct injury causing ecchymosis, bleeding or shearing forces
- Extracerebral hemorrhage
- Subdural hemorrhage
- Subarachnoid hemorrhage
- Epidural hemorrhage
- Intracerebral hemorrhage
- Cerebral contusion
- Cerebral laceration
- Diffuse Axonal injury
SECONDARY INJURY
💡 Chemical cascade with electrolytes imbalance leading to delayed injury
- Diffuse Axonal injury
- Diffuse Brain Swelling
- Hypoxic Injury
- Metabolic Dysfunction
- Diffuse Ischemic Injury
- Hydrocephalus
- Increase in ICP
List 4 complications of Subarachnoid Hemorrhage 🔑🔑
- Focal neurological deficit
- Seizures
- High ICP/hydrocephalus
- Neurogenic pulmonary edema
- Hyponatraemia (CSW/SIADH)
- Rebleeding
- Vasospasm and delayed cerebral ischemia
- Takotsubo cardiomyopathy or “Broken Heart Syndrome”
Secondary Injury. Definition, Location & Mechanism of Injury.🔑
TBI what is the site of diffuse axonal injuries 🔑🔑
Adam’s classification for Grading of DAI 🔑🔑
SECONDARY INJURY
Cascade of biochemical, cellular, and molecular events, which include both endogenous cerebral damage as well as extracerebral damage that comes with trauma.
- Ischemia (pericontusional hypoperfusion), excitotoxicity, energy failure, and apoptosis
- Secondary cerebral swelling (brain swelling and brain edema)
- Axonal injury
- Inflammation and regeneration
ADAM’S CLASSIFICATION
Grade I
- Widespread white matter/axonal damage
- No focal abnormalities on imaging
Grade II
- Widespread white matter/axonal damage
- Focal findings (most common in the corpus callosum)
Grade III
- Damage involving the brainstem
Cuccurollo 4th Editio Chapter 2 pg57 & 59
Locations of diffuse axonal injury other than midbrain and corpus collusum.
- Parasagittal white matter
- Interventricular septum
- Walls of the third ventricle
- Brainstem (midbrain and pons).
Cuccurollo 4th Edition Chapter 2 TBI pg59 & ERABI Module 1 pg12
- Corpus callosum: cognitive dysfunction.
- Parasagittal/periventricular white matter.
- Grey-white matter junction: slowed mental processing, fatigue.
- Superior cerebral peduncles: hemiparesis/tetraparesis.
- Midbrain (dorsolateral quadrant): dysarthria, dysphagia.
- Pons.
DeLisa pg 577-578.
Diffuse Axonal Injury: 2 Mechanism of Injury / Causes 🔑🔑
PRIMARY INJURY → MECHANICAL INJURY
1. Traumatic shearing forces (rapid acceleration or deceleration injury)
- High-speed motor vehicle collisions above 15 mph or 24 km/h.
- High-speed collisions in sports (i.e. football, hockey, soccer, rugby)
- Shaken baby syndrome.
SECONDARY INJURY → PATHOPHYSIOLOGICAL
1. Excitotoxicity
Release of glutamate causes calcium influx causing axonal swelling and breakage
2. Hypoxia
3. Apoptosis
Cuccurollo 4th Edition Chapter 2 TBI pg59
ERABI Module 1 pg13
Most common cause of LOC after TBI?🔑
Axonal injury is the most common cause of unconsciousness during and following the first 24 hours of injury.
Cuccurollo Chapter 2 TBI pg59
Describe some of the clinical features seen following diffuse axonal injuries 🔑
Locations affection by DAI
- Grey-white matter junction - slowed mental processing and fatigue.
- Rostral brain stem - initial loss of consciousness, poor attention and concentration.
- Brainstem injury - dysarthria and dysphagia
- Cerebellar peduncle - ataxia.
- Corticospinal tract - hemiparesis.
Rehabilitation Issues
- Slowed mental processing, fatigue, poor attention and concentration.
- Physical and cognitive stamina may be reduced
- Proper pacing will need to be implemented
ERABI Module 1 pg14
What are the biochemical changes that can occur with TBI?
What is the neurotransmitter that is neurotoxic to the brain?
ELECTROLYTES “Cells dying and pumping K out”
- K (increased extracellular)
- Ca (increased ionized Ca into cell)
- Na (increased Na entering cell)
NEUROTRANSMITTERS
- Serotonin (decrease)
- Dopamine (decrease)
- Glutamate (increase)
GLUTAMATE
After impact, release of excitotoxic neurotransmitters (glutamate) causes calcium influx and a series of events (oxygen-free radical release, mitochondrial failure, and DNA damage) that ultimately lead to nerve cell death.
Cuccurollo 4th Edition Chapter 2 TBI pg59
Describe the lesion, diagnosis, incidence 🔑🔑
FIGURE 2–3 Epidural hematoma
Biconvex acute hemorrhagic mass seen on head CT. Occurs commonly (90%)
FIGURE 2–4 Subdural hematoma
Shearing of the bridging veins. Occurs in 30% of severe head trauma.
FIGURE 2–5 Subarachnoid hemorrhage.
Ruptured cerebral aneurysms and arteriovenous malformations (AVMs)
Cuccurollo 4th Editio Chatper 2 TBI pg58-59
Time interval for SAH Acute vs Chronic 🔑
- Acute SDH: Immediately symptomatic lesions
- Subacute SDH: Those between 3 days and 3 weeks
- Chronic SDH: Lesions >3 weeks
Currucollo 4th Edition Chapter 2 TBI pg59
Definition & Mechanisms of Focal Injury 🔑🔑
Localized injury in the brain occurring immediately after the injury and easily visualized by CT or MRI
- Skull fracture or laceration
- Cerebral contusions
- Focal hemorrhages
- Epidural hematoma (EDH) 90%
- Subdural hematoma (SDH)
- Subarachnoid hemorrhage (SAH)
- Cranial nerve injuries (CN 1, 2 & 8)
- Pituitary stalk tearing
Cuccurollo 4th Edition Chapter 2 pg58
Hematoma can exasperate damage to the brain by
- Placing direct pressure on the underlying brain structures
- Causing a portion of the brain to herniate leading to secondary compression of the brainstem
ERABI Module 1 pg15
General prognosis of epidural hematomas (EDH) vs subdural hematomas (SDH)? 🔑
EDH: often not severe if treated promptly
SDH: Prognosis is poor with a high mortality because of the severity of the underlying brain injury
ERABI Module 1 pg16
Necrosis vs Apoptosis
Apoptosis
- Programmed cell death
- Caused by normal, healthy processes in the body.
Necrosis
- Premature death of cells and living tissue.
- Caused by external factors such as infection, toxins, or trauma
List 4 penetrating injury causing TBI. 🔑🔑
- Bullet
- Stab wound
- Motor vehicle injury
- Occupational injury (e.g., nail).
Cuccurollo 4th Editio Chapter 2 pg59
What causes instant death in penetrating injury following TBI?
If the brain is penetrated at the lower levels of the brainstem, death is instantaneous from respiratory and cardiac arrest.
Cuccurollo 4th Edition Chapter 2 pg59
List 5 recovery mechanisms after TBI 🔑🔑 EXAM
NEUROPLASTICITY
- Functional reorganization/unmasking neural reorganization
- Neuronal regeneration/neuronal (collateral) sprouting
SYNAPTIC ALTERATION
3. Diaschisis
Initial loss of function secondary to depression of areas of the brain connected to the primary injury site, and resolution is parallel to the recovery of the focal lesion.
FUNCTIONAL SUBSTITUTION / BEHAVIORAL
4. Redundancy
Recovery of function based on uninjured brain areas that normally would contribute to that function
5. Vicariation
Functions taken over by brain areas not originally managing that function.
6. Substitution
Techniques/new strategies are learned to compensate for deficits and to achieve a particular task.
Cuccurollo 4th Edition Chapter 2 pg60
Factors help in brain plasticity. 🔑
Think like training for tournament:
- Environment
- Motivation.
- Complexity of stimulation
- Repetition of tasks
Cuccurollo 4th Edition Chapter 2 pg60
What is the only pharmacological intervention supported by American Academy of Neurology’s practice guidelines (2018 update) to improve recovery in traumatic DOC? What is the recommended dosage? 🔑🔑
Amantadine, 100-200 mg twice daily.
ERABI Module 8 pg22
