1. Definitions
   1. A traumatically induced physiologic disruption of brain function, as manifested by one of the following
      1. Any period of loss of consciousness (LOC),
      2. Any loss of memory for events immediately before or after the accident,
      3. Any alteration in mental state at the time of the accident,
      4. Focal neurologic deficits, which may or may not be transient.”
   2. Diffuse Axonal Injury
      1. Lesion to white matter
   3. Head Injury
      1. INjury to head and scalp too
   4. Head Trauma
      1. Can be brain injury without head injurd
2. Types
   1. Presetrating vs Nonprenetrating
      1. Unless specified a TBI is non penetrating
      2. Penetrating
         1. May present other characteristics of TBI
         2. (+) Focal destruciton of tissue
         3. (+) Risk of infection
   2. Mechanisms
      1. Differentiation between primary and secondary injury
         1. Differnt types of lesions
         2. different chronology
         3. Different Imaging and assesment
3. Primary
   1. Contusions
      1. Coup
         1. Blow
      2. Contracoup
         1. After Blow
      3. Mechanisms
         1. Mechanical force of impact
         2. Coup / Contre Coup evein in absence of impact
         3. Sudden acceleration/deceleration
         4. Direct damage from shock/laceration against inner ridge of the skull
      4. SS
         1. Depend on the localization
         2. Anosmia
         3. Orbitofrontal --> Behavoral changes
         4. Prefrontal cortex --> Pure fronal syndrome
      5. Chronology
         1. Immediate damage
         2. Restorative recovery possible for small lesions
         3. Compensatory recovery for large lesions
      6. Imaging and assesment
         1. MRI, CT, fMRI
         2. Neurological Exam
         3. Neuropsychological Exam
   2. Axonal Injury
      1. Mechanism
         1. Shearing and tearing of neurons
         2. acceleratio and deceleration
         3. Rotational forces
      2. Lesions
         1. Diffuse axonal injury
         2. Disorganizaiton of cytoskeleton
         3. Tearing of axon (Mod --> severe)
      3. Symptoms and outcome
         1. General slowing down of cognitive functions
            1. Longer reaction time
            2. Impaired multi processing
         2. Dysexecutivesyndrome if in hemispheres
            1. No visable lesions
            2. Only seen in autopsy
            3. BC frontal lobe is bad
         3. Loss of consciousness if in brainstem
         4. LOC ranges from transcientLOC to coma and
         5. vegetative state
      4. Chronology
         1. Mild DAI may be reversible
         2. Moderate to severe DAI irreversible
         3. Immediate destruction
         4. + Long term walleriandegeneration
      5. Imaging and assessment
         1. Rarely visible on CT scan
         2. Not always visible on conventional MRI
            1. T2* MRI sequence
            2. Diffusion tensor imaging on MRI
            3. Diffusion weighted imaging on MRI
   3. Hemorrhage
      1. mechanism
         1. Shearing/tearing of blood vessels
         2. Cf hemorrhagic stroke lecture
      2. Lesions
         1. Depending on localization
         2. Focal injury if big vessel
         3. Petechial hemorrhage if small vessels (associated with DAI)
      3. Symptoms and outcome
         1. Depending on localization
      4. Chronology
         1. Immediate
      5. Imaging and assessment
         1. CT, MRI
         2. Neuropsychology, neurological exam
   4. From small cortical --> Large regions of the cortex
4. Secondary
   1. "Talks and Dies"
   2. Chronology
      1. Example of person that experiences a minor fall
      2. No SS: no LOC, no dizzyness, no nausea
         1. Alter and will talk and laugh about the fall
      3. Hours later --> Severe headache and condition deteriorates quickly
         1. Ischemia and Hypoxia
         2. Exictotoxictiy and free radical release --> Wallerian Degeneration and cell Death
         3. Edema and inflamation --> INC ICP
      4. Step by Step
         1. Initially decreased Cerebral blood flow Cerebral swelling develops and peaks 24 to 72 hours after the injury Leads to increased intracranial pressure (ICP) May further impair cerebral perfusion -> ischemia, more swelling, herniation, and death. Simultaneous excitotoxicity(release of neurotransmitters in toxic quantities) and oxydativestress Inflammatory response Leads to Walleriandegeneration and cell death Changes in blood-brain-barrier permeability
      5. Dies of raised ICP
   3. Cerebral Ischemia
      1. Inadequate Cerebral blood flow (CBF) and metabolism -->Poor outcome
      2. Impaired reulation of Cerebral blood flow
         1. Impaired constriction and dialation response
         2. May be delayed or dev immediately after trauma
      3. Case of vasospasm
         1. Persistent hypoperfusion
         2. Develops 2 to 15 days after TBI
         3. Associated with inflammation and excitotoxicity
      4. Causes
         1. systemic hypotension
         2. Increased intracranial pressure
         3. cerebral hypoperfusion.
         4. Cardiovascular collapse and other systemic changes may result from the effects of DAI on the medulla.
      5. Underlying causes of secondary hemorrhage
         1. increased intracranial pressure
         2. vascular compression from herniations
         3. Vasospasm (decreased cerebral blood flow)
         4. traumatic vascular tears
      6. Infarcts and HIE greatly increase morbidity and mortality in TBI.
   4. Cerebral Hypoxia
      1. Cerebral metabolism (O2 and glucose) reduced after TBI
         1. Associated with poorer outcome
         2. Related to mitochondrial dysfunction occurring during excitotoxicprocess
         3. Often associated with uncoupling between metabolism and CBF
         4. Results in hypoxia
   5. Excitotoxicitiy
      1. Excitotoxicity
         1. massive release of excitatory neurotransmitters
         2. Mostly glutamate.
         3. extracellular glutamate overstimulatesneurons and astrocytes
         4. Imbalance of Na+/K+ and Ca++
      2. Oxidative stress
         1. Release of oxygen free radicals
         2. Hydrogen peroxide and nitric oxide (NO)
         3. Immediate cell death
         4. Secondary inflammation and apoptosis
      3. Wallerian Degeneration
         1. Use with brain injury and stroke pt
         2. With significant injury the nerve degrades in a anterograde fashion
         3. Axon and surrounding myelin break down durring this process
         4. Degeneration and loss of the distal nerve segment
         5. Can take up to weeks to happen
         6. Reinnervation
            1. New nerve matures
            2. Preinjury cytoarchitechture and function are restored
   6. Oedema and Inflamation
      1. Oedema
         1. Impaired osmotic imbalance
         2. Vasogenic and Cytotoxic oedema may coexsist
         3. Vasogenicoedemais = damaged blood-brain barrier
         4. Vasogenicoedema = increased volume of the extracellular space.
         5. Cytotoxicoedemais = increased permeability of membranes
         6. Cytotoxicoedema = increased volume of the intracellular space.
            1. Swelling from the inside and the outside
      2. Inflamation
         1. Cellular release of cytokines
         2. Macrophages and T cells infiltrate and eliminate injured tissue
         3. --> Scar tissue by astrocytes
         4. Aggracated by oxydative stress and oedema
   7. Herniation
      1. From INC ICP
      2. Bony ridges divide the cranial cavity
         1. Compression of brain leads to herniation (brain is pushed from one side to aother)
            1. Subfalcial herniation
            2. Uncal (transtentorial) herniation
            3. Cerebellar tonsilar herniation
      3. 4 types of herniation
         1. 1. The brain squeezes under the falx cerebri in cingulateherniation
         2. 2. The brainstem herniatescaudally
         3. 3. The uncusand the hippocampal gyrusherniateinto the tentorial notch
         4. 4. The cerebellartonsils herniate through the foramen magnum in tonsillarherniation.
5. Shaken Baby Injury
   1. Subtle brain injury --> Perminant consequences
   2. Most symptoms are resolved in 48-72 hours
   3. Suspect when the baby has SS of head injury where the caretaker says there is no known cause
6. Concussion
   1. Classified into 5 Grades
      1. Grade 1 = only confusion
      2. Grade 5 = LOC more than 10 min
   2. Each Grade has different recomendations for those that play sports
   3. Repeated concussions --> Stop contact sports
   4. Post concussion syndrome
      1. Peaks at 4-6 weeks
      2. SS do not resolve for weeks
      3. SS: Headaches, light and sound sensativity, dizzyness, memory and attention problems, difficulty with directed movements
7. Clinical
   1. Measures of Severity
      1. Used to ID treatment and prognosis
      2. 3 Paramiters
         1. GCS
         2. Durations of Coma
         3. Duration of Poat Traumatic Amnesia
   2. Subacute and Chronic assesmnet
      1. Used for
         1. Provide adequate care
         2. Insurance purpose
         3. Neurorehabilitation
         4. Prognosis
   3. Symptoms and assesments
      1. SS
         1. Neurological symptoms depending ont he side of the focal lesion
         2. INC risk of seizures
         3. DAI
            1. Frontal is esp sensative to DAI
            2. Dorsofrontal
            3. Dysexecutive Syndrome
            4. Impaired: attention, task switching, concentration, working memory ....
            5. Orbito and mediofrontal
            6. Impaired: Judgement, depression, mood swings, irritability...
            7. Independent of Local
            8. Fatigue and slowness
   4. Assesment of Traumatic Brain Injury
      1. Disability Rating Scale (DRS)
         1. 0 = no disability --> 30 exessive vegitative state
      2. Pt may present with no obvious impairment
      3. Need Test Sensative to DAI