Traumatic Brain Injury

Quick Facts

Open Head Injury – discrete, focal lesions; higher risk for seizures Closed Head Injury – generalized/diffuse cerebral involvement Highest incidence males 16-24 Common Causes MVA, falls (also, industrial, assault, sports)

Risk Factors

  • LD
  • Previous hospitalization for TBI
  • Chronic alcoholism
  • Heart disease and hypertension
  • ADHD
  • Psychiatric illness
  • Seizures
  • Drug abuse
  • Divorce
  • Boxing/soccer
  • Low SES/education
  • Unemployment

Neuropathology of Closed Head Injury

  • Diffuse Axonal Injury (DAI) – breaking/shearing/stretching of myelinated axons
    • Due to acceleration/deceleration and rotational injuries (with subsequent LOC)
    • Occurs over time – compression/stretching, swelling, evolving changes (e.g., changes in glucose transport, blood flow, toxins, etc.)
  • Focal or Subcortical Contusion (FCC) – local abrasions (tearing  hemorrhage; swelling  edematous)
    • Due to coup/contrecoup, depressed skull fx, inertial/rotational force, skull features (e.g., orbital frontal, inferior anterior temporal), hematomas, subcortical bleeds  CVA effects
  • Hypoxic-Ischemic Injury (HII) – infarction in distribution of one artery
    • Due to lack of oxygen, often secondary to physical injuries/chest injuries/airway obstructions
    • Get increased ICP and decreased arterial pressure; results in severe and pervasive memory d/o (because hippocampus requires much oxygen)
    • Edema increases ICP, which increases edema, which increases ICP, and so on…
    • Other secondary insults: from multiple/systemic injuries may get hypoxia/anoxia and fat emboli (fx of femur)
    • Delayed Effects: white matter degeneration (ventricular enlargement), disturbed CSF flow (hydrocephalus)

Primary and Secondary Brain Injury after TBI

  • Primary (immediate on impact)
    • Macroscopic Lesions (contusions at site of impact – coup; contrecoup; laceration)
    • Microscopic Lesions (shearing/stretching of nerve fibers)
  • Secondary mechanisms of brain injury
    • Intracranial hemorrhage
    • Edema in white matter – adjacent to lesion
    • Hyperemia (diffuse swelling)
    • Ischemic brain damage
    • Raised ICP
    • Brain shift/herniation
  • Secondary insult from extracerebral events
    • Effects of multiple systemic injury – e.g., hypoxia, fat emboli
  • Delayed Effects
    • White matter degeneration
    • Disturbed flow of CSF

Degenerative Events Following Brain Damage

  • Anterograde degeneration (aka orthograde or Wallerian) – degeneration of severed axon
  • Astrocyte activity – invade to remove debris; may seal or scar the area
  • Calcification – large deposits where neural degeneration takes place
  • Chromatolyses – color dissolution (cell Nissel substance breaks down); therefore, no stain uptake and are colorless for microscope
  • Gliosis – replacement of cell bodies by glial cells
  • Necrosis – localized death of individual or groups of cells
  • Phagocytosis – removal of dead cells by mitochondria and astrocytes
  • Retrograde Degeneration – death of remaining axon, cell body, and dendrites after being severed
  • Terminal Degeneration – shrinkage/degeneration of terminals after axon severed
  • Transneuronal Degeneration – death of neurons that innervate or are innervated by damaged or destroyed neuron

Associated Physiological Events

  • Diaschesis
  • Shock (e.g., spinal) – cells everywhere show temporary depression when input removed
  • Edema
  • Blood Flow – decreased CO2, decreased flow, decreased metabolic activity; therefore, decreased overall brain activity
  • Neurotransmitter Releases – levels change
  • Glucose Uptake – decreased metabolic activity (not just due to edema)
  • Changes in electrical activity – can be an index of posttraumatic function
  • Autoneurotoxicity – delayed tissue death due to increased release of glutamate (due to oxygen deprivation; overexcites cells)

Recovery Mechanisms

  • Spontaneous recovery – due to resolution/absorption of hematomas, decreased swelling, normalization of blood flow, return of electrolyte/neurochemical balance
  • Plasticity – neural and/or behavioral resilience (ability to reorganize)
  • Diaschesis (von Monakow) – recovery following temporary disruption of functioning in areas adjacent to the primary damage; inhibited functions slowly reemerge; i.e., reestablishment of unimpaired neurological systems
  • Axonal growth – regeneration of neural elements following injury (axonal sprouting, collateral sprouting from intact neurons – collateral axons grow to replace lost axons or innervate targets); not necessarily beneficial
  • Denervation supersensitivity – postsynaptic receptor sites become more sensitive to neurotransmitter agents in denervated neurons; proliferation of receptors, therefore an increase in response
  • Substitution (not a popular theory) – existing intact brain structures can assume functions previously held by lesioned areas; or, redundancy or duplication of function; unoccupied/unused brain area assumes functions of damaged area
  • Behavioral compensation – new or different behavioral strategy
  • Disinhibition – removal of inhibitory actions of a system (by destruction or pharmacological blocking)
  • Nerve Growth Factor – protein secreted by glial cells; facilitates growth, regeneration, reenervation
  • Regeneration – neurons/axons/terminals regrow and establish previous connections
  • Rerouting – axons/collaterals seek new targets after destruction of old ones
  • Silent Synapses – (hypothetical) present synapse – no evident function until system is disrupted
  • Sparing – certain behaviors or aspects of behavior survive brain damage
  • Transient Collaterals – at some time during development they innervated targets, but were abandoned
  • Vicaration (not a popular theory) – functions of damaged areas can be assumed by adjacent areas
    • Some mechanisms may result in seizures or increased spasticity
    • Growth factors and Ach levels may offer promise

Variables Affecting Recovery

  • Lesion size
  • Age
  • Sex (females less lateralized)
  • Handedness – left less lateralized
  • Intelligence – though really, actual residual deficit may be equal
  • Personality – good: optimistic, extroverted, easy going
  • Better recovery with TBI than with CVA

Measures of Severity

  • Glasgow Coma Scale – use with more severe injuries; eye opening/motor response/verbal response (3-15); alcohol use will lower score
  • Coma duration (or LOC) – good predictor
  • PTA duration – best predictor; important in recording moment-to-moment events; usually about 4X the length of coma
    • Early Stage Recovery – disorientation (time comes last), confusion, agitation, lethargy, severely impaired attention, PTA

Cognitive Deficits

  • Mild TBI – attention, verbal retrieval, emotional distress, fatigue, depression
    • PCS – fatigue, irritability, decreased attention, headache, dizziness, memory deficits, anxiety, insomnia, phonophobia, photophobia, hypochondriacal concern
  • Moderate TBI – headache, memory problems, difficulty with everyday living, frontal and/or temporal lobe damage
  • Severe TBI – cognitive, emotional, and executive dysfunction (especially attention, memory, executive, anomia, pragmatics), social isolation, social dysfunction
  • Bulk of recovery is in first 6-9 months (memory slower than general IQ)
    • Social interaction/personality often biggest change
    • Often bigger PIQ decline than VIQ

Sensory Alterations Following CHI

  • Anosmia
  • Vision (acuity, field, oculomotor, diplopia, photophobia)
  • Dizziness
  • Balance d/o
  • Hearing defects (tinnitus)


  • Stimulation (early period) is useful
  • Forced use is helpful for body parts
  • Practice should be extensive and excessive
  • Training tasks should be relevant to real life
  • Family members, etc. should be included
  • Motivation is important
  • Continue training after plateaus
  • Break tasks down into simple components

Conclusions Regarding Adult TBI

  • Recovery most likely in complex behaviors with many components through behavioral compensation
  • Recovery most pronounced after incomplete lesions (e.g., concussions, penetrating head injury)
  • Recovery unlikely for specific functions controlled by localized brain areas f entire area removed
  • There are “always” residual and permanent deficits; extensive recovery is the exception

Miscellaneous Stuff

  • Akinetic Mutism – ability to respond, but can’t initiate (bilateral lesions of mesial frontal lobes, mesial temporal, cingulate gyrus)
  • Coma – caused by diffuse, severe destruction of white matter along with decreased circulation to brain (therefore, diffuse ischemic cortical dysfunction) – leads to necrosis
  • Coma secondary to hypoxia lasting more than one month carries very bad prognosis (worse than TBI)
  • Coma stimulation programs – outcome research is fairly equivocal; can train a response using backward chaining (but there is no accompanying change in cortical control)
  • GOAT – evaluates PTA
  • Penetrating Head Injury – focal lesion; shock waves and pressure effects may increase the effects seen; see more focal than diffuse effects; much higher rate of seizures than in closed head injury
  • Lashley (was WRONG) – recovery of function expected and easy to explain; principles of mass action and equipotentiality
  • Second Impact Syndrome – repeated concussions over brief periods of timing; typically following an initial brain injury and while still symptomatic
    • Often observed in contact sports
    • Rapid deterioration observed from conscious state to coma and possibly death, minutes to hours following trauma
    • Autopsies reveal loss of autonomic regulation of blood vessel diameter causing cerebral blood volume to rise which leads to increased ICP, diminishes cerebral perfusion and leads to increased risk of fatal brain herniation
  • GOAT – evaluates orientation, first memory recalled after PTA and last memory recalled before accident – Scale of 0-100; Normal = 76-100; Borderline = 65-75; impaired = <66

Classification of Severity of Brain Injury

(re: some variability across papers, but…)

  • LOC – most authors cite LOC of < 20-30 minutes considered “mild TBI”
  • GCS – Mild = 13-15; moderate = 9-12; severe = 3-8

Malingering and Its Differentials

  • Malingering – intentional production or gross exaggeration of symptoms motivated by external incentives
  • Conversion Disorder – change in functioning suggesting a physical disorder. Psychological factors are considered b/c of a temporal relationship b/t a psychosocial stressor and an initiation or exacerbation of the symptoms. However patient is not conscious of intentionally producing the symptoms. Distinguished from malingering due to the intentional production of symptoms and obvious external motivations in malingering
  • Factitious Disorder – voluntary production of symptoms to assume the “patient role” not associated with other clear incentives. E.g., ganser’s syndrome (faking a neurological symptom) and Munchausen syndrome
  • Simulation – feigning symptoms that do not exist
  • Dissimulation – concealment or minimization of existing symptoms