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Diffuse Axonal Injury
& Concussion
Dr.Nafeeya
Department of Forensic Medicine & Toxicology
Overview
• Introduction
• Classification of TBI
• Causes
• Mechanism
• Grading
• Medicolegal importance
Introduction
• Severe craniocerebral traumas.
• Extensive lesion in white matter tracts spread over wide diffuse areas.
• Brainstem, corpus callosum, and cerebral hemispheres .
• 90 % never regain consciousness
• Survive - face significant impairs.
• This injury is extensive- diffuse rather than focal
• Widespread area of the brain rather than one specific location of the brain.
Classification of TBI
•Mild(concussion)
•Moderate
•Severe
•Closed head injury
•Penetrating head
injury
•Focal -Contusion
•Diffuse -DAI
Gcs-13-15
PTA-<1hr
LOC-<30
min
Severity
Mechanism Location
When an external force traumatically injury the brain.
Causes Of TBI
• Accidental falls
• Assaults
• RTA –head injury
• Child abuse
• Violent shaking of the baby
• Sports related injury
•Behavioural problems
•Cognitive impairement
•Physical disturbances
Mechanism
• Results in acceleration / deceleration injuries.
• Injury
Sudden
movement
of head
Compressive &
tensile force
(perpendicular
to brain surface)
Linear/rotati
onal
acceleration
Brain-
shearing force
(parallel to
brain surface)
Earliest mechanical theory
• Axonal damage
• Trauma – tear during mechanical stress
• Shear strain – axonal injury & rupture
• White matter junction & corpus callosum
Modern biochemical theory
• Stretching of axon during injury
• Disruption of axolemma
•
•Open up Na channels
•Voltage gated ca channel
•Inflow of ca into the axon
•Activated phospholipases
&proteolytic enzymes
•Mitochondria,
•cytoskeleton
damage
•Neuronal death
Grading of DAI
Histopathology
• Grossly – not much findings
• Significant findings -
Bulb formation at
the terminal end of
axon
(retraction balls)
Tear in white matter
Intraparenchymal
haemorrhage
Silver Impregnation
technique &
Immunoperoxidase
methods
Intraparenchymal
haemorrhage
Retraction balls
White matter tear
Cerebral Concussion
• Brain whipping around skull.
• Temporary loss of brain function
• Clinical syndrome- immediate
and transient post- traumatic
impairement of neural function –
LOC, Vision.
Risk factors
High contact
sports
Previous
concussion
Initial Impact
The brain
swells ,the
swelling puts
pressure on
the brain stem
which controls
breathing and
basic life
support
Brain rebounds
The force from the
impact causes the
brain to strike the
inner surface of the
skull
Mechanism
Grading of concussion
Sequelae
• Secondary impact syndrome
• Post concussion syndrome
• Post traumatic epilepsy, headache & vertigo.
• Neuropsychological impairement.
Secondary impact syndrome
• When the brain swells rapidly shortly after a person suffers a second
concussion before symptoms from an earlier concussion have subsided.
Non- fatal
Persistent muscle spasm
Emotional instability,
Hallucinations,
Post-traumatic epilepsy,
Mental disability, Paralysis,
Coma, &
Brain death.
Rowan's Law
• (Concussion awareness resources)
• 2018 makes it mandatory for sports organizations
•
Contusions of the brain
• A contusion is a bruise to the brain in which a small blood vessels leak into
brain tissue.
1. Coup
2. Counter coup
3. Intermediate
4. Fracture
5. Gliding
6. Herniation
Mechanism
Fixed head
Accelerated
Impact –motion
Moving head
Deceleration
Motion – impact
Theories of Counter-Coup
Positive pressure theory –Lindenberg
Stage -1-skull is accelerated .Brain lag
behind due to inertia .
Stage-2-Creates negative pressure –
leading skull surface.
Creates positive pressure-trailing skull
surface
Stage-3- no cushioning effect,countercoup
lesion
Negative pressure theory –
Russel
Skull –rest but brain continues to
move.
Negative pressure created-
trailing skull surface.
Produce –tensile stress
Cavitation occurs,countercoup
lesion
Rotational shear stress theory-Holbourn
Inferior
portion of
temporal
& frontal
lobes
Medicolegal Importance
• Concealed trauma- cause death without any gross signs .
• Difference between concussion & drunkenness
Face-warm,flushed pale
Smell-present Absent
Pupils –Mc Ewen’s sign Absent
Breathing – fast Slow
Memory –no amnesia Retrograde amnesia
Behaviour –talkative Silent
Blood & urine- positive Negative
Pediatric abusive head injury
• Repeated acceleration –
deceleration forces.
• 30%- cause of death, 80%-
permanent neurological damage
• Cinderella syndrome .
• Boxers injury
• Chronic traumatic brain injury (CTBI)
associated with boxing occurs
in approximately 20% of professional
boxers.
• Diffuse axonal injury ,cerebral edema
also common.
• Subdural haemorrhage –death
Punch -drunk syndrome
Reference
• Bardalae principlesof forensicmedicicne& toxicology.
• Anil Aggrawal textbookof forensicmedicineandtoxicology
• Narayanareddy textbookof forensicmedicine andtoxicology
• knights forensicpathology.

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DIFFUSE AXONAL INJURY,CONCUSSION & CONTUSION

  • 1. Diffuse Axonal Injury & Concussion Dr.Nafeeya Department of Forensic Medicine & Toxicology
  • 2. Overview • Introduction • Classification of TBI • Causes • Mechanism • Grading • Medicolegal importance
  • 3. Introduction • Severe craniocerebral traumas. • Extensive lesion in white matter tracts spread over wide diffuse areas. • Brainstem, corpus callosum, and cerebral hemispheres . • 90 % never regain consciousness • Survive - face significant impairs. • This injury is extensive- diffuse rather than focal • Widespread area of the brain rather than one specific location of the brain.
  • 4. Classification of TBI •Mild(concussion) •Moderate •Severe •Closed head injury •Penetrating head injury •Focal -Contusion •Diffuse -DAI Gcs-13-15 PTA-<1hr LOC-<30 min Severity Mechanism Location When an external force traumatically injury the brain.
  • 5. Causes Of TBI • Accidental falls • Assaults • RTA –head injury • Child abuse • Violent shaking of the baby • Sports related injury •Behavioural problems •Cognitive impairement •Physical disturbances
  • 6. Mechanism • Results in acceleration / deceleration injuries. • Injury Sudden movement of head Compressive & tensile force (perpendicular to brain surface) Linear/rotati onal acceleration Brain- shearing force (parallel to brain surface)
  • 7. Earliest mechanical theory • Axonal damage • Trauma – tear during mechanical stress • Shear strain – axonal injury & rupture • White matter junction & corpus callosum
  • 8. Modern biochemical theory • Stretching of axon during injury • Disruption of axolemma • •Open up Na channels •Voltage gated ca channel •Inflow of ca into the axon •Activated phospholipases &proteolytic enzymes •Mitochondria, •cytoskeleton damage •Neuronal death
  • 10. Histopathology • Grossly – not much findings • Significant findings - Bulb formation at the terminal end of axon (retraction balls) Tear in white matter Intraparenchymal haemorrhage Silver Impregnation technique & Immunoperoxidase methods
  • 14. Cerebral Concussion • Brain whipping around skull. • Temporary loss of brain function • Clinical syndrome- immediate and transient post- traumatic impairement of neural function – LOC, Vision.
  • 16. Initial Impact The brain swells ,the swelling puts pressure on the brain stem which controls breathing and basic life support Brain rebounds The force from the impact causes the brain to strike the inner surface of the skull Mechanism
  • 18. Sequelae • Secondary impact syndrome • Post concussion syndrome • Post traumatic epilepsy, headache & vertigo. • Neuropsychological impairement.
  • 19. Secondary impact syndrome • When the brain swells rapidly shortly after a person suffers a second concussion before symptoms from an earlier concussion have subsided. Non- fatal Persistent muscle spasm Emotional instability, Hallucinations, Post-traumatic epilepsy, Mental disability, Paralysis, Coma, & Brain death.
  • 20. Rowan's Law • (Concussion awareness resources) • 2018 makes it mandatory for sports organizations •
  • 21. Contusions of the brain • A contusion is a bruise to the brain in which a small blood vessels leak into brain tissue. 1. Coup 2. Counter coup 3. Intermediate 4. Fracture 5. Gliding 6. Herniation
  • 22. Mechanism Fixed head Accelerated Impact –motion Moving head Deceleration Motion – impact
  • 23. Theories of Counter-Coup Positive pressure theory –Lindenberg Stage -1-skull is accelerated .Brain lag behind due to inertia . Stage-2-Creates negative pressure – leading skull surface. Creates positive pressure-trailing skull surface Stage-3- no cushioning effect,countercoup lesion Negative pressure theory – Russel Skull –rest but brain continues to move. Negative pressure created- trailing skull surface. Produce –tensile stress Cavitation occurs,countercoup lesion
  • 24. Rotational shear stress theory-Holbourn Inferior portion of temporal & frontal lobes
  • 25. Medicolegal Importance • Concealed trauma- cause death without any gross signs . • Difference between concussion & drunkenness Face-warm,flushed pale Smell-present Absent Pupils –Mc Ewen’s sign Absent Breathing – fast Slow Memory –no amnesia Retrograde amnesia Behaviour –talkative Silent Blood & urine- positive Negative
  • 26. Pediatric abusive head injury • Repeated acceleration – deceleration forces. • 30%- cause of death, 80%- permanent neurological damage • Cinderella syndrome .
  • 27. • Boxers injury • Chronic traumatic brain injury (CTBI) associated with boxing occurs in approximately 20% of professional boxers. • Diffuse axonal injury ,cerebral edema also common. • Subdural haemorrhage –death Punch -drunk syndrome
  • 28. Reference • Bardalae principlesof forensicmedicicne& toxicology. • Anil Aggrawal textbookof forensicmedicineandtoxicology • Narayanareddy textbookof forensicmedicine andtoxicology • knights forensicpathology.