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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 Injuries
• Accidental falls
• Assaults
• RTA –90 %
• Child abuse
• Violent shaking of the baby
• Sports related injury
•Behavioural problems
•Cognitive impairement
•Physical disturbances
Commotio
cerebri
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
Autopsy
• No findings
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
GFAP
S100
IDH 1
ATRX
Intraparenchymal
haemorrhage
Retraction balls
BAPP-beta
apoprotein
precursor
Survive – 1hour
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, amnesia etc .
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
•
Medicolegal Importance
• Concealed trauma- cause death
without any gross signs .
Pediatric abusive head injury
• Repeated acceleration –
deceleration forces.
• 30%- cause of death, 80%-
permanent neurological
damage .
• 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
Reference
• Bardalae principlesof forensicmedicicne& toxicology.
• Anil Aggrawal textbookof forensicmedicineandtoxicology
• Narayanareddy textbookof forensicmedicine andtoxicology
• knights forensicpathology.

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DIFFUSE AXONAL INJURY,CONCUSSION

  • 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 Injuries • Accidental falls • Assaults • RTA –90 % • Child abuse • Violent shaking of the baby • Sports related injury •Behavioural problems •Cognitive impairement •Physical disturbances Commotio cerebri
  • 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
  • 11. 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 GFAP S100 IDH 1 ATRX
  • 15. Cerebral Concussion • Brain whipping around skull. • Temporary loss of brain function • Clinical syndrome- immediate and transient post- traumatic impairement of neural function – LOC, amnesia etc .
  • 17. 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
  • 19. Sequelae • Secondary impact syndrome • Post concussion syndrome • Post traumatic epilepsy, headache & vertigo. • Neuropsychological impairement.
  • 20. 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.
  • 21. Rowan's Law • (Concussion awareness resources) • 2018 makes it mandatory for sports organizations •
  • 23. • Concealed trauma- cause death without any gross signs . Pediatric abusive head injury • Repeated acceleration – deceleration forces. • 30%- cause of death, 80%- permanent neurological damage .
  • 24. • 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
  • 25. Reference • Bardalae principlesof forensicmedicicne& toxicology. • Anil Aggrawal textbookof forensicmedicineandtoxicology • Narayanareddy textbookof forensicmedicine andtoxicology • knights forensicpathology.

Editor's Notes

  1. Naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function.
  2. Transient electrophysiological dysfunction of reticular activation system in upper midbrain .
  3. Acceleration & deceleration of the head .This causes shearing or stretching of the nerve fibre & axonal damage. Coronal head motion .Physiological dysfunction.Recover completely.