This document discusses diffuse axonal injury (DAI) and concussion. It provides an overview of traumatic brain injury (TBI) classification, causes, mechanisms of injury, grading scales, and medicolegal importance. DAI results from acceleration/deceleration forces that cause shearing of axons throughout the brainstem, corpus callosum, and cerebral hemispheres. It is characterized by widespread damage rather than focal lesions. Concussion involves temporary dysfunction from brain impact or whipping, with risks including secondary impact syndrome. Both DAI and concussion are important forensically as they can cause death or long-term impairment without obvious anatomical signs.
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.
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.
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
Naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function.
Transient electrophysiological dysfunction of reticular activation system in upper midbrain .
Acceleration & deceleration of the head .This causes shearing or stretching of the nerve fibre & axonal damage. Coronal head motion .Physiological dysfunction.Recover completely.