The document discusses diffuse axonal injury (DAI) and concussion, emphasizing that DAI is a significant cause of traumatic brain injuries in the U.S., primarily resulting from forces like acceleration/deceleration. Concussions, which may arise from various impacts, lead to temporary neurological impairments and can show no structural damage on imaging studies. The document also outlines classification and grading of concussions, management strategies, and long-term effects related to head injuries.

1. Diffuse Axonal Injury and
Concussion
Dr Amit Agrawal, MCh

2. ∗ Due to stretching forces placed on individual nerve cells
∗ Pathology distributed throughout brain
∗ Types
∗ Concussion
∗ Diffuse Axonal Injury (Moderate to Severe)
Diffuse Brain Injury

3. ∗ Accidental Falls
∗ Vehicular accidents
∗ Child Abuse
∗ Assaults
∗ Gunshots
∗ Violent shaking of a child
∗ Sports related injuries
Causes

4. ∗ Diffuse axonal injury (DAI) is the predominant
mechanism of injury in 40% to 50% of traumatic brain
injuries (TBIs) requiring hospital admission in the United
States.
∗ A component of DAI is believed to be present in all motor
vehicle crashes (MVCs) where the patient has lost
consciousness
∗ Widespread axonal damage occurring after a mild,
moderate, or severe TBI
∗ Process takes approximately 12-24 hours
∗ One of the major causes of unconsciousness and
persistent vegetative state after head trauma
Diffuse Axonal Injury

5. ∗ Due to acceleration/deceleration to whtie matter +
hypoxia
∗ Significant mechanical disruption of nerve cells
∗ Cerebral hemispheres and brainstem
∗ High mortality rate
Diffuse Axonal Injury

6. ∗ Mostly microscopic damage, and it is often not visible on
imaging studies
∗ The main mechanical force that causes DAI is rotational
acceleration of the brain, resulting in unrestricted head
movement
∗ Rotational acceleration produces shearing and tensile
forces, and axons can be pulled apart at the microscopic
level
∗ Microscopic evaluation of the brain tissue often shows
numerous swollen and disconnected axons
∗ Rapid stretching of axons is thought to damage the
axonal cytoskeleton and, therefore, disrupt normal
neuron function
Diffuse Axonal Injury:Pathological
feature

7. ∗ Varies from mild to profound
∗ May be permanent or temporary
∗ Symptoms may appear immediately or over weeks,
months, years
∗ Diffuse axonal injury (DAI)
∗ Clinical signs:
∗ ↓ LOC
∗ ↑ ICP
∗ Decerebration or decortication
∗ Global cerebral edema
Diffuse Axonal Injury: Clinical
features

8. Diffuse Axonal Injury: Grading

9. ∗ Defined as the result of the forceful motion of the head
causing a brief change in mental status for less than 30
minutes.
Concussion

10. ∗ Concussion may be caused either by a direct blow to the
head, face, neck or elsewhere on the body with an ‘‘impulsive’’
force transmitted to the head.
∗ Concussion typically results in the rapid onset of short- lived
impairment of neurologic function that resolves spontaneously.
However in some cases symptoms and signs may evolve over
a number of minutes to hours.
∗ Concussion may result in neuropathological changes but the
acute clinical symptoms largely reflect a functional disturbance
rather than a structural injury and as such, no abnormality is
seen on standard structural neuroimaging studies.
∗ Concussion results in a graded set of clinical symptoms that
may or may not involve loss of consciousness. Resolution of
the clinical and cognitive symptoms typically follows a
sequential course. However it is important to note that in
some cases, post-concussive symptoms may be prolonged.
Concussion

11. ∗ Level of consciousness
∗ Variable period of unconsciousness or confusion
∗ Followed by return to normal consciousness
∗ Retrograde short-term amnesia
∗ May repeat questions over and over
∗ Associated symptoms
∗ Dizziness, headache, ringing in ears, and/or nausea
Concussion
Head Trauma -

12. ∗ No structural injury to brain
∗ Mild to moderate form of Diffuse Axonal Injury (DAI)
∗ Nerve dysfunction without anatomic damage
∗ In a concussion, certain chemical levels are altered at the
cellular level
∗ Blood supply to the brain decreases
∗ The brain’s demand for glucose increases
∗ Mismatch in fuel supply and demand
∗ Neuronal tissue vulnerability
∗ Brain needs time to recover
Concussion: Pathophysiology

13. Classification/Grading Guides
Guideline Grade 1 Grade 2 Grade 3
Cantu 1. No LOC
2. Posttraumatic amnesia <30
min
1. LOC > 5 min
OR
2. Posttraumatic amnesia
> 30 min
1. LOC > 5 min
OR
2. Posttraumatic
amnesia >24˚
Colorado 1. Confusion w/out amnesia
2. No LOC
1. Confusion w/ amnesia
2. No LOC
1. LOC
(of any duration)
AAN 1. Transient confusion
2. No LOC
3. Concussion syx, ms change
resolve w/in 5 min
1. Transient confusion
2. No LOC
3. Concussion syx, ms
change >15 min
1. LOC
(brief or prolonged)
Cantu
(Revised)
1. No LOC
OR
2. Posttraumatic amnesia
signs/syx < 30 min
1. LOC < 1 min
OR
2. Posttraumatic amnesia
>30 min, <24˚
1. LOC > 1min
OR
2. Posttraumatic
amnesia >24˚
OR
3. Post concussion
signs/syx > 7d

14. ∗ Neurological examination and assigning a GCS Score.
∗ Neuroimaging helps in determining the diagnosis and
prognosis and proposed treatment
∗ Neuropsychological assessment
Diagnosis

15. ∗ Computed tomography (CT)
∗ Rarely detected on CT ( 20% of DAI lesions are
hemorrhagic)
∗ Magnetic resonance imaging (MRI)
∗ Can show more details than CT as detecting injury
characteristics such as diffuse axonal injury
∗ However, MRI is not used in the emergency setting
∗ X-rays:
∗ Not much role
∗ Angiography:
∗ May be used to detect blood vessel pathology.
∗ Electroencephalography and transcranial doppler may
also be used.
Investigations

16. ∗ ABCD
∗ Pharmacotherapy
● Prolonged symptoms (sleep disturbance, anxiety)
● Modify underlying pathophysiology
∗ Upon return to play should not be on medication that
could mask symptoms
● Antidepressants?
● Physical Rest
● No training, playing, exercise, weights
● Beware of exertion with activities of daily living
● Cognitive Rest
● No television, extensive reading, video games?
● Caution re: daytime sleep
Management

17. ∗ Mild cases: Gradual resolution within 7-10 days
∗ Gradual return to work and social activities that does
not result in significant exacerbation of symptoms
Management

18. ∗ Intracranial Hemorrhage
∗ Skull Fracture
∗ Epidural Hemorrhage
∗ Subdural Hemorrhage
∗ Intracerebral Hemorrhage
∗ Cerebral Hyperemia
∗ Cerebral Edema
∗ Seizures
∗ Migraine Headaches
Associated Secondary Conditions

19. ∗ Majority (80-90%) resolve in short (7-10 day) period
∗ May take longer in children and adolescents
Recovery

20. ∗ Alzheimer's Disease: recent research suggests correlation
between head injury in early adulthood and AD later in life
∗ Parkinson's Disease: rare, but may occur
∗ Dementia Pugilistica: also known as chronic traumatic
encephalopathy, usually acquired from repetitive blows to the
head (boxers)
∗ Post-traumatic Dementia: long term memory problems,
caused by single, severe traumatic brain injury resulting in a
coma
Long Term Effects

21. • In the car...
o Wear seatbelt
o Head rest in proper position
o Children under the age of 13 should ride in the back seat
• Activities
o Wear a helmet
• Sports
o Wear protective gear
Prevention

22. ∗ Traumatic injuries affect more patients than all other
neurological conditions COMBINED
∗ At present, the best treatment is PREVENTION
Conclusion

23. 1.6 to 2.3 million sports concussions per year
Center for Disease Control 2006