Diffuse Axonal Injury and Concussion
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Due to stretching forces placed on individual nerve cells Pathology distributed throughout brain Types Concussion Diffuse Axonal Injury (Moderate to Severe)
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Diffuse Axonal Injury and Concussion
- 1. Diffuse Axonal Injury and Concussion Dr Amit Agrawal, MCh
- 2. β Due to stretching forces placed on individual nerve cells β Pathology distributed throughout brain β Types β Concussion β Diffuse Axonal Injury (Moderate to Severe) Diffuse Brain Injury
- 3. β Accidental Falls β Vehicular accidents β Child Abuse β Assaults β Gunshots β Violent shaking of a child β Sports related injuries Causes
- 4. β 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. β A component of DAI is believed to be present in all motor vehicle crashes (MVCs) where the patient has lost consciousness β Widespread axonal damage occurring after a mild, moderate, or severe TBI β Process takes approximately 12-24 hours β One of the major causes of unconsciousness and persistent vegetative state after head trauma Diffuse Axonal Injury
- 5. β Due to acceleration/deceleration to whtie matter + hypoxia β Significant mechanical disruption of nerve cells β Cerebral hemispheres and brainstem β High mortality rate Diffuse Axonal Injury
- 6. β Mostly microscopic damage, and it is often not visible on imaging studies β The main mechanical force that causes DAI is rotational acceleration of the brain, resulting in unrestricted head movement β Rotational acceleration produces shearing and tensile forces, and axons can be pulled apart at the microscopic level β Microscopic evaluation of the brain tissue often shows numerous swollen and disconnected axons β Rapid stretching of axons is thought to damage the axonal cytoskeleton and, therefore, disrupt normal neuron function Diffuse Axonal Injury:Pathological feature
- 7. β Varies from mild to profound β May be permanent or temporary β Symptoms may appear immediately or over weeks, months, years β Diffuse axonal injury (DAI) β Clinical signs: β β LOC β β ICP β Decerebration or decortication β Global cerebral edema Diffuse Axonal Injury: Clinical features
- 8. Diffuse Axonal Injury: Grading
- 9. β 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. β Concussion may be caused either by a direct blow to the head, face, neck or elsewhere on the body with an ββimpulsiveββ force transmitted to the head. β 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. β Concussion may result in neuropathological changes but the acute clinical symptoms largely reο¬ect a functional disturbance rather than a structural injury and as such, no abnormality is seen on standard structural neuroimaging studies. β 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. β Level of consciousness β Variable period of unconsciousness or confusion β Followed by return to normal consciousness β Retrograde short-term amnesia β May repeat questions over and over β Associated symptoms β Dizziness, headache, ringing in ears, and/or nausea Concussion Head Trauma -
- 12. β No structural injury to brain β Mild to moderate form of Diffuse Axonal Injury (DAI) β Nerve dysfunction without anatomic damage β In a concussion, certain chemical levels are altered at the cellular level β Blood supply to the brain decreases β The brainβs demand for glucose increases β Mismatch in fuel supply and demand β Neuronal tissue vulnerability β 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 >24Λ 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, <24Λ 1. LOC > 1min OR 2. Posttraumatic amnesia >24Λ OR 3. Post concussion signs/syx > 7d
- 14. β Neurological examination and assigning a GCS Score. β Neuroimaging helps in determining the diagnosis and prognosis and proposed treatment β Neuropsychological assessment Diagnosis
- 15. β Computed tomography (CT) β Rarely detected on CT ( 20% of DAI lesions are hemorrhagic) β Magnetic resonance imaging (MRI) β Can show more details than CT as detecting injury characteristics such as diffuse axonal injury β However, MRI is not used in the emergency setting β X-rays: β Not much role β Angiography: β May be used to detect blood vessel pathology. β Electroencephalography and transcranial doppler may also be used. Investigations
- 16. β ABCD β Pharmacotherapy β Prolonged symptoms (sleep disturbance, anxiety) β Modify underlying pathophysiology β Upon return to play should not be on medication that could mask symptoms β Antidepressants? β Physical Rest β No training, playing, exercise, weights β Beware of exertion with activities of daily living β Cognitive Rest β No television, extensive reading, video games? β Caution re: daytime sleep Management
- 17. β Mild cases: Gradual resolution within 7-10 days β Gradual return to work and social activities that does not result in significant exacerbation of symptoms Management
- 18. β Intracranial Hemorrhage β Skull Fracture β Epidural Hemorrhage β Subdural Hemorrhage β Intracerebral Hemorrhage β Cerebral Hyperemia β Cerebral Edema β Seizures β Migraine Headaches Associated Secondary Conditions
- 19. β Majority (80-90%) resolve in short (7-10 day) period β May take longer in children and adolescents Recovery
- 20. β Alzheimer's Disease: recent research suggests correlation between head injury in early adulthood and AD later in life β Parkinson's Disease: rare, but may occur β Dementia Pugilistica: also known as chronic traumatic encephalopathy, usually acquired from repetitive blows to the head (boxers) β Post-traumatic Dementia: long term memory problems, caused by single, severe traumatic brain injury resulting in a coma Long Term Effects
- 21. β’ 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 β’ Activities o Wear a helmet β’ Sports o Wear protective gear Prevention
- 22. β Traumatic injuries affect more patients than all other neurological conditions COMBINED β At present, the best treatment is PREVENTION Conclusion
- 23. 1.6 to 2.3 million sports concussions per year Center for Disease Control 2006