Diffuse Axonal Injury and Concussion
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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.
Diffuse Axonal Injury and Concussion
- 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