Week 5 - Concussion and SCI Flashcards
what are the 2 main types of concussion injuries?
- Coup-contrecoup injury
- torque (rotational) injury
Coup-contrecoup injury
contusion from impact (coup) causes a movement of the brain to impact the opposite side of the skull (contrecoup)
Torque (rotational) injury
- head and neck twists, causing shear stress on neurons
- neurons of the reticular formation most often affected
Concussion pathophysiology
- many neurons injured due to blow and/or shearing
- spontaneous AP firing (axons begin to leak ions)
- excess excitatory NT release (glutamate)
- many neurons stimulated (EPSP)
- massive increase in metabolic activity
- increased demand for blood (glucose) but also a transient decrease in blood to the brain after a concussion
- imbalance of nutrient supply and demand (hours-days)
- neurons are damaged; remain in a low metabolic state for a period of time
Acute concussion symptoms
- confusion
- memory loss
- loss of consciousness
Chronic concussion symptoms
- headache
- dizziness
- nausea
- sensitivity to noise or light
- fatigue
- vision disturbances
- emotional disturbances
- sleep disturbances
Concussion treatment
- rest completely
- avoid activity that could cause excess brain movement
- rehab with support
- avoid repeated concussion
Chronic Traumatic Encephalopathy
- from repeated concussion
- damage build up
- neuronal death
- brain atrophy
- dementia
Spinal Cord Injury (SCI)
- obstructs the transmission of neural messages through the spinal cord; loss of somatic and autonomic control of the trunk, limbs, and viscera below the site of the injury
Phases of SCI: primary injury
- sudden trauma to the spine
- acute spinal cord compression, shear stress, severing (partial vs complete)
- acute impact to neurons, glial cells, and neural parenchyma
Phases of SCI: secondary injury
Primary injury triggers secondary
- involves cascade of biochemical/metabolic and mechanical changes within the neural tissues
- secondary injury is a consequence of these downstream effects (hemorrhage and inflammation)
SCI secondary injury sub-classifications
- acute phase
- sub-acute phase
- chronic phase
SCI secondary injury: acute phase
(0-48hrs)
- hemorrhage, inflammation and edema result in local ischemia
- neural toxicity induces cellular damage
- demyelination and cell death begins
SCI secondary injury: sub-acute phase
(first two-weeks)
- further neurotoxicity, inflammation, cell death, scar tissue formation
- any undamaged tracts begin to resume function (incomplete injury)
- axonal regrowth and sprouting begins if possible
SCI secondary injury: chronic phase
( days to years)
- continued cell death and scar tissue formation
- cyst development
- axonal degeneration and demyelination
- continued regrowth and sprouting if possible