Concussion Flashcards
What are the three types of traumatic head injury?
- Direct impact (something hitting the head)
- Acceleration/Deceleration injury (e.g car crash)
- Blat injury from shock waves
What effect was seen on the somatosensory evoked potentials of rats undergoing concussive blows?
- There was a complete initial loss of the somatosensory evoked potential
- Early components then recovered first, however later components remained depressed after 10 minutes
What are the symptoms of concussion?
- Physical somatic such as headache, diziness, difficulty with balance
- Affective changes such as irritability and mood changes
- Cognitive function deficits including disorientation, confusion, amnesia
- Sleep abnormalities
What are the two ways typically used to model concussion in animals?
Weight drop model - using a weight drop from a certain height on to an animals head
Piston driven models - useing an electromagnetic or pneumatic driven piston to strike the animal head, allows more control over the impact area
Whatis the vascular hypothesis?
Concussion occurs due to brief cerebral ischemia (now widely dismissed)
What is the reticular (centripedal hypothesis and pontine cholinergic system hypothesis)
brain dysfunction results from the direct biomechanical insults to the brainstem where some critical neurons controlling arousal/sleep are located
What is the convulsive hypothesis?
mechanically elicited neuronal excitation results in an initial convulsive neuronal activity and then neuronal “exhaustion” which accounts for the subsequen salient period of paralysis, muscle relaxation and depressed cortical rhythms (currently most supported)
What are the immediate neurometabolic changes after a concussive blow?
- Increase in extracellular glutamate and acetylcholine concentration
- Concentration of K+ and Ca2+ also increase
- Oxidative glucose and lactate concentrations increase
- There is a decrease in cerebral blood flow which can last up to days after the episode
What is the molecular pathophysiology of concussion?
- Ca2+ channels open, causing neurofilament compaction via phosphorylation, potential microtubule dissasembly and axonal swelling. Intracellular Ca2+ can be sequestered by mitcochondria leading to dysfunction.
- At the dendrites and cell body, global depolarisation, can lead to action potentials and release of K+ throught the NMDA and AMPA channels
- Increased effluc occurs to restore ionic homeostasis leading to hyperglycolysis to generate more ATP hence leading to lactate accumulation
What is post-consussion syndrome?
Persistent symptoms lasting weeks to months after the initial injury including multiple “somatic, emotional and cognitive” symptoms
What is second-impact syndrome?
Where a repeat blow or injury to the head happens before the initial resolution of the first concussion resulting in a rapid swelling of the brain
What is chronic traumatic encephalopathy?
Slow progressive neurodegeneration due to repeated head trauma and tau protein deposition. Symptoms can include memory distubances, behaviour changes as well as speech and gait abnormalities
What are the three hypotheses of chronic traumatic encephalopathy?
- Tau phosphorylation and aggrgation
- Amyloid beta metabolism
- Chronic inflammation
How can TBI affect amyloid?
Proposed to increase expression of APP in response to trauma leading to a large resevoir of APP and BACE1 in axonal bulbs which generate amyloid beta forming aggregates
How is chronic inflammation proposed to play a role in TBI?
- Mitochondrial activation is essential for recovery from TBI
- However TBI can cause pathological inflammation of M1 and M2 like microglia leading to an increase in anti-inflammatory/neurotrophic signals
