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Flashcards in Concussions Deck (35)
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What is a Concussion?

Biomechanically induced transient disturbance of neurological function.

Can be associated with a loss of consciousness, temporary loss of brain function, physical, cognitive, and emotional symptoms.


Concussions are also referred to as what?

Mild Traumatic Brain Injuries.


What causes a concussion?

Rapid acceleration/deceleration of the brain.

Brain collides with the skull: front/back or side/side.

Bruising and swelling of brain tissue follows and may persist for up to 48 hours (brain contusion and cerebral edema; increased intracranial pressure).

Impact can be direct or indirect/linear, rotational, or angular.


Does direction of force matter?



What does direction of force dictate?

Presenting symptoms, long-term consequences, extent of damage, and rate of recovery.

It makes it difficult to compare concussions between patients.


What does the magnitude of rotational force dictate?

Concussion severity.


What is Diffuse Axonal Injury?

Shearing forces that cause axons to detach from the cell body.

Damaged axons will display indiscriminate release of the GLUTAMATE excitatory neurotransmitter.

Excitotoxic lesions subsequently occur from 24-48 hours post injury.


Which parts of the brain are most affected by rotational forces?

Midbrain and Diencephalon.


Disruption of normal cellular activities is thought to produce what?

Level of Consciousness.

Also damages frontal and temporal lobes.


What is a Subdural Hematoma?

It is a collection of clotted blood and accompanying increased pressure on the brain.


What causes a Subdural Hematoma?

Unrestricted movement of the head results in axon shearing, which leads to a subdural hematoma.


What is an Epidural Hematoma?

It results from the collection of blood between the dura mater and the skull.


What is Chronic Traumatic Encephalophagy?

Result of multiple, sub-concussive blows to the head.

Not a concussion issue.

It is a progressive degenerative disease found in individuals with repeated head trauma.

Characterized by neurofibrillary tangles, plaques, and neuronal death.


What is Second Impact Syndrome?

Occurs when an individual suffers a concussion while still symptomatic from a previous concussion.

Prior concussions increase the likelihood of a 2nd concussion and cause greater morbidity in both human and animal models.

Repeated concussions have a cumulative effect on the human brain.


What are the mortality and morbidity rates of Second Impact Syndrome?

50% mortality rate and 100% morbidity rate.


What are the 3 methods of detection and diagnosis for Concussions?

Immediate Post Concussion and Cognitive Testing (ImPACT).




What is ImPACT?

Computer-based battery of tests aimed at detecting post-concussive symptoms.

Demographic questionnaire.

Symptom Inventory.

Injury Evaluation.

20-Minute Neurocognitive Test.


What is an MRI?

Allows us to visualize internal structures.


What is an EEG?

Allows us to record electrical activity.


What are the clinical symptoms of a concussion?

Headache, pressure - Vascular injuries

Temporary loss of consciousness - Brain Stem

Confusion - Corpus Collosum

Amnesia surrounding the event - Hippocampus, Frontal Lobes.

Ringing in the ears - Temporal Lobes.

Nausea and/or vomiting - Area Postrema

Changes in Mood and Emotional Disturbances - Amygdala


What do symptoms of a concussion depend on?

Location of structural damage.


What is BBB Permeability (Secondary Injury)?

Anaerobic glucose metabolism (glycolysis) involves production of lactate - lactic acid.

Overproduction of lactic acid results in acidosis and damage to the Blood Brain Barrier (BBB).

BBB permeability ensues, leaving organism vulnerable to external toxins.


What are Secondary Injuries?

Patient's condition may deteriorate in stages, which suggests that brain injuries result in various waves of potential damage (primary vs. secondary effects).

Secondary effects may take days, weeks, or months to develop.

Can persist for weeks, months, and even years.


A concussion can lead to what kind of tissue damage?

Neural and vascular - which leads to a distortion of cell membranes (neurone activity picks up and cerebral blood flow is interrupted).


What is the Acute Metabolic Cascade?

An indiscriminate release of GLUTAMATE will produce a cascade of events known as the METABOLIC CASCADE - this leads to a cerebral energy crisis.


What is an Energy Crisis?

Release of an indiscriminate release of glutamate.

Depolarization of surrounding neurons and firing of action potentials.

Na-K pumps work in overdrive to restore Ionic Homeostasis (which requires a ton of ATP).

Increased demand for ATP results in massive increase in glucose metabolism.

Increased demand for glucose comes when cerebral blood flow is reduced and the mitochondria are dysfunctional.

Hypoglycemia ensues, leading to cognitive deficits and an energy crisis that leads to secondary injuries.


What is Glutamate?

It is the main excitatory neurotransmitter in the brain. and is present in more synapses than any other NT.


Glutamate can bind which three post-synaptic receptors?



AMPA, NMDA, and Kainate allow and cause what?

Allow Na+ entry into the post-synaptic cell, therefore causing depolarization and excitatory post-synaptic potentials.


NMDA receptors are also permeable to what?



What is Necrosis?

Rapid lysis (rupture of cell wall or membrane) of the cell due to osmotic swelling.


What is Apoptosis?

Delayed cascade of biochemical events that lead to DNA break up and ultimately cell death.


What is Glutamate Excitotoxicity?

Too much glutamate being released can cause damage to surrounding neurons.

Excitotoxicity can occur with overexposure to glutamate, which is caused by prolonged depolarization of the postsynaptic neuron.

Cell death.


What happens when Glutamate activates NMDA receptors?

It can, in some cases, allow the entry of calcium into the cell.


How is Ca2+ toxic to a cell?

Overactivation of the NMDA receptors lead to a massive influx of Ca2+ and efflux of Na+ and K+.

Ca2+ is then sequestered into the mitochondria and disrupts normal function.

ATP production is then hindered - which leads to the initiation of apoptosis.