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(Aghan & Burke)
Multiple Sclerosis III
Parkinson's Disease IV
Visual Form Agnosia
Cerebral Palsy IV
(Labbadia & Taplin)
Multiple Sclerosis IV
Cerebellar Ataxia II
Huntington's Disease III
Smooth Pursuit II
Progressive Supranuclear Palsy
Postural Control II
Parkinson's Disease III
Huntington's Disease II
Phantom Limb III
Vestibular Rehabilitation and Concussion
Cerebral Palsy III
Multiple Sclerosis II
Myofascial Referred Pain
Seizure - Cortical Related
Visual Cortical Neurons
Learning to Dance - Observation vs Action
Restless Leg Syndrome
Grand Mal Seizure
Cerebral Palsy II
Duchenne Muscular Dystrophy
Basal Ganglia II
Saccadic Eye Movement
Shaken Baby Syndrome
Parkinson's Disease II
Alcohol & Cerebellum
(Leach & McManus)
Phantom Limbs II
Cerebellum & Motor Learning
Motor Unit Adaptation
Aging Nervous System
Dance & the Brain
Enteric Nervous System
Golgi Tendon Organs
Vestibular Occular Reflex
Concussions, also known as a mild traumatic brain injury (MTBI), is defined as “any transient neurologic dysfunction resulting from a biomechanical force” (Giza 228). The name comes from the Latin word ‘concutere’, which means to “dash together [or] shake violently” (Pearce 113). Concussions are due to either direct impact, such as a blow to the head, or extreme acceleration forces, like whiplash. Symptoms can include confusion, headache, disorientation, vomiting and/or nausea, unsteadiness, light sensitivity, post-traumatic amnesia, difficulty concentrating, and dizziness. Loss of consciousness is also very common. The brain is not damaged structurally; however, there is temporary functional damage to the neurons, which restore completely with time. More specifically, concussions cause ionic shifts, decreased cerebral blood flow, altered metabolism, impaired connectivity, and changes in neurotransmission, which elicit the various symptoms (Giza 230).
Concussions can be caused by many things, including falls, car accidents, being struck by an object, assaults, and many others, as shown in the figure to the left above. Of the 19% of the sports-related concussions (SRC), most are caused by cycling and football, although basketball, soccer, and playground concussions are common. Concussions are a common issue; to put that 19% into perspective, over 300,000 SRCs occur every year in the United States alone (Guskiewicz 2550).
The brain is surrounded by cerebrospinal fluid, which acts as a buffer for the brain to cushion and protect it. This is sufficient to protect against normal bumps and blows; however, the force of a concussion overcomes this. Depending on which direction the force is received from, the brain hits the inside of the skull, and can even bounce back and hit the opposite side of the skull, known as a "counter-blow" (see figure).
The impact caused as the head decelerates causes bruising on the surface of the brain, causing contusion, secondary oedema, swelling, bleeding, or blood clots.
The force of a concussion also causes widespread stretching and tearing of axons in the brain. This is referred to as ‘diffuse axonal injury’ (DAI). Here, subcortical white matter fibres are torn, and immediate loss of consciousness usually results. Other results of DAI include an increased influx of calcium, neurofilament instability and collapse, microtubule breakdown, axon swelling and constriction, and the formation of axon bulbs.
The traumatic force causes excitatory neurotransmitters such as Glutamate to bind to the N-methyl-D-asparate receptor. This causes a further influx of calcium and efflux of potassium, depolarizing the cells. Trying to get back to a normal membrane potential, the sodium-potassium pumps then work extra. This requires increased amounts of ATP, which greatly increses glucose metabolism. This is referred to as hypermetabolism. This hyermetabolism, paired with a sudden decrease in cerebral blood flow, means that there’s not enough glucose in the available blood to keep up with the need. This “energy crisis” decreases the brain’s ability to respond, and can have short- and long-term effects.
Also, the metabolism is depressed due to the excess calcium (which result from the increased Glutamate levels). Abnormally high levels of calcium due to accelerated APT usage causes damage to mitochondria (making the problem worse) and leads to cell death by impairing neurofilaments and microtubules, decreasing “neural connectivity”. The damage to the mitochondria makes cells go anaerobic, and lactic acid is produced. Calcium accumulation can also lead to cell death. Lasting calcium accumulation shows cell death in "distant structures" (Giza 232), such as the thalamus. Cell death can also occur by "overactivation of phospholipases, plasmalogenase, calpains, protein kinases, nitric acid synthase, and endonucleases" (Giza 232). In addition, intracellular magnesium, inflammatory responses and neurotransmission are decreased. This reduction in magnesium is important in "postinjury neurologic deficits" (Giza 232). Decreased magnesium impairs ATP synthesis, cellular membrane potential, and protein synthesis. It can also lead to an even further increase in calcium influx.
The biomechanical impact also disrupts the membranes of neurons, which causes the opening of voltage-gated potassium channels, leading to an excess of extracellular potassium. This is too much for the glial cells (which work to maintain potassium levels), and the neurons are depolarized, causing a mass excitation and then a “wave of relative neuronal suppression” (called ‘spreading depression’) to counteract it. This spreading depression affects widespread areas of the brain all at the same time, which can lead to loss of consciousness, amnesia, or other concussion symptoms.
Concussive forces disrupt the reticular activating system (RAS), which controls the transition between awake and asleep states, at the cellular level. This causes the loss of consciousness that is so common in concussions. Another cause of unconsciousness is an extreme increase in extracellular potassium levels. When extracellular potassium increases to about 20-50 mmol/L (whereas the normal level is about 4-5 mmol/L), action potentials are inhibietd and the person loses consciousness (Ommaya 640).
Amnesia is also common in concussions. This is due to disruptions in neurotransmitter systems. Specifically, excitatory glutamatergic, adrenergic, and cholinergic pathways are damaged by impaired neurons and/or the hippocampus. Inhibitory neurotransmitters, such as GABA, are also lost in a concussion, and can cause memory loss or seizures.
This ionic imbalance is shown in the figures above. The figure to the left shows the chain of events starting with the depolarization of the axons (1). Glutamate is released (2), and there is an influx of calcium and an efflux of potassium (3). The sodium-potassium pumps work in overtime (4), inducing hypermetablism (5-6, 8). High calcium levels damage mitochondria, and lactic acid is produced and there is even less ATP produced (7-9). A-D of that figure show the damage to the axon in DAI.
The figure to the right shows the effects of concussion minutes, hours and days after the initial incident. Calcium levels skyrocket (up to 5 times of what is normal) and stay elevated for up to a week after the injury. This explains the long-term "energy crisis" in the brain. Potassium levels spike about three minutes after the blow and drop back to normal within twelve minutes. This accounts for the overactivity of the sodium-potassium pumps and thus the short-term "energy crisis". The CMRgluc, which stands for the oxidative glucose metabolism, peaks at about seven minutes and normalizes in around a half hour. The damage to mitochondria is widespread, but affect primarily the cortex and hippocampus. Lactate levels follow the CMRgluc curve perefctly as mitochondria are damaged by the excess calcium. Glutamate increases and peaks at around one to two minutes, triggered by the depolarization of the cells and setting off the whole chain of events. CBF, which stands for cerebral blood flow, decreases and stays low for up to ten days. Researchers are still unsure why this happens, although reductions of up to 50% of normal are not uncommon. Coupled with the increase in glucose demand from the overactive sodium-potassium pump, however, this reduction in blood flow and thus glucose supply further adds to the "energy crisis" in the brain, both short- and long-term.
LEVELS OF CONCUSSIONS
There are a few different grading scales for concussions, each with subtle differences. The most widely accepted is from the American Academy of Neurology (AAN), which defines three grades of concussions.
Grade 1 concussions include confusion, and symptoms last less than 15 minutes. Here, there is no loss of consciousness; this is the most mild stage of concussion. In Grade 2 concussions, symptoms last more than 15 minutes, and there is still no loss of consciousness. In Grade 3 concussions, the person loses consciousness for seconds (3A) or minutes (3B). Robert Cantu’s form of grading considers different lengths of post-traumatic amnesia.
Concussions go away by themselvse with time. Rest is usually the only thing recommended for those with concussions--plenty of sleep at night, and rest during the day. Medication for pain such as ibuprofen can be taken for post-concussive headaches, and patients are advised not to drink alcohol or do drugs. The question is more of the timeframe for reentering activity, especially when it comes to sports-related concussions (SRC).
There are many guidelines for when to return to play after a concussion. For the sake of continuity, the AAN's will be used here, although they are all very similar. For a first-time, Grade 1 concussion, the AAN suggests that the patient return to play only when they are asymptomatic for 15 minutes. For a first-time, Grade 2 concussion, patients should return after they are asymptomatic for a week. For a first-time, Grade 3A concussion, they should be taken to the hospital and allowed to return to play after being asymptomatic for a week. For a first-time, Grade 3B concussion, the patient should be taken to the hospital and allowed to return to play after being asymptomatic for two weeks.
Studies by Guskiewicz, Levin, and many others show that having a first concussion greatly increases the likelihood of getting another one. The reason is not known, but is under investigation. Recurrent concussions are usually more serious than the first, and cumulatively can cause long-term memory loss. There is so much of a difference between first and second concussions that the AAN and others have much different guidelines as to when to return to play. For a second concussion, the patient should return to play when they are asymptomatic for one week (for a Grade 1 concussion), asymptomatic for two weeks (Grade 2 concussion), and asymptomatic for one month (Grade 3A and 3B concussion). For a third concussion, patients should terminate their season and return in 3 months (Grade 1), 6 months (Grade 2), or never (Grade 3A and 3B) (Harmon 895).
Post-concussion syndrome, dimentia pugilistica, second-impact syndrome, and memory loss are all possible lasting effects of a concussion and should be monitored closely. People should wear helmets and always take the necessary precautions in potentially dangerous situations.
In conclusion, concussions are a common and complex occurance. The traumatic force of a concussion causes brain bruising, an "energy crisis" from the imbalance between glucose supply and demand, excess calcium, extracellular potassium, and disruption of the RAS and neurotransmitter levels. By these various mechanisms, the patient may experience dizziness, confusion, lack of coordination, amnesia, headache, nausea, loss of consciousness, and other symptoms. There is still much that is not understood about concussions, and further research is being done on those aspects to gain a better understanding of concussions, and neurophysiology as a whole.
Cerebrospinal fluid (CSF):
"the fluid in the ventricles of the brain, between the arachnoid and pia mater, and surrounding the spinal cord."
Diffuse axonal injury (DAI):
widespread stretching and tearing of axons in the brain.
"a syndrome affecting boxers that is caused by cumulative cerebral injuries and is characterized by impaired cognitive processes (as thinking and remembering), parkinsonism, impaired and often slurred speech, and slow, poorly coordinated movements, especially in the legs."
Mild Traumatic Brain Injury (MTBI):
another term for concussion. "Any transient neurologic dysfunction resulting from a biomechanical force" (Giza 228).
"symptoms of a concussion that are experienced up to a year after the initial concussion."
Reticular activating system (RAS):
"a part of the reticular formation that extends from the brainstem to the midbrain and thalamus with connections distributed throughout the cerebral cortex and that controls the degree of activity of the central nervous system (CNS) (as in maintaining sleep and wakefulness and in making transitions between the two states)."
"condition in which the brain swells rapidly and catastrophically after a person suffers a second concussion before symptoms of an earlier one have subsided."
Solomon, Gary, Johnston, Karen, & Lovell, Mark. (2006).
The heads-up on sport concussion
. Champaign, IL: Human Kinetics.
This is an awesome book that starts at the basics and goes all the way through what happens in sports concussions, what to look for, and how to assess and treat concussions, specifically in sports. Everything you need to know.
Giza, Christopher, & Hovda, David. (2001). The neurometabolic cascade of concussion. Journal of Athletic Training, 36(3), 228-235.
Describes in detail the effects of concussion at the cellular level.
Pearce, J. (2008). Observations on concussion. European Neurology, 59(3), 113-119.
Interesting look at concussions from a more statistical viewpoint.
1. Concussions must be caused by some kind of impact.
2. Concussions are temporary and, under normal conditions, heal completely with time.
3. Cerebrospinal fluid surrounds only the brain.
4. Ibuprofen shoud always taken immediately after concussion.
5. DAI is:
a. widespread tearing and stretching of axons.
b. a blow to any body part, causing damage to axons.
c. the act of healing an injured axon.
d. increased axonal sensitivity.
6. is caused by concussions:
a. decreased calium levels.
b. increase in GABA production.
c. increase in magnesium levels.
d. spike in potassium levels.
7. Which of the following is NOT a grade of concussions?
8. Glutamate spikes _ after initial concussive force:
a. 1-2 minutes
b. 5-7 minutes
c. 8-10 hours
d. 3-4 days
9. Name 3 possible long-term effects of concussions.
10. Desribe the differences between the different levels of concussions.
11. What causes the loss of consciousness in concussions?
9. Post-concussion syndrome, dimentia pugilistica, and second-impact syndrome are all possible long-term effects of concussions.
10. Grade 1 concussions have symptoms that last less than 15 minutes and no loss of consciousness. Grade 2 concussions have symptoms that last more than 15 minutes, but still no loss of consciousness. Grade 3A concussions have a loss of consciousness for seconds. Grade 3B concussions have a loss of consciousness for minutes.
11. Damage to the RAS, extremely high extracellular potassium levels, and disruption of neurotransmitter systems can all cause lack of consciousness in concussions.
Anderson, Tim, Heitger, Marcus, & Macleod, A. (2006).
Practical Neurology, 6(10),
Giza, Christopher, & Hovda, David. (2001). The neurometabolic cascade of concussion.
Journal of Athletic Training
Guskiewicz, Kevin. (2003). Cumulative effects associated with recurrent concussion in collegiate football players.
The Journal of the American Medical Association
Guskiewicz, Kevin. (2000). Epidemiology of concussion in collegiate and high school football players.
American Journal of Sports Medicine
Harmon, Kimberly. (1999).
American Family Physician, 25(1).
Joseph, Maroon. (2000). Cerebral concussion in athletes: evaluation and neuropsychological testing.
Levin, Harvey, Eisenberg, Howard, & Benton, Arthur. (1989).
Mild head injury
. New York, NY: Oxford University Press.
Ommaya, Ayub, & Gennarelli, T. (1974). Cerebral concussion and traumatic unconsciousness.
Pearce, J. (2008). Observations on concussion.
European Neurology, 59(3),
Solomon, Gary, Johnston, Karen, & Lovell, Mark. (2006).
The heads-up on sport concussion
. Champaign, IL: Human Kinetics.
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