Concussion pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
In both animals and humans, MTBI can alter the brain's physiology for hours to weeks, setting into motion a variety of pathological events.[1] Though these events are thought to interfere with neuronal and brain function, the metabolic processes that follow concussion are reversed in a large majority of affected brain cells; however a few cells may die after the injury.[2]
Included in the cascade of events unleashed in the brain by concussion is impaired neurotransmission, loss of regulation of ions, deregulation of energy use and cellular metabolism, and a reduction in cerebral blood flow.[2] Excitatory neurotransmitters, chemicals such as glutamate that serve to stimulate nerve cells, are released in excessive amounts as the result of the injury.[3] The resulting cellular excitation causes neurons to fire excessively.[4] This creates an imbalance of ions such as potassium and calcium across the cell membranes of neurons (a process like excitotoxicity).[2] Since the neuron firing involves a net influx of positively charged ions into the cell, the ionic imbalance causes cells to have a more positive membrane potential (i.e. it leads to neuronal depolarization). This depolarization in turn causes ion pumps that serve to restore resting potential within cells to work more than they normally do.[2] This increased need for energy leads cells to require greater-than-usual amounts of glucose, which is made into ATP, an important source of energy for cells.[2] The brain may stay in this state of hypermetabolism for days or weeks.[5] At the same time, cerebral blood flow is relatively reduced for unknown reasons,[6] though the reduction in blood flow is not as severe as it is in ischemia.[2] Thus cells get less glucose than they normally do, which causes an "energy crisis".[6]
Concurrently with these processes, the activity of mitochondria may be reduced, which causes cells to rely on anaerobic metabolism to produce energy, which increases levels of the byproduct lactate.[2]
For a period of minutes to days after a concussion, the brain is especially vulnerable to changes in intracranial pressure, blood flow, and anoxia.[6] According to studies performed on animals, large numbers of neurons can die during this period in response to slight, normally innocuous changes in blood flow.[6]
Concussion involves diffuse brain injury (as opposed to focal brain injury), meaning that the dysfunction occurs over a widespread area of the brain rather than in a particular spot.[7] Concussion is thought to be a milder type of diffuse axonal injury because axons may be injured to a minor extent due to stretching.[8] Animal studies in which primates were concussed have revealed damage to brain tissues such as small petechial hemorrhages and axonal injury.[9] Axonal damage has been found in the brains of concussion sufferers who died from other causes, but inadequate blood flow to the brain due to other injuries may have contributed to the damage.[10]
Mechanism
The brain is surrounded by cerebrospinal fluid, one of the functions of which is to protect it from light trauma, but more severe impacts or the forces associated with rapid acceleration and deceleration may not be absorbed by this cushion.[12] Concussion may be caused by impact forces, in which the head strikes or is struck by something, or impulsive forces, in which the head moves without itself being subject to blunt trauma (for example, when the chest hits something and the head snaps forward).[8]
Forces may cause linear, rotational, or angular movement of the brain, or a combination of these types of motion.[8] In rotational movement, the head turns around its center of gravity, and in angular movement it turns on an axis other than its center of gravity.[8] The amount of rotational force is thought to be the major type of force to cause concussion[13] and the largest component in its severity.[14] Studies with athletes have shown that the amount of force and the location of the impact are not necessarily correlated to the severity of the concussion or its symptoms, and have called into question the threshold for concussion previously thought to exist at around 70-75 g.[15][16]
The parts of the brain most affected by rotational forces are the midbrain and diencephalon.[17][18] It is thought that the forces from the injury disrupt the normal cellular activities in the reticular activating system located in these areas, and that this disruption produces the loss of consciousness often seen in concussion.[18] Other areas of the brain that may be affected include the upper part of the brain stem, the fornix, the corpus callosum, the temporal lobe, and the frontal lobe.[19]
References
- ↑ McAllister TW, Sparling MB, Flashman LA, Saykin AJ (2001). "Neuroimaging findings in mild traumatic brain injury". Journal of Clinical and Experimental Neuropsychology. 23 (6): 775–791. doi:10.1076/jcen.23.6.775.1026. PMID 11910544.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Invalid
<ref>tag; no text was provided for refs namedIverson2005 - ↑ Invalid
<ref>tag; no text was provided for refs namedTeam - ↑ Giza CC, Hovda DA (2001). "The neurometabolic cascade of concussion". Journal of Athletic Training. 36 (3): 228–235. PMID 12937489.
- ↑ Invalid
<ref>tag; no text was provided for refs namedHeegaard07 - ↑ 6.0 6.1 6.2 6.3 Invalid
<ref>tag; no text was provided for refs namedBowen03 - ↑ Hardman JM, Manoukian A (2002). "Pathology of head trauma". Neuroimaging Clinics of North America. 12 (2): 175–187, vii. doi:10.1016/S1052-5149(02)00009-6. PMID 12391630.
- ↑ 8.0 8.1 8.2 8.3 Invalid
<ref>tag; no text was provided for refs namedsivak - ↑ Hall RC, Hall RC, Chapman MJ (2005). "Definition, diagnosis, and forensic implications of postconcussional syndrome". Psychosomatics. 46 (3): 195–202. doi:10.1176/appi.psy.46.3.195. PMID 15883140.
- ↑ Rees PM (2003). "Contemporary issues in mild traumatic brain injury". Archives of Physical Medicine and Rehabilitation. 84 (12): 1885–1894. PMID 14669199.
- ↑ Invalid
<ref>tag; no text was provided for refs namedPellman - ↑ Invalid
<ref>tag; no text was provided for refs namedShaw02 - ↑ Invalid
<ref>tag; no text was provided for refs namedPoirier - ↑ Invalid
<ref>tag; no text was provided for refs namedAndersonT - ↑ Guskiewicz KM, Mihalik JP, Shankar V; et al. (2007). "Measurement of head impacts in collegiate football players: Relationship between head impact biomechanics and acute clinical outcome after concussion". Neurosurgery. 61 (6): 1244–1252, discussion 1252–1253. PMID 18162904.
- ↑ Gever D (December 7, 2007). "Any football helmet hit can cause potential concussion". MedPage Today, LLC. Retrieved 2008-02-27.
- ↑ Invalid
<ref>tag; no text was provided for refs namedPearce - ↑ 18.0 18.1 Invalid
<ref>tag; no text was provided for refs namedpmid17215534 - ↑ Bigler ED (2008). "Neuropsychology and clinical neuroscience of persistent post-concussive syndrome". Journal of the International Neuropsychological Society. 14 (1): 1–22. doi:10.1017/S135561770808017X. PMID 18078527.