Concussion pathophysiology
|
Concussion Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Concussion pathophysiology On the Web |
|
American Roentgen Ray Society Images of Concussion pathophysiology |
|
Risk calculators and risk factors for Concussion pathophysiology |
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.
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. Excitatory neurotransmitters, chemicals such as glutamate that serve to stimulate nerve cells, are released in excessive amounts as the result of the injury.The resulting cellular excitation causes neurons to fire excessively. Giza CC, Hovda DA (2001). "The neurometabolic cascade of concussion". Journal of Athletic Training. 36 (3): 228–235. PMID 12937489. </ref> This creates an imbalance of ions such as potassium and calcium across the cell membranes of neurons (a process like excitotoxicity). 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. 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. The brain may stay in this state of hypermetabolism for days or weeks. At the same time, cerebral blood flow is relatively reduced for unknown reasons, though the reduction in blood flow is not as severe as it is in ischemia. Thus cells get less glucose than they normally do, which causes an "energy crisis".
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.
For a period of minutes to days after a concussion, the brain is especially vulnerable to changes in intracranial pressure, blood flow, and anoxia. 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.
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. 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. </ref> Concussion is thought to be a milder type of diffuse axonal injury because axons may be injured to a minor extent due to stretching. Animal studies in which primates were concussed have revealed damage to brain tissues such as small petechial hemorrhages and axonal injury. 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. </ref> 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.[2]
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.
- ↑ Rees PM (2003). "Contemporary issues in mild traumatic brain injury". Archives of Physical Medicine and Rehabilitation. 84 (12): 1885–1894. PMID 14669199.