Biomechanics and Pathophysiology

    Concussions occur as a result of imparted linear and rotational accelerations to the brain.

    Because of modifying factors (e.g., concussion history, neck strength, anticipatory reaction and varying magnitudes, frequency, and locations of impact), there is currently no known threshold for concussive injury.

    Metabolic changes that occur in the animal model and thought to occur in humans include the following:

  •  Alterations in intracellular/extracellular glutamate, potassium, and calcium.
  •  A relative decrease in cerebral blood flow in the setting of an increased requirement for glucose (i.e., increased glycolysis). This mismatch in the metabolic supply and demand may potentially result in cell dysfunction and increase the vulnerability of the cell to a second insult.


Complications of Concussion

Concussion may cause a wide range of short- or long-term complications, affecting thinking, sensation, language, or emotions. These changes may lead to problems with memory, communication, personality changes, as well as depression and the early onset of dementia. Other complications of concussion are also addressed in this section.

  •     Prior concussions may increase risk for subsequent concussions.
  •     Postconcussion syndrome

        Persistent postconcussion symptoms lasting 3 months or longer

        Indicator of concussion severity

        Precludes RTP while present

        Increased risk of depression

  •     Convulsive motor phenomena

        Tonic posturing or convulsive movements within seconds of the concussion

        Dramatic, but usually benign

        Require no management beyond on-field ABCs

        No anticonvulsant therapy required

  •     Posttraumatic seizures

        Seizures occur days to months after concussion

        Does require seizure management and precautions

        Usually requires anticonvulsant therapy

  •     Second-impact syndrome

Occurs within minutes of concussion in athlete still symptomatic from prior brain injury, which can be earlier in same event.

        Vascular engorgement leads to massive increase in intracranial pressure and brain herniation resulting in severe brain damage or death.

        May occur with associated small subdural hematoma.

        Except for boxing, most cases in literature in adolescents.

  •     Chronic traumatic encephalopathy

        A progressive neurodegenerative disease (tauopathy) caused by total brain trauma, and is not limited to athletes who have reported concussions.

        The incidence and prevalence is unknown.

        Diagnosed only after death by distinctive immunoreactive stains of the brain for tau protein and is not the same disease as Alzheimer.

        Typical signs and symptoms include a decline of recent memory and executive function, mood, and behavioral disturbances (especially depression, impulsivity, aggressiveness, anger, irritability, suicidal behavior, and eventual progression to dementia).

        Initial signs and symptoms do not typically manifest until decades after trauma received (ages 40–50 yr).

        A small subset of individuals with chronic traumatic encephalopathy have developed chronic traumatic encephalomyopathy, a progressive motor neuron disease characterized by profound weakness, atrophy, spasticity, and fasciculation similar to amyotrophic lateral sclerosis.

  •     Depression

        Increased risk after a history of multiple concussions

        May predate concussion and/or occur independent of concussion.

        Athletes with depression who later sustain concussion may experience worsening symptoms.

  •     Mild cognitive impairment

        Increased risk later in life after a history of multiple concussions.

        May predate concussion and/or occur independent of concussion.

        Multiple concussions have been associated with an earlier onset of mild cognitive impairment.