**2. Concussion pathophysiology**

#### **2.1 Biomechanics of the injury**

Biomechanical forces from sports impact that result in traumatic brain injury or concussion leads to functional impairment at the level of individual cells or neurons. This abnormal cellular function results in overall neurological function

**5**

*Sports-Related Traumatic Brain Injury: Screening and Management*

impairment and may lead to microstructural and subsequent macrostructural

Inertial, or acceleration loading, transmitted to the brain is a primary cause of concussive injury. Both linear and rotational accelerations cause transient increases in pressure within the brain and causes shear forces [16]. The forces and pressure experienced within the brain leads to changes at a cellular level. Neuronal axons can become quickly stretched resulting in a complex cascade of ionic, metabolic and

Changes in intracellular ion concentrations occur due to disruption of cell membranes causing an abnormal outflux of potassium causes irregular neuronal depolarization which in turn leads to increased extracellular potassium and neurotransmitter release. Glutamate, an excitatory neurotransmitter, further promotes potassium efflux and binds to N-methyl-D-aspartate receptors which additionally allows for hyperexcitability and continued unhindered depolarization of the neuron. Simultaneously, accumulation of excitatory neurotransmitters also leads to influx of calcium which promotes proteases, reactive oxygen species and mitochondrial impairment all of which contribute to cellular dysfunction, damage and death

Dysfunction in the regulation of neurotransmitters as well as the inciting excitotoxicity of the neuron causes significant stress on the cellular mitochondria to maintain

which require ATP struggle to maintain the cellular ion homeostasis. The glycolysis process is activated in an attempt to provide this increased energy demand which leads to accumulation of lactic acid. This lactic acid breaks down the blood-brain barrier and

There is also a neuroinflammatory response that occurs after brain trauma which increases microglial cells, cytokine mediators, proteases and reactive oxygen species which promotes widespread inflammation and breakdown of the blood-brain barrier. This leads to cerebral blood flow changes [17, 18]. Other cerebral blood flow changes also occur as a result of carbon dioxide that accumulates from the metabolic changes occurring. Carbon dioxide causes decreases in vasoreactivity acutely and chronically. These changes can lead to many of the acute and chronic symptoms experienced by individuals suffering from sportsrelated concussion and also puts them at increased risk for subsequent head injury

Repetitive traumatic brain injury exposure and sub-concussive injuries, in which a substantial injury is sustain however no outward signs or symptoms are apparent, can lead to persistent neurodegenerative changes. The acute neuroinflammatory response discussed above as well as the sustained neuroinflammation that may occur can result in the development of more permanent neurocognitive deficit symptoms and neurodegenerative changes. Additionally, diffuse axonal injury that occurs from concussive impacts can result in further neurodegenerative processes

/K+

) pumps

when the neuron is unable to recover cellular stability [17, 18].

to energy demands through ATP production. The sodium/potassium (Na+

**2.3 Neuroinflammatory response and cerebral blood flow alterations**

*DOI: http://dx.doi.org/10.5772/intechopen.88442*

damage.

pathophysiological events.

leads to cerebral edema [17].

during this recovery period [17, 18].

**2.4 Chronic pathophysiology**

and permanent changes [17, 19].

**2.2 Metabolic cascade**

*Sports-Related Traumatic Brain Injury: Screening and Management DOI: http://dx.doi.org/10.5772/intechopen.88442*

impairment and may lead to microstructural and subsequent macrostructural damage.

Inertial, or acceleration loading, transmitted to the brain is a primary cause of concussive injury. Both linear and rotational accelerations cause transient increases in pressure within the brain and causes shear forces [16]. The forces and pressure experienced within the brain leads to changes at a cellular level. Neuronal axons can become quickly stretched resulting in a complex cascade of ionic, metabolic and pathophysiological events.
