TBI in American Football: Causes, Intact Calvarium, Closed Head Injury - Research Paper

Introduction

Traumatic brain injury in American Football has been attributed to two primary causes. First, traumatic brain injuries occur when there is penetration of calvarium (Viola-Saltzman and Watson 3). However, in some instances, a traumatic brain injury may develop even when the calvarium remains intact. This is referred to as a closed head injury. When it affects a specific region of the brain tissue, such as intracerebral hemorrhage, epidural hematoma, and cerebral contusion, closed head injury is classified as focal. However, if the head injury is not localized, it is known as diffuse. Focal injury may lead to a coup-contrecoup traumatic brain injury mechanism in which a coup injury is found under the site of the impacted and a contrecoup injury occurring on the side opposite the site of impact with an object (Viola-Saltzman and Watson 3). Diffuse injury has been attributed to acceleration/deceleration forces. On the other hand, axonal injury is attributable to shearing forces resulting in increased intracranial pressure, cerebral edema, and microhemorrhages (Viola-Saltzman and Watson 3).

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Traumatic brain injury in American football has also been linked to the style of play. In one of the recent studies, Teramoto et al. (1) sought to examine whether offensive and defensive strategies, styles of play, are linked to the rate of concussions in the National Football League. In this study, Teramoto et al. (1) conducted a retrospective analysis of data from the 2012 to 2014 National Football League regular seasons. Findings of this study revealed that the number of traumatic brain injuries sustained by offensive players was higher among players who adopted the West Coast offense than those who employed non-West Coast offenses and those who utilized the Air Coryell offense. It was further established that athletes most involved in pass plays had more traumatic brain injuries.

Traumatic brain injury has also been reported to occur upon transmission of linear or rotational forces to the brain (Harmon et al. 3). There currently does not exist a known biomechanical threshold for a clinical traumatic brain injury. However, complex pathophysiological, metabolic, and ionic alterations along with microscopic axonal injuries have been established to be the clinical representation of concussion. Following disrupted ionic balance and metabolism, energy is needed to restore homeostasis. However, the demand for increased energy takes place in the presence of mitochondrial dysfunction and reduced cerebral blood flow, leading to mismatched energy supply and demand. Consequently, any subsequent traumatic brain injury leads to significant cognitive deficits (Harmon et al. 3).

Long-Term Effects of Traumatic Brain Injury in Football

Research studies conducted to explore the long-term consequences of traumatic brain injury in football have revealed crucial findings. McAllister and McCrea (313) noted that apart from the neurocognitive and neuropsychiatric changes associated with traumatic brain injury, exposure to repetitive concussions, especially head-related ones, may elevate the footballers' risk for neurodegenerative disorders in their later lives. One of the neurodegenerative disorders associated with traumatic brain injury is an elevated risk for Alzheimer disease. Yuan and Wang (2) noted that in patients with Alzheimer's disease, memory impairment is linked to chronic traumatic encephalopathy. Additionally, Yuan and Wang (2) revealed that traumatic brain injuries lead to low hippocampal volume, a key factor associated with Alzheimer's disease.

Alzheimer's disease is manifested in various ways. One of the key symptoms of Alzheimer's disease is cognitive impairment characterized by the inability to recognize common things, difficulty creating new memories, the difficulty of concentration, mental confusion, increased forgetfulness, disorientation, delusion, difficulty thinking and understanding, and mental decline. Alzheimer's disease is also manifested through behavioral symptoms such as personality changes, irritability, difficulty in self-care, agitation, and aggression.

The impact of traumatic head injury on the likelihood of developing Alzheimer's disease is affected by the age of the affected individual. It has been established that the risk of developing Alzheimer's disease following a head injury is two-fold in young adults. Apart from Alzheimer's disease, head injuries have also been found to lead to dementia. Also, the severity of head injury affects the risk of developing Alzheimer's disease. Specifically, in cases of moderate head injury, there is a 2.3-fold of developing Alzheimer's disease. On the other hand, severe head injury was found to result in a 4-fold increased risk of Alzheimer's disease.

The other long-term effect football-related concussions are Chronic Traumatic Encephalopathy (CTE). CTE has been defined as a neurodegenerative disease that appears many years after an individual recover from the acute or post-acute impacts of head trauma (Gavett et al. 180). It is posited that a series of cytoskeletal, membrane, ionic, and metabolic disturbances arising from frequent axonal perturbation stimulate the pathologic cascade that causes CTE in vulnerable individuals. CTE starts in middle adulthood, usually after the retirement of the athletes from their football careers or other sports associated with head injuries. In some people, early appearances of CTE has an impact on behavior. Specifically, it has been reported that individuals with CTE are more likely to manifest irritability, anger, or apathy. Additionally, evidence has shown that CTE is associated with an elevated risk of suicidality (Gavett et al. 180).

CTE has also been established to lead to cognitive impairment in the affected individuals. Cognitive dysfunctions are manifested through impaired episodic memory (an individual's unique memory of a specific event) and executive functioning. The late stages of CTE are characterized by ocular, speech, and movement anomalies because of deteriorated cognition and worsening comportment. CTE has also been found to lead to the development of dementia before a person's demise.

Traumatic brain injuries have also been reported to lead to depressive symptoms and depression. Many studies have proven that concussions increase the risk of developing depression in old age. In one of these studies, researchers investigated whether a history of traumatic brain injury is responsible for current depressive symptoms in retired professional athletes (Didehbani et al. 418). The sample for this study comprised of 30 American Football athletes with a history of traumatic brain injury and 29 control participants without a history of concussion. All the respondents completed The Beck Depression Inventory (BDI-II), a self-report questionnaire used to evaluate somatic, affective, and cognitive symptoms of depression (Didehbani et al. 420). Findings of this study revealed a modest but statistically significant association between the number of traumatic brain injuries and current self-reported depressive symptoms in former American football players. These results suggest that as the number of traumatic brain injuries increases, there is an increased likelihood of developing depressive symptoms. A further examination of the BDI-II revealed that the Cognitive factor was significantly associated with the number of traumatic brain injury. This is a manifestation that repeated concussions are linked to "cognitive" symptoms of depression, such as critical self-evaluations, feelings of guilt, and sadness (Didehbani et al. 422).

One of the studies conducted to examine depressive symptoms in National Football League (NFL) players with a history of traumatic brain injury explored the role of white matter dysfunction in depression (Strain et al. 25). The sample of this study comprised of 26 retired NFL players who underwent diffusion tensor imaging (DTI) scanning. In this study, symptoms associated with depression (somatic, cognitive, and affective factors) were assessed using BDI-II. Findings of this study revealed that depressive symptoms in retired athletes with a history of traumatic brain injury are linked to disruption of white matter integrity.

Another long-term effect of football-related traumatic brain injury is anxiety. Football athletes with repeated or chronic traumatic brain injuries have been found to have emotional disturbance and to manifest anxiety/mood clinical profile. It has further been established that the etiology of anxiety or mood clinical profile following sport-related traumatic brain injury is complex and involves an interplay of both psychosocial and physiological factors. Many potential mechanisms have been linked to emotional dysregulation following a sport-related traumatic brain injury. One of these factors is pre-injury risk factors.

Various identified pre-injury risk factors increase the likelihood of developing anxiety following sport-related concussion. It has been reported that athletes with a pre-injury history of mental health condition, such as anxiety disorder, are more likely to experience worse emotional disturbances following traumatic brain injury compared to athletes without such history. Apart from mental health history, biological sex (male or female) is another risk factor that affects the severity of anxiety following traumatic brain injury. Because anxiety disorders are more common among the females compared to the males, there is a higher prevalence of anxiety disorders among the female athletes both before and after traumatic brain injury.

Football-related traumatic brain injury has also been reported to lead to sleep disorders (Viola-Saltzman and Watson 4). Specifically, it has been established that the type of sleep disturbance linked to traumatic brain injury depends on the location of the injury, especially in the sleep-regulating brain regions. One of these sleep disorders is posttraumatic hypersomnia. This is experienced by an individual when the brain areas involved in the maintenance of wakefulness are damaged. In this case, the affected brain regions include, posterior hypothalamus and the region neighboring third ventricle and the brainstem reticular formation. Additionally, it has been established that obstructive sleep apnea and sleepiness is linked to high cervical cord lesion.

Moreover, whiplash has been linked to hypersomnia because it triggers sleep-disordered breathing. Narcolepsy, characterized by cataplexy, has been linked to low levels of cerebral spinal fluid hypocretin-1. Viola-Saltzman and Watson (4) further noted that coup and contrecoup injuries following a traumatic brain injury are mostly found at the base of the skull in regions with bony irregularities. These injuries have been found to damage some of the brain regions involved in sleep, especially the basal forebrain associated with sleep initiation.

Insomnia has also been reported to be one of the long-term effects of traumatic brain injury (Quan 241). Insomnia is a sleep disorder that is manifested through difficulty falling or staying asleep. Other symptoms associated with insomnia include waking up frequent waking at night and difficulty going back to sleep, waking up too early, and fatigue after waking. Many people who have a history of acute traumatic brain injury have later been found to have a variety of sleep disturbances, including obstructive sleep apnea. The prevalence of obstructive sleep apnea and insomnia is 23% and 25% respectively. Moreover, it has been established that cognitive functioning is worse in individuals who have both obstructive sleep apnea and previous traumatic brain injury than in those with traumatic brain injury alone. Neuroimaging studies have helped to understand the etiology of...