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Approximately 1.5 million Americans are diagnosed with traumatic brain injuries each year. Traumatic brain injuries (TBI) are classified by a significant physiological change in the function of the brain due to a blunt force trauma to the head (1). The change in brain function is measured on a scale of mild to severe and is calculated by the Glasgow Coma Scale. The Glasgow Coma scale provides a practical technique to evaluate and assess the impairment of conscious level in response to a predetermined stimuli (2).
Diagnosis of TBI requires the patient’s ability to recollect the events preceding the change in cognitive function or blunt injury to the head. Memory loss, loss of consciousness, and physical trauma (i.e., blow to the head) described by the patient will be considered (3).
Mood disorders are common in conjunction with TBI. Major depression is a specific concern for patients with TBI during recovery and after symptoms have subsided (4). Decreased activity, hospital stays, and a diminished quality of life are factors of depression with TBI that are often seen.
However, a genetic link is seen between the Apolipoprotein-[varepsilon]4 allele and poor cognitive function in these patients (5). This fat-binding protein is essential for normal processing and is linked to Alzheimer’s disease and cardiovascular disease. When the allele is present the incidence of mood disorders increases significantly following a TBI. Environmental and genetic factors play a role in recovery from mild and severe injuries.
Concussions are considered to be a mild form of TBI and are increasingly common in the United States with over a million reported cases each year (6).
Concussions are in the spectrum of TBI and are set apart by their short-term responses that have been found to be treatable unlike the permanent effects of more severe cases of TBI. Concussions can be diagnosed on a scale of mild to severe with varying symptoms. A concussion is termed a mild TBI (mTBI) if consciousness is lost for more than 5 minutes but less than 30 minutes according to the American Psychiatric Association and the Center for Disease Control. If mTBI symptoms are undiagnosed future complications from the concussion may also be misdiagnosed (6).
Major depression is one of the mood disorders that may be treated by pharmacological antidepressants or other cognitive therapy drugs (4). These medications come with side effects that may inhibit the rehabilitation of those with TBI and produce worsening symptoms. Placebo trails are utilized in the research of these antidepressant medications to limit or eliminate bias (6). Psychosocial interventions are also widely used and can be combined as treatment for mood disorders. Behavior and cognitive-behavior therapies are sometimes used in coordination with antidepressant medications. One behavior modification, exercise, can have antidepressant effects on those living with TBI. The use of exercise as a treatment for depression has shown positive improvements in the overall mood which leads to high self-efficacy in many cases (4).
Exercise as a treatment modality produces a variety of benefits including improvements in mood disorders to the recovering patient (7). Exercise prescriptions may include resistance or endurance training such as weight lifting and running or jogging. Dynamic styles that involve the movement of joints through the exercise may be incorporated as well as static or isometric movements that require little to no movement through muscle contraction. Exercise prescriptions may utilize a combination of exercise styles and modalities to achieve the desired results. Exercise regimens added to individual’s treatment plans may produce improvement to mood, symptoms, and prognosis.
TBI can produce symptoms and side effects that can last days or span the rest of a patient’s life. These effects can include impairments to an individual’s memory, movement, emotional function, and lifestyle (8). Depression is one of the most common disorders following a traumatic brain injury that clinicians today are listing in their highest concerns (3). Traumatic brain injuries cause 30% of all injury deaths in the United States per year and prevalence rates are increasing. Every day 153 people die in the United States and over 2.8 million visit their local emergency room per year due to TBI (1).
The incidence of TBI in adolescents is increasing in relation to sports and recreational activities. Highest levels of TBI in adolescents are seen in football and soccer players with a relatively equal distribution between boys and girls (1). The effects of early integration into sports continues through both college and professional athletes increasing the risk for mild-moderate injuries in athletes. Treatment of these early signs and symptoms can help prevent permanent mood disorders, cognition, and patient’s lifestyle. Exercise can be used as a cost-effective treatment for combating the effects of depression following TBI (4).
Exercise prior to TBI shows a significant impact on mental and physical health. The research below utilized animal testing with various protocols to determine the effects of pre-conditioning on subjects with lab-induced TBI. This type of recent research has been highly influential confirming the effects of exercise before TBI.
The preconditioning phenomenon has been addressed in a study by Mota et al. in which brain inflammation and toxicity were evaluated in relation to TBI (9). Conditioning began with 90-day old mice that were familiarized with training equipment and concluded after 4 weeks. All animal testing was conducted using standards of care. The TBI was administered through pressure waves to exposed portions of the dura mater.
Mota et al. evaluated motor function with a neuroscore test which is a battery of motor tests in rats and evaluated brain function from normal to severely impaired. Brain samples were extracted in a random subset of the testing population and tested for blood brain barrier (BBB) degree of permeability. Aerobic training was shown to exert prophylactic effects by increasing the endogenous anti-inflammatories, reducing BBB breakdown as well as neuromotor impairment. The findings suggested physical training as a new therapeutic treatment to control acute inflammation that may lead to future cell damage with TBI.
Much like the previous study, Taylor et al. utilized mice and training protocols to evaluate motor function and impairment after administration of a TBI (2). However, unlike Mota et al., there was a randomized placement of subjects into four exercise groups. Subjects assigned to the exercise group were placed into cages containing exercise equipment that was absent in the cages of the other groups. The exercise group had 24hr access to running wheels and were observed for trends in exercise patterns found throughout the experiment. The subjects were kept and observed for the six weeks prior to testing, evaluating, and euthanasia. To produce a TBI a controlled cortical impact (CCI) was implemented. CCI was used with the mice because of its ability to produce similar symptoms of brain injuries in humans allowing for more direct comparison to human research. Sensorimotor function, mRNA, and protein analyses. It was found that exercise increased the expression of neuroprotective proteins and genes such as erythropoietin in the sensorimotor cortex. Improvements in sensorimotor function and spatial learning were observed.
Exercise conditioning prior to a TBI was similarly used in a study produced by Zhao et al. (10). The exercise protocol was comparable in length (4 weeks) to Mota et al. and had similarities to the procedures completed in the Taylor et. al. study including CCI. During administration of CCI all animals were monitored and kept on a heating pad to obtain normal core temperature at 38˚ C and resist changes in physiological processes. After recovery, the mice were evaluated using several tests. A beam walk test reflected the sensorimotor function and showed significant improvement in subjects that completed exercise prior to injury. Anterograde spatial learning and memory was evaluated using the Morris water maze test and substantial improvement in time, escape latency, and strategy was observed in the exercise group. Preconditioning had protective and anti-inflammatory effects on the brain in TBI.
Generally, based on the reviewed studies, the exercise duration before administration of a TBI should range from four to six weeks (2, 9). The exercise can be voluntary or regulated and completed in controlled environments. Placement of running wheels and cage conditions can affect the voluntary exercise performed by the subjects. Testing is completed to evaluate effectiveness of treatment including the evaluation of sensorimotor function and inflammatory response. Pre-conditioning to lab-induced TBI shows similar benefits with varying degree of difficulty, duration, and subject subgrouping (9).
Exercise after TBI affects different aspects of the patient’s health including depression and cardiorespiratory endurance (11). The following studies all explore the benefits of initiating and maintaining an exercise protocol after a TBI. Studies currently focus on individuals with high levels of anxiety and depression and long-term data is limited (11). The studies mentioned below share commonalities with intervention modalities, testing procedures, and result outcomes.
A ten-week protocol described by Wise et al. utilized both in person and at home training for the study participants (11). Following the intervention, there was a six month exercise period in which subjects were encouraged to maintain the exercise regimens and self-reporting. Measurements were taken such as the Back Depression Inventory (BDI) and the Medical Outcomes Study 12-item Short-form Health Survey (SF-12) at the end of the supervised exercise portion and again six months later. Depression was evaluated using the BDI a self-reporting inventory that measures the presence of symptoms and characteristics of depression. The subject’s depression was categorized by the severity, intensity, and level of depression observed. The SF-12 evaluated items such as vitality, mental health, and social functioning. Mental and physical evaluations were performed at baseline, after ten weeks, and at six months following exercise intervention. The data supported the findings of completing a minimum of 90 minutes of exercise per week and its relationship to improvement in depression and quality of life.
Residential rehabilitation was used in a protocol written by Mossberg et al. 6 weeks to 25 months after a motor vehicle accident. Testing and evaluation was completed within a seven-day window (12). Subjects were diagnosed using the Glasgow Coma Scale and a median score of six was reported at the start of the protocol. A modified Balke-Ware protocol was used in which the speed of the treadmill remained constant (3.3 mph) while the incline was increased every minute by 1% and consistent monitoring was present. Each subject was expected to repeat the exercise test four to eight days after preliminary testing. Controls for the study included time of day, equipment used, and staff administering the test. Mossberg et al. also evaluated cardiorespiratory fitness in each subject with TBI. The data suggested that patients with a TBI can produce considerable fitness improvements such as VO2 at submaximal levels of fitness in rehabilitation exercise programs. Mossberg et al. had issues with compliance between testing days and had skewed data that was discarded as result.
In a randomized pilot study by Blake and Batson, Tai Chi Qigong was completed to examine its effects in a supportive community center for those with TBI (13). Qigong incorporates both aerobic and dynamic styles into its programming. The exercise regimen was taught in detail to subjects and practiced only during assigned sessions. Along with a one-hour session per week the participants were also involved with social activities over an eight week period. The study used self-administered health and social surveys unlike the other studies previously mentioned. Psychological health was evaluated by comparing the subject’s baseline data to their final questioner responses. Improvements in depression and self-esteem were reported however inconclusive due to limitations in sample size.
Thornton et al. produced an experiment that integrated balance training and virtual reality games to evaluate its effects in subjects that had a TBI 6 months prior to testing (14). The subject group’s baseline data was taken from their Berg Balance Scale Scores. One exercise group used traditional activities such as walking or running and utilized gym/household equipment for exercising. The other group used virtual reality activities that required full body movement and offered interactive scenarios that may not otherwise be available. The exercise protocol was completed three times a week for 6 weeks. Each exercise session duration was 50 minutes and took place at a rehabilitation center. Thornton et al. measured the participant’s activities of daily living using the Activity-specific Balance Confidence Scale (ABC), lower extremity function scale (LEFS) to evaluate disorders of musculoskeletal system, and functional questioners that were later evaluated. Significant improvements were seen in both the ABC and LEFS. Increased community involvement and general physical activity was also reported among the subjects.
Unlike the studies mentioned above a study by Shen. et al. utilized rats in a treadmill exercise to determine the effects of different intensities following CCI (15). A total of 30 rats were divided into high and low intensity exercise groups and housed with food and water. A brief anesthesia period was induced and CCI was performed on the subjects. The rats were previously trained to run on motorized treadmills. The treadmills were set at a speed of 6-9 miles per minute for 3 consecutive days prior to surgery. The exercise group intervention began 24 hours after the administration of the TBI. The speed and inclination of both groups increased gradually and reported in detail. The sedentary group was placed on the motorized treadmills are zero inclination as they were stationary and did not run. Subjects were tested for neurological deficits every day for 25 days following the CCI. Cognitive function was assessed using the Morris Water Maze Task which indicated spatial learning and memory function.
In a study by Silva et al. a similar protocol described the effects of exercise after fluid percussion injury (FPI) using adult male Wistar rats and treadmill training (16). FPI was administered by the attachment of the devise to the previously implanted injury cannula 12 hours after the last training session. The training protocol was completed blindly and modifications were kept to a minimum. After one week animals were placed on treadmills 5 days a week for three weeks. The fourth week required the subjects have 4 training sessions.
The subjects were connected in a Faraday’s cage to block electromagnetic fields. Seizure monitoring and other abnormalities was completed with a digital encephalographer which recorded an EEG. Biochemical tissue analysis was completed of the injured tissue after decapitation exposure of the brain. A decrease in Na+/K+-ATPase activity after the 5 week exercise protocol had effects on tissue excitability and was linked to post-traumatic epilepsy. Increased latency for convulsive episodes was experienced with the treadmill training and duration was attenuated.
Exercise regimens that are prescribed after a TBI have verifying effects on the individual including attenuated duration of seizures, increased cognitive function, and improvements in activites of daily living (15, 16, 17). Benefits of physical activity and its effects after TBI can be achieved using a variety of exercise modalities including traditional exercise, Qigong, and even virtual reality (11–14). There is agreement among the studies that future research in the field is necessary for further conclusions to be drawn.
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