Traumatic Brain Injury

Traumatic brain injury (TBI) is a major cause of death and disability. In the United States, TBIs affect 1.7 million people annually and are responsible for about 40% of all deaths from acute injuries (CDC, 2017). Annually, 200,000 victims need hospitalization, and 1.74 million people need at least one day off of work after a TBI (Dawodu, 2015). It is estimated that 3.2 million Americans are living with a disability from TBI. TBI is the leading cause of long-term disability in children and young adults worldwide.

TBI is a sudden trauma that damages the brain. Damage is either focal, in one area, or diffuse. When the head hits an object and the skull does not break, the injury is considered a closed head injury. When the skull breaks and the object penetrates brain tissue, the injury is considered a penetrating injury. About 75% of TBIs are mild. Repeated TBIs over a while can lead to multiple problems such as cumulative cognitive or neurological deterioration.

Falls are the leading cause of TBI, accounting for 35.2 percent of TBIs in the United States (CDC, 2017).  Falls lead to 61 percent of all TBIs in those over 65. They also account for about 50 percent of TBIs in children under 15.

Motor vehicle accidents are the second leading cause of TBI, accounting for 17.3 percent of all TBIs. Due to the violent nature of many motor vehicle accidents result in the highest percentage of deaths from TBI (CDC, 2017). 

Running into a stationary object or getting struck in the head is another common cause of TBI, which accounts for 16.5% of TBIs. (CDC, 2017).  Other causes of TBI include violence, assaults, firearms, and blasts (particularly among military personnel).

Sports-related injuries account for many TBIs every year. TBIs commonly occur in football, boxing, ice hockey, soccer, and rugby.

Chun et al. found that the overall concussion rate was highest in girls' judo, followed by football. The concussion rate for boys was higher than that for girls. In four of the five sports in which girls and boys participated, girls had a higher concussion injury rate.

Approximately 20% of professional boxers have a chronic traumatic brain injury with cognitive, motor, or behavioral disturbances. When it becomes severe, it is classified as dementia pugilistica. Pathologically, chronic traumatic brain injury is like Alzheimer's disease. Factors that increase the risk of dementia pugilistica include the number of professional bouts, the total number of head blows, and the number of knockouts. Other sports that have repeated head blows may lead to dementia pugilistica.

Cerebral perfusion pressure is the blood pressure minus the intracranial pressure (ICP) and should be above 70 mm HG in adults and 60 mm Hg in children. The pressure on the brain is critical. If the pressure gets too low, below 12ml/mg/min, irreversible brain damage may occur (Tolias, 2015). Autoregulation helps maintain adequate perfusion to the brain. Autoregulation does not work when a traumatic event and cerebral blood flow are decreased. Maintaining adequate blood pressure during a TBI is critical.

Inside the skull is a closed space, and the pressure in the cavity is constant. On average, the adult has an intracranial volume of about 1500 mL. The brain makes up about 85-90% of the volume. The intravascular cerebral blood volume consumes about 10% of the volume, and cerebrospinal fluid (CFS) accounts for less than three percent of the volume (Ainsworth, 2015). Any alteration in one of the components will result in an alteration of the other. When ICP increases, the brain may herniate; this is when part of the brain is pushed through a natural opening.

The CSF acts as a shock absorber for compressive forces. Certain brain areas are more prone to trauma due to rough spots in the skull, including the frontal lobe floor and the top and floor of the temporal lobes.

A stationary head is most likely damaged at the point of impact. When the head is in motion, the injury most commonly occurs on the opposite side of the trauma because the brain lags slightly behind the body falling, and the brain bounces off the other side of the skull (Ainsworth, 2015).

TBI can be primary or secondary. Primary injures occur at the moment of the injury due to mechanical forces. They can occur when the object strikes the head. The brain hits the inside of the skull, or acceleration-deceleration (Ainsworth, 2015).

Secondary injury happens sometime after the trauma and often leads to long-term problems. Secondary injury often compounds the primary injury. Swelling, bleeding, and increased ICP may result in decreased blood flow to the brain. Reduced blood flow leads to cell death. Secondary injury may be noted clinically by low blood pressure, hyperthermia, hypoxia, intracranial hemorrhage, or malignant brain edema (Dawodu, 2015).

A contusion is bruising of the brain and occurs in two ways:

• Direct trauma
• Acceleration/deceleration injury

Direct trauma causes injury at the site of impact, termed a coup contusion. Acceleration/deceleration causes injury at a site opposite the impact site, termed a contrecoup contusion. Contrecoup typically results in a bruised brain when the brain bounces off the skull and often occurs in shaken baby syndrome or a car accident. It can cause damage to individual nerve cells.

Skull fractures occur when there is a break in the integrity of the skull bone. When the skull pushes into the brain, it is called a dressed skull fracture. When an object penetrates the skull, a penetrating skull fracture occurs.

An intracranial hematoma is bleeding into or around the brain and is a common injury seen in TBI. A hematoma is TBI's most common cause of death (Ainsworth, 2015). A hematoma should be considered when there is neurological deterioration such as worsening headache, confusion, lethargy, focal neurological sign, or loss of consciousness.

Multiple intracranial hematomas can occur, including a subdural hematoma, epidural hematoma, and intracerebral hematoma. A subdural hematoma (SDH) is bleeding into the subdural space. SDH can act as a mass lesion and lead to death or disability.

An epidural hematoma is bleeding between the skull and the dura and is often caused by a break in the temporal bone and rupture of the middle meningeal artery. This type of hematoma can grow rapidly because the bleeding comes from a high-pressure artery and can quickly elevate the pressure in the brain. An intracerebral hematoma is bleeding into the brain.

Diffuse axonal injury is an important feature of TBIs. It results from damage on a microscopic level and, therefore, is not seen in imaging studies. It is believed that the rapid stretching of the axon damages the neuron and reduces its function.

Astrocytes form the blood-brain barrier. It maintains ion concentrations, regulates the flow of elements into the brain, and protects the brain from foreign elements circulating in the bloodstream. TBI compromises the protection of the blood-brain barrier, leading to damage to the brain parenchyma (Younus et al., 2018).

Assessment of the Glasgow Coma Scale (GCS) is a way to measure the impact on brain function. This test is rated from one to fifteen. It assesses eye-opening verbal responses and motor responses. GCS describes the severity of the TBI.

The scores given to each section are added up, and based on the total score, the severity of the head trauma is determined.

Symptom severity is related to the severity of the injury. Some signs and symptoms occur immediately. Other signs and symptoms occur days or even weeks after the injury.

Mild traumatic brain injury is defined as a GSC between 13 to 15. A GSC in that range 30 minutes after the injury is typically a benign problem, but it must be carefully considered because there is potential for significant long-term and short-term complications. Mild TBIs often have subtle symptoms such as the patient acting a little strange, blurred vision, tinnitus, confusion, dizziness, fatigue, mood change, sleep disturbance, and inability to concentrate. Minor head injuries usually do not progress, but about 3% of mild head injuries advance to more severe injuries (Ainsworth, 2015).

A trauma-induced structural injury or physiological disruption of brain function due to an external force may result in a moderate to severe TBI. Symptoms are the new onset or worsening of at least one of the following clinical signs immediately following the event:

1. Loss of or a decreased level of consciousness
2. Loss of memory of events immediately before or after the injury (posttraumatic amnesia)
3. Alteration in mental state at the time of the injury (confusion, disorientation, slowed thinking, and alteration of consciousness/mental state)
4. Neurological deficits (weakness, loss of balance, changes in vision, praxis, paresis/plegia, sensory loss, and aphasia) that may or may not be transient
5. Intracranial lesion (Younus et al., 2018)

Severe brain injury results in loss of consciousness for >6 h and a Glasgow Coma Scale (GCS) of 3–8 (Younus et al., 2018).

Children with head injuries may present with persistent crying, irritability, refusal to eat, abnormal sleeping patterns, tiredness, listlessness, inconsolable, changed behavior or playing patterns, reduced performance in school, regression of development, emesis, or incoordination.

Some symptoms persist long into the recovery period. Six months after mild TBI, some patients will report weakness, fatigue, memory problems, dizziness, and headache. Eighty-three percent of patients with mild TBI report at least one symptom after six months (Ainsworth, 2015).

When evaluating a head injury, it is important to evaluate for other injuries such as neck injury, spinal cord injury, facial fracture, eye injury, or skull fracture.

Posttraumatic seizures (PTS), generalized or partial, are a common complication of head trauma. Seizures are more common with moderate to severe TBIs (brain contusions, hematomas, or penetrating head injuries) than mild TBIs.

Seizures can be early (occurring in <7 days of injury) or late (occurring after seven days of injury). The risk factors for early PTS include:

• GCS score of ≤10
• Immediate seizures
• Posttraumatic amnesia lasting longer than 30 min
• Linear or depressed skull fracture
• Penetrating head injury
• Subdural, epidural, or intracerebral hematoma
• Cortical contusion
• Chronic alcoholism (Younus et al., 2018)

Those with early seizures are at higher risk of developing posttraumatic epilepsy (PTE). PTE is defined as recurrent seizures >7 days following an injury. Reducing PTS should be a clinical goal to avoid PTE and decrease the associated morbidity and mortality rate. In patients with severe TBI, the rate of clinical PTS may be as high as 12%, whereas that of subclinical seizures detected on electroencephalography may be as high as 20% to 25% (Younus et al., 2018).

The Brain Trauma Foundation recommended using anticonvulsants such as phenytoin and valproate to prevent early but not late seizures because of the side effects associated with the chronic use of these medications. Phenobarbital and carbamazepine are avoided because of adverse effects (Younus et al., 2018).

The incidence of abnormal EEGs and seizure activity is the same for levetiracetam and phenytoin for the initial seven days posttrauma. However, the incidence of seizures is lower for patients who use levetiracetam on follow-up. So, levetiracetam is a better option for PTS prophylaxis. Levetiracetam is well tolerated and has fewer side effects (Younus et al., 2018).

Patients using selective serotonin reuptake inhibitors (SSRI) at TBI have a higher risk of epilepsy after TBI. The association may be causal but may also be due to other confounding factors. Underlying disease (depression or anxiety) can be the cause. Behaviors associated with depression, like poor adherence to anti-seizure medications, increased alcohol use, and poorer sleep/self-care, may also be causal (Taiwo et al., 2019).

Brain injuries can lead to coagulopathy (a disorder of blood coagulation) as they lead to a systemic release of tissue factors and brain phospholipids into the circulation, leading to abnormal intravascular coagulation and consumptive coagulopathy (Epstein et al., 2014). Those with coagulopathy after a TBI have a worse prognosis.

The ventricles can dilate when CSF builds up in the brain, leading to hydrocephalus and an increased ICP. It often occurs soon after an injury but can occur after an extended time. Increased ICP may lead to cerebral edema, ischemia, hypoxia, and brain herniation.

Skull fractures are another complication. When the matter between the dura and the arachnoid membrane tears, CSF can leak out in a condition called subdural hygroma. Fluid can leak out of the nose, ears, and mouth. Any tear in the brain's protective matter increases the risk that bacteria can enter these spaces, leading to meningitis.

Hemorrhagic stroke can result from an arterial bleed in the brain. Ischemic stroke can occur when a clot forms in the brain's vessels. Blood clots can occur in the sinuses next to the brain. These clots usually occur within a few days of the injury. They present with seizures, headache, emesis, hemiparesis, and a creased level of consciousness.

The cranial nerves can also be injured when there is a TBI. However, it is more common when there is a fracture near the base of the skull. The most commonly injured cranial nerve is the facial nerve (CN VII), resulting in paralysis of the face. Cranial nerve injury may lead to an impaired sense of smell or taste. If the patients lose their sense of smell, it will likely be permanent if it lasts one year after the injury (Xydakis et al., 2015). Double vision may occur, and cranial nerve IV will likely be affected if it occurs. Damage to the trigeminal nerve (CN V) leads to facial pain.

The post-concussion syndrome can occur days or even months after a TBI and can occur with any degree of head injury from mild to severe. A post-concussion syndrome is characterized by dizziness, vertigo, headache, reduced concentration, apathy, depression, sleep disturbance, confusion, irritability, and anxiety.

Amnesia can also occur after a head injury. Anterograde amnesia is impaired memory of events after the injury, whereas retrograde amnesia is memory deficits of events before the injury.

Brain dysfunction can take many forms after a TBI. The following are problems that may present after a TBI:

• Impaired concentration and attention
• Impaired executive function
• Reduced hand-eye coordination
• Sensory deficits: vision, smelling, touching, hearing
• Tinnitus
• Vertigo
• Aphasia (inability or reduced ability to communicate, which can include impairments in expression or understanding of written or verbal language)
• Dysarthria (cannot speak the proper words due to dysfunction of the muscles used to speak)
• Reduced ability to carry out complex tasks
• Behavior changes or onset of mental illness (depression/anxiety)
• Social inappropriateness or aggression

Most of the recovery from a TBI occurs in the first six months and can be more gradual after six months.

Some problems may occur years after the head injury (CDC, 2017). Alzheimer's disease is the most common type of dementia and is linked to a prior history of head injury. Parkinson's disease can occur when there is a remote history of damage to the basal ganglia. As mentioned above, dementia pugilistica occurs in patients with a history of head trauma. Posttraumatic dementia is dementia that occurs after a single TBI that results in a coma.

Agitation is commonly seen after a head injury. Other causes of agitation seen after a head injury may include pain, depression, infection, side effects of medications, sleep deprivation, or electrolyte imbalance.

A myriad of other problems may occur after a TBI, including:

• Deep vein thrombosis
• Spasticity
• Rigidity
• Gastrointestinal and genitourinary problems
• Pneumonia
• Decubiti
• Organ failure
• Chronic Traumatic Encephalopathy

Athletes who have experienced head injuries over the years may experience chronic traumatic encephalopathy (CTE), a neurodegenerative disease likely caused by repetitive brain trauma. It may result in memory problems, executive dysfunction, poor impulse control, depression, apathy, suicide, aggression, violence, substance abuse, and an increase in high-risk behaviors (e.g., increased food intake, risky sexual behavior, and gambling). Motor disturbances, such as rigidity with a slow shuffling gait, may be present in CTE. It may eventually lead to dementia.

CTE is thought to be secondary to hyperphosphorylated tau and TDP-43 in the brain. Once thought to be only a problem in boxers, it is now prevalent in football players.

CTE is likely caused by repetitive trauma to the brain (both concussions and subconcussive trauma). CTE is difficult to diagnose because it overlaps with multiple other syndromes. CTE may start during the post-concussive syndrome. As the disease progresses, it presents similarly to other dementing illnesses such as frontotemporal dementia and Alzheimer's.

Different diagnostic tests are available to help determine the severity of the injury. Imaging helps determine if there is a fracture and assists in the determination of prognosis.

Computed tomography (CT) scans are the best test for moderate to severe head trauma. CT scans identify bone fractures, hemorrhages, contusions, cerebral edema, hematoma, and tumors. Neuronal damage can be underestimated with a CT. Most mild TBIs have no evident change in neuroimaging, but a mild TBI may be associated with a cortical contusion or an intracranial hemorrhage.

Magnetic resonance imaging (MRI) is another commonly used test in the diagnostic workup of TBI. It is not the best initial test as it is more time-consuming and readily available. The MRI is a more accurate test for detecting contusions and diffuse axonal injury (Morales, 2015).

In mild TBI cases, consideration of a head CT is in order if:

• Glasgow Coma Scale (GCS) score less than 15 two hours after injury
• Vomiting
• Any loss of consciousness
• The individual is 60-65 years old or older
• Scalp lacerations to the bone of greater than 5 cm
• Significant maxillofacial injuries
• Persistent headache
• Amnesia before the impact of 30 minutes or more
• Dangerous mechanism of injury (e.g., pedestrian struck by a motor vehicle, occupant ejected from a motor vehicle, fall from ≥3 feet or ≥five stairs)
• Suspected skull fracture (e.g., CSF leak [clear fluid from the nose or out of ears], raccoon eyes [bruising around eyes], Battle's sign [bruising behind ears], or hemotympanum [blood behind ear drum])

Individuals requiring a CT scan include:

• Seizures
• Neurological deficits
• Taking oral anticoagulants
• Those with bleeding diathesis

Mild TBIs often present at their primary care doctor's office, urgent care clinic, or walk-in patient at an emergency department. More severe cases may present to the emergency department after transport by emergency medical personnel.

Those with severe injuries need to be medically stabilized as a primary priority. Pre-hospital care needs to ensure that the patient is triaged appropriately, stabilized, and assessed for any life-threatening complications, such as increased intracranial pressure and cerebral herniation.

The ABCs are of primary importance in any severe injury. Assuring an airway is present to maintain adequate oxygen flow to the brain and the rest of the body. Intubation is often done on those with moderate or severe head injuries. Blood pressure control is necessary, as is controlling any other injuries that may accompany a head injury. Often, head injury cases are multi-trauma cases, including spinal cord injury, and patients need to be managed systemically as other injuries may be more immediately life-threatening.

Patients discharged with a mild head injury should be awakened every 2 hours and assessed neurologically. Patients and their caregivers should return to the hospital if there is any seizure, confusion, severe/worsening headache, watery discharge from the ear or nose, or persistent nausea and vomiting (Ainsworth, 2015).

Certain indications necessitate consideration for admission (Tolias, 2015). These include:

• An attempted suicide
• No responsible adult supervision
• Epilepsy
• Uncertain diagnosis
• Drug or alcohol abuse
• Co-morbid neurological disease
• Coagulation disorder or someone on warfarin

A CT scan helps determine the degree of intracranial injury and helps predict the outcome. In those with normal CT scans, hospitalization may be avoided. Ct scans help detect skull fracture, hemorrhage, midline shift, mass effect, and herniation. A repeat exam should occur in 4-8 hours for those with coagulopathies or intracranial hemorrhage. Abnormal findings on the CT scan, prolonged unconsciousness, persistent mental changes, or an abnormal neurological exam necessitate referral to a neurosurgeon. Patients with normal CT scans after head injury will clinically improve within hours. Those who fail to improve should have a repeat CT scan (Rangel-Castilla, 2016).

Neurological checks should be done frequently. The patient should consume nothing orally until they are alert. Intravenous fluids will help prevent dehydration and help maintain pressure. Comfort measures should ensue with the use of mild analgesics and an antiemetic. Do not use phenothiazines (e.g., Compazine, Thorazine) as this increases the risk of seizure (Younus et al., 2018).

A Glasgow Coma Score under 8 indicates severe injury. A severe injury requires a CT scan, admission to the hospital, and a neurosurgical referral. ICP should be lowered using a variety of measures, including:

• Maintaining a systolic blood pressure above 90 mm Hg
• Keeping the head of the bed elevated to 30-45 degrees while keeping the neck straight
• Mild sedation and pain control
• Ventilate to normocapnia
• Mannitol intravenously, if agreed upon with the neurosurgical team

Among those with moderate to severe head injury, fewer than 10% have an initial surgical lesion (Ainsworth, 2015). Indications for surgery include an open skull fracture, a depressed skull fracture of more than 1 cm, extra-axial hematoma with a midline shift of greater than 0.5 cm, intra-axial hematoma with a volume greater than 30 ml, or a temporal or cerebellar hematoma more than three cm (Ainsworth, 2015).

Methylprednisolone increases mortality rates in acute traumatic brain injury patients and should not be used. Dexamethasone does not improve ICP levels and may worsen outcomes in patients with an ICP greater than 20mmHg.Triamcinolone may improve outcomes in patients with a focal lesion and a GCS less than 8. Progesterone can improve neurologic outcomes for up to 6 months in acute severe traumatic brain injury patients (Christensen et al., 2019).

An athlete with a diagnosed sports-related concussion should not be allowed to return to play on the day of the injury (McCrory et al., 2016). If an athlete returns to play too quickly, there is a risk of recurrent concussion and cumulative brain injury. With each concussion, there is an increased risk of future concussions.

It is important to ensure that concussion symptoms are fully resolved before the athlete can return to exercise. Some student-athletes may require reduced schoolwork while recovering from a concussion. Student-athletes who are experiencing symptoms from their concussion need to rest the brain from cognitive activity not to worsen or lead to a reemergence in the symptoms.

A stepwise progression is utilized to return the athlete to play gradually. There should be 24-48 hours of physical and cognitive rest before the return to sport progression begins. Each step should take no longer than 24 hours, giving the athlete, at minimum, a one-week rehabilitation period. The athlete can proceed to the next progression if they remain asymptomatic at the current level. If any post-concussion symptoms return during rehabilitation, the athlete should return to the previous step. They can try to progress again after 24 hours of rest and being symptom-free. The athlete whose symptoms persist for more than 10-14 days in adults or more than one month in children should be seen by an expert in the management of concussions.

A 14-year-old boy is playing soccer, and after heading the ball in for a goal, he comes off the field and asks the coach, "Who won the game?" Since it is only the first half, the coach realizes that the player is confused. The player is taken out of the game, and one of the parents, a nurse, comes over to evaluate the athlete. The nurse determines that the athlete has a GCS score of 15, but it is unclear if the game's score (this suggests retrograde amnesia). The nurse tells the coach that the boy should not reenter the game.

After calling his primary doctor, the boy takes the next day off school and has an appointment with his primary care doctor. He complains of a slight headache at the doctor's office and feels a little dizzy. The following day he reports no symptoms; therefore, he goes to school and participates in light running at practice. He feels well after running. He goes back to practice the next day and does some light drills with the team. Since he continues to have no symptoms, he can advance his practice and includes some more intense drills the following day. In the next practice, he fully participates and believes he will be able to participate in the game scheduled for the next day. However, he wakes up the next day with a headache. He sits out the game but does participate in warm-up drills with the team. He can participate in practice the following day without limitations and post-concussion symptoms. He plays without incident the following week.

This scenario is the typical course of a mild traumatic brain injury or concussion. After being successfully identified as having a possible concussion, the patient came off the field. The patient progressed through graded exercise challenges resulting in the resumption of play when symptoms were resolved. The athlete could return to play while reducing his risk for complications because he followed the gradual return to play protocol. The patient will need to be watched in the future for recurrent head injuries.

This patient was managed well. The coach immediately got him out of the game to reduce the risk of further injury. The primary care team followed the patient closely to assure that the patient was symptom-free before resuming activities that may potentially lead to further injury to the brain.

Observation is recommended for at least 24 hours after a concussion because of an intracranial complication risk. Admitting to the hospital may be considered for those with a GCS of less than 15; any seizure activity; CT scan evidence of cerebral edema or intracranial bleeding; those on an anticoagulation medication; or those with a bleeding diathesis. Those with no one to monitor them at home should be admitted to the hospital for observation.

If an athlete is monitored at home, it is important to teach the observer that the athlete should be awakened from sleep every two hours the first night, and if the athlete is unable to be wakened, immediate help should be attained. The athlete should not perform any strenuous activity for 24 hours. Other signs that should prompt the athlete to attain immediate medical help include confusion, somnolence, vision difficulties, urinary or bowel incontinence, severe or worsening headaches, vomiting, stiff neck, fever, seizure, restlessness, and unsteadiness, or weakness/numbness of any body part. These findings suggest a potential intracranial bleed/cerebral edema secondary to a contusion. These signs warrant an evaluation, including a head CT.

Second impact syndrome is a rare complication of a mild head injury. This syndrome is diffuse cerebral swelling after a second concussion during the time the athlete is still symptomatic from the first. If the athlete returns to play too soon and develops another injury, when not fully recovered from the first, swelling of the brain, herniation or death may occur. It is not a common condition, but athletes may die within a few minutes if it does occur.

When evaluating a patient with a TBI, the priority is always airway, breathing, and circulation. It is also important to rule out any spinal cord/cervical spine injury and if suspected immobilization and radiography should occur. Paresthesia, reduced consciousness, posterior midline tenderness/pain, or extremity weakness may suggest spinal cord/cervical spine injury.

Multiple steps should be implemented in the prevention of TBI. These include:

• Wearing a seatbelt and properly securing children in the car
• Drive at or below the speed limit
• Use helmets when riding motorized vehicles or bikes
• Use proper protective gear when playing sports
• Practice gun safety
• Fall prevention methods
• Eliminate tackling from school football for those under 16 to reduce concussions
• More education needs to be included in athletes, coaches, parents, school administrators, and health care providers regarding the assessment, prevention, and management of concussion

An 85-year-old female was admitted to the hospital following an unwitnessed fall at home in the early hours of the day. The client sustained a left humeral fracture and a left hip fracture. The client underwent a total hip replacement, and a sling was applied to her left arm two days ago. The Occupational Therapist arrives to initiate AROM to the elbow, wrist, and hand and begin lower body dressing training with adaptive equipment.

While gathering information regarding the client's home situation, prior level of function, and occupational profile, the client indicates that she does not recall the immediate events leading up to the fall (retrograde amnesia), nor does she believe that her family knows she is here in the hospital. Following ROM and strength assessment, the client begins complaining of a headache, stating, "I have had a headache since this morning. I think it is because of the lights" (photophobia). Wrapping up the OT evaluation, the OT advises the nurse of her findings related to retrograde amnesia and complaints of a headache and sensitivity to light.

This information is then relayed to the MD, who suspects a possible TBI and orders a CT, which proves negative. However, the doctor suspects the client may have a mild concussion and requests 2-hour neuro-checks and that therapy be continued.

The therapist provided ROM exercises to the client in bed with only the over-bed backlight light on and short demonstrations to the client regarding the use of adaptive equipment, beginning with slipper socks and advancing to pants and panties by day 5 of admission. By day 5, the client is no longer complaining of a headache and can now demonstrate the ability to complete lower body dressing with adaptive equipment.

This case is the typical course of a client initially seen by therapy for orthopedic concerns. She was determined later to have sustained a mild TBI due to a fall. The client was able to participate in therapy with modifications made to the environment to reduce stimulation and graded activities until symptoms resolved. The client will need to be monitored to ensure the resolution of symptoms.

Head injuries are common, costly, and at times devastating. Healthcare Professionals should know how to assess, educate, and monitor patients with TBI. With recent information about mild traumatic brain injury in sports, it is becoming more important for all healthcare providers to fully understand TBI, its recognition, management, and prevention.

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