Abstract
Pressurized tank therapy has existed for hundreds of years, gaining success around the turn of the 20th century. Today, hyperbaric oxygen therapy, or HBOT, is used primarily for decompression sickness. However, it is occasionally applied as a second-line treatment for many medical conditions involving cell death and ischemia, such as stroke, infection, and bodily trauma. Within the past several years, scientists discovered the potential for HBOT in the arena of traumatic brain injury (TBI). The therapy is benign, noninvasive, and potentially very beneficial. In preliminary studies, HBOT has demonstrated effectiveness in reducing neuropsychiatric symptoms associated with TBI as well as significantly decreasing trauma to the brain as seen on SPECT scan. There is an increasing need for new therapies to treat TBI, especially in the area of professional contact sports and the military. The potential for HBOT as a first-line treatment for TBI is significant, although more studies must take place to prove its continued efficacy.
Keywords
Apoptosis, Atmosphere (ata), Depression, Glasgow Coma scale (GCS), Hyperbaric, Hyperbaric oxygen therapy (HBOT), Injury, Ischemia, Neuropsychiatric, Oxygen, Pressurized, Regional cerebral blood flow (rCBF), SPECT, Supersaturation, Therapy, Trauma, Traumatic brain injury (TBI)
Introduction
The human body breathes in and out an average of 10–16 times per minute. The air we breathe contains 21% oxygen, 78% nitrogen, and 1% carbon dioxide and other gases. For an average adult body, the volume of each breath is between 400 and 600 mL. This equals roughly 6–8 L of air per minute. Taking 21% of 6 L equals about 1.3 L of oxygen every sixty seconds. The standard pressure of that air is 1 atm equivalent, or 1 ata, which is equal to roughly 14.5 psi, or 760.00 mm Hg on a barometer. The density of air at sea level under standard atmospheric conditions is roughly 1.2 kg/m 3 . At this pressure and density, breathing 21% oxygen provides the average healthy human body with enough oxygen molecules to support normal cellular functions. In other words, our bodies function well when we are breathing in 400–600 mL of 21% oxygen at a pressure of 14.5 psi and a density of 1.2 kg/m 3 .
Under a variety of medical situations, supplemental oxygen is used as an adjunct to general atmospheric oxygen. This can occur in both acute and chronic situations where the body is unable to maintain normal cellular function by breathing air alone. Whether in an emergency room, on an operating table, or even at home, people use supplemental oxygen therapy in a variety of situations to assist the distressed human body. However, this is all done at a standard atmospheric pressure and density. What happens when that supplemental oxygen is delivered at a higher pressure? What effects would this have on the body? This is precisely what scientists have been exploring for many years with hyperbaric oxygen therapy, or HBOT. Hyperbaric oxygen tanks are enclosed capsules in which patients lie flat and receive 100% oxygen at anywhere between 1 and 3 ata, or one to three times normal atmospheric pressure. The purpose of this tank is to provide the body with an ultrahigh concentration of supersaturating oxygen that would be unavailable using standard supplemental oxygen equipment. HBOT is currently used for a variety of ailments including decompression sickness, cyanide poisoning, and necrotizing infections ( ). Only within the past decade has HBOT gained a reputation as being a possible treatment for trauma to the brain. This chapter will explore the use of HBOT for traumatic brain injury (TBI), as a review of what is already known and what additional information we must gather in recommending its standard use of therapy.
A Brief History of HBOT
At 100 ft beneath the surface, the pressure surrounding a scuba diver is about 43 pounds per square inch. With a standard sea level pressure of 14.7 psi, the pressure at that depth is equal to roughly 3 atm of pressure. While being submerged at 100 ft may not pose any inherent danger to the human body, a rapid fall in pressure could be potentially life-threatening. Inert gases, most notably nitrogen, exist in physical solution in the body at high pressure. A sudden decrease in pressure causes the gas molecules to come out of solution and form gas bubbles in the blood stream and other parts of the body. This is exactly what happens when divers surface too quickly and do not allow their bodies to adjust for these dramatic changes in pressure. Professionally called nitrogen sickness, or decompression sickness, popular culture refers to it as “the bends.” The bends can be a potentially fatal condition depending on where the gas bubbles form in the body and must be treated immediately. The signs of decompression sickness include a wide array of neurological, cutaneous, musculoskeletal, audiovestibular, and pulmonic symptoms such as fatigue, loss of balance, seizures, confusion, itching, and joint pain. HBOT is the most effective means of dealing with the bends and requires placing the body in an environment that recreates the condition in which inert gases exist in solution. The pressure is then slowly lowered in a way to simulate a slow return to surface that prevents the gas bubbles from forming.
The hyperbaric tank has existed for close to 350 years. Though attempts to conjure its design were previously attempted with no success, a British physician named Nathaniel Henshaw achieved the first documented closed “hyperbaric” environment in the 17th century. Stemming from his work in 1662, Dr. Henshaw reportedly filled a small capsule called a domicilium with highly compressed air to create a hyperbaric environment. Henshaw based his work off the principles of the Irish physicist and chemist Robert Boyle, who famously identified the inverse relationship between pressure and volume of air in a closed space. Several 100 years of medical experimentation and development passed before the technology was adopted into mainstream medicine. By the 1870s, hyperbaric tank air therapy was commonly used to treat a variety of ailments with various successes. Due to concerns of oxygen toxicity and limited knowledge of treating such ailments, the original hyperbaric tanks used compressed air instead of oxygen. It was not until 1917 that two German brothers Bernhard and Heinrich Dräger began applying pure oxygen to the tanks, resulting in the first successful treatment for decompression sickness caused by diving accidents ( ).
Hyperbaric therapy did not make its way to the United States until 1861, when neurologist James Leonard Corning saw its potential as a unique therapeutic option. Corning was interested in the technique after witnessing severe decompression sickness among site workers in building the Hudson tunnel. He employed the method to treat their collection of symptoms, which was essentially decompression sickness. In 1921, Kansas City-based physician Orval Cunningham built the first hyperbaric tank in the United States with pure oxygen, in treating patients with the flu. Cunningham thought that because there appeared to be a greater incidence of the flu in states with higher altitudes, he could potentially treat the illness with increased pressure. Stunned by his success, Cunningham went on to build the largest known hyperbaric tank in Cleveland, Ohio. The chamber, referred to as the Cunningham Sanitarium, was five stories tall, and contained twelve beds per story. It was considered the “first attempt in history to house people in such a unique structure” ( ). Due to numerous failures in treating infectious diseases, the chamber was dismantled in 1937.
The use of hyperbaric therapy was widely discontinued for nondecompression-related conditions until 1956, when Dutch cardiac surgeon Ite Boerema used the device to aid in cardiopulmonary surgery. In 1961, Boerema’s colleague, Willem Brummelkamp, reported that infections caused by anaerobic bacteria could not survive in a hyperbaric environment, as was postulated by Cunningham and that hyperbaric therapy could provide adequate amounts of oxygen to kill the bacteria. In 1969, the US Navy reported using HBOT to treat patients 3 months following ischemic stroke ( ). When the neurocognitive tests showed significant improvement, the therapy gained interest as a possible option for treatment of acute stroke. Since its renewal into modern medicine, hyperbaric therapy has been used to treat a variety of conditions including carbon monoxide poisoning, wound healing, various types of bacterial infections, and trauma. Even today, some physicians use HBOT in treating medical conditions including gas gangrene, acute traumatic peripheral ischemia, necrotizing infections, osteoradionecrosis, acute peripheral artery insufficiency, and gas embolism. HBOT is unique in that it is the only nonhormonal therapy used for tissue repair and regeneration ( ), including such disorders as diabetic wounds, chronic refractory osteomyelitis, and actinomycosis. It is noninvasive which makes it very desirable for patients in their treatment of disease ( ).
What Is Traumatic Brain Injury?
Brief History
Perhaps the most notable and infamous incident in the history of traumatic brain injury, or TBI, is that of Phineas Gage. Born in 1823, Gage was a railroad construction worker who experienced severe trauma to the head while assisting in the construction of the Rutland and Burlington Railroad in Cavendish, Vermont. The accident occurred in 1848, when at the age of 25 an unexpected explosion sent an iron rod through Phineas’ head and cranium. The rod was three and half feet long, weighed 13 and a half pounds, and had a diameter of one and a fourth inches. The rod entered just under the left cheekbone and flew vertically through his left hemisphere out the top of his head. It landed roughly 30 yards behind him. Even with the substantial head injury, Gage most likely never lost consciousness, as he shortly thereafter walked himself to the office of the physician of Cavendish, Dr. John Martyn Harlow. Gage even explained to Harlow in great detail what had occurred ( ).
Dr. Harlow treated Phineas’ wounds and allowed him to return home 10 weeks after the accident. In 1849, Phineas felt strong enough to return to his work on the railroad. However, the contractor would not rehire Phineas, due to substantial changes in his personality and disposition. Before the accident, Phineas had been a balanced, hard-working, honest individual with a strong intellect and grounded personality. After the accident, Phineas Gage exhibited profanity, would break down in fitful rage, and paraded around like a clown. He became impatient, crude, and obstinate, resorting to immaturity and inappropriate childlike behaviors. These characteristics prevented him from holding any type of intellectual or professional job. Though little is known about the rest of his life, most historians believe that Phineas went on to work remedial jobs as a carriage driver and doorman. His behavior continued to exacerbate throughout his life, causing him to go from one job to another. In 1860, Gage began experiencing epileptic fits, ultimately killing himself that same year ( ).
The importance of Phineas Gage’s story allows us to understand not merely the physical injury that occurred at the time of the accident, but the psychological and personality changes that developed as a result of the trauma. The long-term effects of trauma can be much more hidden and show up slowly over time as a change in behavior and affect. A favorite in the world of neuroscience, Phineas Gage’s story is the seed that grew into modern day TBI and how to treat this complex increasing disorder throughout the world.
Traumatic Brain Injury
TBI is widely considered to be one of the most damaging and misunderstood conditions to the human body. In fact, many believe it to be the leading undiagnosed brain disorder in the United States ( ). Every year, roughly 2 million people suffer from a traumatic brain experience in the United States. More than 500,000 are hospitalized and 50,000 die due to the severity of the injury and lack of adequate treatment. The cost of hyperbaric therapy in the United States is ∼56 billion dollars per year ( ). People, who play contact sports such as football, engage in potentially dangerous hobbies like motorcycling, and members of the military are more likely to experience TBI. While 70–90% of TBI incidents are considered mild, roughly 25% of people do not recover and develop chronic symptoms such as postconcussive syndrome ( ).
Shortly after a TBI, victims can experience symptoms such as confusion, loss of memory, slurred speech, and even seizures ( ). Those living with TBI can struggle with its devastating effects for days, months, years, or potentially the rest of their lives ( ). The actual trauma occurs due to a sudden physical assault on the head that causes damage to the brain. The damage can be focal, confined to one area, or diffuse, involving multiple areas of the brain. The injury itself can be closed-head or penetrating. A closed-head injury occurs when the head suddenly and violently hits an object, but the object does not penetrate through tissue or the skull. A penetrating head injury occurs when an object pierces the skull and enters the brain, destroying tissue and brain matter ( ). While ischemia can also cause significant damage to the brain, it is not usually caused by blunt external force, and thus will not be examined in this chapter.
The Centers for Disease Control and Prevention estimates ( ) that there were 2.5 million cases of TBI in 2010; that same year, TBIs contributed to the deaths of more than 50,000 people; TBI-related emergency department visits increased by 70% from 2001 to 2010; and 249,000 children were treated for TBI that resulted from recreational or sporting activities in 2009. It is important to identify TBI as quickly as possible in part due to the “second-impact syndrome.” When a patient sustains a second head injury before fully recovering from the first, “It leads to an exaggerated response and carries a 50% mortality rate” ( ). While some drugs have shown neuroprotection in animals after a TBI, none have proven very useful in humans. In fact, the standard of care for TBI today consists of allowing the brain to rest and providing symptom relief, primarily for pain ( ). Improved treatment will come through understanding the physical changes in the brain that occur at the microscopic and molecular levels when the brain is subject to trauma. That understanding is only beginning to emerge ( ).
Symptoms of Traumatic Brain Injury
Acute Symptoms
Symptomatology of TBI can be extensive, encompassing a wide variety of both neurological and neuropsychiatric symptoms occurring from the moment of impact. While many symptoms occur shortly after the injury, most long-term effects do not show up until weeks or even months after the incident ( ). Acute and chronic symptoms alike can be mild, moderate, or severe, depending on the extent of damage to the brain ( ). While it is not uncommon to experience a loss of consciousness, many who experience TBI remain conscious during the event ( ). The most immediate symptoms are feeling dazed and not quite normal. Other more immediate symptoms include headache, confusion, lightheadedness, dizziness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue, or lethargy. Within a week, an individual may develop a change in sleep patterns, behavior or mood, and trouble with memory, concentration, attention, and thinking ( ).
A person with a moderate to severe TBI may also experience more significant symptoms, including intractable headache, repeated vomiting or nausea, convulsions or seizures, inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination, and/or increased confusion, restlessness, or agitation ( ). Small children with moderate to severe TBI may display the same symptoms in addition to persistent crying, inability to be consoled, and/or refusal to nurse or eat ( ).
Within days to weeks of the head injury, ∼40% of TBI patients develop a host of troubling symptoms collectively referred to as postconcussion syndrome (PCS) ( ). While this typically occurs after the loss of consciousness, a patient need not have had a loss of consciousness to develop PCS. Symptoms of PCS often include headache, dizziness, vertigo, memory problems, trouble concentrating, sleep problems, restlessness, irritability, apathy, depression, and anxiety and can last for weeks or even months. The syndrome is more prevalent in patients who have had previous psychiatric symptoms, such as depression or anxiety, before the injury. Treatment for PCS is often limited to alleviating the pain, inability to sleep, and psychiatric conditions. People with PCS often engage in psychotherapy and occupational therapy as well as a variety of different coping mechanisms ( ).
Another ailment that affects roughly 15–33% of individuals with severe TBI is called paroxysmal sympathetic hyperactivity (PSH), or cerebral storming. PSH takes place in the deep structures of the brain and causes a series of episodic dysfunctions in the nervous system. It can cause dramatic changes in blood pressure, heart rate, body temperature, and muscle tone. Because these symptoms are also present in a variety of other conditions, such as seizure disorders, neuroleptic malignant syndrome, and expanding cerebral lesions, it is often difficult to diagnose them as associated with TBI ( ).
Chronic Ailments
Long-term disabilities resulting from a TBI depend upon the location and severity of the injury, as well as the age and general health of the patient ( ). While almost any postinjury neurological abnormality can qualify as a symptom of TBI, common disabilities include problems with cognition, sensory processing, communication, and behavior or mental health (mood problems, personality changes, and aggression) ( ).
The most common cognitive impairment among severely head-injured patients is memory loss ( ). This is also referred to as posttraumatic amnesia (PTA), either anterograde or retrograde ( ). Anterograde PTA is impaired memory of events that occurred after TBI, while retrograde PTA is impaired memory before the incident ( ). Many patients with mild to moderate head injuries who experience cognitive deficits become easily confused or distracted and have problems with concentration and attention. They may also have problems with higher level, so-called executive functions, such as planning, organizing, abstract reasoning, problem solving, and making judgments, making it difficult to resume preinjury work-related activities. Unfortunately, recovery from cognitive deficits is greatest within the first 6 months postinjury, becoming slower and more gradual thereafter ( ). Patients with moderate to severe TBI tend have more problems with cognitive deficits than patients with mild TBI, but a history of several mild TBIs may have an additive effect, causing cognitive deficits equal to a moderate or severe injury ( ).
Some TBI patients can develop quite significant sensory and motor changes ( ). Depending on the severity of the injury, patients who develop severe sensory issues may not be able to register what they are seeing or may be slow to recognize objects. This can also be the case in developing problems with hand–eye coordination ( ). These individuals may be prone to bumping into or dropping objects, or may seem generally unsteady ( ). This can affect activities such as driving a car, working complex machinery, or even playing sports ( ). Other sensory deficits may include problems with hearing, smell, taste, or touch ( ). It is not unusual for TBI patients to develop tinnitus, a ringing or roaring in the ears. Damage to that part of the brain that processes taste or smell may result in a persistent bitter taste in the mouth or perceive a persistent noxious smell ( ). Damage to the part of the brain that controls the sense of touch may cause a TBI patient to develop persistent skin tingling, itching, or pain ( ). While these sensory conditions are not extremely common, they are difficult to treat when they occur.
Language and communication problems can also be common disabilities in TBI patients ( ). The most common is called aphasia, defined as difficulty with understanding and producing spoken and written language. Others may have difficulty with the more subtle aspects of communication, such as body language and emotional, nonverbal signals. In nonfluent aphasia, also called Broca’s aphasia or motor aphasia, TBI patients often have trouble recalling words and speaking in complete sentences, in addition to frequent pausing ( ). Patients with fluent aphasia, also called Wernicke’s aphasia or sensory aphasia, display little meaning in their speech, even though they speak in complete sentences and use correct grammar. They often speak in flowing gibberish, drawing out their sentences with nonessential and often invented words. Patients with global aphasia, where damage affects both areas of communication often suffer severe communication disabilities.
Some TBI patients have difficulty with the physical process of speaking, due in part to damage of the brain region that controls speech muscles. In this disorder, called dysarthria, the patient can think of the appropriate language but cannot easily speak the words because he or she is unable to use the muscles needed to form the words and produce the sounds ( ). Speech is often slow, slurred, and garbled. Some may have problems with intonation or inflection, called prosodic dysfunction ( ). These language deficits can lead to miscommunication, confusion, and frustration for the patient as well as those interacting with him or her.
Due to the nature of the injury, some TBI patients develop significant emotional and behavioral problems that are recognized as psychiatric conditions ( ). Family members of TBI patients often find that personality changes and behavioral problems are the most difficult symptoms to handle. Psychiatric problems include depression, apathy, anxiety, irritability, anger, paranoia, confusion, frustration, agitation, insomnia or other sleep problems, and mood swings. Problem behaviors often include aggression and violence, impulsivity, disinhibition, acting out, noncompliance, social inappropriateness, emotional outbursts, childish behavior, impaired self-control, impaired self-awareness, inability to take responsibility or accept criticism, egocentrism, inappropriate sexual activity, and alcohol or drug abuse/addiction ( ). Some patients’ personality problems may be so severe that their symptoms resemble borderline personality disorders, characterized by a combination of several unusual personality traits ( ).
Patients with severe TBI and extensive neural death often suffer from developmental stagnation, meaning that they fail to mature emotionally, socially, or psychologically, after the trauma. This can be a serious problem for both children and young adults, as attitudes and behaviors that are appropriate for a child or teenager become inappropriate in adulthood. It is fortunate that many TBI patients who display psychiatric or behavioral problems can be helped with medication and psychotherapy/support.
The Military and Traumatic Brain Injury
TBI is currently a significant problem in the military, especially among troops returning from the Middle East. It is no surprise that blast injury is the most common cause of war injuries and death ( ). However, due to better equipment and protection, closed-head TBI is occurring at very high rates. Blasts or explosions that would have been fatal in the past are now simply injuries. Because nothing actually penetrates the brain in most explosions, blast-induced TBI can be much more difficult to spot and accurately diagnose. The contribution of the primary blast wave to brain injury is an area of active research. In combat, sources of blast injury include artillery, rocket and mortar shells, mines, booby traps, aerial bombs, improvised explosive devices (IEDs), and rocket-propelled grenades (RPGs) ( ). The severity and pattern of blast injuries depends on the explosive composition and amount of material involved, surrounding environment, delivery method, distance between the victim and the blast, and presence of intervening protective barriers or environmental hazards.
The four basic mechanisms of blast injury are termed primary, secondary, tertiary, and quaternary ( ). Primary injuries occur secondary to a high-order over pressurization shock wave moving through the body. This wave affects gas-filled organs such as the lungs, gastrointestinal tract, and middle ear. These injuries are not necessarily obvious and make diagnosis of any problem rather difficult. Secondary injuries can occur due to flying bomb fragments and other objects propelled by the explosion, resulting in penetration into the body. Tertiary injuries result from the blast wind (in contrast to the high-pressurized shock wave) throwing the victim and can include bone fractures and traumatic amputation. Quaternary injuries are those not included in the first three classes, such as burns, crushing injuries, and respiratory injuries. Blast injuries are often polytraumatic, meaning that they impact more than one body system or organ. It has been estimated that over 60% of blast injuries result in traumatic TBI, and, for this reason, TBI is often referred to as the “signature injury” ( ).
One report published in 2012 in the Journal of Neurotrauma showed substantial improvements on several neuropsychiatric planes in 16 military personnel treated for TBI with 1.5 ata HBOT, using SPECT as a their primary diagnostic tool ( ). A case report in Undersea Hyperbaric Medicine discussed the treatment of two airmen with significant TBI symptoms including irritability, sleep disturbances, memory issues, and headaches. Preinjury neuropsychiatric testing had been completed on both Airmen, who were each treated with 1.5 ata for 3 months. The treatment not only resulted in complete resolution of their symptoms, but neuropsychiatric test scores were almost identical to scores taken preinjury ( ). Because this suggests such positive outcomes, several initiatives have been put in place that would bring HBO tanks to US military bases in the Middle East. A group of scientists from the University of Minnesota have designed a study that would involve troops in Iraq and Afghanistan with the following hypothetical scenario:
A Level III Air Force Theater Hospital located in Balad, Iraq, and Bagram, Afghanistan could support the infrastructure and personnel for an HBO facility. We envision a monoplace tank being installed at these Level III facilities. The tanks would be pressurized with air with the patient breathing 100% oxygen. Hyperbaric technicians would be required to maintain the chambers and technically deliver the HBO treatments. Critical care nurses and respiratory therapists would need training in the management of these patients in the HBO tanks. Treatments would be delivered to TBI victims immediately after appropriate resuscitation/stabilization had occurred. If craniotomy were to be required, including decompressive craniectomy, HBO treatment would be initiated in the recovery ICU setting as soon as the patient was stable. Although early HBO treatments are important, when ischemia is most severe, our research suggests that treatment given at any time during the 5-day post injury period results in positive response. Whenever transport and transfer of the patient to Landstuhl, a Level IV Army Regional Medical Center in Germany, was deemed appropriate, this would be carried out. The Critical Care Air Transport Team would perform transfer in the usual way. Transport time from Balad to Landstuhl is approximately 7 hours and approximately 9 hours from Bagram to Landstuhl. A second HBO facility as described above would be instituted in Landstuhl. HBO treatments would continue every 12 hours for up to 5 days depending upon response. Since the total average time spent in Iraq/Landstuhl is 4–5 days prior to transport to a continental United States (CONUS) hospital, initial HBO treatment would be completed in most cases. If not, treatment could continue at a CONUS hospital.
The goal of this initiative is to gain additional knowledge on the impact of HBOT on blast-induced TBI, while providing immediate care to injured military personnel. This would hopefully improve their outcome before returning to the United States. Because PTSD is also common in returning soldiers, airmen, sailors, and marines, it adds to the complication of how TBI should be treated. The general consensus is that each ailment be treated individually. By reducing the neuropsychiatric effects of TBI, HBOT may assist in decreasing or even eliminating symptoms of PTSD.
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5-Lipoxygenase-Activating Protein Inhibitors: Promising Drugs for Treating Acute and Chronic Neuroinflammation Following Brain Injury
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