Brain Injuries

There are many different types of brain injuries, with many different causes, and a wide range of physical, psychological, emotional, and behavioral consequences. It is now recognized that even “mild” concussions can cause serious brain injuries, especially if they occur repeatedly. Profound brain damage can be fatal.

Traumatic brain injury (TBI), skull fracture, bruising or tearing of brain tissue, or blood clots or bleeding between the skull and brain—subdural hematoma and subarachnoid hemorrhage, respectively— can all damage the brain. A slight blow to the head or even a fall without hitting the head may be sufficient to tear blood vessels in the brain. TBI is the most common cause of coma and subarachnoid hemorrhage. Subarachnoid hemorrhage is an accumulation of blood that compresses the brain as the brain swells, damaging tissue. It occurs with 23%–39% of severe head injuries and is frequently fatal. It can also lead to stroke, seizures, or permanent brain damage. Cerebral edema is swelling caused by excessive fluid in the brain from TBI, stroke, or a tumor. Because the skull leaves very little room for brain swelling, cerebral edema is also referred to as elevated intracranial pressure (ICP). ICP can directly damage or destroy brain cells, displace brain tissue, or cause intracerebral hemorrhaging or disrupted blood flow that deprives the brain of oxygen. Edema can prevent fluids from exiting the brain, thereby increasing swelling and ICP. Cerebral edema can very quickly lead to temporary or permanent brain damage or death.

TBIs

Concussion—the most common TBI—is considered a complex neurobehavioral syndrome. Concussion occurs when the brain jars against the skull with sufficient force to cause temporary loss of function in higher brain centers. The brain movement may be a sudden acceleration, deceleration, and/or rotation. Concussion can be caused by direct or indirect blows to the head or body, violent shaking, whiplash-type injuries, gunshot wounds, or shockwaves from explosions. The actual injury is usually on the opposite side of the head from the initial blow. Concussions may cause a brief loss of consciousness or a dazed feeling. They can also involve skull fracture, bleeding in the brain, diffuse axonal injury (tearing of nerve tissue), or cerebral edema, with temporary or permanent damage. It is not known exactly how brain cells are affected by concussion, but it appears to involve chemical changes that temporarily affect function. During this period of abnormal function, the brain is much more susceptible to a second injury. Although most concussions resolve on their own without lasting effects, even a very mild concussion followed by a second blow to the head before full recovery can have serious, long-lasting consequences—a condition known as second-impact syndrome. The second impact or recurrent TBI is more likely than the initial TBI to cause brain swelling and widespread damage.

There are other types of TBI:

Non-traumatic brain injuries

Non-traumatic brain injuries are sometimes called acquired brain injuries. They can include injuries from:

Brain injuries can also occur before or during birth. For example, cerebral palsy can be caused by damage to the motor control centers in the brain before, during, or after birth, resulting in a spectrum of movement disorders.

Most people experience some form of head injury at least once in their lives, although most are not serious. Nevertheless, about 70% of all accidental deaths and most disabilities following trauma are due to brain injuries. Young children, males aged 15–24, and people over age 75 are most likely to suffer head trauma.

There are about 2.5 million TBIs in the United States each year, of which 75% are concussions or other relatively mild forms. Every year in the United States, TBI results in approximately 373,000 hospitalizations, more than 56,000 deaths, and 99,000 permanent disabilities. Sports-related concussion and other TBIs are now recognized as serious public-health concerns. Studies have shown that approximately one out of every five high-school football players suffers a concussion or more serious brain injury during their brief careers. Approximately 230,000 American military personnel suffered “mild” TBIs between 2001 and 2014, primarily from blasts. Falls account for about 40% of all non-combatrelated TBIs. Motor-vehicle accidents account for about 14%. Other common causes of TBIs are bicycle accidents, assaults, and workplace accidents. Firearms cause the most deaths from TBI, and the overall death rate for TBIs from bullets is 91%.

Signs and symptoms of brain injuries depend on the parts of the brain that are damaged. For example, damage to the frontal lobes can cause difficulties with attention, problem-solving, creativity, and other cognitive functions. Symptoms of brain injuries may include:

Symptoms of even a “mild” brain injury may persist for days or weeks. Up to 60% of people with mild brain injuries continue to experience a range of symptoms—post-concussion syndrome—for as long as six months or a year. The severity of symptoms appears to be significantly influenced by previous head injuries and their recovery times and the patient's age.

The neurological exam assesses:

Imaging of the brain by computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET), as well as electroencephalography (EEG) and other studies, may help diagnose brain injuries. Cerebral angiography is used to locate damaged blood vessels. However, CT, MRI, EEG, and routine neurologic evaluations may all be normal, because it is difficult to detect microscopic damage with diffuse axonal injuries. Mental status evaluations are particularly important when other neurologic and imaging results are normal. Sometimes small changes in memory or other intellectual abilities are the only indication of a problem.

Brain injuries such as concussions are managed with complete physical and mental rest until symptoms are completely gone. Returning to activities can worsen symptoms, prolong recovery, and put the patient at risk for second-impact syndrome. Normal activities are resumed very gradually in a stepwise manner.

Cerebral edema is commonly treated with corticosteroids, diuretics, glycerin, or other medications. Surgery may be required to measure or relieve ICP, close a vein, drain blood or fluid, or remove a clot. A penetrating head wound or skull fracture may also require surgery. Anticonvulsants can prevent or control seizures. Sedatives and medications for pain, nausea, and vomiting are administered as needed. Transcranial magnetic stimulation has had some success in reviving coma patients with severe TBI. Patients with severe brain injuries may need to relearn basic skills.

With proper rest and management, concussions usually resolve within a few weeks, without lasting neurologic effects. However, symptoms can sometimes last for months, and complete recovery from a more severe concussion may take years. Concussions that are not managed with physical and mental rest can lead to permanent problems. The risk of a second concussion is greater than the risk for the first concussion. Frequent concussions, as experienced by boxers and football and hockey players, can lead to chronic, progressive disorders such as CTE, Parkinson disease and other motor problems, Alzheimer's, disease, or post-traumatic dementia.

KEY TERMS

Acquired brain injury—
Non-traumatic brain injury; brain injury resulting from a stroke, tumor, toxin, electric shock, infection, oxygen starvation, or similar events.
Cerebral edema—
Fluid accumulation in the brain causing swelling.
Chronic traumatic encephalopathy (CTE)—
An ultimately fatal neurodegenerative disease with cognitive impairment and dementia, caused by repeated brain injuries.
Coma—
Profound unconsciousness due to injury, illness, or poisoning.
Concussion—
Atraumatic brain injurythat disturbs cerebral function.
Contusion—
Bruising or bleeding in the brain without fracture of the skull.
Diffuse axonal injury—
Brain injury caused by shaking or rotational forces that stretch or tear nerve tissue.
Glascow Coma Scale (GCS)—
An assessment of brain injury severity based on eye opening and verbal and motor responses.
Intracranial pressure (ICP)—
Pressure inside the skull.
Second-impact syndrome—
A more severe brain injury following a previous injury.
Stroke—
Sudden diminishing or loss of consciousness, sensation, or voluntary movement from a rupture or obstruction of a blood vessel in the brain.
Subarachnoid hemorrhage—
Bleeding on the surface of the brain.
Subdural hematoma—
A collection of blood or a clot trapped under the dura mater—the outermost membrane surrounding the brain.
Traumatic brain injury (TBI)—
Injury to the brain from sudden trauma.

PHINEAS GAGE




Skull of Phineas Gage on display at the Warren Anatomical Museum at the Countway Library of Medicine at the Harvard.





Skull of Phineas Gage on display at the Warren Anatomical Museum at the Countway Library of Medicine at the Harvard.
(© Boston Globe/Getty Images.)

The story of Phineas Gage is a classic study in neuropsychology. The 25-year-old railroad foreman was the first documented person to survive brain damage, and his case was the first to demonstrate the relationship between the frontal lobes and personality. It is used today in the study of the biological basis of personality and personality changes caused by lesions or damage to frontal lobes.

Phineas Gage's case history was first reported in a letter to the editor in the Boston Medical and Surgical Journal by John Martyn Harlow, the physician who treated Gage.

On September 13, 1848 Phineas Gage was working on the Rutland and Burlington Railroad near Cavendish, Vermont, when an accidental explosion sent a tamping iron into the left side of his face. It entered under his left cheekbone, passing behind the left eye, through the left frontal lobe, exiting the skull and landing about 25 yards behind him. The tamping iron was three feet seven inches long, 1 inch in diameter and weighed 13 pounds. The impact threw Gage onto his back, but after a few convulsions of the extremities he was reportedly speaking within a few minutes, and rode upright in a cartto receive medical treatment. Despite the brain injury and hemorrhage, Gage was fully conscious when Dr. Harlow arrived. “He recognized me at once and said he hoped he was not much hurt,” Harlow reported. Gage also told the doctor, with confirmation from workmen who observed the accident that “the iron struck his head and passed through.” The iron caused the most significant damage to the left frontal lobe, as well as damage to some other parts of the brain.

Gage was restricted to bed rest, treated and meticulously observed by Dr. Harlow for 10 weeks, at which point he was able to return to his home in Lebanon, New Hampshire.

Dr. Harlow gave a follow-up report on Gage in 1868, 20 years following his initial case study. This report provides most of the information we have on the last 12 years of Gage's life following the accident, and the nature of his personality changes due to frontal lobe injury.

Following his recovery Gage demonstrated significant changes to his behavior and personality. In 1849 he applied for his previous job as railroad foreman, but the contractors found the changes in his personality so drastic they refused to rehire him. Before the accident, Gage was said to be “a great favorite” of the workmen, of eventempered demeanor, and a very competent and efficient businessman. However now he was found to be fitful, profane, showing little regard for his fellow workers, impatient and capricious. His behavior was referred to as both childish and animal-like. His friends and coworkers said he was “no longer Gage.”

Gage kept the tamping iron as his “constant companion for the remainder of his life” and exhibited himself at Barnum's American Museum in New York City. He also worked as a stagecoach driver in Chile and New Hampshire and later joined his family in San Francisco, where he worked on a farm before dying in 1861 following a series of epileptic fits. No autopsy was performed, but Gage's mother and friends gave his skull to Harlow for further study.

Gage's condition following the brain injury has been likened to that of patients given prefrontal lobotomies, and some have even gone so far as to call Gage's case the first lobotomy, though there is no evidence to suggest that the development of the lobotomy was in any way related to or influenced by Gage's case history. Gage's case history remains a critical early example of the relationship between the frontal lobe and personality in humans.

Resources

BOOKS

Arciniegas, David B., editor. Management of Adults with Traumatic Brain Injury. Washington, DC: American Psychiatric Publishing, 2013.

Elliott, Clark. The Ghost in My Brain: How a Concussion Stole My Life and How the New Science of Brain Plasticity Helped Me Get It Back. New York: Viking, 2015.

Fainaru-Wada, Mark, and Steve Fainaru. League of Denial: The NFL, Concussions, and the Battle for Truth. New York: Crown Archetype, 2013.

Goldsmith, Connie. Traumatic Brain Injury: From Concussion to Coma. Minneapolis: Twenty-First Century, 2014.

Muenchberger, Heidi, and Elizabeth Kendall. Health and Healing After Traumatic Brain Injury: Understanding the Power of Family, Friends, Community and Other Support Systems. Santa Barbara, CA: Praeger, 2013.

Padgett, Jason, and Maureen Ann Seaberg. Struck by Genius: How a Brain Injury Made Me a Mathematical Marvel. Boston: Houghton Mifflin Harcourt, 2014.

Stoler, Diane Roberts, and Barbara Albers Hill. Coping with Concussion and Mild Traumatic Brain Injury: A Guide to Living with the Challenges Associated with Post Concussion Syndrome and Brain Trauma. New York: Avery, 2013.

PERIODICALS

Alexander, Caroline. “The Invisible War on the Brain.” National Geographic 227, no. 2 (February 2015): 30–53.

Shifflett, C. M. “Women & Concussion: An Under-Recognized Danger.” Women's Health Activist 39, no. 6 (November/ December 2014): 6–7.

“Your Brain on Trauma.” Time 184, no. 12 (September 29, 2014): 36.

WEBSITES

“About Brain Injury.” Brain Injury Association of America. October 12, 2012. http://www.biausa.org/about-braininjury.htm (accessed June 22, 2015).

MedlinePlus. “Traumatic Brain Injury.” U.S. National Library of Medicine, National Institutes of Health. June 10, 2015. http://www.nlm.nih.gov/medlineplus/traumaticbraininjury.html (accessed June 22, 2015).

National Center for Injury Prevention and Control, Division of Unintentional Injury Prevention. “Traumatic Brain Injury.” Centers for Disease Control and Prevention. March 27, 2015. http://www.cdc.gov/TraumaticBrainInjury/index.html (accessed June 22, 2015).

Office of Communications and Public Liaison. “Traumatic Brain Injury: Hope Through Research.” National Institute of Neurological Disorders and Stroke. February 3, 2015. http://www.ninds.nih.gov/disorders/tbi/detail_tbi.htm (accessed June 22, 2015).

ORGANIZATIONS

American Psychiatric Association, 1000 Wilson Blvd., Ste. 1825, Arlington, VA, 22209, (703) 907-7300, (888) 35PSYCH (357-7924), apa@psych.org, http://www.psychiatry.org .

American Stroke Association, 7272 Greenville Ave., Dallas, TX, 75231, (888) 4-STROKE (478-7653), http://www.strokeassociation.org/STROKEORG .

Brain Injury Association of America, 1608 Spring Hill Rd., Ste. 110, Vienna, VA, 22182, (703) 761-0750, (800) 4446443, Fax: (703) 761-0755, info@biausa.or, http://www.biausa.org .

Centers for Disease Control and Prevention, 1600 Clifton Rd., Atlanta, GA, 30333, (800) CDC-INFO (232-4636), http://www.cdc.gov .

National Institute of Neurological Disorders and Stroke, NIH Neurological Institute, PO Box 5801, Bethesda, MD, 20824, (301) 496-5751, (800) 496-5751, http://www.ninds.nih.gov .