3/20/18: BRAIN INJURY AWARENESS DAY: Considering Concussions and Comas; TBI, Part 2


Good grief, Charlie Brown. How many concussions did you have?

In my St. Patrick’s Day blog post, I defined a traumatic brain injury (TBI) as occurring whenever the brain is wounded by a penetrating object, such as a bullet, shrapnel, knife, or other weapon, or by a non-penetrating external physical force such as a bump, blow, or jolt to the head. A person can suffer both penetrating and non-penetrating TBIs, most typically with an explosion, a natural disaster, or other extreme event.

I further explained that a TBI is caused by two mechanisms: impact to the brain and movement of the brain within the skull. The brain’s two cerebral hemispheres are not fixed rigidly inside the skull and have a lot of room in which to move. With both impact and movement, mechanical forces compress or lacerate the brain’s surface and create shock waves that travel through it and injure parts remote from the impact site.

March is Brain Injury Awareness Month, and today is Brain Injury Awareness Day. I believe everyone should reflect today upon precautions that they and their loved ones can take to prevent such injuries, such as fall-proofing an older person’s home or wearing a helmet while cycling.

Since my earlier post, I’ve read about two newsmakers who died as the result of TBIs: 88-year-old Rep. Louise M. Slaughter (N.Y.), the oldest sitting member of Congress, who, The Washington Post reported, died after being hospitalized, treated, and monitored for consequences of a fall-related concussion; and 7-year-old Tripp Halstead, who succumbed to a lung infection more than five years after he suffered a severe brain injury when a tree branch fell on him during Hurricane Sandy.

The impact of the branch damaged both of Tripp’s cerebral hemispheres and other parts of his brain, and he was not expected to survive. The toddler was comatose for weeks. He left the hospital after 10 months, a paralyzed and otherwise severely compromised child who struggled with basic functioning, including breathing.

Congresswoman Slaughter and young Tripp each fit into one of the three age groups that experience the highest TBI rate in this country. They are 1) newborn to 4 years old; 2) 15 to 19 years old; and 3) over 75 years old.

According to Georgetown neuroscientist Dr. Mark Burns, who was the inspiration for my earlier post, the 40-to-50 age group is fast becoming the fourth TBI at-risk group because of extreme-sports playing and other physical risk-taking. Dr. Burns actually counts himself among such daredevils.

(Men are more than twice as likely as women to suffer a TBI.)

According to the U.S. Centers for Disease Control and Prevention, TBI-related deaths in children age 4 and under are most often the result of assault (such as violent shaking); and in young adults 15 to 24, motor vehicle accidents are the most likely cause. TBI-related deaths in the oldest age group are usually attributable to a fall.


The damage to the brain from traumatic injury can range from mild, which a concussion is, to severe and life-threatening. (For more about the nature of TBIs, their potential damage, and brain anatomy, see my 3/17 post.)

A mild TBI can become a severe TBI if secondary damage occurs in the hours, days, or even weeks after a penetrating or non-penetrating injury. Primary damage is that which happens immediately.

When hematomas develop, for example—as I presume happened with Congresswoman Slaughter—severe bleeding pools in and around the brain. Such bleeding is toxic to brain cells and can lead to brain swelling (edema). When brain tissue swells, the pressure within the skull, known as intracranial pressure, rises. Intracranial hypertension, which I previously defined, prevents blood from flowing to the brain, thus depriving it of vital oxygen and causing permanent brain damage.

Dr. Burns defined concussion in a lecture I attended last week as the “rapid onset of short-lived impairment of neurological function that resolves spontaneously.”

Short-lived. Spontaneous resolution. 

“We shouldn’t be as afraid of concussions as we are,” he said. “The brain fixes itself.”

An extreme-sports aficionado, Burns claimed to have had three concussions in his lifetime.

I ended my 3/17/18 blog post with wondering if I had suffered a concussion when I fell on black ice years ago and hit my head. Based on all that I know now, I can confidently answer, yes.

According to the online National Institute of Neurological Disorders and Stroke (NINDS), a concussion is a “type of mild TBI that may be considered a temporary injury to the brain [that] could take minutes to several months to heal.” Elaborating, the NINDS says:

After “a bump, blow, or jolt to the head, a sports injury or fall, a motor vehicle accident, a weapons blast, or a rapid acceleration or deceleration of the brain within the skull” (such as when a toddler is violently shaken), a person with a concussion “either suddenly loses consciousness or has sudden altered state of consciousness or awareness, and is often called ‘dazed’ or said to have [had] his/her ‘bell rung.’”

I wrote of experiencing a “Teflon” effect after my head injury and of feeling detached from my physical environment. My consciousness was altered. Dazed fits the bill.

Dr. Burns described a concussion as “an energy crisis,” brought on by a sudden release of potassium and free calcium stores that leads to an ionic imbalance in the brain. The brain then responds chemically to restore homeostasis. In the absence of secondary damage, the energy crisis of concussion should resolve in seven to 10 days, said Burns, noting that 90 percent of all concussions are fully resolved within a month, as mine was.

Concussions can become more than mild energy crises, however, when more than one occurs, especially in quick succession.

The “second hit” phenomenon, also called second-impact syndrome, describes the catastrophic damage that can occur when a second concussion closely follows a first, before brain healing has taken place. The second hit triggers “overwhelming physiologic reactions,” said the NINDS. The previously injured brain swells rapidly, usually causing severe permanent disability or death.

Chronic traumatic encephalopathy (CTE), which has been best documented in boxers and U.S. football players, is a progressive neurodegenerative disease that results as a delayed consequence of extraordinary exposure to multiple blows to the head. These are typically multiple concussions (and worse) that are not sequential brain insults.

According to Dr. Burns, the average time of CTE onset in a professional boxer is 14 years after the start of his or her career. About 17 percent of professional boxers are estimated to have CTE.

The most common symptoms of CTE, the Georgetown neuroscientist said, are “aggression, depression, cognitive impairment, dementia, and parkinsonism.” More specifically, a person with CTE has memory disturbances, speech abnormalities, motor disorders, problems with impulse control, confusion, and irritability.

Like Parkinson’s disease, CTE is a tauopathy, meaning it is a pathology characterized by abnormal clumps of the protein tau in the brain. Tau aggregation kills nerve cell bodies. In CTE, according to Dr. Burns, tau exists in dense deposition in the hippocampus (the memory center) and medial temporal lobe structures. There is also prominent tau deposition in the medial thalamus.

Dr. Burns specializes in the biochemical connection between TBIs and dementia. Fifty percent of patients with CTE, he said, are estimated to have deposits of beta-amyloid, a hallmark of Alzheimer’s disease, in their brains.

Whenever nerve axons are broken as the result of a TBI—see my 3/17 post for more about axonal connections—the potential exists for the development of a neurodegenerative-disease type pathology, he said.

Besides athletes, CTE cases have been found in women who have suffered chronic domestic abuse and in individuals who have chronically harmed themselves with repetitive head damage.

Evaluating a Concussion

A mild TBI can have serious health implications if it quickly worsens. Physicians, therefore, recommend that all TBIs be assessed by a professional who has experience with evaluating head injuries. That professional should be able to conduct a neurological exam that would assess motor and sensory skills and the functioning of one or more cranial nerves. Hearing and speech, coordination and balance, mental status, and changes in mood or behavior should all be evaluated.


The CDC has prepared an acute concussions evaluation (ACE) form to assist physicians and other healthcare providers with initially assessing the severity of a concussion. I think it is useful to laypeople. You may access it here: https://www.cdc.gov/headsup/pdfs/providers/ace-a.pdf.

The ACE provides an evidence-based clinical protocol. It enables a medical professional to obtain TBI characteristics; ascertain the patient’s symptoms from a checklist; assess risk factors for a protracted recovery (such as a concussion history); identify red flags for deteriorating neurological functioning; make a diagnosis; and develop a follow-up plan, which typically involves physician monitoring for three to five days and, if symptom reduction does not occur, referral to a specialist.

According to Dr. Burns, the assessment tool used in the National Football League by team doctors and trainers is not as comprehensive.

When necessary, medical providers will use brain CT scans (computed tomography) to evaluate the extent of primary brain injuries and to determine if surgery is required. CT scans are helpful in people with suspected moderate to severe TBI, but Dr. Burns characterized the number of CT scans given to people with mild TBIs as excessive and unduly expensive. They are, however, standard procedure in hospital emergency rooms.

Neuropsychological tests are often used in conjunction with CT imaging in people with mild TBIs. Such tests involve having the patient perform cognitive tasks that depend on “memory, concentration, information processing, executive functioning, reaction time, and problem solving,” according to the NINDS.

Five percent of all patients who suffer a concussion also experience post-concussion syndrome, a complex disorder in which various symptoms, such as headache, dizziness, fatigue, insomnia, loss of concentration and memory, etc.—I list concussion-related symptoms in my 3/17 post—last for weeks or even months after the initial traumatic injury. According to the Mayo Clinic, the risk of post-concussion syndrome does not appear to be associated with the severity of the initial injury.

For more about this syndrome, see the Mayo Clinic at https://www.mayoclinic.org/diseases-conditions/post-concussion-syndrome/symptoms-causes/syc-20353352.


Concussions usually involve no loss of consciousness. If unconsciousness occurs, it is of brief duration, defined as less than an hour.

At the other end of the TBI-damage spectrum, short of death, is the brain injury that induces a coma.

According to the NINDS, a comatose person is “totally unconscious, unaware, and unable to respond to external stimuli such as pain or light.”

The Glasgow Coma Scale is the most widely used tool for assessing a person’s level of consciousness after a TBI. The standardized 15-point test measures a person’s ability to open his or her eyes (called the best eye response); to respond to prompts for movement (best motor response); and to respond to spoken questions (best verbal response).

In this test, the higher a patient’s score is, the better.

For example, the scores and choices for verbal response are:

5–Alert and oriented

4–Confused, yet coherent, speech

3–Inappropriate words and jumbled phrases consisting of words

2–Incomprehensible sounds

1–No sounds

Total scores and their interpretations are as follows: 13-15, a mild TBI; 9-12, moderate disability (loss of consciousness greater than 30 minutes); 3-8, severe disability (unconscious state); less than 3, vegetative state.

When a vegetative state lasts longer than a month, it is considered persistent. People in a vegetative state have suffered widespread brain damage and are unconscious and unaware, but they can have periods of unresponsive alertness, and they may groan, move, or show reflex response, according to the NINDS.

When there is no measurable brain function and activity, brain death has occurred. Such death may be confirmed by studies showing that there is no blood flow to the brain.

To access a complete Glasgow Coma Scale, please click on http://www.traumaticbraininjury.com/symptoms-of-tbi/glasgow-coma-scale/.

According to Dr. Burns, a coma rarely lasts more than two to four weeks.

How many movies or TV shows have you seen in which people who have been comatose for years suddenly awaken and are fully functional? Even novelists cheat on this one.


According to Dr. Burns, about 4 million TBIs occur annually in the United States. The CDC says 2.2 million people with TBIs visit hospital emergency departments each year; and 280,000 TBI patients are hospitalized. Traumatic brain injuries cause 50,000 deaths per year.

The hospital emergency-department numbers are on the rise, Dr. Burns said, because of the thousands of soldiers returning from Iraq and Afghanistan with TBIs related to explosions. Blast injuries are particularly devastating to the brain.

Ann, 3/20/18

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