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Sports Concussion And Neck TraumaPreventing Injury for Future Generations
By Kelly J. Roush
AuthorHouseCopyright © 2012 Dr. Kelly J. Roush
All right reserved.
Chapter OneDefinition of Head Injury/What Is a Concussion? Types of Head Injury/What Is Second-Impact Syndrome?
There are various types of injuries to the head, with the most common being a concussion or traumatic brain injury, sometimes referred to as a TBI. A traumatic brain injury is defined as a blow or jolt to the head or related structure that disrupts the normal function of the brain.
Depending on the extent of damage to the brain, symptoms of a traumatic brain injury may be mild, moderate, or severe. Mild cases may result in a brief change in mental state or consciousness, while severe cases may result in extended periods of unconsciousness, coma, or even death. Loss of consciousness is not required for an injury to be a concussion. The distinction between the degrees of consciousness is based on signs and symptoms. Signs/symptoms of a concussion can show up right away or may take days or weeks to appear. Following is a list of the most common signs/symptoms of a sports-related concussion:
PHYSICAL SIGNS/SYMPTOMS OF A CONCUSSION
HEADACHE * DIZZINESS * NAUSEA * SENSITIVITY TO LIGHT * BALANCE PROBLEMS VISUAL PROBLEMS * VOMITING * CONFUSION * SLURRED SPEECH SENSITIVITY TO NOISE * FATIGUE * NUMBNESS/TINGLING OF HEAD, FACE, OR HANDS
COGNITIVE SIGNS/SYMPTOMS OF CONCUSSION
HAS DIFFICULTY CONCENTRATING * REPEATS QUESTIONS * ANSWERS QUESTIONS SLOWLY FEELS MENTALLY IN A FOG * HAS DIFFICULTY REMEMBERING * IS CONFUSED ABOUT EVENTS IS FORGETFUL OF RECENT INFORMATION
EMOTIONAL SIGNS/SYMPTOMS OF CONCUSSION
IRRITABILITY * SADNESS * EXCESSIVE DISPLAYS OF EMOTION * NERVOUSNESS
SLEEP-RELATED SIGNS/SYMPTOMS OF CONCUSSION
DROWSINESS * SLEEPING LESS THAN NORMAL * SLEEPING MORE THAN NORMAL * TROUBLE FALLING ASLEEP ("Concussion Facts")
Coaches may notice the athlete appears dazed or is confused about an assignment, particular plays, or position on the field. The athlete may appear to be clumsy, answer questions slowly, and/or show behavioral or personality changes. The athlete may not be able to recall events prior to or after the hit or specific tackling event. The athlete may argue or laugh excessively. Coaches and other team members should observe any behavior that is not normal for the athlete and report it to the medical professional—such as the licensed athletic trainer or team physician—immediately.
When a football player takes a hit to the head, the force of that blow averages ninety-eight times the force of gravity. Most hits occur from a blow to the side of the head, often on the lower half of the face. The pressure from the hit passes through the brain and bounces off the skull. The concussion occurs on the opposite side of the brain (contre coupe injury; "School of Hard Knocks").
Sports-related trauma causes many types of head injuries. A common complication of a blow to the head is cerebral contusion, causing increased intracranial pressure in the skull due to an increase of cerebrospinal fluid and/or occurrence of an intracranial bleed. Computer tomography (CT) is commonly used to detect this type of injury, and surgical decompression is typically performed if herniation is present.
Hematomas, localized swelling filled with blood resulting from a break in a blood vessel, in the intracranial cavity are categorized by three anatomical locations.
1. Subdural Hematoma: A subdural hematoma is the most fatal athletic head injury and occurs between the dural surface and the leptomeninges covering the brain. These hematomas are venous in nature and are often associated with contusion of the white matter of the brain. Acute subdural hematomas result from bleeding within the subdural space as a result of stretching and tearing of subdural veins. Athletes with an acute subdural hematoma may be alert and awake, neurological deficits may not show up immediately and could take up to a three-week duration to appear). However, the majority of athletes with any sizable acute subdural hematoma present with an altered state of consciousness, major neurological deficits, and coma. Athletes with an acute subdural hematoma are often unconscious and sustain diffuse, irreversible brain damage ("Subdural Hematoma").
Symptoms of a subdural hemorrhage/hematoma have a slower onset than those of an epidural hemorrhage because veins bleed slower than arteries as a result of their lower pressure. Signs/symptoms of a subdural hematoma may show up within twenty-four hours but may be delayed as much as two weeks. Subdural hematomas occur around the top and side of the frontal and parietal lobes. They also occur in the posterior cranial fossa and near the falx cerebri and tentorium cerebelli. Athletes on blood thinners, taking aspirin, or drinking alcohol are more susceptible to a subdural hematoma and may develop a bleed from even a minor head injury.
A chronic subdural hematoma is rare but can be dangerous (over three-week duration). This type of hematoma results in a small amount of bleeding that becomes surrounded by a semipermeable membrane. This membrane then attracts tissue fluid through osmotic pressure. The fluid passes through the membrane, which increases the size of the hematoma. This process may continue for several months as the brain gradually adapts to the increasing pressure. A chronic subdural hematoma is defined as a hematoma present three weeks or more after a traumatic injury (Bailes and Hudson). The athlete may present with clinical symptoms, such as mental disturbance, personality changes, focal transient neurologic deficits, nuchal rigidity, photophobia (sensitivity to light), or a slow progression of neurological signs of severe and progressive headache (Robinson). A CT scan is commonly performed to detect subdural hematoma, which typically reveals a concave appearance. Treatment may include monitoring with CT imaging, anti-epileptic medication, and, if mass effect or neurologic deficits, surgical evacuation.
2. EPIDURAL HEMATOMA: An epidural hematoma is located between the dura and the skull and is caused by a rupture of the middle meningeal artery, commonly caused by a linear fracture of the temporal bone. Most epidural hematomas are associated with a skull fracture that leads to a laceration of the middle meningeal artery or vein. Epidural hematomas are typically characteristic of an isolated injury to the skull, dura, and dural vessels. The athlete may clinically present with a lucid interval. The athlete will lose consciousness and then appear asymptomatic and may have a normal neurological exam. However, the injury to the skull or vessels leads to a slow accumulation of blood in the epidural space, compressing the brain stem and causing a rapid progression toward neurologic dysfunction, brain hemorrhage, and possibly death (Bailes and Hudson).
SYMPTOMS OF A SKULL FRACTURE
*LEAKAGE OF CSF FLUID FROM THE NOSE, MOUTH, OR EAR (clear, sweet fluid)
*VISIBLE DEFORMITY OR DEPRESSION OF HEAD OR FACE
*AN EYE THAT CANNOT MOVE OR IS DEVIATED TO ONE SIDE
*BRUISING OF THE EYES OR FACE
3. SUBARACHNOID HEMORRHAGE: A subarachnoid hemorrhage is an abnormal dilation of an artery that causes vasospasm and, most often, a stroke. This may occur in athletics yet be completely unrelated to head trauma— possibly caused by a congenital aneurysm. It may also occur in conjunction with diffuse cerebral damage resulting from a serious head trauma caused by impact. A subarachnoid hemorrhage is a common cause of sudden death in young people.
An aneurysm is a saclike protrusion of an artery caused by a weakened area within the vessel wall. If a cerebral aneurysm ruptures, the escaping blood within the brain may cause severe neurological complications and/ or death. A person with a ruptured cerebral aneurysm may complain of the sudden onset of the worst headache of his or her life, may complain of a popping sensation in the head, a stiff neck, loss of vision, or nausea. The individual may begin vomiting and have a seizure. This injured athlete needs to be transported to the nearest trauma center immediately.
Diagnosis for this condition is confirmed with a CT of the brain, a lumbar puncture to test for CSF in blood, and angiogram, or an MRI of the brain. Treatment options include surgery or coiling to stop bleeding, placement of a ventricular catheter in the ventricles of the brain to drain fluid and relieve the cranial pressure. (Mayfield) Vasospasm and hypertension also needs to be closely monitored and controlled.
SECOND IMPACT SYNDROME
In 1973, neurosurgeon R. C. Schneider and his colleagues presented a clinical case of an athlete who died from a second blow to the head before recovering fully from the initial concussion. This condition has been termed second-impact syndrome (qtd. in Cantu).
Second-impact syndrome is a condition that occurs when an athlete who has sustained a head injury— usually a concussion or cerebral contusion— sustains a second head injury before symptoms associated with the first injury have cleared. This condition creates accumulative neurologic and cognitive deficits, such as in the cases of many boxers and football players. If the recurrent trauma occurs within a short period of time (hours, days, weeks) and there is repeated head trauma with probable concussions that may be considered mild, accumulative injuries can be fatal. There needs to be more research to prove clearly these catastrophic injuries were solely due to repetitive head trauma.
Bleeding or swelling in the brain can cause pressure that forces the brain downward in the skull, which causes a herniation. The most common type of herniation is a transtentorial herniation, where the temporal lobe is forced through the tentorial notch (Maiese). The pupil of the eye dilates and may not constrict in response to light. A transtentorial herniation can cause paralysis, stupor, coma, abnormal heart rhythms, disturbance or cessation of breathing, cardiac arrest, and death.
As the injured brain bleeds or swells, this increases the pressure on the brain, because there is nowhere for it to go within the confines of the skull. As the pressure increases, the athlete's symptoms increase. The athlete will complain of sensitivity to light, increased headache, confusion, nausea, and vomiting; he or she may lose consciousness. The herniation can cause a coma or death, as the vital portion of the brain stem— which controls heart rate and breathing— is compromised.
When an athlete has sustained a traumatic brain injury, the brain may be injured in a specific location, or the injury may be diffused to many parts of the brain. It is important to understand that the brain coordinates its different parts to function as a whole.
The portion of the brain injured can reveal particular deficits or abnormalities. The cerebral cortex is located in the frontal lobe, under the forehead. The cerebral cortex is responsible for our awareness of our surroundings and controls emotional responses, our expressive language, and memory for habits and motor activities. Injury to the cerebral cortex could cause paralysis, inability to multitask, inability to focus, persistence of a single thought, mood changes, personality changes, inability to express language, and difficulty with problem solving.
The parietal lobe, located near the back of the brain and on top of the head, assists us with visual attention, touch perception, and integrating thought processes for understanding a single concept. An injury to the parietal lobe would make it difficult to attend to more than one task at a time, name an object, locate words for writing, read, and draw. It also makes it difficult to distinguish the left side from the right side. It shows deficits in eye-hand coordination, lack of awareness of certain body parts, and an inability to focus visual attention.
The occipital lobe is at the back of the head and is primarily responsible for vision. An injury to the occipital lobe would lead to difficulty locating objects in the environment, difficulty identifying colors, possible hallucinations, an inability to recognize movement of an object, and difficulty reading and writing.
The temporal lobes are located on the sides of the head, just above the ears. They are responsible for hearing, memory, visual perception, and categorization of objects. An injury to a temporal lobe could result in difficulties in recognizing faces, understanding spoken words, and identifying objects, as well as short-term memory loss, long-term memory loss, inability to categorize objects, and an increase in aggressive behavior. Damage to the right lobe can cause persistent talking.
The brain stem is located deep in the brain, and it controls breathing, heart rate, swallowing, visual and auditory components sweating, blood pressure, and temperature regulation, and it affects the level of alertness, the ability to sleep, and the sense of balance. A brain stem injury can cause dizziness, breathing problems, speech problems, difficulty swallowing, balance problems, and insomnia.
The cerebellum is located at the base of the skull and is responsible for equilibrium. An injury to the cerebellum can cause an inability to coordinate fine movements, make rapid movements, walk, and reach out and grab objects. An injury may also cause tremors and slurred speech.
Location of the swelling and/or pressure on the brain explains the huge difference in how an athlete responds following a traumatic brain injury (concussion). I have seen some athletes become extremely emotional and cry. Others become angry, shove you away, and have personality changes. Some react by laughing constantly; they think every question you ask is hysterically funny. I was working a football game several years ago, and the referee brought a kid off of the field and said, "This kid's in trouble." The ref said he blew his whistle to start the play, and this athlete walked up to him and asked, "Lunchtime; did you bring your lunch?" When I evaluated this kid, he sang the answer to every question, and he laughed at everything.
Recent research reveals a correlation with genetic factors and the significance of apolipoprotein (Apo) Ey (APO E). APO E promotes gene, tau polymerase, and other genetic markers that may be possible reasons for increased effects of a head trauma. Evidence from human and animal studies of more severe traumatic brain injury shows induction of a variety of genetic and cytokine factors, such as insulin-like growth factor-1 (IGF- 1), IGF binding protein-2, fibroblast growth factor, Cu-Zn superoxide dismutase, superoxide dismutase-1(SOD-1), and nerve growth factor glial fibrillary acidic proteins (GFAP and S100)(Peng et al.). More research on this correlation needs to be performed
Chapter TwoAssessment of Head Injury: Signs/Symptoms, Sideline Evaluation vs. Clinical Evaluation
Proper documentation and initial assessment of head and/or neck trauma are essential to the subsequent management of the injury. There are more than twenty-five recognized guidelines for the assessment and management of concussion. I have included several of these assessment tools for your review. I have also included one of the assessment tools I utilize in my own sports injury practice as an additional tool.
Sports medicine professionals are continuously searching for standardized methods to obtain a more objective evaluation of head trauma. These methods assist the athletic trainer/physician to quantify the severity of injury and measure the athlete's progress as he or she recovers. Data from objective measures of cognitive function, postural stability, and post-concussion signs and symptoms are most helpful in making a determination about severity of injury and post injury recovery. An emerging model of sport concussion assessment involves the use of brief screening tools to evaluate post-concussion signs and symptoms, cognitive function, and postural stability on the sideline immediately after an injury in conjunction with physical exam of the athlete.
Excerpted from Sports Concussion And Neck Trauma by Kelly J. Roush Copyright © 2012 by Dr. Kelly J. Roush. Excerpted by permission of AuthorHouse. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
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Table of Contents
Chapter 1 Definition of Head Injury/What Is a Concussion? Types of Head Injury/What Is Second-Impact Syndrome?....................1
Chapter 2 Assessment of Head Injury: Signs/Symptoms, Sideline Evaluation vs. Clinical Evaluation....................9
Chapter 3 Grades of Concussion/Return-to-Play Decisions/Treatment Options for Brain Bleeds....................35
Chapter 4 Cervical Spine Injury: Types of Injury/Evaluation and Treatment/Return-to-Play Decisions....................39
Chapter 5 How to Care for an Athlete with Head/Neck Trauma on the Field....................47
Chapter 6 Prevention of Head/Neck Trauma....................59
Chapter 7 The Role of Legislation in Prevention of Concussion and Chronic Traumatic Encephalopathy....................84
Chapter 8 Matt's Story: A Football Player Who Collapsed After a Football Game and Died of a Brain Hemorrhage, Written by His Mother/MJ's Story: A Fifteen-Year-Old Who Had a Bicycle Wreck Without a Helmet and Sustained a Life-Threatening Head Trauma/Sk Fracture, Written by His Father/Other Case Studies of Athletes Who Suffered Concussion and/or Neck Trauma....................87
Chapter 9 The Long-Term Effects of Repetitive Head Trauma/Chronic Traumatic Encephalopathy....................95
Chapter 10 Common Questions Asked About Head/Neck Trauma and an Interview with Dr. Bill Moreau, US Olympic Committee Director of Sports Medicine Clinics....................99
About the Author....................115