Immediate and transient loss of consciousness accompanied by a brief period of amnesia following a blow to the head.
A functional manifestation of mild traumatic brain injury.
Can have physical, cognitive, and psychological implications in both short and long-term.
Defined as a clinical syndrome of biomechanically induced alteration of brain function typically affecting memory and orientation, which may involve loss of consciousness.
Results in a neurometabolic cascade that causes the brain to be more sensitive to stress and further injury until it is fully recovered.
Can occur after motor vehicle accidents, sports related injuries, falls, or assaults.
Gross structural changes are often not apparent on non-functional brain imaging.
Acute changes in brain physiology can occur after concussion and include alterations in cerebral blood flow, cerebral blood flow autoregulation, cerebral metabolism, neurotransmitter release, neurotransmitter receptors expression, blood brain barrier integrity, and expression of inflammatory cytokines.
These changes in brain physiology account for headache, lethargy, memory impairments, sleep disturbances, and psychiatric symptoms ref2242ed to as post concussive syndrome.
Affects about 50 persons per 100,000 population annually in the U.S.
Mildest form refers to momentary sensation of being dazed without a loss of consciousness.
A complex pathophysiological process induced by external traumatic forces and capable of producing long-term functional disturbance.
A cerebral concussion is generally defined as a brief, temporary int2242uption of neurologic function following head trauma; it can occur with or without loss of consciousness.
Patients appear dazed initially and may stare blankly for several seconds or minutes.
Associated often with headache, dizziness or vertigo. that may last for a few minutes or several hours.
Post-traumatic amnesia(PTA) and confusion are often present with more severe concussions, and duration of these processes are directly proportional to the severity of the injury.
Loss of consciousness may accompany more severe concussions.
As many as 300,000 sports-related concussions are diagnosed each year in the United States, but that underestimates the true incidence.
The CDC estimates 1.6 million to 3.8 million sport related concussions Re sustained in the US each year across all competitive sports and recreational activities.
More than the 62,000 concussions occur annually at the high school level.
Contact sports such as football, hockey, rugby, and soccer have the highest incidence of concussion, but athletes across all sports are at risk.
The greatest risk factor for a concussion is a history of concussion, which increases an athletes likelihood of repeated concussion by 2-5.8 times.
It is estimated that approximately one in 30 youth league football players, one in 14 high school football players and one in 20 collegiate football players sustain a concussion each year.
Many concussive injuries are not recognized.
4 of 5 professional football players with concussion are unaware that they had suffered this injury.
Symptoms are largely subjective, and recognition often relies on individual or family reports.
Headache and dizziness of the most common post concussion symptoms.
Clinical symptoms of acute concussion may be somatic, cognitive, or emotional in nature and may include loss of consciousness, amnesia, slow reaction time, confusion, disinhibition or headaches.
About 10% of patients with concussion manifest significant clinical symptomatology.
Many patients outwardly appear normally, but still experience substantial sequelae internally.
Neurologic examinations and mental status evaluations frequently failed to detect findings that often characterize concussion.
Symptoms may last several hours to several weeks, however the potential of chronic symptoms may not present for several years, making it difficult to link those symptoms with the sentinel event.
McGill Concussion Protocol enables evaluation the severity of a CNS injury and to gauge the progress of recovery.
Some patients may be ataxic immediately after the injury.
There are generally no focal neurologic deficits associated with concussion.
CT scans of the brain are normal; however, small petechial hemorrhages are seen on MRI in a few patients with mild traumatic brain injury.
Chronic traumatic encephalopathy has been attributed to repetitive concussions.
The signs and symptoms of concussion may be confused injuries to the vestibular system of the inner ear or to other head and neck structures.
The initial complaints of poor concentration, forgetfulness, and sleep-wake disturbances are usually caused by neural injuries.
Anxiety, mood disorders, and irritability may result and be attributable to neuronal injury, but they may also be caused by pain from other injuries or psychological factors.
Severity of concussions:
Grade 1. This is the mildest and most common form of concussion.
Grade I is the most difficult to recognize.
Defined by transient confusion without loss of consciousness.
If post traumatic amnesia occurs, it lasts for less than 30 minutes.
Moderate concussion with loss of consciousness with complete recovery in less than 5 minutes.
Transient confusion that lasts more than 15 minutes, and post traumatic amnesia that lasts more than 30 minutes.
Severe concussion with any loss of consciousness, whether brief or prolonged of more than 5 minutes, and/or post traumatic amnesia that lasts more than 24 hours.
The McGill Grading System subdivides mild concussions into 3 classes.
A Grade 1a concussion involves no post traumatic amnesia and only seconds of confusion.
A Grade 1b concussion features post traumatic amnesia and/or confusion that resolves within 15 minutes.
A Grade 1c concussion is characterized by postconcussion syndrome or confusion that does not resolve in 15 minutes.
Features of concussion include: stare, confusion, inability to focus, disorientation of time, space or direction, dizziness, vertigo, headaches, slurred speech, impaired coordination, emotional lability, impaired memory, delayed verbal and motor responses, and any level of loss of consciousness and nausea of vomiting.
Following concussion patients may experience headaches, light-headedness, poor attention and concentration abilities, impaired memory, fatigue biliary, irritability, frustration, depression, anxiety, tinnitus, noise sensitivity, light sensitivity, and sleep disturbance.
All patients should be assessed medically and not return to physical exertion if signs or symptoms persist.
Follow-up examinations of concussed patients are required.
The treatment of concussion is standardized for each grade or level of injury.
Grade 1. If asymptomatic 15 to 20 minutes later and there is completely normal neurologic assessment return to the event is allowed.
If the patient has a second Grade 1 concussion in the same event, they should not resume play that day, but may return if asymptomatic for 1 week at rest and during exertion.
If 3 Grade 1 concussions occur in the same event, the patient is disallowed from play for the season.
Second-impact syndrome refers to a second or third concussion that can cause severe neurologic injury or death.
Second-impact syndrome is a likely process if subsequent concussions occur during the post-concussive period.
Grade 2 concussion patients should be stopped from further participation of the event, and the patient requires frequent on-site evaluations to check for signs of evolving neurologic changes..
Grade 2 concussed patients must be re examined the next day.
Grade 2 concussed patients can return to activities if asymptomatic, and with a normal neurologic evaluation after 1 week.
CT or MRI should be performed if headache or other symptoms worsen or persist longer than 1 week.
If a second Grade 2 concussion occurs, defer return to play until he has been symptom-free at rest and with exertion for at least 2 weeks.
If there is any abnormality on CT scanning or MRI consistent with brain swelling, contusion, or other intracranial pathology further activity is prohibited.
Grade 3. The patient requires a complete neurologic evaluation, including appropriate neuroimaging procedures. Neuro imaging studies include: CT of brain in most cases, although MRI can be obtained if more details are needed in evaluation.
Normal imaging studies in grade 3 injury the patient may return to the sport after 1 week if the LOC was brief and he is completely asymptomatic.
After a prolonged LOC, the athlete should be disallowed from play until asymptomatic for 2 weeks at rest and with exertion.
If two Grade 3 concussions occur, the athlete should not play until at least 1 month has passed with no symptoms.
Any abnormal findings on CT or MRI should discourage future competition.
Patients with post concussion syndrome may experience headache, dizziness, difficulty in concentration, impaired memory, variable amnesia, depression, apathy, and anxiety.
In the first few days after a concussion, deficits in arousal are often present.
Impairments in sleep-wake cycles and attention are more long-lasting.
Results in disturbances in new learning, attention, and speed of information processing.
Cognitive deficits that can be documented with neuropsychological tests within 24 hours of the injury.
Rapid return to preconcussion performance level is often observed 5 to 10 days after concussion, even in patients still symptomatic.
More complex mental functions may be abnormal for 7-10 days, but these deficits generally resolve during the next several weeks to months.
In patients with a brief loss of consciousness, and posttraumatic amnesia of less than 1 hour recover usually occurs within 6 to 12 weeks.
In patients with loss of consciousness longer than 10 minutes and/or duration of post traumatic amnesia for more than 4 to 6 hours may require months or even years to return to normal, and some may never do so.
By 3 months after concussion neurologic recovery is usually substantial.
After 3 months after concussion only a small number of patients still have limitations.
Patients who recover are susceptible to occasional impairment during periods of increased physiologic or psychological stress.
Most patients with a mild to moderate concussion become asymptomatic within a few minutes or days.
Approximately 10% to 15% of patient with a mild to moderate concussion have symptoms that persist for more than 1 year.
Even with mild concussion frequent postconcussive symptoms may persist for 3 months and include:headache, forgetfulness, poor memory, fatigue, irritability, easy to be angered, dizziness and poor concentration.
It is the mild end of the traumatic brain injury continuum.
Highest rates in young children.
Majority of concussions among 5-14 year olds related to sports and bicycle related accidents.
In adults falls and auto accidents are most common causes.
The direct cause is a rapid acceleration-deceleration at the time of a blow to the head, jarring of the brain inside the skull and stretching the neurons so that they temporarily are impaired.
Stretching and shearing of axons causes a pathological release of neurotransmitters which leads to ion level fluctuations.
Such fluctuations in ion levels cannot be seen on brain imaging.
Results in a rapid onset and neuro physiologic and neurologic dysfunction that usually resolves spontaneously over a short period of time.
Symptoms include headache, confusion, amnesia, altered level of consciousness, nausea and vomiting, mood swings, ringing in the ears, impaired speech, balance, coordination, judgment, difficulty with concentration, learning, difficulty sleeping, blurred vision, photosensitivity, phonosensitivity, slower reaction times, insomnia, emotional liability, irritability. or depression, and drowsiness.
Severity related to the length of amnesia and unconsciousness.
Extent of amnesia correlates with duration of loss of consciousness and severity of head trauma.
Amnesia can be anterograde with inability to retain new information and retrograde extending usually moments or rarely to longer periods of time.
Anterograde memory loss tends to be briefer than retrograde amnesia, but both improve over a period of hours or less.
Does not cause loss of autobiographical information or confabulation.
Brief loss of consciousness results from rotational forces exerted at junction of upper midbrain and thalamus causing transient disruption of reticular neuron function that maintains alertness.
Multiple concussions over months result in cumulative neuropsychologic deficits.
Attention at site of injury includes keeping the airway clear, seeing that the neck is stable or if it requires immobilization and then transport to an emergency department for evaluation.
Clinical evaluation of an individual’s alertness, orientation, memory, and neurologic status is performed immediately.
Diagnostic imaging such as CT scan of the brain or MRI of the brain to exclude skull fractures, brain swelling or bleeding may be done after initial evaluation.
Postconcussion evaluation is repeated until symptoms resolve.
Sports related concussive injury is generally related to functional or metabolic changes rather than structural dysfunction since neuroimaging results are usually normal.
Most patients improve rapidly, while 10 to 20% of patients with sports related concussions may remain symptomatic, particularly children and adults.
Among collegiate football athletes there is a inverse relationship of concussion and years of football played with hippocampal volume.
Concussion causes prolonged disruptive cognitive performance in college athletes.
The accumulation of subconcessive hits across a high school football season inversely correlates with behavioral and neuroimaging measures of working memory performance.
Patients involved in trauma may also have other injuries such as fractures, intra-abdominal injuries and can cause hypotension, hypoxemia, anemia, and hyperglycemia.