Most recent update: February 2, 2018 : This page is not written for or intended for use in legal endeavors.
Concussion comes from the Latin word, "to shake violently" (Webster). Most concussions in adults are caused by direct blows to the head. However, it is also accepted that occasionally, such as in the "shaken baby" syndrome, concussions can occur without a direct blow to the head after a very forceful acceleration/decelerations.
There are an immense number of publications with "concussion" in their title -- roughly 300/year. Thus it seems that concussion is a topic of great interest.
The American Academy of Neurology (AAN) defined concussion in 1997 as "any trauma-induced alteration in mental status that may or may not include loss of consciousness". In other words, they defined it as the combination of a change in mental status associated with "trauma". (Practice Parameter, 1997). We think that this definition is so all-inclusive as to be almost meaningless as by this a "concussion" could be a change in one's mood after an acorn fell on one's head.
Another attempt was made in 2001. Criteria for concussion proposed by the 2001 "Concussion in Sport" international symposium are as follows:
- Concussion may be caused either by a direct blow to the head, face, neck, or elsewhere on the body with an “impulsive” force transmitted to the head.
- Concussion typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously.
- Concussion may result in neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than structural injury.
- Concussion results in a graded set of clinical syndromes that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course.
- Concussion is typically associated with grossly normal structural neuroimaging studies.
(Aubry et al, 2001).
As shown above, sports researchers in 2001 also used vague words to "define" concussion. In #1, they specified that a concussion must be caused by trauma that transmits an "impulsive" force to the head. At least they are saying that the head must be affected, which is more precise than the earlier AAN definition that didn't specify whether the trauma affected the head or not.
More recently, the "Zurich" consensus statement as of the 4th international conference on concussion in sport occured in 2012. (McCrory et al, 2013). The revised definition statement says (with italics denoting the new material):
- Concussion may be caused either by a direct blow to the head, face, neck, or elsewhere on the body with an “impulsive” force transmitted to the head.
- Concussion typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously. However in some cases, symptoms and signs may evolve over a number of minutes to hours.
- Concussion may result in neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than structural injury, and as such, no abnormality is seen on standard structural imaging studies.
- Concussion results in a graded set of clinical syndromes that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course. However, it is important to note that in some cases symptoms may be prolonged.
(McCrory et al, 2013)
The definition statement for concussion in 2012 was tightened from 2001 from Aubry et al above. This is good. They stated that "no abnormality is seen on standard structural neuroimaging studies". In other words, they took out the "typically associated" clause. They also tightened the onset in the new statement, "symptoms and signs may evolve over a number of minutes to hours". We presume that they meant to exclude "days", leaving out symptoms that appear a week later (for example).
With respect to what "impulsive means, Conidi (2015) distinguishes between "impact loading" and "impulse loading". Impact loading was defined by Conidi as a direct blow transmitted primarily through the center of mass of the head causing linear acceleration. He further considered impulse (inertial) loading caused by sudden movement of the brain relative to the skull that results in angular and rotational acceleration. Classical physics considers an "impulse" to be the integral of force, and has no particular connection to inertia. In signal processing, the "impulse" generally refers to a very short duration input, such as the Dirac delta function. Impact is another vague term. So, we have some imprecise words here that would better have been defined in a very precise way as is done in physics. What it seems to boil down to in the end, is that force is transmitted to the head, (and presumably the brain), and that the force be either linear or angular. As there are only two kinds of mechanical force -- linear or angular -- the 2001 definition boils down to requiring that force is transmitted to the head. It seems to us that the word "brain" should have been used, to eliminate the possibility of a nose-bleed or other superficial head injuries being designated a "concussion".
Conidi (2015) also stated that "At present there is no accepted threshold (i.e. angular and rotational) for concussion. Omaya and Gennarelli published a landmark study on cerebral concussion in 1974, and noted that translation (linear force) produced focal injuries such as contusions, while diffuse effects, including concussion and subdural hematoma were only produced when rotational loading was present. "
In criteria 2 of the Zurich Concussion in Sports statement from 2001 and 2012, they suggest that concussion "typically" results in the "rapid" onset of short-lived impairment of "neurological function". The "typically", "rapid", and "short term" qualifiers as well as the use of the term "neurological function" here make criterian 2 vague. We prefer the AAN definition that requires a change in mental status rather than "impairment of neurological function". Otherwise, by the sports criterian 2, an injury to a nerve in the big toe associated with an "impulsive" type force, might qualify as a concussion. We think the injury in concussion should be limited to the brain.
Criteria 3-4 are are improved in 2012, and are probably useful in medicolegal contexts.
In criterian 5 from 2001 (merged into item 3 of the 2012 statement), they also indicated that concussion is typically associated with normal structural imaging studies. In other words, a normal MRI and CT scan of the brain. Logically, one might both have a bleed of the brain as well as additional disruption of the brain due to "concussion". We think the "typically" word is justified here.
Whether or not a concussion occurred after in a "whiplash" type accident, where there was no or minimal force to the head, is often debated by personal injury attorneys. Considering the vagueness of the definitions adopted by the groups above, nearly anything (including feeling distressed after a ping-pong ball dropping on one's head) would qualify as a concussion. This moves the legal discussion into the territory of clinical judgement and out of the territory of science. In whiplash, there is certainly the potential for rotational acceleration, and thus could meet the criteria for "concussion". On the other hand, the neck is more vulnerable than the brain -- and it takes almost an order of magnitude more force to cause a significant brain injury than a neck injury (see whiplash page).
We prefer a more constrained definition of a concussion as a mental disturbance (including poor memory, slowed or otherwise disturbed thinking) which follows a direct impact of the head within 24 hours at the most, and that is without a new imaging abnormality. We realize that it fails in unusual situations such as the "shaken baby" syndrome, and some leeway must be provided. The obvious remaining difficulty with this narrower definition is that it depends on a subjective judgement (concerning memory or abnormal thinking), and thus is vulnerable to bias. Thus to conclude someone has a concussion, one must also accept that the individual is reporting their internal thought processes accurately. It has been our experience that frequently individuals involved in auto accidents are not clear about whether they were "dazed" or not, and in addition, the individuals mind can change later on. Frequently, the only unambiguous definition of impaired consciousness in these situations is unresponsiveness. This requires an observer, and if required, would exclude some situations (such as an unwitnessed fall) where no data is available.
Post concussion syndrome is often attributed to "Traumatic Brain Injury", or TBI, which is a general term for a head injury caused by trauma, affecting the brain. Again, there is looseness to this term. Exactly how "injured" do you have to be to collect money from litigation for "TBI". Is it enough to forget your cousin's phone # ? Does it require one standard deviation lower IQ testing ? We think this term should be either tightened up -- perhaps dividing it up into minimal, moderate, severe with hard criteria, or discarded.
One must differentiate "significant", or maybe "real" concussions from events that meet the literature's criteria (i.e. almost anything), but that no reasonable person would accept as being a cause impairment or disability. For example, one might be involved in a motor vehicle collision and not remember the second of impact.
Our general impression is that "significant" concussions are unlikely to be consequences of whiplash mechanism accidents, that are unaccompanied by significant cervical spine injury. We are also dubious that "significant" cognitive symptoms should persist for long periods of time after a head injury unaccompanied by a loss of consciousness. Not impossible, but uncommon.
Theories regarding the source of cognitive symptoms in concussion fall into several broad categories (Choe et al, 2012).
- Diffuse axonal injury
- metabolic impairment
- alterations in neural activation
- cerebral blood flow
Each theory has its advocates.
Signoretti et al(2011) suggested that "energetic metabolism disturbances caused by the initial mitochondrial dysfunction seem to be the main biochemical explanation for most postconcussion signs and symptoms".
Johnson et al (2013) suggested that diffuse axonal injury was one of the "most common and important pathological features of traumatic brain injury). McAllister et al (2014) compared concussed to nonconcussed athletes, and suggested that diffusion tensor imaging diffusivity on MRI correlates with both the magnitude of impact as well as neuropsychological measures. In most instances however, a pre-injury MRI with DTI is not available for comparison, making inference regarding the source of DTI changes difficult in individuals.
Len et al (2011) reviewed blood flow abnormalities post mild traumatic brain injury.
Some studies suggest that there is increased amyloid accumulation in individuals who have had brain injuries. This would suggest a link between Alzheimer's disease and cognitive disturbances after brain injury.
Chronic traumatic encephlopathy (CTE) is a pathological diagnosis (i.e. made at autopsy) in which a neurofibrillary protein (tau) is found deposited in the brain, in persons who have had repeated head injuries. CTE has been found most often in professional athletes who have experienced repetitive head impacts -- e.g. boxers and American football players. A 2015 study found CTE neuropathology in about 1/3 of former amateur contact sports athletes (Bieniek et al, 2015). This is frightening. It would seem to us that if one value's one's intellect, it is prudent to avoid contact sports with a risk of head injury.
Concussion diagnosis is a combination of screening for other diagnoses (like bleeding in the brain), and assessment of vulnerable brain systems such as thinking and balance.
Neuropsychological testing is the preferred method of assessing thinking. Recently, a short neuropsychological test called the "IMPACT" test has become widely available for sports concussions. It is much quicker (and cheaper) than the formal "neuropsych battery", and can be performed using a proctored computer. While designed for sports concussions, it is actually generally applicable to concussions of all causes. The Zurich statement suggested that neuropsychological testing would best be done by a "trained neuropsychologist". (McCrory, 2012), presumably as an alternative to online screeners such as the IMPACT test. This recommendation to us seems safe, but not very practical as it is not possible to have a trained neuropsychologist evaluate every individual who may have had a concussion. Furthermore, it is difficult to see how care would be substantially changed. We offer the IMPACT test in our dizzy practice, and we think it is valuable.
Regarding balance testing, moving platform posturography, ENG and rotatory chair testing all are useful. Posturography is the most sensitive of these three for concussion looking for nonspecific effects. ENG and rotatory chair testing are useful primarily to exclude ear damage.
All of these tests have the problem of detecting invalid tests. Athletes typically are eager to return to play, even though they may be mentally impaired. On the other hand, individuals who are hoping to benefit financially from their injury, such as persons in litigation or seeking disability compensation, may exaggerate their balance or cognitive deficits. Both the IMPACT test and the posturography test have methods suggested to detect invalid or "aphysiologic" patterns. These sorts of procedures are difficult to validate however.
It is common to encounter patients with concussion who have been seen by clinicians who claim that there are oculomotor abnormalities -- i.e. abnormal eye movements. For example, the "King-Devick" test has been used as a visual performance measure (Ventura et al, 2016). While this may be true up to 48 hours after a concussion, we are dubious that more than a very few patients have long term oculomotor deficits. We say this because individuals with very large structural lesions of the brain, generally become impossible to distinguish from normal after a few months. We are frankly dubious that concussion patients have objective visual disturbances as reported by Master et al (2016).
In any case, while dizziness and nausea symptoms accompanying the entity called "concussion" in the literature usually resolve over 6 weeks, cognitive symptoms and headaches may persist longer. The Mayo clinic (2015) suggests that 70-80% of persons who experience symptoms, no longer experience them 2 weeks later. Hoffer et al (2004) suggested that dizziness symptoms persisted an average of 39 weeks -- about 9 months, and that return to work usually occurred at about 16 weeks. Hoffer was reporting symptoms from military trauma rather than sports. In athletes, concussion symptoms resolve quickly -- within 2 weeks(d'Hemecourt, 2011). Of course, sports concussions usually involve a population of people who are otherwise very healthy, while military personnel may have less motivation to report recovery.
According to Chorney et al (2017), in "1,647 recorded sports-related concussions, with athletes reporting dizziness (68.2%), imbalance (35.8%), disorientation (31.4%), noise sensitivity (29.9%), and tinnitus (8.5%)." This is remarkably high number of symptoms. "Concussion symptoms resolved within 1 day (17.1%), within 2 to 7 days (50.0%), within 8 to 30 days (25.9%), or persisted over 1 month (7.0%). Return to participation occurred within 1 week (38.3%), within 1 month (53.0%), or over 1 month (8.7%)". Individuals with more symptoms, especially imbalance and dizziness, predicted longer duration and slower return. Thus it seems that only about 8% of college athletes have concussion symptoms persisting longer than a month.
Occasionally symptoms are permanent. Acording to Mayo clinic (2015), "1 in 5 people don't recover within seven to 10 days. Thats a huge population at risk". This seems a little vague to us. As noted above, in many cases, chronic symptoms post concussion are psychological in origin. Balance symptoms after concussion generally (i.e. 50% of the time) resolve by 10 days (Peterson et al, 2003). Nevertheless, there are many persons who have longer lasting symptoms (looks like about 9% from the paper above last longer than a month).
Our experience has been that balance symptoms post neck injury can take much longer to resolve.
The longer duration of symptoms is strongly correlated with psychiatric variables -- and in particular somatization (Nelson et al, 2016). It is possible that when health care workers suggest to their concussion patients in a compassionate way that they may have symptoms for months or years, they are prolonging the duration of the patient's impairment through suggestion.
There sometimes seems to be a perverse incentive for therapists to nurture patients symptoms which results in greater use of health care resources. Someone who goes back to work does not need to attend therapy sessions, while the person who is getting neck massages or psychotherapy sessions twice/week may be a source of income for the health care organization billing their insurance. We have encountered situations where compassionate and supportive psychotherapists encourage patients to "take control of their lives" and just stop working. This improves the quality of life for those who do not want to work, but it may create a group whose symptoms are nutured by the perverse incentives of the health care system. When there is litigation involved, examining every possible symptom as being potentially related to an injury, can also incentivize the patient to recognize and cherish trivial symptoms. The risk of compensating patients for entirely subjective symptoms is obvious.
In spite of all of the above, repeated concussions is associated with pathological change in the brain resembling Alzheimer's disease. The "dose" effect remains to be worked out, but it is possible to have permanent decline in one's intellect after concussion.
It is currently thought that there is a period of increased vulnerability to repeated injury following a concussion and that its duration is variable. (Giza et al, 2011) Accordingly, athletes with a concussion should not return to play on the same day.
Dolan et al (2011) put forth their recommendations for "retiring", an athlete from sports activities:
- Prolonged post-concussion symptom--note that in athletes, concussion symptoms commonly resolve in only 2 weeks -- much more quickly than the same injury outside of sports, (d'Hemecourt, 2011)
- three or more concussions in a single season
- two or more severe concussions in a single season
- decreased academic and athletic performance
- clinical relevant imaging abnormality.
- Pathologic abnormality such as Chiari, intracranial hemorrhage, clinically relevant imaging abnormality (such as a subdural)
- Diminished academic performance or cognitive performance
- Persistent prolonged post-concussion syndrome
- Decreased threshold for concussion
- Three or more major concussions
- Symptoms consistent with chronic traumatic encephalopathy
Protocol for returning athlete to sports (also from Doolan, 2011)
- No activity until asymptomatic
- Light activity at about 70% intensity until asymptomatic
- Sports-specific exercise until asymptomatic
- Full contact practice -- allow assessment of skills by coach
- Return to play
In the 2012 Zurich consensus statement (Mccrory et al, 2013), they state that "current published evidence evaluating the effect of rest following a sports-related concussion is sparse". They suggest that an "initial period of rest ... (24-48 hours) may be of benefit.
It is difficult for us to see a rationale for "cognitive rest", as is often suggested for concussion. In other words, we do not know of any reasonable physiological reason for those who have headaches, or who are confused after a head injury, should be withdrawn from all job and educational activity for long periods (i.e. months). The Zurich statement continues that "a sensible approach involves the gradual return to school and social activities .." This is very vague. It seems to us that they are leaving some room for different procedures, but are basically suggesting 1-2 days is reasonable.
Regarding evidence concerning rest, Brown et al (2014) reported that athletes who self-reported more cognitive activity after a concussion took longer to recover than those who reported less cognitive activity. Of course, self-report is vulnerable to bias. On the other hand, Thomas et al (2015) reported that patients aged 11-22 who were prescribed 5 days rest reported more daily postconcussive symptoms than patients who were prescribed 2 days rest with progressive return to activity. There was no difference in outcome between groups other than the more symptoms reported in the longer rest group.
Individuals that somaticize may be particularly vulnerable to the effect of practitioners that suggest that patients are sicker through longer periods of "cognitive rest". Root et al (2016) and Nelson et al (2016) both reported that patients with higher pre-injury somatization had higher concussion symptom scores over time. This would seem rather obvious -- persons who tend to imagine symptoms in other contexts also might imagine more symptoms after concussion.
It does seem reasonable to us that more sleep than usual might help the brain repair, and also reasonable that accomodations should be made for the injured persons impairment. On the other hand, clinical management procedures that eliminate the need for the injured individual to work or go to school obviously increase the potential for secondary gain in individuals who are not inclined to return to school or work. Furthermore the system of providing academic advantages (called accomodations) to students who have signed doctor's notes indicating that they had a concussion, provides an avenue for unscrupulous individuals to take advantage of the concussion care system. Given the subjective nature of almost all concussion symptoms, an individual who can provide positive answers to concussion questions, can game the system and do better in school than the person who does not know the "right" concussion answers.
Vision rehabilitation done under the supervision of optometrists is sometimes recommended after concussion. Like the situation with cognitive rest, it is difficult to see a rationale for extensive vision rehabilitation after concussion. Still, we think there is a place for these procedures in the "outliers" who are still not back to normal activities after a month or more and who have substantial vision complaints. A home protocol for the optometry type of vision rehabilitation can be found here.
Common sense would suggest that it is imprudent to return to a contact sport, if one wishes to minimize risk of adding more thinking disturbance. It would also suggest that sports such as boxing, where concussions are routine, are very likely to result in impaired thinking over time. We are puzzled why people expose themselves to the risk of being demented. While participating in activities where there is a substantial risk of being hit on the head over and over seems extremely unwise to the author of this page, the proper response of society is debatable. While we do legislate that seat belts should be worn when in a motor vehicle, we do not stop people from engaging in many dangerous activities such as driving cars, mountain climbing, or smoking tobacco. There is an assumption made that adults who participate in dangerous activities have the right to direct their own activities. On the other hand, society does have a mandate to protect its members from harm, and inviting concussion by participating in concussion seems very risky.
No medication has been established to speed recovery in concussion. Unfortunately, this includes commonly prescribed medications such as amantidine. They may have some place as placebos.
Medications that may help other aspects of concussion include:
- Sleep medications
- Mood altering medications
- Migraine medications (if an underlying migraine has been triggered).