The American Academy of Neurology (AAN)—an association of more than 22,500 neurologists and neuroscience professionals dedicated to providing the best possible care for patients with neurological disorders—is an advocate for policy measures that promote high quality, safe care of individuals participating in contact sports.
Concussion is a common consequence of trauma to the head in contact sports, estimated by the Centers for Disease Control and Prevention to occur three million times in the United States each year. Among people aged 15 to 24 years, sports are now second only to motor vehicle accidents as the leading cause of traumatic brain injury. While the majority of concussions are self-limited injuries, catastrophic results can occur and the long-term effects of multiple concussions are unknown.
Members of the AAN specialize in treating disorders of the brain and nervous system, and some members have particular interest and experience caring for athletes and are best qualified to develop and disseminate guidelines for managing athletes with sports-related concussion. Based on the clinical experience of these experts, the AAN supports the implementation of policy that supports the following recommendations:
Recommendations
- Any athlete who is suspected to have suffered a concussion should be removed from participation until he or she is evaluated by a physician with training in the evaluation and management of sports concussions
- No athlete should be allowed to participate in sports if he or she is still experiencing symptoms from a concussion.
- Following a concussion, a neurologist or physician with proper training should be consulted prior to clearing the athlete for return to participation.
- A certified athletic trainer should be present at all sporting events, including practices, where athletes are at risk for concussion.
- Education efforts should be maximized to improve the understanding of concussion by all athletes, parents, and coaches.
Position Statement History
Approved by the AAN Sports Neurology Section, Practice Committee, and Board of Directors
October 2010 (AAN Policy 2010-36).
One of the issues I see in head trauma that is less fully discussed is the
impact on the sense of smell. In TBI some people report changes in the
taste of food or the sense of smell, and when this is closely investigated
they have had damage to the connections between the olfactory bulb of the
limbic system under the base of the frontal lobe, and the sensory input from
the nose through the boney base of the skull (cribiform plate). These
fragile connections can be torn, and the unfortunate permanence of the loss
is never good news to have to deliver.
As a symptom, this sensory loss points to the severity of the TBI, and it
immediately makes the case something other than a mild traumatic brain
injury, as the effect is not mild.
The loss of sense of smell is not something that has an EEG signature,
though often the severity of the TBI will have caused some cortical issue,
which may be seen as a temporary loss of rhythmic faster content (see
previous postings for the spectral impact of gray matter injury and the
time-course for those changes).
The new American Academy Of Neurology paper suggests that in MOST mild
traumatic brain injuries there is no long term effect. This does not speak
to the cases that look mild until they looked with better imaging technology
than human sight, like CT scans or MRI to see bleeding (see the post of the
paper regarding my father’s mild TBI and large subdural hematoma removal),
or better clinical workup which can reveal things like the loss of sense of
smell associated with the TBI. The circular logic of changing the
definitional diagnosis of a case as “mild TBI” as soon as a “real” finding
is identified to a TBI (note the lack of the term “mild” now?) has never
seemed like a real good clinical practice, but it is the current situation,
given the pre-defined nature of MTBI as being “benign”.
If the MTBI were really benign, then a series of them should also be
benign… and this logical fallacy reveals the difficulty at the heart of
the AAN position on MTBI. A series of these MTBI events is known to cause
an exponential increase in the likelihood of seeing a finding which is not
normal.
Repetitive TBIs have a developing literature showing increased levels of a
substance “Tau” with repeated injury, which is much like the amyloid plaque
of Alzheimer’s Dementia.
The AAN position on this is obviously undergoing an acute change, and even
more change is expected, since the neuroscience is getting better and as the
politics of evaluation of the MTBI in court starts to dissolve with the use
of better neuroscience tools, including the ERP and the EEG/qEEG.
The failure of MTBI discriminants to be both sensitive and specific should
not discourage professionals from using EEG and ERP to characterize their
client’s brain function, as these tools can and do show a head trauma’s
impact on brain function, and without the discriminant, can often get
admitted into court along with good neurocognitive testing as valid evidence
of brain function/dysfunction. Even in the absence of litigation or severe
findings (like a subdural), the data can help direct neuromodulatory
treatment options such as Neurofeedback to help in thee remediation.
I personally prefer the path of remediation to that of diagnostic
specificity and litigation, and find the EEG and ERP invaluable in
optimizing the design of an individual’s remediation.
Jay