Concussion

General

Occurs in a subset of patient with mild traumatic brain injury (mTBI).

It is considered “mild” because it is usually not life-threatening by itself.

While most victims recover completely, effects of concussion can be serious and lifelong.

Most data from concussion in sports

There has been a move away from grading scales for concussion, and the current recommendation is for the diagnosis to be determined in the judgment of an experienced examiner with the assistance of various assessment tools, ideally with the availability of pre-injury baseline metrics for comparison.

Concussion can occur without a direct blow to the head, e.g. with violent shaking of the torso and head.

Concussion symptoms can present soon after an insult or in a delayed fashion.

The subject may not be aware that they have sustained a concussion.

Definition

There is no universally accepted definition for concussion.

Opinions differ e.g. whether there is any long-term effect of concussion or if that necessitates a different diagnosis.

Of the many contemporary definitions, most key elements are contained in the Concussion in Sport Group 2012 consensus definition summarized below.

Definition

A form of mild head injury where there is an alteration of brain function due to blunt trauma.
Without identifiable abnormality in standard structural imaging.

The Concussion in Sport Group elaborates on this definition as follows:

Results in a graded set of neurological symptoms that may or may not involve loss of consciousness (LOC).
Symptom onset is usually rapid, short-lived and resolves spontaneously.

Transient deficits in balance, coordination, memory/cognition, strength, or alertness.

May result in neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury.
Resolution of the clinical and cognitive features typically follows a sequential course.

The United States (US) Centers for Disease Control and Prevention (CDC) for both mTBI/concussion as a

Transient neurological disturbance
Caused by

Rapid linear and/ or
Rotational acceleration and deceleration forces

Resulting in a disruption in cerebral structural or vascular physiology.

The American Congress of Rehabilitation Medicine (ACRM) defines mTBI by one or more of the following:

Loss of consciousness (LOC),
Loss of memory immediately before or after the incident,
Alteration in

Mental state,
Focal neurologic deficit that may or may not be transient.

The U.S. Department of Veterans Affairs and Department of Defense (VA/ DOD) provide similar clinical guidelines while specifying that presence of intracranial lesions classify the patient with, at minimum, moderate TBI.

Epidemiology

Incidence: 1.6–3.8 million concussions occur per year in the United States from sports and recreational activities.

75% of TBI patients are classified as ‘mild’

An underestimate as most of these patients do not present to the ED.
50% of concussions go unreported.

After mild head injury

7.1% prevalence of severe intracranial injury

Absence of Canadian CT Head Rule features lowers severe injury probability to 0.31%
Absence of New Orleans Criteria findings lowers severe injury probability to 0.61%

0.9% prevalence of injuries leading to death or requiring neurosurgical intervention

Concussion genetics

There is no clear evidence to support a genetic predisposition to concussion.

Apolipoprotein E4, Apo E G-219 T promoter and tau exon 6 have been studied in small retrospective and prospective trials without definitive association.

Concussion versus mTBI

Concussion	Mild TBI
A subcategory of mTBI
No abnormalities on imaging	Abnormalities present in imaging
	Part of spectrum of TBI based on GCS
Evaluated directly after injury	Evaluated 6hrs after injury

Risk factors

History of previous concussion increases risk for further concussion

Being involved in an accident: bicyclist, pedestrian or motor vehicle collision

Combat soldier

Victim of physical abuse

Falling (especially paediatrics or elderly)

Sports

Males are diagnosed with sports-related concussion more than females
Due to increased number of male participation in sports studied) but females have a higher risk overall when compared to males who play in the same sport (i.e., soccer and basketball)
Participating in sports with high risk of concussion:

American football
Australian rugby
Ice hockey
Boxing
Soccer is the highest risk for females

BMI> 27kg/m2 and less than 3 hours of training per week increase risk of sports-related concussion
For contrast, sports with the lowest risk of concussion:

Baseball
Softball
Volleyball
Gymnastics

Grading

Multiple concussion grading scales currently exist without definitive consensus.

Due to

Lack of evidence in imaging studies, perhaps due to lack of sensitivity, is a challenge to the clinical diagnosis of mTBI/ concussion.

Recent efforts in utilization of magnetic resonance imaging (MRI), including MR Spectroscopy, for TBI diagnosis has shown promise in identifying a subset of patients with structural changes post- mTBI.

Diagnosis

Triggers

Findings suggestive of concussion are listed in

Physical	Cognitive	Emotional	Sleep
- Vacant stare or befuddled expression - Dazed or stunned - headache or pressure sensation in the head - Nausea - Vomiting - Fatigue - "Seeing stars" - Photophobia - Phonophobia - Ringing in the ears (tinnitus) - Delayed verbal & motor responses: difficulty focusing attention - Inability to perform normal activities - Speech alterations: slurred or incoherent, disjointed or incomprehensible statements - Incoordination stumbling - Any period of LOC, paralytic coma, unresponsiveness to stimuli	- Feeling like being in a fog - Slow to answer questions or follow instructions - Easy distractibility - Disorientation (e.g. walking in the wrong direction) - Unaware of date, time or place - Memory deficits: amnesia for the event - Repeatedly asking same question that has been answered	- Exaggerated emotionality: inappropriate crying - Distraught appearance - Irritability - Nervousness	- Drowsiness - Insomnia - Hypersomnia - Difficulty falling asleep or staying asleep

In pre-verbal children

Listlessness and easy fatigability, change in sleeping patterns
Irritability
Appearing dazed
Balance impairment
Excessive crying
Change in eating habits
Loss of interest in favourite toys

Acute pathophysiology

A sudden change in momentum of the head → causing mechanical stretching or compression of the partially tethered brain against the cranial vault → initiating diffuse neuronal firing, discharge, and axonal shearing.

Biomechanical force results in

Unregulated ionic (K+ efflux, Na+/Ca2+ influx) flux

Unrestricted hyperacute glutamate release from sublethal mechanoporation of lipid membranes at the cellular level.

Inc. glucose utilization and hyperglycolysis sustain the indiscriminate neuronal depolarization and firing

Levels of glutamate rise after concussion and the brain enters a hyperglycotic and hypermetabolic state which may persist for 7-10 days after injury (i.e. the period after which the vast majority of patients are symptom free again),

This triggers voltage/ligand gated ion channels causing a cortical spreading depression-like state that is thought to be the substrate behind immediate post concussive symptoms.

Diffuse neuronal suppression (e.g. spreading depression) is characterized by

Near- complete breakdown of ion gradients,
Loss of electrical activity,
Vasoconstriction → infarct growth + initiate cascades leading to apoptotic cell death

Subsequently, ATP-dependent ionic pumps are extensively upregulated to restore cellular homeostasis causing widespread intracellular energy reserve depletion and an increase in ADP.

Cells then pass into a state of impaired metabolism (energy crisis) that can last up to 7–10 days and may be associated with alterations in CBF.

This impaired metabolic state is associated with vulnerability to repeat injury as well as behavioral and spatial learning impairments.

Cells also undergo cytoskeletal damage, axonal dysfunction, and altered neurotransmission with the as yet unproven impression that each of these pathologic processes correlate with a separate symptomology

Physiologic perturbations and their proposed corresponding symptomatology

Perturbation	Symptom
Ionic influx →	Migraine headache, photophobia, phonophobia
Energy crisis →	Vulnerability to second injury
Axonal injury →	Impaired cognition, slowed processing, slowed reaction time
Impaired neurotransmission →	Impaired cognition, slowed processing, slowed reaction time
Protease activation, altered cytoskeletal proteins, cell death →	Chronic atrophy, persistent impairments

Later stages

Physiological disturbances persist after mTBI/ concussion and increase susceptibility to further injury.

After the initial hypermetabolism, hypometabolism and reduction in CBF may persist for up to 4 weeks.
Additional excitation (e.g. direct cortical stimulation or recurrent concussion) prolongs cellular recovery and induced cell death due to inability to match increased metabolic demand in part due to decoupling between neuronal activation and CBF after concussion.
Dependent on the severity of impact, intracellular accumulation of Ca2+ also remains elevated, which impairs mitochondrial metabolism and initiates programmed cell death.
In the surviving cells, reduction in cellular plasticity is associated with neurotransmission changes, particularly in subunits of NMDA receptors.
Make the brain more susceptible to a second impact as altered cerebral autoregulation may produce much more severe sequelae (malignant cerebral edema resistant to treatment and almost certainly fatal).

Neurocognitive deficits tend to occur with minimal detectable pathology and can resolve over time.

General diagnostic information

Clinical evaluation

No physiologic measure has been identified to detect concussion.

Diagnosis relies on:

Self-reporting of abnormal function (symptoms),
Observed physiologic abnormalities (signs) including assessment of cognitive dysfunction, sometimes with the assistance of imaging tests to rule out a structural substrate.

A clinical diagnosis of concussion is made if there are abnormal findings in balance, coordination, memory/cognition, strength, reaction speed, or alertness after a traumatic insult to the head.

Findings include

Confusion,
Amnesia,
Headache,
Drowsiness
LOC

LOC is not a requirement for diagnosing concussion, patients themselves may be unaware whether or not they experienced LOC

Approach

Take a concussion specific symptom survey including inquiries about: H/A, N/V, light sensitivity, tinnitus, feeling like being in a fog, sleep disturbances

History of diagnoses that might have an impact on the assessment or on a current concussion

History of prior concussions
H/A history
ADD/HD
Learning disabilities
Medications (prescribed and other) that might affect alertness or cognition

Include a concussion specific neuro exam

Check orientation
Assess for amnesia and impaired verbal memory
Balance:

Romberg test (look for significant sway or breaking stance),
Single leg stance

Eye movements:

Optokinetic nystagmus (OKN),
Smooth pursuit

Simultaneous task performance: e.g. snap fingers while walking
Include assessment aides (“sideline tools”) as appropriate

Assessment aids

Diagnosis may be aided by concussion assessment tools such as the SCAT3, ImPACT™.

❌ No test has shown high validity on independent testing, and no test should be used as the sole method of diagnosing concussion or for determining suitability for return to play.
Athletes have also learned to “game” some baseline tests to avoid removal from play after possible concussion

SCAT3 (Sports Concussion Assessment Tool – 3rd Edition):

Derived from the 2012 Zurich Conference.
The SCAT has become the most commonly used standardized tool for sideline assessment of sport concussion.
The sensitivity and specificity of concussion assessment tools change over the course of a concussion so a tool designed for sideline use is not appropriate for office use
SCAT3™ is a trademarked tool developed by the Concussion in Sports Group for use only by medical professionals for assessing sports-related concussion
It can be found at http://bjsm.bmj.com/content/47/5/259.full.pdf
To be used in athletes of 13 years or older (for 12 and younger, use Child SCAT313)
Is a multimodal assessment tool with 8 sections that includes self-reported symptoms and evaluation of functional domains such as cognition, memory, balance, gait and motor skills
Takes 8–10min to administer
A “normal” SCAT3 does not rule out concussion
It has not been validated

Other types of sports concussion assessment tools (many can be viewed on YouTube):

Neurocognitive testing (may take up to 20 minutes to administer)
SAC (Standardized Assessment of Concussion): a neurocognitive test that includes tests of immediate memory, delayed recall, serial 7’s, digit span
ImPACT™ (Immediate Post-Concussion Assessment and Cognitive Testing):

A widely used commercially produced computer test (https://www.impacttest.com).
Independent validation studies have yielded conflicting results and results can diverge from observations

PCSS (Post-Concussive Symptom Scale)
CSI (Concussion Symptom Inventory)
BESS (Balance Error Scoring System):

The subject stands in each of various standardized positions for 20 seconds each, and the number of errors are recorded (breaking stance, opening eyes, taking hands off hip…).

SOT (Sensory Organization Test)
“Concussion Quick Check” app for mobile devices produced by the AAN
King-Devick eye movement testing:

Only takes 2–3 minutes to administer.
On printed cards or tablet computer (http://kingdevicktest.com/for-concussions/)

Formal neuropsychological testing:

It is recommended that this be reserved for patients with prolonged cognitive symptoms

Concussion serum biomarkers:

No moiety has been identified that can reliably diagnose concussion on serum or saliva testing.
Neuron-specific enolase,

Another study involving pediatric patients with mTBI showed no difference in levels of neuron-specific enolase or S100B in asymptomatic and symptomatic children.

S100,

Has only a 33.3% sensitivity for post concussive symptoms
93% sensitivity for an Extended Glasgow Outcome Scale <5 at 1 month.

Cleaved tau protein

A prospective study found no significant correlation between cleaved tau protein and postconcussive syndrome in patients with mTBI16

On-site/sideline evaluation

Any individual suspected of having a concussion should be removed from the activity (for athletes, stopped from playing) and assessed by a licensed healthcare provider trained in the evaluation and management of concussions with attention to excluding a cervical spine injury.

If no provider is available, return to the activity is not permitted and urgent referral to a physician should be arranged.
After ruling out emergency issues, the provider should perform a concussion assessment (may employ standardized tools such as SCAT3™ or other methodologies).
The patient should not be left alone, and serial evaluations for signs of deterioration should be made over the following few hours. For return to play guidelines, see below

Indications for imaging or other diagnostic testing

Imaging in concussion is typically used to rule out more serious traumatic injuries.

Most predictive features of severe intracranial injury on CT:

Skull fracture signs
GCS score 13/15
Multiple vomiting episodes
Decline in GCS
Pedestrians struck by vehicles

Indications for CT or MRI imaging:

General

Adults with or without LOC or amnesia

Focal neurologic deficit
GCS<15
Severe headache
Coagulopathy
Vomiting
Age>65 years old
Seizures

Peds

LOC> 60 secs
Evidence of skull fracture
Focal neurologic deficit

Other imaging studies:

Diffusion Tensor Imaging (DTI):

Used to quantify white matter tract integrity throughout the brain with 4 types of analysis methods

Voxel analysis
Region of interest (ROI) analysis
Histogram analysis
Tractography.

There is no strong consensus regarding the best method for utilizing DTI for diagnosis or prognosis in the individual patient but multiple studies have shown group differences in DTI parameters between mTBI and control patients.

Functional MRI (fMRI):

Consists of 2 types

Task-based fMRI
Resting state fMRI)

Based on the blood oxygen level dependent (BOLD) effect, in which specialized MRI sequences measure/ detect regions of increased oxygen rich blood flow to areas of upregulated neuronal activity.

Both task-based and resting state fMRI modalities have shown group differences between mTBI and control patients (specifically in frontal lobe dysfunction), but further studies need to be completed on both a single time point and longitudinal basis before these techniques can be widely adopted for individual diagnosis and therapeutic guidance.

Imaging studies that are currently used primarily in concussion research:

Positron emission tomography (PET),

Patients with GCS score 13– 15 present with acute and subacute glucose metabolic disturbances on positron emission topography (PET) and require careful assessment for postconcussive risks

Single photon emission CT (CT-SPECT),

MR-spectroscopy (MRS).

Quantitative EEG (QEEG)

Is another research tool for concussion that assesses brain activity, patterns of cortical activation and neuronal networks.

The concept is that post-concussion studies are compared to baseline.

Currently undergoing proof of concept evaluation.

Postconcussive EEG was excitatory and epileptiform in nature comparable to generalized seizures.

Sensory evoked potential was completely lost

Cerebral microdialysis

Immediately following mTBI/ concussion contains elevated levels of excitatory amino acids and ionic fluxes throughout hemispheric regions, the hippocampus, and the brainstem

Specifically, there is a sharp increase of extracellular K+ through voltage- gated channels.

Prevention of concussion

Helmet/head gear

AAN guidelines conclude that protective headgear in rugby is “highly probable” to decrease the incidence of concussion.

However, the AMSSM (American Medical Society for Sports Medicine) hold that there is no clear evidence that soft or hard helmets reduce the severity or incidence of concussion (in football, lacrosse, hockey, soccer, and rugby).

Biomechanical studies have shown helmets reduced impact forces on the brain

But this has not translated into concussion prevention.

There is insufficient data to determine whether one type of football helmet protects better than another in preventing concussions

No significant evidence that a mouthpiece protects against concussion

Management of concussion and post-concussion syndrome

Return to Play (RTP)

No system of return to play (RTP) guidelines has been rigorously tested and proven to be scientifically sound

After sustaining a concussion,

Athletes should not return to play the same day.
❌ a symptomatic player should not return to competition.
If there is any uncertainty: “When in doubt, sit them out”

Evaluation should proceed in a stepwise fashion.

A player needs to be completely asymptomatic both at rest and with provocative exercise before full clearance is given.
Each player’s progression should be individualized.
Generally, the athlete’s level of activity should be gradually increased over 24-hour increments from light aerobic activity to full contact practice.
The athlete is evaluated after each progression.
If post concussive symptoms occur then the player is dropped back to the previous asymptomatic level and then allowed another attempt at progression after a 24-hour rest period.
80–90% of concussions resolve within 7–10 days.
This recovery time may be longer for children or adolescents.

The CDC endorses a graded 5-step return to play for student athletes

Step	Description
Baseline	Athlete is back to regular school activities without symptoms
1	Light aerobic activity: only to increase heart rate for 5-10 minutes. No weight lifting
2	Moderate activity: increase heart rate with body or head movement. May include moderate intensity weight training (less time and intensity than their typical routine)
3	Heavy, non-contact activity: may include running, high-intensity stationary biking, regular weight training, non-contact sports-specific drills
4	Practice & full contact: in controlled practice
5	Competition

The athlete should move to the next step only if they have no new symptoms.
If symptoms return or new ones develop, then medical attention should be sought and after clearance the student can return to the previous step.

Contraindications for return to play:

Persistent post concussion symptoms
Permanent CNS sequelae from head injury (e.g. organic dementia, hemiplegia, homonymous hemianopsia)
Hydrocephalus
Spontaneous SAH from any cause
Symptomatic (neurologic or pain producing) abnormalities about the foramen magnum (e.g. Chiari malformation)

Management of post-concussive syndrome

Complicated topic

Because of potential for litigation
The symptoms are often vague and nonspecific
There may be no objective findings to corroborate subjective symptoms.

Most symptoms from concussion resolve within 7–10 days and do not require treatment.

The most common exception to this is posttraumatic headache, the most common subtype being acute posttraumatic migraine.

Typical symptoms include: H/A, dizziness, insomnia, exercise intolerance, depression, irritability, anxiety, memory loss, difficulty concentrating, fatigue, light or noise hypersensitivity.

Patients with protracted symptoms may require more directed treatment.

Psychological and neuropsychological involvement is often employed
Pharmacologic treatment: there are no evidence-based studies of the utility of medications for post-concussive symptoms (aside from H/A)
Intractable headaches: occurs in ≈ 15% of concussions

Expert neurology consultation is usually required for difficult-to-control headaches
The first line drugs are Over-the-counter medicine
Triptans are usually employed for non responders
Third line drugs include Ketorolac or DHE-45 (dihydroergotamine)
Steroids may be beneficial for some
Avoid: narcotics, butalbital/caffeine preparations (Fioricet, Esgic…), beta blockers, and calcium channel blockers