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Tracey A. Littrell, BA, DC, DACBR, DACO, CCSP

www.littrellradiology.com

� � http://youtu.be/yyRBlSAfb_k

� CNN Dr. Sanjay Gupta

� http://youtu.be/wb6Bm5skuBA � Zachary Lystedt

� http://youtu.be/f0xJT53SZqQ � Preston Plevretes

� Chiropractors can play a key role in helping to prevent mild traumatic brain injury (mTBI) and in identifying, diagnosing, and managing mTBI when it does occur

� Chiropractors can improve patient outcomes when mTBI is suspected or diagnosed by implementing early management and appropriate referral

� mTBI symptoms can appear mild, but can lead to significant, life-long impairment affecting physical, cognitive, and psychological functioning

� Appropriate diagnosis, referral, and patient education are critical for helping patients with mTBI achieve optimal recovery and to reduce significant sequelae

What is our role? �

� Concussion and mTBI are terms used interchangeably � mTBI is a complex pathophysiologic process affecting

the brain, induced by traumatic biomechanical forces secondary to direct or indirect forces to the head

� mTBI is caused by a blow or jolt to the head or body that disrupts brain function

� Typically, neuroimaging reveals no pathological findings

Concussion Defined

� � The consensus statement of the fourth and latest

international conference in Zurich, held in November 2012, defines concussion as “a complex pathophysiological process affecting the brain, induced by traumatic biomechanical direct or indirect forces with rapid onset of short-lived symptoms and impairments, largely functional, with spontaneous resolution (in most cases) and normal neuroimaging studies.”

Zurich Consensus Statement

� � mTBI may demonstrate a constellation of physical,

cognitive, emotional, and/or sleep-related symptoms � mTBI may or MAY NOT involve a loss of

consciousness � The duration of mTBI symptoms is highly variable—

minutes, days, weeks, or months

mTBI

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� � Approximately 75-90% of the 1.4 million TBI-related

deaths, hospitalizations, and ER visits each year are mTBIs

� Approximately 1.6-3.8 million sports and recreation-related TBIs occur in the US each year—most are not treated in a hospital or ER � Why? Athletes vs non-athletes?

� Direct and indirect health care costs are an estimated $12 billion per year in the US

mTBI Significance �

� Falls � Motor vehicle accidents � Unintentionally being struck by or against something � Assaults � Sports

Leading causes of mTBI

� � Infants and children (under 4) � Children and young adults (5-25) � Older adults (75-older)

Highest Risk Groups �

� Unlike severe TBIs which may result in structural injury to the brain, mTBIs alter brain function by causing dysfunctional brain metabolism

� Current understanding of mTBI focuses on neuronal dysfunction involving a cascade of ionic, metabolic, and physiological events

Neuropathophysiology

� �  In the adult, as little as 80gs (g-force) of translation acceleration

may be enough to begin the biochemical change �  For perspective, one study documented the average translation

force for over 11,000 non-injurious collegiate-level football impacts to be 20.1g

�  Jogging or jumping jacks result in about 5 gs; heading a soccer ball causes about 40 gs

�  The concussive force causes either a collision between the brain and skull or a strain to the neurological tissue and/or vasculature

�  The force is hypothesized to cause the symptoms of concussion through a cascading series of events that can broadly be summarized as “rapid neuronal depolarization, release of excitatory neurotransmitters, ionic shifts, altered glucose metabolism and cerebral blood flow, and altered axonal function.”

Forces Required �

� An impact of sufficient force causes glutamate and other excitatory neurotransmitters to attach to N-methyl-D-aspartate receptors, or NMDA receptors

� This causes a rapid ion shift across the cell membrane; within the cell, the loss of potassium and the entry of calcium forces up-regulation of the sodium-potassium pumps in an attempt to return the cell to its normal resting membrane potential

� The sodium-potassium pumps rid the supply of adenosine triphosphate or ATP, which then triggers hyperglycolysis

� Because the potassium outside the cell continues to rise, neuronal depolarization continues, and the excitatory neurotransmitters are discharged, resulting in widespread neurotransmission and more glucose consumption to the point of glucose deficit

Pathophysiology

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� � Ultimately this cascade results in reduced cerebral

blood flow at a critical stage when demand is high � The cycle causes calcium accumulation in the

mitochondria and it causes ATP deficits, which rob the energy from the cell, prompting further glycolysis

� The energy required for this process produces lactic acid, which the cell cannot metabolize in this weakened state

� As lactic acid levels rise, the pH of the cell decreases, causing cellular acidosis, which then results in cell membrane damage and permeability of the blood-brain-barrier, causing cerebral edema

Pathophysiology �

�  Intracellular magnesium, which is necessary for ATP production, protein synthesis, and cell membrane integrity, is also affected by this cascade

� As magnesium is depleted, ATP production is reduced, protein synthesis ceases, the cell membrane is weakened, and calcium accumulates

� All of these events combine to weaken the cellular membrane, causing it to leak and causing cerebral edema

� At this point, because the reserve stores of the brain have been depleted, the brain is at its most vulnerable state, should additional trauma, or even overstimulation, occur

Pathophysiology

� � A rare condition known as second impact syndrome

(SIS) can occur, especially in adolescents who have sustained two minor impacts in close proximity

� It is hypothesized that these closely occurring injuries can result in a catastrophic increase in intracranial pressure due to dysfunction of autoregulation of the cerebrovascular system

� Identifying concussions in order to allow full neurologic recovery is critical to avoid further injury and to facilitate prudent return-to-play (RTP) decisions

Second Impact Syndrome �

� Beyond the cellular membrane, concussions can stretch and shear the white matter of the brain and axons, called Diffuse Axonal Injury or DAI

� This injury may cause enough hemorrhage to be seen with advanced imaging procedures

� DAI occurs most commonly in the corpus callosum, the brain stem, and the frontal hemispheres

� The frontal and temporal lobes, cerebral cortex, superior cerebral peduncles, basal ganglia, thalamus, and deep hemispheric nuclei also demonstrate DAI changes

Pathophysiology

� � Most DAI injuries occur at the junction of the white and

grey matter, probably because of the density differences between the adjoining tissues

� All three grades of DAI severity include widespread axonal damage

� Grade I DAI has no focal neurological deficits � Grade II DAI demonstrates focal deficits, often of the

corpus callosum � Grade III DAI has focal deficits and rostral brain stem

injury �  These injuries are potentially devastating and currently there

are no specific treatment approaches beyond stabilization of the patient and management of intracranial pressure

Pathophysiology �

� Diffuse amyloid plaques appear within six days in more than 30% of concussion sufferers

� Beta-amyloid deposits occur throughout the brain after acute traumatic stress, such as cerebral ischemia, increased intracranial pressure, cerebral contusions, DAI, or cerebral edema

� Beta-amyloid derives from amyloid precursor protein (APP), which normally functions to protect the cell from hypoglycemia, but is abnormally processed with TBI, resulting in the Beta-amyloid deposition

�  In-vivo studies have correlated Beta-amyloid in Alzheimer disease, a finding that prompts the correlation of beta-amyloid deposition and cognitive impairment in TBI patients

Pathophysiology

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� � Other degenerative neurological diseases have been

associated with traumatic brain injury, like Parkinson disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease)

� Repetitive concussions and even sub-concussive brain traumas have been shown to be primary risk factors for developing the progressive neurodegenerative disease Chronic Traumatic Encephalopathy and the motor neuron disease variation called Chronic Traumatic Encephalomyelopathy

� Beta-amyloid deposits are found in 40-45% of patients with CTE, in contrast to the extensive deposition that is seen in Alzheimer Disease

Pathophysiology �

� Thus far, one retrospective study found a prevalence of Alzheimer Disease on autopsy in patients with histories of traumatic brain injury

� Beta-amyloid deposition and phosphorylation of a protein called Tau, may be the cause

� Chronic Traumatic Encephalopathy, or CTE, is a progressive neurodegenerative process caused by repeated concussive and subconcussive forces

� The symptoms of CTE are progressive memory loss, deterioration of executive functioning, mood and behavior changes, including depression, impulsiveness, anger, irritability, aggression, and suicidal ideation; Parkinsonian-like gait changes; and, eventually, dementia

� After CTE starts, the mean survival time is 18 years after symptom onset

Pathophysiology

� � Chronic Traumatic Encephalopathy is marked by Tau

deposition � Tau proteins are found in neurons and they normally

serve to stabilize microtubules � In CTE, higher numbers of neurofibrillary tangles,

neuropil threads, and glial tangles are found � The main protein of neurofibrillary tangles is the Tau

protein � CTE is similar microscopically to Alzheimer Disease

and other chronic neurodegenerative disorders

Pathophysiology �

� Though repetitive head trauma is required for CTE, it is not enough by itself to cause the cascade of neuropathological changes

� The apolipoprotein E gene on chromosome 19 is the primary genetic source of late-onset Alzheimer Disease

� The gene has 3 allele variants and it is the apolipoprotein E 4 variant that increases the risks for both Alzheimer Disease and may increase the risk for CTE, even in patients with only subconcussive head trauma histories and no reported concussion incidences

Pathophysiology

� � http://www.cnn.com/2012/01/27/health/big-hits-

broken-dreams-brain-bank

Am J Geriatr Psychiatry. 2013 Feb;21(2):138-44. doi: 10.1016/j.jagp.2012.11.019. Epub 2013 Jan 22. PET Scanning of Brain Tau in Retired National Football League Players: Preliminary Findings. Small GW, Kepe V, Siddarth P, Ercoli LM, Merrill DA, Donoghue N, Bookheimer SY, Martinez J, Omalu B, Bailes J, Barrio JR. Abstract OBJECTIVE: Mild traumatic brain injury due to contact sports may cause chronic behavioral, mood, and cognitive disturbances associated with pathological deposition of tau protein found at brain autopsy. To explore whether brain tau deposits can be detected in living retired players, we used positron emission tomography (PET) scans after intravenous injections of 2-(1-{6-[(2-[F-18]fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene)malononitrile (FDDNP). METHODS: Five retired National Football League players (age range: 45 to 73 years) with histories of mood and cognitive symptoms received neuropsychiatric evaluations and FDDNP-PET. PET signals in subcortical (caudate, putamen, thalamus, subthalamus, midbrain, cerebellar white matter) and cortical (amygdala, frontal, parietal, posterior cingulate, medial and lateral temporal) regions were compared with those of five male controls of comparable age, education, and body mass index. RESULTS: FDDNP signals were higher in players compared with controls in all subcortical regions and the amygdala, areas that produce tau deposits following trauma. CONCLUSIONS: The small sample size and lack of autopsy confirmation warrant larger, more definitive studies, but if future research confirms these initial findings, FDDNP-PET may offer a means for premorbid identification of neurodegeneration in contact-sports athletes. Copyright © 2013 American Association for Geriatric Psychiatry. Published by Elsevier Inc. All rights reserved.

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� �  Symptoms of mTBI are challenging and non-specific and

are common to other health conditions �  Headache syndromes, PTSD, depression

� The onset of symptoms may occur days or weeks after the initial injury

� The National Collegiate Athletic Association Concussion study showed that most athletes who suffered a concussion had resolution of symptoms and cognitive impairments resolve within 7 days and balance deficits resolve within 5 days

� This finding is consistent with other studies demonstrating that concussion sufferers usually experience symptom resolution within a few weeks or months, but for some, symptoms can last for long periods of time and can even result in permanent disability

Signs and Symptoms �

� Headache � Nausea � Vomiting � Balance disturbances � Dizziness � Visual disturbances �  Fatigue �  Sensitivity to light (photophobia) �  Sensitivity to noise � Numbness/tingling � Dazed or stunned

Physical Symptoms

� � Feeling “foggy” � Feeling slowed down � Difficulty concentrating � Difficulty remembering � Forgetful of recent information or conversations � Confused about recent events � Answers questions slowly � Repeats questions

Cognitive Symptoms �

� Irritability � Sadness � Emotional lability � Nervousness

Emotional Symptoms

� � Drowsiness � Sleeping more than usual � Sleeping less than usual � Trouble falling asleep

Sleep Symptoms �

� http://www.cdc.gov/concussion/HeadsUp/physicians_tool_kit.html

� The Acute Concussion Evaluation (ACE) is used for

the initial evaluation and diagnosis of patients � The ACE can be used for serial evaluation of

symptoms � The ACE consists of three components

� Characteristics of the injury � Types and severity of the symptoms � Risk factors that may cause protracted recovery periods

Systematic Assessment

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� � High speed activities (MVA, bike crashes, skateboarding) �  Sports and recreation activities �  Falls, especially from heights �  Suspected child physical abuse � Exposure to blasts (workplace and military) �  Injuries to external head or scalp

� Concussions are often not recognized among children with orthopedic injuries, as attention is paid to the more symptomatic or visible extremity injury

Who should be evaluated? �

� 1. Injury description: how did the injury occur, type of force, location on the head or body the force was received

� 2. Cause: the cause of the injury may help to estimate the force of the hit or blow to the patient—the greater the force of the injury, the more likely the patient will present with severe symptoms; importantly, significant symptoms associated with light force may indicate increased vulnerability to mTBI, especially in patients with a history multiple mTBIs or pre-existing history of migraine headaches

A. Injury Characteristics (7)

� � 3. Amnesia (Retrograde): determine the presence of

any memory loss for events before the injury and the length of time of loss � Research indicates even a few seconds of memory

amnesia may predict more serious injury � 4. Amnesia (Anterograde): determine the presence of

any memory loss for events after the injury and the length of time of loss � Anterograde amnesia is AKA post-traumatic amnesia

A. Injury Characteristics (7) �

� 5. Loss of Consciousness (LOC): determine if LOC occurred and the length of time � Up to 90% of mTBIs do NOT demonstrate LOC

� 6. Early signs observed by others: get input from family members and friends about specific signs of mTBI

� 7. Seizures: uncommon, but determine if any seizures were observed

A. Injury Characteristics (7)

� � 1. Signs and Symptoms

� Record symptoms in 4 areas (physical, cognitive, emotional, sleep)

�  If present within past 24 hours, record “1” � 2. Exertion

� Do any symptoms worsen with physical or cognitive activity?

� 3. Overall “Difference” Rating � Does the patient or the parent/spouse perceive a

change from the pre-injury status? 0-6 grading scale

B. Symptom Checklist �

�  24-48 hours of observation, looking for: �  Headaches that worsen �  Seizures �  Focal neurological signs �  Drowsiness or can’t be awakened (hypersomnolence) �  Repeated vomiting �  Slurred speech �  Can’t recognize people or places �  Increasing confusion or irritability �  Weakness or numbness in arms or legs �  Neck pain �  Unusual behavior change �  Significant irritability �  Any LOC greater than 30 seconds

C. Signs of Deteriorating Neurological Function

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� � 1. Concussion/mTBI history

� Multiple mTBIs may be cumulative, especially if there is minimal time between events or less force is required to cause an mTBI

� 2. Headache history � Migraine headaches can result in protracted recovery

� 3. Developmental history � Learning disabilities and AD/HD may result in

protracted recovery

� 4. Psychiatric history � Depression or mood disorder, anxiety, sleep disorder

D. Risk Factors Complicating Recovery �

� 850.0 (Concussion with no LOC): � 850.1 (Concussion with brief LOC < 1 hour) � 850.9 (Concussion, unspecified)

� If LOC is > 1 hour, or if there is evidence of skull fracture, and/or intracranial injury, code 854 should be considered

� 959.01 Head injury, unspecified is not recommended for concussion due to its lack of specificity

E. ICD-9-CM codes

� � Infants, toddlers, and preschoolers frequently sustain

bumps and bruises due to falls, direct impacts, MVA, tricycle/bike accidents, and child abuse

� Some of these events could cause concussions � Young children may be unable to express the

symptoms of mTBIs as older children and adults � We should have a low threshold for considering

mTBI in young children who may not be able to describe nausea, amnesia, or cognitive changes

Special Considerations for Young Children �

� Vomiting � Headache � Crying and inability to be consoled � Restlessness or irritability � Seizures � Dizziness or confusion � Change in personality

Acute Signs and Symptoms for Children

� � Inquire about the following during follow-up visits: � Excessive crying � Persistent headache � Poor attention � Change in sleep patterns � Change in nursing or eating habits � Becoming upset easily/temper tantrums � Sad or lethargic mood � Lack of interest in favorite toys

Follow-up for Young Children �

� Approximately 1400 cases of TBI occur in the US each year due to abuse

� These injuries are often unrecognized and underreported

� Recognition is critical � Is the history of the injury developmentally appropriate

for the child’s age? � Consider abuse even in the absence of a history of

trauma…may be from a caregiver other than the parent

Abusive TBI

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� � 1. Monitor the patient in your office

� Office monitoring is appropriate if the number and severity of symptoms are steadily decreasing over time or fully resolve within 3-5 days

� 2. Make a referral to an mTBI specialist �  If symptom reduction is not evident, or if symptoms

worsen, refer (national brain injury associations) � 3. Refer the patient for diagnostic testing

� CT, MRI, neuropsychological testing can aid in return to play-work-school assessments

Clinical Management �

� Rest and careful management of physical and cognitive exertion are the keys to recovery

� Returning to daily home/community activities � Returning to school

�  Section 504 Plans may be needed

� Returning to play � Returning to work

Management Approaches

� � When the behavioral, cognitive, or somatic

symptoms of concussion persist beyond the typical recover period, the patient may have Post Concussion Syndrome

� Post concussion syndrome is the most common entity to be diagnosed in people who have suffered TBI and is present in up to 64% of patients

� As many as 15% of people with a history of mTBI still suffer from deficits one year after injury

Post Concussion Syndrome (PCS) �

� At one year post-injury, the most common symptoms are a combination of physical, psychosocial, and cognitive, with reports of headaches, dizziness, disturbances of senses, light and noise sensitivity, and various psychiatric symptoms, including depression, anxiety, coping issues, and psychosocial disability

� Some studies have suggested that women are more likely to develop PCS, both in terms of more symptoms reported and a longer duration of impairment

PCS

� � Although PCS is considered to be fully recoverable

with proper treatment, patients suffering from PCS-related symptoms for an extended time may not be able to return to work, resulting in additional social and economic costs

� The inability to return to work could exacerbate a pre-existing depression or impair the ability to adequately cope with stress

PCS in Adults �

� The experience of PCS in children and young adults is similar to adults with the same behavioral, emotional, and somatic difficulties following mTBI

� But, some studies using neuropsychological testing have reported that high school athletes take longer to recover.

� Younger patients’ risks for PCS has been expanded to include sports beyond football and to other activities, and the increased risk is perhaps explained by the fact that the frontal lobes do not fully develop until late adolescence

� Animal models have also suggested that the immature brain is more susceptible than the adult brain to apoptosis following mTBI

PCS in Children and Adolescents

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� �  Children differ significantly from adults and adolescents, not

only in size, but also biomechanically, pathophysiologically, neurobehaviorally, and developmentally

�  Because the developing brain is more plastic than the mature brain, younger age at the time of injury was originally thought to have a beneficial effect on recovery and expected outcome

�  However, current literature indicates that this is not the case; the developing brain appears to be more vulnerable to diffuse brain injury

�  Traumatic injury to the immature brain results in a prolonged period of pathogenesis in both cortical and subcortical structures, leading to progressive neurodegeneration, hyperactivity, and sustained cognitive impairments

PCS in Children and Adolescents

� �  Some thorough studies have found that children report

worse cognitive symptoms over one year after concussion than adults

� These deficits are first reported months after the original injury and affect the child’s schoolwork or abilities to function at home

� Children aged 6-12 years with mTBI have impaired executive functioning and attention one year post-injury as compared to non-injured controls

� Even mTBI can affect linguistic skills, conduct, and personality changes

PCS in Children and Adolescents

� � Wear a seatbelt every time � Use child safety seats/booster seats/seatbelts

appropriately � Never drive under the influence � Wear a helmet while on a bike, motorcycle,

snowmobile, ATV � Wear a helmet for contact sports (football, ice hockey,

lacrosse, boxing) � Wear a helmet for skating or skateboarding, riding a

horse, skiing, sledding, snowboarding, batting and running bases

Primary Prevention �

� Install window guards to keep children from falling out

� Use safety gates at the top and bottom of steps � Keep stairs clear of clutter � Secure rugs and use rubber mats in bathtubs � Use shock-absorbing material, such as mulch or

sand, around outdoor play areas

Safer Living Areas

� � In the early post-injury phase, the patient with mTBI

may have difficulty communicating with you as he or she did before

� Expression: may have trouble thinking of specific words or expressing the specifics of their symptoms or functional difficulties

� Comprehension: may become confused if too much information is given at once; may need extra time to understand; may have trouble following multi-step directions; may take longer than expected to respond; may read slowly or have trouble with complex formats, small print, or filling out forms

� What should you do to help?

Improving Communication �

Additional Slides

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� Protective Equipment

� Impact forces to the head and dental and orofacial injuries are reduced by helmets and mouthpieces

� Helmets reduce skull fractures and other head injuries in many sports, such as cycling, motor sports, equestrian sports, alpine sports

� BUT, these findings do not translate to a reduction of concussion injuries

� False sense of protection? Possibly

� Girls and Concussion

� Girls are 68% more likely to suffer sports related concussions.

� The reasons for this are anatomy and biomechanical differences: �  Heads are smaller �  Neck muscles are not as strong �  Different styles of play �  Different training techniques �  Cultural norms �  Increasing numbers of highly competitive female athletes.

�  In basketball girls were 300 percent more likely to get a concussion

�

Concussion Management

� The cornerstone of concussion management is physical and cognitive rest until symptoms resolve

� Then, graduated (stepwise) program of exertion � Graduated Return to Play Protocol

� KEY: The athlete (and parents) must understand that physical AND cognitive rest is necessary

� http://www.iowadcs.org/Dynamic.aspx?Id=271

�

RTP Protocol: Each Step = 24 hours

� �

Pre-participation Assessment

� History!! � Reveals high risk categories � Offers opportunity for education

� # of past concussions � Symptoms associated (or not) with concussions � Head injuries � Facial injuries � Cervical spine injuries � Protective equipment use

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�

Modifying Factors of RTP

Home Instructions

� 1. Avoid strenuous activity for 24 hours after the injury � 2. Do not take mediations without consulting your

physician � 3. Eat a “regular” diet, but avoid alcohol � 4. Do not drive until you are fully recovered � 5. Do Not take aspirin, sleeping pills, or ibuprofen

6. Call your doctor or go to the ER if any of the following occur: a. Becomes sleepy or is difficult to awaken b. Vomiting c. Trouble with balance d. The eyes move oddly, difficulty with focusing, unequal pupil size e. Persisting or increasing headache f. Restlessness or irritability, personality changes g. Convulsions or seizures h. New swelling at the area of the head injured i. Increased neck stiffness j. Numbness k. Ringing in the ears l. Shortness of breath m. Confusion n. Visual problems

� Home Instructions

� No need to: � Check eyes with flashlight � Wake up every hour � Test reflexes �  Stay in bed (but do rest) � Use alcohol

� Hospital Admission

� Hospital admission for further observation or treatment is indicated when: � An athlete has persistent confusion � Lethargy �  Focal neurologic signs � Abnormal findings on the brain CT scan � When the clinical picture is confounded because of

seizures.

� Admission should also be considered if no responsible person is available at home to monitor the patient for progression of symptoms.

� � http://www.cdc.gov/concussion/headsup/pdf/

Concussion_in_Sports_palm_card-a.pdf � Palm card for field assessment

� http://www.cdc.gov/concussion/headsup/pdf/ACE_care_plan_school_version_a.pdf � ACE Care Plan for School

� http://www.cdc.gov/concussion/headsup/pdf/ACE_care_plan_returning_to_work-a.pdf � ACE Care Plan for Work

� www.knowconcussion.org � www.parachutecanada.org

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� � Please contact me anytime

� Tracey A. Littrell � 563-650-6797 � www.littrellradiology.com

Questions?