osteopathic approach in the treatment of concussions

V I K R A M A G N I S H D . O & S A U N D R A H O L S E T H , D . O

MILD TRAUMATIC BRAIN INJURY

DISCLOSURES

• Disclosures• 49ERS Fan• Amazon Prime and Netflix subscriber

OUTLINE

• Key Concepts• Acute management• Legal landscape• Treatment

• Osteopathic treatment of concussion• Literature• Techniques• Outcomes

www.westrehab.com

EPIDEMIOLOGY

• 1.5 Million people sustain a brain injury annually • 80% of these injuries are mild in severity (Ruff 2005)

• 3.8 million concussions are sports related as per CDC • Underestimated number due to no reporting.

• Global annual incidence of m-TBI is100-500/100,000 people (Belanger et al., 2007)

• M-TBI is the most common Neurological disorder• Herpes zoster and Migraines having a higher incidence• Migraines have a higher prevalence

FOOTBALL AND CONCUSSION

PHYSIOLOGY OF CONCUSSION

AMERICAN COLLEGE OF REHABILITATION MEDICINE (ACRM) DEFINITION

• Alteration of brain function one or more of the following:• LOC: lasting 0-30mins• PTA: lasting less than 24 HRS• GCS: 13-15 after 30 min• +/- Focal neurologic deficit – may be transient• Other:

• AMS • Confusion• Disorientation• Slowed thinking

CDC DEFINITION

• Any period of observed or self reported:• LOC: lasting 0-30mins• PTA: Not required• GCS: Not required• +/- Focal neurologic deficit• Other:

• Confusion• Disorientation• Impaired consciousness,• Dysfunction of memory around the time of the incident.

WORLD HEALTH ORGANIZATION (WHO) DEFINITION

• Any period of observed or self reported:• LOC: lasting 0-30mins• PTA: <24 Hours• GCS: 13-15 at time of presentation to a healthcare

professional instead of restricting the score to within 30 minutes.

• +/- Focal neurologic deficit• Other: None

DEPARTMENT OF VETERANS AFFAIRS (VA) DEFINITION

• Any period of observed or self reported:• LOC: lasting 0-30mins• PTA: <24 Hours• GCS: Best score 13-15 in first 24h• +/- Focal neurologic deficit• Other:

• AMS <24hrs • Imaging normal

www.triaxtec.com

AMERICAN ACADEMY OF NEUROLOGY 1997 GRADING SYSTEM

• AAN updated guidelines in 2013 and abandoned the 1997 grading system (shown right) à

Grade Cantu Colorado Medical Society and American Academy of Neurology

Grade 1-mild No LOCPTA < 30 min

No LOCConfusion < 15 min

Grade 2-moderate LOC < 5 minPTA > 30 min

No LOCConfusion > 15 min

Grade 3-severe LOC > 5 min (??—suspect mistake in Cuccurullo)PTA > 24 h

3a—brief LOC, on order of seconds3b—prolonged LOC, on order of minutes

(PCS)/PCD - ICD 10 DEFINITION (2004)

• 3/8 symptoms are present following head trauma:• Headache• Dizziness• Fatigue• Irritability• Difficulty concentrating• Memory impairment• Insomnia• Intolerance to stress, emotion or alcohol

saveinjurekids.org

PCS/(PCD) - DSM IV CRITERIA (1994)

• At least 3/8 symptoms following head trauma:• Headache• Dizziness• Fatigue• Irritability• Difficulty concentrating• Memory impairment• Insomnia• Intolerance to stress, emotion or alcohol• Impairment in concentration/memory be present on NP testing• Significant impairment in social or occupational functioning• Present for at least 3 months.

4TH INTERNATIONAL CONFERENCE ON CONCUSSION IN SPORTSZURICH, SWITZERLAND

• Concussion:• “a complex pathophysiological process affecting the brain,

induced by traumatic biomechanical forces”

• PCS: • “graded set of clinical symptoms” w/wo LOC• Resolution that “typically follows a sequential course”• That “in a small percentage of cases may be prolonged”

• 5th International Conference on Concussion in Sport (10/2016, Berlin, Germany)

PATHOPHYSIOLOGY

BRAIN INJURIES IN BOXING

PATHOPHYSIOLOGY

• Caused by shearing forces• Disrupts fragile structures running in the long axis of

the brain, axons and small vessels• Affecting intracellular transport & membrane stability

in the axon• Leading to swelling, wallerian degeneration and release of

excitatory NT’s• Vascular injuries produces white matter petechial

hemorrhages and edema• AKA – DAI (Diffuse Axonal Injury)

DIAGNOSIS

• Clinical Diagnosis

• Serum Biomarkers:• S100b and NSE (Neuron-specific enolase)

• High sensitivity and low specificity

• Eye Motility (Research – Maruta et al., 2010):• “Gaze error variability has shown significant correlation with

attention and working memory measures on neuropsychological testing, indicating that this may serve as a useful screening tool for mild TBI”

DIAGNOSIS: EARLY PHASE SYMPTOMS

• Peak in hours to days and resolve over days to weeks in vast majority:• Headache• Dizziness• Imbalance• Fatigue• Sleep disruption• Difficulty concentrating• Trouble remembering

DIAGNOSIS: LATE PHASE DISORDER (PCS/PPCS)

• Estimated at 10-15% of original cohort (months to years)

• Often worsening set of symptoms dominated by:• Psychological & emotional factors• Somatic symptoms• Cognitive symptoms• Impact in functioning and participation in life roles.

• These symptoms have no specificity for brain injury and may be present in other groups:• Depression, anxiety, PTSD, chronic pain, and even

substantial portion of healthy population.

DIAGNOSIS: LATE PHASE DISORDER (CTE)

• Rare progressive Neurological Disorder• Initially described as “Punch Drunk” syndrome in boxers • (1928 Martland)

• Symptoms presenting years to decades after exposure:• Cognitive: Memory, Attention, Executive function• Mood: Apathy, depression, suicidality• Behavioral: Poor impulse control, Substance abuse, Violence• Neurologic: Dysarthria, Parkinsonian features

• Much remains unknown about CTE:• Histopathological, Dx w/ Autopsy: A distinct tauopathy• Current literature: Correlation but can not prove causality.• Permanent PCS is not known to cause CTE

MANAGEMENT

• Assessment (“when in doubt, sit them out”):• Sideline assessment:

• SAC (Standardized Assessment of Concussion)• SCAT3 (Sport Concussion Assessment Tool)• Postural stability: BESS (Balance Error Scoring System)

• Pre-participating NP testing:• ImPACT• HeadMinder• Digit Symbol Substitution Test

• Post concussion testing:• Post concussion symptom scale• McGill Abbreviated Concussion Evaluation (ACE)• Concussion Symptom Inventory

• Imaging Criteria (primarily CTH)• ACEM: Headache, vomiting, 60+, intoxication,

deficits in short –term memory, evidence of trauma above clavicle, seizures, GCS less than 15

MANAGEMENT – RETURN TO PLAY

• Rest is the cornerstone of initial therapy

• Graded return to play:• No same day return to play

• Endorsed by most state laws and athletic organizations

• Exceptions for professional athletes • Sufficient sideline resources to show recovery

• Graded return should take minimum 24 hours for each step:• Nonimpact aerobic exercise → Sport-specific

exercise (nonimpact drills) → Noncontact training drills → Full Contact practice → Return to normal play

News.ivhn.org

RECOVERY AND PROGNOSIS

• 80-90% of injuries improve with natural resolution• 10-15% of symptoms persist for months to years

• High risk groups include:• <18 years or > 65 years• Specific symptoms lasting >60hours• LOC more than 60 seconds• Amnesia• Previous history of concussion• Co morbid conditions, e.g. Psychiatric conditions• Dangerous style of athletic play • High risk sport (contact, collision)

LEGAL LANDSCAPE OF CONCUSSION

• Zackery Lysted: October 12, 2006 game• 13 year-old middle school football player

• Lysted Law (WA2009): Concussion laws in all 50 states.

Myheadfirst.wordpress.com

LEGAL LANDSCAPE OF CONCUSSIONLYSTED LAW (WA 2009)

• Concussion laws in US:• Education for coaches,

athletes, and guardian• Signed release by

parent/guardian in contact sports

• No same day return to play

• Clearance by a healthcare provider for RTP

HIGH RISK SPORTS

HOW ABOUT HEADING A FOOTBALL?

• No sport is completely without risk, even chess!• Heading alone (ball to head contact only) not

identified as cause of any head or neck injury. Anderson BJSM ’04, Fuller BJSM ’05

• Purposeful heading not identified as causing concussion • Agel JAT ’07• Dick JAT ‘07

HOW COME WOODPECKERS DON’T GET A CONCUSSION?

• An experiment in nature

• Woodpecker Drilling Behavior• Motor Coordination before impact

• Eyelids close ms before impact• Linear acceleration

• Design of beak• Shock is dampened by flexible cartilageConnecting base of beak to the bones of skull

• Design of head• Woodpecker’s brain is tightly backed byrelatively dens yet spongy bone

allaboutbirds.org

WHAT HAVE WE LEARNED FROM THE WOODPECKER

• U-shaped device at the c-spine • Pressure on jugular veins àdecrease venous return à IC ‘cushion’• Rat and monkey models is showing promise• Human trials to undergo 2017

Ideaconnection.com

STILL NOT FEELING BETTER?A FEW DAYS TO MONTHS LATER…

• “Doc I still have…”• Poor concentration • Forgetful• Neck pain• Headache• Dizziness• Anxiety

• What’s wrong with me doctor?• PCS (Post concussion syndrome)-ICD-10• PCD (Post concussive Disorder)-DSM-IV

NATURAL HISTORY OF PCS (6-9 MONTHS)

• Most pts will continue to improve & recover• Pts still susceptible to periodic impairments,

especially during times of physiologic or psychological stress

• Increased sensitivity to modest alcohol use, sleep deprivation, lengthy travel schedules, or increase work demands

• Pharmacologic interventions may be used including antidepressants & psycho stimulants• Off Label Use

BUT DOC…A FEW MONTHS TO YEARS LATER…

• Doc, since my accident one year ago, I still have:• Poor concentration• Forgetfulness • Headaches

• What’s wrong with me doctor?• PPCS (Persistent Post Concussive Syndrome)• General predictors include:

• Female Gender• Ongoing litigation• Low socioeconomic status• Prior mild TBI• Prior Headaches• Serious associated systemic injury

CLINICAL MANAGEMENT AND SUMMARY

BUT DOC…I’M STILL HAVING THESE SYMPTOMS... WHAT

DO I DO?• Well, you have come to the right doctor…

• I am an Osteopath!• By far, the best treatment for your symptoms of mild TBI and post-

concussive syndrome…but of course this is my biased opinion.• But don’t take my word for it…

• OMT was effective at reducing overall symptoms related to concussion. A substantial subset of concussive symptoms on the SCAT2 had significant reduction with the use of OMT. The integration of OMT into concussion management appears to immediately reduce symptom burden.

POST CONCUSSIVE SYNDROME

• Description-• Mild form of brain injury with symptoms that included, but are

not limited to tinnitus, dizziness, headache, nausea, vomiting, depression and cognitive impairment

• Parasympathetic dysfunctions• Increased tone= constricted pupils, increased nasal, lacrimal

and submandibular secretions • Cranial dysfunctions of facial nerve (CN VII) and

glossopharyngeal nerve (CN IX)• Vagus nerve dysfunction- OA, AA, C2: tenderpoints, TART, OA

and osteomastoid compression• Sympathetic dysfunctions

• Increased tone= vasoconstriction and decreased secretions, increased blood flow to skeletal muscle

• T1-T5: tenderpoints, TART


• Motor dysfunctions• C1-C8, spinal accessory nerve (CN XI)- levator scapula,

longus capitus, longus colli, scalenes, splenius, SCM, rectus capitis: tenderpoints, TART, SD

• Somatic Dysfunctions• Hypertonicty of the cervical and cranial muscles• Cervical dysfunctions • Cranial dysfunctions• Temporomandibular joint dysfunction• Fascial restriction


• Osteopathic Manipulative Treatment• Head: vagus- OA release, decreased CRI- CV4 hold,

compressed cranial sutures- V spread, cranial strain- vault hold, cranial techniques, TMJ- direct inhibition to medial pterygoid, genioglossal and posterior digastric muscles


• Osteopathic Manipulative Treatment• Cervical: FPR, MFR, ME, Soft tissue and or HVLA• Thoracic: MFR, FPR, ME, Soft tissue and or HVLA• Sternum/ribs: Still, HVLA, CS and MFR

• * All techniques will be demonstrated during the hands on portion of seminar

V- Spread

HEADACHE

• Description- pain in the head that is localized to the cranial vault, although it may include the region of the eyes and upper neck

• Parasympathetic• Increased tone= constricted pupils, increased secretions • Facial, glossopharyngeal and vagus nerve- cranial and

cervical dysfunctions• OA and occipitomastoid suture compression

• Sympathetic• Increased tone= vasoconstriction and decreased secretions,

increased blood flow to skeletal muscle • T1-T5: tenderpoints, TART and SD

• Motor• C2-C8: tenderpoints, hypertonicity of musculature, Cervical

vertebrae dysfunction, TMJ

HEADACHE

• Osteopathic Manipulative Treatment• Head: OA release, CV4 hold, TMJ treatment• Cervical: MFR, FPR, ME, HVLA and PINS techniques • Thoracic: MFR, ME (seated), HVLA • Ribs: MFR, Still• Viscerosomatic: Chapman’s Reflexes corresponding to the

head

EMESIS

• Description: vomiting is a symptoms of another disease process.

• Parasympathetic • Vagus Nerve- OA, AA, C2: tenderpoints, TART, SD • OA and occipitomastoid compression

• Sympathetic • T5-T10: tenderpoints, TART, SD • Celiac ganglion restriction

• Motor• Cranial dysfunctions • Respiratory diaphragm restriction in motion at all attachments • GI Chapman’s reflex

EMESIS

• Osteopathic Manipulative Treatment• Head: OA release • Cervical: C2, C3-C5: MFR, FPR, ME, HVLA• Thoracic: T5-T10: MFR, FPR, ME, HVLA• Abdomen: diaphragm- re-doming, MFR• Visceral: Chapman’s reflexes, especially for stomach and

esophagus

Re-doming of the Diaphragm

LABYRINTHITIS

• Description: inflammation of the vestibular labyrinth often leading to vertigo, dizziness and tinnitus

• Parasympathetic- not applicable• Sympathetic

• T1-T4: tenderpoints, TART, SD • Motor

• Spinal Accessory Nerve (CN XI): to SCM• Trigeminal Nerve (CN V3): to temporalis muscle

• Other SD• Eustachian tube dysfunction • Trigger points to facial muscles and medial clavicle • Cranial dysfunctions- especially torsions and side bending• Lymphatic congestion- preauricular, post auricular,

submaxillary, submental, and supraclavicular

LABYRINTHITIS

• Osteopathic Manipulative Treatment• Head: Muncie technique, periauricular drainage technique,

OA release, sphenopalatine ganglion stimulation, CV4 hold, counter strain, direct inhibition

• Cervical: MFR, FPR, Still, ME, HVLA• Viscerosomatic: Chapman’s Reflexes- for ear sinuses,

pharynx

TEMPOROMANDIBULAR JOINT DYSFUNCTION

• Description: collection of symptoms caused by either TMJ dysfunction or muscle spasm of mastication muscles. Often characterized by clicking or popping sound of jaw when moved. Includes pain in the TMJ, facial pain, headache, ear ache and neck pain

• Parasympathetic• Increased tone= vasodilatation and copious secretions of

submandibular glands • Facial Nerve (CN VII) and Glossopharyngeal Nerve (CN XI)

dysfunction• Sympathetic

• Increased tone= vasoconstriction and decreased secretions of submandibular glands

• T1-T5: tenderpoints, TART, SD


• Motor• Genioglossal- hypoglossal (CN XII), glenohyoid C1 via

hyoglossal; myohyoid, digastric, medial pterygoid muscles via trigeminal (CNV3)

• Other Somatic Dysfunctions• Eustachian tube dysfunction • Cranial dysfunction• Lymphatic congestion- preauricular, post auricular,

submaxillary, submental, and supraclavicular• Anterior fascial restrictions (cervical to sternum):

tenderpoints


• Osteopathic Manipulative Treatment• Head: direct inhibition to medial pterygoid, genioglossal

and digastric muscles. Massage, ME to mandible, Muncie technique, OA release, periauricular drainage technique, galbreath technique

• Cervical: MFR, ME, Still, HVLA• Thoracic: MFR, ME, HVLA• Sternum: Counterstrain, MFR• Viscerosomatic: Chapman’s Reflexes especially ear, sinuses,

pharyngitis

Galbreath Technique

THORACIC OUTLET SYNDROME

• Description: pain or paresthesias of UE from compression/ irritation of brachial plexus or vascular structure of thoracic outlet. • Thoracic outlet defined by: anterior and middle scalenes,

the clavicle, the first rib, and beneath the pectoralis minor muscle

• Parasympathetic: not applicable• Sympathetic:

• Increased tone= dilated arterioles of muscles (cholinergic and adrenergic β2), constricted arterioles of the muscles (adrenergic α2)

• T5-T7: tenderpoints, TART, SD


• Motor• C5-T1: tenderpoints, TART, SD

• Somatic Dysfunction• Anterior and middle scalene, Pectoralis minor, levator

scapulae, teres major and minor, and latissimus dorsi hypertonicity, tenderpoints and restricted motion

• Inhalation dysfunction of ribs 1 and 2


• Osteopathic Manipulative Treatment• Cervical: MFR, FPR, ME, Still, HVLA, counterstrain• Thoracic: MFR, FPR, ME, HVLA• Upper extremity: counterstrain, ME, Still, MFR• Ribs 1 & 2: FPR and HVLA• Clavicle: MFR and ME

DEPRESSION

• Description: mood disorder- altered emotional states, anhedonia, altered appetite, and sleep. Associated with somatic complaints and chronic illness.

• Parasympathetic• Increased tone= decrease acid secretion, nausea and

peristalsis• OA and occipitomastoid compression• Vagus Nerve: OA, AA, C2- tenderpoints, TART, SD• Pelvic Splanchnic nerves: S2-S5- tenderpoints

• Sympathetic• T1-S2: tenderpoints, TART, SD• Celiac ganglion, Superior mesenteric ganglion, and inferior

mesenteric ganglion- fascial restriction

DEPRESSION

• Somatic Dysfunction• Abdominal, pelvis, sacral, and cranial dysfunctions most

common • Other Dysfunctions

• GI complaints- commonly due to serotonin’s affects • Compensatory changes due to poor posturing

DEPRESSION

• Osteopathic Manipulative Treatment• Head: OA release, vault hold, CV4, direct and indirect

treatment of cranial dysfunctions• Cervical: MFR, ME, FPR, HVLA• Thoracic: MFR, ME, FPR, HVLA• Lumbar: MFR, ME, FPR, HVLA• Ribs: rib raising• Innominate: MFR, ME• Sacrum: cranial, MFR, ME • Abdomen: ganglion treatment: MFR• Viscerosomatic: Chapman’s reflexes • Lymphatic drainage techniques

Cranial Vault Hold

CHAPMAN’S REFLEXES

SPHENOPALATINE GANGLION BLOCK

• The sphenopalatine ganglion blockade is nothing new. In fact, it goes back to 1909, to Geenfield Sluder. Dr. Sluder was a professor and Director of the Department of Otolaryngology at Washington University School of Medicine in St. Louis.

• After looking for some form of therapy for the treatment of head pains, he concluded that the little ganglion situated in the head just above the top of the nose, was an important pathway for pain.

• What is a sphenopalatine ganglion block?• A nerve block is a procedure to stop pain transmission through anesthesia

to the nerve. In an SPG block, an anesthetic agent is administered to the collection of nerves in the ganglion. The least invasive way to access the SPG is through the nose.


Anatomy• Sphenopalatine ganglion consists of the largest

aggregate of neurons in the head outside of the brain and is conveniently located in the sphenopalatine (pterygopalatine) fossa at the back or the nose. This location which makes it very accessible to be blocked.

• The Sphenopalatine ganglion receives sensory connections from the maxillary nerve of the Trigeminal Nerve (V) system. There are also some autonomic connections to the Facial Nerve (VII).

• One also has to keep in mind that the upper cervical nerve roots (C2,C3,C4,) have some indirect connection with the sphenopalatine ganglion which in turn is connected with the trigeminal nerve system via the maxillary nerve.

• Therefore it would not be unreasonable to appreciate that pain from the upper cervical spine can cause referred symptoms into the head and facial area, and vice versa, this might explain why sphenopalatine ganglion block would relieve headache, facial pain, pain in the neck and upper back.


Procedure• The procedure is done in the office

or clinic. • The patient is instructed to lie on

his/her back with the head tilted back and to the side (usually of the pain).

• Then, a small applicator or catheter is inserted through the nostril to the very back of the nasal cavity.

• An anesthetic agent applied using a cotton swab or catheter drips onto the back of the nasal cavity, is absorbed through the bone and into the SPG, and is left there for up to 30 minutes.

• Depending on the type of headache disorder being treated, the procedure may be repeated in the other nostril


Risk and Results• The risks of the procedure are

typically minimal. They include discomfort during and after the procedure, a numb sensation when swallowing, bitter taste from the anesthesia, bleeding from the nose and light-headedness. These side effects typically resolve within minutes to a few hours. There is a very small risk of seizures, infection, and allergic reactions

• The duration of pain relief is highly variable, as some patients may not respond while others improve over days to weeks.

What it treats• Cluster headache• Migraine• Trigeminal neuralgia• Herpes zoster• Paroxysmal hemicrania• Cancer of the head or neck• Facial pain that is atypical• Complex regional pain

syndrome (CRPS)• Temporomandibular disorder• Nasal contact point

headache• Vasomotor rhinitis

ABBREVIATIONS

• TBI-traumatic brain injury• GCS-Glasgow coma

scale• LOC-loss of

consciousness• PTA-posttraumatic

amnesia• PCS/D-Post concussion

syndrome/disorder• PPCS-Persistent post

concussive syndrome• DAI-Diffuse Axonal injury• NP- NeuroPsychological• mTBI-Mild traumatic brain

injury (AKA Concussion)• PTSD-Post-traumatic

stress disorder• CTE-Chronic Traumatic

Encephalopathy

• CT-computed tomography• MRI-magnetic resonance

imaging• DWI/DW-MRI-Diffusion-

weighted Imaging/MRI• DTI- Diffusion tensor imaging

(special kind of DWI to map white matter tractography)

• DfMRI-diffusion functional MRI

• Diffusion – refers to diffusion of water in blood vessels, also evaluates tissue perfusion.

• MRS – Magnetic resonance spectroscopy

REFERENCES

1. Evaluation and treatment of the concussed athlete – update. Kaufman MS, Concannon LG, Herring SA. PhysMed Rehabil Clin N Am. 2014 Nov;25(4):707-22. doi: 10.1016/j.pmr.2014.06.002. Epub 2014 Aug 2. Review.

2. Biomechanism of impact resistance in the woodpecker's head and its application.Wang L, Lu S, Liu X, Niu X,Wang C, Ni Y, Zhao M, Feng C, Zhang M, Fan Y. Sci China Life Sci. 2013 Aug;56(8):715-9. doi: 10.1007/s11427-013-4523-z. Epub 2013 Jul 10. Review.

3. Current concepts in concussion: evaluation and management. Scorza KA, Raleigh MF, O'Connor FG. Am FamPhysician. 2012 Jan 15;85(2):123-32. Review.

4. The Legal Landscape of Concussion: Implications for Sports Medicine Providers. Albano AW Jr, Senter C, AdlerRH, Herring SA, Asif IM. Sports Health. 2016 Sep;8(5):465-8. doi: 10.1177/1941738116662025. Epub 2016 Aug 16.

5. Mild traumatic brain injury. Katz et al. Handbook of Clinical Neurology. Vol. 127 (3rd series)6. Woodpecker drilling behavior. An endorsement of the rotational theory of impact brain injury. May PR, Fuster

JM, Haber J, Hirschman A. Arch Neurol. 1979 Jun;36(6):370-3.7. New Collar Promises to Keep Athletes’ Brains from “Sloshing” During Impact. Mike Orcutt. MIT Technology

Review. Feb 2016. Online.8. Assessing the Immediate Effect of Osteopathic Manipulation on Sports Related Concussion Symptoms. Chapell et al.

Osteopathic Family Medicine. July/August 2015. Vol7. No 4.9. Punch Drunk. Martland HS. JAMA .1928; 91 (15): 1103-7.10. The 5 Minute Osteopathic Manipulative Medicine Consult. M.K. Channell D.O. MA, D.C Mason D.O. FACOFP. 2009 Lippincott

Williams and Wilkins11. Atlas of Osteopathic Techniques 2nd Ed. Alexander S Nicholas DO FAAO, Evan A. Nicholas DO. 2012 Lippincotts Williams and

Wilkins12. Foundations for Osteopathic Medicine 2nd Ed. 2003 Lippincott Williams and Wilkins

osteopathic approach in the treatment of concussions

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