Pennsylvania Academy of Family Physicians Foundation & UPMC 43rd Refresher Course in Family Medicine CME Conference March 10-13, 2016

Transcription

1 Pennsylvania Academy of Family Physicians Foundation & UPMC 43rd Refresher Course in Family Medicine CME Conference March 10-13, 2016 Disclosures: Concussion Management in Children and Adolescents Justin Berthold, MD Speaker has no disclosures and there are no conflicts of interest. The speaker has attested that their presentation will be free of all commercial bias toward a specific company and its products. The speaker indicated that the content of the presentation will not include discussion of unapproved or investigational uses of products or devices.

2 A Comprehensive Approach to Concussions 1 JUSTIN BERTHOLD, D.O. PHYSICAL MEDICINE & REHABILITATION PENNSYLVANIA ACADEMY OF FAMILY PHYSICIANS MARCH 11 TH, WHO AM I? Physical Medicine & Rehabilitation (PM&R) Physician Also known as Physiatry Focus on restoring function and quality of life Lake Erie College of Osteopathic Medicine (D.O.) University of Pittsburgh Medical Center (PM&R, Chief Resident) The Children s Institute Medical Director of PM&R Rehabilitation Physicians of Pittsburgh MSK/NEURO JUSTIN BERTHOLD D.O. FINANCIAL DISCLOSURES The speaker has no conflict of interest, financial agreement, or working affiliation with any group or organization. 3 1

3 4 LECTURE OBJECTIVES FACILITATE FURTHER AWARENESS OF CONCUSSION AND RELATED SEQUELAE REVIEW PHYSICAL EXAM AND DIAGNOSTIC TOOLS DISCUSS EFFECTIVE TREATMENT APPROACHES THAT CAN BE USED BY FAMILY PHYSICIANS ICD-10 Diagnostic Criteria 5 After head trauma (usually involving LOC) At least 3 of the following features: (No objective evidence is necessary) Headache Dizziness (not true vertigo) Fatigue Irritability Difficulty concentrating and performing mental tasks Impairment of memory Insomnia Reduced tolerance to stress, emotional excitement, alcohol, depression /anxiety, loss of self-esteem, fear of permanent brain damage; Potentially escalating to hypochondriacal features and permanent sick role Concussion Defined 6 Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. Consensus Statement on Concussion in Sport the 4 th International Conference on Concussion in Sport Held in Zurich, November

4 Epidemiology 7 In the United States: Estimated 1.7 million people sustain a TBI (traumatic brain injury) annually million emergency room visits 275,000 hospitalizations annually $60 billion in direct and indirect costs CDC estimates 1.6 to 3.8 million concussions occur in sports and recreational activities annually Daneshvar et al- The Epidemiology of Sport-Related Concussion; Clin Sports Med Jan; 30(1):

5 Pathophysiology 10 Concussion is a metabolic brain injury, rather than structural excitatory amino acids induce ionic shifts Giza and Hovda Pathophysiology 11 Concussion is a metabolic brain injury, rather than structural excitatory amino acids induce ionic shifts Giza and Hovda Differential Diagnosis 12 Depression Somatization Chronic fatigue Chronic pain Cervical injury Vestibular dysfunction Visual dysfunction Migraine 4

6 Typical Recovery Time 13 Sports related: 7-10 days %: have symptoms that last longer than 2 weeks. Non-sports related: 2 weeks. 33% have symptoms longer than 3 months. Leddy et al, 2012 Risk factors for Persistence of Symptoms 14 Agreed Upon Age Sex Prior history of concussions History of cognitive dysfunction Leddy et al, 2012 Affective disorders Less Important Length of Post-traumatic amnesia Loss of consciousness Cognitive difficulties (on testing) Injury Severity Environmental/Behavioral 15 Sleep hygiene Rest breaks Work/school accommodations Minimize screen time Maintain a schedule Stress management 5

7 Sleep Alterations Increased latency Fragment ed sleep Too much/too little sleep Cognitive Symptoms Fogginess Difficulty concentrating Memory deficits Cognitive Fatigue Mood Disruption Irritability Feeling sad Anxiety Somatic Symptoms Headach es Dizziness Nausea Light/Soun d Sensitivity 16 Symptom Questionnaire 17 Physical Examination 18 Cranial Nerves Disruption of smooth pursuit saccadic eye movements Vestibular Screen (VOMS) Balance testing: Romberg, BESS, tandem gait Cervical spine Strength Reflexes 6

8 Balancing Act 19 1.Proprioception (dorsal columns, cerebellum, thalamus) 2.Vision 3.Vestibular input FRANKCHAMBERS.COM Vestibular System 20 Balancing Act 21 Between 37% and 48% of patients experience vestibularrelated impairments. A study of 48 athletes, aged 9 to 23 years, with a diagnosed protracted concussion, showed that patients with vestibular dizziness had significantly lower scores in gauging reaction time compared with those without the impairment (P =.05), as did athletes with vestibulo-ocular symptoms (P =.04). If this system is compromised in some way following concussion, it makes sense that a reaction time would be slowed. This is an important point, as athletes with this impaired reaction time may be at greater risk for subsequent injury until they are no longer impaired. Anthony Kontos, PhD, University of Pittsburgh Medical Center's Sports Medicine Concussion Program 7

9 Balancing Act 22 Patients with protracted recovery from concussion frequently have dysfunction involving the vestibular system. Lau et al 2011: Dizziness is the immediate symptom most predictive of prolonged recovery Balancing Act 23 Vestibulo-ocular Pathway 24 8

10 Vestibular-ocular Motion Sensitivity Testing 25 Smooth Pursuits: Visually tracking Abnormal: Rapid, choppy movements Saccadic pursuit: Looking rapidly between 2 objects in a stationary plane Overshooting, undershooting, 3 or more movements: abnormality in eye movement Vestibulo-ocular Reflex (VOR) 26 To maintain focus on an object regardless of head position Thumb out, maintain gaze while moving head rapidly Symptoms or saccadic pursuits: unilateral or bilateral vestibular lesion Vestibulo-Spinal Reflex (VSR) Head and target move together Coordinate head/neck movement with the trunk/body Contracts limb muscles for postural support Symptoms of postural instability indicate problem 27 9

11 Vestibular Therapy 28 Gradual progression Develop home exercises Treatments: Visual tracking exercises Pencil pushups Walk while throwing a ball from hand to hand Walking backwards Disco ball When it s a Vision Problem 29 Concussions can have effects on the visual system: Accommodative Insufficiency Convergence Insufficiency Light Sensitivity Ocular-Motor Dysfunction Reduced Cognitive Abilities With Visual Tasks Reduced Visual Processing Speed or Reaction Time Post concussion Headaches 30 Musculoskeletal (myofascial) Cervicogenic Rebound headaches Neuralgia Post traumatic migraine Tension/Fatigue related headaches Convergence Insufficiency 10

12 Physical Exam of Head/Neck 31 Cervical range of motion Spurling s test (radicular sx) Tender points/trigger points Palpation of facet joints (supine) Occipital neuralgia Trigger Points 32 Tender to palpation, with radiation into an expected pattern, reproducing discomfort Cervical Facets 33 Palpated while patient lying supine Gentle manual traction If potential pain generators, Consider X-rays or MRI Based on results cervical PT 11

13 Occipital Neuralgia 34 Reproduction of pain or burning upon palpation of the occipital nerves: 1/3 of distance from greater occipital protuberance to mastoid process Examine while supine Mark and inject while prone GoN Block (Greater Occ. Nerve) 35 Injectate: Depo-medrol 40 mg/ml and lidocaine 36 Headaches: Treatment Musculoskeletal/Myofascial/Tension Osteopathic Manipulative Treatment (OMT) Physical Therapy: ROM, modalities, massage Analgesics/Anti inflammatories/muscle relaxants Trigger Point Injections Nerve block (GON) Relaxation techniques Biofeedback and behavior modification Acupuncture Yoga 12

14 Headaches: Treatment 37 Inhibition of cortical excitation Restoring nociceptive dysregulation Ca channel blockers verapamil Anticonvulsants topiramate gabapentin valproic acid Beta blockers propranolol Antidepressants fluoxetine duloxetine amitriptyline venlafaxine Magnesium, ALA, Vitamin B2, Coenzyme Q10: RCTs show decrease migraine frequency w/ chronic supplementation Migraine Abortives: Triptans PO Migraine Cocktail Nucynta Concussion Pharmacology 38 Clearly define the target symptoms Are there certain symptoms that are driving others? Therapeutic trial of all medications Spontaneous recovery? Taper meds after remission Start low and go slow One medication at a time Monitor for side effects and drug drug interactions Concussion Pharmacology 39 Ease of use is important Dosing frequency Simplicity of dose titration Where possible, use agents with benefits on multiple target symptoms Augment partial treatment responses using agents with complementary pharmacologic properties 13

15 Sleep Alterations Increased latency Fragment ed sleep Too much/too little sleep Cognitive Symptoms Fogginess Difficulty concentrating Memory deficits Cognitive Fatigue Mood Disruption Irritability Feeling sad Anxiety Somatic Symptoms Headach es Dizziness Nausea Light/Soun d Sensitivity 40 Sleep Cycle Disruptions 41 Up to 70% of patients after TBI Severity of head injury inversely associated with severity of sleep disturbance mild head injuries report more insomnia than severe In adolescents, sleep disturbance was significantly larger for those who experienced minor head injury when compared to control subjects 42 Sleep Alterations: Treatment Behavioral strategies Sleep hygiene education No TV, computer, phone, ipad in bed/hour before bed Relaxation therapies Sleep restriction 14

16 Sleep Dysregulation 43 Difficulty with sleep initiation: Melatonin Difficulty with sleep maintenance: Melatonin XR, Trazodone Other options: Remeron, Lunesta, Flexeril, Restoril, anti-anxiety Cognitive Fatigue 44 Citicoline (CDP choline) Amantadine (Reddy et al 2012) Reaction time, Verbal Memory, symptoms. Ritalin, Adderall, Concerta Strattera, Vyvanse (non-stimulant release of norepinephrine) * Difficult to get approved for adults * Beware with using in anxious or bipolar patients, or those with CAD Mood Disorders 45 Antidepressants: Activating: Prozac, Wellbutrin, Effexor Sedating: Zoloft, Celexa, Paxil Anxiolytics: *Benzodiazepines (Klonopin, Ativan) Buspar Mood Stabilizers: Depakote Lamictal *Counseling and Resolve Crisis 15

17 When to taper 46 Feeling better subjectively May have missed a few doses Neurocognitive data at baseline Daily routine with manageable symptoms Return to Play Protocol 47 Graded return to activity with increased heart rate within tolerable level of symptoms Static ->Dynamic->Sports Specific exercises- > Drills-> Non-contact practice ->Full contact practice Exit test and cleared Return to Play Protocol 48 Consensus Statement on Concussion in Sport (2013) Asymptomatic at Rest Asymptomatic with exertion (all stages) Neurocognitive data at baseline *Off all medications 16

18 Return to School/Work 49 Part time vs. full-day With or without accommodations: No gym class Academics: Decreased work load, longer time on tests Tutoring Environmental: Testing in a quiet room, early dismissal from classes, rest breaks in nurses office Progress as tolerated High Definition Fiber Tracking Uses anisotropy of fibers to determine orientation and then outline where fibers are missing/asymmetric Research studies, not done routinely 50 Chronic Traumatic Encephalopathy (CTE) 51 Tau protein tangles on tissue analysis Requires multiple traumatic events Symptoms include: Cognitive dysfunction-dementia, executive dysfunction Mood disorders/suicidal ideation Headaches Parkinsonism, ataxia, and dysarthria, appear in a subset of cases, predominantly boxer 17

19 Chronic Traumatic Encephalopathy (CTE) 52 Separated in time from concussion and symptoms Genetics may play a role Current Treat Options Neurology (2014) 16:306 DOI /s Traumatic Brain Injury (JR Couch, Section Editor) Current Understanding of Chronic Traumatic Encephalopathy Christine M. Baugh, MPH1,2 Clifford A. Robbins, BA1 Robert A. Stern, PhD1,2,3,4,* Ann C. McKee, MD1,2 Chronic Traumatic Encephalopathy (CTE) 53 CTE is the only known neurodegenerative dementia with a specific identifiable cause; in this case, the cause is head trauma. It is unknown whether a single blow to the head is sufficient to initiate the metabolic cascade that precedes the clinical and neuropathological changes characteristic of CTE, as all confirmed cases of CTE to date have had a history of multiple head injuries. Therefore, the most obvious way to prevent CTE is, in theory, to prevent repetitive head injuries from occurring. Chronic Traumatic Encephalopathy: A Potential Late Effect of Sport-Related Concussive and Subconcussive Head Trauma 1; Brandon E. Gavett, Ph.D., a,b Robert A. Stern, Ph.D., a,b and Ann C. McKee, M.D. a; Clin Sports Med Jan; 30(1): 179 xi. doi: /j.csm