Learning Objectives. Sports Concussion. Learning Objectives (Cont.) Definitions. Marc Norman, Ph.D. & Amanda Gooding, Ph.D. Department of Psychiatry

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1 Learning Objectives Sports Concussion Marc Norman, Ph.D. & Amanda Gooding, Ph.D. Department of Psychiatry Definitions Mechanisms Neuroimaging Assessment Sideline Clinic Impact Symptoms Vestibular Cognitive Sex Differences Symptom Recovery NP assessment Baseline testing Physiologic vs. Clinical Recovery Post-concussion Syndrome Other Factors Hx, migraine, social, mood 2 Learning Objectives (Cont.) Return to Play Return to School Effects of Multiple Concussions Pediatric Issues Clinical Subtypes & Treatments Reduction & Prevention Equipment Rules Guidelines Zurich, Berlin Ontario Long-term Risks CTE Neuropath (McKee) Clinical (Stern) 1.6 million ED visits for mtbi/concussion per year mtbi/concussion accounts for 75% of all TBI-related hospital visits Estimated 30-50% receive no medical attention 70% of ED-related visits for sports concussion are age American Congress of Rehabilitation Medicine (1993) Traumatically induced physiological disruption of brain function manifested by at least one of the following: Any LOC Loss of memory for events immediately before/after (PTA) Altered Mental Status (feeling dazed, disoriented, confused) Focal neurologic deficits Severity does not exceed: LOC 30 min 30 min GCS is Definitions Problems w/ ACRM definition Focal deficits that persist may suggest more severe TBI Feeling dazed, disoriented or confused are non-specific No significant differences between other injury (no TBI) and mtbi groups in feeling dazed (52% vs. 71%), disoriented (42% vs. 33%) or confused (65% vs. 67%) (Lees-Haley et al., 2001, Archives Clinical Neuropsychology, ) Posttraumatic amnesia (PTA) is 24 hours 5 6 1

2 VA/DoD 2016 Criteria for TBI Traumatically induced structural injury and/or physiological disruption of brain function as a result of external force. At least one of the following immediately following : LOC or decreased LOC PTA Alteration in mental state at the time of injury (confusion, disorientation, slowed thinking, looking and feeling dazed) Neurological deficits (weakness, loss of balance, change in vision) Intracranial lesion 7 VA/DoD Definition (Cont.) Does not require direct external trauma Acceleration/deceleration movement Blast injuries Presence of intracranial abnormality à moderate TBI classification in someone who otherwise meets criteria for mtbi 8 VA/DoD Classification of Severity DSM-5 Major or Mild Neurocognitive Disorder Criteria met for major or minor NCD Evidence of TBI: either LOC or PTA or disorientation and confusion or abnormal imaging or neurologic signs NCD presents immediately after the TBI and persists past the acute post-injury period Bottom Line Definition of Coma Concussion is a clinical diagnosis. No diagnostic guideline is a substitute for sound clinical judgment. Concussion should be diagnosed based on evidence of an acute biomechanical force causing immediate neurologic disturbance Not on signs/ symptoms that appear weeks or months later. 11 Plum and Posner (1980) Total absence of awareness of the self and environment, even when the subject is externally stimulated Absence of consciousness, the state of awareness of self and the environment Teasdale and Jennett (1974) State in which there is no eye opening, an inability to obey commands, and no utterance of recognizable words 12 2

3 Glasgow Coma Scale Range is 3 (unresponsive) to 15 Eye opening (1 = none, 2 = to pain, 3 = to voice, 4 = spontaneous) Verbal (1 = none, 2 = makes unintelligible sounds, 3 = nonsensical speech, 4 = confused/disoriented, 5 = oriented times 3) Motor (1 = none, 2 = decerebrate posturing, 3 = decorticate posturing, 4 = withdraws from pain, 5 = localizes pain, 6 = follows commands) 13 Concussion Mechanisms Linear force Rotational Force Impact location Impact magnitude 14 Impact Magnitude Neuroimaging CT (early bleeds and bony pathology) MRI (subacute pathology, DTI) MEG SPECT/ Cerebral Blood Flow (CBF) Sideline Subjective symptoms Assessment Vestibular function (VOMS) Cognitive function Balance (BESSIE) ED Neuroimaging Clinic ImPACT CogSport HeadMinder RBANS SCAT-5 Sideline: Red Flags Observable signs Memory Assessment GCS Cervical Spine Assessment

4 SCAT-5 Symptoms Clinic: Symptom Evaluation Cognitive Screening Orientation Immediate/delayed memory Digits backwards (concentration) Months in reverse Neuro screen/ balance exam Decision-making Sex Differences Sex Differences in Sport-Related Concussion: Incidence, Outcomes, and Recovery Tracey Covassin Males Cognitive Amnesia Disorientation Female Headache Dizziness Irritability Nausea / vomit Fatigue 21 Females have higher rates of concussion in Fútbol, basketball, softball (but not lacrosse) Impact Females Player-surface and player-equipment Males Player-player Women in luteal phase (high progesterone) have worse outcomes than those in follicular phase 22 Symptom Recovery Symptom Recovery

5 When to do NP Testing? 25 Assessment: NP Attention/ Processing Speed Impaired concentration Decreased sustained attention Variable response time Diminished processing speed Memory Difficulty absorbing new information Poor recall of episodic information Deficits in error monitoring 26 Takes time Costs money Poor reliability Baseline Testing Berlin Conference (2017) Adults Recommend AGAINST baseline testing Pediatrics Should not be mandatory is it worth it? Levels of Awareness No universally accepted definition of consciousness

6 Coma Absence of arousal and consciousness Unarousable unresponsiveness Eyes closed and no awareness of self or surroundings Reflex activity Failure of reticular activating system and cortex Vegetative State Awake but unaware of self and environment 3 months is permanent following non-tbi and 12 months following TBI arbitrary and may be untrue Minimally Conscious State Unable to follow instructions reliably or communicate Inconsistent but reproducible behavioral evidence of awareness of the environment or self-awareness Locked-in Syndrome Quadriplegia and anarthria Disruption of corticospinal and corticobulbar pathways Relative preservation of cognition Vertical eye movement intact because the pontine tegmentum is spared Physiologic vs. Clinical Recovery Physiologic dysfunction may outlast clinical symptoms McCrea et al. (2010) 28 concussed athletes vs. 28 non-concussed athlete controls Symptom report, cognition and balance recovered by 5-8 days QEEG did not normalize until 45 days Reliable studies of MR Spectroscopy and CBF show physiological disturbance for >15 but <30 days after injury. Integrated Investigation of Recovery After Sport-Related Concussion: Findings from the CARE Consortium - Mike McCrea Recovery and risk >80% achieve recovery in 7-10 days 75% of repeat concussions within first 7 days 92% of repeat concussions within first 10 days Cerebral vulnerability window

7 CARE Natural history of acute injury and recovery Recovery Increased risk within 10 days % of athletes recovered by 14 days % of athletes recovered by 14 days 71% recovered by 30 days Advocate increased exercise (except for early awakening migraine) Persistent Symptoms >2 weeks in adults >4 weeks in children/adolescents Post-concussion Syndrome (PCS) Refers to nonspecific symptomatology that persists A syndrome = a group of signs and symptoms that occur together and characterize a particular abnormality or condition. PCS is not a true syndrome because: No widely accepted pathology Symptoms following concussion are nonspecific Nonetheless Strongest predictors for acute PCS are Previous mental health or anxiety disorder Pre-existing problems with ETOH Females 3.33x more likely than males Other significant predictors: Prior life stressors, prior psych treatment, prior psych/neuro/pain medications, $ compensation, history of LD/ADHD Other Factors to Consider Family/ personal history of: Migraine Motion sickness/ sensitivity Anxiety/ mood disorder Strabismus, nystagmus, lazy eye Confounding health issues History of prior mtbi/concussions

8 Return to Play in Sports Concussion Determined thorough clinical assessment No standard biomarker(s) of underlying vulnerability Physiological metrics reserved for research Insufficient evidence to recommend a change in the current graded return to play progression CDC 5-Step Progression Baseline: Back to school first Step 1: light aerobic activity Step 2: moderate activity Step 3: heavy, non-contact activity Step 4: practice & full contact Step 5: competition Effects of Multiple Concussions Longer duration of symptoms after recurrent concussion (6.5% symptomatic > 1 month) vs. 1 st concussion (0.6% symptomatic > 1 month) Cumulative effects NCAA Concussion study History of 3 concussions à 3x more likely to have incident concussion than those with 0 prior concussions Slowed recovery associated with history of multiple prior concussions Most repeat injuries happen with 7-10 days of the first injury

9 Effects of Multiple Concussions 226 potential NFL draft picks Self reported history of 0, 1, and 2 concussions There was no relationship of concussion history to Wonderlic (brief IQ measure) or ImPACT. Those with more concussions did no worse. (Solomon & Kuhn (2014, American Journal of Sports Medicine, 42, ) Effects of Multiple Concussions Meta-analysis (614 with 2 concussions vs. 926 controls sustaining a single concussion), evaluated symptom complaints and 7 domains of NP performance Overall effect size of.06 Non-significant significant effects for Executive functions (d = 0.24) and Delayed Memory (d = 0.16) (Belanger et al. 2010, JINS, 16, ) Pediatric Issues Treatment of Concussion in Kids: What We Know, What We Think We Know, and What We Need to Learn Chris Vaughn Prolonged recovery Concussion Clinical Profiles and Targeted Treatments: Building the Evidence Michael Collins, Anthony Kontos Collins / Kontos Clinical subtypes

10 Ontario Guidelines (2015) 96 recommendations for diagnosing & treating mtbi and persistent symptoms Education & expectations Expected symptom outcomes Normalizing Reassurance & positive expectations Gradual return to activities Stress management 55 Ontario Guidelines (2015) Persistent Symptoms: Differential diagnosis of chronic pain, depression, anxiety, other comorbidities Review prescription and OTC medications, substance use Evaluate & treat: Headache (pharmacological & non) Sleep/wake disturbances Sleep hygiene CBT Supplements/ medications Stress reduction, exercise, acupuncture 56 Ontario Guidelines (2015) Persistent mental health disorders CBT Medications Persistent cognitive dysfunction NP assessment Evaluate ADHD/ LD Implement accommodations & compensatory strategies Ontario Guidelines (2015) Persistent vision/vestibular dysfunction Neuro exam to evaluate vision, vestibular, balance, coordination, hearing BPPV, Dix-Hallpike maneuver, Epley Vestibular therapy Refer to vision specialists/ vision therapy Ontario Guidelines (2015) Persistent audiologic dysfunction Review medications for ototoxicity Refer to audiologist Persistent fatigue Increase physical activity, sleep hygiene Education & reassurance Identify contributing factors, motivation Evidence for Active Recovery from Concussion and Post-Concussion Syndrome - Leddy Athletes have diminished autonomic response and cerebral blood flow following SRC High focus on exercise tolerance Buffalo Concussion Bike Test Buffalo Concussion Treadmill Test Aerobic, not anaerobic

11 Equipment Rules Reduction & Prevention Head Impact in Football: Can We Predict Concussion? Steve Broglio Impact Mechanics Rotational force Cumulative impact Impact Density Equipment Head bands in fútbol Broglio Rule changes Restricted practices Hockey checking Changing technique Prevention Neck Strength negative finding Long-term Risks Question: Are there any long-term risks of either multiple sport-related concussions or repetitive head trauma incurred over many years of playing contact sports? Answer: We have absolutely no idea Hypothetical Risks 1. Recurrent concussion may be a risk factor for late-life MCI, dementia (Guskiewicz et al., 2005) 2. Repetitive sub-concussive trauma over a long playing career may result in diminished cerebral reserve, leading to the earlier clinical expression of late-life neurodegenerative disorders (Randolph & Kirkwood, 2009) 3. Single or multiple concussions, or possibly repetitive trauma, produces a unique neurodegenerative disorder that has been termed chronic traumatic encephalopathy (Omalu et al., 2005; McKee et al., 2009) 65 Dementia Pugilistica Also known as punch drunk syndrome A condition in boxers attributed to repetitive head trauma Corsellis et al., 1970: Reported autopsy results on 15 boxers. Septum pellucidum damage Focal scarring of cerebellum Loss of neurons in substantia nigra Numerous cortical neurofibrillary tangles, but few plaques identified by silver/congo red staining Conclusion was that pathology was similar to AD, but the lack of plaques (in 11/15 cases) was a distinguishing feature suggesting unique pathophysiology 66 11

12 Dementia Pugilistica (Cont.) Roberts et al., 1990: Examined brain material from 14/15 Corsellis cases, added 6 more boxers, and compared to AD cases (20) and controls (20), using newly-developed immunocytochemical staining for β-amyloid Boxers and AD cases had same pathologic features of both plaques and tangles Their conclusion: head injury may precipitate the pathological processes which give rise to AD 67 DP to CTE CTE first used as a term by Geddes (1999) in 4 reported autopsy cases: Professional boxer died of SDH Professional boxer with schizophrenia and a seizure disorder A mentally subnormal man with a long history of head banging, died from a head injury in a fall A footballer with a history of one severe TBI in the past, died of SDH CTE first used by Omalu et al. in 2005 (football player) 68 Neuropath Criteria McKee et al. (2016) Clinical Criteria

13 New syndrome, called Traumatic Encephalopathy Syndrome Extraordinarily broad Symptoms encompass people with depression, angercontrol problems, late-stage dementia The Problems with CTE Diverse neuropathologic findings. The only consistent hallmark of CTE is abnormal phosphorylated tau (p-tau) accumulation. The specificity has yet to be substantiated alongside control subjects with CTE-like symptoms (without head trauma) No definable clinical syndrome. Does not differ from other psychiatric and neurologic conditions. Diverse psychiatric problems. Samples biased by self-selection. (Castellani et al., 2015, J Neuropathol Exp Neurol, 74, ). 77 CTE (Cont.) CTE lacks statistical evidence for: Relationship between concussions and the described clinical syndrome Relationship between concussions and p-tau accumulation Relationship between clinical syndrome and p-tau accumulation Is this actually a unique pathologic syndrome?? 78 13

14 Is CTE the Early Onset of FTD? Contrasting Clinical, Neuroimaging, and Neuropathologic Features Paul Schulz Lack of CTE clinical features No evidence of neurodegeneration Absent CTE in retired NFL players CTE in pt with no h/o TBI Players who filled in during strike had higher rates of (earlier) mortality Inconsistent data of depression in NFL retirees 79 TBI (in general) increases risk of dementia Hypothesis CTE is a new form of dementia CTE neuropathology is scaring 2/2 TBI and is similar to TBI risk of dementia Bottom line: preliminary data suggest such risks may be increased but there is no compelling evidence to suggest the existence of a unique syndrome such as CTE 80 14