Essential Neurology for Concussion Evaluations Aftab Merchant, MBBS, FCPS Professor Pre-Clinical Sciences Cleveland University Kansas City
Learning Objectives Recognize the clinical features of concussion Differentiate between concussion and structural head injury Recognize the sequelae and complications of concussive injury Outline the assessment procedures for patients with concussion
Traumatic Brain Injury (TBI) Mild TBI occurs with head injury due to contact and/or acceleration/deceleration forces
Glasgow Coma Scale Credit: First aid for free
Rutland-Brown et al. J Head Trauma Rehabil 2006 Liaa CC et al. J Neurol Neurosurg Psychiatry 2012
Pathophysiology of TBI Primary Brain Injury Occurs at the time of trauma Results in focal contusions and hematomas Due to Direct impact Rapid acceleration / deceleration Penetrating injury Blast waves Surgical treatment
Pathophysiology of TBI Secondary Brain Injury Cascade of molecular injury mechanisms Includes Electrolyte imbalances Inflammatory responses Secondary ischemia from vasospasm Focal microvascular occlusion Free-radical injury Neurotransmitter-mediated excitotoxicity
Structural Brain Injury Cerebral contusions Epidural hematoma Subdural hematoma Subarachnoid hemorrhage
Cerebral Contusion Most frequently encountered lesions Permanent damage to small blood vessels on the surface of the brain Acceleration-deceleration injury Coup-contrecoup injuries
Epidural Hematoma Collection of blood between skull and dura Caused by fracture of the bone Rupture of middle meningeal artery Lens shaped lesion on CT Intracranial pressure increases herniation and death Lucid interval may precede neurologic deterioration
Pterion
Subdural Hematoma Venous bleeding between the dura and arachnoid membranes Pathogenesis Bridging veins between brain and dural sinuses are torn Slowly enlarging blood clot covers the convexity of the brain
Subdural Hematoma Causes Blunt trauma Anticoagulants, hemophilia Child abuse, shaken baby syndrome Spontaneous Risk Factors Elderly persons Alcoholics
Subdural Hematoma Clinical Features Progressive neurological signs Fluctuating consciousness level Complications Herniation and death may occur Dementia (chronic subdural hematoma) Diagnosis: CT scan (imaging test of choice)
Subarachnoid Hemorrhage Bleeding into subarachnoid space MCC is rupture of saccular (berry) aneurysm Berry aneurysm lacks a media layer Most are located in anterior circle of Willis
Subarachnoid Hemorrhage Clinical Features Sudden onset of a severe headache Described as the worst headache ever Nuchal rigidity LP shows xanthochromia
Subarachnoid Hemorrhage Diagnosis CT scan without contrast (best test) MRI is most useful for posterior fossa infarcts Complications Further hemorrhage Hydrocephalus Permanent neurologic deficits
Vascular Pathologies Cerebral vessels associated with vascular pathologies: Epidural hemorrhage Subdural hemorrhage Subarachnoid hemorrhage Middle meningeal artery Bridging veins draining into the sagittal sinus Berry aneurysms in the circle of Willis
Concussion Concussion is a mtbi In severe concussions as the brain rebounds, it twists.
Concussions in 14 NCAA sports 2014-15 NCAA Sports Medicine Handbook
Concussion Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. McCrory P. et al. Br J Sports Med 2013;47:250
Pathophysiology Diffuse Axonal Injury Mild TBI results in diffuse axonal injury DAI affects individual nerve fibers Axons are severed Disruption of communication Neuron may die or swell
Pathophysiology Rotation of head at the time of impact can also damage the axons. Department of Neurological Surgery, Weill Cornell Medical College
Concussion causes an Energy Crisis in the brain Matthew et al. Pediatric Annals 2012; 41:9
Pathophysiology Disruption of axonal neurofilament organization impairs axonal transport Release of excitatory neurotransmitters Generation of free radicals Concussive injury reflects a physiological disturbance rather than a structural injury to the brain Mardissi M et al. Aus Fam Phy 2014; 43:3
In concussion, the exterior remains unbroken and intact while the inside contents are completely misplaced.
Etiology Mild traumatic brain injury (mtbi) Due to sudden movement of brain in the skull Chemical changes makes brain more sensitive to any increase stress or injury The management of concussion in sports. Neurology 1997; 48:581
Clinical Presentation Asymptomatic Regular symptoms Asymptomatic becomes symptomatic Dramatic symptoms
No loss of consciousness Lopez V et al. Medicine & Science in Sports & Exercise (2016)
Diagnosis Clinical symptoms Physical signs Cognitive impairment Neurobehavioral features Sleep disturbances
Signs and Symptoms Somatic Cognitive Emotional Sleep Disturbances Headache Pressure in head Neck pain Dizziness Blurred vision Balance problems Sensitivity to light Sensitivity to noise Feeling like in a fog Fatigue Low energy Difficulty: Concentrating Remembering Confusion More emotional Irritability Sadness Nervous or anxious Drowsiness Trouble falling asleep
Hallmark Symptoms The hallmark symptoms of concussion are confusion and amnesia Alteration in mental status characteristic of concussion can occur without loss of consciousness Duhaime AC et al. J Neurosurg 2012 Collins ME et al. JAMA 1999
Headache worsens Seizures Focal neurologic signs Neck pain Repeated vomiting Slurred speech Red Flags Can t recognize people or places Increasing confusion Weakness / numbness in arms or legs Unusual behavioral change Decreasing state of consciousness Very drowsy or cannot be awakened
Complications Second impact syndrome Acute, progressive diffuse cerebral edema Disordered autoregulation Post-concussion syndrome Seen in <1% of cases Symptoms lasting >3 months
Complications Post-traumatic headaches Onset of headache within 7 days after injury Post-traumatic epilepsy Two fold increase in the risk of epilepsy for the first five years Seizures occurring within the first week are not considered epilepsy
Complications Post-traumatic vertigo Direct injury to cochlea or vestibular structure Labyrinthine concussion due to blunt trauma to membranous labyrinth Cranial nerve injuries Anosmia (CN I) Diplopia (CN III, IV, VI) Facial pain (CN V)
Complications Chronic traumatic encephalopathy Cognitive impairment Neuropsychological symptoms (behavior, personality changes, depression, and suicide) Parkinsonism Speech and gait abnormalities
Chronic Traumatic Encephalopathy CTE is a progressive disease of the brain found in athletes (and others) with a history of repetitive brain trauma CTE Center, Boston University
CTE Tau protein buildup and tissue degeneration CTE Center, Boston University
International Conferences on Concussion in Sport 2001: Vienna 2004: Prague 2008: Zurich 2012: Zurich
Assessment Three main points where assessment is valuable: Pre-participation evaluation On-site at the time of injury Post-injury in office setting
Pre-participation Evaluation Ask specific questions about: previous symptoms about concussion length of recovery perceived number of concussions previous head, face, cervical spine injuries details regarding protective equipment used at the time of injury
On-site Evaluation Address first-aid issues first If there is a loss of consciousness then document the length of time the person remained unconscious
Glasgow coma scale (GCS) Record level of consciousness using Glasgow coma scale A person suspected of having a concussion should not return to activities (play) on the same day.
On-site Assessment Evaluate orientation and cognitive functioning Conduct serial monitoring Standard orientation questions like time, place, and person have been shown to be unreliable in the sporting situation.
Modified Maddocks Maddock s questions are used to determine the impact of the patient s memory at the time of the incident Review SCAT3 with the following slides
Onsite Standardized Assessment of Concussion (SAC) Onsite SAC is used for cognitive assessment Includes: Orientation questions Immediate memory of a five word list Concentration using digits backwards Delayed recall
SAC: Delayed Recall Perform delayed recall after completion of the Balance and Coordination Examination. Ask the person to recall words from the list of words read earlier.
In-office Assessment Comprehensive history Neurological examination should include Mental status Cognitive functioning Gait and balance Determine the clinical status Determine the need for neuroimaging
Comprehensive History Determine if the impact was directly to the head or transmitted to the head. Find out if there was any loss of consciousness, if so, how long. Ask if there is any amnesia for the event. Determine if there is an observer to collaborate what happened. Find out if baseline assessments were done (SAC) Ask if there is history of concussions. If so, what are the details?
Neurological Examination Neurological examination should include Mental status Cognitive functioning Gait and balance Test of memory, orientation, and concentration as provided in the SAC is recommended.
Standardized Assessment of Concussion (SAC) SAC is used for cognitive assessment Includes: Orientation questions Immediate memory of a five word list Concentration using digits backwards Delayed recall
Balance and Gait Balance and Error Scoring System (BESS) Double leg stance Single leg stance Tandem stance Tandem Gait Postural stability testing assesses the motor domain of neurological functioning
BESS: Common Errors Hands lifted off iliac crest Opening eyes Step, stumble, or fall Moving hip into > 30 degrees abduction Lifting forefoot or heel Remaining out of test position for > 5 sec
SAC: Delayed Recall Perform delayed recall after completion of the Balance and Coordination Examination. Ask the person to recall words from the list of words read earlier.
Coordination Examination Upper limb coordination Finger-to-nose task (5 correct repetitions in < 4 seconds = 1)
Clinical Status Assess for the presence and severity of the symptoms using a Likert scale (0 to 6) 22 common symptoms are listed on SCAT3 evaluation form
Clinical Status Determine if the symptoms have changes Do symptoms worsen with activity? Has patient experienced any retrograde or anterograde amnesia? Is there any change in behavior?
Neuroimaging Conventional structural neuroimaging is typically normal in concussion injuries Consider neuroimaging if: prolonged disturbance of conscious state focal neurological deficit worsening symptoms
Neuropsychology Testing Conduct clinical NP assessment including cognitive function on all your patients suspected of having a concussion Formal NP testing is not required for all patients Formal NP testing, if needed, should be performed by a neuropsychologist Routine baseline NP testing not recommended
Sport Concussion Assessment Tool 3 (SCAT3) Tool developed by a group of international experts at the 4th International Consensus meeting on Concussion in Sport held in Zurich, Switzerland in November 2012 Published in The BJSM Injury Prevention and Health Protection, 2013, Volume 47, Issue 5
SCAT3 and Child SCAT3 SCAT3 is used primarily for patients aged 13 and older Child SCAT3 is used for children aged 5 to 12 years old SCAT3 should not be used as a stand alone method for diagnosis and management of concussion
Special Considerations Children and adolescents Child SCAT3 to assess children (5-12 years) Modified Maddock s score with ageappropriate questions Symptom evaluation to include both child and parent reporting SAC with age-appropriate questions and concentration test
Special Considerations Elite vs. Non-elite athletes All athletes regardless of the level of participation should be managed using the same treatment and return to play protocol.
Treatment and Follow-up Physical and cognitive rest Pharmacology in some cases Graded return to activities
Rest Rest both from physical and cognitive exertion for at least first 24-48 hours Physical and cognitive activity increases post-concussive symptoms severity and prolongs recovery. In most cases, no other intervention is required.
Pharmacology Two situations where pharmacology plays a role. In the management of specific prolonged symptoms, e.g., sleep disturbance and anxiety. To modify the underlying pathophysiology of the condition with the aim of shortening the duration of concussion symptoms
Return to Activities Protocol Step 1 Step 2 Step 3 Step 4 Step 5 No activity, complete rest until asymptomatic. Proceed to step two when symptoms are gone. Light aerobic exercise Sport-specific exercise and training. No contact or risk of contact. Half days at school or work Non-contact training drills Light resistance training and progress to heavy weights Full days at school or work Full contact training after medical clearance Step 6 Return to competition
Treatment and Follow-up Majority of the patients with concussion will recover spontaneously in less than 10 days If symptoms last beyond 10 days or become worse then the patient s treatment plan might need to be modified.
Prevention Recognition of the concussive injury is of primary importance Helmets are not concussion-proof Mouthguards are a controversial area Rule changes to reduce injury
Concussion An injury to the brain that causes a brief disruption in mental status Not life-threatening Often no STRUCTURAL damage but FUNCTIONAL damage is present Potential to cause long-term damage
References McCrory, P., et al. Consensus statement on concussion in sport: the 4 th International Conference on Concussion in Sport held in Zurich, November 2012. British Journal of Sports Medicine 2013; 47:250-258. McCrory, P., et al. Sport Concussion Assessment Tool 3 rd Edition. British journal of Sports Medicine 2013; 47: 259-262. Makdissi M, Davis G, McCrory P. Updated guidelines for the management of sports-related concussion in general practice. Australian Family Physician 2014; 43(3):94-99. Rutland-Brown W, Langlois JA, Thomas KE, Xi YL. Incidence of traumatic brain injury in the United States, 2003. J Head Trauma Rehabil 2006;21:544. Liao CC, Chiu WT, Yeh CC, et al. Risks and outcomes for traumatic brain injury in patients with mental disorders. J Neurol Neurosurg Psychiatry 2012; 83:1186. Grady GF, Master CL, Gioia GA. Concussion Pathophysiology: Rationale for Physical and Cognitive Rest. Pediatric Annals 2012; 41(9):377-382. Crossman, A.R., Neary D. Neuroanatomy: An Illustrated Colour Text, 5 th ed. New York: Churchill Livingstone Elsevier, 2015. Bickley, L.S., Szilagyi, P.G. Bates Guide to Physical Examination and History Taking, 12 th ed. Philadelphia: Wolters Kluwer, 2017. Report of the Quality Standards Subcommittee of the American Academy of Neurology. Practice Parameter: The management of concussion in sports (summary statement). Neurology 1997;48:581-585. Lopez V, Ma R, Weinstein MG, Cantu RC, Myers LS, Nadkar NS, et al. Concussive Injuries in Rugby 7s. Medicine & Science in Sports & Exercise. 2016;48(7):1320 30. Duhaime AC, Beckwith JG, Maerlender AC, et al. Spectrum of acute clinical characteristics of diagnosed concussions in college athletes wearing instrumented helmets: clinical article. J Neurosurg 2012 Dec;117(6):1092-9.