Concussions Christopher P. Demers, M.D. Sierra Neurosurgery Group, Reno, NV Clinical Instructor, Univ. of NV School of Medicine
Concussion What is it? What to Watch for? Treatment?
Concussion: What is it?
Are Concussions a Problem?
Mild Traumatic Brain Injury
Jan. 15, 2004: Federal judge rejects NFL $765 million initial settlement because it’s likely not enough
No gross structural damage Normal CT Likely normal MRI
Nov. 2013: 10 ex-NHL players file suit against league for improper head injury prevention
Concussion Incidence
Concussion Incidence
Gessel, et al., 2007
Concussion Incidence
Gessel, et al., 2007
Concussion Incidence J. Pediatrics Sept. 2013 468 male football players ages 8-12 in PA 45% of concussions from head-to-head contact Incidence Practice: 0.24/1000 exposures Games: 6.16/100 exposures
Gessel, et al., 2007
Concussion Incidence
Traumatic Brain Injuries
JAMA Pediatrics study Jan 2014
1,365,000 Emergency Room visits / yr
Young women’s soccer ages 11-14 in Puget Sound
275,000 Hospitalizations
59 concussions per 43,742 exposure hours (1.2/1000)
52,000 Deaths
9.4 day mean length of sx
$76 Billion in direct and indirect costs
Heading accounted for 30.5% 58.6% played with sx 44.1% sought medical attention
173,000 sports / recreation-related TBI each year from 0-19yo
Concussion: Primary Injury
Concussion: Secondary Injury
Axonal disruption
Impaired blood flow regulation
Acceleration / deceleration Shear Tensile Compressive forces
Mass Lesions SDH/EDH/Contusion/Edema
Nonhuman primate models ½ of concussion potential related to head rotation Other ½ related to the contact phenomena
3-phases in severe TBI 1. acute hypoperfusion lasting for ~1 day 2. increased CBF begins on days 2 3. vasospasm begins ~day 4 and lasts for weeks
Concussion: Secondary Injury
Concussion: Secondary Injury
Structural changes in microtubules and neurofilaments
Excitotoxicity
Blebbing (focal swelling)
Shear stress causes dysregulation of protein channels
Impaired axonal transport
Uncontrolled ion flux
Can be seen within 4 hours, may last for days to weeks
Release of K and glutamate Release of glutamate causes release of Ca (NMDA receptors) ATP-dependent pumps overworked to restore homeostasis Hypermetabolic state can be seen within 30 minutes
Concussion: Secondary Injury
Concussion: Secondary Injury
Hypometabolic state
Blood/brain Barrier Breakdown
Happens after 5-6 hours
Can last for weeks to months after injury
Can persist for days
Shear forces disrupt endothelium
Glycolysis / anaerobic respiration
Increased small vessel permeability
Further membrane permeability
Exudation causes cerebral edema Excitatory molecule influx
Concussion: Secondary Injury
Concussion: Secondary Injury
Inflammation
Mitochondrial dysfunction
Microglia activated Release of inflammatory products Present from 1hr to up to 30
Downregulated cytochrome oxidase for up to 10 days in rat model Caused by increased Ca
Concussion Mechanism
Why Does it Matter?
Rat Model
Chronic Traumatic Encephalopathy
Period of vulnerability after a mild injury
Significant similarities with Alzheimer’s Ds
Two mild TBIs within 3 days had same morality as single severe TBI
Tau-protein neurofibrillary tangles: brain scarring
Why Does it Matter?
Why Does it Matter?
Chronic Traumatic Encephalopathy
Second Impact Syndrome
Motor Symptoms Speech difficulty, tremors, poor coordination, can lead to parkinsonism Cognitive Symptoms slowed thought, speech, attention deficits, poor executive function Psychiatric Symptoms can range from emotional lability to frank psychosis
Concussion: Symptoms
Period of brain vulnerability after even a mild injury Second Injury occurs before brain has a chance to heal from first injury More likely in kids/teens Malignant, uncontrolled brain swelling Mortality 50-100% Of people who survive, most have severe, permanent deficits
Kort Breckenridge, Teton High, ID
Concussion: Symptoms
Loss of Consciousness not required!!! Physical Loss Of Consciousness (
