concussions

Traumatic Brain Injury

A brain injury that is caused by an outside force

• Forceful bump

• Blow

• Jolt to the head or body

• From an object entering the brain

types of TBI

• direct impact injury

• acceleration - deceleration injury

• shock wave injury

two broad types of TBI

penetrating

non-penetrating

penetrating TBI

• open TBI

• happens when an object pierces the skull (e.g., a bullet, shrapnel, bone fragment, etc.) and enters the brain tissue

non penetrating TBI

• (closed head injury or ”blunt TBI”)

• caused by an external force strong enough to move the brain within the skull

  Causes include falls, motor vehicle crashes, sports injuries, blast injury, or being struck by an object

TBI risk factors

• adults >65

• men

top 4 causes of TBI (sports)

football

basketball

bicycles

soccer

concussion

trauma-induced brain dysfunction without structural injury on neuroimaging and symptoms include headache, dizziness, confusion, drowsiness, nausea, amnesia, irritability, and transient loss of consciousness

concussion is a considered a

traumatically induced transient disturbance of brain function

• mild TBI

highest percentage of concussions in female athletes

soccer

• twice as often as males in the same sport

acute symptoms of concussion

• due to functional disturbance rather that structural damage

• negative MRI, CT

neurochemical and neurometabolic events after mTBI

• acute axonal injury via disruption of neurofilament organization

• release of electrolytes through ion channel depolarization leads to a release of neurotransmitters and subsequent neurologic dysfunction

• changes to glucose metabolism with decreased cerebral blood flow

• Mitochondrial dysfunction

diffuse axonal injury (DAI)

• most common brain injury

• widespread damage

• Can disrupt and break down communication among nerve cells in the brain

• Can also lead to the release of brain chemicals that can cause further damage

neuron following concussion

• metabolic dysfunction results in energy crisis (may last for up to 10 days)

• massive release of neurotransmitters interferes with cell communication

cellular crisis: potassium flows out of the neuron, soium and calcium flow in

• trigger voltage gated channels throughout brain

• widespread neuronal depression

• primes cells for barrier dysfunction

• inability to clear debris, resolve inflammation, and release trophic factors to repair neuronal connections

cell attempts to restore homeostasis via membrane ionic pumps

• pumps require energy, which is quickly exhausted

• The ability to deliver energy, via ATP, to the cell is also impaired after a concussion, resulting in an “energy crisis”

• a high demand for energy to restore homeostasis (i.e. ionic pumps) paired with the simultaneous decreased ability to deliver energy (i.e. altered cerebral blood flow)

mitochondrial dysfunction

•due to the increased calcium present with the cell, worsening the mismatch between demand for energy and the ability to produce or deliver energy

concussion baseline

• clinical history (including any symptoms)

• physical and neurologic evaluations

• measures of motor control (eg, balance)

• neurocognitive function

concussion evaluation

brief concussion-evaluation tool (e.g., Standardized Assessment of Concussion [SAC]) should be used in conjunction with a motor-control evaluation and symptom assessment to support the physical and neurologic clinical evaluation

Most important component is the medical history

•What happened

•Was trauma involved

•Any recent head-trauma events or prior concussions

•Any loss of consciousness

•Most patients (greater than 90%) diagnosed with a concussion do not have an associated loss of consciousness

•loss of consciousness is an important sign of a potentially serious head injury

emotional concussion s/s

irritability

changes in mood

cognitive concussion s/s

confusion/ disorientation

Amnesia

Mental fogginess

Difficulty concentrating

physical/ somatic concussion s/s

Headache

Dizziness

Difficulties with balance

Visual changes

sleep concussion s/s

Drowsiness

Sleeping less than usual

Sleeping more than usual

Difficulty falling asleep

most commonly reported concussion s/s 1-7 days post injury

1. headache

2. difficulty concentrating

3. fatigue

4. drowsiness

5. dizziness

6. foggy

7. feeling slowed down

8. light sensitivity

9. balance problems

10. difficulty with memory

concussion physical exam

• hed and neck for structural injury

• neurologic exam

• cognitive fxn

• emotional state

neurologic exam

• assessment of strength

• sensation

• reflexes

• ocular asessment (saccades and nystagmus)

• balance and vestibular

SCAT6

• standardized tool used by medical professionals and qualified health care professionals to aid in evaluation of athletes suspected of having sustained a concussion

• can also be used to obtain baseline data among health athletes for future reference

• > 13 years

SCAT6 components

An immediate/on-field assessment tool and an off-field assessment tool

on field SCAT6 assessment

•Taking note of red flags

•Checking for observable signs of concussion

•Memory assessment using Maddock's questionnaire

•Examining the level of consciousness using the Glasgow Coma Scale

•Cervical spine assessment

SCAT6 off field assessment

•Taking a comprehensive history of the player’s condition

•Symptom evaluation

•A cognitive screen (measures orientation and immediate memory)

•Spell first name backwards, recite months of the year in reverse order

•A measure of concentration

•A neurological screen

•Delayed recall (reciting 3 words that were clearly stated minutes earlier)

Child SCAT6

designed as a standardized tool to screen for concussion with children aged from 5 to 12

• It is to be used exclusively by a physician or licensed healthcare professional

• Immediate or On-Field Assessment

• Symptom Evaluation

• Cognitive Screening

• Neurological Screen

• Delayed Recall

• Decision

child SCAT6 immediate on field assessment

•Taking notes of red flags

•Observable signs

•Glasgow Coma Scale (GSC)

•Cervical spine assessment

•History - of concussion and recovery and other past medical history

glasgow coma scale

eye opening

verbal response

motor response

glasgow coma eye opening

spontaneous > 4

to sound > 3

to pressure >

none > 0

glasgow coma verbal response

orientated > 5

confused > 4

words > 3

sounds > 2

none > 1

glasgow coma motor response

obey commands > 6

localising > 5

normal flexion > 4

abnormal flexion > 3

extension > 2

none > 1

glasgow coma scale score

mild: 13-15

moderate: 9-12

severe: 3-8

child SCAT6 cognitive screening

• testing immediate memory

• concentration

child SCAT6 neurological screening

• testing if the child could follow instruction

• Cervical movement and pain

• Coordination

• Walking pattern

• BESS Balance test

child SCAT6 delay recall

Recall words from immediate memory session after 5 minutes

post concussive syndrome (PCS)

• set of symptoms that occurs in prolonged mild TBI

• PCS is an array of physical, cognitive, behavioral, and emotional symptoms including headache, fatigue, vision changes, disturbances in balance, confusion, dizziness, insomnia, and difficulty with concentration

• S/S persist > 3 months

second impact syndrome

• repeat blow or injury to the head before the complete resolution of the initial concussion

• diffuse cerebral swelling, brain herniation, and death can occur

• young, healthy patients may die within a few minutes

enhanced vulnerability of the brain after an initial insult can be explained by..

• characteristic ionic fluxes

• acute metabolic changes

• cerebral blood flow alterations that occur immediately after cerebral concussions

what makes the brain more vulnerable and susceptible to death after a second sub-lethal insult of even less intensity?

Extracellular potassium concentration can increase massively in the brain after concussion, followed by hypermetabolism lasting up to ten days

what happens to the brain in second impact syndrome?

brain loses its ability to auto regulate intracranial and cerebral perfusion pressures

chronic traumatic encephalopathy (CTE)

• axonal injury, micro-hemorrhage with subsequent loss of blood-brain barrier integrity, and the inflammatory cascade caused by activation of glial cells ultimately results in the deposition of both tau protein and neurofibrillary tangles in specific regions of the brain characteristic of CTE

• tauopathy

what percentage of people with repetitive concussion or mild TBI will develop CTE?

approximately 17%

concussion associated learning difficulties

those associated with light and noise sensitivity

cognitive fatigue

attention deficits

problems with memory

slower processing speed

why is the concussion grading scale no longer used?

•evidence indicates that a brief loss of consciousness in association with concussion does not predict clinical course of long-term cognitive impairment

•the absence of loss of consciousness in concussion should not be used to justify more rapid return to play

define sport related concussion

• traumatic brain injury induced by biomechanical forces

• cause by…

  • direct blow to head or body

  • results in repid onset of short-lived impairment of neurological function (resolves min-hrs)

  • acute s/s indicate functional disturbance

return to a learning environment

• return to play should not come before return to learning

• brief absence from school

• temporary academic adjustments (eg, extra time, reduced load), formal accommodations (eg, 504 plan), and academic modifications (eg, Individualized Education Program [IEP])

Return to Activity after concussion

• initial period of relative rest (24 to 48 hours)

• symptom-limited cognitive and physical activity as well as symptom-tolerated aerobic exercise treatment and clinician-directed activities may be appropriate

• steadily increasing aerobic exercise duration and intensity, avoiding more than a mild increase in symptoms

  • Mild = <2pt increase in symptoms on a 10-point scale

what do “stakeholders” need to know about concussions?

Prevention

Mechanism

recognition and referral

appropriate return to participation

physical and cognitive restrictions for patients with concussion

including driving post-concussion when relevant

ramifications of improper concussion management

what kind of injury is a concussion?

biopsychosocial

essential components of concussion asessment

• visual- vestibular

• cervical spine

• neurologic

subsymptom threshold aerobic exercise training

can begin as soon as 1–2 days after injury

concussion protocol

• an organization’s set of policies, tools, and assessments for caring for a concussion

• implies a strict, written policy that instructs healthcare providers to treat every patient and every concussion the same, but a concussion protocol (policy) is used to ensure everyone involved knows what to do when a concussion happens

Natasha’s Law (Texas)

The student cannot practice or compete again until:

• He or she has been evaluated, using established medical protocol based on peer-reviewed scientific evidence, by a treating physician chosen by the student or by the student's parent

• He or she has successfully completed each requirement of the return-to-play protocol established by the concussion oversight team

• The treating physician has provided a written statement indicating that, in his or her professional judgment, it is safe for the student to return to play

• The student and the student's parent acknowledge that the student has completed the requirements of the return-to-play protocol

minimum concussion protocol steps

Concussion definition

Concussion education including signs, symptoms, and immediate recognition. (Use this removal from activity guide to educate stakeholders on the importance of reporting concussion symptoms.)

Pre-season baseline testing

Removal from activity criteria

Sideline assessment procedures

Clinical evaluation procedures

Academic adjustment guidelines

Return to activity procedures and guidelines

Notification procedure to education staff

If a student has a concussion diagnosis, all stakeholders in the student’s education must be notified

oregon return to academics protocol

1. total rest

2. light mental activity

3. part -time school

4. part time school

5. full time school

6. full time school

return to activity checklist

1. medical assessment

2. rest

3. symptom limited activity

4. non - contact training

5. sport specific training

6. light exercise

7. medical clearance

8. full contact practice

9. return to life

ATs in cases of negligence after concussion

• improper evaluation

• improper documentation

• misunderstood communications with the patient

• lack of education of the patient or the patient’s family

documentation of concussion

mechanism of injury

initial signs and symptoms

state of consciousness

findings of the physical and neurologic examinations, symptoms, neurocognitive function, and motor control (noting any deficits compared with baseline)

instructions given to the patient or parent (or both)

recommendations provided by the physician

graduated RTP progression, including dates and specific activities

relevant information on the patient’s history of prior concussion and associated recovery pattern(s)