Bryan Sloane
Trauma Research Associate Program
2010
MILD TRAUMATIC BRAIN INJURY
BRAIN ANATOMY
MILD TRAUMATIC BRAIN INJURY

Also more commonly known as a Concussion
 Differs
from Cerebral Contusion
Very common in contact sports
 Acute but transient effects

 Emotional,
physical and cognitive effects
Frequent MTBIs can add to each other, causing
cumulative brain damage
 Loss of brain function, similar to a petite mal Sz

MECHANISM OF INJURY
Injury to a portion of the brain resulting from
rapid acceleration or deceleration of the brain
 Impact against the skull causes edema and
loss of functionality

Damage can last from hours to weeks
Neurotransmitters released in excess as a result of injury
(mechanical depolarization)
->Causes deregulation of membrane potential and
unfocused depolarization
-> ATPase pumps (Na/K) work in excess to restore balance
->Cells become hypermetabolic, and Glucose levels can be
depleted. Decreased cerebral blood flow adds to this effect
and can create long lasting damage.
Axonal damage can occur due to stretching or sheering of the
neuronal Axons when they experience the force (DIA)
SYMPTOMS
Confusion/ disorientation/ amnesia/ emotional
changes
 LOC
 Headache, Dizziness, vomiting, nausea
 Lack of motor coordination
 Audio/visual disturbances
 Tinnitus
 Convulsions

MTBI SCALE AND CLINICAL SCALES

MTBI can be broken down into three categories as defined by the
American Academy of Neurology Guidelines

Grade I


Grade II




Confusion and disorientation with symptoms lasting more than 15 mins
Grade III Loss of Consciousness


Confusion, no LOC and symptoms last less than 15 mins
IIIa LOC lasts seconds
IIIb LOC last for minutes
EEGs obtained after concussive injury in animal models show the same
electrical activity as generalized Sz activity (confusion is similar to postictal state after a Sz)
Clinically measured using Glasgow Coma Scale and A&Ox4 questions

Person, Place, Time, Event
GLASGOW COMA SCALE

MTBI usually presents with high GCS
 Confusion
and disorientation could present at 14
TREATMENT
Mortality is very low, but repeated MTBI can cause
long term damage with the injury increasing in
severity with each successive incident
 Most of the time observation and non ASA
analgesics are used.
 Trauma patients are frequently observed until
other factors that could mask a more severe Brain
Injury wear off (sedation, drugs, EtOH)
 Most of the time there are no structural changes
visible on a head CT.

COMPLICATIONS
Cumulative effects
 Increased risk of Alzheimer’s disease and
memory problems
 Second-impact syndrome

 Fatal
in many cases
 Occurs
when a second minor blow to the head is
experienced after a recent MTBI
 Could be due to Blood Vessels in the brain losing the
ability to regulate blood flow and ICP rapidly increases.
EPIDEMIOLOGY

Of the 1.4 million who sustain a TBI each year in the United States:




Among children ages 0 to 14 years, TBI results in an estimated:




2,685 deaths;
37,000 hospitalizations; and
435,000 emergency department visits annually.1
The leading causes of TBI are:





50,000 die;
235,000 are hospitalized; and
1.1 million are treated and released from an emergency department.1
Falls (28%);
Motor vehicle-traffic crashes (20%);
Struck by/against events (19%); and
Assaults (11%).1
$60 Billion in costs to the US yearly
SOURCE MATERIAL
http://www.cdc.gov/ncipc/tbi/TBI.htm
 Shaw, Nigel. "The neurophysiology of
concussion." Progress in Neurobiology 67.4
(2002): 281-344. Print.
 http://studentlanka.com/images/brain-insideskull.jpg
 http://www.pollsb.com/photos/o/57124ever_concussion.jpg
