CONCUSSION RESOURCE CENTER

Mild Traumatic Brain Injury (MTBI)

Physicians can play a key role in helping to prevent mild traumatic brain injury (MTBI or concussion), and appropriately identifying, diagnosing, and managing it when it does occur. Physicians can also improve patient outcomes when MTBI is suspected or diagnosed by implementing early management and appropriate referral. Concussion symptoms may appear mild, but can lead to significant, life-long impairment in an individual's ability to function physically, cognitively, and psychologically. Appropriate diagnosis, referral, and patient and family/caregiver education are critical for helping patients with MTBI achieve optimal recovery and to reduce or avoid significant sequelae.

The term mild traumatic brain injury (MTBI) is used interchangeably with the term concussion. An MTBI or concussion is defined as a complex pathophysiologic process affecting the brain, induced by traumatic biomechanical forces secondary to direct or indirect forces to the head. Concussion, in Latin, means "to shake violently" and MTBI is caused by a blow or jolt to the head that disrupts the normal function of the brain. Disturbance of brain function is related to neurometabolic dysfunction, rather than structural injury, and is typically associated with normal structural neuroimaging findings (i.e., CT scan, MRI). MTBI may or may not involve a loss of consciousness (LOC). In fact, recent research suggests that up to 90% of concussions do not involve an LOC (ref). MTBI results in a constellation of physical, cognitive, emotional and sleep-related symptoms. Duration of symptoms are highly variable and may last for as short as several minutes and last as long as several days, weeks, months, or even longer in some cases.^1-3 Concussion is a highly variable process and differential outcomes are associated with multiple factors, including the associated biomechanical forces of injury, pre-existing risk factors, and likely other unknown factors or considerations.

TBI
TBIs contribute to a substantial number of deaths and cases of permanent disability annually.

• Of the 1.4 million who sustain a TBI each year in the United States:
• 50,000 die;
• 235,000 are hospitalized; and
• 1.1 million are treated and released from an emergency department.⁴
• Among children ages 0 to 14 years, TBI results in an estimated:
• 2,685 deaths;
• 37,000 hospitalizations;
• 435,000 emergency department visits; and
• Approximately 125,000 pediatric office visits annually.^4,5
• The number of people with TBI who are not seen in an emergency department or who receive no care is unknown.
• Direct medical costs and indirect costs such as lost productivity of TBI totaled an estimated $60 billion in the United States in 2000.⁶
• At least 5.3 million Americans currently have a long-term or lifelong need for help to perform activities of daily living as a result of a TBI.⁷
• An estimated 1.6 - 3.8 million sports- and recreation-related TBIs of mild to moderate severity occur in the United States each year.⁸

• About 75% of TBIs that occur each year are concussions or other forms of MTBI.⁹
• Direct medical costs and indirect costs such as lost productivity of MTBI totaled an estimated $12 billion in the United States in 2000.⁶
• An estimated 15% of persons who sustain an MTBI continue to experience negative consequences one year after injury, including physical, cognitive, emotional, and sleep problems, such as:¹⁰
  

      Physical
• Headache
• Fatigue
• Dizziness
• Sensitivity to light and/or noise
• Nausea
• Balance problems

      Cognitive
• Difficulty remembering
• Difficulty concentrating
• Feeling slowed down
• Feeling mentally foggy

      Emotional
• Irritability
• Sadness
• Feeling more emotional
• Nervousness

      Sleep
• Drowsiness
• Sleeping less than usual
• Sleeping more than usual
• Trouble falling asleep
• Symptoms or deficits that continue beyond 3 months may be a sign of post-concussion syndrome.
• With proper diagnosis and management of MTBI most patients recover fully.^11,12

Unlike more severe traumatic brain injuries, the disturbance of brain function in MTBI is related more so to dysfunction of brain metabolism rather than to frank structural injury or damage. The current understanding of the underlying pathology of MTBI involves a paradigm shift away from a hardware/ anatomic damage model to a software/ neuronal dysfunction model (Giza & Hovda, 2001) involving a complex cascade of ionic, metabolic and physiologic events. The cascade includes shifts in ionic concentrations, indiscriminate release of excitatory amino acides (glutamate), altered brain glucose metabolism (first hyperglycolysis, then hypoglycolysis), reduced cerebral blood flow, with possible axonal injury - resulting in impaired connectivity and changes in neurotransmission as indicated in Figure 1. Clinical signs and symptoms of MTB such as poor attention, memory, speed of processing, and motor function are manifestations of this underlying neurometabolic cascade. Further work by the Hovda and Giza group also has demonstrated adverse effects of experimentally induced TBI on the developmental plasticity (i.e., dendritic arborization) of the brain in young animals with implications for the unique effects of the injury upon the child. Animal models investigating the effects of post-injury exertional activity demonstrate that both excessive overuse and underuse of an impaired limb following experimental unilateral brain injury can lead to worse neurological and behavioral recovery (Humm, Kozlowski, et al., 1998; Leasure & Schallert, 2003). These findings have critical implications for post-injury rehabilitation and highlight the importance of a mild degree of activity and not significant over-exertion.

Figure 1. Neurometabolic cascade following experimental concussion. (Giza & Hovda, 2000)

Functional imaging studies of patients have demonstrated a variety of physiological and metabolic changes in the brain following MTBI using (1) PET with findings of reduced glucose metabolism following TBI lasting 2-4 weeks post-injury (Bergsneider, Hovda, Lee et al., 2000 J of Neurotrauma), (2) SPECT, with abnormalities in cerebral perfusion 3 months post-injury correlating with post-concussive symptoms (Jacobs, Put, Ingels et al., 1996), (3) Event-Related Potentials (ERP) indicating electrophysiological abnormalities during attentional tasks (Lavoie, Dupuis, Johnston et al., 2004), and (4) fMRI studies which have found abnormal brain activitation patterns during working memory task performance one month post-injury (McAllister, Sparling, Flashman et al., 2001). The findings from the animal and human work have important implications in explaining the variability in symptom presentation and cognitive dysfunction, reasons for increased vulnerability to repeat injuries within a short timeframe, increased risks and vulnerabilities in the developing brains of children, and strategies for rehabilitation planning (, Giza & Hovda, 2001).