Traumatic brain injury, the "signature injury" among wounded soldiers of the current military engagement in Afghanistan and Iraq, can cause major long-term disability in survivors. Protective gear has improved overall survival rates—We have gotten very good at saving lives, but not as good at saving life.

    Traumatic brain injury (TBI) occurs when trauma damages the brain. TBI often results when the head suddenly and violently hits an object, when an object pierces the skull and enters brain tissue, or from an explosive force. Earlier studies suggested that 20 percent of soldiers wounded in Iraq experience traumatic brain injury (TBI), most caused by IEDs. Neurologists associated with the U.S. military now estimate that as many as 30 percent of the troops active in Iraq and Afghanistan for 4 months or longer are at risk for debilitating neurological damage. While official statistics indicate around 22,600 TBI casualties, there may actually be as many as 150,000 struggling with it. Of all patients who had been exposed to a blast and who were admitted to Walter Reed between January 2003 and February 2005, 59 percent (450) were diagnosed with TBI. Of these, 56 percent were moderate or severe and 44 percent were mild. Closed brain injuries outnumbered those caused by penetration.

    Closed head injuries far outnumber the penetrative injuries the original estimates were based on. A closed head injury is not the result of a direct blow to the head, but caused by the tremendous pressure changes from explosions. Often there are no external signs of injury, and if there are other, external wounds, the medics may not test for neurological damage. The effects of the TBI may go undetected for years or even decades. Many closed head injuries are confusingly similar to post-traumatic stress disorder (PTSD).

    Imaging tests reveal the location and extent of brain injury and associated injuries and help determine diagnosis and probable outcome. Sophisticated imaging tests can help the doctor differentiate among the variety of unconscious states associated with TBI and determine their anatomical basis. X-rays of the skull and neck, MRIs, or computed tomography (CT) scans can help diagnose the extent and nature of the injury. More recent studies have shown that the damage may not be easy to diagnose with traditional imaging tests.

    The delicate brain tissue and the hard, bony skull are two completely different materials. If you shake a glass of water, the glass itself never changes shape, even as the water sloshes around. With an explosive force, the brain can be shaken hard enough against the skull to get bruised (contusion), even when there is no visible external injury. The resulting injury is probably evident.

    Less easy to recognize is the injury that occurs at a cellular or sub-cellular level, damage which can cause permanent and continuing neurological deterioration and premature aging.Current theory is that compressed sound waves from an explosive blast lead to the formation of small air bubbles. These can form emboli (blood vessel blockages) that travel to the brain and cause parts of it to die due to lack of oxygen. Contusions and hemorrhage in both the cortical and subcortical brain regions, programmed tissue death around the areas of hemorrhage, and the activation of immune system at the sites of brain injury have been observed.

    Damage to the axons, the conductive part of the nerves, begins within minutes of the injury and can continue for days after that. The cause of this damage is not yet understood. Often, initial trauma-induced brain damage cannot be reversed and it is essential to prevent further injury. Loss of neural connections may lead to many of the symptoms associated with brain injuries, and the gradual replacement of lost synapses by the sprouting of nearby, undamaged axons probably underlies the recovery process.

     A mild TBI may cause a loss of consciousness, headache, confusion, lightheadedness, dizziness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, a change in sleep patterns, behavioral or mood changes, and trouble with memory, concentration, attention, or thinking. Seizures, fluid in the brain, cerebrospinal fluid leaks, infection, and organ failure are complications. The damage is often irreversible, but it is vitally important to prevent further damage.

    Cognition (thinking, memory, and reasoning), sensory processing (sight, hearing, touch, taste, and smell), communication (expression and understanding), and behavioral or mental health (depression, anxiety, personality changes, aggression, acting out, and social inappropriateness) can all be affected. More serious head injuries or those not properly treated may result varying degrees of unconsciousness. The symptoms of TBI may occur immediately or they may develop slowly over several hours, especially if there is slow bleeding into the brain or gradual swelling. Depending on the cause, mechanism, extent, and location of injury, the severity TBI symptoms can be mild, moderate, or severe.

    One-quarter of patients having brain contusions or hematomas and half of with penetrating head injuries develop seizures within the first 24 hours. Seizures can also occur as much as a year later. Approximately 40% of patients with TBI develop post-concussion syndrome within days to weeks. Syndrome symptoms include headache, dizziness, memory and concentration problems, disturbed sleep, restlessness, irritability, depression, and anxiety, and may persist for several weeks.

    With more severe injuries, patients may experience numbness, weakness, blindness, deafness, inability to speak or understand speech, slurred speech, lethargy with difficulty staying awake, persistent vomiting, loss of coordination, disorientation, or agitation. Less obvious are difficulties in thinking or concentrating.

    Medicating TBI patients for psychiatric and physical problems can be difficult because TBI patients are more sensitive to side effects.

    Hydrocephalus (fluid accumulation in the brain) usually occurs within the first year of TBI and causes increased intracranial pressure. Unfortunately, it is associated with neurological deterioration, impaired consciousness, behavioral changes, poor coordination or balance, or loss of bowel and bladder control.

     Long-term TBI disabilities depend on the severity and location of the injury, the age and general health of the individual, and how quickly the patient received medical intervention to prevent the secondary brain damage that occurs within days of a head trauma.

    Moderate or severe TBI may cause the same symptoms. If the initial headache worsens or persists, or the person has vomiting or nausea, convulsions or seizures, an inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination, and increased confusion, restlessness, or agitation, prompt medical attention is essential.

    Long-term survivors of TBI may suffer from persistent problems with behavior, thinking, and communication disabilities, as well as epilepsy; loss of sensation, hearing, vision, taste, or smell; ringing in the ears (tinnitus), coordination problems, and/or paralysis. Recovery from cognitive deficits is most dramatic within the first six months after TBI, and less apparent subsequently.

     Sometimes the onset of symptoms is delayed. Patients with moderate to severe TBI may never fully recover their p re-injury function. Many with severe TBI will require health support services and treatment for life.

     About half of severely head-injured victims require surgery to repair or remove blood clots (hematomas) or bruised brain tissue (contusions). Occupational, physical, and speech/language therapy may also be required to ensure maximum recovery of function. Problems with orientation, thinking, and communication should be addressed early, often during the hospital stay. The focus is typically on improving alertness, attention, orientation, speech understanding, and swallowing problems.

©2008 Florida Oxygen