The casualties of the Iran missile attack: not your father’s concussion

Recently, revelations indicated that the Iran missile strike on the U.S. base in Iraq actually did cause head injuries.  So why did the U.S. initially claim no “casualties”?   From the limited reports available, it appears that most of the soldiers’ symptoms were consistent with concussions.  Let’s define terms:  In the wars of the 20th century, our soldiers would have been labeled with “shell shock.”  In the past, diagnosing concussion required a direct blow to the head, at least transient loss of consciousness, and some degree of amnesia for the event.

In today’s medical world, a concussion is diagnosed when any traumatic force is applied to the brain, including air pressure waves (as in a bomb blast) or violent head shaking despite the absence of any direct blow, loss of consciousness, or even initial headache. Now, any subjective complaints of headache, dizziness, and mental fuzziness suffice, but overlap with symptoms of certain mood disorders such as anxiety, posttraumatic stress disorder, and depression. Mild traumatic brain injury (mTBI) is the final diagnosis in such cases when imaging studies and objective examinations fail to reveal a structural lesion in the brain. 90 percent of those afflicted with mTBI recover completely, Most, if not all, of us have had a blow to the head with a subsequent headache for a short period of time – thus, we are subjects of mTBI.

Those whose symptoms linger beyond 3 to 4 weeks are labeled with the diagnosis of post-concussive syndrome. That unfortunate minority can include patients who become convinced by the diagnostic process that they have had permanent brain damage, a label that can paint the remainder of their lives in a darker color.  Some go on to fear lifetime limitation and subsequent risk of developing chronic traumatic encephalopathy or Alzheimer’s.

All this is not meant to discount the impact of such symptoms on those who suffer them; rather, it aims to educate as to their risk of permanent brain damage.  The recognition that chronic traumatic encephalopathy is associated with repeated concussions, as studied in boxers and football players, led to the precautionary raising of consciousness regarding brain injuries, particularly in adolescents.  A 2013  study found that over 500,000 adolescents annually required hospital care for head injury  (defined as loss of consciousness or overnight hospitalization) – half in sports activities.   It suggested much higher numbers likely went untreated.  A relationship to poorer academic performance, substance abuse, and mood disorders was also raised.

Heightened awareness stimulated the broader definition of concussion and thus mTBI, resulting in the current state of perhaps exaggerated fear regarding the actual consequences, indirectly lowering the threshold for a self-fulfilling prophecy. The power of secondary suggestion, particularly in medical management, is well-recognized, and the lack of definitive diagnostic methodologies for the lowest levels of concussion and its consequences exacerbates the confusion.

Let’s clarify the science: At its truly transient level, a concussion disturbs neurotransmitter release.  A sufficient force flushes out what are otherwise finely modulated amounts of these substances mediating normal brain cell interactions, thus altering their subsequent electrical propagation of the nerve cell impulse down their axons (or “wires”), the constant backdrop for our conscious lives. Fluctuation in neurotransmitters affects our mood and cognition, including sensory perceptions. With sufficient force, a gross neurotransmitter disruption occurs, an event like tripping a circuit breaker–   “the lights go out.” We lose consciousness. With the replenishment of the normal neurotransmitter molecular balance, everything returns to normal.

A greater force can actually cause stretching of the axons and disruption of the molecular cascade within them that propagates the electrical current. Significant stretching can lead to permanent axonal damage. Only when sufficient force occurs to rupture of tiny little blood vessels supplying the axon bundles, can an MRI definitively detect structural damage in the brain to diagnose a TBI. At that point, such an injury is labeled as “moderate.”   Unfortunately, the lesser degrees of mTBI described above have no definitive bright line to separate reversible from permanent, nor is there any certainty as to when sufficient accumulation of injury will actually affect individuals clinically.

This lack of verifiable proof leads to the conundrum clinicians face when evaluating individuals such as our soldiers in Iraq and prognosticating conscientiously. Undoubtedly, soldiers caught in such a horrific missile attack will experience high degrees of stress, ground shaking, air pressure waves, etc., even without a blow to the head. Again, no surprise that the explosions could lead to headaches, and the nonspecific symptoms that blur the distinction between a physiologic mTBI, versus a posttraumatic stress disorder that can include many similar disabling symptoms. The distinction likely doesn’t matter much to those afflicted, unless they are erroneously labeled with the diagnosis of permanent structural brain damage. That could be a true casualty of the event.

Michael Brant-Zawadzki is a senior physician executive, and endowed chair, Pickup Family Neurosciences Institute, Hoag Hospital, Newport Beach, CA.

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