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Experience with mild traumatic brain injuries and postconcussion syndrome at Kandahar, Afghanistan.


In this article, we describe the in-theater experience with mild traumatic brain injuries (TBIs) and the changing approach to management, with the emphasis on in-theater evaluation that maximizes return to duty status and minimizes evacuation to Germany or to the United States. We also discuss the incidence, pathophysiology, recognition, and treatment of both TBI and its aftermath, postconcussion syndrome.


Every war seems to have its singular pattern of distinctive injuries or illnesses. Examples include the extremity amputations of our American Civil War and the cold weather injuries that were so prevalent during the Korean conflict. For Operation Enduring Freedom (OEF) [Afghanistan], the signature injury has become TBIs secondary to improvised explosive device (IED) exposures. (1) This situation is the result of a variety of reasons, but the additional protection provided by the enhanced body armor and the greater protection provided by the newer armored vehicles have reduced the number of fatalities from these blasts, and increased the number who suffer blast effects and survive.

The Department of Defense definition (below) of TBI is one of many available (2):

A traumatically induced structural injury and/or physiological disruption of brain function as a result of an external force that is indicated by the new onset or worsening of at least one of the following clinical signs, immediately following the event:

* Any period of loss or a decrease in the level of consciousness.

* Any loss of memory for events immediately before or after the injury.

* Any alteration in mental state at the time of the injury (confusion, disorientation, slowed thinking, etc).

* Neurological deficits (weakness, loss of balance, change in vision, praxis, paresis/ plegia, sensory loss, aphasia, etc) that may or may not be transient.

* Intracranial lesion.

We favor the above definition for its cause and effect relationship and the fact that it is reliant upon input not just from the affected individual, but requires input from a trained, objective provider.

Published data from the mid phases of the Iraq conflict show an incidence of 5% of Soldiers suffered a TBI with some effect on the loss of consciousness (LOC) and up to 10% suffered a TBI without any effect on LOC. (3) These reports are likely an underrepresentation since this was drawn from retrospective and self-reported data. Current efforts are underway to improve real-time tracking and reporting, but we feel the incidence in OEF is even higher, especially as troops are subject to multiple tours and repeated exposures to IEDs. The exposure to IED blast is a very common event among actively patrolling troops. We expect that eventually the published figures will show numbers beyond that experienced in Operation Iraqi Freedom. (4) An empirical observation is that repetitive subclinical injury from prior event(s) over time, often suffered over multiple tours, lowers the threshold for induction of TBIs by the next blast.


A long term assumption was that since typical central nervous system imaging studies (ie, computerized tomography (CT) scans of the head) are normal in the vast majority of those with mild TBI, no structural damage had occurred. We now know from a variety of sources that microscopic level damage occurs diffusely throughout the brain. (5) This has been confirmed in examinations of pathologic specimens and is also evident in functional central nervous system imaging studies, such as single photon emission computed tomography and positron emission tomography scans. The damage is to the level of the axons and often involves axonal stretching or even separation. Additionally, numerous excitatory neurotransmitters are released, as well as the typical acute phase reactants of tissue injury. (6) While recovery of the structural and biochemical damage is anticipated, the central point is that this is not a feigned injury. The damage is quite real.


The cardinal immediate phase symptoms can be defined into neurocognitive, somatic, and behavioral categories as follows:

* Neurocognitive--attention deficit, reduced speed in processing new information, or language dysfunction in the form of difficulty in finding words for expression.

* Somatic--focal neurologic deficits, headache, nausea with or without vomiting, sleep disturbance, visual complaints, fatigue, seizures, or vestibular symptoms, usually in the form of a sense of imbalance.

* Behavioral--depression, anxiety, irritability, impulsive behavior (including disinhibition) and, on rare occasion, symptoms of mania or psychosis. (7)

The cardinal symptoms are confusion and amnesia. Amnesia is typically for the period immediately following the injury. It is generally measured in minutes but can be retrograde and encompass longer time frames. The confusion is typically more evident to observers than the victim. The simplest approach is to ask the squad members: is this the same person or is he/she acting differently? (8) Simple questions as to whom, what, and why (ie, the sideline sports screen used for decades), are poor screening tools and suffer considerably in terms of sensitivity. More formalized screening tools are strongly suggested. In the civilian sector, the best validated tool is the Westmead Posttraumatic Amnesia Scale (9) (Figure 1), but the military now uses the Military Acute Concussion Evaluation (10) (MACE) (Figure 2). No head-to-head comparisons of the 2 tools are available, but the Westmead is more subjective while the MACE is more quantitative. In addition, the MACE scale can be used to follow serial responses and after physical exertion to see if replication of the physical stressors that a Soldier faces will cause worsening of the neurocognitive symptoms. The postexertional MACE functions as a poor man's central nervous system "stress test."

Other symptoms seen in the first 24 hours can include a constellation of complaints including escalating headaches, dizziness, true vertigo, insomnia, tinnitus, nonspecific visual complaints, nausea and vomiting (primarily in the first 24 hours), difficulty concentrating, short-term memory dysfunction, and a sense of imbalance. Our experience is that a grief reaction is frequently intertwined as the blasts often involve others in the squad who have been wounded-in-action/killed-in-action (WIA/KIA). Some component of immediate posttraumatic stress disorder is common in the form of flashbacks and nightmares. Effects of secondary soft tissue injuries are often more noticeable in the delayed phase as the fright and flight response begins to wane.

Signs can include a multitude of findings including the "thousand-yard stare," delayed verbal responses, an apparent concentration deficit, alterations in speech pattern, visible but subtle cerebellar findings, and emotional responses that are atypical or disproportionate for the individual. Many of these parallel what would be seen in a driving under the influence setting. Since the medical observers at the scene are typically medics and may not know the baseline appearance and function of the individual Soldier, the question should be posed to the battle buddies: is this the same guy you saw before the injury?
Figure 1. The Westmead Posttraumatic Amnesia Scale questions
used by civilian healthcare providers to screen patients with
possible traumatic brain injury. (9)

What is your name?

What is the name of the place you are in now?

Why are you here?

What month is this?

What year are we in now?

In what town/area are you from?

How old are you?

What is your date of birth?

What time of day is it? (morning, afternoon, evening)

Show three pictures and ask for delayed recall. (within one to two

Since presentation may be delayed to a medical treatment facility, the evaluation is best begun in the field by the medic or corpsman. MACE cards for use in the field are becoming available. The importance of the field evaluation is that it establishes an immediate baseline that then can be referenced as the casualty moves though the various echelons of the evacuation system. In particular, the MACE questionnaire provides an index that is quantifiable and simple to administer. If the MACE scores are regressing versus improving, it is a "red flag" to all concerned, and serves as a prompt to search for a reversible structural central nervous system injury, eg, a subdural hematoma.

While discussed in detail in prior TBI literature, prospective data shows seizures are relatively rare events, in mild to moderate TBI patients with an incidence of no greater than 5%. (11) Of those who suffer seizures, most are seen in the first 24 hours. The earlier seizures occur, however, the greater the likelihood of recurrences long term. Prophylactic antiepileptics have not been shown to be effective in prior prospective studies. Onset of seizures, however, is a red flag and should prompt immediate neuroimaging, even if previously done.

Prior reviews show CT head scan abnormalities in about 5% of those who present with a Glasgow Coma Scale* (GSC) score of 15 and are routinely scanned, as is often the case in civilian settings. As anticipated, the percentage of abnormal scans goes up as the severity of injury worsens, with up to 30 % of those with GSC of 13 (or less) showing demonstrable CT changes. Even these latter figures may be misleading in that only 1% of patients scanned have an abnormality that warrants neurosurgical intervention. (13) Sensitivity is excellent for CT scanning but specificity is poor. This has lead to criteria such as the Canadian CT head rule that help to select those who warrant scanning for lesions that have immediate clinical import. (14) The Canadian rules suggest scanning based on the following presenting clinical criteria:

* GSC score of less than 15 at 2 hours postinjury. The emphasis is on the individual who is failing to show signs of improvement in the immediate postinjury phase.

* Suspected skull fracture, especially with a history of blunt trauma.

* Physical findings of basilar skull fracture, such as hemotympanum, raccoon eyes, Battle's sign, or evidence of a cerebrospinal leak.

* Repetitive vomiting, defined as 2 or more episodes in the first 24 hours.

* Aged 65 years or older.

* A mechanism of injury that involves projection or a fall from a significant height, typically 3 feet or more, or a fall down 5 or more stairs.


We are not aware of any studies that have validated the Canadian rule in military field settings, but the rule has held up well in civilian trauma centers. CT scans may be difficult to access in theater, and we think the Canadian criteria provide an excellent triage tool.

Patients can and will deteriorate after a seemingly benign initial presentation. A variety of intracranial catastrophes can occur in the hours following initial presentation. Fortunately, these declines are rare. The key to recognition is the initially stable patient who deteriorates for no obvious and apparent reason. Then, immediate central nervous system imaging is mandatory to exclude treatable abnormalities such as epidural and/or subdural hematomas and/or intracranial hemorrhage. (15)

Although much discussed in the civilian literature, such postpresentation degradation is rarely seen and reported. The presentation is one of a seemingly benign TBI, typically seen in the context of a sports participant who suffers a mild TBI, returns to competition, and suffers a second concussion, in short succession. The affected patient then undergoes a rapid downhill course with features of diffuse cerebral edema and often suffers either death or severe disability. (16) Since many mild TBI patients have returned to play or duty and not suffered this sequence of events, the question remains as to whether there is some preceding genetic or structural process that makes these individuals uniquely susceptible. Since one cannot predict who is at higher or lower risk for this rare event, no one should be exposed to further risk of head trauma, in short sequence, unless it is absolutely unavoidable. The sports equivalent of "shake it off and get back in" no longer applies, either in the military or civilian sectors.


No specific drug interventions are typically suggested in the immediate phase outside of simple analgesics as needed. The time-honored dictum of avoiding drugs with central nervous system depressant effects remains true as they may color interpretation of evolving signs and symptoms. In fact primum non nocere [first do no harm] holds especially true as no drug interventions, including systemic steroids, have proven effective in ameliorating brain damage, even in those with the most severe of injuries. It remains best to keep any and all drugs to a minimum until stability is insured over the first 24 hours. (17)

Beyond the window of the first day, one can be more liberal with medications, though drug use remains reactionary and treats the symptoms but not the root cause, the injured brain. The intervention we have found to be of greatest benefit after the first 24 hours of insured stability are efforts at restoration of a more normal sleep-wake cycle. For a variety of reasons, insomnia is extremely common in the field setting and is typically a combination of difficulty with sleep initiation and sleep maintenance. We are not aware of any direct drug trials, but we have had empiric success with the older sedating antidepressants such as amitriptyline or trazodone. The most important thing for the injured brain is time and rest.

As anticipated, the earlier in the course we were able to see the patient and intervene, the better the outcome, with the vast majority returning to duty. If presentation was delayed to the care level of the combat support hospital, outcome was more suspect. Is this selection bias or a real phenomenon? We have no hard data to confirm this but observations from the field are by nature often empiric.

Adjunctive therapies can be used in the immediate phase that is nonpharmacologic and therefore low risk, if not necessarily high reward. A concussion class and/ or Soldier directed handouts explain in common terminology the anticipated course of events. This helps reassure affected individuals that what they are experiencing is very real, and describes the expected course and progress in recovery of their symptoms. It also reemphasizes the idea to the patient that the goal is to return them to duty, but full recovery will take time. A 20-year old Soldier is not blessed with the utmost of patience. We felt that the group rehabilitation milieu was beneficial because "misery loves company." We had a low threshold to involve mental health and/or combat stress control, especially if fellow squad members were WIA/KIA or if the patient had preinjury mental health difficulties. In this situation, "talk is cheap," and effective. If combat stress control resources are not available, chaplains can fill a similar role.

We also used physical and occupational therapy for the secondary soft tissue injuries that are not uncommon, especially to the neck or back. Lastly, we had the luxury of having acupuncturists available who were helpful with soft tissue injuries and also helped with certain aspects of the of the postconcussion component, mainly cervical pain. Overall, we found the busier we kept the patients, the less they dwelled on the event, and the more quickly they recovered. Our TBI clinic kept the patients on base for as short a period as possible and aimed to return them to their forward operating base as soon as our "hard court press" was completed. In reality, our clinic was a program.

In the immediate phase, the question is whether or not the individual should be hospitalized. We were liberal about initial hospitalization. Any hint of regression of GSC or MACE scores was a trigger. In addition, a history of blunt head trauma was often a trigger to hospitalize. Since these patients were often brought from outlying bases and were separated from their battle buddies, ** we did not always have the luxury of using the civilian equivalent of sending them home with a head trauma sheet for a "family" to follow in the first 24 hours postinjury. With all of those provisos, the vast majority of those with a mild TBI, even in a battlefield environment, still do not need to be hospitalized, and their entire course of management can be performed on an outpatient basis.

Unit leaders want their Soldiers, Marines, Sailors, and Airmen back to fill their ranks immediately. Although the goal must be to preserve the fighting strength, this must not trump the need for the brain to have adequate time to recover. As a general rule of thumb, we found that a minimum of 2 to 4 weeks was necessary to stabilize the injury. Recovery did not mean that the service member needed to stay at our facility or under our guise for the entire length of the rest and recovery phase. It did mean that they could not be exposed to potential head trauma during the minimal time frame of rest. Further, even if they did return to their forward operating base, they were not to go "beyond the wire" for whatever time period we determined to be necessary for recovery.

An evolving and very important question is whether there is a point at which we must say too many cumulative injuries have occurred and a long-term modification of duties is absolutely necessary. The Marines have taken the lead in this regard. The current USMC intheater guidelines (18) are:

* First injury: "brain rest" for between 2 to 4 weeks.

* Second injury: a minimum of 4 weeks (and possibly longer) of no risk or very low risk exposure.

* Third injury: the line is drawn and that individual will not go beyond the wire for the remainder of his or her tour.

The above guidelines are defined by injuries within a given tour. However, there are no current guidelines to address the common scenario of multiple exposures over multiple tours. In our experience, individuals were often not "back to baseline" by the time of their redeployment, and the next injury that occurred on the current tour was the breaking point. On occasion, the 3 strikes rule was not exceeded, but the clinical line was undoubtedly crossed, and we had to insist that the individual be withdrawn from exposure on a permanent basis. This is a grave decision that affects the individual, the unit, and the higher command, and it is not taken lightly. We invoked such limitations only if we were convinced that return to preinjury status was unlikely, and that further exposures bring a high likelihood of an irrevocably injured brain.


There is no clear separation between the acute injury and the potential aftermath. Studies have shown that up to 80% of head injury patients have symptoms of a postconcussion syndrome. (19) Unfortunately, we do not have good data from the battlefield environment, particularly for those with multiple blast exposures and head injuries over multiple tours. Most published data for postconcussion syndrome is drawn from the civilian sector, but we suspect that carefully gathered information from the current active theaters would show similarly high rates of occurrence. Only data from predeployment information which is compared to postdeployment information will be objective enough to qualify, since retrospective data is subject to considerable recall bias.

Symptoms far outweigh signs, and nondynamic CNS imaging studies, if done, are typically normal. This means that the postconcussive syndrome is defined almost entirely based on subjective symptoms. There is no current objective test to separate those with superimposed secondary gain. Perhaps the currently used Automated Neuropsychological Assessment Metrics (20) screening will help to fill this information gap, but since predeployment screening was only recently begun, it will not be of any use for the thousands who have been injured prior to late 2009.

In our experience and that of others, the most frequent symptoms were headaches and cognitive dysfunction. Other symptoms include mood liability, continued sleep disturbance, and a residual sense of imbalance. To the previously invulnerable 20-year old, the most frightening symptom is cognitive dysfunction. The pattern most often seen is a combination of short-term memory difficulty and an overall sense of difficulty in concentration. These mimic in many ways the early stages of the memory dysfunction often seen in the elderly such as the subtle syndrome of mild cognitive disorder. A parallel exists in what has been observed in some former professional and amateur athletes, the worst being dementia pugilistica seen in professional boxers who have suffered repeated head trauma. A limited number of former professional football players have experienced a neuropathologic entity called chronic traumatic brain injury or chronic traumatic encephalopathy. (21) The disturbing pathologic information is that the visible macro- and microscopic damage is quite similar to that seen in traditional dementia. While all of these tantalizing bits of information are nothing more than food for thought, the aggregate harkens back to the concept that structural damage does occur even with a mild TBI, the changes may not be fully reversible in all, and cumulative damage may occur.

Treatment of the headaches includes a variety of therapies, both reactive as well as prophylactic in nature. Most of these have existed in the civilian literature for decades. As discussed previously, one caution is to avoid agents with sedative capacity, for obvious reasons, in field settings. Fortunately for most patients, the headaches do diminish in severity and frequency over time.

Unchartered territory exists in terms of how to address the cognitive dysfunction. Are cholinergic agents such as donepezil appropriate for those with features of mild cognitive dysfunction? Are stimulant agents such as the amphetamine compounds of value for those with features of attention deficit disorder? Considerable research is ongoing to address these questions, but for now they remain unanswered and considerable empiricism is necessary.

Our experience was that a considerable admixture of depression and posttraumatic stress disorder coexists in those who suffer long term symptoms. (22,23) This raised a logical question as to the efficacy of any of a variety of psychotropic medications, in particular, antidepressants, in treatment of those individuals. Since these drugs are, in general, medications with excellent therapeutic/toxic ratios, we had little hesitation to use these medications, if the mood component was becoming dominant and time was not providing alleviation. Obviously, the hope is that the use of antidepressants is a short-term rather than a long-term requirement. We consider major and minor tranquilizers to be inappropriate at the front and more rear echelon type interventions, and consciously avoided their use. Psychiatric treatment, if available, can be of considerable help. However, it may be a limited resource, especially at the level of the forward operating base and the battalion aid station's level 1 care must by necessity often assume this role. Combat stress control assets can provide counseling, but again, availability may be limited.

Both short- and long-term sleep disturbance is common. A variety of sopoforic agents are now available, most of which again have favorable side effect profiles and minimal capacity for dependence. Very few of us sleep well in-theater, but patients with structural and somatic overlay have an especially difficult time sleeping. The net debt from chronic sleep fragmentation is well-described. We felt that part of both the immediate and long-term treatment was liberal use of drugs, such as low dose trazodone, to restore some semblance of a more normalized sleep pattern. At low dose, those are drugs with low toxic risk, though we purposely limited the volume of the distributed medication to minimize risk of an intentional overdose.

While not the intention of this article, some comments about the experience in the United States with severe TBI patients is not only of interest, but also relevant as we providers encounter such patients when we return to our US facilities, be they military, Veterans Affairs, or civilian. Severe injuries are more commonly caused by penetrating head injuries and are typically associated with very low Glasgow Coma Scores on presentation. Salient observations of this unfortunate subset of individuals include the following (24):

* As anticipated, presenting Glasgow Coma Scores correlate with both survival and residual morbidity.

* However, severe injuries do not always equate to poor outcomes; the young and previously healthy brain can have amazing recuperative powers.

* Overall survival rates are high (95%) among those who survive long enough to be evacuated to the United States.

* In-hospital complication rates are high and include a variety of events that have both short- and long-term import. Some of these include:

* Systemic infections are common (46%).

* Pulmonary embolism is common, especially since anticoagulation prophylaxis is contraindicated (7%).

* Cerebrospinal fluid leaks and infections are not infrequent (9%).

* Early onset seizures are not infrequent (12%).

* Spinal cord and column injuries often accompany the initial injury (10%).

* Posttraumatic aneurysms and arteriovenous malformations are surprisingly common (8%).


From mid November of 2009 through mid April 2010, 125 new patients were seen in the TBI clinic at the combat support hospital at Kandahar Air Field. Most were referrals from outlying forward operating bases (FOBs), and virtually all patients were seen for at least one follow-up visit. The time from initial injury to presentation to our clinic varied from days to months, but since the beginning of 2010, most were seen in the immediate phase, allowing better evaluation and treatment. A total of 360 patient encounters occurred prior to our departure. No patients required hospitalization, and well over 90% returned to duty and to their prior military occupation specialty functions and duty assignments, in particular the combat roles. The goal is to return to the referring FOB immediately, drawing from the model of combat stress control to make the recovery process FOB-centric. Whatever time is necessary for limited duties and activities inside the wire is best spent within the environment of the squad and unit.


Traumatic brain injury is common in the current operational environment. Diffuse brain injury is the norm, though this condition cannot be readily measured by current means, including standard central nervous system imaging. Screening for a significant injury is best accomplished by a standardized format, such as the MACE scale, which can be initiated at the level of the squad medic. While recovery is anticipated, a significant percentage suffers long-term sequalae, especially in the form of mood disturbances and cognitive dysfunction. The point at which the individual must be removed, at least short-term if not permanently, from further blast exposures is a looming concern. For now, we concur with the "3 strikes and you're out" policy practiced by the Marines. However, at present this is defined by exposures during a single tour and does not address the more common situation of multiple TBIs occurring in an interspersed manner over multiple tours.

Treatment is largely supportive, though this is an area of intense interest for effective immediate phase therapies. Brain rest is imperative in the immediate phase of injury, and a minimum time spent inside the wire (at least 2 to 4 weeks) is absolutely mandatory. As one moves into the area of the postconcussion syndrome, long-term treatment involves maintenance of sleep and treatment of depression and posttraumatic stress syndrome, if they coexist. At present, no known and proven treatment exists for the neurocognitive sequalae. Whether use of dementia and attention deficit disorder drugs used in the civilian sector will be of benefit remains to be determined. As we move further away from the initial military TBI injuries of the early 2000s, both military and civilian caregivers will likely be forced to use such therapies more and more in this atypical subset of young/old brains to maintain function. This will be necessary within both the military and civilian environments as the injured experience the lingering effects of cumulative damage and deterioration brought about by time and the aging process.



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(2.) Assistant Secretary of Defense, Health Affairs. Memorandum: Traumatic Brain Injury: Definition and Reporting. Washington, DC: US Dept of Defense; October 1, 2007. Available at http:// Accessed June 14, 2010.

(3.) Hogge CW, McGurk D, Thomas JL, et al. Mild traumatic brain injury in US soldiers returning from Iraq. New Engl J Med. 2008; 358:453-463.

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(7.) French LM, Parkinson GW Assessing and treating veterans with traumatic brain injury. J Clin Psychol. 2008;64:1004-1013.

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(9.) Marosszeky NEV, Ryan L, Shores EA, Batchelor J, Marosszeky JE. The PTA Protocol. Glebe, New South Wales, Australia: Wild & Wooley; 1998. Available at: index.html. Accessed June 14, 2010.

(10.) Defense and Veterans Brain Injury Center. Military Acute Concussion Evaluation (MACE) Information Paper. Available at: pdfs/providers/MACE-Information-Paper-V3.aspx. Accessed June 16, 2010.

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(16.) Saunders RL, Harbaugh RE. The second impact in catastrophic contact-sports head trauma. J Am Med Assoc. 1984;252(4):538-539.

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(18.) Defense and Veterans Brain Injury Center. Joint Theater Trauma System Clinical Practice Guideline. Management of Mild Traumatic Brain Injury (mTBI)/ Concussion in the Deployed Setting. November 2008. Available at: /Management%20of%20Mild%20TBI%20(mTBI) Concussion%20in%20the%20Deployed%20 Setting.pdf. Accessed June 25, 2010.

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(20.) Ivins BJ, Kane R, Schwab KA. Performance on the automated neuropsychological assessment metrics in a nonclinical sample of soldiers screened for mild TBI after returning from Iraq and Afghanistan: a descriptive analysis. J Head Trauma Rehabil. 2009;24 (1):24-31.

(21.) Loosemore M, Knowles CH, Whyte GP. Amateur boxing and risk of chronic traumatic brain injury: systematic review of observational studies. Br Med J. 2007;335(7624):809.

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(23.) Hill JJ, Mobo BH, Cullen MR. Separating deployment-related traumatic brain injury and posttraumatic stress disorder in veterans: preliminary findings from the Veterans Affairs traumatic brain injury screening program. Am J Phys Med Rehabil. 2009;88(8):605-614.

(24.) Bell RS, Ho AH, Ned CJ, et al. Military traumatic brain and spinal column injury: a 5 year study of the impact blast and other military grade weaponry on the central nervous system. J Trauma Inj Infect Crit Care. 2009;66(suppl 4):S104-S111.

* The Glasgow Coma Scale is a quick, practical, standardized system for assessing the degree of consciousness in the critically ill and for predicting the duration and ultimate outcome of coma, primarily in patients with head injuries. The system involves eye opening, verbal response, and motor response, all of which are evaluated independently according to a rank order that indicates the level of consciousness and degree of dysfunction. (12)

** Generally defined as the person to whom a Soldier can turn in time of need, stress, and emotional highs and lows who will not turn the Soldier away, no matter what. This person knows what the Soldier is experiencing because of experience with similar situations or conditions, either current, previous, or both.

LTC Ralph D. Caldroney, MC, USAR

CAPT James Radike, MC, USN

LTC Caldroney has been an internal medicine physician in Lexington, Kentucky, for 30 years. When this article was written, he was the Command Surgeon, 135th Expeditionary Sustainment Command, Kandahar Air Field, Afghanistan.

CAPT Radike is an internist at the Naval Hospital, Pensacola, Florida. When this article was written, he was the Senior Medical Officer and Director of Clinical Services at the NATO Role 3 Hospital, Kandahar, Afghanistan.
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Author:Caldroney, Ralph D.; Radike, James
Publication:U.S. Army Medical Department Journal
Article Type:Report
Geographic Code:9AFGH
Date:Jul 1, 2010
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