Blast Injury

Posted on January 15, 2009 by Tim Titolo


A commonly held belief is that the pressure alone from an explosive blast injury is sufficient to cause brain injury in human beings. While this would intuitively seem to make sense, what many people do not realize is that there are no published, peer reviewed, prospective research studies with human subjects that have demonstrated this to be the case. The evidence to date is based on a few old single case studies, military documents that were not scientific research studies, and data from animal research.

There is no doubt that explosive blasts are associated with brain injury. However, there are many components to a blast that can cause injury to the body. First, there is the primary pressure wave injury, which is injury caused by the changes in the atmosphere caused by the explosion. The organs that are most vulnerable to this type of injury are those with air-fluid interfaces, such as the lungs, intestines, or inner ear. These tend to be hollow body parts. The most common type of injury from a primary pressure wave explosion is an eardrum rupture.

Then there are secondary blast injuries, in which the force of the explosion causes objects to fly through the air and strike someone. There is no doubt that this can cause a brain injury, since an object can fly through the air at considerable force and cause blunt trauma to the skull and its underlying contents. A tertiary injury is when the force of the explosion causes the person to be thrown into solid object. Clearly, this can also cause brain injury, if the person is thrown forwards with enough force.

One of the problems in stating that primary pressure waves causes brain injury in humans is that it is often impossible to know whether or not someone (such as a soldier) was only exposed to a primary blast injury or whether secondary or tertiary injuries also occurred. As Hurley and colleagues (2006) stated, “A still unresolved controversy is whether primary blast forces directly injure the brain” (p. 143, emphasis added). Similarly, Bochicchio and colleagues (2008) noted “...it is difficult to clearly distinguish between primary versus secondary or tertiary blast injury” (p.270). It is important to emphasize that no one denies this is possible, or even that it is likely, but caution needs to be taken before it is stated as a scientific fact in humans.
 


The word “humans” is emphasized because there is evidence that primary pressure waves alone can cause brain injury in animals. However, generalizing from animal studies to humans is not always possible. To begin with, the brains of mice, which is the animal group most often researched in these types of studies, are extremely small, structurally different, and not at all identical to the brains of humans. Secondly, the animal studies typically involve exposing them to blast forces at the end of a giant shock tube. While this may be something you see in an episode of a Tom and Jerry cartoon, it is not necessarily something that can be generalized to what soldiers experience during war time. To quote Hurley and colleagues, “The vulnerability of the human brain to primary blast injury is controversial and an area of active research” (p. 145).

As the committee of the Institute of Medicine (IOM) reported in December 2008, "There is a paucity of information in the scientific literature regarding the sequelae of blast injury, and there is a need for prospective, longitudinal studies to confirm reports of long-term effects of exposure to blasts." The IOM report was commissioned by the Department of Veterans Affairs and based on an analysis of 1,900 peer-reviewed studies.

MTBIFacts.com fully supports future research in this area but cautions against definitive statements on this topic until such research has been performed, replicated, and accepted by the general scientific community.

REFERENCES

Bochicchio et al. (2008). Blast injury in a civilian trauma setting is associated with a delay in diagnosis of traumatic brain injury. The American Surgeon, 74, 267-270.

Hurley et al. (2006). Blast-related traumatic brain injury: What is known? J Neuropsychiatry Clin Neurosci, 1, 141-145.

Copyright © 2009, MTBIFacts.com.

Dr. Carone offers paid lectures on MTBI, “post concussion syndrome,” and symptom validity testing upon request. He can be contacted at info@mtbifacts.com.

 
 

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All Brain Injuries are the Same Myth

Posted on January 12, 2009 by Tim Titolo


 

I have published articles on this topic previously but it is worth reprinting.  This one is by neuropsychologist Dr. Carone.  He  offers paid lectures on MTBI, “post concussion syndrome,” and symptom validity testing upon request. He can be contacted at info@mtbifacts.com.

Another one of the most popular myths perpetuated by some health care providers and some in the media is that mild traumatic brain injuries (TBIs) can be equated with moderate to severe traumatic brain injury. While this is not usually stated in such precise language, the way the topic is discussed often conveys this impression. This occurs when the effects of “brain injury” are discussed with patients or the public. What often happens is that findings from patients with moderate to severe TBIs are misapplied to those with injuries on the mild end of the spectrum. The assumption seems to be that a brain injury is a unitary construct when this is not actually true. As Dr. Michael McCrea (2008) writes in his evidence based text, moderate to severe TBI is a completely different animal than mild TBI. There are many examples, which are nicely summarized in McCrae’s text and the interested reader should read that book for specific references supporting the statements below. Some of these examples are presented and expanded upon below.

1. USEFULNESS OF SEVERITY GRADING TOOLS: In moderate to severe TBI, there are measures available that are useful for grading the severity of the injury whereas the scales on the mild end of the spectrum are not as helpful. The most commonly used severity index is the score on the Glasgow Coma Scale (Teasdale & Jennett, 1974) which assesses level of consciousness. The scale ranges from 3 to 15 points and provides a way to rate patients on their eye movements, motor responses, and verbal responses. The TBI classification scheme based on the GCS is as follows: 13-15 (mild), 9-12 (moderate), and 3-8 (severe). While a significant injury and/or alteration in consciousness is required to obtain a GCS score between 3 and 12, the same cannot be said for the mild end of the TBI severity range. For example, consider a person who merely bumps his head into a wall with a minimal degree of force that was not significant enough to cause a brain injury. Assume, however, that the person develops a headache and is concerned that he has a brain injury, causing him/her to go to the ER. When the person goes to the ER, he/she is physically examined and a GCS score of 15 is assigned because there were no abnormalities with eye movements, motor responses, or verbal responses. According to the criteria above, a GCS score of 15 is equated with a mild TBI. Clearly, however, this example shows a GCS score of 15 does not always equate to brain injury.

2. ACUTE INJURY CHARACTERISTICS: In moderate to severe TBIs, the acute injury characteristics are the strongest predictors of outcome. In mild TBIs, there is only a limited correlation between acute injury characteristics and outcome. For example, in mild TBI, a brief and transient loss of consciousness is not strongly predictive of outcome. Conversely, loss of consciousness in a severe TBI patient, which could last for weeks and beyond, is strongly correlated with outcome. One of the problems is that acute injury characteristics are not as clearly documented in MTBI cases because of a lack of witnesses and the transient nature of the event. For example, a mild TBI patient may lose consciousness for a few minutes but if no one was present to witness this, it cannot be confirmed. Conversely, in a moderate to severe TBI case, LOC usually lasts long enough such that paramedics or some other observer would be able to confirm its presence.

3. CRITERIA FOR DIAGNOSIS: The criteria for diagnosing moderate to severe TBI tends to be more consistent throughout the literature compared to mild TBI. The criteria used to diagnose MTBI are largely based on self-reported subjective symptoms (e.g., altered mental status) without collaborating and/or objective data (e.g., witnesses, neuroimaging findings). In moderate to severe TBI, objective data are often sufficient enough (e.g., diffuse bleeds throughout the brain) such that self-report is not required to make the diagnosis.

4. NEUROIMAGING: In moderate to severe TBI, the results of neuroimaging are critical to deciding how to manage the patient. For example, if a bleed is large enough, this might require neurosurgery to remove pressure on the brain. This sometimes requires repeat brain scans in the acute injury phase to monitor the size and effects of an intracranial lesion (e.g., a brain bleed). In MTBI cases, initial neuroimaging results in the ER do not show abnormalities between 90 to 95% of the cases. Thus, after an initial negative brain CT scan, clinical management of the MTBI patient is often based on subjective symptoms (e.g., headache) rather than objective findings.

5. COURSE: In moderate to severe TBI, the recovery course is well-defined and empirical, with the most drastic improvement occurring in the first six months, additional recovery over the next six months, and slower recovery up to 18 to 24 months. In mild TBI, the course of recovery is clear for the vast majority of people which would suggest that most recover within a week to a few months. However, the course of recovery for those who experience persisting symptoms (more than three months) is less clearly understood.
 


6. OUTCOME: As noted above, outcome is strongly related to acute injury characteristics in moderate to severe TBI cases and it is generally an exception when psychological factors confound outcome (although this certainly can occur). Conversely, in mild traumatic brain injury, outcome is poorly related to acute injury characteristics. Rather, non-injury related factors tend to be the most predictive of outcome. Examples of non-injury factors include litigation/compensation-seeking, psychological distress, pre-injury psychiatric history, post-injury stressors, substance abuse, and various other psychosocial issues.

7. DISABILIY: In moderate to severe TBI, disability (a form of outcome) is more clearly attributed to injury severity, the functional neuroanatomy of the injury, and resulting impairments. In mild TBI, there is a less clear association between the clinical presentation of the patient and the degree to which neurological and psychological factors play a role.

These examples show that one cannot speak of traumatic brain injury as if it has the same meaning across the severity spectrum. The media and health care providers are strongly encouraged to clearly distinguish between mild and moderate to severe brain injuries when discussing this topic with patients and the public.

REFERENCES

McCrea, M. (2008). Mild traumatic brain injury and postconcussion syndrome. The new evidence base for diagnosis and treatment. New York: Oxford University Press.

Teasdale, G, Jennett, B. (1974). Assessment of coma and impaired consciousness. A practical scale. Lancet, 2:81–84.

 Copyright © 2009, MTBIFacts.com.
 

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