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  #1  
Old 31-01-2008, 02:22 PM
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anthony anthony is offline Gender Male
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Default Disentangling Mild Traumatic Brain Injury and Stress Reactions

The study by Hoge and colleagues in this issue of the Journal provides an important profile of the sequelae of mild traumatic brain injury in military personnel after combat.1 The findings demonstrate that mild traumatic brain injury results in increased rates of psychological, health, and functional problems. Although the study provides strong evidence for impairments in military personnel serving in Iraq and Afghanistan, it also raises a number of critical questions concerning the impairments that may be attributed to mild traumatic brain injury.

One striking finding from this study is that although mild traumatic brain injury predicted a range of health problems, its effects became nonsignificant after post-traumatic stress disorder (PTSD) and depression were considered. This pattern is in accordance with other studies2 and points out that one must use caution when attributing health problems to mild traumatic brain injury, because associated PTSD and depression may be the primary problem. This is an important point because mild traumatic brain injury typically occurs in the context of a traumatic event, and psychological stress will probably be influential in many cases of mild traumatic brain injury.

If Hoge and colleagues had not assessed for PTSD and depression, the possible conclusion from this study would have been that mild traumatic brain injury is the causative agent for the impairment observed in many soldiers. This mistaken conclusion often has been made in clinical settings, and impairment observed in the aftermath of mild traumatic brain injury has been attributed incorrectly to neurologic insult, rather than psychological distress.

One of the classic features of mild traumatic brain injury, and the presumed cause of impairment after mild traumatic brain injury, is postconcussive symptoms. These symptoms can include problems with memory, balance, and concentration, as well as ringing in the ears, sensitivity to light or sound, and irritability. There has been a long-standing debate about the extent to which postconcussive symptoms are a result of organic or psychological factors, or an interaction between the two.3 Incontrovertible evidence now shows that psychological factors play a significant role in postconcussive symptoms; one recent study showed that postconcussive symptoms occur at similar rates in persons with mild traumatic brain injury and in those with no traumatic brain injury.2 Misattributing postconcussive symptoms to brain injury may have unfortunate implications, because it may be concluded that recovery depends on neurologic factors. The evidence suggests that participation in educational programs that normalize the reactions can alleviate postconcussive symptoms.4 The evidence from Hoge and colleagues, as well as from other studies,5 that psychological factors account for many postconcussive symptoms suggests that more effective interventions may involve augmenting educational programs with strategies that aim to reduce PTSD and depression.

The finding that mild traumatic brain injury is associated with an increased incidence of PTSD raises interesting possibilities about how mild traumatic brain injury may compound PTSD. Biologic models posit that a fundamental mechanism underpinning PTSD involves an exaggerated response of the amygdala, resulting in impaired regulation by the medial prefrontal cortex.6 The amygdala is central to the development and expression of conditioned fear reactions, and studies in humans and animals have shown that learning to inhibit these fear reactions involves inhibition by the medial prefrontal cortex. Consistent with this model, patients with PTSD have diminished activation of the medial prefrontal cortex during the processing of fear.7 Mild traumatic brain injury often involves damage to the prefrontal cortex due to shearing forces of the frontal regions against the skull. It is possible that a person's capacity to regulate the fear reaction may be impaired after mild traumatic brain injury because the neural networks involved in the regulation of anxiety may be damaged as a result of the mild traumatic brain injury.8

Cognitive models propose that PTSD is maintained when trauma survivors have inadequate cognitive resources to manage their trauma memories and to engage adaptive cognitive strategies to manage the traumatic experience (e.g., they are unable to appraise a distressing state as temporary and, therefore, have heightened anxiety).9 Mild traumatic brain injury can impair cognitive resources10 and may compromise the capacity to engage in cognitive strategies to manage the aftermath of a psychological trauma. There is overwhelming evidence that maladaptive cognitive strategies (e.g., ruminating that one will never recover from the traumatic experience) after trauma are a major predictor of PTSD.9 Therefore, it is possible that people with mild traumatic brain injury have insufficient cognitive resources to engage appropriate cognitive strategies, which results in a greater incidence of PTSD.

The current study also highlights the need for clear operational definitions of mild traumatic brain injury. The study retrospectively assessed for mild traumatic brain injury by inquiring about having a loss of consciousness, being dazed, or not remembering the injury. Each of these reactions can be attributed to acute stress responses.11 There are no reliable means to differentiate between symptoms involving impaired awareness that are caused by severe stress or mild traumatic brain injury,3 so differential diagnosis is problematic. This problem is highlighted by retrospective accounts of injury, because during recall of trauma reactions, people with severe psychological disturbance overestimate the symptoms that they had in the acute phase12 and also their exposure to harm.13 It is preferable to use validated measures of post-traumatic amnesia in the immediate aftermath of the suspected mild traumatic brain injury to determine the extent of impaired awareness.

There are two very important outcomes of the study by Hoge and colleagues. First, soldiers who have mild traumatic brain injury are at greater risk for health-related problems. Second, soldiers should not be led to believe that they have a brain injury that will result in permanent change. Previous military conflicts have led to syndromes that have involved specific constellations of symptoms that are ascribed to some cause. After the first Gulf War, many soldiers had unexplained somatic symptoms — the so-called Gulf War syndrome — which many commentators ascribed to concern about chemical agents, even though exhaustive tests failed to determine a neurologic basis for the symptoms.14 If troops currently serving in Iraq or Afghanistan are informed about a postconcussive syndrome and persistent problems emerging from mild traumatic brain injury, a new syndrome could arise from the current conflict in which soldiers attribute a range of common stress reactions to the effects of brain injury. This could be damaging to morale and to the person's future mental health, because it could lead to the expectation of poor recovery. In contrast, the normalization of many of these reactions and the recognition that stress-related conditions can be managed with evidence-based strategies may minimize the unnecessary attribution of common stress reactions to pathology and facilitate resilience after mild traumatic brain injury.

No potential conflict of interest relevant to this article was reported.

Source Information

From the School of Psychology, University of New South Wales, Sydney.

References

1. Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro CA. Mild traumatic brain injury in U.S. soldiers returning from Iraq. N Engl J Med 2008;358:453-463. [Free Full Text]
2. Meares S, Shores EA, Taylor AJ, et al. Mild traumatic brain injury does not predict acute postconcussion syndrome. J Neurol Neurosurg Psychiatry (in press).
3. Bryant RA. Posttraumatic stress disorder and traumatic brain injury: can they co-exist? Clin Psychol Rev 2001;21:931-945. [CrossRef][ISI][Medline]
4. Mittenberg W, Tremont G, Zielinski RE, Fichera S, Rayls KR. Cognitive-behavioral prevention of postconcussion syndrome. Arch Clin Neuropsychol 1996;11:139-145. [CrossRef][ISI][Medline]
5. Bryant RA, Harvey AG. Postconcussive symptoms and posttraumatic stress disorder following mild traumatic brain injury. J Nerv Ment Dis 1999;187:302-305. [CrossRef][ISI][Medline]
6. Rauch SL, Shin LM, Phelps EA. Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research -- past, present, and future. Biol Psychiatry 2006;60:376-382. [CrossRef][ISI][Medline]
7. Lanius RA, Bluhm R, Lanius U, Pain C. A review of neuroimaging studies in PTSD: heterogeneity of response to symptom provocation. J Psychiatr Res 2006;40:709-729. [CrossRef][ISI][Medline]
8. Kennedy JE, Jaffee MS, Leskin GA, Stokes JW, Leal FO, Fitzpatrick PJ. Posttraumatic stress disorder and posttraumatic stress disorder-like symptoms and mild traumatic brain injury. J Rehabil Res Dev 2007;44:895-920. [Medline]
9. Ehlers A, Clark DM. A cognitive model of posttraumatic stress disorder. Behav Res Ther 2000;38:319-345. [CrossRef][ISI][Medline]
10. Landre N, Poppe CJ, Davis N, Schmaus B, Hobbs SE. Cognitive functioning and postconcussive symptoms in trauma patients with and without mild TBI. Arch Clin Neuropsychol 2006;21:255-273. [CrossRef][ISI][Medline]
11. Harvey AG, Bryant RA. Acute stress disorder: a synthesis and critique. Psychol Bull 2002;128:886-902. [CrossRef][ISI][Medline]
12. Harvey AG, Bryant RA. Memory for acute stress disorder symptoms: a two-year prospective study. J Nerv Ment Dis 2000;188:602-607. [ISI][Medline]
13. Wessely S, Unwin C, Hotopf M, et al. Stability of recall of military hazards over time: evidence from the Persian Gulf War of 1991. Br J Psychiatry 2003;183:314-322. [Free Full Text]
14. Jones E, Hodgins-Vermaas R, McCartney H, et al. Post-combat syndromes from the Boer war to the Gulf war: a cluster analysis of their nature and attribution. BMJ 2002;324:321-324. [Erratum, BMJ 2002;324:397.] [Free Full Text]
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  #2  
Old 03-02-2008, 09:23 AM
Beachbum Beachbum is offline Gender Female
 
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Default questionable research?

As I have been researching PTSD and TBI/ABI for some time now, I was pretty shocked to read the conclusions from this 'study' by Hoge. I wonder where the funding came from as it is a clearly biased study. My guess would be funding from the military, and/or drug companies (who are making millions of dollars fom medications such as antidepressants that actually CAUSE some brain/neurological/neurotransmitter etc damage) perhaps supported by medics (who get taken on 'jollies' by the drug companies in their efforts to get as many patients as possible onto their medications)? I haven't yet checked the sources used here but there is a lot of conflicting 'evidence' in all these areas: it appears possible to 'prove' whatever is required, the more I learn in this area the less I trust just one piece of research!

1. It says:"one recent study showed that postconcussive symptoms occur at similar rates in persons with mild traumatic brain injury and in those with no traumatic brain injury".
This is ridiculous! MRI scans often do no show mild TBI/ABI - is that the 'evidence' used for determining which people had brain injury & which didn't, or WHAT was used? 'Postconcussive symptoms' are caused by concussion - a brain injury. There is generally a very high incidence of brain injury going undetected (up to 50%) - doctors (if they even bother to do an MRI scan) use the apparent lack of 'evidence' of injury as 'there is no injury' - a dreadful fallacy that has been proved bad practice for many years now and doesn't even hold up in court. Most often, if any scan is done, it is done too soon after the event, with incorrect settings, and/or only with CT.

2.It says: "There are no reliable means to differentiate between symptoms involving impaired awareness that are caused by severe stress or mild traumatic brain injury, so differential diagnosis is problematic."
Yes, it can be problematic and it requires a WILL to WANT to find the difference, and for various reasons, this will is often lacking, but there are however neuropsychological tests that if done properly & at the correct time, can differentiate between the two (& including Aquired, non-traumatic brain injury fom eg anoxia/toxins etc). There are several studies that have looked at this. Also, to suddenly have a brain injury and the terror that can cause: to not be able to do or see or understand all the things you could before, is VERY shocking and that can cause very severe stress reactions and depression etc, as can DENIAL that this is the case, on top of the injury. Betrayal trauma on top of brain injury is extremly damaging, treating a patient as if they are 'somatising' their symptoms is one of the cruellest things a doctor or psychologist can do. I have come across many people whose brain tumours were not 'diagnosed' early on by medics who chose not to listen to their patients - thinking they, the docs, of course know better! Instead these people were prescribed antidepressants and told they were 'imagining' their symptoms for so long that their tumours grew so large that eventual surgery was much more dangerous as extensive brain damage had occurred from the greatly enlarged tumour.

3. It says: "After the first Gulf War, many soldiers had unexplained somatic symptoms — the so-called Gulf War syndrome — which many commentators ascribed to concern about chemical agents, even though exhaustive tests failed to determine a neurologic basis for the symptoms."
To call these purely SOMATIC symptoms is ridiculous now, there is too much evidence to the contrary, although the military (from both sides) has done its best to cover up info on the neurotoxins etc they used, just as in Portan Down, England. Whose 'exhaustive tests' are being referred to? There is clear neurological involvement in very many (probably almost all if truth were actually told) of Gulf War syndome sufferers. This smacks rather of early medical views on ME: some yars ago patients were told they were somatising symptoms & were 'psychiatric' cases whereas now it's clear there are clusters of what is now known to be a real physical illness (with CNS damage) & evidence of virus involvement etc - rather sad that soldiers are being tarred with this same brush by psychologists who should know better. Interestingly, neurotoxic damage often does not show on MRI scan and the best tests that would show it are often not done at all, eg muscle biopsy, specific blood tests - I wonder why?! Yes, it might frighten soldiers, frighten & educate & mak them AWARE, NOT make them somatise, it mght also allow them to not be afraid to REPORT! Clearly because it is cheaper for the military to 'treat' PTSD, rather than brain damage. It is true that it's good for patients to HOPE that they can recover when 'only' PTSD rather than brain damage, but when this is a wrong diagnosis it is preventing correct treatment & rehab, that if done early on would ensure maximum possible recovery. The more I find out about PTSD & TBI/ABI/neurological damage, the more I am led to believe that many many more cases of 'just' PTSD now will, with correct diagnosis, turn out to be TBI/ABI/neurological damage - including damage to neurotransmitters - but of course the military and medical & motor insurance companies etc all have enormous financial incentives to NOT 'recognise' an even more serious diagnosis than PTSD.
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  #3  
Old 03-02-2008, 10:36 AM
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anthony anthony is offline Gender Male
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You should never trust one piece of research, because as you state is actually quite correct, all research shows bias because they are looking for a particular answer before they begin, not allowing the study to find its own answers. The moment they look for an expected outcome is the same moment the study is tainted with bias.

Yes, other factors are prevalent from pharmaceutical companies, military and the like. I have seen this first hand, so it does happen.
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Old 07-02-2008, 12:23 AM
tiltmonster tiltmonster is offline Gender Male
 
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Default conflict?

Now I am really confused. I think I need to read the actual report? Perhaps that is a monumental task? Does the Hoge report claim TBI is psycological; or is this the extracted meaning by the editor(psycologist association)? PTSD is still a syndrome, is it not? I thought it was the editor's opinion, that TBI was more psycological (not taken from the report)? Just because the report rules out classic physical trauma(from the impact), does not mean PTSD is not physical. If the editor is a psycologist; this is like asking Phillip Morris whether smoking is dangerous. Psycologists make money, treating the non-physical, manifestation of symtoms. Chemical imbalance(DNA methylation) is a physical dynamic, just as much as outright nerve/cell damage. To me, this just gave more credibility to PTSD being physical; all these physical manifestations(TBI), are now PTSD synromes. Is the report itself too long to post? How can there be no conflict of interest; when this editor(source) treats the symptoms of the extracted conclusion, FOR PROFIT? I presume, the Hoge report might say exactly what this editorial says it does. No telling with the military; but I would like some clarification of actual conclusion by someone other than the psych community, or some Scientologist paradigm. Is there anyone with limited bias, that has read this report?
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Old 08-02-2008, 08:11 AM
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anthony anthony is offline Gender Male
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Oh... nicely said tiltmonster, and welcome to the forum. I do love healthy opinion....
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