Elsevier

NeuroImage

Volume 54, Supplement 1, January 2011, Pages S76-S82
NeuroImage

Cerebrocerebellar hypometabolism associated with repetitive blast exposure mild traumatic brain injury in 12 Iraq war Veterans with persistent post-concussive symptoms

https://doi.org/10.1016/j.neuroimage.2010.04.008Get rights and content

Abstract

Disagreement exists regarding the extent to which persistent post-concussive symptoms (PCS) reported by Iraq combat Veterans with repeated episodes of mild traumatic brain injury (mTBI) from explosive blasts represent structural or functional brain damage or an epiphenomenon of comorbid depression or posttraumatic stress disorder (PTSD). Objective assessment of brain function in this population may clarify the issue. To this end, twelve Iraq war Veterans (32.0 ± 8.5 [mean ± standard deviation (SD)] years of age) reporting one or more blast exposures meeting American Congress of Rehabilitation Medicine criteria for mTBI and persistent PCS and 12 cognitively normal community volunteers (53.0 ± 4.6 years of age) without history of head trauma underwent brain fluorodeoxyglucose positron emission tomography (FDG-PET) and neuropsychological assessments and completed PCS and psychiatric symptom rating scales. Compared to controls, Veterans with mTBI (with or without PTSD) exhibited decreased cerebral metabolic rate of glucose in the cerebellum, vermis, pons, and medial temporal lobe. They also exhibited subtle impairments in verbal fluency, cognitive processing speed, attention, and working memory, similar to those reported in the literature for patients with cerebellar lesions. These FDG-PET imaging findings suggest that regional brain hypometabolism may constitute a neurobiological substrate for chronic PCS in Iraq combat Veterans with repetitive blast-trauma mTBI. Given the potential public health implications of these findings, further investigation of brain function in these Veterans appears warranted.

Introduction

There is intense controversy regarding the etiology, course, and treatment of persistent somatic, cognitive, and behavioral symptoms experienced by many military personnel and Veterans following exposure to blast concussion (Connors et al., 2009, Eibner et al., 2009, Hoge et al., 2009, Sigford et al., 2009). It is universally accepted that blast exposed personnel frequently meet American Congress of Rehabilitation Medicine (ACRM) criteria for acute mild traumatic brain injury (mTBI) (Kay et al., 1993). But the term “mTBI” increasingly has been applied to a very different chronic post-concussive syndrome of subtle cognitive deficits, headache, tinnitus, sleep disruption, daytime fatigue, irritability and other symptoms that persists for months and often years after the blast-induced acute mTBI. Whether these chronic symptoms reflect persistent structural or functional brain damage is not clear. An epidemiologic study in military personnel found that chronic post-concussive symptoms (except for headache) were more correlated with posttraumatic stress disorder (PTSD) and depression (Schneiderman et al., 2008). These data would argue against persistent brain damage providing a neurobiologic basis for blast-related chronic post-concussive symptoms. On the other hand, many clinicians are convinced that war combatants’ chronic post-concussive symptoms suggest real albeit subtle persistent brain damage (Connors et al., 2009, Eibner et al., 2009, Ruff et al., 2008, Schneiderman et al., 2008, Sigford et al., 2009).

Demonstrating the presence of regional brain hypometabolism by fluorodeoxyglucose positron emission tomography (FDG-PET) in combat Veterans with chronic post-concussive symptoms years after their last blast exposure mTBI, compared to a control group, would inform this debate. Here we report consistent regional hypometabolism in infratentorial and medial temporal brain regions in a sample of Iraq war combat Veterans with multiple episodes of blast exposure mTBI and persistent post-concussive symptoms.

Section snippets

Participants

The Veterans Affairs Puget Sound Health Care System (VAPSHCS) and University of Washington (UW) institutional review boards approved all procedures and all the participants provided written informed consent before enrollment into the study. The mTBI Veteran participants were a convenience sample of 13 male Veteran warriors recruited from the VAPSHCS, all of whom had documented hazardous duty experience in Iraq with the US Armed Forces and had reported experiencing at least one blast exposure in

Demographic characteristics

One mTBI Veteran participant was dropped from the study due to TOMM scores suggesting poor effort. His scores and imaging findings are not included in the results presented here. The remaining 12 mTBI Veteran participants were 32.0 ± 8.5 years of age (range 24–49 years) at the time of study enrollment. They had 13.8 ± 1.9 years of education (range 11–16 years). The cognitively normal community volunteer controls were 53.0 ± 4.6 years of age (range 49–56 years) and had 15.5 ± 2.0 years of education (range 12–19 

Discussion

This is the first report of FDG-PET in military blast-exposure mTBI. We demonstrated consistent regional hypometabolism in infratentorial (cerebellum, vermis, and pons) and medial temporal brain regions in Iraq combat Veterans with multiple episodes of blast-related mTBI. These participants also exhibited subtle impairments in complex information processing, with mild reductions in verbal fluency, processing speed, and aspects of attention and working memory. These findings suggest the

Conflict of interest statement

The authors declare that there are no conflicts of interest.

Acknowledgments

This material is based upon work supported, in part, by the Northwest Network Mental Illness, Research, Education, and Clinical Center (MIRECC) and Office of Research and Development Medical Research Service, Department of Veterans Affairs; by grants P50 AG05136, K08 AG023670, and R01 NS045254 from the National Institutes of Health; and by a grant from an anonymous foundation.

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