A prospective examination of Axis I psychiatric disorders in the first 5 years following moderate to severe traumatic brain injury

Alway, Yvette; Gould, Kate Rachel; Johnston, Lisa Susan; McKenzie, Dean Philip; Ponsford, Jennie Louise

doi:10.1017/s0033291715002986

Cited by 117 publications

(103 citation statements)

References 46 publications

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“…Psychiatric diagnoses, including mood, anxiety, and substance abuse disorders, were reported in 75.2% of individuals across the first 5 years post-TBI, with the majority of these (77.7%) emerging in the first year,7 similar to another study indicating clinically significant psychiatric symptoms in 42% of adults with TBI at 6 months post-injury 8. The majority of all psychiatric disorders (56.5%) post-TBI, and two-thirds of PTD diagnoses specifically,9 were first-time diagnoses.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, being unemployed or impoverished at the time of injury or substance abuse before or at the time of injury also conferred a higher likelihood of developing PTD 8,12,13,15,94. Personality characteristics and pre-injury psychiatric conditions that increase the risk of sustaining a TBI95,96 may also put individuals at greater risk for developing PTD 7,85,94. In fact, one of the biggest predictors of PTD was a pre-injury history of depression or other psychiatric disorder 7,94,97.…”

Section: Discussionmentioning

confidence: 99%

“…Personality characteristics and pre-injury psychiatric conditions that increase the risk of sustaining a TBI95,96 may also put individuals at greater risk for developing PTD 7,85,94. In fact, one of the biggest predictors of PTD was a pre-injury history of depression or other psychiatric disorder 7,94,97. However, the extent to which pre-injury mental health conditions contribute to PTD development through biological versus psychological pathways is unknown.…”

Section: Discussionmentioning

confidence: 99%

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A narrative literature review of depression following traumatic brain injury: prevalence, impact, and management challenges

Juengst¹,

Kumar²,

Wagner³

2017

PRBM

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Depression is one of the most common conditions to emerge after traumatic brain injury (TBI), and despite its potentially serious consequences it remains undertreated. Treatment for post-traumatic depression (PTD) is complicated due to the multifactorial etiology of PTD, ranging from biological pathways to psychosocial adjustment. Identifying the unique, personalized factors contributing to the development of PTD could improve long-term treatment and management for individuals with TBI. The purpose of this narrative literature review was to summarize the prevalence and impact of PTD among those with moderate to severe TBI and to discuss current challenges in its management. Overall, PTD has an estimated point prevalence of 30%, with 50% of individuals with moderate to severe TBI experiencing an episode of PTD in the first year after injury alone. PTD has significant implications for health, leading to more hospitalizations and greater caregiver burden, for participation, reducing rates of return to work and affecting social relationships, and for quality of life. PTD may develop directly or indirectly as a result of biological changes after injury, most notably post-injury inflammation, or through psychological and psychosocial factors, including pre injury personal characteristics and postinjury adjustment to disability. Current evidence for effective treatments is limited, although the strongest evidence supports antidepressants and cognitive behavioral interventions. More personalized approaches to treatment and further research into unique therapy combinations may improve the management of PTD and improve the health, functioning, and quality of life for individuals with TBI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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A narrative literature review of depression following traumatic brain injury: prevalence, impact, and management challenges

Juengst¹,

Kumar²,

Wagner³

2017

PRBM

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“…Traumatic brain injury (TBI), whereby mechanical forces to the head disrupt brain physiology and structure, is a leading cause of hospital utilization and disability in the United States (Faul, Xu, Wald, & Coronado, ; Selassie et al, ). Furthermore, TBI is associated with increased risk for psychiatric comorbidities (Alway, Gould, Johnston, McKenzie, & Ponsford, ; Whelan‐Goodinson, Ponsford, Johnston, & Grant, ) and neuropathology (Crane et al, ; Hong et al, ) that present and persist beyond the acute post‐injury window. Positron emission tomography (PET) and post mortem studies show that glial reactivity persists over a decade after injury (Cherry et al, ; Coughlin et al, ; Ramlackhansingh et al, ).…”

Section: Introductionmentioning

confidence: 99%

Traumatic brain injury‐induced neuronal damage in the somatosensory cortex causes formation of rod‐shaped microglia that promote astrogliosis and persistent neuroinflammation

Witcher

Bray

Dziabis

et al. 2018

Glia

125

119

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Microglia undergo dynamic structural and transcriptional changes during the immune response to traumatic brain injury (TBI). For example, TBI causes microglia to form rod‐shaped trains in the cerebral cortex, but their contribution to inflammation and pathophysiology is unclear. The purpose of this study was to determine the origin and alignment of rod microglia and to determine the role of microglia in propagating persistent cortical inflammation. Here, diffuse TBI in mice was modeled by midline fluid percussion injury (FPI). Bone marrow chimerism and BrdU pulse‐chase experiments revealed that rod microglia derived from resident microglia with limited proliferation. Novel data also show that TBI‐induced rod microglia were proximal to axotomized neurons, spatially overlapped with dense astrogliosis, and aligned with apical pyramidal dendrites. Furthermore, rod microglia formed adjacent to hypertrophied microglia, which clustered among layer V pyramidal neurons. To better understand the contribution of microglia to cortical inflammation and injury, microglia were eliminated prior to TBI by CSF1R antagonism (PLX5622). Microglial elimination did not affect cortical neuron axotomy induced by TBI, but attenuated rod microglial formation and astrogliosis. Analysis of 262 immune genes revealed that TBI caused profound cortical inflammation acutely (8 hr) that progressed in nature and complexity by 7 dpi. For instance, gene expression related to complement, phagocytosis, toll‐like receptor signaling, and interferon response were increased 7 dpi. Critically, these acute and chronic inflammatory responses were prevented by microglial elimination. Taken together, TBI‐induced neuronal injury causes microglia to structurally associate with neurons, augment astrogliosis, and propagate diverse and persistent inflammatory/immune signaling pathways.

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“…TBI can also increase the risk for other neurological disorders such as seizures (D'Ambrosio et al, 2004; D'Ambrosio and Perucca, 2004; Curia et al, 2011), Alzheimer’s disease (Sullivan et al, 1987; Schofield et al, 1997; Fleminger et al, 2003; Ikonomovic et al, 2004; DeKosky et al, 2007; Gupta and Sen, 2016; Scott et al, 2016) and Parkinson’s disease (Marras et al, 2014; Acosta et al, 2015; Tanner et al, 2015; Taylor et al, 2016), which further exacerbate neurologic dysfunction. Psychiatric comorbidities, such as major depression, generalized anxiety disorder, and post-traumatic stress disorder are also escalated after TBI (Rogers and Read, 2007; Ponsford et al, 2012; Na et al, 2014; Warren et al, 2015; Alway et al, 2016; Scholten et al, 2016) and further limit the successful integration of patients to society and the workforce. Lastly, while the affective toll of TBI on interpersonal relationships with family, friends, and coworkers is incalculable, the economic cost to society accounts for billions of dollars each year (Max et al, 1991; Selassie et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Combination therapies for neurobehavioral and cognitive recovery after experimental traumatic brain injury: Is more better?

Kline

Leary

Radabaugh

et al. 2016

Progress in Neurobiology

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Traumatic brain injury (TBI) is a significant health care crisis that affects two million individuals in the United Sates alone and over ten million worldwide each year. While numerous monotherapies have been evaluated and shown to be beneficial at the bench, similar results have not translated to the clinic. One reason for the lack of successful translation may be due to the fact that TBI is a heterogeneous disease that affects multiple mechanisms, thus requiring a therapeutic approach that can act on complementary, rather than single, targets. Hence, the use of combination therapies (i.e., polytherapy) has emerged as a viable approach. Stringent criteria, such as verification of each individual treatment plus the combination, a focus on behavioral outcome, and post-injury vs. pre-injury treatments, were employed to determine which studies were appropriate for review. The selection process resulted in 37 papers that fit the specifications. The review, which is the first to comprehensively assess the effects of combination therapies on behavioral outcomes after TBI, encompasses five broad categories (inflammation, oxidative stress, neurotransmitter dysregulation, neurotrophins, and stem cells, with and without rehabilitative therapies). Overall, the findings suggest that combination therapies can be more beneficial than monotherapies as indicated by 46% of the studies exhibiting an additive or synergistic positive effect versus on 19% reporting a negative interaction. These encouraging findings serve as an impetus for continued combination studies after TBI and ultimately for the development of successful clinically relevant therapies.

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A prospective examination of Axis I psychiatric disorders in the first 5 years following moderate to severe traumatic brain injury

Abstract: Findings suggest the first year post-injury is a critical period for the emergence of psychiatric disorders. Disorder frequency declines thereafter, with anxiety disorders showing greater resolution than mood and substance-use disorders.

Cited by 117 publications

References 46 publications

A narrative literature review of depression following traumatic brain injury: prevalence, impact, and management challenges

A narrative literature review of depression following traumatic brain injury: prevalence, impact, and management challenges

Traumatic brain injury‐induced neuronal damage in the somatosensory cortex causes formation of rod‐shaped microglia that promote astrogliosis and persistent neuroinflammation

Combination therapies for neurobehavioral and cognitive recovery after experimental traumatic brain injury: Is more better?

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