A Review of Chronic Pain and Cognitive, Mood, and Motor Dysfunction Following Mild Traumatic Brain Injury: Complex, Comorbid, and/or Overlapping Conditions?

Grandhi, Ramesh; Tavakoli, Samon; Ortega, Catherine; Simmonds, Maureen J.

doi:10.3390/brainsci7120160

Cited by 50 publications

(27 citation statements)

References 55 publications

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“…The most common pain type related to mild TBI is headache, with a prevalence of 57.8%. Other frequent pain forms include neck or back pain and musculoskeletal pain [60].…”

Section: Chronic Central Npmentioning

confidence: 99%

Therapeutic Approaches for Peripheral and Central Neuropathic Pain

et al. 2019

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Neuropathic pain is a chronic secondary pain condition, which is a consequence of peripheral or central nervous (somatosensory) system lesions or diseases. It is a devastating condition, which affects around 7% of the general population. Numerous etiological factors contribute to the development of chronic neuropathic pain. It can originate from the peripheral part of the nervous system such as in the case of trigeminal or postherpetic neuralgia, peripheral nerve injury, painful polyneuropathies, or radiculopathies. Central chronic neuropathic pain can develop as a result of spinal cord or brain injury, stroke, or multiple sclerosis. As first-line pharmacological treatment options, tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and gabapentinoids are recommended. In trigeminal neuralgia, carbamazepine and oxcarbazepine are the first-choice drugs. In drug-refractory cases, interventional, physical, and psychological therapies are available. This review was structured based on a PubMed search of papers published in the field from 2010 until May 2019.

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“…The most common pain type related to mild TBI is headache, with a prevalence of 57.8%. Other frequent pain forms include neck or back pain and musculoskeletal pain [60].…”

Section: Chronic Central Npmentioning

confidence: 99%

Therapeutic Approaches for Peripheral and Central Neuropathic Pain

et al. 2019

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“…Clinically, presence of sleep disorders—specifically insomnia—reduces community integration following TBI and acts as either a mediator or contributor to depression through lowering quality of life (159). Also, sleep disturbances have been heavily implicated in either mediating or contributing to post-TBI sequelae such as PTSD (160), pain (161), and psychiatric disorders (162). For example, self-reports of depression and poor sleep quality are significantly associated with fMRI changes in the lateral orbitofrontal, dorsolateral prefrontal, and cingulate cortices (163).…”

Section: Experimental Stress Models Provide Insight To the Relationshmentioning

confidence: 99%

A Tilted Axis: Maladaptive Inflammation and HPA Axis Dysfunction Contribute to Consequences of TBI

2019

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Each year approximately 1.7 million people sustain a traumatic brain injury (TBI) in the US alone. Associated with these head injuries is a high prevalence of neuropsychiatric symptoms including irritability, depression, and anxiety. Neuroinflammation, due in part to microglia, can worsen or even cause neuropsychiatric disorders after TBI. For example, mounting evidence demonstrates that microglia become “primed” or hyper-reactive with an exaggerated pro-inflammatory phenotype following multiple immune challenges. Microglial priming occurs after experimental TBI and correlates with the emergence of depressive-like behavior as well as cognitive dysfunction. Critically, immune challenges are various and include illness, aging, and stress. The collective influence of any combination of these immune challenges shapes the neuroimmune environment and the response to TBI. For example, stress reliably induces inflammation and could therefore be a gateway to altered neuropathology and behavioral decline following TBI. Given the increasing incidence of stress-related psychiatric disorders after TBI, the degree in which stress affects outcome is of particular interest. This review aims to highlight the role of the hypothalamic-pituitary-adrenal (HPA) axis as a key mediator of stress-immune pathway communication following TBI. We will first describe maladaptive neuroinflammation after TBI and how stress contributes to inflammation through both anti- and pro-inflammatory mechanisms. Clinical and experimental data describing HPA-axis dysfunction and consequences of altered stress responses after TBI will be discussed. Lastly, we will review common stress models used after TBI that could better elucidate the relationship between HPA axis dysfunction and maladaptive inflammation following TBI. Together, the studies described in this review suggest that HPA axis dysfunction after brain injury is prevalent and contributes to the dynamic nature of the neuroinflammatory response to brain injury. Experimental stressors that directly engage the HPA axis represent important areas for future research to better define the role of stress-immune pathways in mediating outcome following TBI.

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“…Inhibition of fractalkine with anti-fractalkine antibodies improved experimental autoimmune myositis in the mouse model [35]. At the same time, LHVS was shown to produce neuroprotective effects in mice after traumatic brain injury, which often ends in the preservation of symptoms common for FM for several months [36,37]. The mechanism of immunomodulatory effects of LHVS has been established.…”

Section: Pathogenesis Of Fm: Neuroinflammationmentioning

confidence: 99%

Neuroimmunology: What Role for Autoimmunity, Neuroinflammation, and Small Fiber Neuropathy in Fibromyalgia, Chronic Fatigue Syndrome, and Adverse Events after Human Papillomavirus Vaccination?

Ryabkova

Чурилов

Shoenfeld

2019

IJMS

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Fibromyalgia is a disorder characterized by chronic widespread pain and non-pain symptoms, such as fatigue, dysautonomia, and cognitive and sleep disturbances. Its pathogenesis and treatment continue to be the subject of debate. We highlight the role of three mechanisms—autoimmunity, neuroinflammation, and small fiber neuropathy—in the pathogenesis of the disease. These mechanisms are shown to be closely interlinked (also on a molecular level), and the review considers the implementation of this relationship in the search for therapeutic options. We also pay attention to chronic fatigue syndrome, which overlaps with fibromyalgia, and propose a concept of “autoimmune hypothalamopathy” for its pathogenesis. Finally, we analyze the molecular mechanisms underlying the neuroinflammatory background in the development of adverse events following HPV vaccination and suggesting neuroinflammation, which could exacerbate the development of symptoms following HPV vaccination (though this is hotly debated), as a model for fibromyalgia pathogenesis.

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A Review of Chronic Pain and Cognitive, Mood, and Motor Dysfunction Following Mild Traumatic Brain Injury: Complex, Comorbid, and/or Overlapping Conditions?

Cited by 50 publications

References 55 publications

Therapeutic Approaches for Peripheral and Central Neuropathic Pain

Therapeutic Approaches for Peripheral and Central Neuropathic Pain

A Tilted Axis: Maladaptive Inflammation and HPA Axis Dysfunction Contribute to Consequences of TBI

Neuroimmunology: What Role for Autoimmunity, Neuroinflammation, and Small Fiber Neuropathy in Fibromyalgia, Chronic Fatigue Syndrome, and Adverse Events after Human Papillomavirus Vaccination?

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