Effects of trauma-related audiovisual stimulation on cerebrospinal fluid norepinephrine and corticotropin-releasing hormone concentrations in post-traumatic stress disorder

Geracioti, Thomas D.; Baker, Dewleen G.; Kasckow, John; Strawn, Jeffrey R.; Mulchahey, J. Jeffrey; Dashevsky, Boris A.; Horn, Paul S.; Ekhator, Nosa N.

doi:10.1016/j.psyneuen.2007.12.012

Cited by 90 publications

(54 citation statements)

References 53 publications

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“…The NPY system has been shown to operate as a physiological "brake" system which dampens the CNS activity of the stress-signaling transmitters corticotropin-releasing hormone (CRH) and norepinephrine (NE) in the amygdala, bed nucleus of stria terminalis (BNST) and brain stem (Morris et al, 1997;Kash and Winder, 2006;Giesbrecht et al, 2010). In this regard, CNS abnormalities in both CRH and NE are observed in PTSD patients (for example, Baker et al, 1999;Geracioti et al, 2001Geracioti et al, , 2008.…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid neuropeptide Y in combat veterans with and without posttraumatic stress disorder

Sah

Ekhator

Jefferson-Wilson

et al. 2014

Psychoneuroendocrinology

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SummaryAccruing evidence indicates that neuropeptide Y (NPY), a peptide neurotransmitter, is a resilience-to-stress factor in humans. We previously reported reduced cerebrospinal fluid (CSF) NPY concentrations in combat-related posttraumatic stress disorder (PTSD) subjects as compared with healthy, non-combat-exposed volunteers. Here we report CSF NPY in combat-exposed veterans with and without PTSD. We quantified NPY concentrations in morning CSF from 11 male subjects with PTSD from combat in Iraq and/or Afghanistan and from 14 combat-exposed subjects without PTSD. NPY-like immunoreactivity (NPY-LI) was measured by EIA. The relationship between CSF NPY and clinical symptoms, as measured by the ClinicianAdministered PTSD Scale (CAPS) and Beck Depression Inventory (BDI), was assessed, as was the relationship between combat exposure scale (CES) scores and CSF NPY. As compared with the combat-exposed comparison subjects without PTSD, individuals with PTSD had significantly lower concentrations of CSF NPY [mean CSF NPY was 258.6 ± 21.64 pg/mL in the combat trauma-no PTSD group but only 180.5 ± 12.62 pg/mL in PTSD patients (p = 0.008)]. After adjusting for CES and BDI scores the two groups were still significantly different with respect to NPY. Importantly, CSF NPY was negatively correlated with composite CAPS score and intrusive (re-experiencing) subscale scores, but did not significantly correlate with CES or BDI scores. Our current findings further suggest that NPY may regulate the manifestation of PTSD symptomatology, and extend previous observations of low CSF NPY concentrations in the disorder. Central nervous system NPY may be a clinically important pharmacotherapeutic target, and/or diagnostic measure, for PTSD.

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Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid neuropeptide Y in combat veterans with and without posttraumatic stress disorder

Sah

Ekhator

Jefferson-Wilson

et al. 2014

Psychoneuroendocrinology

Self Cite

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“…Heightened sympathetic tone in the form of increased catecholamine secretion has been described consistently in individuals with PTSD (Southwick et al, 1999). Peripheral and central concentrations of norepinephrine are augmented in individuals with PTSD at baseline (Delahanty et al, 2005;Geracioti et al, 2001;Southwick et al, 1999) and following exposure to threatening stimuli (Blanchard et al, 1991;Geracioti et al, 2008). This increased norepinephrine production in PTSD in response to stressful or threatening stimuli can induce cytokine release (Bierhaus et al, 2003).…”

Section: Mechanisms Of Increased Inflammation In Fearand Anxiety-basementioning

confidence: 99%

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

Michopoulos

Powers

Gillespie

et al. 2016

Neuropsychopharmacol

545

376

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The study of inflammation in fear-and anxiety-based disorders has gained interest as growing literature indicates that proinflammatory markers can directly modulate affective behavior. Indeed, heightened concentrations of inflammatory signals, including cytokines and C-reactive protein, have been described in posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, social phobia, etc.). However, not all reports indicate a positive association between inflammation and fear-and anxiety-based symptoms, suggesting that other factors are important in future assessments of inflammation's role in the maintenance of these disorders (ie, sex, co-morbid conditions, types of trauma exposure, and behavioral sources of inflammation). The most parsimonious explanation of increased inflammation in PTSD, GAD, PD, and phobias is via the activation of the stress response and central and peripheral immune cells to release cytokines. Dysregulation of the stress axis in the face of increased sympathetic tone and decreased parasympathetic activity characteristic of anxiety disorders could further augment inflammation and contribute to increased symptoms by having direct effects on brain regions critical for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus). Taken together, the available data suggest that targeting inflammation may serve as a potential therapeutic target for treating these fear-and anxiety-based disorders in the future. However, the field must continue to characterize the specific role pro-inflammatory signaling in the maintenance of these unique psychiatric conditions.

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“…(11) measured CRH in serial CSF after presenting a stressful psychological suprahypophysial stimulus. Similar to us, they unpredictedly observed a missing increase in serial CSF CRH in patients with posttraumatic stress disorder during and after exposure to traumatic stimuli.…”

Section: Discussionmentioning

confidence: 99%

Corticotropin-releasing hormone and copeptin as acute stress markers in serial cerebrospinal fluid – first evidence for non-response during insulin hypoglycemia test

Wortmann

Kober

Pulic

et al. 2017

MRAJ

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Background: During stress, arginine vasopressin (AVP) and corticotropin-releasing hormone (CRH) can act as potent hypothalamic stimulators of the hypothalamic pituitary adrenocortical (HPA) axis. Recently, plasma CT-proAVP, also termed copeptin, was found to be a stable and sensitive surrogate marker for AVP release. A valid assessment of both CRH and copeptin in cerebrospinal fluid (CSF) might directly quantify an individual's current stress level. Here we investigated how concentrations of CRH and copeptin in CSF alter during insulininduced hypoglycemia test (IHT) -which has been shown to activate both hypothalamic AVP and CRH -and hypothesized an increase of both.

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Effects of trauma-related audiovisual stimulation on cerebrospinal fluid norepinephrine and corticotropin-releasing hormone concentrations in post-traumatic stress disorder

Cited by 90 publications

References 53 publications

Cerebrospinal fluid neuropeptide Y in combat veterans with and without posttraumatic stress disorder

Cerebrospinal fluid neuropeptide Y in combat veterans with and without posttraumatic stress disorder

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

Corticotropin-releasing hormone and copeptin as acute stress markers in serial cerebrospinal fluid – first evidence for non-response during insulin hypoglycemia test

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