Conceptualising the neurobiology of fatigue

Hegerl, Ulrich; Lam, Raymond W.; Malhi, Gin S; McIntyre, Roger S.; Demyttenaere, Koen; Mergl, Roland; Gorwood, Philip

doi:10.1177/0004867413481505

Cited by 18 publications

(15 citation statements)

References 32 publications

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“…Extending the previous cross-sectional investigations2425, this raises the question whether or not upregulated arousal regulation separates a core group of depressed patients responding to AD from atypical depression with hypersomnia or fatigue. The latter often show signs of a downregulated arousal regulation and might respond to psychostimulants4344. Concerning the prediction of response to specific antidepressants, the iSPOT-D data set indicated that the group of treatment responders receiving a SSRI showed a faster decline of CNS-arousal than non-responders, whereas those patients effectively treated with the SNRI had an increase in heart rate activity17.…”

Section: Discussionmentioning

confidence: 99%

Brain arousal regulation as response predictor for antidepressant therapy in major depression

Schmidt

Sander

Dietz

et al. 2017

Sci Rep

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A tonically high level of brain arousal and its hyperstable regulation is supposed to be a pathogenic factor in major depression. Preclinical studies indicate that most antidepressants may counteract this dysregulation. Therefore, it was hypothesized that responders to antidepressants show a) a high level of EEG-vigilance (an indicator of brain arousal) and b) a more stable EEG-vigilance regulation than non-responders. In 65 unmedicated depressed patients 15-min resting-state EEGs were recorded off medication (baseline). In 57 patients an additional EEG was recorded 14 ± 1 days following onset of antidepressant treatment (T1). Response was defined as a ≥50% HAMD-17-improvement after 28 ± 1 days of treatment (T2), resulting in 29 responders and 36 non-responders. Brain arousal was assessed using the Vigilance Algorithm Leipzig (VIGALL 2.1). At baseline responders and non-responders differed in distribution of overall EEG-vigilance stages (F2,133 = 4.780, p = 0.009), with responders showing significantly more high vigilance stage A and less low vigilance stage B. The 15-minutes Time-course of EEG-vigilance did not differ significantly between groups. Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance levels from baseline to T1 than non-responders (F2,130 = 4.978, p = 0.005). Higher brain arousal level in responders to antidepressants supports the concept that dysregulation of brain arousal is a possible predictor of treatment response in affective disorders.

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Section: Discussionmentioning

confidence: 99%

Brain arousal regulation as response predictor for antidepressant therapy in major depression

Schmidt

Sander

Dietz

et al. 2017

Sci Rep

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“…In this context, VIGALL could be helpful in elucidating whether the experienced fatigue is a hypo-aroused state, i.e. associated with unstable arousal regulation, or a state where patients feel exhausted due to chronic hyperarousal [69] . Olbrich et al [70] found signs of an unstable arousal regulation in patients with cancer-related fatigue, which might explain the reported efficacy of stimulants in this condition.…”

Section: Application Of Vigallmentioning

confidence: 99%

Assessment of Wakefulness and Brain Arousal Regulation in Psychiatric Research

Sander¹,

Hensch²,

Wittekind³

et al. 2015

Neuropsychobiology

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tion of wakefulness to the environmental and situational needs so that the optimal balance between energy conservation and responsiveness can be obtained. Since one approach to the assessment of brain arousal regulation is the classification of EEG vigilance stages, a computer-based algorithm (Vigilance Algorithm Leipzig) has been introduced, allowing classification of EEG vigilance stages in EEG recordings under resting conditions. The time course of EEG vigilance stages in EEGs of 15-20 min duration allows estimation of the individual arousal regulation (hyperstable, adaptive, or unstable vigilance pattern). The vigilance model of affective disorders and attention-deficit/hyperactivity disorder links a disturbed arousal regulation to the pathogenesis of psychiatric disorders and accordingly helps to explain and possibly also predict treatment effects of pharmacological and nonpharmacological interventions for these conditions. AbstractDuring the last few decades, much knowledge has been gained about sleep being a heterogeneous condition with several distinct sleep stages that represent fundamentally different physiological states. The same applies for the wake state which also comprises distinct global functional states (called vigilance stages). However, various terms and concepts have been introduced describing different aspects of wakefulness, and accordingly several methods of assessment exist, e.g. sleep laboratory assessments (Multiple Sleep Latency Test, Maintenance of Wakefulness Test), questionnaires (Epworth Sleepiness Scale, Karolinska Sleepiness Scale), behavioural tasks (Psychomotor Vigilance Test) or electroencephalography (EEG)-based assessments (Alpha Attenuation Test, Karolinska Drowsiness Test). Furthermore, several theoretical concepts about the regulation of sleep and wakefulness have been put forward, and physiological correlates have been identified. Most relevant for healthy functioning is the regulation of brain arousal and the adap-

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“…The term fatigue is used by patients and clinicians for a syndrome associated with increased daytime sleepiness and short sleep onset latencies as found in many nondepressed COPD patients. However, it is also used to describe a syndrome with decreased sleepiness and prolonged sleep onset latencies, as typically found in patients with major depression [16,17].…”

Section: Risk Of Major Depression In Patients With Copdmentioning

confidence: 99%

Depression and suicidality in COPD: understandable reaction or independent disorders?

Hegerl

Mergl

2014

Eur Respir J

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Both depression and chronic obstructive pulmonary disease (COPD) are prevalent, severe and often comorbid disorders. There is a risk of undertreatment for depression in patients with COPD as depressive symptoms, including suicidal tendencies, can erroneously be conceptualised as an understandable reaction to COPD and not as signs of an independent depressive disorder. In this context, the comorbidity rates of COPD and depression, the risk of suicidal behaviour in patients with COPD, and the evidence base for pharmaco-and psychotherapy in these patients are reviewed.Because symptoms of depression and COPD overlap it remains unclear how far the prevalence of major depression in COPD exceeds that in the general population. The suicide risk appears to be increased in COPD. Methodological studies providing evidence for the antidepressant efficacy of antidepressants or psychotherapy in patients with COPD are lacking. Recommendations for clinicians on how to separate depression from an understandable reaction to COPD are provided.Given the profound effects of depression on quality of life, life expectancy, COPD prognosis and suicide risk it is important to carefully diagnose and treat depression in patients with COPD according to national guidelines. @ERSpublications Comorbid depression has profound effects on COPD prognosis and should not be seen as understandable reaction to COPD

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Conceptualising the neurobiology of fatigue

Cited by 18 publications

References 32 publications

Brain arousal regulation as response predictor for antidepressant therapy in major depression

Brain arousal regulation as response predictor for antidepressant therapy in major depression

Assessment of Wakefulness and Brain Arousal Regulation in Psychiatric Research

Depression and suicidality in COPD: understandable reaction or independent disorders?

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