Sleep markers in psychiatry: do insomnia and disturbed sleep play as markers of disrupted neuroplasticity in mood disorders? A proposed model

2021 ◽  
Vol 28 ◽  
Author(s):  
Laura Palagini ◽  
Pierre Alexis Geoffroy ◽  
Dieter Riemann

Introduction: Since insomnia and disturbed sleep may affect neuroplasticity, we aimed at reviewing their potential role as markers of disrupted neuroplasticity involved in mood disorders. Method: We performed a systematic review, according to PRIMA, on PubMed, PsycINFO and Embase electronic databases for literature regarding mood disorders, insomnia, sleep loss/deprivation in relation to different pathways involved in the impairment of neuroplasticity in mood disorders such as 1] alterations in neurodevelopment 2] activation of the stress system 3] neuroinflammation 4] neurodegeneration/neuroprogression, 4] deficit in neuroprotection. Results: Sixty-five articles were analyzed and a narrative/ theoretical review was conducted. Studies showed that insomnia, sleep loss and sleep deprivation might impair brain plasticity of those areas involved in mood regulation throughout different pathways. Insomnia and disrupted sleep may act as neurobiological stressors that by over-activating the stress and inflammatory systems may affect neural plasticity causing neuronal damage. In addition, disturbed sleep may favor a deficit in neuroprotection hence contributing to impaired neuroplasticity. Conclusions: Insomnia and disturbed sleep may play a role as markers of alteration in brain plasticity in mood disorders. Assessing and targeting insomnia in the clinical practice may potentially play a neuroprotective role, contributing to “repairing” alterations in neuroplasticity or to the functional recovery of those areas involved in mood and emotion regulation.

BJPsych Open ◽  
2018 ◽  
Vol 4 (4) ◽  
pp. 167-179 ◽  
Author(s):  
Danny Phelan ◽  
Patricio Molero ◽  
Miguel A. Martínez-González ◽  
Marc Molendijk

BackgroundMagnesium (Mg2+) has received considerable attention with regards to its potential role in the pathophysiology of the mood disorders, but the available evidence seems inconclusive.AimsTo review and quantitatively summarise the human literature on Mg2+intake and Mg2+blood levels in the mood disorders and the effects of Mg2+supplements on mood.MethodSystematic review and meta-analyses.ResultsAdherence to a Mg2+-rich diet was negatively associated with depression in cross-sectional (odds ratio = 0.66) but not in prospective studies. Mg2+levels in bodily fluids were on average higher in patients with a mood disorder (Hedge'sg = 0.19), but only in patients treated with antidepressants and/or mood stabilisers. There was no evident association between Mg2+levels and symptom severity. Mg2+supplementation was associated with a decline in depressive symptoms in uncontrolled (g = −1.60) but not in placebo-controlled trials (g = −0.21).ConclusionOur results provide little evidence for the involvement of Mg2+in the mood disorders.Declaration of interestNone.


2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Dominika Justyna Ksiazek-Winiarek ◽  
Piotr Szpakowski ◽  
Andrzej Glabinski

Multiple sclerosis is an autoimmune neurodegenerative disorder resulting in motor dysfunction and cognitive decline. The inflammatory and neurodegenerative changes seen in the brains of MS patients lead to progressive disability and increasing brain atrophy. The most common type of MS is characterized by episodes of clinical exacerbations and remissions. This suggests the presence of compensating mechanisms for accumulating damage. Apart from the widely known repair mechanisms like remyelination, another important phenomenon is neuronal plasticity. Initially, neuroplasticity was connected with the developmental stages of life; however, there is now growing evidence confirming that structural and functional reorganization occurs throughout our lifetime. Several functional studies, utilizing such techniques as fMRI, TBS, or MRS, have provided valuable data about the presence of neuronal plasticity in MS patients. CNS ability to compensate for neuronal damage is most evident in RR-MS; however it has been shown that brain plasticity is also preserved in patients with substantial brain damage. Regardless of the numerous studies, the molecular background of neuronal plasticity in MS is still not well understood. Several factors, like IL-1β, BDNF, PDGF, or CB1Rs, have been implicated in functional recovery from the acute phase of MS and are thus considered as potential therapeutic targets.


2019 ◽  
Vol 28 (6) ◽  
Author(s):  
Laura Palagini ◽  
Celyne H. Bastien ◽  
Donatella Marazziti ◽  
Jason G. Ellis ◽  
Dieter Riemann

2016 ◽  
Vol 224 (2) ◽  
pp. 102-111 ◽  
Author(s):  
Carsten M. Klingner ◽  
Stefan Brodoehl ◽  
Gerd F. Volk ◽  
Orlando Guntinas-Lichius ◽  
Otto W. Witte

Abstract. This paper reviews adaptive and maladaptive mechanisms of cortical plasticity in patients suffering from peripheral facial palsy. As the peripheral facial nerve is a pure motor nerve, a facial nerve lesion is causing an exclusive deefferentation without deafferentation. We focus on the question of how the investigation of pure deefferentation adds to our current understanding of brain plasticity which derives from studies on learning and studies on brain lesions. The importance of efference and afference as drivers for cortical plasticity is discussed in addition to the crossmodal influence of different competitive sensory inputs. We make the attempt to integrate the experimental findings of the effects of pure deefferentation within the theoretical framework of cortical responses and predictive coding. We show that the available experimental data can be explained within this theoretical framework which also clarifies the necessity for maladaptive plasticity. Finally, we propose rehabilitation approaches for directing cortical reorganization in the appropriate direction and highlight some challenging questions that are yet unexplored in the field.


2021 ◽  
pp. 000486742110314
Author(s):  
Samantha J Groves ◽  
Katie M Douglas ◽  
Melissa Milanovic ◽  
Christopher R Bowie ◽  
Richard J Porter

Objective: Neurocognitive impairment is considered a core feature of mood disorders. Research has shown that neurocognitive impairment often persists beyond mood symptom resolution and can have significant deleterious effects on interpersonal relationships, academic achievement, occupational functioning and independent living. As such, neurocognitive impairment has become an important target for intervention. In this systematic review, we aimed to examine the extant literature to ascertain whether current standard evidence-based psychotherapies can improve neurocognitive functioning in mood disorders. Method: Studies examining changes in neurocognitive functioning following evidence-based psychotherapy were identified using MEDLINE, PsycINFO and Web of Science databases. Given the heterogeneity of study procedures, treatment protocols and patient samples, a narrative rather than meta-analytic review technique was employed. Results: Nineteen studies (21 articles) met inclusion criteria. There was preliminary evidence of improved executive functioning following evidence-based psychotherapy for Major Depressive Disorder and Bipolar Disorder. There was also some signal of reduced negative biases in emotional information processing following psychotherapy in depression. Due to methodological variability across studies however, it was difficult to draw clear conclusions. Conclusion: Findings from the current review suggest that evidence-based psychotherapies may influence some aspects of neurocognitive functioning in mood disorders. This continues to be an ongoing area of importance and warrants further research.


Author(s):  
Reza Heidari ◽  
Mostafa Akbariqomi ◽  
Yazdan Asgari ◽  
Diako Ebrahimi ◽  
Hamid Alinejad-Rokny

2021 ◽  
pp. 101490
Author(s):  
Johanna M. Boardman ◽  
Kate Porcheret ◽  
Jacob W. Clark ◽  
Thomas Andrillon ◽  
Anna W.T. Cai ◽  
...  

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