Persistent Suppression of Postexercise Facilitation of Motor Evoked Potentials During Alternate Phases of Bipolar Disorder

Chroni, Elisabeth; Lekka, N.P.; Polychronopoulos, Panagiotis; Beratis, Stavroula

doi:10.1097/wnp.0b013e31816ef739

Cited by 3 publications

(5 citation statements)

References 18 publications

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“…Studies using transcranial magnetic stimulation paradigms showed a significant deficit in cortical inhibition in BD patients compared to healthy controls (Levinson et al, 2007 ; Chroni et al, 2008 ), which is in agreement with the data showing increased glutamatergic neurotransmission in BD patients. The hippocampus, another brain region affected in BD, also is the site of adult neurogenesis (Vadodaria and Gage, 2014 ).…”

Section: Glutamatergic Neurotransmission and Hyperexcitabilitysupporting

confidence: 83%

Molecular Mechanisms of Bipolar Disorder: Progress Made and Future Challenges

Kim

Santos

Gage

et al. 2017

Front. Cell. Neurosci.

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Bipolar disorder (BD) is a chronic and progressive psychiatric illness characterized by mood oscillations, with episodes of mania and depression. The impact of BD on patients can be devastating, with up to 15% of patients committing suicide. This disorder is associated with psychiatric and medical comorbidities and patients with a high risk of drug abuse, metabolic and endocrine disorders and vascular disease. Current knowledge of the pathophysiology and molecular mechanisms causing BD is still modest. With no clear biological markers available, early diagnosis is a great challenge to clinicians without previous knowledge of the longitudinal progress of illness. Moreover, despite recommendations from evidence-based guidelines, polypharmacy is still common in clinical treatment of BD, reflecting the gap between research and clinical practice. A major challenge in BD is the development of effective drugs with low toxicity for the patients. In this review article, we focus on the progress made and future challenges we face in determining the pathophysiology and molecular pathways involved in BD, such as circadian and metabolic perturbations, mitochondrial and endoplasmic reticulum (ER) dysfunction, autophagy and glutamatergic neurotransmission; which may lead to the development of new drugs.

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Section: Glutamatergic Neurotransmission and Hyperexcitabilitysupporting

confidence: 83%

Molecular Mechanisms of Bipolar Disorder: Progress Made and Future Challenges

Kim

Santos

Gage

et al. 2017

Front. Cell. Neurosci.

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“…The articles reviewed here provide neurophysiological evidence for altered cortical excitability (Maeda et al., 2000; Fitzgerald et al., 2004; Levinson et al., 2010; Spampinato et al., 2013; Concerto et al., 2013; Croarkin et al., 2013; Veronezi et al., 2016) and synaptic plasticity (Chroni et al., 2008; Bajwa et al., 2008; Spampinato et al., 2013; Croarkin et al., 2013; Player et al., 2013; Kuhn et al., 2016) in MDD. These data confirm the findings of previous investigations that have used different approaches (Debener et al., 2000; Normann et al., 2007; Teyler and Cavus, 2007; Salustri et al., 2007; Nissen et al., 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, a number of studies have shown that there is a significant decrease in postexercise facilitation in these individuals (Samii et al., 1996; Shajahan et al., 1999a, 1999b; Reid et al., 2002; Chroni et al., 2008) that is probably linked to an imbalance between inhibitory and excitatory inputs at the level of cortical-spinal neurons. This observation, which has also been reported in schizophrenia (Reid et al., 2002; Chroni et al., 2002), might explain the symptoms reported by these patients, which can include fatigue, weakness, motor inertia, and apathy, and indicates the existence of a potentially strong relationship between psychiatric disorders and motor output.…”

Section: Discussionmentioning

confidence: 99%

“…Abnormal activity in the glutamatergic system that regulates synaptic plasticity is centrally important to the pathological mechanism underlying and treatment for MDD (Sanacora et al., 2008). The excessive glutamatergic activation of NMDA receptors induces LTD, which may be responsible for the disruptions observed in glutamatergic receptor plasticity-related processes, including reduced motor cortex excitability and postexercise facilitation and insensitivity to PAS protocols (Samii et al., 1996; Shajahan et al., 1999a; Maeda et al., 2000; Reid et al., 2002; Fitzgerald et al., 2004; Chroni et al., 2008; Levinson et al., 2010; Spampinato et al., 2013; Concerto et al., 2013; Player et al., 2013). …”

Section: Discussionmentioning

confidence: 99%

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Cortical Plasticity in Depression

et al. 2017

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Neural plasticity is considered the neurophysiological correlate of learning and memory, although several studies have also noted that it plays crucial roles in a number of neurological and psychiatric diseases. Indeed, impaired brain plasticity may be one of the pathophysiological mechanisms that underlies both cognitive decline and major depression. Moreover, a degree of cognitive impairment is frequently observed throughout the clinical spectrum of mood disorders, and the relationship between depression and cognition is often bidirectional. However, most evidence for dysfunctional neural plasticity in depression has been indirect. Transcranial magnetic stimulation has emerged as a noninvasive tool for investigating several parameters of cortical excitability with the aim of exploring the functions of different neurotransmission pathways and for probing in vivo plasticity in both healthy humans and those with pathological conditions. In particular, depressed patients exhibit a significant interhemispheric difference in motor cortex excitability, an imbalanced inhibitory or excitatory intracortical neurochemical circuitry, reduced postexercise facilitation, and an impaired long-term potentiation-like response to paired-associative transcranial magnetic stimulation, and these symptoms may indicate disrupted plasticity. Research aimed at disentangling the mechanism by which neuroplasticity plays a role in the pathological processes that lead to depression and evaluating the effects of modulating neuroplasticity are needed for the field to facilitate more powerful translational research studies and identify novel therapeutic targets.

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“…As cortical inhibition processes are under the control of GABAergic interneurons, these results show GABAergic pathway involvement in depressive pathologies. The one longitudinal study in bipolar patients was led by Chroni et al (2008). The authors evaluated the post-exercise facilitation of MEP in two patients during different phases of rapid cycling depressive-manic disorder.…”

Section: Introductionmentioning

confidence: 99%

Saccadic Performance and Cortical Excitability as Trait-Markers and State-Markers in Rapid Cycling Bipolar Disorder: A Two-Case Follow-Up Study

Malsert¹,

Guyader²,

Chauvin³

et al. 2013

Front. Psychiatry

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Background: The understanding of physiopathology and cognitive impairments in mood disorders requires finding objective markers. Mood disorders have often been linked to hypometabolism in the prefrontal dorsolateral cortex, and to GABAergic and glutamatergic neurotransmission dysfunction. The present study aimed to discover whether saccadic tasks (involving DPLFC activity), and cortical excitability (involving GABA/Glutamate neurotransmission) could provide neuropsychophysical markers for mood disorders, and/or of its phases, in patients with rapid cycling bipolar disorders (rcBD). Methods: Two rcBD patients were followed for a cycle, and were compared to nine healthy controls. A saccade task, mixing prosaccades, antisaccades, and nosaccades, and an evaluation of cortical excitability using transcranial magnetic stimulation were performed. Results: We observed a deficit in antisaccade in patients independently of thymic phase, and in nosaccade in the manic phase only. Cortical excitability data revealed global intracortical deficits in all phases, switching according to cerebral hemisphere and thymic phase. Conclusion: Specific patterns of performance in saccade tasks and cortical excitability could characterize mood disorders (trait-markers) and its phases (state-markers). Moreover, a functional relationship between oculometric performance and cortical excitability is discussed.

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Persistent Suppression of Postexercise Facilitation of Motor Evoked Potentials During Alternate Phases of Bipolar Disorder

Cited by 3 publications

References 18 publications

Molecular Mechanisms of Bipolar Disorder: Progress Made and Future Challenges

Molecular Mechanisms of Bipolar Disorder: Progress Made and Future Challenges

Cortical Plasticity in Depression

Saccadic Performance and Cortical Excitability as Trait-Markers and State-Markers in Rapid Cycling Bipolar Disorder: A Two-Case Follow-Up Study

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