Cortical Excitability of Psychiatric Disorders: Reduced Post-Exercise Facilitation in Depression Compared to Schizophrenia and Controls

Reid, P; Daniels, Brett A.; Rybak, Marzena; Turnier‐Shea, Yvonne; Pridmore, Saxby

doi:10.1046/j.1440-1614.2002.01082.x

Cited by 20 publications

(12 citation statements)

References 12 publications

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“…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: Discussionsupporting

confidence: 87%

“…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%

“…This sequence has been demonstrated in both nonmedicated and medicated MDD subjects (Shajahan et al., 1999a; Reid et al., 2002). These studies support the view that the motor cortex is less dynamically excitable in depressed patients and that this phenomenon may be a neurophysiological sign of an imbalance between the excitatory and inhibitory mechanisms involved in plasticity.…”

Section: Tms In Depressionmentioning

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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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Tms In Depressionmentioning

confidence: 99%

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Cortical Plasticity in Depression

et al. 2017

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“…However, these authors recognized the limitation of considerable intersubject MEP amplitude variability. Moreover, the view that reduced postexercise facilitation is a neurophysiologic marker characteristic of the depressed state is weakened by findings suggesting that schizophrenic patients too, have similarly impaired facilitation (Chroni et al, 2002;Reid et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

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

Chroni¹,

Lekka²,

Polychronopoulos³

et al. 2008

Journal of Clinical Neurophysiology

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The current study sought to longitudinally evaluate the postexercise facilitation of motor evoked potentials (MEP) in two patients during different phases of short-circle depressive-manic disorder. Each study included 50 baseline MEP elicited by transcranial magnetic stimulation, followed by 50 MEP immediately after nonfatiguing exercise of the examined muscle. Postexercise MEP facilitation, expressed as percentage of baseline value, varied from 71% to 119% and from 99% to 107% in each patient, respectively, being significantly lower than our mean normal control value (268%). No differences in MEP facilitation between phases of short-circle depressive-manic disorder were revealed. Reduced postexercise facilitation was independent of the bipolar disorder phases, suggesting an invariable underlying association of the psychiatric pathophysiological mechanisms to impaired cortical excitability.

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