Mitochondrial myopathy and comorbid major depressive disorder: effectiveness of dTMS on gait and mood symptoms

Rapinesi, Chiara; Janiri, Delfina; Kotzalidis, Georgios D.; Serata, Daniele; Casale, Antonio Del; Scatena, Paola; Dacquino, Claudia; Gentile, Giovanna; Manfredi, Giovanni; Danese, Emanuela; Raccah, Ruggero; Brugnoli, Roberto; Callovini, Gemma; Ferri, Vittoria Rachele; Ferracuti, Stefano; Zangen, Abraham; Simmaco, Maurizio; Angeletti, Gloria; Girardi, Paolo

doi:10.1016/j.genhosppsych.2015.03.002

Cited by 6 publications

(7 citation statements)

References 11 publications

(13 reference statements)

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“…Several studies reported that dTMS reduced anxiety in patients with comorbid depression [21,[36][37][38][39]. It is possible that dTMS acts indirectly on CUD by reducing anxiety, in addition to the drugs which were ineffective on their own for this purpose.…”

Section: Discussionmentioning

confidence: 99%

Add-on high frequency deep transcranial magnetic stimulation (dTMS) to bilateral prefrontal cortex reduces cocaine craving in patients with cocaine use disorder

Rapinesi

Casale

Pietro

et al. 2016

Neuroscience Letters

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Section: Discussionmentioning

confidence: 99%

Add-on high frequency deep transcranial magnetic stimulation (dTMS) to bilateral prefrontal cortex reduces cocaine craving in patients with cocaine use disorder

Rapinesi

Casale

Pietro

et al. 2016

Neuroscience Letters

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“…91 An anxiety disorder as a manifestation of a MID has been described in nsMIDs. 91 Psychosis has been reported in MELAS, 86 KSS, 92 POLG1-related disorders, 93 infantile onset spinocerebellar ataxia, 94 Leigh syndrome, 95 and nsMIDs. 96 Psychiatric abnormalities particularly occur in patients with MELAS, in which 50% of cases are affected.…”

Section: Psychiatric Abnormalitiesmentioning

confidence: 99%

Cerebral Manifestations of Mitochondrial Disorders

Finsterer

Carvalho

2017

Can. J. Neurol. Sci.

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This review aims at summarizing and discussing previous and recent findings concerning the cerebral manifestations of mitochondrial disorders (MIDs). MIDs frequently present as mitochondrial multiorgan disorder syndrome (MIMODS) either already at onset or later in the course. After the muscle, the brain is the organ second most frequently affected in MIMODS. Cerebral manifestations of MIDs are variable and may present with or without a lesion on imaging or functional studies, but there can be imaging/functional lesions without clinical manifestations. The most well-known cerebral manifestations of MIDs include stroke-like episodes, epilepsy, headache, ataxia, movement disorders, hypopituitarism, muscle weakness, psychiatric abnormalities, nystagmus, white and gray matter lesions, atrophy, basal ganglia calcification, and hypometabolism on 2-deoxy-2-[fluorine-18]fluoro-D-glucose positron-emission tomography. For most MIDs, only symptomatic therapy is currently available. Symptomatic treatment should be supplemented by vitamins, cofactors, and antioxidants. In conclusion, cerebral manifestations of MIDs need to be recognized and appropriately managed because they strongly determine the outcome of MID patients.

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“…32 Several cases of subjects with CPEO and other mitochondrial disorders and comorbid mood disorders have been recorded. 32 , 84 – 86 Similar homozygous (and to a smaller extent heterozygous) mutations cause motor symptoms in mice. 87 In addition to motor dysfunction, these mice exhibit age-dependent increase in the number of mtDNA deletions, specifically in brain and muscle, 87 providing a potential link between CPEO and psychiatric disorders.…”

Section: The Comorbidity Of Psychiatric and Mitochondrial Disordersmentioning

confidence: 99%

Mitochondrial dysfunction in psychiatric morbidity: current evidence and therapeutic prospects

Toker¹,

Agam²

2015

NDT

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Cumulating evidence for the involvement of mitochondrial dysfunction in psychiatric disorders leaves little to no doubt regarding the involvement of this pathology in mood disorders. However, mitochondrial abnormalities are also observed in a wide range of disorders spanning from cancer and diabetes to various neurodegenerative and neurodevelopmental disorders such as Parkinson’s, Alzheimer’s, Huntington’s, autism, and amyotrophic lateral sclerosis. The apparent lack of specificity questions the role of mitochondrial dysfunction in psychiatric disorders, in general, and in mood disorders, in particular. Is mitochondrial dysfunction a general phenomenon, simplistically rendering brain cells to be more vulnerable to a variety of disease-specific perturbations? Or is it an epiphenomenon induced by various disease-specific factors? Or possibly, the severity and the anatomical region of the dysfunction are the ones responsible for the distinct features of the disorders. Whichever of the aforementioned ones, if any, is correct, “mitochondrial dysfunction” became more of a cliché than a therapeutic target. In this review, we summarize current studies supporting the involvement of mitochondrial dysfunction in different psychiatric disorders. We address the question of specificity and causality of the different findings and provide an alternative explanation for some of the aforementioned questions.

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Mitochondrial myopathy and comorbid major depressive disorder: effectiveness of dTMS on gait and mood symptoms

Abstract: dTMS may be an alternative antidepressant strategy in patients with MMs, provided that they are free from seizures. The mechanism of improvement of motor disturbance may relate to dorsolateral prefrontal cortex stimulation and improved executive function and needs further investigation.

Cited by 6 publications

References 11 publications

Add-on high frequency deep transcranial magnetic stimulation (dTMS) to bilateral prefrontal cortex reduces cocaine craving in patients with cocaine use disorder

Add-on high frequency deep transcranial magnetic stimulation (dTMS) to bilateral prefrontal cortex reduces cocaine craving in patients with cocaine use disorder

Cerebral Manifestations of Mitochondrial Disorders

Mitochondrial dysfunction in psychiatric morbidity: current evidence and therapeutic prospects

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