Functional neurological disorder is characterized by neurological symptoms that cannot be explained by typical neurological diseases or other medical conditions. This review will critically discuss the literature on the pathophysiology of functional movement disorders (FMD), including functional neuroimaging studies, neurophysiological studies, studies on biomarkers and genetic studies. According to PRISMA guidelines for systematic reviews, we selected 39 studies. A complex scenario emerged, with the involvement of different areas of the brain in the pathophysiology of FMD. Our findings showed a hypoactivation of the contralateral primary motor cortex, a decreased activity in the parietal lobe, an aberrant activation of the amygdala, an increased temporo-parietal junction activity and a hyperactivation of insular regions in patients with FMD. Functional connectivity (FC) findings underlined aberrant connections between amygdala and motor areas, temporo-parietal junction and insula. We proposed amygdala hyperactivation as a possible biological marker for FMD and FC alterations between amygdala and other areas of the brain as consequent epiphenomena, accounting for the pathophysiological complexity of FMD. These conclusions might drive novel treatment hypotheses.
Demartini, B., Nistico', V., Edwards, M., Gambini, O., Priori, A. (2021). The pathophysiology of functional movement disorders. NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS, 120, 387-400 [10.1016/j.neubiorev.2020.10.019].
The pathophysiology of functional movement disorders
Nistico' V.Secondo
;
2021
Abstract
Functional neurological disorder is characterized by neurological symptoms that cannot be explained by typical neurological diseases or other medical conditions. This review will critically discuss the literature on the pathophysiology of functional movement disorders (FMD), including functional neuroimaging studies, neurophysiological studies, studies on biomarkers and genetic studies. According to PRISMA guidelines for systematic reviews, we selected 39 studies. A complex scenario emerged, with the involvement of different areas of the brain in the pathophysiology of FMD. Our findings showed a hypoactivation of the contralateral primary motor cortex, a decreased activity in the parietal lobe, an aberrant activation of the amygdala, an increased temporo-parietal junction activity and a hyperactivation of insular regions in patients with FMD. Functional connectivity (FC) findings underlined aberrant connections between amygdala and motor areas, temporo-parietal junction and insula. We proposed amygdala hyperactivation as a possible biological marker for FMD and FC alterations between amygdala and other areas of the brain as consequent epiphenomena, accounting for the pathophysiological complexity of FMD. These conclusions might drive novel treatment hypotheses.File | Dimensione | Formato | |
---|---|---|---|
Demartini-2021-Neurosci Biobehav Rev-VoR.pdf
Solo gestori archivio
Tipologia di allegato:
Publisher’s Version (Version of Record, VoR)
Licenza:
Tutti i diritti riservati
Dimensione
1.2 MB
Formato
Adobe PDF
|
1.2 MB | Adobe PDF | Visualizza/Apri Richiedi una copia |
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.