A complex relation between depression and multiple sclerosis: a descriptive review

• Published in: Neurological sciences Vol. 40; no. 8; pp. 1551 - 1558
• Main Authors: Corallo, Francesco, Lo Buono, Viviana, Genovese, Roberto, Palmeri, Rosanna, Di Cara, Marcella, Rifici, Carmela, Sessa, Edoardo, D’Aleo, Giangaetano, Galletti, Francesco, Bonanno, Lilla, Marino, Silvia
• Format: Journal Article
• Language: English
• Published: Cham Springer International Publishing 01.08.2019; Springer Nature B.V
• Subjects: Brain injury; Central nervous system; Demyelination; Depression - etiology; Humans; Limbic system; Medicine; Medicine & Public Health; Mental depression; Multiple sclerosis; Multiple Sclerosis - complications; Multiple Sclerosis - pathology; Multiple Sclerosis - psychology; Neurodegenerative diseases; Neurology; Neuroradiology; Neurosciences; Neurosurgery; Psychiatry; Review Article; Structure-function relationships; Depressive symptoms; Multiple sclerosis; Organic lesions; Anatomical–functional abnormalities; Magnetic resonance; Hippocampus
• ISSN: 1590-1874; 1590-3478
• DOI: 10.1007/s10072-019-03889-1

Background Multiple sclerosis (MS) is a demyelinating neurodegenerative disease that affects central nervous system (CNS). MS patients are more likely to develop depressive symptoms than patients with other chronic diseases. Objective In this review, we have analysed if there is a correlation between brain lesions (BL), structural damage (SD) and depressive symptoms (DS). Methods We Searched on PubMed and Web of Science databases and screening references of included studied and some review article for additional citations. From initial 745 studies, only 9 met the inclusion criteria. All studies conducted research on 389 patients with MS associated with DS and 120 HC (healthy controls). Results The selected researches highlighted the involvement of limbic system, the role of hippocampus and the impact of brain lesions on the emotional status of MS patients. Discussion In the genesis of depression are implicated many mechanisms including genetic, biochemical, immunological and psychosocial factors, even if a prominent role in the onset of DS seem to be associated with structural and functional brain alterations.