Hippocampal subfield volumes in short‐ and long‐term lithium‐treated patients with bipolar I disorder

Simonetti, Alessio; Sani, Gabriele; Dacquino, Claudia; Piras, Fabrizio; Rossi, Pietro De; Caltagirone, Carlo; Coryell, William; Spalletta, Gianfranco

doi:10.1111/bdi.12394

Cited by 36 publications

(29 citation statements)

References 50 publications

(64 reference statements)

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“…However, insufficient information on the duration of exposure has to be considered a limitation of our study. In fact, differences in hippocampal volume were found in BP patients with short‐term and long‐term lithium treatment . Moreover, we found differences in the lifetime use of antidepressants and antipsychotics.…”

Section: Discussionmentioning

confidence: 60%

“…In fact, differences in hippocampal volume were found in BP patients with short-term and long-term lithium treatment. 57 Moreover, we found differences in the lifetime use of antidepressants and antipsychotics. As expected from clinical practice, BP-I patients presented a lower lifetime use of antidepressants and a higher lifetime use of antipsychotics than BP-II patients, 58,59 except in the case of BP-II patients who presented childhood trauma.…”

Section: Discussionmentioning

confidence: 78%

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Amygdala and hippocampus volumes are differently affected by childhood trauma in patients with bipolar disorders and healthy controls

et al. 2017

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 78%

Amygdala and hippocampus volumes are differently affected by childhood trauma in patients with bipolar disorders and healthy controls

et al. 2017

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“…19,58 A recent cross-sectional study, which included only patients with BD-I, showed that long-term, but not short-term, exposure to lithium treatment was associated with larger total hippocampal volumes and bilateral CA2–3, left CA4-DG, left presubiculum, and right subiculum volumes. 63 In addition, it was showed that erythropoietin was associated with memory improvement and reversal of brain matter loss in the left hippocampal CA1–3 and subiculum in patients with mood disorders. 64 Regarding diagnostic implications, future studies should consider the hippocampus subfield changes presented in the current study as well as other relevant brain regions that are altered in mood disorders to build a neuroanatomical network signature using machine learning techniques, so that we are able to differentiate patients with mood disorders in regards to the diagnosis and stage of the disorder.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal subfield volumes in mood disorders

et al. 2017

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Volume reduction and shape abnormality of the hippocampus have been associated with mood disorders. However, the hippocampus is not a uniform structure and consists of several subfields, such as the cornu ammonis (CA) subfields CA1–4, the dentate gyrus (DG) including a granule cell layer (GCL) and a molecular layer (ML) that continuously crosses adjacent subiculum and CA fields. It is known that cellular and molecular mechanisms associated with mood disorders may be localized to specific hippocampal subfields. Thus, it is necessary to investigate the link between the in vivo hippocampal subfield volumes and specific mood disorders, such as bipolar disorder (BD) and major depressive disorder (MDD). In the present study, we used a state-of-the-art hippocampal segmentation approach, and we found that patients with BD had reduced volumes of hippocampal subfields, specifically in the left CA4, GCL, ML, and both sides of the hippocampal tail, compared to healthy subjects and patients with MDD. The volume reduction was especially severe in patients with bipolar I disorder (BD-I). We also demonstrated that hippocampal subfield volume reduction was associated with the progression of the illness. For patients with BD-I, the volumes of the right CA1, ML and Sub decreased as the illness duration increased, and the volumes of both sides of the CA2/3, CA4, and hippocampal tail had negative correlations with the number of manic episodes. These results indicated that among the mood disorders the hippocampal subfields were more affected in BD-I compared to BD-II and MDD, and manic episodes had focused progressive effect on the CA2/3 and CA4 and hippocampal tail.

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“…Lithium has received more clinical assessment of its neuroprotective capacity than any other agent, most notably in bipolar disorder. Crosssectional studies of bipolar patients have associated lithium treatment with: (a) attenuation of cortical grey matter loss and (b) maintained white matter integrity (Table 1) (Giakoumatos et al, 2015;Gildengers et al, 2015;Hajek et al, 2012Hajek et al, , 2014Hartberg et al, 2015;Pfennig et al, 2014;Poletti, Locatelli, Radaelli, Colombo, & Benedetti, 2014;Simonetti et al, 2016;van Erp et al, 2012;Zung et al, 2016), though few have correlated lithium's structural benefits with a similar improvement in brain function.…”

Section: Lithiummentioning

confidence: 99%

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

Robertson

Coronado

Sethi

et al. 2019

Early Intervention Psych

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Aim: Neuropsychiatric disorders including depression, bipolar and schizophrenia frequently exhibit a neuroprogressive course from prodrome to chronicity. There are a range of agents exhibiting capacity to attenuate biological mechanisms associated with neuroprogression. This review will update the evidence for putative neuroprotective agents including clinical efficacy, mechanisms of action and limitations in current assessment tools, and identify novel agents with neuroprotective potential.Method: Data for this review were sourced from online databases PUBMED, Embase and Web of Science. Only data published since 2012 were included in this review, no data were excluded based on language or publication origin.Results: Each of the agents reviewed inhibit one or multiple pathways of neuroprogression including: inflammatory gene expression and cytokine release, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophin dysregulation and apoptotic signalling. Some demonstrate clinical efficacy in preventing neural damage or loss, relapse or cognitive/functional decline. Agents include: the psychotropic medications lithium, second generation antipsychotics and antidepressants; other pharmacological agents such as minocycline, aspirin, cyclooxygenase-2 inhibitors, statins, ketamine and alpha-2-delta ligands; and others such as erythropoietin, oestrogen, leptin, N-acetylcysteine, curcumin, melatonin and ebselen.Conclusions: Signals of evidence of clinical neuroprotection are evident for a number of candidate agents. Adjunctive use of multiple agents may present a viable avenue to clinical realization of neuroprotection. Definitive prospective studies of neuroprotection with multimodal assessment tools are required.

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Hippocampal subfield volumes in short‐ and long‐term lithium‐treated patients with bipolar I disorder

Abstract: Long-term, but not short-term, exposure to lithium treatment may exert neuroprotective effects on specific hippocampal subfields linked to disease progression.

Cited by 36 publications

References 50 publications

Amygdala and hippocampus volumes are differently affected by childhood trauma in patients with bipolar disorders and healthy controls

Amygdala and hippocampus volumes are differently affected by childhood trauma in patients with bipolar disorders and healthy controls

Hippocampal subfield volumes in mood disorders

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

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