Motivated behaviours are thought to lead to enhanced performances. In the neurorehabilitation field, motivation has been demonstrated to be a link between cognition and motor performance, therefore playing an important role upon rehabilitation outcome determining factors. While motivation-enhancing interventions have been frequently investigated, a common and reliable motivation assessment strategy has not been established yet. This review aims to systematically explore and provide a comparison among the existing motivation assessment tools concerning stroke rehabilitation. For this purpose, a literature search (PubMed and Google Scholar) was performed, using the following Medical Subject Headings terms: “assessment” OR “scale” AND “motivation” AND “stroke” AND “rehabilitation”. In all, 31 randomized clinical trials and 15 clinical trials were examined. The existing assessment tools can be grouped into two categories: the first mirroring the trade-off between patients and rehabilitation, the latter reflecting the link between patients and interventions. Furthermore, we presented assessment tools which reflect participation level or apathy, as an indirect index of motivation. In conclusion, we are left to put forth a possible common motivation assessment strategy, which might provide valuable incentive to investigate in future research.

The triazolopyridine derivative trazodone is approved for the treatment of major depressive disorder (MDD) in adults; according to the available literature, this molecule, through a specific dose-dependent profile of action, was found to be a potential therapeutic option in some neurological conditions. This systematic review aimed to synthesise the available evidence on the use of trazodone in neurological patients. PubMed was searched for articles published from inception until March 2025. Article reference lists were screened, and relevant articles were retrieved for consultation. Clinical trials specifically investigating trazodone in neurological populations were included, following PRISMA guidelines for systematic reviews. Out of 69 records initially retrieved, 14 studies met the inclusion criteria, comprising 13 randomised controlled trials and 1 retrospective study, with a total of 608 patients. Most of the included studies focused on individuals with dementia, while others explored its use in different neurological disorders. Despite being an older antidepressant, trazodone remains widely prescribed. Beyond treating depression in neurological patients, it may may be useful in the treatment of some neurological aspects. However, current evidence remains limited. Further high-quality research is necessary to better define the therapeutic potential of trazodone in the management of neurological conditions.

Traumatic brain injury (TBI) is a major cause of long-term neurological and psychiatric morbidity and is frequently associated with persistent cognitive impairment. Deficits in attention, memory, processing speed, and executive dysfunctions are among the most commonly reported cognitive sequelae and may significantly compromise everyday functioning, social integration, and quality of life. Importantly, cognitive dysfunction following TBI often co-occurs with a wide range of psychiatric manifestations, including depression, anxiety, irritability, emotional dysregulation, and post-traumatic stress symptoms, which may further exacerbate functional disability. These cognitive and psychiatric disturbances arise from complex pathophysiological processes, including diffuse axonal injury, which involves cytoskeletal disruption, axolemmal permeability changes, calcium influx, and Wallerian degeneration, and neuroinflammation, characterized by microglial M1/M2 polarization and reactive astrogliosis that alter synaptic plasticity and promote excitotoxicity. These cellular events collectively disrupt large-scale neural networks involved in cognitive control and emotional regulation, underpinning the observed deficits. This narrative review aims to provide an overview of the mechanisms underlying cognitive impairment after TBI, describe the most common clinical cognitive profiles and associated psychiatric manifestations, and discuss their implications for cognitive remediation and functional recovery. Particular attention is given to the role of cognitive rehabilitation strategies in addressing both cognitive dysfunction and functional outcomes. Emerging approaches integrating digital technologies and neuromodulation are also discussed as potential avenues to enhance rehabilitation and improve psychiatric and functional outcomes in individuals with TBI.

Introduction: Emotional ambivalence - the coexistence of conflicting positive and negative feelings toward the same object, event, or person - has been historically emphasized in psychiatry and psychoanalysis and is increasingly studied in affective neuroscience. While Bleuler identified ambivalence as central to schizophrenia and Freud described its coexistence of love and hate, contemporary psychology extends the concept to mixed emotions, decision-making, and attitudes such as nostalgia. This review aims to synthesize evidence on the neural basis of ambivalence, clarify its distinction from uncertainty, and explore its clinical and therapeutic implications. Methods: A narrative review methodology was adopted, integrating findings from functional neuroimaging, electrophysiology, and meta-analyses. Studies of ambivalent evaluation, decision-making under conflict, and mixed affective states were examined. Analyses focused on distributed neural networks and their dynamic spatiotemporal organization, including oscillatory EEG and ERP dynamics. Results: Ambivalence consistently engages a distributed network involving the anterior cingulate cortex (conflict monitoring), insula (interoception), prefrontal regions (valuation/regulation), and salience circuits, together with temporoparietal and posterior midline regions involved in meta-cognitive and social-cognitive integration. Evidence from electrophysiological studies further indicates that ambivalence unfolds dynamically over time, reflecting rapid interaction between positive and negative affective representations rather than static co-activation. Pharmacological and neuromodulatory interventions show potential to recalibrate dysfunctional circuits. Conclusions: Ambivalence represents a distinct neurobiological state whose dysregulation contributes to psychopathology. It can be conceptualized as a transdiagnostic dimension of affective integration, reflecting the capacity to integrate competing emotional representations. Therapeutic strategies may enhance tolerance of ambivalence and improve clinical outcomes.