Deep brain stimulation (DBS) is a neuro-psychosurgical technique widely accepted in movement disorders, such as Parkinson’s disease. Since 1999, DBS has been explored for severe, chronic and treatment-refractory psychiatric diseases. Our review focuses on DBS in obsessive-compulsive disorder (OCD), considered as a last treatment resort by most of learned societies in psychiatry. Two main stimulation areas have been studied: the striatal region and the subthalamic nucleus. But, most of the trials are open-labeled, and the rare controlled ones have failed to highlight the most efficient target. The recent perspectives are otherwise encouraging. Indeed, clinicians are currently considering other promising targets. A case series of 2 patients reported a decrease in OCD symptoms after DBS in the medial forebrain bundle and an open-label study is exploring bilateral habenula stimulation. New response criteria are also investigating such as quality of life, or subjective and lived-experience. Moreover, first papers about cost-effectiveness which is an important criterion in decision making, have been published. The effectiveness of tractography-assisted DBS or micro-assisted DBS is studying with the aim to improve targeting precision. In addition, a trial involving rechargeable pacemakers is undergoing because this mechanism could be efficient and have a positive impact on cost-effectiveness. A recent trial has discussed the possibility of using combined cognitive behavioral therapy (CBT) and DBS as an augmentation strategy. Finally, based on RDoc Research, the latest hypotheses about the understanding of cortico-striato-thalamo-cortical circuits could offer new directions including clinical predictors and biomarkers to perform adaptive closed-loop systems in the next future.
Primary progressive aphasias (PPAs) are a group of neurodegenerative diseases presenting with insidious and relentless language impairment. Three main PPA variants have been described: the non-fluent/agrammatic variant (nfvPPA), the semantic variant (svPPA), and the logopenic variant (lvPPA). At the time of diagnosis, patients and their families’ main question pertains to prognosis and evolution, but very few data exist to support clinicians’ claims. The objective of this study was to review the current literature on the longitudinal changes in cognition, behaviours, and functional abilities in the three main PPA variants. A comprehensive review was undertaken via a search on PUBMED and EMBASE. Two authors independently reviewed a total of 65 full-text records for eligibility. A total of 14 group studies and one meta-analysis were included. Among these, eight studies included all three PPA variants. Eight studies were prospective, and the follow-up duration was between one and five years. Overall, svPPA patients showed more behavioural disturbances both at baseline and over the course of the disease. Patients with lvPPA showed a worse cognitive decline, especially in episodic memory, and faster progression to dementia. Finally, patients with nfvPPA showed the most significant losses in language production and functional abilities. Data regarding the prodromal and last stages of PPA are still missing and studies with a longer follow-up observation period are needed.
Knowledge on the natural history of the three main variants of primary progressive aphasia (PPA) is lacking, particularly regarding mortality. Moreover, advanced stages and end of life issues are rarely discussed with caregivers and families at diagnosis, which can cause more psychological distress. We analyzed data from 83 deceased patients with a diagnosis of PPA. We studied survival in patients with a diagnosis of logopenic variant (lvPPA), semantic variant (svPPA), or non-fluent variant (nfvPPA) and examined causes of death. From medical records, we retrospectively collected data for each patient at several time points spanning five years before the first visit to death. When possible, interviews were performed with proxies of patients to complete missing data. Results showed that survival from symptom onset and diagnosis was significantly longer in svPPA than in lvPPA (p = 0.002) and nfvPPA (p < 0.001). No relevant confounders were associated with survival. Mean survival from symptom onset was 7.6 years for lvPPA, 7.1 years for nfvPPA, and 12 years for svPPA. The most common causes of death were natural cardio-pulmonary arrest and pneumonia. Aspiration pneumonia represented 23% of deaths in nfvPPA. In conclusion, this pilot study found significant differences in survival between the three variants of PPA with svPPA showing the longest and nfvPPA showing more neurologically-related causes of death.
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