Surgery:

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Abstract: Neuroleptic-induced dystonia is a source of great concern in clinical practice because of its iatrogenic nature which can potentially lead to life-threatening conditions. Since all neuroleptics (antipsychotics) share the ability to block the dopamine D-type receptors (DRs) that are highly enriched in the striatum, this drug-induced dystonia is thought to be caused by decreased striatal DR activity. However, how associations of striatal DR inactivation with dystonia are formed remains elusive.A growing body of evidence suggests that imbalanced activities between DR-expressing medium spiny neurons and DR-expressing medium spiny neurons (D-MSNs and D-MSNs) in the striatal striosome-matrix system underlie the pathophysiology of various basal ganglia disorders including dystonia. Given the specificity of the striatal dopamine D system in 'humans', this article highlights the striatal striosome hypothesis in causing 'repetitive' and 'stereotyped' motor symptoms which are key clinical features of dystonia. It is suggested that exposure to neuroleptics may reduce striosomal D-MSN activity and thereby cause dystonia symptoms. This may occur through an increase in the striatal cholinergic activity and the collateral inhibitory action of D-MSNs onto neighbouring D-MSNs within the striosome subfields. The article proposes a functional pathology of the striosome-matrix dopamine system for neuroleptic-induced acute dystonia or neuroleptic-withdrawal dystonia. A rationale for the effectiveness of dopaminergic or cholinergic pharmacotherapy is also provided for treating dystonias. This narrative review covers various aspects of the relevant field and provides a detailed discussion of the mechanisms of neuroleptic-induced dystonia.

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CONCLUSIONS: VitD levels before DMT start affect the risk of disease activity in MS. Genetic predisposition to higher VitD levels confers a lower risk of disease activity and is associated with delayed MS onset. Our work prompts future prospective studies regarding VitD supplementation and lifestyle interventions to hamper disease activity in MS.

The cerebral blood volume index (CBV index) is a perfusion-based marker of collateral status. Several real-world data analyses from observational stroke cohorts have established relationships between this parameter and a range of favorable and unfavorable stroke outcomes. In this review, an overview is provided of the CBV index, within the context of thrombectomy-treated large vessel and medium vessel occlusion ischemic strokes. The current literature is summarized describing the CBV index and its association with a variety of efficacy, safety, and clinical outcome measures during the thrombectomy course and post-treatment recovery in both large vessel occlusion and medium vessel occlusion strokes. The range of CBV index value thresholds that have been identified and are able to differentiate between favorable and unfavorable outcomes across different clinical scenarios are summarized. This review underscores the need for additional analyses to further explore the CBV index in other clinical outcome contexts and for future prospective studies to validate the CBV index in thrombectomy-treated large vessel and medium vessel occlusion strokes, especially with increasing use of thrombectomy for treating medium vessel occlusions.

CONCLUSIONS: While previous studies have dismissed a causal role of in ALS, our results strongly support as a novel ALS-causing gene.

CONCLUSIONS: The use of SR Classic or SR Combination was more likely to achieve first pass eTICI 2c or 3 reperfusion. There were no significant differences in clinical outcomes and safety endpoints.

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