A Standardized Ward Round Proforma Improves Documentation in a Specialist Stroke Unit.

Background and aim Ward-round documentation is important for clinical communication and patient safety. Standardized checklists have improved ward-round documentation in surgical and medical settings. This quality improvement project aimed to introduce a standardized ward round proforma to improve documentation in a UK specialist stroke unit. Methods Ward round entries were assessed against internally agreed standardized criteria. A stroke-specific ward round proforma was designed and introduced with input from the multidisciplinary team. A repeat audit was performed, including assessment of the use of different proforma sections. Multidisciplinary team members were invited to provide feedback via an anonymous online survey. Results A total of 111 ward round entries were reviewed before the proforma was introduced. Ninety-five ward round entries were reviewed following introduction of the proforma, and 84.2% of these used the proforma for documentation. Overall documentation of standardized criteria improved from 48.7% to 62.1% with substantial improvement seen in documentation of neurological examination, presence/absence of mechanical venous thromboembolism prophylaxis, and blood test results. Multidisciplinary team feedback was positive. Conclusions The stroke-specific ward round proforma improved the quality and consistency of documentation in the unit. An updated proforma was designed using these results and multidisciplinary team feedback.

Quantitative patterns of motor cortex proteinopathy across ALS genotypes.

Degeneration of the primary motor cortex is a defining feature of amyotrophic lateral sclerosis (ALS), which is associated with the accumulation of microscopic protein aggregates in neurons and glia. However, little is known about the quantitative burden and pattern of motor cortex proteinopathies across ALS genotypes. We combined quantitative digital image analysis with multi-level generalized linear modelling in an independent cohort of 82 ALS cases to explore the relationship between genotype, total proteinopathy load and cellular vulnerability to aggregate formation. Primary motor cortex phosphorylated (p)TDP-43 burden and microglial activation were more severe in sporadic ALS-TDP disease than C9-ALS. Oligodendroglial pTDP-43 pathology was a defining feature of ALS-TDP in sporadic ALS, C9-ALS and ALS with OPTN, HNRNPA1 or TARDBP mutations. ALS-FUS and ALS-SOD1 showed less cortical proteinopathy in relation to spinal cord pathology than ALS-TDP, where pathology was more evenly spread across the motor cortex-spinal cord axis. Neuronal pTDP-43 aggregates were rare in GAD67+ and Parvalbumin+ inhibitory interneurons, consistent with predominant accumulation in excitatory neurons. Finally, we show that cortical microglia, but not astrocytes, contain pTDP-43. Our findings suggest divergent quantitative, genotype-specific vulnerability of the ALS primary motor cortex to proteinopathies, which may have implications for our understanding of disease pathogenesis and the development of genotype-specific therapies.

The elephant in the room: understanding the pathogenesis of Charles Bonnet syndrome.

PURPOSE: Charles Bonnet syndrome (CBS) is a syndrome characterised by complex visual hallucinations in individuals who are cognitively normal, though often elderly and visually impaired. Although first described over 250 years ago, the condition remains poorly understood and difficult to treat. RECENT FINDINGS: Our understanding of CBS pathogenesis has advanced little since it was first described, and much of the recent literature consists of case studies strikingly similar to the first published account of CBS. However, imaging studies have provided some indication as to the cortical areas implicated in the genesis of complex visual hallucinations, and the existence of similar hallucinatory syndromes in other sensory modalities suggests a common underlying mechanism. SUMMARY: This review begins by describing what is currently known about CBS, focusing on epidemiology, clinical presentation and diagnosis. It then explores potential starting points for better understanding the pathogenesis of CBS, namely the existence of similar conditions in other sensory modalities and the reproduction of complex visual hallucinations in sensory deprivation scenarios. Finally, it discusses how CBS should be approached in clinical practice.