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Olfactory dysfunction is a common symptom in patients with neurodegenerative disorders, including Huntington’s disease (HD). Understanding its pathophysiology is important in establishing a preventive and therapeutic plan. In this literature review, we cover the physiology of olfaction, its role in neurodegeneration, and its characteristics in patients with HD. In the general population, olfactory dysfunction is present in 3.8–5.8%and the prevalence increases significantly in those older than 80 years. For HD, data regarding prevalence rates are lacking and the scales used have been inconsistent or have been restructured due to concerns about cross-cultural understanding. Pathogenic huntingtin deposits have been found in the olfactory bulb of individuals with HD, although no studies have correlated this with the grade of olfactory impairment. Olfactory dysfunction is present in both premanifest and manifest patients with HD, showing a progressive decline over time with more severe deficits at advanced stages. No specific treatment for olfactory impairment in HD has been proposed; identifying and avoiding potential medications that cause olfactory dysfunction, as well as general safety recommendations remain the basis of the therapeutic strategy.

Introduction: Stroke code simulation training is effective at reducing door to needle times (DTNT) for tPA administration. We aimed to evaluate the effect on DTNT from simulation training specifically for Neurology residents. Method: Stroke code simulation was implemented at our comprehensive stroke center in July 2017, targeting PGY2 adult neurology residents and PGY3 pediatric neurology residents who were first responders at stroke codes during off-hours. Training was completed at the beginning of the residents’ respective training years. An interrupted time series analysis of DTNT for tPA before and after the implementation of simulation training from July 2016 to July 2019 was performed. Demographics, tPA metrics, and safety and hospital metrics were compared pre and post intervention among the residents. No other quality improvement projects targeting DTNT were implemented during this time. Results: Between July 2016 and July 2019, 305 patients received thrombolysis from a resident first responder - 118 (39%) of whom were treated pre-simulation and 187 (61.3%) treated during the simulation period. There was no significant difference in patient baseline characteristics between the two groups (Table 1). Median DTNT was 49.5 (IQR 40-71) min during the pre-simulation period and 48 (IQR 37-60) min during the post-simulation period (p= 0.04). Compared to pre-simulation, there were no months in which the median DTNT exceeded 60 min post-simulation. IQR for the DTNT appeared both clinically and statistically different. Pre and post simulation, there was no difference in incidence of symptomatic intracranial hemorrhage nor in 90-day outcomes. Conclusion: In our analysis of the effect of stroke code simulation training among neurology residents, improvement in DTNT after simulation training appears more driven by improvement in the variation in times rather than a clinically significant decrease in median times.

Neurodegenerative disorders encompass a range of conditions in which neuronal structure and function are altered affecting the brain and spinal cord [central nervous system (CNS)] and worsening over time. Concomitant with the increase in longevity that has occurred over the past five decades, there has been a rise in the incidence of neurodegenerative disorders. For a number of these neurodegenerative disorders, the initiating pathoetiology involves an inflammatory process in a response to a diverse array of CNS insults, whose purpose is to protect and repair the tissues involved and restore homeostasis. A sustained inflammatory response or a change from acute to chronic neuroinflammation constitutes a fundamental process in the progression of several of these neurodegenerative disorders. The CNS inflammatory response is orchestrated by an interaction of microglial cells, infiltrating myeloid cells, astrocytes, oligodendrocytes, the blood-brain barrier (BBB), and signaling molecules (cytokines, chemokines, and growth factors) that produces a reaction that is both central and peripheral. This review examines the role of neuroinflammation in the most prevalent neurodegenerative disorders including Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD).