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Parkinson’s disease (PD) is a common neurodegenerative disorder arising from an interplay between genetic and environmental risk factors. Studies have suggested that the pathological hallmarks of intraneuronal α-synuclein aggregations may start from the olfactory bulb and the enteric nervous system of the gut and later propagate to the brain via the olfactory tract and the vagus nerve. This hypothesis correlates well with clinical symptoms, such as constipation, that may develop up to 20 years before the onset of PD motor symptoms. Recent interest in the gut–brain axis has led to vigorous research into the gastrointestinal pathology and gut microbiota changes in patients with PD. In this review, we provide current clinical and pathological evidence of gut involvement in PD by summarizing the changes in gut microbiota composition and gut inflammation associated with its pathogenesis.

Contains fulltext : 235596.pdf (Publisher’s version ) (Open Access) Several COVID-19 vaccines have recently been approved for emergency use according to governmental immunization programs. The arrival of these vaccines has created hope for people with Parkinson's disease (PD), as this can help to mitigate their risk of becoming infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which can lead to serious, life-threatening disease, at least among those with more advanced PD. However, both persons with PD and physicians looking after these individuals have expressed concerns about the vaccine's efficacy and safety in the specific context of PD and its symptomatic treatment. Here, we discuss our perspective on these concerns, based on our interpretation of the literature plus the unfolding experience with widespread vaccination in the population at large. Because the benefits and risks of COVID-19 vaccines do not appear to be different than in the general population, we recommend COVID-19 vaccination with approved vaccines to persons with PD, unless there is a specific contraindication. Some caution seems warranted in very frail and terminally ill elderly persons with PD living in long-term care facilities.

Background: Efficacy of thrombolytic therapy decreases with time elapsed from symptom onset. We sought to identify the impact of code stroke on the thrombolytic therapy. Methods: Code stroke is activated by the emergency physician when a patient is eligible for thrombolytic therapy. We retrospectively reviewed patients with acute ischemic stroke between January 2011 and December 2014. Results: In total, 1809 patients were enrolled. Code stroke was activated in 233 of 351 patients arriving at the emergency room (ER) within 3 h of symptom onset, and in 21 patients arriving >3 h. The sensitivity, specificity, and positive and negative predictive values of code stroke were 76%, 46%, 72%, and 51%, respectively. Thrombolytic therapy was provided to 58 patients, accounting for 3.4% of all cerebral infarcts. Code stroke was activated in 40 of these patients. The most common reasons for excluding thrombolytic therapy were: National Institute of Health Stroke Scale (NIHSS) 80 years. Mean liaison-to-neurological evaluation time was only 6 min. Code stroke activation significantly reduced all the intervals, except for the onset-to-ER and door-to-order times. During the 4-year study period, there were significant reductions of the door-to-neurology liaison time by 28 min and door-to-laboratory time by 22 min. The proportion of door-to-needle time within 60 min improved from 33% in 2011 to 67% in 2014. Improved NIHSS scores during hospitalization were most prominent in tPA-treated patients. Symptomatic ICH occurred in 3.6% patients arriving within 3 h. Death occurred in 50% of patients received tPA treatment on family's request, and only 13% of those patients had favorable outcome. Conclusion: Code stroke is effective in reducing in-hospital delays. The accuracy of code stroke activation has acceptable sensitivity but low specificity. Rapid patient assessment by neurologists increases the number of patients eligible for thrombolytic therapy. Keywords: Acute stroke, Brain infarction, Code stroke, In-hospital delays, Thrombolytic therapy

Background and aims Renal dysfunction is a potent risk factor for cardiovascular diseases, including stroke. This study aimed to evaluate the impact of admission estimated glomerular filtration rate (eGFR) levels on short-term (1-month) and long-term (1-year) mortality in patients with acute ischemic stroke. Methods From the Taiwan Stroke Registry data, we classified ischemic stroke patients, identified from April 2006 to December 2015, into 5 groups by eGFR at admission: ≥ 90, 60–89, 30–59, 15–29, and Results Among 52,732 ischemic stroke patients, 1480 died within one month. The 1-month mortality rate was over 5-fold greater in patients with eGFR Conclusions After acute ischemic stroke, patients with reduced eGFR are at elevated risks of short-term and long-term deaths in a graded relationship.

We investigated the impact of serum cholesterol levels on 30-day mortality after ischemic stroke in dialysis patients.From the Taiwan Stroke Registry data, we identified 46,770 ischemic stroke cases, including 1101 dialysis patients and 45,669 nondialysis patients from 2006 to 2013.Overall, the 30-day mortality was 1.46-fold greater in the dialysis group than in the nondialysis group (1.75 versus 1.20 per 1000 person-days). The mortality rates were 1.64, .62, 2.82, and 2.23 per 1000 person-days in dialysis patients with serum total cholesterol levels of 120 mg/dL, 120-159 mg/dL, 160-199 mg/dL, and ≥200 mg/dL, respectively. Compared to dialysis patients with serum total cholesterol levels of 120-159 mg/dL, the corresponding adjusted hazard ratios of mortality were 4.20 (95% confidence interval [CI] = 1.01-17.4), 8.06 (95% CI = 2.02-32.2), and 6.89 (95% CI = 1.59-29.8) for those with cholesterol levels of 120 mg/dL, 160-199 mg/dL, and ≥200 mg/dL, respectively.Dialysis patients with serum total cholesterol levels of ≥160 mg/dL or 120 mg/dL on admission are at an elevated hazard of 30-day mortality after ischemic stroke.

Parkinson’s disease (PD) is a neurodegenerative disorder related to nigrostriatal dopaminergic neuron degeneration and iron accumulation. As a cellular oxygen sensor, prolyl hydroxylase domain containing protein 2 (PHD2, encoded by egl-9 family hypoxia inducible factor 1, EGLN1) modifies hypoxia-inducible factor alpha (HIF-α) protein for proteasomal destruction under normoxic condition. In addition, 2-oxoglutarate- (OG-) dependent dioxygenase activity of PHD2 is involved in the oxygen and iron regulation of iron-responsive element binding protein 2 (IRP2) stability. Previously increased expression of EGLN1 was found in the substantia nigra of the parkinsonian brain. We investigated the possible role of c.380 G > C (p.C127S) of EGLN1 gene in Taiwanese patients with PD. 479 patients and 435 healthy controls were recruited. Polymerase chain reaction and BsmAI restriction enzyme analysis were applied for analysis. An association between CC genotype and reduced PD risk in the recessive model (CC vs. GG + GC) was found. Our study provides a link between EGLN1 c.380 G > C SNP and the development of PD.

Objective Emerging evidence suggests that gut microbiome composition alterations affect neurodegeneration through neuroinflammation in the pathogenesis of Parkinson’s disease (PD). Here, we evaluate gut microbiota alterations and host cytokine responses in a population of Taiwanese patients with PD. Methods Fecal microbiota communities from 80 patients with PD and 77 age and gender-matched controls were assessed by sequencing the V3–V4 region of the 16S ribosomal RNA gene. Diet and comorbidities were controlled in the analyses. Plasma concentrations of IL-1β, IL-2, IL-4, IL-6, IL-13, IL-18, GM-CSF, IFNγ, and TNFα were measured by a multiplex immunoassay and relationships between microbiota, clinical characteristics, and cytokine levels were analyzed in the PD group. We further examined the cytokine changes associated with the altered gut microbiota seen in patients with PD in another independent cohort of 120 PD patients and 120 controls. Results Microbiota from patients with PD was altered relative to controls and dominated by Verrucomicrobia, Mucispirillum, Porphyromonas, Lactobacillus, and Parabacteroides. In contrast, Prevotella was more abundant in controls. The abundances of Bacteroides were more increased in patients with non-tremor PD subtype than patients with tremor subtype. Bacteroides abundance was correlated with motor symptom severity defined by UPDRS part III motor scores (rho = 0.637 [95% confidence interval 0.474 to 0.758], P

Primary orthostatic tremor (POT) is a rare movement disorder characterised by a tremor of 13–18 Hz in the legs with female preponderance. POT typically causes severe unsteadiness on standing which, when severe, may persist during walking. This can greatly impact day-to-day functions, including activities that require prolonged standing, such as showering. The response to medications is often limited. There are few data on medications for POT. Clonazepam and gabapentin are probably the two most efficacious medications to treat POT, whereas other medications such as levodopa may also have a role.1 On the other hand, case studies have shown favourable outcomes in patients treated with ventralis intermedius medialis (VIM) thalamic nucleus deep brain stimulation (DBS). Blahak et al also reported that four patients responded well to chronic spinal cord stimulation (SCS), at the cost of stimulation-induced paraesthesias.2 Here, we report the surgical treatment response and electrophysiology findings of two additional patients with severe POT. ### Case 1 The patient is a 74-year-old woman who developed progressive unsteadiness and tremor in the legs when standing at age 50. The symptoms improved when she leant on something to support and disappeared when she walked. There was also low-amplitude, high-frequency tremor of the outstretched hands. Surface electromyography (sEMG) showed a short duration (

BACKGROUND AND PURPOSE The requirement for neurology liaison is increasing in accordance with the growing health care demands associated with aging populations. The aim of this study was to characterize the nature of neurological inpatient liaisons (NILs) to help plan for the appropriate use of neurology resources. METHODS This was a retrospective cross-sectional study of NILs in a secondary referral hospital over a 12-month period. RESULTS There were 853 neurological consultations with a liaison rate of 3% per admission case. Chest medicine, gastroenterology, and infectious disease were the three most frequent specialties requesting liaison, and altered consciousness, seizure, and stroke were the three most frequent disorders for which a NIL was requested. Infection was the most common cause of altered consciousness. Epilepsy, infection, and previous stroke were common causes of seizure disorders. Acute stroke accounted for 44% of all stroke disorders. Electroencephalography was the most recommended study, and was also the most frequently performed. Ninety-five percent of emergency consultations were completed within 2 hours, and 85% of regular consultations were completed within 24 hours. The consult-to-visit times for emergency and regular consultations were 44±47 minutes (mean±standard deviation) and 730±768 minutes, respectively, and were shorter for regular consultations at intensive care units (p=0.0151) and for seizure and stroke disorders (p=0.0032). CONCLUSIONS Altered consciousness, seizure, and stroke were the most common reasons for NILs. Half of the patients had acute neurological diseases warranting immediate diagnosis and treatment by the consulting neurologists. Balancing increasing neurologist workloads and appropriate health-care resources remains a challenge.