Health Care Workers and Patients as Trojan Horses: a COVID19 ward outbreak.

BACKGROUND: Transmission in healthcare settings can result in significant infections in healthcare workers and patients. Understanding infection dynamics has important implications for methods employed in hospitals to prevent nosocomial transmission events. METHODS: In this case series report we describe a cluster of COVID-19 (Coronavirus disease 2019) in a tertiary care university hospital, in the early phases of the epidemic, after hospital visiting had been stopped and when the UK lockdown was in place. FINDINGS: A 48 year old patient developed COVID-19 31 days post-admission and four days after admission to a medical ward from ITU. Infection was likely acquired from an asymptomatic or minimally symptomatic healthcare worker (HCW). Subsequent investigation over a 14 day period revealed symptoms in 23 staff members and five linked cases in patients on the same ward.Nine of the 23 affected staff members provided care for and had direct exposure with the index case. Four staff reported caring for the index case without use of personal protective equipment. One was coughed on directly by the patient 24 hours prior to the onset of symptoms. CONCLUSION: SARS CoV2 infection can be introduced to a ward area by asymptomatic and minimally symptomatic healthcare workers. Staff members and patients can act as Trojan horses carrying infection into and around the hospital, setting up unexpected transmission events.Transmission of infection from pre-symptomatic, asymptomatic and minimally symptomatic individuals means that universal use of measures to prevent transmission is required for successful reduction of transmission events in the hospital setting.

Ropinirole in the treatment of restless legs syndrome: results from the TREAT RLS 1 study, a 12 week, randomised, placebo controlled study in 10 European countries.

OBJECTIVE: To assess the efficacy, safety, and tolerability of ropinirole in the treatment of patients with restless legs syndrome. METHODS: A 12 week, prospective, double blind, randomised comparison involving 284 patients from 10 European countries. All participants had a score of > or =15 on the international restless legs scale (IRLS). Patients were randomised (1:1) to receive either ropinirole 0.25-4.0 mg once daily or placebo. The primary efficacy end point was mean change from baseline to week 12 in total IRLS score. Global improvements (clinical global impression (CGI) scale) and improvements in sleep, health related quality of life (QoL; using generic and disease specific measures), work, and other activities were also assessed. RESULTS: 112/146 patients (76.7%) taking ropinirole and 109/138 (79.0%) taking placebo completed the study. Improvement in IRLS at week 12 with ropinirole (mean (SD) dose, 1.90 (1.13) mg/day) was greater than with placebo (mean (SE): -11.04 (0.719) v -8.03 (0.738) points; adjusted difference = -3.01 (95% confidence interval (CI), -5.03 to -0.99); p = 0.0036). More patients in the ropinirole group (53.4%) showed improvement on the CGI scale at week 12 than in the placebo group (40.9%; adjusted odds ratio = 1.7 (1.02 to 2.69); p = 0.0416). Significant differences on both IRLS and CGI scales favouring ropinirole were apparent by week 1. Ropinirole was also associated with significantly greater improvements in sleep and QoL end points. The most common adverse events were nausea and headache. CONCLUSIONS: Ropinirole improves restless legs syndrome compared with placebo, with benefits apparent by week 1. It is generally well tolerated.

Neuronal intranuclear inclusion disease and juvenile parkinsonism.

Juvenile parkinsonism (onset age <20 yrs) is uncommon and few cases with neuropathologic confirmation have been reported. We present the case of a 17-year-old boy who presented with asymmetric arm tremor and bulbar symptoms. His paternal great aunt had parkinsonism with onset at age 22 years. Examination revealed parkinsonism in the absence of additional neurologic signs except for delayed pupillary responses to light. He responded well to levodopa but developed motor fluctuations and disabling dyskinesias after 3 years of treatment. Following attempted withdrawal of levodopa at age 24 years, he developed severe aspiration pneumonia complicated by cardiorepiratory arrests and he died 6 months later. At autopsy, the dominant histologic feature was wide-spread neuronal hyaline intranuclear inclusions. Neuronal depletion was observed in the substantia nigra, locus ceruleus, and, to a lesser extent, in the frontal cortex, and inclusions were particularly prominent in these areas. Inclusions were immunoreactive for ubiquitin and were typical of those seen in neuronal intranuclear inclusion disease (NIID), a rare, multisytem neurodegenerative disease. NIID should be considered in the differential diagnosis of juvenile parkinsonism. A link between NIID and hereditary neurodegenerative disorders characterized by expanded polyglutamine tracts is supported by the similar appearance of intranuclear inclusions in both conditions and by a family history in some cases of NIID.

Cognitive outcome after aneurysm rupture: relationship to aneurysm site and perioperative complications.

We evaluated cognitive outcome in a group of 37 patients who had undergone surgery for rupture and repair of a single intracranial aneurysm at least 6 months previously. We compared outcome--assessed by tests of intelligence, attention, executive functions sensitive to frontal lobe lesions, memory, neglect, and mood, as well as by a specially devised questionnaire--between a group of 20 patients who had aneurysms of the anterior communicating artery and 17 patients who had aneurysms located on other branches of the internal carotid artery. There were no differences in cognitive outcome between patients with anterior communicating artery aneurysms and those with aneurysms on other branches of the internal carotid artery. The patient group as a whole, however, showed impairment in executive functions and some aspects of memory in comparison with normative data. Overall, 65% of the patients were impaired in at least one cognitive domain, with 19% showing executive impairments alone, 14% showing memory impairments alone, and 32% showing deficits in both domains. Cognitive outcome was most strongly predicted by postoperative neurologic events, although clipping of an anterior cerebral artery was associated with a higher impairment rating on a symptom profile completed by patients' relatives, and although preoperative rebleeding of aneurysms predicted impairment of executive function.

Slowed central processing in simple and go/no-go reaction time tasks in Parkinson's disease.

Studies of cognition and motor control have independently suggested that patients with Parkinson's disease show deficits in both attentional control and the preprogramming of movement. However, few studies have examined directly the involvement of cognitive processes in the origin of their slowed response. We examined the performance of 100 Parkinson's disease patients on simple reaction time (SRT) and a series of go/no-go cross-modality choice reaction time (CRT) tasks, in which motor response was constant; correct positive responses required attention to a progressively increasing number of dimensions of visual and auditory stimuli. The results showed that Parkinson's disease patients became increasingly impaired in response speed as choice complexity increased. Slowed response speed in Parkinson's disease involved two factors: (i) a 'perceptuomotor' factor which was constant across conditions and independent of choice complexity. Depression affected this factor selectively and independently of confounding associations with impoverished motor control; (ii) a 'cognitive-analytical' factor, which played an increasingly important role as complexity of choice increased. The characteristics of the relationship between response latency and cognitive complexity indicate that the deficit was due to a constant proportional slowing in cognitive speed across all SRT and CRT conditions. A cognitive deficit affecting the monitoring of stimulus-response compatibility may contribute to delayed response in Parkinson's disease. This cognitive-analytical deficit is present in early, untreated cases and, in contrast to perceptuomotor processes, is weakly related to depression.

Different effects of dopaminergic and anticholinergic therapies on cognitive and motor function in Parkinson's disease. A follow-up study of untreated patients.

The cognitive performance of a group of 82 newly diagnosed patients with Parkinson's disease who had never been treated was reassessed approximately 4 mths after randomization to one of three monotherapies (levodopa, bromocriptine or anticholinergic drugs). Dopaminergic and anticholinergic treatments both led to improvement in motor control but their effects upon cognitive performance dissociated. Anticholinergic drugs produced impairment in processes underlying the immediate registration of information whilst dopaminergic therapy produced improvement on a task dependent on working memory and cognitive sequencing. Other cognitive measures showed no change on treatment. The deficits that were affected by cholinergic and dopaminergic modulation are those that were most compromised in the early, untreated state in Parkinson's disease. The data support the notion that cognitive impairment in Parkinson's disease is multifactorial in origin: short-term memory processes are served by both dopaminergic and cholinergic subcortico-frontal systems but much of the cognitive impairment of Parkinson's disease is independent of this subcortical neurochemical pathology and may be due to early neuronal dysfunction within the cerebral cortex.