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The NSW Government has proposed a blanket lifting of COVID-19 restrictions when the proportion of fully vaccinated people rate reaches 70% of the adult population. If implemented, this would have devastating effects on Aboriginal populations. At the present time, vaccination rates in Aboriginal communities remain low. Once restrictions are lifted unvaccinated people will be at high risk of infection. The risks of serious illness and death among Aboriginal people from a variety of medical conditions are significantly greater than for the wider population. This is also the case with COVID-19 in First Nations populations around the world. The vulnerability of Aboriginal people is an enduring consequence of colonialism and is exacerbated by the fact that many live in over-crowded and poorly maintained houses in communities with under-resourced health services. A current workforce crisis and the demographic structure of the population have further hindered the effectiveness of vaccination programs. Aboriginal organisations have called on state and federal governments to delay any substantial easing of restrictions until full vaccination rates among Aboriginal and Torres Strait Islander populations aged sixteen years and older reach 90-95%. They have also called for additional support in the form of supply of vaccines, enhancement of workforce capacity and appropriate incentives to address hesitancy. Australia remains burdened by the legacy of centuries of harm and damage to its First Nations people. Urgent steps must be taken to avoid a renewed assault on Aboriginal and Torres Strait Islander health. This article is protected by copyright. All rights reserved.

A 48-year-old woman presents to your office with upper and lower left-sided facial weakness she noticed while applying mascara that morning. Other than the peripheral pattern of left facial weakness and absent taste of the left tongue, her neurologic examination is normal. You see no signs to suggest Ramsay Hunt syndrome1 and your practice is not in a Lyme disease endemic area. You make a diagnosis of idiopathic Bell's palsy.

Key message: Direct, non-invasive X-ray microtomography and optical technique observations applied in stems and leaves of intact seedlings revealed that laurel is highly resistant to drought-induced xylem embolism. Contrary to what has been brought forward, daily cycles of embolism formation and refilling are unlikely to occur in this species and to explain how it copes with drought. Context: There has been considerable controversy regarding xylem embolism resistance for long-vesselled angiosperm species and particularly for the model species for refilling (Laurus nobilis L.). Aims: The purpose of this study was to resolve the hydraulic properties of this species by documenting vulnerability curves of different organs in intact plants. Methods: Here, we applied a direct, non-invasive method to visualize xylem embolism in stems and leaves of intact laurel seedlings up to 2-m tall using X-ray microtomography (microCT) observations and the optical vulnerability technique. These approaches were coupled with complementary centrifugation measurements performed on 1-m long branches sampled from adult trees and compared with additional microCT analyses carried out on 80-cm cut branches. Results: Direct observations of embolism spread during desiccation of intact laurels revealed that 50% loss of xylem conductivity (Psi(50)) was reached at - 7.9 +/- 0.5 and - 8.4 +/- 0.3 MPa in sterns and leaves, respectively, while the minimum xylem water potentials measured in the field were - 4.2 MPa during a moderate drought season. Those findings reveal that embolism formation is not routine in Laurus nobilis contrary to what has been previously reported. These Psi(50) values were close to those based on the flow-centrifuge technique (- 9.2 +/- 0.2 MPa), but at odds with microCT observations of cut branches (- 4.0 +/- 0.5 MPa). Conclusion: In summary, independent methods converge toward the same conclusion that laurel is highly resistant to xylem embolism regardless its development stage. Under typical growth conditions without extreme drought events, this species maintains positive hydraulic safety margin, while daily cycles of embolism formation and refilling are unlikely to occur in this species.

If we have learned anything from a decade's worth of litigation, it is that the pharmaceutical industry pays the vast majority of physicians for one reason: to market their drugs. And why would we have ever thought otherwise? Pharma companies are not charitable organizations. They are not in the business of education, or philanthropy, or poverty relief, or even—let's be honest—health care. Their business is to manufacture and sell drugs. Unlike most any other businesses, however, pharmaceutical companies must go through an intermediary in order to sell their product. This places physicians in a position of singular trust. They stand between corporations and the vulnerable, sometimes desperate patients that those corporations call “customers.”

The lack of clinical trial data demonstrating efficacy of disease-modifying treatments (DMTs) for nonrelapsing forms of multiple sclerosis (MS) does not prove that DMTs are ineffective for nonrelapsing MS. It has been argued that DMTs have met primary endpoints in relapsing MS, but not in nonrelapsing forms of the disease. This does not prove that such treatments are ineffective for nonrelapsing phenotypes. It could mean that clinical trial endpoints are ineffective in identifying true differences between treatment and placebo arms, or do not properly account for individual variation within clinical trial cohorts.

[Graphic][1] The evaluation of a patient with cognitive impairment or dementia is part of many neurologists' daily practice. Once it has been established that a patient has mild cognitive impairment (MCI) or dementia, our job is to determine the etiology. Why is this important? Although specific pharmacologic treatment options are still limited at present for most dementias, there are a growing number of clinical trials in which patients may participate. Furthermore, it is imperative for the neurologist to guide a comprehensive approach to the treatment of cognitive impairment and dementia including management of behavioral symptoms, programs and strategies to optimize functional independence, caregiver education and support, and assistance with prognostication, planning, and connection with specific resources to assist with these issues. In 2011, new diagnostic criteria were published for Alzheimer disease (AD),1 behavioral variant frontotemporal dementia (FTD),2 and primary progressive aphasia,3 and a new consensus statement was published on vascular cognitive impairment.4 All of these criteria emphasize the value of structural and functional/molecular neuroimaging (including fluorodeoxyglucose PET [FDG-PET]), as well as CSF markers, in increasing diagnostic confidence or specificity. Although these criteria were in large part aimed at the clinical research communities studying these diseases, they also serve as guidance for practicing clinicians. These reports emphasize elements that can be summarized as the practitioner's 2 major goals: 1) start by establishing a diagnostic hypothesis based on a … [1]: /embed/inline-graphic-1.gif

[Graphic][1] Symptomatic internal carotid artery (ICA) stenosis is a common cause of ischemic stroke. The goal of management is to decrease the risk of stroke. This objective can be reached with a combination of medical therapy and revascularization with either carotid endarterectomy (CEA) or carotid artery stenting (CAS). At this time, evidence-based medicine provides guidance for our decision regarding which revascularization procedure is the most appropriate for the patient with routine, symptomatic carotid stenosis, i.e., with no clinical or radiographic exclusions for either procedure. The choice of treatment for revascularization comes down to 3 questions: 1) If the goal is to reduce stroke, which treatment option provides the best short and long-term outcomes? 2) Which treatment is cost-effective? 3) Which treatment provides the best patient-centered outcomes? Two recent trials evaluating the difference between CEA and CAS are the Carotid Revascularization Endarterectomy vs Stent Trial (CREST)1 and the International Carotid Stenting Study (ICSS).2 In CREST, the primary composite endpoint of any stroke, myocardial infarction (MI), or death within 30 days following treatment plus any ipsilateral stroke during long-term follow-up (median 2.5 years) was similar for CAS and CEA (7.2% vs 6.8%, hazard ratio [HR] 1.1, 95% confidence interval [CI] 0.8–1.5). There was no differential treatment effect according to symptomatic status. In contrast, the ICSS interim safety analysis evaluating the 120-day rate of stroke, death, or procedural MI reported that more patients in the CAS group reached the combined endpoint of stroke, MI, or death than the CEA group (8.5% vs 5.2%, HR 1.69, 95% CI 1.16–2.45, p = 0.006).2 In addition, a subanalysis of 231 patients in ICSS underwent MRI and demonstrated more ischemic brain lesions on diffusion-weighted imaging after treatment with CAS than … [1]: /embed/inline-graphic-1.gif

[Graphic][1] The results of recent carotid artery stenting (CAS) vs carotid endarterectomy (CEA) randomized studies (CREST,1 SPACE,2 EVA3S,3 and ICSS4) have created conflict among surgical and endovascular communities over which procedure is preferred for secondary stroke prevention for symptomatic carotid stenosis. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST) established CEA as the gold standard for surgical treatment in the early 1990s. Carotid stenting has been held to the high standard of CEA, and in order to present a viable alternative surgical therapy, it must be effective at preventing strokes, durable, and safe, with complication rates comparable to CEA. Carotid stenting is a clinically effective procedure. CREST, SPACE, and EVA3S showed equivalent annual stroke rates for the 2 treatments in symptomatic patients after the initial 30 days (CEA vs CAS: 0.8 vs 0.6, 1.3 vs 1.4, and 0.7 vs 0.4, percent per year, respectively). The stroke-free survival curves in CREST for CEA and CAS are parallel after the perioperative period out to 4 years, indicating clinical durability. > The increase in minor stroke in the CAS group and the increase in perioperative MI in the CEA group offset one another, leading to the equivalent primary endpoint. Perioperative safety remains the controversial point; the 30-day stroke and death rate for the stented patients was over 2 times that of the surgical group in the EVA3S trial. In the ICSS trial, the CAS group suffered stroke or death twice as often as the CEA group. Complications rates were, at best, equivalent in the 2 groups in the SPACE trial (6.3% for CEA and 6.8% for CAS), with CAS not achieving noninferiority. Why the … [1]: /embed/inline-graphic-1.gif

All who practice medicine face, on a daily basis, conflicts of interest (COIs) that have the potential to affect patient care. COIs may exist within our own practice. We may choose to perform (or not perform) a procedure that may (or may not) benefit the patient but clearly brings income to the practice; we may see patients in the office for services that might just as easily be taken care of by phone.

Contains fulltext : 49234.pdf (Publisher’s version ) (Closed access) This report describes the long-term follow-up data of three consecutive Dutch Childhood Oncology Group acute myeloid leukemia (AML) protocols. A total of 303 children were diagnosed with AML, of whom 209 were eligible for this report. The first study was the AML-82 protocol. Results were inferior (5-year probability of overall survival (pOS) 31%) to other available regimes. Study AML-87 was based on the BFM-87 protocol, with prophylactic cranial irradiation in high-risk patients only, and without maintenance therapy. This led to a higher cumulative incidence of relapse than that reported by the Berlin-Frankfurt-Munster (BFM), but survival was similar (5-year pOS 47%), suggesting successful retrieval at relapse. The subsequent study AML-92/94 consisted of a modified BFM-93 protocol, that is, without maintenance therapy and prophylactic cranial irradiation. However, all patients were to be transplanted (auto- or allogeneic), although compliance was poor. Antileukemic efficacy was offset by an increase in the cumulative incidence of nonrelapse mortality, especially in remission patients, and survival did not improve (5-year pOS 44%). Our results demonstrate that outcome in childhood AML is still unsatisfactory, and that further intensification of therapy carries the risk of enhanced toxicity. Our patients are currently included in the MRC AML studies, based on the results of their AML 10 trial.

Drug formularies have existed since the 1940s. The formulary in any health system is not a static list of drugs; it is not a “light switch” or a “yes” and “no” system. The formulary is part of a system for quality drug therapy within that system. The formulary in hospitals and large systems is established by the Pharmacy and Therapeutics Committee (or similar body) by a medical staff committee establishing policies for the effective, safe, and cost-effective use of drugs. Overall, a formulary should meet the needs of individual patients based on the best available evidence. The formulary is part of quality improvement and education programs within a health system.

Multiple sclerosis (MS) is a damaging CNS disease. Because the CNS has inherent properties that prevent the damage from manifesting readily (e.g., redundancy, plasticity, repair), often irreversible damage is not appreciated until very late. Pathologically it is apparent that permanent and irreversible damage occurs very early in MS plaque formation.1 Treatment of the disease course can therefore be viewed as having 3 goals: 1. Damage control to prevent or limit further damage 2. To protect injured axons and neurons from further injury 3. To encourage repair of reversibly damaged tissue It is clear that once patients are diagnosed with MS, or at high risk of developing MS (clinically isolated syndrome), they have already sustained damage to their CNS. How much damage it takes before patients actually present is variable: it is astounding at times to see patients even after one attack who have accumulated substantial disease loads on their MRI scans or already demonstrate symptoms and signs of chronic disease, such as cognitive or even physical impairment. It can be argued that current therapies are inadequate for some of these patients, though the goals of therapy are still probably reasonable but more difficult to realize. Once a patient enters the progressive phase of illness, with few relapses and minimal activity on MRI, it may be too late with our current armamentarium of agents to attain any of the stated goals of treatment. The exact etiopathogenesis of damage in MS is still …

Taking action to protect patients from impaired colleagues is a long-standing ethical and professional obligation. In 2010, this responsibility was codified in law with the introduction, across Australia, of a new mandatory reporting regimen. While several concerns remain to be addressed, mandatory reporting has the potential not only to reinforce the primacy of patient safety, but also to open internal dialogue about the profession's response to concerns about practitioner health and well-being. Four years after the introduction of the scheme, key challenges include ensuring the reporting threshold is appropriately defined and clearly understood, improving access to evidence-based health programmes for practitioners, and strengthening upstream protections to prevent and minimise impairment at its roots.

The American Academy of Neurology (AAN) recently chartered the Choosing Wisely Working Group to identify 5 recommendations for improving value and reducing waste in neurologic care. One of these recommendations was “Do not prescribe interferon-β or glatiramer acetate to patients with disability from progressive, nonrelapsing forms of multiple sclerosis.” Release of this recommendation precipitated an emotional, strongly negative response from many multiple sclerosis (MS) neurologists, and this discontent was enhanced when it was recognized that an administrative oversight prevented this recommendation from being vetted by the MS Section of the AAN before it was released. It has been argued that the evidence used to support this recommendation is fundamentally flawed and suggested that the resultant absence of evidence should not preclude treatment of the individual patient with MS.1

The goal of treating an individual with epilepsy is to have no seizures and no side effects. Limiting availability of medications appears to be a simple way of controlling costs of patient care. This approach potentially jeopardizes both efficacy and safety. We argue, in this edition of Current Controversies, that limiting costs by restricting formularies is detrimental to the patients from an efficacy, safety, and cost perspective.

[Graphic][1] Imaging with [18F]fluorodeoxyglucose-positron emission tomography (FDG-PET) offers excellent insights into regional brain dysfunction but fails to deliver tangible benefits in most clinical settings in persons with suspected cognitive impairment. The radiation exposure from a single FDG-PET brain scan is 1.3 rem, equivalent to about 3 chest X-rays or 4 months of background radiation; therefore, while unnecessary exposure to radiation is to be avoided, my view is not driven by risks of PET scanning. It is the realities of clinical diagnostics and the lack of potent interventions for specific dementing illnesses that limit the value of FDG-PET. Diagnoses of mild cognitive impairment (MCI) or dementia are entirely based on information obtained from the history and cognitive examination. Distinguishing abnormal cognition from normal cognition can sometimes be very challenging. As clinicians, we are often confronted with patients who report cognitive complaints that seem discordant with their level of daily functioning. Because there is a wide range of what is considered normal based on education, occupation, and cultural background, and because mood or motivation issues sometimes cloud performance, the distinction between normal and impaired can be very difficult. An FDG-PET scan will not solve this problem. The availability of FDG-PET offers a seductive but flawed logic that goes something like this: “Even though I don't know clinically whether the person has cognitive impairment or not, an abnormal FDG-PET would confirm that the cognitive complaints … [1]: /embed/inline-graphic-1.gif

[Graphic][1] Multiple sclerosis (MS) is a serious disease that, if left untreated, often leads to disability and reduced quality of life.1 Some of the newer and emerging MS therapies (e.g., natalizumab, fingolimod) hold potential for enhanced efficacy in comparison to more established treatments (i.e., interferon and glatiramer acetate).2 However, the increased efficacy appears to sometimes come at the costs of safety and monitoring. In assessing the risk/benefit ratio for the individual patient, clinicians must synthesize many factors to decide upon an ideal treatment strategy. Acknowledging that there may be the rare patient with fulminant and rapidly disabling early MS who may need a highly effective treatment at the beginning, agents with considerable safety concerns should generally be used as “second line.” The initiation of a safe and effective first-line agent should include a comprehensive plan for monitoring disease activity, with potential for rapid changes in therapy if necessary. ### Rationale for a stepped approach to treat patients with MS 1. New agents will require several years and tens of thousands of patients before we understand their full safety profile. While recent phase III MS clinical trials are relatively large and reasonably long, important adverse events may be discovered only after the approved medicine is launched. Serious safety concerns may be missed if they are uncommon or associated with a long latency. For example, the … [1]: /embed/inline-graphic-1.gif

On April 29, 1996, Dr. Quill offered testimony at an Oversight Hearing on "Assisted Suicide in the United States," before the Subcommittee on the Constitution of the House of Representatives Committee on the Judiciary. That testimony is reproduced here, with permission of the author.