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Background and ObjectivesTo describe the current landscape of gender and racial diversity among adult neurology residency and fellowship program directors (PDs). Diversity in medicine affects the quality of care provided to a diverse patient population. There are efforts in nearly every field of medicine to increase the diversity of the physician workforce. While there has been improvement in some of the known disparities in medicine such as gender disparities, these disparities have persisted in more senior academic positions in medicine.MethodsA data set was generated by the Association of American Medical Colleges for the purpose of this study using a variety of sources. The data included deidentified, person-level variables, including self-reported gender, race, or ethnicity, and the type of program for all PDs of Accreditation Council for Graduate Medical Education–accredited residencies and fellowships. This retrospective descriptive survey study sought to (1) describe the current gender and race climate of neurology PDs and (2) identify groups that may be disproportionally underrepresented in these positions compared with those in other specialties and levels of medical training. Descriptive statistics and tests of nonrandom association were performed to address the objectives.ResultsWe found that 56.7% of residency PDs and 58% of fellowship PDs are male. The male to female ratio of PDs was similar to current neurology residents who are 53.4% male. There were significantly more female medical students (51.5%) compared with all other categories of academic rank other than neurology residency PDs (41.1%). Only 4.3% of residency PDs were Black and only 3.7% were Hispanic. There were no Black fellowship PDs, and 5.1% were Hispanic. There were significantly more non-White medical students and trainees compared with each PD group. The breakdown of gender and ethnic diversity of neurology PDs was similar to that of PDs from all residencies and fellowships.DiscussionWhile there are many barriers to achieving diversity in medicine, program leadership in graduate medical education may be one of them. This report describes the current landscape of diversity among PDs of residency and fellowship programs in the United States. This study shows one snapshot in time, which can be used as a baseline during this era of change.

Inclusion is the deliberate practice of ensuring that each individual is heard, all personal traits are respected, and all can make meaningful contributions to achieve their full potential. As coronavirus disease 2019 spreads globally and across the United States, we have viewed this pandemic through the lens of equity and inclusion. Here, we discuss how this pandemic has magnified preexisting health and social disparities and will summarize why inclusion is an essential tool to traverse this uncertain terrain and discuss strategies that can be implemented at organizational and individual levels to improve inclusion and address inequities moving forward.

The Humanities section of the February 12 issue of Neurology® included an article titled “Lucky and the root doctor.” In this piece, the author describes his previous encounters with a black patient and his wife, and recounts dialogues in which the author is introduced to some of the patient's health beliefs, which differ widely from his own. Unfortunately, and perhaps unintentionally, the piece frames these interactions in the context of a highly problematic portrayal of race. Many Neurology readers reacted to the article, expressing concern over the negative racial overtones and calling for immediate corrective action. The article was quickly retracted, and a formal letter of apology and action plan was subsequently issued by the editor-in-chief of Neurology .1

Evolution of the US health care system has been punctuated by periods of rapid change. In the coming decades there will be meaningful and potentially disruptive developments in health care delivery mechanisms, the policy environment, and the populations for whom we provide care. Neurologists will need to adapt to changing patient expectations, market dynamics, and regulatory structures to thrive in the future health care environment. This article describes a forecast of potential changes in the US health care system by 2035, an assessment of the implications for the field of neurology, and a rationale for long-term strategic planning to prepare.

In a thriving and just society, all constituents must have equitable access to basic human needs, without which all components of that society will eventually fail. This is the basis for the fundamental necessity of health equity, which can be described as the absence of health disparities or disadvantages that are conferred on individuals or particular societal groups. More constructively, health equity requires that every individual has a just and fair chance to attain the highest standard of health possible. The coronavirus disease 2019 (COVID-19) pandemic provides a striking example of health inequity as evidenced by the disproportionate burden of disease observed in certain groups, particularly Black and Latino patients. While compelling, the racial and ethnic disparities related to COVID-19 are neither unique nor surprising. A large and growing body of literature describes significant inequities in health care broadly and within the field of neurology specifically.1,2

GNE myopathy is a rare autosomal recessive muscle disease caused by mutations in GNE, the gene encoding the rate-limiting enzyme in sialic acid biosynthesis. GNE myopathy usually manifests in early adulthood with distal myopathy that progresses slowly and symmetrically, first involving distal muscles of the lower extremities, followed by proximal muscles with relative sparing of the quadriceps. Upper extremities are typically affected later in the disease. We report a patient with GNE myopathy who presented with asymmetric hand weakness. He had considerably decreased left grip strength, atrophy of the left anterior forearm and fibro-fatty tissue replacement of left forearm flexor muscles on T1-weighted magnetic resonance imaging. The patient was an endoscopist and thus the asymmetric hand involvement may be associated with left hand overuse in daily repetitive pinching and gripping movements, highlighting the possible impact of environmental factors on the progression of genetic muscle conditions.

A 34-year-old man with diffuse large B-cell lymphoma in complete remission presented with painful paresthesias of the thorax and proximal legs with loss of patellar reflexes bilaterally. Laboratory studies showed no evidence of autoimmune or infectious processes. CSF cytology was unremarkable. MRI showed enlarged, enhancing dorsal root ganglia (DRG) at L3-L4 bilaterally (figure, A). Whole-body PET showed avidity in these nerve roots and in T2 and T8 (figure, C) . Abnormalities on nerve conduction studies were isolated to sensory nerves affecting the same roots. Sensory ganglionopathies can occur with lymphomatous infiltration of the DRG, known as neurolymphomatosis, and can be the initial manifestation of lymphoma relapse.1,2

Although it is known that elective cyclosporine (CsA) withdrawal increases the risk for acute rejection, few studies have been large enough to identify risk factors for acute rejection after CsA withdrawal. We examined risk factors for acute rejection in 464 kidney transplant recipients who underwent elective CsA withdrawal. The incidence of acute rejection within 6 months of CsA withdrawal was 20/141 (14.2%) in the period January 1986 to May 1989, but only 14/323 (4.5%) since May 1989 (p = 0.0002). Among those transplanted since May 1989, the incidence was 5/20 (25%) for those with both 2 HLA-B and 2 HLA-DR mismatches, compared with only 9/298 (3.0%) for those with fewer mismatches (p < 0.0001). In Cox proportional hazards analysis, risk factors for acute rejection within 6 months, or at any time after elective CsA withdrawal, were date of transplant January 1986 to May 1989 (compared with more recently May 1989 to March 1999), younger age, obesity, as well as B and DR mismatches. Recipient race (83% were white), acute rejection during the first year before withdrawal (31%), mycophenolate mofetil (17%), and other variables failed to predict postwithdrawal acute rejection. We concluded that avoiding CsA withdrawal in the relatively small number of recipients with both 2 HLA-B and 2 HLA-DR mismatches could further reduce our already low incidence of acute rejection following elective CsA withdrawal.

The study by Young and colleagues1 in this issue of Neurology® used a technique called magnetic resonance spectroscopy (MRS) to examine the brain chemistry of patients with HIV. MRS is a noninvasive method of measuring the levels of certain chemicals, or “metabolites,” in the brain. One metabolite, N -acetylaspartate (NAA), is a marker of healthy brain cells. Three other metabolites, choline (Cho), myo-inositol (MI), and glutamate (Glu), are markers of damaged brain cells and inflammation (see table).

Few studies have systematically investigated what changes in chronic renal allograft function best predict subsequent graft failure, when these changes occur, and whether they occur soon enough to allow possible intervention. We collected serum creatinine values (mean, 183 +/- 75 values/patient) measured over a maximum follow-up of 22 years in 101 consecutive renal transplant recipients (excluding creatinine levels from periods of acute rejection). We determined the dates of first decline in inverse creatinine (Delta1/Cr;-20%, -30%, -40%, -50%, and -70%), declines in estimated creatinine clearance (CCr;55, 45, 35, 25, and 15 mL/min), and declines in measured slope of 1/Cr over time. We used time-dependent covariates in Cox proportional hazards analyses to determine the relative effect of each renal function parameter on outcomes while adjusting for other risk factors. The best predictor of subsequent graft failure was Delta1/Cr. Delta1/Cr less than -40% first occurred at a median of 1.28 years after transplantation in 73 patients, and 67 patients went on to have graft failure a median of 3.28 years after Delta1/Cr less than -40%. The independent relative risk for graft failure attributable to Delta1/Cr less than -40% was 5.91 (95% confidence interval, 3.25 to 10.8; P0.0001). A decline in CCr, eg, less than 45 mL/min, also was a strong predictor of subsequent graft failure. Conversely, declines in allograft function estimated from slopes of 1/Cr were poor predictors of graft failure. In analysis limited to patients followed up for 2.5 years or less, Delta1/Cr continued to predict graft failure, suggesting that Delta1/Cr will be a useful predictor in populations with shorter follow-up. If confirmed in other populations, eg, patients treated with calcineurin inhibitors, this simple marker of chronic allograft dysfunction may prove to be a practical tool for defining patients at high risk for late graft failure.