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Prior studies report that most published medical education research is unfunded. We sought to determine the extent and sources of funding for medical education research articles published in leading journals, and how these have changed in the last two decades. All research articles published in Academic Medicine, Advances in Health Sciences Education, Medical Education and Medical Teacher in 1999, 2004, 2009, 2014, and 2019 were reviewed for funding declarations. Funding sources were categorised as: government; university; healthcare organisation; private not-for-profit organisation; and for-profit company. Time trends were analysed using the Cochran-Armitage test. 1822 articles were analysed. Over the aggregate 20-year period, 44% of all articles reported funding, with the proportion increasing from 30% in 1999 to 50% in 2019 (p <.001). The proportion of articles with government (10% to 16%, p =.049), university (6% to 17% p <.001), and not-for-profit funding sources (15% to 20%, p =.04) increased. Proportions of healthcare (3% to 4%, p =.45) and for-profit funding (2% to 1%, p =.25) did not significantly change with time. Over the last 20 years, the proportion of funded published medical education research has significantly increased, as has funding from government, universities, and not-for-profit sources. This may assist researchers in identifying funders with a track record of supporting medical education research, and enhances transparency of where research funding in the field originates. [ABSTRACT FROM AUTHOR]

Objective. Spinal cord injury (SCI) results in disruption of descending tonic activation of sympathetic circuits in the spinal cord. The authors determined whether different stimuli that increase sympathetic activity induced [...]

Multiple system atrophy (MSA) and pure autonomic failure (PAF) represent distinct pathological models of autonomic failure in humans. We have investigated the neuroendocrine, behavioural and autonomic cardiovascular responses to the 35% CO2 challenge. Nine patients with MSA, nine with PAF and five control subjects received a single breath of 35% CO2. Peripheral autonomic failure (i.e., PAF) was associated with significantly lower resting noradrenaline levels. All groups demonstrated a significant pressor response to CO2. In controls, the mean pressor response was +60.2 mm Hg, which was significantly smaller in both the PAF (+26.8 mm Hg, P < 0.01) and MSA (+18.3 mm Hg, P < 0.001) patients. In addition, the onset of the response was significantly delayed in both MSA (140.2 s) and PAF (154.2 s) patients compared with controls (32.4 s, P = 0.04 and P = 0.03, respectively). Noradrenaline levels increased only in controls. Central autonomic impairment (i.e., MSA) was associated with lower cortisol release (+8.8% in MSA compared with +35.2% in control and +23.7% in PAF) and fewer somatic symptoms of emotional arousal. Both MSA and PAF exhibit marked sympathetic autonomic impairment, however, residual (albeit differing) sympathetic pathways can still maintain a partial cardiovascular response. A central autonomic lesion, however, also appears to be associated with blunting of both cortisol and emotional responses to this stress paradigm. [ABSTRACT FROM AUTHOR]

Objective: To report a case of a disturbance of taste and smell associated with the alpha-adrenoceptor agonist midodrine., Case Summary: A 64-year-old white man with autonomic failure was started on midodrine 5 mg/day as treatment for orthostatic hypotension. After 3 months, the dose was increased to 12.5 mg/day, whereupon he noted a new onset of taste and smell disturbance. These symptoms made eating so unpleasant that the man greatly reduced his food intake, leading to significant weight loss. In addition, he experienced well-recognized adverse effects of midodrine, such as scalp pruritus, after the dose increase. All symptoms resolved with a dose reduction of midodrine (to 5 mg/day), and the patient increased his food intake, resulting in a return to his initial body weight., Discussion: Midodrine is commonly associated with dose-dependent adverse effects, such as scalp pruritus and cutis anserina. Disorders of taste and smell have not been previously reported with midodrine, although it has been suggested that other sympathomimetic drugs may have effects on the olfactory threshold. Severe disorders of taste and smell may impact not only on a patient's quality of life, but also on their physical well-being, with significant weight loss being reported in this case. According to the Naranjo probability scale, this patient's taste and smell disturbance was probably associated with midodrine., Conclusions: The use of midodrine may be associated with taste and smell disturbance. This case suggests that such an association is likely to be dose dependent.