Considering Burnout and Well-Being: Emergency Medicine Resident Shift Scheduling Platform and Satisfaction Insights from a Quality Improvement Project.

Few studies explore emergency medicine (EM) residency shift scheduling software as a mechanism to reduce administrative demands and broader resident burnout. A local needs assessment demonstrated a learning curve for chief resident schedulers and several areas for improvement. In an institutional quality improvement project, we utilized an external online cross-sectional convenience sampling pilot survey of United States EM residency programs to collect information on manual versus software-based resident shift scheduling practices and associated scheduler and scheduler-perceived resident satisfaction. Our external survey response rate was 19/253 (8%), with all United States regions (i.e., northeast, southeast, midwest, west, and southwest) represented. Two programs (11%) reported manual scheduling without any software. ShiftAdmin was the most popularly reported scheduling software (53%). Although not statistically significant, manual scheduling had the lowest satisfaction score and programs with ≤30 residents reported the highest levels of satisfaction. Our data suggest that improvements in existing software-based technologies are needed. Artificial intelligence technologies may prove useful for reducing administrative scheduling demands and optimizing resident scheduling satisfaction.

Survival of midbrain dopaminergic cells after lesion or deep brain stimulation of the subthalamic nucleus in MPTP-treated monkeys.

We have examined dopaminergic cell survival after alteration of the subthalamic nucleus (STN) in methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys. The STN was lesioned with kainic acid (B series) or underwent deep brain stimulation (DBS) at high frequency (C series). In another series, MPTP-treated and non-MPTP-treated monkeys had no STN alteration (intact animals; A series). Animals were treated with MPTP either after (B1, C1) or before (B2, C2) STN alteration. We also explored the long-term ( approximately 7 months) effect of DBS in non-MPTP-treated monkeys (D series). Brains were aldehyde-fixed and processed for routine Nissl staining and tyrosine hydroxylase immunocytochemistry. Our results showed that there were significantly more (20-24%) dopaminergic cells in the substantia nigra pars compacta (SNc) of the MPTP-treated monkeys that had STN alteration, either with kainic acid lesion or DBS, compared to the non-MPTP-treated monkeys (intact animals). We suggest that this saving or neuroprotection was due to a reduction in glutamate excitotoxicity, as a result of the loss or reduction of the STN input to the SNc. Our results also showed that SNc cell number in the B1 and C1 series were very similar to those in the B2 and C2 series. In the cases that had long-term DBS of the STN (D series), there was no adverse impact on SNc cell number. In summary, these results indicated that STN alteration offered neuroprotection to dopaminergic cells that would normally die as part of the disease process.

SPECT imaging, immunohistochemical and behavioural correlations in the primate models of Parkinson's disease.

Dopamine active transporter (DAT) single photon emission computerised tomography (SPECT) is considered a useful and practical technique for early diagnosis of Parkinson's disease (PD) and assessment of its progression. The application of this technique, particularly as a surrogate marker for therapeutic and neuroprotective trials in Parkinsonism, however, is dependent on pathological validation. In the absence of human studies, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) primate models of Parkinsonism to verify correlation between the SPECT, immunohistochemical and behavioural data. The DAT SPECT data correlated strongly and significantly with the substantia nigra pars compacta tyrosine hydroxylase and Nissl cell counts as well as the behavioural scores. Within the limitations of small numbers inherent to such studies, this data provides the first attempt at pathological validation of SPECT in primates.

Differential survival patterns among midbrain dopaminergic cells of MPTP-treated monkeys and 6OHDA-lesioned rats.

We explore the patterns of survival among dopaminergic cells of the midbrain in MPTP-treated macaque monkeys and 6OHDA-lesioned Sprague-Dawley rats. For the monkeys, animals were injected intramuscularly with MPTP for 8 days consecutively and then allowed to survive for 21 days. For the rats, 6OHDA was injected into the midbrain and then allowed to survive for either 7, 28 or 84 days. Brains were processed for tyrosine hydroxylase (TH) and calbindin immunocytochemistry to label populations in the ventral and dorsal tiers of midbrain dopaminergic cells. In monkeys, while there was a decrease in the TH+ cell number in the ventral tier of MPTP-treated cases (65%), there was an overall increase (22%) in the TH+ and calbindin+ cell number in the dorsal tier. Double labelling studies indicate that approximately 50% of TH+ cells of the dorsal tier contain calbindin also. In rats, there was a decrease in TH+ cell number in the ventral tier of 6OHDA-lesioned cases (97%), and to a lesser extent, in the TH+ and calbindin+ cell number in the dorsal tier ( approximately 40%). In conclusion, we show a surprising increase in TH+ and calbindin+ cell number in the dorsal tier in response to MPTP insult; such an increase was not evident after 6OHDA insult. We suggest that the increase in antigen expression relates to the dopaminergic reinnervation of the striatum in MPTP-treated cases. We also suggest that the greater loss of dopaminergic cells in the ventral tier when compared to the dorsal tier relates to glutamate toxicity.

Cell survival patterns in the pedunculopontine tegmental nucleus of methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkeys and 6OHDA-lesioned rats: evidence for differences to idiopathic Parkinson disease patients?

We explore the patterns of cell loss in the pedunculopontine tegmental nucleus (PpT), a major locomotor and muscle tone suppression centre of the brainstem, in two animal models of Parkinson disease, namely MPTP (methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-treated monkeys and 6-hydroxydopamine(6OHDA)-lesioned rats. Although there have been many studies documenting the loss of dopaminergic cells from the substantia nigra in these animal models, there has been little, if any, documentation of a loss of cells in the PpT. Results were obtained from macaque monkeys (Macaca fascicularis) and Sprague-Dawley rats. For the monkey series, animals were injected intramuscularly with MPTP (0.2 mg/kg) for 8 days consecutively and then allowed to survive for 21 days thereafter. Each monkey underwent behavioural assessment for parkinsonian symptoms. For the rat series, 6OHDA was injected into the midbrain using stereotactic coordinates. Rats were then allowed to survive for either 7, 14, 28, or 84 days thereafter. Monkey and rat brains were aldehyde-fixed and processed for routine tyrosine hydroxylase (TH; to label nigral dopaminergic cells) and nitric oxide synthase (NOs; to label PpT cholinergic cells) immunocytochemistry. In monkeys, the morphology, distribution and number of NOs(+) cells in the controls and MPTP-treated cases were very similar. In fact, in terms of number, there was only a 1% difference in the mean cell number between the controls and MPTP-treated cases. A comparable pattern was evident in 6OHDA-lesioned rats; there was no substantial difference in morphology, distribution and number of NOs(+) cells on the 6OHDA-lesioned cases when compared to the controls at each of the survival periods post-surgery. In summary, we show no loss of the large cholinergic/NOs(+) cells in the PpT in two animal models of Parkinson disease. This is in contrast to the heavy loss of these cells reported by previous findings in idiopathic Parkinson disease in patients.

Deep brain stimulation for the treatment of chronic, intractable pain.

Deep brain stimulation (DBS) was first used for the treatment of pain in 1954. Since that time, remarkable advances have been made in the field of DBS, largely because of the resurgence of DBS for the treatment of movement disorders. Although DBS for pain has largely been supplanted by motor cortex and spinal cord stimulation during the last decade, no solid evidence exists that these alternative modalities truly offer improved outcomes. Furthermore, nuclei not yet fully explored are known to play a role in the transmission and modulation of pain. This article outlines the history of DBS for pain, pain classification, patient selection criteria, DBS target selection, surgical techniques, indications for DBS (versus ablative techniques), putative new DBS targets, complications, and the outcomes associated with DBS for pain.

Chemoarchitectonic heterogeneities in the primate zona incerta: clinical and functional implications.

In view of the recent focus on the zona incerta (and surrounding regions) as a target for deep brain stimulation in patients with Parkinson Disease, we have explored incertal cyto and chemoarchitecture in normal and MPTP (methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-treated macaque monkeys. Brains were processed for routine tyrosine hydroxylase (TH), nitric oxide synthase (NOs), parvalbumin (Pv) and calbindin D 28k (Cal) immunocytochemistry, as well as for Nissl staining. We show four main sectors in the zona incerta, namely rostral, dorsal, ventral and caudal, each with a largely distinct cytoarchitecture. Each of the antibodies screened had signature distribution patterns across the zona incerta; TH+ cells were localised within the rostral sector, NOs+ cells were concentrated in the dorsal sector, Pv+ cells were found mainly in the ventral sector and Cal+ cells were distributed uniformly across all sectors. These patterns match closely those reported in non primates. We found no major differences in the distribution and shape of labelled cells in the zona incerta of MPTP-treated monkeys when compared to control. In conclusion, we report that the primate zona incerta shows considerable cyto and chemoarchitectonic heterogeneity; that it forms a nucleus with distinct sectors presumably associated with diverse functions--from generating arousal to shifting attention, and from controlling visceral activity to influencing posture and locomotion. These functions have been proposed for the zona incerta of non primates. Our results have clinical implications, in that deep brain stimulation of the zona incerta (or parts thereof) could manifest in signs and symptoms other than those associated with the motor system. Such clinical stimulations could well involve other systems, including those of arousal, attention and visceral control.