Modeling factors influencing the demand for emergency department services in ontario: a comparison of methods

<p>Abstract</p> <p>Background</p> <p>Emergency departments are medical treatment facilities, designed to provide episodic care to patients suffering from acute injuries and illnesses as well as patients who are experiencing sporadic flare-ups of underlying chronic medical conditions which require immediate attention. Supply and demand for emergency department services varies across geographic regions and time. Some persons do not rely on the service at all whereas; others use the service on repeated occasions. Issues regarding increased wait times for services and crowding illustrate the need to investigate which factors are associated with increased frequency of emergency department utilization. The evidence from this study can help inform policy makers on the appropriate mix of supply and demand targeted health care policies necessary to ensure that patients receive appropriate health care delivery in an efficient and cost-effective manner. The purpose of this report is to assess those factors resulting in increased demand for emergency department services in Ontario. We assess how utilization rates vary according to the severity of patient presentation in the emergency department. We are specifically interested in the impact that access to primary care physicians has on the demand for emergency department services. Additionally, we wish to investigate these trends using a series of novel regression models for count outcomes which have yet to be employed in the domain of emergency medical research.</p> <p>Methods</p> <p>Data regarding the frequency of emergency department visits for the respondents of Canadian Community Health Survey (CCHS) during our study interval (2003-2005) are obtained from the National Ambulatory Care Reporting System (NACRS). Patients' emergency department utilizations were linked with information from the Canadian Community Health Survey (CCHS) which provides individual level medical, socio-demographic, psychological and behavioral information for investigating predictors of increased emergency department utilization. Six different multiple regression models for count data were fitted to assess the influence of predictors on demand for emergency department services, including: Poisson, Negative Binomial, Zero-Inflated Poisson, Zero-Inflated Negative Binomial, Hurdle Poisson, and Hurdle Negative Binomial. Comparison of competing models was assessed by the Vuong test statistic.</p> <p>Results</p> <p>The CCHS cycle 2.1 respondents were a roughly equal mix of males (50.4%) and females (49.6%). The majority (86.2%) were young-middle aged adults between the ages of 20-64, living in predominantly urban environments (85.9%), with mid-high household incomes (92.2%) and well-educated, receiving at least a high-school diploma (84.1%). Many participants reported no chronic disease (51.9%), fell into a small number (0-5) of ambulatory diagnostic groups (62.3%), and perceived their health status as good/excellent (88.1%); however, were projected to have high Resource Utilization Band levels of health resource utilization (68.2%). These factors were largely stable for CCHS cycle 3.1 respondents. Factors influencing demand for emergency department services varied according to the severity of triage scores at initial presentation. For example, although a non-significant predictor of the odds of emergency department utilization in high severity cases, access to a primary care physician was a statistically significant predictor of the likelihood of emergency department utilization (OR: 0.69; 95% CI OR: 0.63-0.75) and the rate of emergency department utilization (RR: 0.57; 95% CI RR: 0.50-0.66) in low severity cases.</p> <p>Conclusion</p> <p>Using a theoretically appropriate hurdle negative binomial regression model this unique study illustrates that access to a primary care physician is an important predictor of both the odds and rate of emergency department utilization in Ontario. Restructuring primary care services, with aims of increasing access to undersupplied populations may result in decreased emergency department utilization rates by approximately 43% for low severity triage level cases.</p

Detecting stress from imaging photoplethysmography using high frame rate video and a yellow-green filter: A pilot study

We investigate the use of a yellow-green filter to increase the signal-to-noise ratio (snr) in imaging photoplethysmography (iPPG) and test if high frame rate (HFR) video improves the accuracy of the derived heart rate variability (HRV). This pilot study is associated with a broader program to use iPPG to detect and monitor stress levels using HRV. To improve the snr of the iPPG signal, we employ two HFR colour video cameras of which one was fitted with a yellow-green filter (corresponding to the haemoglobin absorption peak within the visible spectrum). To our knowledge, the benefit of a yellow-green filter has never been explored. The predominant influence on HRV comes from the autonomic nervous system (ANS), which connects directly to the heart and cues the human body to relax or to stress. The linkage of HRV to the ANS makes HRV a proxy for stress levels. The HRV is derived from the iPPG signal by first using a cubic spline interpolation for more precise peak detection, and then calculating the inter-beat intervals from the peak-to-peak time differences. Instead of interpolating the signal, we hypothesise that a more accurate HRV measurement can be obtained using a HFR video camera, in our case at 200 frames per second. References E. B. Blackford, J. R. Estepp, and D. J. McDuff. Remote spectral measurements of the blood volume pulse with applications for imaging photoplethysmography. In G. L. Cote, editor, Optical Diagnostics and Sensing XVIII: Toward Point-of-Care Diagnostics, volume 10501, page 105010Z. International Society for Optics and Photonics, SPIE, 2018. doi:10.1117/12.2291073. M. Brayne. Trauma and Journalism: A Guide For Journalists, Editors and Managers. DART Center for Journalism and Trauma, 2007. https://dartcenter.org/sites/default/files/DCE_JournoTraumaHandbook.pdf. L. F. C. Martinez, G. Paez, and M. Strojnik. Optimal wavelength selection for noncontact reflection photoplethysmography. In Proceedings of the 22nd Congress of the International Commission for Optics: Light for the Development of the World, volume 8011, page 801191. International Society for Optics and Photonics, SPIE, 2011. doi:10.1117/12.903190. Y. Sun, S. Hu, V. Azorin-Peris, R. Kalawsky, and S. E. Greenwald. Noncontact imaging photoplethysmography to effectively access pulse rate variability. J. Biomed. Optics, 18(6):061205, 2013. doi:10.1117/1.JBO.18.6.061205. A. M. Unakafov. Pulse rate estimation using imaging photoplethysmography: generic framework and comparison of methods on a publicly available dataset. Biomed. Phys. Eng. Exp., 4(4):045001, 2018. doi:10.1088/2057-1976/aabd09

Neurodegeneration exposes firing rate dependent effects on oscillation dynamics in computational neural networks.

Traumatic brain injury (TBI) can lead to neurodegeneration in the injured circuitry, either through primary structural damage to the neuron or secondary effects that disrupt key cellular processes. Moreover, traumatic injuries can preferentially impact subpopulations of neurons, but the functional network effects of these targeted degeneration profiles remain unclear. Although isolating the consequences of complex injury dynamics and long-term recovery of the circuit can be difficult to control experimentally, computational networks can be a powerful tool to analyze the consequences of injury. Here, we use the Izhikevich spiking neuron model to create networks representative of cortical tissue. After an initial settling period with spike-timing-dependent plasticity (STDP), networks developed rhythmic oscillations similar to those seen in vivo. As neurons were sequentially removed from the network, population activity rate and oscillation dynamics were significantly reduced. In a successive period of network restructuring with STDP, network activity levels returned to baseline for some injury levels and oscillation dynamics significantly improved. We next explored the role that specific neurons have in the creation and termination of oscillation dynamics. We determined that oscillations initiate from activation of low firing rate neurons with limited structural inputs. To terminate oscillations, high activity excitatory neurons with strong input connectivity activate downstream inhibitory circuitry. Finally, we confirm the excitatory neuron population role through targeted neurodegeneration. These results suggest targeted neurodegeneration can play a key role in the oscillation dynamics after injury

The epilepsy phenotype of ST3GAL3‐related developmental and epileptic encephalopathy

Abstract Objective ST3GAL3‐related developmental and epileptic encephalopathy (DEE‐15) is an autosomal recessive condition characterized by intellectual disability, language and motor impairments, behavioral difficulties, stereotypies, and epilepsy. Only a few cases have been reported, and the epilepsy phenotype is not fully elucidated. Methods A retrospective chart review of two siblings with ST3GAL3‐related DEE was completed. In addition, we reviewed all published cases of ST3GAL3‐related congenital disorder of glycosylation. Results Two brothers presented with global developmental delay, motor and language impairment, hypotonia, and childhood‐onset seizures. Seizures started between 2.5 and 5 years and had tonic components. Both siblings had prolonged periods of seizure freedom on carbamazepine. Tremor was present in the younger sibling. Whole exome sequencing revealed two novel pathogenic variants in ST3GAL3, (a) c.302del, p.Phe102Serfs*34 and (b) c.781C>T, p.Arg261*, which were inherited in trans. Magnetic resonance imaging showed T2 hyperintensities and restricted diffusion in the brainstem and middle cerebellar peduncle in the older sibling, also described in two reported cases. A review of the literature revealed 24 cases of ST3GAL3‐related CDG. Twelve cases had information about seizures, and epilepsy was diagnosed in 8 (67%). The median age of seizure onset was 5.5 months. Epileptic spasms were most common (67%). Four children were diagnosed with Infantile Epileptic Spasms syndrome and Lennox Gastaut syndrome (57%). Most children (n = 6, 75%) had seizures despite anti‐seizure medication treatment. Significance Seizures related to ST3GAL3‐related DEE often occur in infancy and may present as epileptic spasms. However, seizure onset may also occur outside of infancy with mixed seizure types and show good response to treatment with prolonged seizure freedom. Tremor may also be uniquely observed in this condition

Significant vomiting and weight loss in a pediatric epilepsy patient secondary to vagus nerve stimulation: A case report and review of the literature

Vagus nerve stimulation is a neuromodulatory treatment option for individuals with drug resistant epilepsy who are not resective surgical candidates. As the vagus nerve has widespread neural connections, stimulation can lead to an array of adverse effects. While vomiting and weight loss are known side effects of vagus nerve stimulation, these are typically transient, mild, and do not limit the ability to continue treatment. We describe a 17-year-old female with drug resistant focal epilepsy secondary to tuberous sclerosis complex, who began to experience daily emesis and significant weight loss approximately 2.5 years after VNS device insertion. Her body mass index progressively fell from between the 75th–85th percentiles to less than the first percentile. She underwent extensive workup by neurology, gastroenterology, and adolescent medicine services with no obvious cause identified. Prior to the insertion of an enteral tube for feeding support and urgent weight restoration, her vagus nerve stimulator was switched off, resulting in immediate cessation of her vomiting and a dramatically rapid recovery of weight over the ensuing few months. This case emphasizes the need to consider adverse effects of vagus nerve stimulation in the differential diagnosis of patients with otherwise unexplained new medical sequelae, and provides evidence potentially linking vagal stimulation to significant malnutrition-related complications. Outside of GI-related effects, few studies have shown late-onset adverse effects from VNS, including laryngeal and facial pain as well as bradyarrhythmia. Further research is needed to elucidate the exact mechanisms of vagus nerve stimulation to better anticipate and mitigate adverse effects, and to understand the pathophysiology of late-onset adverse effects in previously tolerant VNS patients

Ovarian Failure Related to Eukaryotic Initiation Factor 2B Mutations

Ovarian failure (OF) at age <40 years occurs in ∼1% of all women. Other than karyotype abnormalities, very few genes are known to be associated with this ovarian dysfunction. We studied eight patients who presented with premature OF and white-matter abnormalities on magnetic resonance imaging. Neurological signs may be absent or present after OF. In seven patients, we report for the first time mutations in three of the five EIF2B genes (EIF2B2, -4, and -5) that were recently shown to cause childhood ataxia with central nervous system hypomyelination/vanishing white-matter disease leukodystrophy. The correlation we observed between the age at onset of the neurological deterioration and the severity of OF suggests a common pathophysiological pathway

Functional Effects of Epilepsy Associated <i>KCNT1</i> Mutations Suggest Pathogenesis via Aberrant Inhibitory Neuronal Activity

KCNT1 (K+ channel subfamily T member 1) is a sodium-activated potassium channel highly expressed in the nervous system which regulates neuronal excitability by contributing to the resting membrane potential and hyperpolarisation following a train of action potentials. Gain of function mutations in the KCNT1 gene are the cause of neurological disorders associated with different forms of epilepsy. To gain insights into the underlying pathobiology we investigated the functional effects of 9 recently published KCNT1 mutations, 4 previously studied KCNT1 mutations, and one previously unpublished KCNT1 variant of unknown significance. We analysed the properties of KCNT1 potassium currents and attempted to find a correlation between the changes in KCNT1 characteristics due to the mutations and severity of the neurological disorder they cause. KCNT1 mutations identified in patients with epilepsy were introduced into the full length human KCNT1 cDNA using quick-change site-directed mutagenesis protocol. Electrophysiological properties of different KCNT1 constructs were investigated using a heterologous expression system (HEK293T cells) and patch clamping. All mutations studied, except T314A, increased the amplitude of KCNT1 currents, and some mutations shifted the voltage dependence of KCNT1 open probability, increasing the proportion of channels open at the resting membrane potential. The T314A mutation did not affect KCNT1 current amplitude but abolished its voltage dependence. We observed a positive correlation between the severity of the neurological disorder and the KCNT1 channel open probability at resting membrane potential. This suggests that gain of function KCNT1 mutations cause epilepsy by increasing resting potassium conductance and suppressing the activity of inhibitory neurons. A reduction in action potential firing in inhibitory neurons due to excessively high resting potassium conductance leads to disinhibition of neural circuits, hyperexcitability and seizures