Adherence to Clinical Practice Guidelines for Treatment of Bell's Palsy.

BACKGROUND: Bell's palsy is the most common cause of acute facial nerve paresis and paralysis with devastating disability yet high rate of spontaneous recovery. Patients who do not fully recover have functional disability that may require reconstructive surgery. The Clinical Practice Guideline: Bell's Palsy recommends treatment with high-dose steroids as it shows a higher likelihood of complete recovery. However, guideline adherence rates are inconsistent and unstudied. OBJECTIVE: To identify the frequency at which hospital-based clinicians at the University of Wisconsin-Madison follow recommended clinical guidelines and prescribe high-dose steroid medication. METHODS: Charts were reviewed from a single hospital (University Hospital) to evaluate Bell's palsy guideline adherence. All hospital-based encounters from 2008 through 2018 with primary diagnosis of Bell's palsy (ICD-9 351.0 and ICD-10 G51.0) were identified. Encounters were excluded if they had a diagnosis of Bell's palsy within 1 year prior (n=250) and did not have a medication list available (n=353). We examined patient demographics, common comorbidities, and any radiology and lab orders. RESULTS: We identified 565 patients with a primary diagnosis of Bell's palsy with available medication lists; 77.70% received the recommended treatment. The patients' median age was 47 (interquartile range 34-59), 52.16% were male, and 82.46% were treated by emergency medicine clinicians. Other treating clinicians were hospital-based primary care, otolaryngology and plastic surgery, and others. Multivariate analysis showed that treating clinician specialty was the only significant positive predictor. CONCLUSIONS: A significant portion of clinicians followed treatment guidelines for Bell's palsy. Further and larger research is needed to better identify points of intervention to improve guideline adherence.

Impaired cerebral angiogenesis in the fetal lamb model of persistent pulmonary hypertension.

BACKGROUND: Persistent pulmonary hypertension of the newborn (PPHN) is associated with increased risk of neuro-developmental impairments. Whether relative fetal hypoxia during evolution of PPHN renders the fetal brain vulnerable to perinatal brain injury remains unclear. We hypothesized that in utero ductal constriction, which induces PPHN also impairs cerebral angiogenesis. METHODS: Fetal lambs with PPHN induced by prenatal ligation of the ductus arteriosus were compared to gestation matched twin controls. Freshly collected or fixed brain specimens were analyzed by immunohistochemistry, Western blot analysis, and RT-PCR. RESULTS: Cortical capillary density was decreased in PPHN lambs compared to controls (Glut-1, isolectin B-4 and factor VIII, n=6, p<0.05). Hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) protein levels were decreased in cortical cell lysates of PPHN lambs. PPHN increased angiopoetin-1 (Ang-1) and tyrosine-protein kinase receptor (Tie-2) protein expression while angiopoetin-2 (Ang-2) protein levels were decreased (n=6, p<0.05). PPHN did not change mRNA levels of these proteins significantly (n=6). CONCLUSIONS: PPHN decreased cortical capillary density in fetal lamb brain. PPHN decreased the expression of proteins involved in angiogenesis. These findings suggest that PPHN is associated with impaired cortical angiogenesis.

Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons.

Previous work has shown that hindbrain catecholamine neurons are required components of the brain's glucoregulatory circuitry. However, the mechanisms and circuitry underlying their glucoregulatory functions are poorly understood. Here we examined three drugs, glucosamine (GcA), phloridzin (Phl) and 5-thio-d-glucose (5TG), that stimulate food intake but interfere in different ways with cellular glucose utilization or transport. We examined feeding and blood glucose responses to each drug in male rats previously injected into the hypothalamic paraventricular nucleus with anti-dopamine-ß-hydroxylase conjugated to saporin (DSAP), a retrogradely transported immunotoxin that selectively lesions noradrenergic and adrenergic neurons, or with unconjugated saporin (SAP) control. Our major findings were 1) that GcA, Phl, and 5TG all stimulated feeding in SAP controls whether injected into the lateral or fourth ventricle (LV or 4V), 2) that each drug's potency was similar for both LV and 4V injections, 3) that neither LV or 4V injection of these drugs evoked feeding in DSAP-lesioned rats, and 4) that only 5TG, which blocks glycolysis, stimulated a blood glucose response. The antagonist of the MEK/ERK signaling cascade, U0126, attenuated GcA-induced feeding, but not Phl- or 5TG-induced feeding. Thus GcA, Phl, and 5TG, although differing in mechanism and possibly activating different neural populations, stimulate feeding in a catecholamine-dependent manner. Although results do not exclude the possibility that catecholamine neurons possess glucose-sensing mechanisms responsive to all of these agents, currently available evidence favors the possibility that the feeding effects result from convergent neural circuits in which catecholamine neurons are a required component.