Creation of an advancing adult and pediatric neurology resident EEG curriculum.

BACKGROUND: The Accreditation Council for Graduate Medical Education (ACGME) milestones state that neurology residents should be able to "interpret common EEG abnormalities, recognize normal EEG variants, and create a report." Yet, recent studies have shown that only 43% of neurology residents express confidence in interpreting EEG without supervision and can recognize less than half of normal and abnormal EEG patterns. Our objective was to create a curriculum to improve both confidence and competence in reading EEGs. METHODS: At Vanderbilt University Medical Center (VUMC), adult and pediatric neurology residents have required EEG rotations in their first and second years of neurology residency and can choose an EEG elective in their third year. A curriculum consisting of specific learning objectives, self-directed modules, EEG lectures, epilepsy-related conferences, supplemental educational material, and tests was created for each of the three years of training. RESULTS: Since the implementation of an EEG curriculum at VUMC from September 2019 until November 2022, 12 adult and 21 pediatric neurology residents completed pre- and post-rotation tests. Among the 33 residents, there was a statistically significant improvement in post-rotation test scores, with a mean score improvement of 17% (60.0 ± 12.9 to 77.9 ± 11.8, n = 33, p < 0.0001). When differentiated by training, the mean improvement of 18.8% in the adult cohort was slightly higher than in the pediatric cohort, 17.3%, though it was not significantly different. Overall improvement was significantly increased in the junior resident cohort with a 22.6% improvement in contrast to 11.5% in the senior resident cohort (p = 0.0097 by Student's t-test, n = 14 junior residents and 15 senior residents). DISCUSSION: With the creation of an EEG curriculum specific to each year of neurology residency, adult and pediatric neurology residents demonstrated a statistically significant mean improvement between pre- and post-rotation test scores. The improvement was significantly higher in junior residents in contrast to senior residents. Our structured and comprehensive EEG curriculum objectively improved EEG knowledge in all neurology residents at our institution. The findings may suggest a model which other neurology training programs may consider for the implementation of a similar curriculum to both standardize and address gaps in resident EEG education.

Aquaporins in Brain Edema and Neuropathological Conditions.

The aquaporin (AQP) family of water channels are a group of small, membrane-spanning proteins that are vital for the rapid transport of water across the plasma membrane. These proteins are widely expressed, from tissues such as the renal epithelium and erythrocytes to the various cells of the central nervous system. This review will elucidate the basic structure and distribution of aquaporins and discuss the role of aquaporins in various neuropathologies. AQP1 and AQP4, the two primary aquaporin molecules of the central nervous system, regulate brain water and CSF movement and contribute to cytotoxic and vasogenic edema, where they control the size of the intracellular and extracellular fluid volumes, respectively. AQP4 expression is vital to the cellular migration and angiogenesis at the heart of tumor growth; AQP4 is central to dysfunctions in glutamate metabolism, synaptogenesis, and memory consolidation; and AQP1 and AQP4 adaptations have been seen in obstructive and non-obstructive hydrocephalus and may be therapeutic targets.

Effect of histamine on Ca(2+)-dependent signaling pathways in rat conjunctival goblet cells.

PURPOSE: The purpose of this study was to determine the Ca(2+)-dependent cellular signaling pathways used by histamine to stimulate conjunctival goblet cell secretion. METHODS: Cultured rat goblet cells were grown in RPMI 1640. Goblet cell secretion of high molecular weight glycoconjugates was measured by an enzyme-linked lectin assay. Intracellular [Ca(2+)] ([Ca(2+)](i)) was measured by loading cultured cells with the Ca(2+) sensitive dye fura-2. The level of [Ca(2+)](i) was measured using fluorescence microscopy. Extracellular regulated kinase (ERK) 2 was depleted using small interfering RNA (siRNA). RESULTS: Histamine-stimulated conjunctival goblet cell secretion of high molecular weight glycoproteins was blocked by removal of extracellular Ca(2+) and depletion of ERK2 by siRNA. Histamine increase in [Ca(2+)](i) was desensitized by repeated addition of agonist and blocked by a phospholipase C antagonist. Histamine at higher doses increased [Ca(2+)](i) by stimulating influx of extracellular Ca(2+), but at a lower dose released Ca(2+) from intracellular stores. Activation of each histamine receptor subtype (H(1)-H(4)) increased [Ca(2+)](i) and histamine stimulation was blocked by antagonists of each receptor subtype. The H(2) receptor subtype increase in [Ca(2+)](i) was cAMP dependent. CONCLUSIONS: We conclude that histamine activates phospholipase C to release intracellular Ca(2+) that induces the influx of extracellular Ca(2+) and activates ERK1/2 to stimulate conjunctival goblet cell mucous secretion, and that activation of all four histamine receptor subtypes can increase [Ca(2+)](i).

Signaling pathways used by EGF to stimulate conjunctival goblet cell secretion.

The purpose of this study was to identify the signaling pathways that epidermal growth factor (EGF) uses to stimulate mucin secretion from cultured rat conjunctival goblet cells and to compare the pathways used by EGF with those used by the known secretagogue muscarinic, cholinergic agonists. To this end, goblet cells from rat conjunctiva were grown in culture using RPMI media. For immunofluorescence experiments, antibodies against EGF receptor (EGFR) and ERK 2 as well as muscarinic receptors (M(1)AchR, M(2)AchR, and M(3)AchR) were used, and the cells viewed by fluorescence microscopy. Intracellular [Ca(2+)] ([Ca(2+)](i)) was measured using fura 2/AM. Glycoconjugate secretion was determined after cultured goblet cells were preincubated with inhibitors, and then stimulated with EGF or the cholinergic agonist carbachol (Cch). Goblet cell secretion was measured using an enzyme-linked lectin assay with UEA-I or ELISA for MUC5AC. In cultured goblet cells EGF stimulated an increase in [Ca(2+)](i) in a concentration-dependent manner. EGF-stimulated increase in [Ca(2+)](i) was blocked by inhibitors of the EGF receptor and removal of extracellular Ca(2+). Inhibitors against the EGFR and ERK 1/2 blocked EGF-stimulated mucin secretion. In addition, cultured goblet cells expressed M(1)AchR, M(2)AchR, and M(3)AchRs. Cch-stimulated increase in [Ca(2+)](i) was blocked by inhibitors for the M(1)AchRs, matrix metalloproteinases, and EGF receptors. Inhibitors against the EGF receptor and ERK 1/2 also blocked Cch-stimulated mucin secretion. We conclude that in conjunctival goblet cells, EGF itself increases [Ca(2+)](i) and activates ERK 1/2 to stimulate mucin secretion. EGF-stimulated secretion is dependent on extracellular Ca(2+). This mechanism of action is similar to cholinergic agonists that use muscarinic receptors to transactivate the EGF receptor, increase [Ca(2+)](i), and activate ERK 1/2 leading to an increase in mucin secretion.