Clinical Features and Headache Diagnoses in Patients With Chief Complaint of Craniofacial Pain.

OBJECTIVES: Investigate the use of nasal endoscopy, sinus imaging, and neurologic evaluation in patients presenting to a rhinologist primarily for craniofacial pain. METHODS: This was a retrospective analysis of consecutive outpatients presenting to a rhinologist between 2016 and 2019 with chief complaints of craniofacial pain with or without other sinonasal symptoms, who were then referred to and evaluated by headache specialists. Data analyzed included sinusitis symptoms, Sino-Nasal Outcome Test (SNOT-22) scores (and facial pain subscores), pain location, nasal endoscopy, computed tomography (CT) findings, and headache diagnoses made by headache specialists. RESULTS: Of the 134 patients with prominent craniofacial pain, the majority of patients were diagnosed with migraine (50%) or tension-type (22%) headache, followed by multiple other non-sinogenic headache disorders. Approximately 5% of patients had headaches attributed to sinusitis. Amongst all patients, 90% had negative nasal endoscopies. Patients with negative endoscopies were significantly less likely to report smell loss (P = .003) compared to those with positive endoscopies. Poor agreement was demonstrated between self-reported pain locations and sinus findings on CT (kappa values < 0.20). Negative nasal endoscopy showed high concurrence with negative CT findings (80%-97%). CONCLUSIONS: Patients presenting with chief complaints of craniofacial pain generally met criteria for various non-sinogenic headache disorders. Nasal endoscopy was negative in 90% of patients, and CT demonstrated poor agreement with pain locations. Nasal endoscopy and CT shared high concurrence rates for negative sinus findings. The value of nasal endoscopy over sinus imaging in craniofacial pain evaluation should be explored in future studies.

Glycogenic Acanthosis: An Unusual Cause of Vocal Fold Leukoplakia.

Glycogenic acanthosis is a common benign lesion of the esophagus; however, reports of extra-esophageal manifestations are exceedingly rare. This case represents the first report of laryngeal glycogenic acanthosis found in a living patient, presenting as vocal fold leukoplakia. Glycogenic acanthosis may be considered among the differential diagnoses of conditions presenting as vocal fold leukoplakia. Laryngoscope, 132:1641-1643, 2022.

Impact of a specialty trained billing team on an academic otolaryngology practice.

PURPOSE: To determine how the incorporation of specialty specific training for coders within a focused billing team affected revenue, efficiency, time to reimbursement, and physician satisfaction in an academic otolaryngology practice. MATERIALS AND METHODS: Our academic otolaryngology department recently implemented a new billing system, which incorporated additional training in otolaryngology surgical procedures for medical coders. A mixed model analysis of variance was used to compare billing outcomes for the 6 months before and 6 months after this new approach was initiated. The following metrics were analyzed: Current Procedural Terminology codes, total charges, time between services rendered and billing submission, and time to reimbursement. A survey of department physicians assessing satisfaction with the system was reviewed. RESULTS: There were 4087 Current Procedural Terminology codes included in the analysis. In comparing the periods before and after implementation of the new system, statistically significant decreases were found in the mean number of days to coding completion (19.3 to 12.0, respectively, p < 0.001), days to posting of charges (27.0 to 15.2, p < 0.001), days to final reimbursement (54.5 to 27.2, p < 0.001), and days to closure of form (179.2 to 76.6, p < 0.001). Physician satisfaction with communication and coder feedback increased from 36% to 64% after initiation of the new program. CONCLUSIONS: The implementation of additional specialty training for medical coders in the otolaryngology department of a large medical system was associated with improved revenue cycle efficiency. Additionally, this model appears to improve physician satisfaction and confidence with the coding system.

Nucleus accumbens GABAergic inhibition generates intense eating and fear that resists environmental retuning and needs no local dopamine.

Intense fearful behavior and/or intense appetitive eating behavior can be generated by localized amino acid inhibitions along a rostrocaudal anatomical gradient within medial shell of nucleus accumbens of the rat. This can be produced by microinjections in medial shell of either the γ-aminobutyric acid (GABA)A agonist muscimol (mimicking intrinsic GABAergic inputs) or the AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) antagonist DNQX (6,7-dinitroquinoxaline-2,3-dione), disrupting corticolimbic glutamate inputs). At rostral sites in medial shell, each drug robustly stimulates appetitive eating and food intake, whereas at more caudal sites the same drugs instead produce increasingly fearful behaviors such as escape, distress vocalizations and defensive treading (an antipredator behavior rodents emit to snakes and scorpions). Previously we showed that intense motivated behaviors generated by glutamate blockade require local endogenous dopamine and can be modulated in valence by environmental ambience. Here we investigated whether GABAergic generation of intense appetitive and fearful motivations similarly depends on local dopamine signals, and whether the valence of motivations generated by GABAergic inhibition can also be retuned by changes in environmental ambience. We report that the answer to both questions is 'no'. Eating and fear generated by GABAergic inhibition of accumbens shell does not need endogenous dopamine. Also, the appetitive/fearful valence generated by GABAergic muscimol microinjections resists environmental retuning and is determined almost purely by rostrocaudal anatomical placement. These results suggest that nucleus accumbens GABAergic release of fear and eating are relatively independent of modulatory dopamine signals, and more anatomically pre-determined in valence balance than release of the same intense behaviors by glutamate disruptions.