Vagal sensory neurons mediate the Bezold-Jarisch reflex and induce syncope.

Visceral sensory pathways mediate homeostatic reflexes, the dysfunction of which leads to many neurological disorders1. The Bezold-Jarisch reflex (BJR), first described2,3 in 1867, is a cardioinhibitory reflex that is speculated to be mediated by vagal sensory neurons (VSNs) that also triggers syncope. However, the molecular identity, anatomical organization, physiological characteristics and behavioural influence of cardiac VSNs remain mostly unknown. Here we leveraged single-cell RNA-sequencing data and HYBRiD tissue clearing4 to show that VSNs that express neuropeptide Y receptor Y2 (NPY2R) predominately connect the heart ventricular wall to the area postrema. Optogenetic activation of NPY2R VSNs elicits the classic triad of BJR responses-hypotension, bradycardia and suppressed respiration-and causes an animal to faint. Photostimulation during high-resolution echocardiography and laser Doppler flowmetry with behavioural observation revealed a range of phenotypes reflected in clinical syncope, including reduced cardiac output, cerebral hypoperfusion, pupil dilation and eye-roll. Large-scale Neuropixels brain recordings and machine-learning-based modelling showed that this manipulation causes the suppression of activity across a large distributed neuronal population that is not explained by changes in spontaneous behavioural movements. Additionally, bidirectional manipulation of the periventricular zone had a push-pull effect, with inhibition leading to longer syncope periods and activation inducing arousal. Finally, ablating NPY2R VSNs specifically abolished the BJR. Combined, these results demonstrate a genetically defined cardiac reflex that recapitulates characteristics of human syncope at physiological, behavioural and neural network levels.

Hidradenitis Suppurativa and Concomitant Down Syndrome: Literature Review of Other Associated Mucocutaneous Manifestations in Adults.

This contribution describes hidradenitis suppurativa (HS) occurring in Down disease that presented with morphology conforming to an overlap of stages 1 and 2 of the Hurley staging system, namely the formation of solitary or multiple isolated abscesses without scarring or sinus tracts, recurrent abscesses, and single or multiple widely separated lesions with sinus tract formation, occupying apocrine sweat gland-bearing areas: the inner thighs, groin, and buttocks. The lesions were bilateral and symmetrical, of rare occurrence. In addition, the clinical and pathognomonic features of several other concomitant diseases are defined and reviewed; these include elastosis perforans serpiginosa, fissured tongue/macroglossia, syringomas, palmoplantar keratodermas, cheilitis, xerosis, atopic dermatitis, seborrheic dermatitis, vitiligo, cutis marmorata, and alopecia areata.

Necrotizing fasciitis.

Necrotizing fasciitis is an uncommon, rapidly spreading infection, affecting primarily the deep fascia, which may result in secondary necrosis of the subcutaneous tissue, fascia and muscle. We report a patient that had the cardinal features; namely, excruciatingly painful lesions, demonstration of gas in the tissue and an obnoxious foul odor, prominent erythema, induration, patchy necrosis, and loss of sensation in the left buttock and thigh. Its onset probably followed inadvertent trauma/injury of the left buttock. Corroborative microscopic pathology confirmed the diagnosis. Debridement and intensive supportive therapy comprising antibiotics, analgesics and fluids were given. The outcome of the therapy was gratifying.