[Physiopathology of obstructive sleep apnea syndrome]. / Physiopathologie du syndrome d'apnées-hypopnées obstructives du sommeil.

An excellent grasp of the physiopathology of obstructive sleep apnea syndrome (OSAS) is essential to understanding its diagnostic and therapeutic modalities. A systematic review of the literature was performed on data specific to humans. Two aspects are involved: on one hand, the mechanisms contributing to intermittent obstruction of the upper airways (UA) during sleep and, on the other hand, the impact of this obstruction, e.g. neurocognitive disorders, cardiovascular disease and metabolic dysregulation. UA obstruction can be explained by anatomical, mechanical and neuro-functional conditions, especially the proprioceptive and chemical feedback of UA neuromuscular activity. Our understanding of the impact of OSAS has benefited from the recently developed concepts of oxidative stress and low-grade systemic inflammation, the discovery of hypoxia-sensitive agents and of the role of cytokines. The onset of this chain of events is determined by chronic intermittent hypoxia.

Sinonasal involvement in sarcoidosis: a case-control study of 20 patients.

We conducted a retrospective single-center study to describe the clinical features of sinonasal sarcoidosis (SNS) and to determine whether SNS is associated with a particular clinical phenotype of sarcoidosis. Twenty patients with histologically proven SNS (men/women, 7/13; mean age, 32 +/- 9 yr) were compared with control patients with sarcoid but without sinonasal (SN) involvement. Each patient was matched with 2 controls for the date of admittance in our institution. SN involvement occurred in the course of previously known sarcoidosis in 8 patients, whereas it preceded disease diagnosis in 12 patients. Among these 12 patients, 4 initially presented with strictly isolated SNS and 8 had other associated signs related to sarcoidosis. The most common symptoms were stuffiness (90%), anosmia (70%), and rhinorrhea (70%). Lupus pernio was frequent (50%). Local examination was constantly abnormal and showed hypertrophy (75%) and purplish coloring of the nasal mucosa with granulations (50%) on the septum and/or inferior turbinates. Computed tomography scans showed medial lytic lesions, mainly of the septum and/or the turbinates in about half the cases. All patients had negative antineutrophil cytoplasmic antibodies. Patients with SNS had significantly more frequent and severe involvement of vital organs than controls, had a longer history of sarcoidosis, and required systemic treatment more frequently (100% vs. 57.7%, p < 0.001) and for a longer time (78 +/- 42 mo vs. 29 +/- 18 mo, p < 0.0001). Corticosteroids maintenance dosage was high (10.5 +/- 6 mg daily) and mainly depended on SN involvement. Although rare, SN involvement is a severe and recalcitrant manifestation of sarcoidosis representing a therapeutic challenge.

Wegener granulomatosis involving the pterygopalatine fossa: an unusual case of trigeminal neuropathy.

We report on a case of Wegener granulomatosis in the pterygopalatine fossa that was associated with trigeminal neuropathy. MR and CT examinations were useful in depicting the extent of the lesion and suggesting a perineural spread. Diagnosis was confirmed with positive serum assay findings for the presence of cytoplasmic antineutrophil cytoplasm antibody.