Obstructive sleep apnoea syndrome (OSAS) is characterized by repeated upper airway obstruction during sleep, which induces interruption of ventilation, intermittent desaturation, microarousals and a transient increase of sympathetic tone [
1]. Severe OSAS is responsible for accidents related to excessive daytime sleepiness [
2] and cardiovascular [
3], cognitive [
4] and metabolic [
5] consequences. Nocturnal continuous positive airway pressure (CPAP) ventilation [
3], the reference treatment, and mandibular advancement devices, the most frequent alternative treatment in patients not supporting CPAP [
6,
7], prevent obstructive events by modifying upper airway anatomy, to enlarge and maintain an open airway. However, although obstructive apnoeas often have an anatomical origin (excessively narrow upper airways, macroglossia) [
8], more than 50% of patients experience obstructive apnoeas with no major anatomical abnormality [
9]. This suggests that functional abnormalities of the upper airways also contribute to the pathophysiology of OSAS. The maintenance of upper airway patency throughout the respiratory cycle is dependent of upper airways dilator muscles, which are mainly innervated by the hypoglossal nerve [
10]. In OSAS patients, these muscles comprise a smaller proportion of type I muscle fibres [
11] and present reduced metabolic activity [
12]. Moreover, alteration of the neural control of upper aiways are also present in OSA patients: peripheral sensory neuropathy [
13], hypoglossal motor neuropathy [
14], and abnormal respiratory-related cortical adaptations [
15] have been reported. These abnormalities may contribute to obstructive events during sleep by promoting upper airways unstability [
16]. This probably explains why “functional” treatment, such as pharyngeal muscle retraining which acts via a combination of increased strength of the genioglossus, the main dilator muscle of the upper airways, and neuromodulating adaptations [
17], has been shown to effectively reduce the apnoea-hypopnoea index (AHI) [
18].
The sphenopalatine ganglion (SPG) is an autonomic nervous system ganglion that relays mixed cranial nerves innervating the upper airways. The SPG is situated in the pterygopalatine fossa, posterior to the posterior wall of the maxillary sinus and inferior to the junction of the body of the sphenoid, the greater wing and pterygoid process of the sphenoid, lateral to the perpendicular plate of the palatine bone, and medial to the pterygomaxillary fissure. It receives parasympathetic and sympathetic sensory afferents via fibres derived from the accessory branch of the facial nerve (VIIb) and the maxillary branch of the trigeminal nerve (V2). It distributes these fibres to the nasal mucosa, lacrimal glands, nasopharynx and soft palate, including some of the upper airway dilator muscles [
19]. It could therefore play an important role in control of upper airway stability, by modulating nasal congestion, and/or upper airways muscles tone throughout the respiratory cycle. The SPG is targeted in the treatment of cluster headache, based on the fact that parasympathetic hyperactivity plays an important role in its physiopathology [
20]. Postganglionic parasympathetic blockade of the SPG by local anaesthesia or implanted stimulation alleviates pain and nasal congestion in cluster headache [
20,
21].
Intraoral myofascial therapy of the SPG is widely used in osteopathic practice, for the management of nasal obstruction, chronic rhinitis and snoring [
22]. It is possible that this therapy allows to obtain muscle relaxation and to relieve pain in patients with temporomandibular dysfunction [
23]. Clinical experience and upublished observations also suggest reduction of snoring (reflecting upper airway instability during sleep) after osteopathic manipulative treatment (OMT) of the SPG. On the basis of the above reasoning, weakly supported by unpublished reports from practitionners, it seemed interesting to test the hypothesis that OMT of the SPG could improve upper airway stability in OSAS patients. We designed a randomized, crossover, double-blind, controlled (active manipulation vs. sham manipulation) proof-of-concept trial, in which the primary endpoint was determination of upper airway critical closing pressure in awake subjects (Pcrit; defined as the negative pressure beyond which the upper airways collapse, and recognized as an index of upper airway collapsibility [
24]). This study was retrospectively registered in the
clinicaltrial.gov registry on 1st September 2010 under reference NCT01193738. The first patient was included on 19 May 2010 and the last visit of last patient was done on 25 May 2011. The trial ended when the needed number of patients was reached. The results were presented in an oral communication to the congress of the
Société Française de Médecine du Sommeil (SFRMS) [(French society of sleep medicine] in November 2015.