DDSP- expanding etiology

Introduction: There are two forms of DDSP: intermittent (iDDSP) associated with airway obstruction and persistent (pDDSP) associated with airway obstruction and often dysphagia. DDSP results in a marked airway obstruction during exhalation and therefore, performance impairment occurs quickly after the occurrence of palate displacement which is referred to using terms such as “choking down” or “hitting a wall” by trainers and/or riders, The dysphagia may be associated with a neurological dysfunction of the soft palate or it may be a result of tracheal aspiration leading to tracheitis.

Objectives: Review of the literature on etiopathological causes of DDSP and contrast those with our experiences in clinical patients at either Cornell clinic.

Methods: Cases tabulated from electronic medical records (EMR).

Results and discussion: There are multiple etiopathogenesis to this condition. The evidence-based data that we have are from experimental studies in experimental horses where three reproducible models of this disease have been reported: 1) desensitization of the pharyngeal branch of the vagus(1,2) 2) bilateral resection of the thyrohyoideus muscle(3), and 3) bilateral desensitization of the hypoglossal nerves at the level of the ceratohyoid bones.(4) The first model introduced by Holcombe et al., 1998 hypothesized that DDSP was secondary to a dysfunction of the palatinus and palatopharyngeus muscle. The model did reproduce DDSP at rest and at exercise and therefore was a more severe form of palate displacement than most naturally-occurring cases. However this model also resulted in dysphagia which is not a feature of iDDSP. In this model the cause of DDSP is a neuromuscular dysfunction of the nasopharynx. In their study glossopharyngeal and hypoglossal desensitization at the level of the guttural pouch did not result in DDSP.(5) The latter two models were able to recreate iDDSP and do so only at exercise and without dysphagia. These latter two models of DDSP indicated that factors other than the intrinsic neuromuscular structure of the nasopharynx were implicated in iDDSP namely the thyrohyoideus muscle and/or one or more of the following muscles: genioglossus, styloglossus, geniohyodeus and hyoglossus. More recent observations supported that early muscle fatigue may be at the root cause of some iDDSP.(6) The current working hypothesis is that cervical descent of the larynx is the underlying cause of iDDSP. Strap muscle resection and laryngeal tie-forward appears to be effective in preventing caudal descent of the larynx.

The non evidence-based data are centered on observation of intermittent or persistent DDSP associated with structural abnormalities surrounding the soft palate and/or epiglottic areas: palatal cysts, sub-epiglottic masses, granuloma and epiglottic chondritis. These structural abnormalities as a cause for DDSP are anecdotal, yet frequently observed. The mechanisms by which they are associated with displacement was thought to be structural: interfering with laryngo-palatal seals. However, we have observed recently that sensory input may play a role because blocking the sensory afferent results in near immediate resolution of the palate displacement on endoscopy. In summary, at the level of the nasopharynx, neuromuscular deficits, sensory abnormalities, and structures that interfere with the laryngo-palatal seal represent the intrinsic pathway to DDSP. Extrinsic pathway appears to be tied to early fatigue of the external musculature that controls the position of the larynx.