In 1908 Sluder described a clinical picture of unilateral facial pain, lachrymation, rhinorrhea and mucosal congestion deriving from the Sphenopalatine Ganglion (SPG) irritation. We described a case of monolateral xerophthalmia, dry palate and mouth, deriving from SPG lesion after septoplasty that we called “SPG Deficit Syndrome”.
In our study a woman complaining functional nasal disorders and Computer Tomography (CT) images of a huge condro-vomerian septal spur in right nasal cavity, was underwent to septoplasty. After surgery she complained monolateral xerophthalmia, xerostomia and migraine.
We formulated hypothesis of parasympathetic postgangliar nerve transmission interruption due to a lesion of effector fibers, supported by post-operative CT images of posterior wall of maxillary sinus lesion and by endoscopic evaluation of dryness of palatal mucosa and right nasal cavity.
To the best of our knowledge this is the first case of this kind of symptomatology reported as complication after septoplasty.
Sluder was the first to highlight the role of the SPG.
“SPG deficit syndrome”, is subtended by a lesional mechanism.
“SPG deficit syndrome”, is related to a ganglion injury.
SPG deficit syndrome s’: xerophthalmia, dryness and hypoesthesia of palate and nose.
In 1908, Sluder proposed that a high-grade inflammatory reaction in the posterior ethmoid and sphenoid sinuses may be involved in certain cases of unilateral facial pain associated with lachrymation, rhinorrhea, and mucosal congestion. These symptoms are related to the inflammation or neuropeptides release that cause vessel dilation and/or activation of the trigeminal nociceptor fibres into the sphenopalatine ganglion (SPG) [ ]. The SPG, even called Meckel’s ganglion, is the largest extra cranial neural structure located into pterygopalatine fossa (PPF). The ganglion has sensory, motor and autonomic components, for the sensibility of the palate, the motility of the velum palatinum elevator muscle, but the most representative fibers are the parasympathetic fibers, which inputs derive from the superior salivatory nucleus (SSN) in the brainstem. The efferent postganglionic fibers provide secretomotor function to the mucous membrane of the nose, soft palate, tonsils, uvula, roof of the mouth, upper lip and gums, upper part of the pharynx, lacrimal gland, and meningeal vessels [ ] ( Fig. 1 a).
The aim of our study is to describe the physiopathological bases underlying an unusual syndromic clinical picture characterized by monolateral xerophthalmia, dry palate and mouth, deriving from the lesion of the SPG after septoplasty. We have called this lesional picture as “SPG Deficit Syndrome” to underline the differences with the one described by Sluder due to an irritative stimulus. To the best of our knowledge this is the first time description of such a kind of syndromic clinical picture reported as a complication after septoplasty.
A 43 years-old woman, who complained functional nasal disorders with a sense of obstruction and breathing difficulty, was admitted to our Maxillo-Facial Surgery Unit on July 2013 for elective septoplasty. To the medical history no prior trauma or surgery was declared, she only suffered for Gastro-Esophageal Reflux Diseases (GERD), under treatment with Proton-pump inhibitors (PPIs). Pre-surgical Computer Tomography (CT) showed a huge condro-vomerian septal spur in the right nasal cavity ( Fig. 1 b and c).
On September 2013, a closed septoplasty was performed under general anesthesia. Through a trans -columellar incision, the right septal spur was removed with use of a nasal osteotome. Total operation time was 65 min, and no anomalies were found during the surgical procedure. Nasal packing was applied, and the awakening from anesthesia occurred without complications. After nasal packing removal, at day three, the patient began to complain a symptomatology characterized by right xerophthalmia, dryness and hypoesthesia of palate and nose. The patient also began to suffer of frequent episodes of right migraine without aura, never complained before. Post-surgical CT showed a linear bone lesion at the posterior wall of the maxillary sinus extended to the PPF. The PPF impairment, appearing blocked due to scattered bone fragments, was evident ( Fig. 2 a–c).