Nasal Septal Spur Associated with Rhinogenic Contact Point Otalgia and Tinnitus

Abstract

Rhinogenic contact point otalgia is a new term in medicine and it represents earache as a form of facial pain that is caused by intranasal mucosal contact points between the nasal septal spur or septal deviation and lateral nasal wall. It is a referred otalgia without any signs of inflammation. The author reports an unusual case of a 19-year-old male who complained of a 5-year history of right-sided otalgia and tinnitus. On physical exam, a big, right-sided nasal septal spur was seen in contact with the right lateral nasal wall. Other findings are unremarkable. Placement of anesthetic and vasoconstrictor solution provided relief of symptoms. After the exclusion of other causes of otalgia, and after surgical removal of septal spur, the patient experienced a significant relief of symptoms.

Earache and tinnitus are common entities in otolaryngologic clinical practice. Rhinogenic contact point headache (RCPH) is a pain of noninflammatory origin caused by contact and pressure between adjacent mucosal surfaces in the nasal cavity due to the presence of anatomical variations, especially of nasal septum and nasal turbinates [1]. RCPH was added in 2004 as a separate form of secondary headache in the Appendix (A11.5.1—“Mucosal contact point headache”) of second revision of International Classification of Headache Disorders [2]. Recently, Kim [3] presented a case of a 17-year-old male patient who presented with intermittent and intractable otalgia which was supposed to be induced by nasal septal deformation. After surgical correction of nasal mucosal contact point, the symptom in this patient has been alleviated. It was the first such case reported in the English literature and the author suggested for new disease entity of rhinogenic contact point otalgia. Here, the author reports an unusual case of otalgia and tinnitus which could be related to contact between the septal spur and lateral nasal wall, and, to the best of the author’s knowledge, this is the first report on two associated otological symptoms, otalgia and tinnitus, which were supposed to be induced by nasal mucosal contact point.

Case Report

A 19-year-old man was presented with a 5-year history of right-sided otalgia and tinnitus. The pain was deep and penetrating in character, intermittent, and lasted for 4 to 5 h, radiating to the right mastoid region. Tinnitus was in the form of whistle and also intermittent with the same duration as otalgia. The patient reported the right-sided nasal obstruction only during the attacks of otalgia and tinnitus. He had no history of head trauma and surgery and he was treated for migraine and otitis media without success. The otoendoscopic examination revealed normal right-sided external auditory canal and tympanic membrane (Figure 1) and the audiological evaluation showed a normal hearing. During rhinoscopic and nasal endoscopic examination, there was no sign of inflammation. The author found a normal nasal mucosa with a mucosal contact between the large, right-sided septal spur and lateral nasal wall, which was confirmed by computed tomographic (CT) scan of the paranasal sinuses (Figure 2a,b). During an otalgia attack, the author placed a small 5% lidocaine and epinephrine-soaked cotton pledget on the contact point and, after 15 min, the patient experienced a significant reduction in intensity of earache and tinnitus. The patient underwent a septoplasty under general anesthesia. A few days postoperatively, the patient was free of otalgia, with significant improvement in tinnitus intensity, and without the right-sided nasal discharge. At 12 months follow-up, the patient reported no further otalgia and tinnitus.

Discussion

Only one case of nasal septal deviation–induced contact point otalgia as a subtype of RCPH has been previously reported. This was a case of a 17-year-old boy [3]. The diagnosis was confirmed by lidocaine test and the patient was successfully treated by septoplasty. This headache has been attributed to referred pain through the system of n. trigeminus. Back in 1948, Wolff hypothesized that stimulation of various points of the nasal mucosa can cause pain that was felt in the cutaneous distribution of ophthalmic and maxillary division of trigeminal nerve [1,3]. Previous investigations demonstrated that neuropeptide substance P has the most important role as a mediator of rhinogenic pain [4]. Some mechanical stimuli, such as pressure on the nasal mucosa, may cause the release of substance P in the trigeminal system through the central orthodromic impulse and peripheral, local, antidromic impulse. The release of substance P in the nasal mucosa leads to vasodilatation, edema, plasma extravasation, and gland hypersecretion, which further intensifies the pressure of contact surfaces [4]. Pseudostratified respiratory epithelium of the nasal mucosa produces enzyme neural endopeptidase (NEP), which is able to degrade substance P. However, in small areas of mucosal contacts, the epithelium is affected and the basement membrane which contains a larger number of sensory nerves is exposed. So, in contact point areas, this degrading action of NEP may be disturbed and this leads to an increase of pain [5]. In the central nervous system, the release of substance P causes the sensation of pain, which is similar to migraine without aura and the onset and duration of pain coincide with the beginning and duration of nasal cycle [4]. In case of this patient, the attacks of right-sided otalgia were presented synchronously with the right-sided nasal obstruction. In a previously reported case, [3] otalgia was associated with mucosal contact caused by septal spur. In one previous retrospective study evaluating the diagnosis and surgical treatment of RCPH patients, the author found the most intensive pain sensation in patients with mucosal contacts between the lateral nasal wall and septal spur [1]. The author suggested that this form of mucosal contact may imply more intense production and local mucosal release of substance P than contacts associated with other forms of anatomical variations [1]. The relationship between nasal mucosal contact point and otalgia, and especially between contact point and tinnitus, is not completely clear. This is a difficult association to understand given the paucity of randomized studies in the area of mucosal contact points in general. However, contact point otalgia, as a form of referred pain could be explained by previously well-described trigeminal sensory innervation of the middle ear and Eustachian tube mucosa [6]. The referred pain is pain that is not felt at its origin, but may be projected onto corresponding dermatomes. Pressure between two opposing mucosal surfaces initiates the release of substance P, which mediates central orthodromic impulses to the cortex by afferent C fibers of branches of the trigeminal nerve [7]. The orthodromic impulse is diffuse and is poorly localized by higher cortical centers and the pain is projected and perceived in dermatomes corresponding to the trigeminal branches [8]. So, the patient with mucosal contact in the nasal cavity may have the sensation of pain in the ipsilateral ear. On the other hand, trigeminal fibers play a role in maintaining normal vascular tone and causing pathophysiological vascular responses in the cochlea [9]. Accordingly, auditory symptoms often occur with some kinds of headaches, such as migraine, which may be related to trigeminal vascular disturbances. So, tinnitus presenting synchronously with earache could be explained by disturbances in function of trigeminal neurons in maintaining normal vascular tone and physiological vascular responses in the cochlea [9]. Vass et al. [10] using the horseradish peroxidase tracer method, have observed that significant number of trigeminal fibers innervate spiral modiolar artery. Those fibers originated in the medial part of the trigeminal ganglion, mainly in the area of the ophthalmic nerve which has important role in sensory innervation of the nasal mucosa.

To the author’s knowledge, this is the first reported case of association between nasal mucosal contact point otalgia and tinnitus. Diagnosis of rhinogenic contact point otalgia and tinnitus requires a multidisciplinary approach. The patients without the signs of inflammation of nasal/paranasal sinuses mucosa and external/middle ear and with normal audiological tests should be sent to the examination of neurologist, dentist, and internist. After exclusion of other causes of pain, rhinoscopic and endoscopic examination and CT scan of the nasal cavity/paranasal sinuses should be performed for the evaluation of mucosal contact point. The patient should have a positive lidocaine test, that is, he should experience relief of pain and tinnitus after placement of topical anesthetic/ vasoconstrictor on the nasal contact point. It is very important to include rhinogenic contact point otalgia as a differential diagnosis for headaches. However, further prospective studies are necessary to validate the existence of rhinogenic contact point otalgia with tinnitus.

Conclusions

In cases of otalgia and tinnitus without the confirmation of inflammation of middle and external ear and nasal and paranasal sinuses mucosa, it is necessary to exclude other causes of otalgia. Diagnosis should be made by nasal endoscopic examination and CT scan of the paranasal sinuses and confirmed by lidocaine test. In this report, the patient was successfully treated by septoplasty. The relationship between nasal mucosal contact point otalgia and tinnitus is not well investigated, but previous investigations suggested the role of trigeminal sensory innervation of the middle ear mucosa and cochlear arterial vessels. It is important to include rhinogenic contact point otalgia associated with tinnitus as a differential diagnosis for headaches.