By Marcello Cherchi, MD PhD
For patients
A glomus tympanicum (GT) is a vascular tumor in the middle ear, usually in just one ear. It is more common in adults, and more common in women. Over half of cases cause pulsatile tinnitus, and about a third of cases cause hearing loss. If you have these symptoms, and if your physician sees a red pulsatile mass behind your eardrum, then you will be referred to an otolaryngologist (ENT), who may order imaging studies to confirm the diagnosis. Depending on the location and extent of the GT, the ENT may consider surgery, or radiation therapy, or a combination. GTs do not usually recur.
For clinicians
Overview
A glomus tympanicum (GT) tumor is a paraganglioma arising at various locations in the middle ear. It is highly vascular, and the classic appearance under otomicroscopy/otoscopy is a red pulsatile mass behind the eardrum. It is usually a disease of adulthood, and is more common in women. A number of diseases can resemble GTs, and GTs can mimic other lesions. About 15% of GTs secrete catecholamines. The most common presenting symptoms are pulsatile tinnitus and hearing loss. Rarely GTs can cause disequilibrium and epistaxis. GTs are usually unilateral; they can occur with other paragangliomas anywhere along the sympathetic chain. Audiometry usually shows mixed conductive and sensorineural hearing loss. CT is usually the imaging modality of choice, but MRI and various forms of angiography may also play a role. Treatment is usually surgical, though radiation therapy has become more common. Recurrence is uncommon, and occurs more frequently in surgically-treated cases. If a clinician observes a red pulsatile mass behind the eardrum, referral to a neuro-otologic otolaryngologist is appropriate.
Introduction
Glomus tympanicum (GT) tumors are a type of paraganglioma.
“Extra-adrenal paragangliomas (PGOMAs) are rare and can occur anywhere along the sympathetic chain including the carotid body, glomus jugulare, vagal bodies, ganglium tympanicum, larynx, ciliary bodies, organs of Zuckerkandl, urinary bladder, and other locations” (Snitzer, Sheeler et al. 1995).
Embryologically, paragangliomas originate from non-chromaffin (Neto, Vuono et al. 2005) neural crest cells (Mafee, Raofi et al. 2000, Fountarlis, Hajiioannou et al. 2022) of the autonomic nervous system (Ma, Ji et al. 2012).
Of particular interest in neuro-otology are paragangliomas arising from the tympanic membrane; these are usually called “glomus tympanicum” (GT) tumors, and “are benign arising from paraganglion cells of the tympanic plexus in the middle ear” (Sweeney, Carlson et al. 2015) “located on promontory” (Fountarlis, Hajiioannou et al. 2022).
Terminology
The term “glomus” derives from a Latin word usually translated as “ball of yarn,” reflecting the vascular nature of these lesions.
Sometimes paragangliomas are referred to as “glomus tumors,” but some authors reserve the term “glomus tumor” to refer to “hyperplasia of glomus bodies” rather than to paragangliomas (Wieser, Gilley et al. 2022).
Histopathology
Despite the common embryologic origin, GTs differ histopathologically from other paragangliomas (Branica, Sprem et al. 1993).
Pathophysiology
GTs cause symptoms by virtue of occupying the middle ear space (where they can impinge on the ossicular chain and cause conductive hearing loss) and invasion into other areas, and by virtue of the fact that they are heavily vascularized (and thus can produce pulsatile tinnitus).
A minority of GTs secrete catecholamines. Anand and colleagues report 15% of GTs to be secreting (Anand, Leonetti et al. 1993). In such cases, laboratory studies may detect elevated levels of noradrenalin in the serum, and vanillylmandelic acid in the urine (Kouzaki, Fukui et al. 2008).
Laterality
GTs usually present unilaterally, but cases of bilateral involvement have been reported (Fukushima, Hara et al. 2018).
Co-occurrence with other paragangliomas
GT can occur with other paragangliomas, such as glomus vagale and glomus jugulare (Balatsouras, Eliopoulos et al. 1992), or with glomus of the carotid body (Balatsouras, Eliopoulos et al. 1992).
Epidemiology
GT is primarily a disease of adults, but has also been reported in children (Busby and Hepp 1974, Yaniv and Sade 1983, Jacobs and Potsic 1994). GT are more common in women (Rohit, Jain et al. 2003).
Presentation: tinnitus
Tinnitus is the most common presentation of GT (Larson, Reese et al. 1987, O’Leary, Shelton et al. 1991, Baguley, Irving et al. 1994, Liscak, Vladyka et al. 1998, Weissman and Hirsch 2000, Rohit, Jain et al. 2003, Tatla, Savy et al. 2003, Neto, Vuono et al. 2005, Devuyst, Defreyne et al. 2016, Daneshi, Asghari et al. 2017, Ohki and Kikuchi 2019, Lee, Lee et al. 2021, Ghate, Bhatnagar et al. 2022), and is the primary symptom in over half of cases (O’Leary, Shelton et al. 1991). The tinnitus is almost always pulsatile, but non-pulsatile tinnitus has been reported (Fukushima, Hara et al. 2018).
Presentation: hearing loss
GT is often associated with hearing loss (Larson, Reese et al. 1987, O’Leary, Shelton et al. 1991, Alshaikhly, Hamid et al. 1994, Baguley, Irving et al. 1994, Tatla, Savy et al. 2003, Neto, Vuono et al. 2005, Kumar, Andreou et al. 2014, Devuyst, Defreyne et al. 2016, Daneshi, Asghari et al. 2017, Ghate, Bhatnagar et al. 2022). Hearing loss is the second most common presenting symptom of GT, occurring in about a third of cases (O’Leary, Shelton et al. 1991). The hearing loss is usually mixed conductive and sensorineural (Daneshi, Asghari et al. 2017).
Presentation: disequilibrium
Disequilibrium is an uncommon presentation of GT, but has been reported (Liscak, Vladyka et al. 1998, Reddy 2011).
Presentation: epistaxis
Rarely, GT can present with epistaxis (Lum, Keller et al. 2001, Tatla, Savy et al. 2003).
Physical examination
A compatible clinical history should prompt examination of the external auditory canal with binocular otomicroscopy, or at least with otoscopy. The classic presentation is a red, sometimes visibly pulsatile, mass behind the eardrum.
The Figure below from Lee and Park (Lee and Park 2010) shows a red mass behind the eardrum.
The Video below from Lee and Park (Lee and Park 2010) shows video endoscopy of GT.
Glomus tympanicum can be mimicked by other diseases
A number of other pathologies can appear similar to GT, including middle ear adenomatous tumors (Bierry, Riehm et al. 2010), extramedullary hemopoietic masses (Chen, Espinel et al. 2018), carcinoid tumor of the middle ear (Chang, Silva et al. 2022), malignant hemangioendotheioma of the temporal bone (Goldstein, Bowen et al. 1994), metastatic carcinoma of the temporal bone (Hellier, Crockard et al. 1997), promontory hemangioma (Karatas, Durucu et al. 2012), endolymphatic sac tumor (Muller, Zammit-Maempel et al. 2010), aberrant petrous carotid artery (McKiever, Carlson et al. 2014), persistent stapedial artery (Sullivan, Curtin et al. 2019), jugular bulb diverticulum (Te, Ong et al. 2021), middle ear cholesterol granuloma (Olcott and Strasnick 2017) and middle ear polyp (Shew, Bush et al. 2017).
Glomus tympanicum can mimic other diseases
GT can “transgress the tympanic membrane and appear as an inflammatory polyp in the external auditory canal” (Rohit, Jain et al. 2003).
The clinical behavior of GT can mimic Ménière’s disease (Fitzgerald 1985).
Glomus tympanicum can be comorbid with other otologic diseases
Unusually, GT can co-occur with other otologic diseases, such as cholesteatoma (Gulati 2020) or otosclerosis (Yanagisawa and Principato 1970).
Location
Some GTs arise from the tympanic nerve (Jacobson’s nerve) which traverses the middle ear, and in such cases the lesions may originate from any location along the medial wall of the middle ear (Weissman and Hirsch 1998).
Anatomical extension
In some cases GT can extend intracranially (Anand, Leonetti et al. 1993), including into the middle cranial fossa (Carlson, Sasaki et al. 1987). GT can also extend into the nasopharynx (Hirunpat, Riabroi et al. 2006) or even the cervical region (Ma, Ji et al. 2012).
Testing
Audiologic findings are well-reported in GT (Black, Berger et al. 1979, Baguley, Irving et al. 1994, Thiede, Stoll et al. 2004, Papaspyrou, Mewes et al. 2011, Medina, Prasad et al. 2014, Patnaik, Prasad et al. 2015, Devuyst, Defreyne et al. 2016, Daneshi, Asghari et al. 2017, Walker and Babu 2019). While this is interesting, diagnosis of GT does not rely on audiometry.
The role of audiometry is more important when comparing hearing at diagnosis with post-treatment outcomes.
Imaging: CT
Most investigators endorse high-resolution temporal bone CT as the imaging modality of choice in diagnosing GT (Mafee, Valvassori et al. 1983, Phelps and Lloyd 1983, Som, Reede et al. 1983).
Imaging: MRI
A few studies recognize complementary roles of CT and MRI in the diagnosis of GT (Amin and El Ameen 2013).
Imaging: angiography
Some studies report a potential role for MR angiography, digital subtraction angiography or transcranial spectral Doppler in the diagnosis of GT (De Candia, Como et al. 2002).
Treatment
Surgery was the mainstay of treatment for decades, and there is a lively debate in the literature regarding optimal surgical approaches (Cannon 1962, Smith and Shinn 1976, Farrior 1984, Sillars and Fagan 1993, Jackson 2001, Alaani, Chavda et al. 2009, Sanna, Fois et al. 2010, Chou, Huang et al. 2011, Papaspyrou, Mewes et al. 2011, Patnaik, Prasad et al. 2015, Pollak and Soni 2017, Noel and Sajjadi 2018, Ohki and Kikuchi 2019, Kaul, Filip et al. 2020, Fermi, Ferri et al. 2021).
More recently radiation therapy has become an accepted treatment modality (Konefal, Pilepich et al. 1987, Hansen and Thomsen 1988, Boyle, Shimm et al. 1990, Powell, Peters et al. 1992, Pemberton, Swindell et al. 2005, Lee, Pan et al. 2011, Kunzel, Iro et al. 2012, Liscak, Urgosik et al. 2014, Jansen, Timmers et al. 2018, Sahyouni, Mahboubi et al. 2018, Scheick, Morris et al. 2018, Fatima, Pollom et al. 2021, Kalhoro and Hashim 2023), and is often combined with surgery. As with any radiation therapy, complications include damage of healthy tissue, accelerated atherosclerosis, and subsequent increased risk of malignancy.
Embolization (sometimes followed by surgery) has been another fairly well-studied treatment modality (Boyle, Shimm et al. 1990, Tasar and Yetiser 2004, Kouzaki, Fukui et al. 2008, Sawlani, Browing et al. 2009, Devuyst, Defreyne et al. 2016), though like any embolization procedure carries a risk of stroke (Sawlani, Browing et al. 2009, Kajtazi, Manzoor et al. 2022).
Less studied treatment modalities include laser coagulation (Robinson, Grant et al. 1993, Molony, Salto-Tellez et al. 1998, Durvasula, De et al. 2005, Kouzaki, Fukui et al. 2008, Noel and Sajjadi 2018) and piezoelectric surgery (Salami, Mora et al. 2008, Salami, Dellepiane et al. 2009).
Recurrence
Recurrence of treated GT is uncommon.
A case series of 8 surgically-treated GTs reported no recurrences at up to 15 years (Cole 1979). A case series of 16 radiation-treated GTs reported no recurrences at a mean follow-up of 10.5 years (range 4 – 24 years).
One series of 17 surgically-treated cases of GT reported recurrence in 1 patient (6%) after 9 years (Rohit, Jain et al. 2003). Another series of 73 surgically-treated cases reported a recurrence rate of 5% (O’Leary, Shelton et al. 1991). One series noted persistence and/or recurrence of surgically-treated GT only in patients in whom the tumor had invaded the central nervous system (Spector and Sobol 1980).
Some series report a lower rate of recurrence with radiation-treated GT compared to surgically-treated cases (Contrera, Yong et al. 2020).
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