DOI: 10.1148/radiol.2302021108
(Radiology 2004;230:413-416.)
© RSNA,
Case 67: Persistent Stapedial Artery1
Rajan Jain, MD,
Dheeraj Gandhi, MD,
Sachin Gujar, MD and
Suresh K. Mukherji, MD
1 From the Division of Neuroradiology, Department of Radiology B2B3110030, University of Michigan Health System, 1500 E Medical Center Dr, Ann Arbor, MI 48109-0030. Received September 3, 2002; revision requested November 6; revision received November 7; accepted January 15, 2003. Address correspondence to R.J. (e-mail: rajanjee@yahoo.com).
Index terms: Arteriovenous malformations, cranio-facial, 2129.14 Cerebral blood vessels, abnormalities, 2129.14 Cerebral blood vessels, CT, 2129.12118 Diagnosis Please Ear, abnormalities, 2129.12118
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HISTORY
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A 4-year-old girl presented with hearing loss in her left ear that had begun 1 year earlier. She had chronic otitis media of the left ear 2 years ago, which was treated with antibiotics and insertion of a tympanostomy tube. She also had one instance of substantial bleeding from the left ear during the course of otitis media. She did not have a history of meningitis. The findings of an otoscopic examination were unremarkable. Audiologic evaluation revealed profound conductive hearing loss in the left ear but normal hearing in the right. Computed tomographic (CT) (Hispeed; GE Medical Systems, Milwaukee, Wis) evaluation of the temporal bones was performed, and 1-mm sections were obtained in the transverse and coronal imaging planes. All images were subjected to unilateral retargeting and postprocessing with a thin-section bone algorithm and a small field of view (9.6 cm). Relevant CT scans of the left temporal bone were obtained. The findings of a CT examination of the right temporal bone were unremarkable.
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Imaging Findings
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Thin-section CT (1-mm-thick transverse and coronal sections) of the left temporal bone revealed ossification in the basal turn of the cochlea (Figs 1, 2). This finding was consistent with a diagnosis of labyrinthitis ossificans. Additionally, a small area of abnormal soft-tissue attenuation was seen along the cochlear promontory (Figs 1, 2). This originated from the petrous part of the carotid artery (Figs 2b, 3a) and entered the middle ear cavity. It continued as a small area of soft-tissue attenuation in the region of the obturator foramen of the stapes (Fig 1d). Subsequently, it merged with the tympanic part of the facial nerve, which can be seen as an enlargement of the facial nerve canal (Fig 2c).

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Figure 1a. (a-c) Transverse CT scans of the left temporal bone at the cochlear level show ossification of the basal turn of the cochlea (black arrow) and persistent stapedial artery (PSA) (white arrow) coursing along the cochlear promontory. (d) Transverse CT scan at oval window level shows PSA (arrow) in obturator foramen of stapes.
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Figure 1b. (a-c) Transverse CT scans of the left temporal bone at the cochlear level show ossification of the basal turn of the cochlea (black arrow) and persistent stapedial artery (PSA) (white arrow) coursing along the cochlear promontory. (d) Transverse CT scan at oval window level shows PSA (arrow) in obturator foramen of stapes.
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Figure 1c. (a-c) Transverse CT scans of the left temporal bone at the cochlear level show ossification of the basal turn of the cochlea (black arrow) and persistent stapedial artery (PSA) (white arrow) coursing along the cochlear promontory. (d) Transverse CT scan at oval window level shows PSA (arrow) in obturator foramen of stapes.
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Figure 1d. (a-c) Transverse CT scans of the left temporal bone at the cochlear level show ossification of the basal turn of the cochlea (black arrow) and persistent stapedial artery (PSA) (white arrow) coursing along the cochlear promontory. (d) Transverse CT scan at oval window level shows PSA (arrow) in obturator foramen of stapes.
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Figure 2a. (a-c) Coronal CT scans at cochlear level show calcification and/or ossification of the basal turn of the cochlea (black arrow) and PSA (white arrow) arising from the petrous part of carotid artery ( ) and coursing superiorly along the cochlear promontory. Prominence of the tympanic part of the facial nerve (arrowhead) is also seen.
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Figure 2b. (a-c) Coronal CT scans at cochlear level show calcification and/or ossification of the basal turn of the cochlea (black arrow) and PSA (white arrow) arising from the petrous part of carotid artery ( ) and coursing superiorly along the cochlear promontory. Prominence of the tympanic part of the facial nerve (arrowhead) is also seen.
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Figure 2c. (a-c) Coronal CT scans at cochlear level show calcification and/or ossification of the basal turn of the cochlea (black arrow) and PSA (white arrow) arising from the petrous part of carotid artery ( ) and coursing superiorly along the cochlear promontory. Prominence of the tympanic part of the facial nerve (arrowhead) is also seen.
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Figure 3a. (a) Transverse CT scan of the left skull base shows absence of the foramen spinosum posterolateral to the foramen ovale (arrow). (b) Transverse CT scan of the right skull base shows the normal foramen spinosum (arrowhead) posterolateral to the foramen ovale (arrow).
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Figure 3b. (a) Transverse CT scan of the left skull base shows absence of the foramen spinosum posterolateral to the foramen ovale (arrow). (b) Transverse CT scan of the right skull base shows the normal foramen spinosum (arrowhead) posterolateral to the foramen ovale (arrow).
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Transverse CT scans obtained at the level of the skull base revealed absent foramen spinosum on the left side (Fig 3a) and normal findings on the right (Fig 3b). These findings are highly characteristic of a diagnosis of PSA and labyrinthitis ossificans.
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DISCUSSION
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PSA is a rare congenital vascular anomaly of the middle ear (1). The prevalence of PSA was 0.02%0.05% in surgical series (2,3) and was slightly higher (0.48%) in a temporal bone study (4). PSA usually manifests as a pulsatile mass in the middle ear cavity, an incidental finding during middle ear surgery, or pulsatile tinnitus. It can also manifest as conductive hearing loss due to associated stapes ankylosis (5). In rare instances, however, PSA may erode the otic capsule and result in sensorineural hearing loss (6). A PSA can be associated with an aberrant internal carotid artery or other middle ear anomalies, especially of the stapes and facial nerve. Rarely, PSA has been detected in patients with trisomy 13, second branchial arch anomalies, Paget disease, otosclerosis, or thalidomide deformities (7).
The stapedial artery is transiently present in fetal life and connects the branches of the future external carotid artery to the internal carotid artery. The stapedial artery arises at 45 weeks of fetal life from the hyoid artery, which is a derivative of the second branchial arch, near its origin from the proximal internal carotid artery (third branchial arch). It extends cranially and passes through the mesenchymal primordium of the stapes (second branchial arch) and forms the obturator foramen of the stapes. The stapedial artery gives rise to two branches after entering the cranial cavity. The upper, or supraorbital, branch becomes the middle meningeal artery and also transiently anastomoses with the opthalmic artery. The lower, or maxillomandibular, division has two branches, a mandibular branch and an infraorbital branch, which persist in adult life as inferior alveolar and infraorbital arteries, respectively. This lower division leaves the cranial cavity via the foramen spinosum. Ventral pharyngeal arteries from the aortic sac form adult external carotid arteries. Normally, anastomoses develop between the ventral pharyngeal arteries and the lower division branches of the stapedial artery, which involutes during the 10th week of fetal life with reversal of flow at the foramen spinosum level. The hyoid artery persists as the caroticotympanic branch of the internal carotid artery in adult life (8).
Persistence of the stapedial artery in postnatal life leads to the middle meningeal artery typically arising from it. The foramen spinosum remains hypoplastic or aplastic, which is an indirect sign of PSA; however, absence of the foramen spinosum is seen in up to 3% of skull base CT studies (9). It can be a normal variation, particularly when the middle meningeal artery arises from the ophthalmic artery. The PSA arises from the petrous part of the internal carotid artery, enters the anteromedial hypotympanum, and is contained in the Jacobson canal. After leaving the osseous canal, it crosses the cochlear promontory and passes through the obturator foramen of the stapes. It then enters the fallopian canal through a dehiscence just behind the cochleariform process and travels anteriorly in the anterior facial canal. This leads to prominence of the tympanic part of the facial nerve, another indirect imaging sign of PSA. Finally, the PSA exits just before the geniculate ganglion, entering into the extradural space of the middle cranial fossa.
Ossification of the membranous labyrinth (labyrinthitis ossificans) occurs as the final result of many inflammatory processes, such as meningitis, blood-borne septic emboli, middle ear infection, and cholesteatoma. Labyrinthine ossification may also occur as a result of previous labyrinthectomy or secondary to trauma (10). In the present case, a diagnosis of labyrinthitis ossificans was made on the basis of visible findings of cochlear ossification. This diagnosis did not, however, explain the patients conductive hearing loss, as labyrinthitis ossificans usually presents as sensorineural hearing loss. A closer look at the CT scan revealed a very small vessel that arose from the petrous part of the internal carotid artery and coursed through the middle ear cavity. Prominence of the tympanic part of the facial nerve and absence of the foramen spinosum, the indirect signs of PSA, were also seen. Thus, identification of PSA, along with labyrinthitis ossificans, was important for two reasons. First, PSA was correlated with the patients conductive hearing loss, probably attributed to stapes ankylosis because of pulsations of the PSA; hence, the management plan changed. Second, the treating surgeon was alerted if the patient underwent stapedotomy to correct stapes ankylosis or was considered for a cochlear implant because of labyrinthitis ossificans. PSA has been known to prevent successful cochlear implantation (11) and to cause unexpected hemorrhage during middle ear interventions if not detected at preprocedure imaging. To our knowledge, there is no reported association of PSA with labyrinthitis ossificans. In the present case, the association is probably incidental, without any causal relationship.
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FOOTNOTES
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Part 1 of this case appeared 4 months previously and may contain larger images.
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REFERENCES
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- Schuknecht H. Pathology of the ear Cambridge, Mass: Harvard University Press, 1974; 186-187.
- Pirodda A, Sorrenti G, Marliani AF, Cappello I. Arterial anomalies of the middle ear associated with stapes ankylosis. J Laryngol Otol 1994; 108:237-239.[Medline]
- Kelemen GD. Arteria stapedia in bilateral persistence. Arch Otolaryngol 1958; 67:668-677.
- Boscia R, Knox RD, Adkins WY, Holgate RC. Persistent stapedial artery supplying a glomus tympanicum tumor. Arch Otolaryngol Head Neck Surg 1990; 116:852-854.[Abstract]
- Silbergleit R, Quint DJ, Mehta BA, Patel SC, Metes JJ, Noujaim SE. The persistent stapedial artery. AJNR Am J Neuroradiol 2000; 21:572-577.[Abstract/Free Full Text]
- Ginsberg LA, Pruett SW, Chen MY, et al. Skull base foramina of the middle cranial fossa: reassessment of normal variation with high resolution CT. AJNR Am J Neuroradiol 1994; 15:283-291.[Abstract]
- Swartz JD, Mandell DM, Faerber EN, et al. Labyrinthine ossification: etiologies and CT findings. Radiology 1985; 157:395-398.[Abstract/Free Full Text]
- Wardrop P, Kerr AI, Moussa SA. Persistent stapedial artery preventing successful cochlear implantation: a case report. Ann Otol Rhinol Laryngol Suppl 1995; 166:443-445.[Medline]
Congratulations to the 70 individuals who submitted the most likely diagnosis (persistent stapedial artery) for Diagnosis Please, Case 67. The names and locations of the individuals, as submitted, are as follows:
- Arangasamy Anbarasu, MD, FRCR, Coventry, United Kingdom
- Angus Baird, Birmingham, Ala
- Ken Baliga, Rockford, Ill
- Sandip Basak, MD, Somerset, NJ
- Debra M. Berger, MD, New York, NY
- K. Boubagra, Grenoble, France
- Peter R. Bream, Jr, MD, Nashville, Tenn
- Eric L. Bressler, MD, Minnetonka, Minn
- Luisa F. Cervantes, Miami, Fla
- Bharath Chinta, Rochester Hills, Mich
- Y. S. Cordoliani, MD, Paris, France
- Kenneth R. Curtin, MD, Chicago, Ill
- Marc G. de Baets, MD, Lugano, Switzerland
- Manuel de Juan-Delago, MD, PhD, Barcelona, Spain
- Jose Luiz F. De Mendonca, MD, Brasilia, Brazil
- Jon De Witte, Phoenix, Ariz
- Mustafa Kemal Demir, Ataköy, Istanbul, Turkey
- David Donovan, BMBS, FRANZCR, Adelaide, Australia
- Namik Erdag, MD, Norwalk, Conn
- Steven J. Fagan, DO, Mt Pleasant, SC
- Akira Fujikawa, Tokyo, Japan
- Dr Gilles Genin, Annecy, France
- Mark Goldshein, MD, Andover, Mass
- W. Zev Goldstein, MD, Poughkeepsie, NY
- Jean Pierre Gurret, MD, Annecy, France
- Robert Hermans, MD, PhD, Leuven, Belgium
- Thomas Charles Hoffer, MD, El Paso, Tex
- Alberto Iaia, MD, Wilmington, Del
- Nurettin Katranci, MD, Antalya, Turkey
- Timo Kyyronen, MD, Kaarina, Finland
- Stefanos Lachanis, MD, Athens, Greece
- Mario Laguna, West Allis, Wis
- Walter S. Lesley, MD, St. Louis, Mo
- Peter Leyman, MD, Aalst, Belgium
- John T. Lim, MD, Newport Coast, Calif
- Michael L. Lipton, MD, Bronx, NY
- David A. Lisle, Brisbane, Australia
- N. B. S. Mani, MD, Nassau, Bahamas
- Frank McKowne, MD, Vancouver, Wash
- Edward Menges, MD, Aptos, Calif
- Philippe Meriot, MD, Brest, France
- Sankar Ranjan Mondal, MD, Nassau, Bahamas
- Tammam Nehme, Wenatchee, Wash
- Jim Nugent, MD, Victoria, British Columbia, Canada
- Robert Oot, MD, Nashua, NH
- Juan C. Pallares, MD, Woodlands, Tex
- Harish Panicker, MD, Washington, DC
- Hilton Pittman, Pensacola, Fla
- Mario Pliego, MD, Bloomington, Minn
- John M. Plotke, Naperville, Ill
- Shawn P. Quillin, MD, Charlotte, NC
- Barry M. Rabin, MD, Northbrook, Ill
- Pierre J. Sauvage, MD, Mâcon, France
- Joel Schwartz, MD, Irvington, NY
- Matt Shapiro, MD, Staunton, Va
- Taro Shimono, MD, Osaka, Japan
- Dr Manohar Shroff, Toronto, Ontario, Canada
- Jeffrey A. Simon, MD, Orlando, Fla
- David Sobel, La Jolla, Calif
- James D. Sprinkle, Jr, MD, Spotsylvania, Va
- Ellen K. Tabor, MD, Allison Park, Pa
- Douglas L. Teich, MD, Brookline, Mass
- Eugene Tong, MD, Austin, Tex
- Glenn Tsukada, MD, San Diego, Calif
- Herminia Tyminski Al-Saffar, MD, Manama, Kingdom of Bahrain
- Piet Vanhoenacker, MD, Aalst, Belgium
- Raimo Virkki, MD, Turku, Finland
- Christopher Vittore, MD, Rockford, Ill
- Susan W. Weathers, MD, Houston, Tex
- Joe Yut, Olathe, Kan