Clin. O/ohryngo/. 1992, 17, 300-302

Fenestration and occlusion of the posterior semicircular canal for benign positional vertigo A N N F.DINGLE, MAURICE R . H A W T H O R N E & B . U . K U M A R North Riding Infirmary, Middlesbrough , Cleveland, U K Accepted for publication 10 January 1992 DINGLE A . F . , HAWTHORNE M . R . & K U M A R R . U .

(1992) Clin. Otolaryngol. 17, 300-302

Fenestration and occlusion of the posterior semicircular canal for benign positional vertigo Benign positional vertigo is a potentially disabling condition characterized by episodic vertigo following certain provocative head movements. In most patients i t is self limiting; however, in a few it may prove intractable, causing considerable social morbidity. In these patients surgery may be considered. Surgery previously involved section of the vestibular or singular nerves, involving a significant risk to hearing and to the facial nerve. Ablation of the labyrinth may even be considered. The new surgical technique of occlusion of the posterior semicircular canal has proved to be curative in most patients with benign positional vertigo with little risk to hearing. This paper describcs our experience of fenestration and occlusion of the posterior semicircular canal in four patients. Keywords

benign positional vertigo

labyrinth

Barany’ (1921) first described cases of episodic short-lived nystagmus related to certain head movements. He noted the relationship of the nystagmus to head position and so attributed the condition to a disorder of the otoliths. Dix and Hallpike2 (1952) reviewed 100 patients with benign positional vertigo and found more than 50% had some evidence of gross middle ear or labyrinthine disease. They studied the utricular macula of the patients who had suffered from benign positional vertigo and found absence of the otolithic membrane and disorganization of the sensory epithelium. They postulated that benign positional vertigo was caused by chronic tissue changes of the saccular and utricular macula as a result of trauma, chronic infection or vascular disease. Lindsay and Hemenway3 (1956) described occlusion of the anterior vestibular artery in a patient who had suffered vertigo of several weeks duration followed by positional vertigo. Histological examination showed degeneration of the superior vestibular nerve and they suggested this as the pathological process in positional vertigo. Schuknecht4 (1969) first suggested the posterior semicircular canal as the site of the lesion in benign positional vertigo. He demonstrated the presence of large basophilic deposits on the Correspondence: Mr M.R.Hawthorne, North Riding Infirmary, Middlesbrough, Cleveland TS1 5JE, UK.

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cupulae of patients with clinical benign positional vertigo and postulated that the gravitational effect on these deposits gave rise to the symptoms of vertigo. He introduced the term ‘cupulolithiasis’ and suggested that these deposits arose from degeneration of the otolithic membrane of the macula of the saccule and utricle. Subsequent investigations have shown these cupular deposits in all three semicircular canals and in patients with no clinical evidence of benign positional vertigo.s Despite these findings, cupulolithiasis is still the most widely accepted theory of the pathogenesis of benign positional vertigo. We describe 4 patients with intractable benign positional vertigo who have been operated upon in this unit by fenestration and occlusion of the posterior semicircular canal (FOP). We use a technique originally described by Parnes and McClure.6 In all cases the posterior semicircular canal was exposed by a transmastoid approach. The semicircular canal was blue-lined 2-3 mm proximal to the site at which the facial nerve crosses the posterior semicircular canal. The remaining thin shell of bone was then curetted. The membranous labyrinth was not entered but was compressed using bone pate. The fenestration was then covered with temporalis fascia. All 4 patients have been relieved of their vertigo and shown no significant change in their audiograms.

Fenestration and occlusion of the posterior semicircular canal for vertigo 301

Case 1 A 45-year-old man presented with a 3-year history of episodic vertigo precipitated by movement, in particular on turning to the right. It was not relieved by medication. There was no history of tinnitus or of recent deterioration in hearing. 25 years previously he had undergone a radical right rnastoidectomy. An audiogram showed normal hearing on the left and a mixed hearing loss on the right. Caloric testing of the right mastoid cavity by air calorics showed no hypofunction compared to the left ear, but positional testing showed nystagmus on positioning the right ear undermost. A diagnosis of intractable positioning vertigo was made and the patient underwent the FOP procedure on the right side. After an initial period of nausea, vertigo and nystagmus lasting 2 days the patient was fully mobilized and was discharged home on the 6th post-operative day. One month post-operatively there was no history of vertigo and an audiogram showed no change in hearing. Two months postoperatively caloric testing showed no response in the right ear. He remains symptom free 7 months following surgery.

Case 2 A 32-year-old woman presented with an 18-month history of episodic vertigo, precipitated by turning to the left. This had been of sudden onset and was not relieved by any medication. On examination she was found to have a non-fatiguable vertigo on positional testing with the left ear undermost. An audiogram was normal and caloric testing showed a symmetrical response. Six months later the vertigo was still present and despite its non-fatiguable nature a diagnosis of intractable benign positional vertigo was made. She therefore underwent the FOP procedure to the left side. Post-operatively there was initially some nystagmus and unsteadiness, but this settled over a period of 3 days. She was discharged 6 days post-operatively. Two months after operation she had no vertigo on movement and no unsteadiness on walking. Caloric testing showed 28% hypofunction of the left labyrinth compared to the right. 4 months after surgery she developed tinnitus in the operated ear with pure tone audiometric thresholds better than 20 dB at all tested frequencies (i.e. up to 8 kHz). Six months following surgery she has remained free of vertigo.

Case 3 A 55-year-old man presented with a 10-year history of vertigo precipitated by movement, in particular turning to the left. This was associated with nausea. It had frequently woken him during the night and lasted for a period of a few seconds to 1 or 2 minutes. His symptoms had been aggravated by an assault a year before presentation. He also complained of intermittent tinnitus, but no deterioration in

hearing. He felt that his symptoms were helped by prochlorperazine. On examination positional testing with the right ear undermost produced dramatic nystagmus with latency and fatigue. Positioning with the left ear undermost also produced mild vertigo. An audiogram was normal and caloric testing showed symmetrical responses. A diagnosis of intractable benign positional vertigo was made and the patient underwent the FOP procedure on the right side. During the procedure the incus was touched by the drill. Post-operatively the patient initially complained of mild vertigo associated with nystagmus, but this settled very rapidly and the patient was discharged 3 days postoperatively. One month following surgery the patient complained only of mild unsteadiness. An audiogram showed a conductive loss on the right averaging 20 dB, which was presumed to be due to damage to the incus. Three months post-operatively his vertigo had settled except on very violent movements. Caloric testing showed 20% hypofunction of the right vestibular system and an audiogram showed only a mild conductive hearing loss on the right. This patient reported no further episodes of benign positional vertigo when last reviewed 5 months following surgery.

Case 4 A 64-year-old man presented with a 5-year history of episodic rotatory vertigo, of sudden onset. It was precipitated by movement, in particular by bending and by rolling over in bed. The periods of vertigo lasted 5-10 s and on some occasions were associated with vomiting. He had bilateral tinnitus, but did not complain of hearing loss. He obtained little benefit from any medication for his vertigo. On examination he was found to have no spontaneous nystagmus and no evidence of any other abnormality of his cranial nerves. Positional testing t o the left produced a fatiguable left rotatory nystagmus. Positional testing to the right produced a fatiguable right rotatory nystagmus associated with vomiting. An audiogram showed a bilateral high frequency sensorineural hearing loss of a minor degree. Caloric testing had been performed some 3 years previously and had produced profound, distressing, vertigo. This was therefore not repeated. A diagnosis of intractable benign positional vertigo was made and the patient underwent the FOP procedure on the right side. He experienced some vertigo for 3 days post-operatively, but was fit enough to be discharged on the 6th day. Three months following surgery he had no positional vertigo on either side and only an occasional mild unsteadiness on walking. An audiogram did not show any change in thresholds.

Discussion Most patients with benign positional vertigo have a spontaneous remission after a period of weeks or months.

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Vestibular habituation training has been advocated as a method of controlling benign positional vertigo, either by repeated challenging causing loosening and disruption of the cupular deposits, for example by Semont’s procedure,’ or by enhancing ccntral control over the peripheral lesion. However, in those patients with intractable vertigo and no evidence of resolution, surgery may be the only treatment available. Labyrinthectomy of the affected ear in patients with a hearing loss on that side is an effective way of eliminating benign positional vcrtigo. However, except in patients with profoundly debilitating vertigo the hearing loss incurred by this surgery is difficult to justify. Vestibular neuroncctomy, in addition to the inherent risks of craniotomy, carries a significant risk to the facial and cochlear nerves. Gacek’ in 1974 described section of the singular nerve. Selective section of the nerve supplying the semicircular canal has been curative in more than 80% of Gacck’s patients. However, thcre is also a significant risk of sensorineural deafness (in his series 7.3%). Ohmici,‘ in a study of human temporal bones, showed that the singular nerve was inaccessible in 14% of bones due to the position of the labyrinth. Occlusion of the posterior semicircular canals was first described by Money and Scott (l962).“ They occluded individual canals in cats and demonstrated the interruption of impulses from each canal without affecting the other vestibular organs. This study was taken a step further by Parncs and McClure ( 1990)6who studied the effect of posterior Semicircular canal occlusion on auditory brain-stem evoked responses in guinea-pigs. Their results suggested that there was no cochlear damage. They then postulated that in patients with bcnign positional vertigo occlusion of the posterior semicircular canal on the affected side would relieve symptoms of vertigo. Posterior canal occlusion by a transmastoid approach was felt to be technically easier and safer than a singular neurectomy. The theory of this operation is that by preventing endolymph flow in the posterior semicircular canal deflection of the cupula is prevented. In the first of Parnes’ patients the osseous and membranous labyrinth of the posterior semicircular canal was punctured and occluded by bone chips and tissue glue. This patient suffered transient nystagmus and vertigo following surgery, which was felt to be secondary to a labyrinthitis. Subsequent operations were performed with only the osseous labyrinth being entered and the membranous labyrinth being compressed by bone chips and tissue glue. This appears to lessen the degree of nystagmus and vertigo suffered post-operatively. In our patients there was no case of sensorineural hearing loss and only one case of a mild conductive hearing loss, presumed to be due to damage to the incus (we no longer feel it is necessary to expose the incus and this lessens the risk of a conductive hearing loss). There appears to be mild reduction in caloric function in those patients who had normal caloric tests prior to surgery. However, one patient had a

total loss of caloric response when tested 6 weeks postoperatively. Whether the previous mastoid surgery predisposed to an increased risk of vestibular damage is unknown. Patient 4 underwent resolution of bilateral symptoms following a unilateral FOP procedure on the worse affected side. The authors are unable to explain this phenomenon. We recommend that patients who have had symptoms of positional vertigo for more than 12 months should be considered for surgery. Patients are warned of the risk of a total hearing loss and of damage to the facial nerve and are warned to expect a mild unsteadiness in the initial postoperative period. While the pathogenesis of postional vertigo is still not fully understood it does appear to be related to the posterior semicircular canal. Occlusion of this canal docs appear to be effective in alleviating the symptoms of the disease. It is too early to predict the long-term results of this surgery. However, the first patient has now been symptom free for 7 months and we feel that the FOP technique shows considerable promise for the relief of intractable benign positional vertigo.

Acknowledgements We wish to acknowledge Mrs Janet Pye for typing the manuscript and the Ear, Nose, Throat and Eye Research Foundation. North Riding Infirmary, Middlcsbrough, for its support.

References I BARANY R. (1921) Diagnose von Krankheitscrscheinungen im Bereiche des Otolithaparates. A c / u Oioltryngol iStockh.j 2,

434-437 2 Dix R . & HALLPIKE C.S. (1952) The pathology, symplomatology and diagnosis of certain common disorders of the vestibular system. Ann. Uiol. Rhino/. I,aryngol. 61, 987-1016 J.R. & ~ I E M E N W W.G. A Y (1956)Postural vertigo due to 3 LINDSAY unilateral sudden partial loss of vestibular function. Ann. Otol. Rhinol. Laryngol. 65, 692-708 H.F. (1969) Cupulolithiasis. Arch. Otolaryngol. 90, 4 SCHUKNHCHT

765-778 H.F. & RUBYR . R . F . (1973). Cupulolithiasis. Adv. 5 SCHUKNECHT Olorhinolaryngol. 20, 434-443 L.S. & MCCLURE 6 PARNES (1990) Posterior semicircular canal

occlusion for intractable benign paroxysmal positional vertigo. Ann. Otol. Rhiriol. Loryngol. 99, 330-334 7 SEMONT A,, FREYSSG. & VITTE E. (1988) Curing benign paroxysmal vertigo with the liberating manoeuvrc. A d v . Otorhinolaryngol. 42, 290- 293 8 GACEK R.R. (1974)Transection of the posterior ampullary nerve for the relief of benign paroxysmal positional vcrtigo. Ann. Otol. Rhinol. Laryngol. 83, 596-605 9 OHMICIT., RUTKAJ. & HAWKEM. (1989) Histopathologic consequences of surgical approaches to the singular nerve. Laryngoscope 99, 963-970 10 MOSEYK.E. & SCOTT J.W. (1962) Functions of separate sensory receptors of non-auditory labyrinth of the cat. Am. J . Physiol. 202, 1211-1220

Fenestration and occlusion of the posterior semicircular canal for benign positional vertigo.

Benign positional vertigo is a potentially disabling condition characterized by episodic vertigo following certain provocative head movements. In most...
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