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Show Journal of Neum- Ophlhalmology 19( 3): 173- 175, 1999. © 1999 I. ippincoll Williams & Wilkins. Inc., Philadelphia Transient Vertical Diplopia and Silent Sinus Disorder Francois- Xavier Bormat, MD, Bertrand Jaques, MD, and Jacques Diirig, MD A 57- year- old man had isolated transient recurrent vertical diplopia. Left hypoglobus and enophthalmos were present. Investigations revealed an otherwise asymptomatic left maxillary chronic aspecific sinusitis, with 8 mm lowering of the left orbital floor. Transient diplopia was thought to be secondary to transient fusion impairment. Orbital floor reconstruction cured the patient. Key Words: Transient diplopia- Silent sinus syndrome. Transient diplopia is not a frequent complaint and etiologies include myasthenia, dysthyroidism, multiple sclerosis, decompensation of a preexisting phoria, dorsal mesencephalic syndrome, ocular neuromyotonia, and giant cell arteritis. Sinus disorders can involve the orbit and produce proptosis, enophthalmos, diplopia, pain, or visual loss. However, in most cases the clinical presentation is typical enough to suggest the sinus origin. We report an unusual case of a patient who complained of isolated transient vertical diplopia as the sole symptom of an underlying otherwise silent sinus disorder. CASE REPORT In April 1994, a healthy 57- year- old man complained for the first time of isolated vertical diplopia while driving his car. The episode lasted a few minutes, resolving spontaneously. Despite disappearance of symptoms, ophthalmologic examination revealed vertical ocular dissociation diagnosed as right trochlear palsy. With prisms, evolution was stationary until May 1994 when transient vertical diplopia recurred. Magnetic resonance imaging ( MRI) was performed with angiography sequences. Neither brain nor brainstem lesions was found. Left maxillary sinus was homogeneously filled, but this finding was not considered. A neurologist diagnosed an isolated left inferior oblique palsy. In November 1994, because of persistent and Manuscript received April 13, 1999; accepted April 22, 1999. From the Hopital Ophtalmiquc Jules Gonin ( FXB, JD), Lausanne, Switzerland, Centre Ophtalmologiquc dc La Source ( FXB), and De-partement d'ORL ( BJ), CHUV. Address correspondence and reprint requests to Dr. Francois- Xavier Borruat, Hopital Ophtalmiquc Jules Gonin, Avenue de France 15, CH- 1004 Lausanne, Switzerland. fluctuating vertical diplopia, the patient was examined by another ophthalmologist who diagnosed paresis of the left superior rectus and inferior oblique muscles with a comitant deviation and excyclotorsion of the left eye. Myasthenia was suspected but excluded by neurologic examination. The neurologist noted a slight increase in vertical deviation and concluded to a probable decompensation of a preexisting vertical phoria. The patient was referred for neuro- ophthalmologic examination in December 1994. Visual function was normal in both eyes ( visual acuity 20/ 20 in both eyes, Ishi-hara color plates 13/ 13 OU, visual fields full to confrontation), and slit lamp and fundus examination were normal in both eyes. Intraocular pressure was 16 mmHg in the right eye and 14 mmHg in the left eye. A slight asymmetry of the patient's face was noticeable with a narrowed left palpebral fissure ( 10 mm right side, 9 mm left side), a lower positioned left eye, and 2 mm of left enophthalmos ( Fig. 1). Oculomotility examination showed a right variable hypertropia; smooth pursuit and saccades were normal. Trigeminal and facial nerve examination was normal. A CT scan was performed, showing the left maxillary sinus to be homogeneously filled and 8 mm of inferior displacement of the left orbital floor, which was markedly thinned ( Fig. 2). On repeat questioning the patient recalled that sinus surgery was performed twice in 1957. An ears, nose, and throat examination and left maxillary sinus exploration was performed. The left maxillary sinus was lined by polypoid mucosa and filled with thick mucoid material, without bacteria, fungi, or malignant cells. The pathologic diagnosis was chronic nonspecific sinusitis. Two months later, orbital floor reconstruction was performed and the patient has since been asymptomatic. COMMENT Over the course of 37 years, our patient developed a chronic asymptomatic sinusitis that resulted in progressive thinning of the orbital floor, which was fully preserved. Thus, enophthalmos and hypoglobus were not related to orbital floor disruption, but were caused by an inferior displacement of the orbital content probably secondary to a contraction of the sinus cavity. / n? 174 F.- X. BORRUAT ET AL. : : - - ••' i8[ . . : • • • i : \$ 0Sm ••''^ 0'- i : W-' ^ -.- b\- Sx •• l^ pr^- fe- . b . . • • ' • ; • • * * " • ' . & i % ^^ H^ WH| H ^^^ HI ^ ' ' i - i i ^ ^ .-••'••' i^ BB^ i.. ^(^; " M '^ W ^ ^ ^ ' Jr ^ hui' ^ 1 F y # VF I r * T FIG. 1. Eight months after the onset of transient vertical diplopia, left hypoglobus, a slight narrowing of the left palpebral fissure, and left enophthalmos were present. Silent sinus syndrome is a rare disorder resulting in spontaneous enophthalmos and hypoglobus ( l). Lowering of the orbital floor occurs secondary to asymptomatic maxillary sinus disease with secondary thinning of the bony orbital floor. Most of the cases reported by Soparkar et al. ( l) presented mild to moderate hypoplasia of the ipsilateral maxillary sinus. From their retrospective multicentric study, they collected 14 cases but none with diplopia. Five other patients have been reported in the literature, also none with diplopia ( 2- 5). All these patients were diagnosed secondary to the development of enophthalmos and hypoglobus, none complaining of diplopia. Our patient complained of transient vertical diplopia in association with a silent sinus disease. He was the oldest of all published similar cases ( average age, 37 years; range, 29- 46 years) ( 1) and his amount of hypoglobus ( 8 mm) was the highest ( average, 3.4 mm; range, 2- 6 mm) ( 1). Evolution was slow, spanning over 37 years. Most likely, transient vertical diplopia was caused by progressive inability to compensate for 8 mm of hy-poglobia. Silent sinus syndrome should be kept in mind FIG. 2. Axial ( Top left), coronal ( Top right), and reconstructed sagittal CT scans ( Bottom) showed lowering and thinning without disruption of the left orbital floor. The left maxillary sinus was moderately contracted and filled with homogenous material. .1 Neum- Oplillialuwl, Vol. 19, No. J, 1999 SILENT SINUS 175 as a diagnostic possibility in patients with fluctuating transient vertical diplopia. REFERENCES Soparkar CNS, Palrinely JR, Cuaycong MJ, el al. The silent sinus syndrome. A cause of spontaneous cnophthalmos. Ophthalmology 1994; 101: 772- 8. 2. Montgomery WW. Mucocele of the maxillary sinus causing enophlhalmos. Eye Ear No. se Throat Moil 1964; 43: 41- 4. 3. Trauslason 01, Fcklon SE. Cause of cnophthalmos secondary to maxillary sinus mucocele. Am .1 Ophthalmol 1983; 95: 838- 40. 4. Hayes EJ, Weber AL. Chronic sinus disease: a rare cause of cnophthalmos. Ann Otol Rhinol Ijnyngol 1987; 96: 351- 3. 5. Kallreider SA, Dorlzbach RK. Destructive cysts of the maxillary sinus affccling the orbit. Arch Ophthalmol 1988; 106: 1 398- 1402. J Neum- Ophllwlmol, Vol. IV. No. .(, I9W |
