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PubMed1995

[Vestibular neuritis: a frequently unrecognized cause of diplopia].

The vestibular function plays an essential role in the stabilization of the image on the retina. In addition, when the head is tilted, it contributes to maintain horizontally the plane of the gaze. Vestibular changes can result in oscillopsia and/or diplopia. The latter is related to occurrence of a skew deviation. The authors emphasize the frequent occurrence of diplopia following disorders of the vestibular nerve, specially after vestibular neuritis. In clinical practice, the causal relationship between vestibular neuritis and diplopia is often unrecognized.

Adult↗
PubMed1993

[Evaluation of visual field defects, motility disorders and diplopia within the scope of accident insurance law].

Visual Field: The determination of the level of compensation for loss of integrity is based on the Goldmann Perimetry. In case of concentric loss of the visual field the SUVA Tables 1989 are used. Hemi- and Quadrantanopsias are still evaluated according to the Rintelen Tables from 1954. No guidelines are available for the evaluation of central and paracentral skotomas. It is uncertain if automatic perimetry can be used routinely in the future for the evaluation of visual function. Motility Disorders and Diplopia: The evaluation of functional loss caused by diplopia is very difficult. Therefore a big variation of 5-30% has been determined. It is up to the specialist to evaluate the extent of the damage. In this study we looked for a correlation between the objective findings and the subjective complaints. Such a correlation could not be found so that an arbitrary classification depending on the extent of the diplopia must be recommended. This would create an analogy to the evaluation of the loss of visual acuity and visual field where no freedom is left to the judgement of the physician. Some reflections are given on the sense and benefit of the unique Swiss law concerning compensation for loss of integrity.

Diplopia↗
PubMed1989

Evidence of direct damage to extraocular muscles as a cause of diplopia following orbital trauma.

Vertical diplopia following orbital trauma has frequently been attributed to entrapment of the inferior rectus muscle. The high incidence of spontaneous recovery and negative forced ductions suggests that a significant percentage of these patients have other causes for their diplopia, such as direct damage to the extraocular muscles or their innervating nerves. In five patients with blunt trauma to the orbit, high-resolution computed tomography (CT) scanning showed evidence of hemorrhage or edema within the inferior rectus or inferior oblique muscle that was paretic on clinical exam. No evidence of entrapment was noted in any of the five patients. The course was variable. Three patients had almost complete recovery, whereas two demonstrated improvement but with residual restriction or paresis. Our findings support direct extraocular muscle (EOM) damage as the primary cause of diplopia in these patients. High-resolution CT scanning helps in selecting such patients in whom orbital intervention is unnecessary. The clinical goals of binocular single vision in primary and reading positions are emphasized.

Adult↗
PubMed1986

Magnetic resonance imaging in patients with diplopia. A review.

Magnetic resonance imaging may be the procedure of choice for evaluating patients with diplopia; the absence of signals from cortical bone enables the brain stem and individual cranial nerves to be visualized and the imaging planes selected easily, and there is excellent contrast resolution of pathologic lesions. A clinical assessment of diplopia including the identification of associated neurologic disturbances is necessary prior to MR imaging, however, to assure that appropriate anatomic areas are studied and imaging sessions kept within acceptable time limits. The relevant physiology and anatomy critical to normal ocular motility are reviewed and the value of MR imaging for diplopia demonstrated by selected patient examples.

Adult↗
PubMed1977

Monocular central-field occlusion for intractable diplopia.

This report describes several methods of degrading imagery through the central portion of a spectacle lens to provide a cosmetically acceptable means of obtaining single vision in the central field of patients with intractable diplopia. For 2 strabismic patients with annoying diplopia, we applied to 1 spectacle lens a centrally placed disc (about 1 inch diameter) consisting of (1) translucent tap,a (2) a +7 D Fresnel lens,b or (3) stippled, clear lacquer. For 1 patient, the lacquer was the most acceptable; for the other, the tape was best. We present here the case reports for these 2 patients, showing why they preferred different image-degrading methods and how these and other methods of central-field image degrading can be advantageous even when diplopia is present across most of the visual field.

Adolescent↗
PubMed1991

Bilateral monocular diplopia secondary to occult diabetes mellitus.

A 68-year-old man presented with transient, bilateral, vertical, monocular diplopia as an initial manifestation of diabetes mellitus. The diplopia was determined to be of lenticular origin, but was not found to be secondary to the usual refractive changes. Rather, it is presumed to be due to prismatic alterations caused by index of refraction differences within the crystalline lenses. It is not known what other factors relate to the development of this type of diplopia in the diabetic patient.

Aged↗
PubMed1993

Persistent diplopia associated with strabismus surgery.

The primary therapeutic goal for patients with binocular vision problems is comfortable, single, clear, normal binocular vision at all distances and directions of gaze. Strabismus surgery is frequently used to assist in achieving this therapeutic goal. Strabismus surgery is also used for those patients who cannot achieve single normal binocular vision but who have a cosmetically noticeable ocular deviation. However, one of the complications of cosmetic strabismus surgery is persistent diplopia. This possibility must be considered seriously before any cosmetic strabismus surgery is performed. The purpose of this paper is to present a case report of a patient who had diplopia after cosmetic strabismus surgery to emphasize the need for careful consideration of the possibility of persistent diplopia after cosmetic strabismus surgery and how to avoid it.

Adult↗
PubMed1998

Diplopia following transconjunctival blepharoplasty.

The resurgence of popularity of the transconjunctival approach to lower eyelid fat removal as a component of cosmetic blepharoplasty has been highlighted by a number of publications in recent years. There has been, however, minimal discussion in the literature of the complications of this procedure. Although the mechanism of muscle injury is similar in transcutaneous and transconjunctival surgery, there is a much more direct route to the inferior extraocular musculature via the latter approach. Herein, we present a series of six patients with diplopia status post-transconjunctival lower eyelid blepharoplasty referred to the Manhattan Eye, Ear, and Throat Hospital for evaluation. Transconjunctival lower lid blepharoplasty was performed as a primary procedure in four patients and as a secondary procedure following transcutaneous blepharoplasty in two patients. Patients were evaluated with ocular examination and orthoptic measurements. Magnetic resonance imaging was obtained in two cases. The inferior rectus and inferior oblique muscles were found to be equally injured in these cases (4 of 6), and the lateral rectus was encountered in one case. Two patients required strabismus surgery to correct their diplopia, whereas four patients improved with observation alone. The possible etiologies of postoperative diplopia following transconjunctival lower lid blepharoplasty are manifold. Mechanisms of extraocular muscle injury may include intramuscular hemorrhage and edema, cicatricial changes within the muscle, and accidental incorporation of extraocular muscle in closure of orbital septum. Avoidance of these complications is probably best achieved through intimate understanding on the part of the surgeon of eyelid anatomy from the transconjunctival perspective.

Adult↗
PubMed2005

Isolated vertical diplopia as the initial manifestation of presumed pretectal and anterior hypothalamic germinomas.

A 21-year-old man with a 5-month history of diplopia caused by isolated vertical ocular misalignment had normal laboratory studies, including brain magnetic resonance imaging (MRI). Eight months after the onset of diplopia, he reported dry mouth, polydipsia, polyuria, and absent sweating. Examination now disclosed light-near dissociation of the pupillary responses, convergence-retraction nystagmus, and upgaze palsy. MRI revealed enhancing suprasellar and pretectal masses presumed to be germinomas. Two years after brain irradiation and systemic chemotherapy, no lesions are apparent on MRI and hypothalamic dysfunction has partially resolved. In a young patient with isolated vertical diplopia and normal brain imaging, one should consider an early pretectal syndrome and inquire after manifestations of hypothalamic dysfunction.

Adult↗
PubMed2004

"Retinal diplopia" associated with macular wrinkling.

Binocular diplopia is usually due to misalignment from ocular motor dysfunction. Three patients with chronic binocular vertical diplopia and small comitant hypotropic deviations due to macular displacement (heterotopia) associated with monocular retinal wrinkling are described. This maculopathy was idiopathic in two and secondary to treated retinal detachment in the third. Displacement of the macula by vitreoretinal traction is an unusual cause of binocular diplopia that requires careful ophthalmoscopy to diagnose.

Aged↗
PubMedDate not supplied

[Opaque intraocular lens in intractable diplopia: case report].

Intractable diplopia has been described in many situations but poor results are the rule with standard treatment modalities. The authors report a case of a woman with long-standing strabismus and diplopia who failed to improve following surgery, prism, and occlusive spectacles or contact lenses. Then, she was submitted to phacoemulsification and opaque intraocular lens implantation, which successfully neutralized diplopia.

Aged↗
PubMedDate not supplied

Is abnormal focal steepening of the cornea related to persistent monocular diplopia?

PURPOSE: Some case reports have shown that abnormal focal steepening of the cornea appears to cause monocular diplopia by prismatic effect. The purpose of this study was to ascertain prospectively if the pattern of corneal distortion was related specifically to persistent monocular diplopia. METHODS: We selected 16 visually normal eyes (controls) and two groups of volunteers in which abnormal focal steepening of the cornea was expected to be found: 40 eyes of 20 volunteers who wore rigid gas-permeable contact lenses (RGP) for myopia and 10 eyes of seven patients with keratoconus. New charts that consisted of white dials on a black background were prepared for detection and measurement of secondary images. Any secondary image that could not be eliminated by any trial lens correction was defined as a persistent secondary image, using the charts. Corneal topography from all subjects was classified: round or oval, symmetric or asymmetric bowtie, abnormal focal steepening accompanied by contact lens-induced corneal warpage or keratoconus, or amorphous. We analyzed the relationship between the persistent secondary image and the corneal topographical patterns. RESULTS: A persistent secondary image was detected from seven eyes of RGP wearers and all keratoconus eyes. All corneal topographies of the seven RGP eyes with a persistent secondary image showed abnormal focal steepening related to contact lens-induced corneal warpage. The direction of the persistent secondary image was approximately consistent with the location of the focal steepening as seen on the corneal topography. CONCLUSION: Abnormal focal steepening of the cornea that appeared to produce a prismatic difference between two parts of the cornea was specifically related to persistent monocular diplopia.

Adolescent↗
PubMedDate not supplied

Hemorrhagic Rathke's cleft cyst presenting as diplopia.

OBJECTIVE: To report a case of uncommon presentation of hemorrhagic Rathke's cleft cyst (RCC) extending into the cavernous sinus, causing diplopia. METHOD: We present clinical, radiologic, and histologic findings on this patient, and review related medical literature. RESULTS: A 34-year-old man presented with a 4-month duration of worsening left-sided headache with acute development of diplopia which worsened upon looking to the left. Magnetic resonance imaging identified a left pituitary mass with posterior extension and involvement of the cavernous sinus. Hormone level evaluation revealed a low free thyroxine index and elevated prolactin levels, and normal levels of thyroid stimulating hormone, growth hormone, insulin-like growth factor type 1, and cortisol. The patient underwent transsphenoidal resection of a yellow fibrous mass from the left side of the sella. Tumor tissue pathology was consistent with a RCC that may have undergone secondary hemorrhage and rupture. Postoperatively, this patient developed transient diabetes insipidus, and required levothyroxine therapy for hypothyroidism. The diplopia improved, though he continues to complain of episodic headaches. CONCLUSION: RCCs are challenging to diagnose, as they can cause symptoms related to enlargement and hemorrhage. Imaging studies and other diagnostic measures may, therefore, describe heterogeneous features. The most common clinical presentation of this disorder is a manifestation of pituitary dysfunction, such as hyperprolactinemia, diabetes insipidus, and, occasionally, apoplexy. These symptoms may be accompanied by headache. Visual disturbances often appear, usually as visual field defects and decreased visual acuity. This case demonstrates that nonpituitary masses such as RCC can hemorrhage and extend into the cavernous sinus, causing acute ophthalmoplegia.

Adult↗
PubMed1999

Divergence paresis: a nonlocalizing cause of diplopia.

OBJECTIVES: To determine the causes, clinical characteristics, and localizing value of divergence paresis, which is characterized by acquired and uncrossed diplopia when viewing distant targets, fusion when viewing near targets, and no limitation of ocular ductions. Controversy persists regarding the diseases underlying divergence paresis and the existence of a divergence "center." MATERIALS AND METHODS: The charts of 15 patients with divergence paresis examined between 1983 and 1998 were reviewed. All patients underwent neuroimaging and detailed ocular motility testing, with measurement of esotropia in prism diopters in 14 patients. RESULTS: Divergence paresis in 15 patients was idiopathic in three patients, was associated with central nervous system microangiopathy or infarct in seven patients, and clivus lymphoma, chronic lymphocytic leukemia with sinusitis, Wernicke ophthalmoplegia, Parkinson disease, myasthenia gravis, cryptic cerebellar vascular malformation, and childhood esotropia in one patient each (two patients had two diagnoses). The mean maximum esotropia was 10.4 prism diopters, and there was no significant correlation (Fisher exact test) between the magnitude of esotropia and vasculopathic etiology or posterior fossa lesion site. Although six patients had posterior fossa disease, neuroimaging showed no common circumscribed lesion site or evidence of increased intracranial pressure. CONCLUSIONS: Divergence paresis is an uncommon cause of acquired diplopia. Divergence paresis is associated with diverse central nervous system diseases and can be mimicked by myasthenia. The absence of a single consistent lesion in our study, which is the largest reported series, suggests that divergence paresis is a nonlocalizing cause of horizontal diplopia and that multiple or diffusely distributed neural structures may govern divergence. Alternatively, elusive divergence "centers" may not exist, and divergence paresis may arise from impaired inhibition or from defective passive antagonism of orbital structures to convergence.

Adolescent↗
PubMedDate not supplied

Phacoemulsification and opaque intraocular lens implantation for the treatment of intractable diplopia.

Intractable diplopia secondary to paralytic strabismus may be treated with the occlusion of the affected eye. Established treatments include occlusion with a patch, opaque spectacles or contact lenses, and performing upper lid lowering procedures or tarsorrhaphies. Two cases are presented in which intractable diplopia was resolved by performing clear lens phacoemulsification and the insertion of an opaque intraocular lens. Both patients reported a resolution of their diplopia having been dissatisfied with other forms of treatment. Although opaque intraocular lens insertion is not recommended as the initial treatment of choice in such cases, it offers a valuable treatment option for those patients in whom other forms of therapy have failed.

Diplopia↗
PubMed2001

Diplopia as a complication of local anesthesia: a case report.

Diplopia caused by local anesthesia at the superior posterior alveolar nerve for the removal of the maxillary third molar is a rare complication. The diplopia is due to facial palsy of the oculomotor muscles of the globe. This paper describes the case of a 22-year-old woman, in whom diplopia was observed after an overall uncomplicated removal of the semi-impacted third molar. Possible causes of the anesthetic effects are reported. The most accepted explanation is that the anesthetic diffuses on the abducent nerve in the cavernous sinus. The necessary actions that the dental surgeon must perform are reported.

Abducens Nerve↗
PubMed1975

[Some clinical aspects concerning diplopia after retinal detachment surgery with cryopexy and episcleral silastic sponge (author's transl)].

The aetiology of diplopia following retinal detachment surgery after the Lincoff-Custodis method is examined. Of 140 patients operated, 16 (i.e. 11.4%) developed diplopia. The authors believe that this diplopia is due to a fixation of the eyeball at the point of the silastic sponge placement. As responsible factors, which depend on the manner of sponge fixation and the size of the sponge, they regard: Alteration of the bulb curvature, shortening of the Tenon's capsule placed over the sponge, and changes in the conditions of muscular action.

Adolescent↗