Cause Of Diplopia Research Articles

Parkinson's Disease and Diplopia

Objective: To describe the spectrum of ocular dysconjugacy in Parkinson's disease (PD). Methods: Forty-four consecutive PD patients with diplopia (and 9 PD controls without diplopia) were examined for ocular dysconjugacy, including convergence insufficiency (CI). Results: Forty-two PD patients had CI with or without diplopia (2 could not be tested), and 15/44 PD patients also had distance diplopia (hypertropia-9, exotropia-4, variable horizontal heterotropia-1, esotropia-1) of diverse etiologies. All (9/9) control patients had CI. These patients of similar age without diplopia and with shorter duration of PD (P = 0.05) had CI with significantly greater (p < 0.0001) convergence fusional amplitudes than PD patients with diplopia. Conclusions: Prior studies underestimate the frequency of CI in PD patients with visual complaints. In this series 100% of tested patients with diplopia had CI. Comparison of PD patients with and without diplopia demonstrates that convergence fusional amplitudes decrease as disease duration increases. CI is a common accompaniment of PD, the most frequent cause of diplopia, and may reflect extranigral pathology.

Partial avulsion of the inferior rectus: An unusual cause of diplopia after blunt orbital trauma

A 14-year-old boy had a severe blow to the right orbit, which caused a blow-out fracture of the orbital floor and damage to the inferior rectus with resultant diplopia. After two operations his vision is still not perfect.

Persistent diplopia after retrobulbar anesthesia

Reply: We thank Chan and coauthors for their interest in our article. They noticed the predominance of superior rectus involvement in our study and suggest that our use of a bridle suture may be the potential cause of diplopia. Bridle suture injury to the superior or inferior rectus muscle was believed to cause strabismus after cataract surgery.1 However, recent studies indicate that myotoxicity from local anesthetics may play an important role in the development of postoperative strabismus.2–7 Rainin and Carlson2 first suggested the myotoxic effects of local anesthesia on extraocular muscles, and their report was followed by many others.3–7 Munoz and coauthors3 reported 7 cases with superior rectus overaction and 4 cases of superior rectus paresis; a bridle suture was not used in cataract surgery in any patient. Esswein and von Noorden4 demonstrated no correlation between pareses and the use of a bridle suture, antibiotic or corticosteroid injection, or surgical technique and concluded that permanent paresis of a vertical rectus muscle may be caused by the myotoxic effect of the local anesthetic. Chan and coauthors mentioned 3 references for the bridle suture as a “well-recognized” cause of persistent postoperative vertical diplopia. However, no patient in the first study had bridle sutures8 and the third reference states that “our data do not support the theory that bridle suture injury to the superior rectus muscle has a major pathogenic role in vertical strabismus after cataract surgery.”9 One author of the third reference later found that some patients had received a misdiagnosis of bridle suture injury.10 In the remaining reference, Catalano et al.1 found scarring around the superior rectus and superior oblique muscles at surgery in 2 of 8 patients and believed the complications were related to bridle suture placement. Their patients showed hypertropia that worsened with down gaze or contralateral gaze, restriction on forced duction test, and, finally, fibrosis at surgery. On the other hand, our patients showed hypertropia that increased with up gaze and ipsilateral gaze and no marked restriction on forced duction test; inspection of the muscle at surgery did not disclose fibrosis (except in the same case), thus satisfying the criteria of overactive strabismus pattern.11,12 Besides, most of our patients typically reported they saw double on patch removal, which might be more compatible with paresis by anesthetics. Capó et al.6 demonstrated how the tip of a needle can touch the superior rectus muscle in cadaveric dissection. Because only the tip of the needle touches the superior rectus muscle, limited segmental damage might cause an overaction, whereas diffuse contracture from more extensive muscle damage produces restrictive patterns.6,7 In fact, overaction is more common when the superior rectus muscle is involved, and restriction is more common when the inferior rectus muscle is involved.3,6 The affected muscle in local anesthesia depends to some extent on the type of anesthesia. The muscle struck during a peribulbar block is usually the inferior rather than the superior rectus muscle, but for a retrobulbar injection, the 2 muscles are equally likely to be struck.6 Because most reports of diplopia after local anesthesia enrolled mixed populations with retrobulbar and peribulbar anesthesia and none of our patients had peribulbar anesthesia, we found a lower incidence of inferior rectus muscle involvement with retrobulbar anesthesia only. Grimmett and Lambert13 also identified 4 patients with superior rectus muscle overaction after retrobulbar injection among 7 cases with strabismus that developed after cataract extraction. Muñoz and coauthors3 found 11 cases of superior rectus overaction or paresis, and 10 cases of inferior rectus fibrosis or overaction, but did not describe the type of anesthesia used. As we mentioned in the Discussion,11 the smaller anatomical orbit dimensions in Asians, especially the shorter vertical diameter,14–16 might contribute to the remarkable frequency of superior rectus involvement in our study compared with the frequency in previous studies of white patients. We believe that the predominance of superior rectus involvement in our study may be attributed to the application of retrobulbar anesthesia and an anatomical difference of orbit. We appreciate that Chan and coauthors gave us the opportunity to clarify 1 of the points in our article. Soo Kyung Han MD Jeong Hun Kim MD Jeong-Min Hwang MD

Diplopia after cataract surgery

Purpose To evaluate the cause of diplopia after cataract surgery. Setting Cataract surgery at 7 hospitals and examination of diplopia at a central eye hospital. Methods This study comprised 18 eyes of 17 patients with diplopia that developed after cataract surgery in which retrobulbar anesthesia was used. The Hess screen test was done to diagnose oculomotor dysfunction. Results Several cases showed superior or inferior deviation of the globe, but most patients had nonuniform disturbances of eye movement. Examination of 3 patients by the Hess chart within 1 week after surgery showed paralysis of eye muscles but an overaction at a later stage, evident by reversal of eye position 1 month later. Surgery for strabismus was performed in 6 cases. One case with diplopia improved spontaneously 3 months after cataract surgery and achieved good alignment. Conclusions The Hess screen test was useful for comparing changes in oculomotor function before and after surgery. Oculomotor dysfunction after cataract surgery may be caused directly by traumatic injury during administration of anesthesia or surgery using bridle sutures or indirectly from sensitivity to anesthetic agents.

Diplopia: from symptom to diagnosis

This overview gives a rough frame how to proceed to a quick diagnosis and possible differential diagnosis in patients with diplopia. A thorough interview concerning the onset of symptoms, invariability, and subjective perception is mandatory. The first step before examining ocular motility is to verify monocular or binocular double vision. When the reported diplopia is binocular, the examiner can carry out the red-glass test to determine the site of the double image. In a next step monocular range of movement in the 9 directions of gaze is evaluated to search for incomitance. The main causes of diplopia are palsies of the oculomotor nerves, mechanical restriction--posttraumatic or inflammatory--, supranuclear lesions and disturbed neuromuscular junction. With a simple and clear diagnostic diagram ist is easy to work out the underlying cause of diplopia.

Mechanisms of extraocular muscle injury in orbital fractures.

The gross and microscopic events that occur after orbital blowout fractures were evaluated to assess the mechanisms of diplopia and muscle injury. Intramuscular and intraorbital pressures were evaluated in experimental animals, in cadavers, and at the time of orbital fracture explorations for repair of orbital fractures in humans. Histologic and circulatory changes, muscle pressure recordings, and operative observations were evaluated. Creation of a compartment syndrome was evaluated to include a histologic evaluation of the orbital fibrous sheath network for the extraocular muscles and the intramuscular vasculature. These experiments and observations do not support the role of a compartment syndrome in ocular motility disturbances because (1) intramuscular pressures were subcritical in both humans and animals; (2) no limiting fascial compartment could be demonstrated; and (3) microangiograms and histologic evaluations did not confirm areas of compartmental ischemic necrosis. Muscle contusion, scarring within and around the orbital fibrous sheath network, nerve contusion, and incarceration within fractures remain the probable causes of diplopia, with the most likely explanations being muscle contusion and fibrosis or incarceration involving the muscular fascial network.

Diplopia Following Subcutaneous Injections of Botulinum A Toxin for Facial Spasms

To study the incidence, cause, recovery time, and prevention of diplopia following subcutaneous injection of botulinum A toxin for the treatment of facial spasms. Patients who experienced diplopia after botulinum A toxin injections had their deviations examined in detail. When the muscle that caused diplopia was identifiable, the injection closest to that muscle was omitted in the next treatment in an attempt to prevent diplopia. Of 250 patients receiving about 1500 sets of injections, 25 (1.7%) incidents of diplopia occurred in 10 patients. Excluding two patients who declined further treatment after having diplopia on their first botulinum A toxin treatment, seven of the remaining eight patients had multiple incidents of diplopia. The most common pattern of diplopia was "uncertain diagnosis." The most common identifiable cause of diplopia was paresis of the inferior oblique muscle. Omission of the injection into the central portion of the lower eyelids in the next treatment prevented recurrence of diplopia in only one of the four patients. No significant correlation between botulinum A toxin doses injected and times to recovery was noted. Diplopia following botulinum A toxin treatment is uncommon. Seven patients (3% of patients studied) had 22 episodes of diplopia (88% of episodes). When diplopia occurs, it tends to recur on reinjection, sometimes with a prolonged recovery time. This response may not be dose dependent. The extraocular muscles of some patients may be more susceptible to chemodenervation than others, or botulinum A toxin may diffuse to extraocular muscles more easily in some patients than in others.

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.

An unusual cause of diplopia in a cancer patient

A 47-year-old woman with metastatic infiltrating lobular carcinoma of the breast developed diplopia. Computed tomography of the orbits showed enlargement and irregularity of the right inferior rectus and inferior obliques muscles. Biopsies of these muscles contained breast carcinoma cells. This case report discusses the causes of diplopia in cancer patients, with special attention to the diagnostic problems of metastasis in extraocular muscles. The possible combined occurrence of metastasis in the leptomeninges and extraocular muscles is also to be borne in mind if the latter diagnosis is not to be missed.

Eye Movement Disorders

Section I: Anatomy and physiology.- 1: Anatomy of the oculomotor system.- 2: The physiology of eye movement.- 3: Pathophysiology of horizontal and vertical eye movement disorders.- Section II: Clinical and paraclinical examination.- 4: Bedside examination.- 5: Orthoptic investigation of ocular motor disturbances.- 6: Fundamentals and basic properties of clinical eye movement recording techniques.- Section III: Ophthalmic causes of diplopia.- 7: Interocular causes of diplopia.- 8: Diplopia in concomitant strabismus and other disturbances of fusion.- 9: Diplopia resulting from mechanical causes in the orbit.- 10: Vascular causes of diplopia.- Section IV: Myogenic disorders.- 11: Histochemical fibre types in extra-ocular muscles.- 12: Ocular myopathies: syndromes with chronic progressive external ophthalmoplegia (CPEO).- 13: Signs and symptoms of ocular myasthenia: a clinician's view.- 14: Blepharoptosis.- Section V: Neurology.- 15: The interpretation of nystagmus.- 16: Vestibular eye movement disorders.- 17: Disorders of horizontal and vertical gaze.- 18: Syndromes of the medial longitudinal fasciculus.- 19: Oculomotor disturbances in extra-pyramidal disorders: a review of the literature.- 20: Eye movement disorders caused by lesions of the cerebral hemispheres.- 21: Psychogenic eye movements.- Section VI: Treatment.- 22: The conservative management of diplopia.- 23: Eye muscle surgery in peripheral third, fourth and sixth nerve palsy.- 24: Treatment of disturbances of ocular motility and diplopia: causal and cosmetic therapeutical possibilities.- 25: Neurosurgical aspects of tumour induced diplopia.- Index of subjects.

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.

The Incidence of Extraocular Muscle and Cranial Nerve Palsy in Orbital Floor Blow-out Fractures

The frequency of extraocular muscle (EOM) or cranial nerve (CN) palsy as the sole cause of diplopia in orbital floor blow-out fractures has not been previously determined. Of 40 blow-out fracture patients studied prospectively, seven had motility disturbances consistent with palsy of one EOM or CN. All seven patients had negative forced ductions, making entrapment, edema, or orbital hemorrhage unlikely causes of diplopia. The diplopia resolved in four patients in l year. Persistent diplopia is a common indication for repair of such fractures. If, however, diplopia is due only to EOM or CN palsy, orbital surgery should be deferred (in the absence of significant enophthalmos) in favor of observation and/or later strabismus surgery.

Orbital Floor Fractures-Reply

In Reply. —Dr. Putterman objects to our suggestion that all fractures of the floor of the orbit with clinical symptoms and demonstrable x-ray evidence should be explored. He agrees with the need for early treatment of fractures of the zygomati-comaxillary complex, which involves the orbital floor (impure blow-out) but insists that these should be separated from fractures of the floor alone (pure blow-out). In fact, we carefully separated these two major classifications and suggested the use of coexisting and isolated groupings to emphasize this separation. Limiting the discussion to the isolated, pure blow-out fracture, Putterman and his associates reject the entrapment of the inferior rectus muscle or penetration of the orbital fat through the damaged floor, or both as a cause of diplopia and enophthalmos. This pathogenesis has been documented in the experimental laboratory and repeatedly at surgery by direct observations and forced traction tests since the early reports of

Distance ESO Deviation—A Basic Deviation or Paralysis of Divergence

A Group of one hundred patients is described with the condition of distance eso deviation or convergent squint which is present for distance viewing together with an exo deviation for near viewing and in-between distance and near there is a neutral point or crossing distance where there is no deviation. The crossing distance determines the distance at which an exo deviation will be present. Accommodation increases the degree of eso deviation and shortens the crossing distance, especially in younger patients, but does not have much effect in presbyopic patients. Distance eso deviation occurs at all ages and varies in degree from a small phoria to an obvious tropia. It is a cause of diplopia in elderly patients, and may be the underlying cause of convergent squint in young patients. It is distinct from the rare condition of divergence paresis.