Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Diplopia Clinical Presentation

  • Author: Jitander Dudee, MD; Chief Editor: Andrew G Lee, MD  more...
 
Updated: Nov 16, 2015
 

History

A clear and comprehensive history is the single most useful evaluation in treating patients with diplopia. The patient typically presents with a history of double vision, where single objects appear as double. Specific inquiry as to onset, progression, and variability with head posture or gaze direction, as well as previous similar episodes (especially if associated with other neurologic symptoms) and/or spontaneous resolution, is very helpful in the diagnosis and management of diplopia.

Three important symptoms should be elicited, as follows:

  • Does covering either eye make the diplopia disappear? This test helps to rule out monocular diplopia, which persists in one eye even if the other eye is covered.
  • Is the deviation the same in all directions of gaze or by tilting and rotating the head into different positions? This suggests a comitant deviation, with no difference in separation of the images in all directions of gaze. When the extent of deviation changes (and indeed possibly disappears in a given direction), then the deviation is incomitant and suggests a problem with innervation, most likely a paretic muscle.
  • Is the second object displaced horizontally (side-by-side images) or vertically (images above each other)? Oblique diplopia (images separated horizontally and vertically) should be considered as a manifestation of vertical diplopia.

The traditional and detailed evaluation of the chief complaint includes onset (abrupt or slow), severity, duration, location, associated symptoms, and aggravating and relieving factors. A comprehensive and complete review of all these aspects, if necessary with a questionnaire, is more important than the appropriate physical examination or special tests.

Other significant aspects include a review of systems (eg, history of diabetes, vascular disease, or hypertension; headache and other neurologic complaints; muscle fatigue or weakness; medications and drugs being used[5] ), as well as a past medical and surgical history.

Inquire about recent trauma to the face and the head. Blunt injury to the cheek can result in a blow-out fracture of the orbit with hematoma or entrapment of the soft tissues and extraocular muscles, restricting upward and downward eye movement. Entrapment of the inferior rectus muscle can be confirmed by a forced duction test. Blunt head injury may also be associated with nonspecific sixth cranial nerve (abducens) weakness and severe diplopia when gazing to the affected side.

Next

Physical

Evaluate the ocular system with respect to 2 specific aspects: first, physiologically (in turn also with 2 aspects, ie, sensory function and motor function), and, second, anatomically.

The first aspect of the physiologic evaluation includes the sensory component.

Confirm that the symptom is monocular or binocular. Does covering each eye in turn alleviate the problem, or does the diplopia persist despite covering the "good" opposite eye? Monocular diplopia is very uncommon. Possible causes include severe corneal deformity or marked astigmatism (keratoconus), multiple pupils or openings in the iris, refractive anomalies within the eye (early cataracts or partially displaced lenses as in Marfan syndrome), as well as retinal abnormalities (macular scarring and distortion).

Evaluate the magnitude of difference in spectacle correction required for each eye. Marked differences between the eyes (anisometropia) will frequently produce disabling diplopia, especially in extremes of gaze.

Determine the visual acuity in each eye separately, with and without spectacle correction and with a pinhole. Does a pinhole improve the visual acuity, or does it improve monocular diplopia? Major improvement in visual acuity with a pinhole suggests intraocular or refractive problems.

Evaluate the visual field by confrontation testing or formal visual field mapping to detect possible space occupying masses impinging on the visual pathways and/or cranial motor nerves. With severely constricted fields, the peripheral clues for fusion may be lacking, resulting in diplopia.

Determine how various directions of gaze modify the diplopia. Is the diplopia the same in the 9 cardinal directions of gaze? This includes straight ahead (primary gaze), to each side as well as up and down while looking toward that side, and straight up and down from the primary position. This evaluation can enhance subtle weaknesses of individual muscles that may not be apparent during testing of the range of movements.

Evaluate how tilting the head to the left or to the right alters the diplopia. The double vision will increase when the head is tilted to the same side if vertical diplopia is present due to weakness of the superior oblique muscle (innervated by the fourth cranial nerve [trochlear nerve]). Eliciting increases or decreases in the separation of the 2 images is an essential part of the Park three-step test.

Evaluate the integrity of the other cranial nerves (eg, facial sensation [trigeminal nerve], facial muscle movements).

The motor aspect of the physiologic evaluation includes the following:

  • Determine the existence of a normal range of ocular movements. First observe each eye separately (ocular ductions), and then observe both eyes together (ocular versions). Careful consideration of the extraocular muscle anatomy clarifies the effect of each muscle and why one direction of gaze isolates each muscle's effects.
  • Determine that each eye is able to fully adduct (turn inward) and abduct (turn outward) and to fully elevate and depress in abduction and adduction (as if the eye is tracing a capital letter "H").
  • This helps to determine which eye muscle is responsible for diplopia; normal contraction of the medial rectus muscle produces adduction, while abduction is caused by the lateral rectus muscle. Because the vertical eye muscles diverge from their origination at the apex of the orbit to the insertion on the globe, the superior and inferior recti muscles can be evaluated best with the eye abducted.
  • With the eye abducted, the eye will move down by the inferior rectus muscle, while the superior rectus muscle will move it upward in abduction. Likewise, the oblique muscles can be isolated with the eye adducted; with the eye turned in, the inferior oblique muscle elevates and the superior oblique muscle depresses the eye. A simple rule for superior oblique weakness is "the eye that is looks highest in adduction is pointing at the affected superior oblique muscle."
  • Determine if diplopia worsens when the muscles are fatigued (eg, after strenuous use, at the end of the day). Myasthenia gravis can affect any muscle or group of muscles, and a common presenting symptom is variable diplopia. If myasthenia gravis is suspected, its diagnosis can be confirmed by intravenously injecting a short-acting anticholinesterase (ie, 10 mg/mL edrophonium chloride [Tensilon]). See Other Tests.

Determine that other ocular motor functions are normal, as follows:

  • Is the lid in a normal position?
  • Is the pupil response normal and symmetric with the other pupil? Pupil asymmetry is a sinister sign when associated with diplopia because it indicates involvement of the third cranial nerve (oculomotor nerve). An important diagnostic clue is provided by detecting pupil sparing but otherwise complete third nerve palsy (eg, ptosis; inability to elevate, depress, or abduct the eye). A pupil whose function is spared, particularly if associated with complaints of headache or pain around the orbit, is virtually diagnostic of diabetic third nerve palsy. This can avoid expensive and unnecessary imaging studies. Complete and spontaneous recovery after approximately 6 weeks is virtually the rule. Similar temporary mononeuritis multiplex processes can affect the sixth cranial nerve (abducens) with temporary loss of abduction.

The anatomical evaluation includes inspection, palpation, percussion, and auscultation.

Inspect the head position, eyes, eyelids, orbits, and face for symmetry or displacement (upward, downward; proptosis, enophthalmos). Ptosis of the upper eyelid indicates possible third nerve lesions, while eyelid retraction suggests thyroid ophthalmopathy. Abnormal head position (especially tilting the head to one side) suggests superior oblique muscle palsy.

Note inflammation or vascular congestion that may be suggestive of orbital cellulitis, orbital tumors (rhabdomyosarcoma), arteriovenous malformation (carotid cavernous fistula), and thyroid ophthalmopathy. Palpate the orbital rim for fractures and any absences (eg, encephalocele). Palpate soft tissues surrounding the eye for tumors. Gently push on the closed eyelid to determine increased resistance (fullness of the orbit), comparing one eye to the other eye. This may disclose orbital disorders (eg, fractures, tumors).

Perform percussion over the bony orbital rim to disclose focal tenderness from sinus inflammation.

Auscultate the closed eye for the bruit of a carotid cavernous fistula.

Previous
Next

Causes

See Pathophysiology.

Previous
 
 
Contributor Information and Disclosures
Author

Jitander Dudee, MD MA Cantab(Hons), FACS, FRCOphth, Ophthalmologist, Medical Vision Institute, PSC

Jitander Dudee, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Society of Cataract and Refractive Surgery, Kentucky Medical Association, Royal College of Ophthalmologists

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Andrew G Lee, MD Chair, Department of Ophthalmology, Houston Methodist Hospital; Clinical Professor, Associate Program Director, Department of Ophthalmology and Visual Sciences, The University of Texas Medical Branch; Clinical Professor, Department of Surgery, Division of Head and Neck Surgery, University of Texas MD Anderson Cancer Center; Professor of Ophthalmology, Neurology, and Neurological Surgery, Weill Medical College of Cornell University; Clinical Associate Professor, University of Buffalo, State University of New York School of Medicine

Andrew G Lee, MD is a member of the following medical societies: American Academy of Ophthalmology, Association of University Professors of Ophthalmology, American Geriatrics Society, Houston Neurological Society, Houston Ophthalmological Society, International Council of Ophthalmology, North American Neuro-Ophthalmology Society, Pan-American Association of Ophthalmology, Texas Ophthalmological Association

Disclosure: Received ownership interest from Credential Protection for other.

Additional Contributors

Andrew W Lawton, MD Neuro-Ophthalmology, Ochsner Health Services

Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, Southern Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Izak F Wessels, MBBCh, MMed, FRCSE, FACS Adjunct Associate Professor, Loma Linda University; Private Practice in Comprehensive and Surgical Ophthalmology, Allied Eye Associates

Izak F Wessels, MBBCh, MMed, FRCSE, FACS is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Medical Association, and Royal College of Surgeons of England

Disclosure: Nothing to disclose.

Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

References
  1. Rucker JC. Oculomotor disorders. Semin Neurol. 2007 Jul. 27(3):244-56. [Medline].

  2. Stager DR Sr, Black T, Felius J. Unilateral lateral rectus resection for horizontal diplopia in adults with divergence insufficiency. Graefes Arch Clin Exp Ophthalmol. 2013 Mar 22. [Medline].

  3. Migliorini R, Fratipietro M, Segnalini A, Arrico L. Persistent vertical diplopia after cataract surgery: a case report. Clin Ter. 2013. 164(1):e31-3. [Medline].

  4. Morris RJ. Double vision as a presenting symptom in an ophthalmic casualty department. Eye (Lond). 1991. 5 ( Pt 1):124-9. [Medline].

  5. Fraunfelder FW, Fraunfelder FT. Diplopia and fluoroquinolones. Ophthalmology. 2009 Sep. 116(9):1814-7. [Medline].

  6. Shah HA, Shipchandler TZ, Sufyan AS, Nunery WR, Lee HB. Use of fracture size and soft tissue herniation on computed tomography to predict diplopia in isolated orbital floor fractures. Am J Otolaryngol. 2013 Mar 22. [Medline].

  7. Murchison AP, Gilbert ME, Savino PJ. Neuroimaging and acute ocular motor mononeuropathies: a prospective study. Arch Ophthalmol. 2011 Mar. 129(3):301-5. [Medline].

  8. Hatt SR, Leske DA, Holmes JM. Comparing methods of quantifying diplopia. Ophthalmology. 2007 Dec. 114(12):2316-22. [Medline].

  9. Holmes JM, Leske DA, Kupersmith MJ. New methods for quantifying diplopia. Ophthalmology. 2005 Nov. 112(11):2035-9. [Medline].

  10. Phillips PH. Treatment of diplopia. Semin Neurol. 2007 Jul. 27(3):288-98. [Medline].

  11. Holmes JM, Liebermann L, Hatt SR, Smith SJ, Leske DA. Quantifying Diplopia with a Questionnaire. Ophthalmology. 2013 Mar 23. [Medline].

  12. Anderson MW, Sharma K, Feeney CM. Wound botulism associated with black tar heroin. Acad Emerg Med. 1997 Aug. 4(8):805-9. [Medline].

  13. Astin CL. The use of occluding tinted contact lenses. CLAO J. 1998 Apr. 24(2):125-7. [Medline].

  14. Batocchi AP, Evoli A, Majolini L, et al. Ocular palsies in the absence of other neurological or ocular symptoms: analysis of 105 cases. J Neurol. 1997 Oct. 244(10):639-45. [Medline].

  15. Berman EL. Clues in the eye: ocular signs of metabolic and nutritional disorders. Geriatrics. 1995 Jul. 50(7):34-6, 43-4. [Medline].

  16. Bielschowski A. Disturbance of vertical motor muscles of the eyes. Arch Ophthalmol. 1938. 20:175-200.

  17. Brazis PW, Lee AG. Binocular vertical diplopia. Mayo Clin Proc. 1998 Jan. 73(1):55-66. [Medline].

  18. Campbell C. Corneal aberrations, monocular diplopia, and ghost images: analysis using corneal topographical data. Optom Vis Sci. 1998 Mar. 75(3):197-207. [Medline].

  19. Capo H, Roth E, Johnson T, et al. Vertical strabismus after cataract surgery. Ophthalmology. 1996 Jun. 103(6):918-21. [Medline].

  20. Dengis CA, Steinbach MJ, Ono H, et al. Learning to look with one eye: the use of head turn by normals and strabismics. Vision Res. 1996 Oct. 36(19):3237-42. [Medline].

  21. Fingeret M. Forced duction test. Atlas of Primary Eyecare Procedures. Norwalk, Conn: Appleton & Lange; 1990. 138-44.

  22. Fowler MS, Wade DT, Richardson AJ, et al. Squints and diplopia seen after brain damage. J Neurol. 1996 Jan. 243(1):86-90. [Medline].

  23. Galimberti CA, Versino M, Sartori I, et al. Epileptic skew deviation. Neurology. 1998 May. 50(5):1469-72. [Medline].

  24. Gladstone GJ. Ophthalmologic aspects of thyroid-related orbitopathy. Endocrinol Metab Clin North Am. 1998 Mar. 27(1):91-100. [Medline].

  25. Goldenberg AS. Transient diplopia as a result of block injections. Mandibular and posterior superior alveolar. N Y State Dent J. 1997 May. 63(5):29-31. [Medline].

  26. Hahn JS, Berquist W, Alcorn DM, et al. Wernicke encephalopathy and beriberi during total parenteral nutrition attributable to multivitamin infusion shortage. Pediatrics. 1998 Jan. 101(1):E10. [Medline].

  27. Hayreh SS, Podhajsky PA, Zimmerman B. Occult giant cell arteritis: ocular manifestations. Am J Ophthalmol. 1998 Apr. 125(4):521-6. [Medline].

  28. Ing E, Kennerdell JS. The evaluation and treatment of extraocular motility deficits. Otolaryngol Clin North Am. 1997 Oct. 30(5):877-92. [Medline].

  29. Kasner SE, Liu GT, Galetta SL. Neuro-ophthalmologic aspects of aneurysms. Neuroimaging Clin N Am. 1997 Nov. 7(4):679-92. [Medline].

  30. Kolling GH. [Reflections on expert assessment of double vision and forced head position]. Klin Monatsbl Augenheilkd. 1996 Jan. 208(1):63-5. [Medline].

  31. Kushner BJ, Kowal L. Diplopia after refractive surgery: occurrence and prevention. Arch Ophthalmol. 2003 Mar. 121(3):315-21. [Medline].

  32. Kutschke PJ. Taking a history of the patient with diplopia. Insight. 1996 Sep. 21(3):92-5. [Medline].

  33. Lasley DJ, Kivlin J, Rich L, et al. Stereo-discrimination between diplopic images in clinically normal observers. Invest Ophthalmol Vis Sci. 1984 Nov. 25(11):1316-20. [Medline].

  34. Marzo ME, Perez Lopez-Fraile I, Capablo JL, et al. [Ocular myasthenia: clinical course and strategies for treatment]. Rev Neurol. 1998 Mar. 26(151):398-400. [Medline].

  35. Miller NR. Lesions of the supranuclear ocular motor pathways. Walsh and Hoyt's Clinical Neuro-Ophthalmology. 4th ed. Baltimore, Md: Lippincott Williams & Wilkins; 1985. 707-715.

  36. Muneer A, Jones NS, Bradley PJ, et al. ENT pathology and diplopia. Eye. 1998. 12 (Pt 4):672-8. [Medline].

  37. Ottar WL. Diplopia: double the fun! Part 1: History taking. Insight. 1998 Dec. 23(4):119-25. [Medline].

  38. Richardson LD, Joyce DM. Diplopia in the emergency department. Emerg Med Clin North Am. 1997 Aug. 15(3):649-64. [Medline].

  39. Safran AB, Vibert D, Häusler R. [Vestibular neuritis: a frequently unrecognized cause of diplopia]. Klin Monatsbl Augenheilkd. 1995 May. 206(5):413-5. [Medline].

  40. Schachat AP. Diplopia. Diagnostic Diagrams: Ophthalmology. Baltimore: Lippincott Williams & Wilkins; 1984. 101-107.

  41. Seminari E, Cocchi L, Antoniazzi E, et al. [Clinical significance of diplopia in HIV infection. Assessment of a personal caseload and review of the literature]. Minerva Med. 1996 Nov. 87(11):515-23. [Medline].

  42. Shumrick KA, Kersten RC, Kulwin DR, et al. Criteria for selective management of the orbital rim and floor in zygomatic complex and midface fractures. Arch Otolaryngol Head Neck Surg. 1997 Apr. 123(4):378-84. [Medline].

  43. Stangler-Zuschrott E. [Disturbing physiologic diplopia (author's transl)]. Klin Monatsbl Augenheilkd. 1979 Mar. 174(3):370-3. [Medline].

  44. Werner SC. Modification of the classification of the eye changes of Graves' disease: recommendations of the Ad Hoc Committee of the American Thyroid Association. J Clin Endocrinol Metab. 1977 Jan. 44(1):203-4. [Medline].

  45. Woods RL, Bradley A, Atchison DA. Monocular diplopia caused by ocular aberrations and hyperopic defocus. Vision Res. 1996 Nov. 36(22):3597-606. [Medline].

 
Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.