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| colspan="1" rowspan="2" |Neuromuscular junction dysfunction
| colspan="1" rowspan="2" |Neuromuscular junction dysfunction

Revision as of 17:37, 18 February 2019

Diplopia Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Diplopia may be caused by disorders of the orbit, extraocular muscles, neuromuscular junction dysfuntion, paralysis of the oculomotor, trochlear and abducens nerves, and injuries affecting the central nervous system (CNS). Given the various causes of diplopia, it is important to differentiate between the different causes that lead to diplopia.

Differentiating Diplopia From Other Diseases

Diplopia may be caused by disorders of the orbit, extraocular muscles, neuromuscular junction dysfuntion, paralysis of the oculomotor, trochlear and abducens nerves, and injuries affecting the central nervous system (CNS). Given the various causes of diplopia, it is important to differentiate between the different causes that lead to diplopia. The following table differentiates between various causes of diplopia:

Dilopia causing disorder Subcategory Mechanism Distinguising Features Exam Findings
Orbital disorder Trauma
  • Direct injury to the orbit or eye
  • Ecchymosis
  • Bone fracture
  • Hematoma formation
  • Altered mental status
Orbital apex mass[1]
  • Inflitration or mass effect in the orbital apex or cavernous sinus
  • Compression of the oculomotor nerve
  • Palsies of oculomotor, trochlear and/or abducens nerves
  • Periorbital or facial numbness
  • Retro-orbital pain
  • Proptosis
  • Signs of venous congestion
  • Multi-directional horizantal and vertical diplopia
  • Down and out pupil
  • Pupillary dilation
  • Deterioration of visual acuity
  • Exophthamos
  • Prominent choroidal folds
  • Optic atrophy
  • Bone destruction
Orbital cellulitis[2][3]
  • Spread of infection from contiguous sinuses (especially ethmoidal suinus)
  • Culprit organisms include S. aureus and S. pneumoniae
  • Proptosis
  • Eyelid edema
  • Ophthalmoplegia
  • Ocular pain
  • Presence of risk factors:
    • Recent upper respiratory illness
    • Sinus infection
    • Younger age
    • Retained foreign bodies within the orbit
    • Trauma
    • Immunosuppression
    • Systemic infection
    • Dental infections
  • Eyelid swelling
  • Conjunctival chemosis
  • Axial proptosis
  • Restriction of eye movements
  • Retinal venous congestion
  • Papilledema
Thyroid-associated ophthalmopathy (Grave's disease)[4][5]
  • Autoimmune
  • Proptosis
  • Restriction of elevation and abduction of the eyes
  • Tachycardia
  • Intolerance to heat
  • Weight loss
  • Insomnia
  • Fatigue
  • Diarrhea
  • Dysthyroid orbitopathy (involvement of medial and inferior rectii muscles)
  • Von Grafe's sign (lid lag on downward gaze)
  • Joffroy sign (Absent creases on forehead on upward gaze)
  • Stellwag sign (Infrequent and incomplete blinking)
  • Boston sign (jerky irregular movements on downward gaze)
  • Vigouroux sign (eyelid fullness)
  • Dalrymple’s sign
  • Optic disc edema
  • Choroidal folds
  • Optic disc paleness
Extraocular muscle disorder Extraocular muscle injury or hematoma[6][7]
  • Facial trauma
  • Sinus surgery
  • Extreme strabismus
  • Hematoma
  • Entrapment of muscle in the fractured orbital wall
  • Damage to the oculomotor nerve entry zone
  • Muscle transection
  • Partial or complete muscle destruction with entrapment in scar tissue.
  • Restriction of eye movements
  • Hematoma formation
  • Down and out eyes in case of damage to oculomotor nerve
  • Absent oculocardiac reflex of affected muscle
  • Bone damage
Mitochondrial myopathies[8]
  • Dominant optic atrophy (OPA1 gene mutation)
  • Leber hereditary optic neuropathy (point mutation in mitochondrial DNA)
  • Chronic progressive external ophthalmoplegia also known as Kearns-Sayre syndrome (TYMP, ANT1, PEO1, POLG, POLG2, and even OPA1 gene mutations)
  • Retinal ganglion cells and nerve fiber layer of the retina affected in dominant optic atrophy (may lead to blindness)
  • Acute and painless central vision loss of both eyes in Leber hereditary optic neuropathy (days to months)
  • Extraocular muscle mobility impairment in chronic progressive external ophthalmoplegia
  • Chronic progressive external ophthalmoplegia:
    • Restriction of eye movements
    • Visual acuity is spared
    • Ptosis
  • Leber hereditary optic neuropathy:
    • Disc pseudoedema
    • Thickening of the retinal nerve fiber layers
  • Dominant optic atrophy:
    • Blindness
    • Thinning of the neuroretinal rim
    • Cup to disc ratio > 0.5
    • Peripapillary atrophy
    • Sectoral pallor of the optic nerve
Muscular dystrophy[9]
  • Oculopharyngeal muscular dystrophy (Mutations of the polyadenylate binding protein nuclear 1, PABPN1 gene)
  • Oculopharyngodistal myopathy
  • Dysphagia
  • Weakness of proximal muscles (distal muscles in case of oculopharyngodistal myopathy)
  • Atrophy of the tongue
  • Weakness of facial muscles
  • Dysphonia
  • Ptosis
  • Ophthalmoplegia
Neuromuscular junction dysfunction Myasthenia gravis[10][11]
  • Auto-antibodies against nicotinic acetylcholine receptors
  • Fluctuating muscular weakness
  • Ptosis
  • Diplopia and weakness worsens with activity and improves with rest
  • Ptosis
  • Incommitant strabismus or/and external ophthalmoplegia
  • Cogan’s lid-twitch sign
  • Weakness of the orbicularis oculi muscle
Botulism[12]
  • Inhibition of acetylcholine release due to toxin at cholinergic synapse and pre-synaptic myoneural junction
  • Dysathria
  • Dysphagia
  • Autonomic dysreflexia
  • Pupillary dysfunction
  • Ptosis
  • Blurred vision
  • Ophthalmoplegia
Palsies of the third, fourth or sixth cranial nerves Oculomotor nerve palsy
  • Microvascular ischemia:
    • Diabetic neuropathy
  • Hemorrhage
  • Tumor
  • Vascular malformation
  • Aneurysm
  • Meningitis
  • Multiple sclerosis
  • Muscles affected:
    • Medial, inferiorn superior rectii
    • Inferior oblique muscle
    • Levator palpebrae muscle
    • Ciliary and constrictor pupillae muscles
  • Multi-directional horizantal and vertical diplopia
  • No diplopia on lateral gaze to the affected side
  • Eyelid droop (ptosis)
  • Down and out pupil
  • Pupillary dilation
Trochlear nerve palsy
  • Muscles affected:
    • Superior oblique muscle
  • Rotational diplopia that is worse on looking downwards and towards the nose
  • Extorsion on downward gaze
Abducens nerve palsy
  • Muscles affected:
    • Lateral rectus muscle
  • Horizontal diplopia on gaze towards the affected side
  • Lateral gaze palsy
Central nervous system injury (pathways and cranial nerve nuclei) Basilar artery thrombosis[13][14]
  • Occlusive thrombosis of the basilar artery
  • Brainstem ischemia
  • Dysarthria
  • Vertigo
  • Cranial nerve palsies
  • Presence of risk factors for ischemic stroke
  • Nystagmus
  • Visual field defects
  • Restriction of eye movements (maybe internuclear ophthalmoplegia)
Vertebral dissection[15][16]
  • Vertebrobasilar insufficiency
  • Acute onset
  • Neck pain
  • Vertigo
  • Presence of risk factors for vertebral dissection
  • Occipital and nuchal pain
  • Monocular blindness
  • Hemianopsia
  • Bilateral visual field defects
  • Amaurosis fugax
  • Ptosis
  • Miosis
Aneurysm
  • Enlarging aneurysm causes direct compression of the cranial nerves
  • Oculomotor nerve palsy
  • Pupillary involvement
  • Aneurysm visible on fundoscopy
Wernicke's encephalopathy[17][18]
  • Thiamine deficiency leads to metabolic failure and tissue injury
  • Nystagmus
  • Ataxia
  • Altered mental status
  • Ophthalmoplegia
  • Malnutrition
  • History of alcoholism
  • Optic disc edema
  • Preretinal hemorrhage

References

  1. "thejns.org".
  2. Chaudhry IA, Al-Rashed W, Arat YO (January 2012). "The hot orbit: orbital cellulitis". Middle East Afr J Ophthalmol. 19 (1): 34–42. doi:10.4103/0974-9233.92114. PMID 22346113.
  3. Lee S, Yen MT (January 2011). "Management of preseptal and orbital cellulitis". Saudi J Ophthalmol. 25 (1): 21–9. doi:10.1016/j.sjopt.2010.10.004. PMID 23960899.
  4. Şahlı E, Gündüz K (April 2017). "Thyroid-associated Ophthalmopathy". Turk J Ophthalmol. 47 (2): 94–105. doi:10.4274/tjo.80688. PMID 28405484.
  5. Barrio-Barrio J, Sabater AL, Bonet-Farriol E, Velázquez-Villoria Á, Galofré JC (2015). "Graves' Ophthalmopathy: VISA versus EUGOGO Classification, Assessment, and Management". J Ophthalmol. 2015: 249125. doi:10.1155/2015/249125. PMID 26351570.
  6. Thacker NM, Velez FG, Demer JL, Wang MB, Rosenbaum AL (2005). "Extraocular muscle damage associated with endoscopic sinus surgery: an ophthalmology perspective". Am J Rhinol. 19 (4): 400–5. PMID 16171176.
  7. Chen J, Kang Y, Deng D, Shen T, Yan J (September 2015). "Isolated Total Rupture of Extraocular Muscles". Medicine (Baltimore). 94 (39): e1351. doi:10.1097/MD.0000000000001351. PMID 26426604.
  8. Schrier SA, Falk MJ (September 2011). "Mitochondrial disorders and the eye". Curr Opin Ophthalmol. 22 (5): 325–31. doi:10.1097/ICU.0b013e328349419d. PMID 21730846.
  9. "Oculopharyngeal Muscular Dystrophy - NORD (National Organization for Rare Disorders)".
  10. "Update on the Diagnosis of Ocular Myasthenia Gravis - American Academy of Ophthalmology".
  11. Nair AG, Patil-Chhablani P, Venkatramani DV, Gandhi RA (October 2014). "Ocular myasthenia gravis: a review". Indian J Ophthalmol. 62 (10): 985–91. doi:10.4103/0301-4738.145987. PMC 4278125. PMID 25449931.
  12. Khakshoor H, Moghaddam AA, Vejdani AH, Armstrong BK, Moshirfar M (May 2012). "Diplopia as the primary presentation of foodborne botulism". Oman J Ophthalmol. 5 (2): 109–11. doi:10.4103/0974-620X.99375. PMC 3441016. PMID 22993467.
  13. Demel SL, Broderick JP (July 2015). "Basilar Occlusion Syndromes: An Update". Neurohospitalist. 5 (3): 142–50. doi:10.1177/1941874415583847. PMID 26288672.
  14. von Campe G, Regli F, Bogousslavsky J (December 2003). "Heralding manifestations of basilar artery occlusion with lethal or severe stroke". J. Neurol. Neurosurg. Psychiatry. 74 (12): 1621–6. PMID 14638878.
  15. Park KW, Park JS, Hwang SC, Im SB, Shin WH, Kim BT (September 2008). "Vertebral artery dissection: natural history, clinical features and therapeutic considerations". J Korean Neurosurg Soc. 44 (3): 109–15. doi:10.3340/jkns.2008.44.3.109. PMID 19096659.
  16. Gottesman RF, Sharma P, Robinson KA, Arnan M, Tsui M, Ladha K, Newman-Toker DE (September 2012). "Clinical characteristics of symptomatic vertebral artery dissection: a systematic review". Neurologist. 18 (5): 245–54. doi:10.1097/NRL.0b013e31826754e1. PMID 22931728.
  17. Serlin T, Moisseiev E (2017). "Fundus Findings in Wernicke Encephalopathy". Case Rep Ophthalmol. 8 (2): 406–409. doi:10.1159/000478924. PMID 28924437.
  18. "Nystagmus from Wernicke's Encephalopathy | NEJM".

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