Diplopia differential diagnosis: Difference between revisions

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| colspan="1" rowspan="4" |Central nervous system injury (pathways and cranial nerve nuclei)
| colspan="1" rowspan="4" |Central nervous system injury (pathways and cranial nerve nuclei)
| colspan="1" rowspan="1" |Basilar artery thrombosis
| colspan="1" rowspan="1" |Basilar artery thrombosis<ref name="pmid26288672">{{cite journal |vauthors=Demel SL, Broderick JP |title=Basilar Occlusion Syndromes: An Update |journal=Neurohospitalist |volume=5 |issue=3 |pages=142–50 |date=July 2015 |pmid=26288672 |doi=10.1177/1941874415583847 |url=}}</ref>
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* Occlusive thrombosis of the basilar artery  
* Occlusive thrombosis of the basilar artery  
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* Presence of risk factors for ischemic stroke
* Presence of risk factors for ischemic stroke
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* Nystagmus
* Visual field defects
* Restriction of eye movements (maybe internuclear ophthalmoplegia)
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|Vertebral dissection  
|Vertebral dissection  

Revision as of 23:33, 17 February 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:

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:[1]

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
  • 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 Thyroid-associated ophthalmopathy due to ocular surgery
Extraocular muscle injury or hematoma
Congenital myopathie
Mitochondrial myopathies,
Muscular dystrophy
Neuromuscular junction dysfunction Myasthenia gravis
  • Auto-antibodies against nicotinic acetylcholine receptors
  • Fluctuating muscular weakness
  • Ptosis
  • Diplopia and weakness worsens with activity and improves with rest
Botulism
  • Inhibition of acetylcholine release due to toxin at cholinergic synapse and pre-synaptic myoneural junction
  • Dysathria
  • Dysphagia
  • Autonomic dysreflexia
  • Pupillary dysfunction
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[6]
  • 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
  • Vertebrobasilar insufficiency
  • Acute onset
  • Neck pain
  • Vertigo
  • Presence of risk factors for vertebral dissection
Aneurysm
  • Enlarging aneurysm causes direct compression of the cranial nerves
  • Oculomotor nerve palsy
  • Pupillary involvement
Wernicke's encephalopathy
  • Thiamine deficiency leads to metabolic failure and tissue injury
  • Nystagmus
  • Ataxia
  • Altered mental status
  • Ophthalmoplegia
  • Malnutrition

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. Demel SL, Broderick JP (July 2015). "Basilar Occlusion Syndromes: An Update". Neurohospitalist. 5 (3): 142–50. doi:10.1177/1941874415583847. PMID 26288672.

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