Literature DB >> 27056464

Natural history of idiopathic abducens nerve paresis in a young adult.

Jameel Rizwana Hussaindeen1, Revathy Mani2, Archayeeta Rakshit3, Srikanth Ramasubramanian2, Smitha Vittal Praveen2.   

Abstract

The natural history of idiopathic abducens nerve paresis and the role of conservative management such as vision training during the recovery process is not well documented in the literature to the best of our knowledge. This case report presents the natural recovery process of idiopathic abducens nerve paresis in a young adult and the role of vision therapy in the recovery process.
Copyright © 2016 Spanish General Council of Optometry. Published by Elsevier España, S.L.U. All rights reserved.

Entities:  

Keywords:  Diplopia; Diplopía; Esotropia; Esotropía.; Historia natural; Idiopathic abducens nerve paresis; Natural history; Parálisis facial idiopática; Terapia visual; Vision therapy

Mesh:

Year:  2016        PMID: 27056464      PMCID: PMC5030314          DOI: 10.1016/j.optom.2016.02.002

Source DB:  PubMed          Journal:  J Optom        ISSN: 1989-1342


Introduction

Abducens nerve palsy is the most common of the ocular paresis in adults,1, 2 with sudden onset of binocular horizontal diplopia as the bothersome symptom. Sixth cranial nerve palsies can be secondary to etiologies such as vascular, viral illness, inflammation, trauma, and undetermined in few cases. In younger patients it is important to rule out malignant causes such as life threatening neoplasms. The incidence of idiopathic sixth nerve palsies varies between 9.3 and 13.2/100,000 in the Caucasian population, with idiopathic reasons contributing to 26% of the total incidence. This case report deals with an acute onset esotropia due to abducens nerve paresis in a 25 year young adult presumably due to an idiopathic etiology or a viral illness. The natural history of the clinical presentation, findings, and role of vision therapy is emphasized through this case report.

Case history

A 25-year-old male presented with chief complaint of sudden onset, binocular horizontal, uncrossed diplopia during the past 1 week associated with eye pain in right eye. He also complained of vomiting and a radiating headache precipitated by stress, computer work and other near work. There was no history of significant systemic illness or any ocular or head injury, and he denied any recent viral illness. The local ophthalmologist had administered a 10-day course of Intravenous methyl prednisolone injection along with Tablet Prednisolone 5 mg (10 tab/day) for three days. Brain imaging (MRI scan) had been done and was within normal limits.

Clinical findings

Uncorrected visual acuity was 20/20, N6 @ 30 cm in both eyes. Subjective and objective refraction revealed emmetropia. The Worth four dot test showed uncrossed diplopia for both distance and near. Cover test revealed a 35 prism diopter right esotropia at distance and a 25 prism diopters right esotropia at 40 cm. Ocular motility showed mild restriction of abduction (−1) in the right eye and rest of the movements were full. There was no significant head posture. Rest of the ocular findings were within normal limits. MRI brain results (Plain and contrast) were within normal limits and no lesions/demyelination were identified. Diplopia charting identified the paretic muscle to be right lateral rectus. Binocular vision assessment revealed poor stereopsis, normal monocular accommodation, unmeasurable fusional vergence due to constant diplopia and reduced monocular accommodative facility and gradient AC/A ratio of 4:1. The diagnostic data is provided in Table 1. Due to constant diplopia and poor fusional ranges, a trial of prisms was recommended. The patient could fuse with 40 base-out Fresnel prisms in front of the right eye. As the patient was a frequent traveler he preferred using frosted glasses instead of Fresnel prisms.
Table 1

Clinical assessment details.

BaselineAfter 3 monthsPost VT
Chief complaintC/O double vision for 8 days with a sudden onset after prolonged near work (12 h) with computer; associated with eye pain and vomiting. C/O unilateral right temporal headache for 8 daysReduction of double visionC/O headache and eye painNo C/O diplopia, headache/dizziness.
Vision (best corrected)OU: 20/20, N6 @ 30–40 cmOU: 20/20, N6 @ 30–40 cmOU: 20/20, N6 @ 30–40 cm
DuochromeOU: balancedOU: balancedOU: balanced
Stereopsis>400 (wirt circles)50 arc seconds50 arc seconds
Worth four dot testUncrossed diplopiaUncrossed diplopiaFusion (D & N)
EOMOD: abduction restriction −1OS: fullOD: fullOS: fullOD: fullOS: full
CTCover test D & N: right esotropiaEsophoria(D > N)D: orthoN: esophoria
PBCTD: 30 BON: 20 BOD: 16 BON: 10 BOD: orthoN: 2 BO
NPC (accommodative target) (BREAK/RECOVERY)Uncrossed diplopia till 20 cm6 cm9 cm/11 cm
NPC (pen light with R/G glasses/red filter) (BREAK/RECOVERY)Subjective: diplopiaAlternating suppression9/11 cm
NPAOD 10 cmOS 9 cmOU DIPLOPIAOD 12 cmOS 12 cmOU 10 cmOD 7 cmOS 8 cmOU 7.5 cm
Amplitude of accommodationOD 10 DOS 11.1 DOD 8.3 DOS 8.3 DOU 10 DOD 14.3 DOS 12.5 DOU 13.3 D
MEMOD + 0.50 DSOS + 0.50 DSOD +0.50 DSOS + 0.50 DSOD + 0.50 DSOS + 0.50 DS
NRADeferred+2.50 DSNot done
PRADeferred−1.00 DSNot done



Fusional Vergence Amplitudes (step vergence)
 NFV (Distance)Diplopia – fusional ranges not measuredX/4/2X/6/4
 NFV (Near)Diplopia – fusional ranges not measuredX/4/2X/6/4
 PFV (Distance)Diplopia – fusional ranges not measuredX/25/18X/35/30
 PFV (Near)Diplopia – fusional ranges not measuredX/30/20X/30/25
 Vergence facility (12 BO/3 BI flippers/Diplopia1 CPM6 cpm
 Accommodative facility (+2.00/−2.00 DS)OD: 0 CPM (fails both)OS: 2.5 CPM (difficulty with plus > minus)OU: DeferredOD: 0 CPM (fails both)OS: 1.5 CPM (difficulty with plus > minus)OU: 2 CPM (difficulty with plus > minus)OD:5 CPMOS: 4.5 CPMOU:6 CPM
 AC/A ratio4/1 (Gradient Method)4/1 (Gradient Method)
 Impression• Non-comitant, right esotropia secondary to 6th nerve paresis• Poor Stereopsis• Normal Monocular NPA• Reduced negative fusional Vergence• Reduced accommodative facility• Normal NPC• Esophoria D > N• Normal NPA• Reduced vergence amplitudes (NFV)• High AC/A• Reduced accommodative facilityS/O Divergence insufficiency• Near Esophoria• Normal NPC• Reduced NFV Amplitudes (Improved from baseline)• Reduced Accommodative Facility
 AdviceTrial of prismsFollow-up after 3 monthsIn-office Vision Therapy (IVT) with prisms; Wean off prisms during therapyHome Vision Therapy (HVT)Eccentric Circles for distance and near, Transparent Life Saver Card, Brock String, Accommodative Flippers +/− 2.00Ds with N10, N8 targets

Three month follow UP

At the 3 month follow-up, diplopia had reduced considerably except in extreme right gaze. The frequency of the diplopia decreased, although diplopia persisted in right gaze, and this was stable for the past one month with no improvement noticed by the patient. Eyestrain and frontal headache were present with near work. On re-assessment, visual acuity was 20/20, N6 in both the eyes and worth four dot test showed fusion for distance and near. Stereopsis was 50 arc seconds with Randot stereo test. The cover test revealed a 16 PD esophoria at distance and 10 PD esophoria at near. Ocular motility was full, free and painless. Binocular vision assessment revealed improved vergence amplitudes compared to baseline. However, there were still significant reduced negative fusional vergence, and accommodative facility (Table 1). Although there has been considerable improvement probably due to spontaneous recovery, the NFV amplitudes and accommodative facility were still reduced and the patient was symptomatic. Considering no significant improvement over the past month, vision therapy was recommended to improve divergence amplitudes and to improve accommodative facility. Base out prisms were considered to facilitate training due to the large eso component. Three broad goals were established for vision therapy, developing divergence amplitudes for distance and near, improving accommodative facility (monocularly and binocularly), and improving saccadic/pursuit eye movements (due to diplopia in lateral gaze). On re-assessment at the end of 10 sessions, asthenopic symptoms were reduced, and no diplopia was noticed for distance and near. The patient demonstrated fusion for distance and near with the Worth four dot. The distance and near angles reduced significantly from 16 PD esophoria to orthophoria for distance and 2 PD esophoria at near. The diagnostic data at follow-up is provided in Table 1. The goals of vision therapy and details of vision therapy is sequenced in Table 2, Table 3 respectively. After 10 sessions of in-office vision therapy, he was advised to continue home-based therapy using the transparent Eccentric Circles, Life Saver Card, Brock string and accommodative flippers. A six month follow-up revealed stable alignment, and no symptoms with good compliance to home vision therapy.
Table 2

Goals of vision therapy.

ExercisesGoals
Brock stringTo improve convergence and kinesthetic awareness of convergence and divergence
Computer orthoptics (VTS4 - www.visiontherapysolutions.net)Improve Accommodation, vergence and Stereo
Variable tranaglyphs and vectogramsFusion with varying accommodation and vergence demands (Free space fusion techniques)
Accommodative flippers: +/−1.50Stimulate and relax Accommodation
Variable tranaglyphs & vectograms (Clowns and Quoits)Peripheral fusion awareness
Aperture Rule (Base in)To train divergence
Eccentric Circles and Life saver cardFusion with varying vergence demands in different gazes (Free space fusion techniques)
Computer Exercises – RotationsStereo awareness in all gazes
Eccentric circles at all gazesFusion awareness in all gazes (Free space fusion techniques)
Large eccentric circles at 3 mFusion awareness for distance
Bernelloscope (Base in)To train divergence
Table 3

Details of vision therapy given at Each Session.

Day1: Brock string, Computer orthoptics
Day2: Variable Tranaglyphs and Vectograms, Computer Orthoptics, Accommodative flippers: +/−1.50
Day 3: Computer orthoptics, Variable Vectograms (Quoits), Accommodative flipper: +/−1.50 and rock
Day 4: Computer orthoptics, Variable Tranaglyphs & Vectograms (Quoits), Accommodative flipper: +/−1.50 and rock
Day 5: Variable Tranaglyphs (Quoits & Clowns), Computer orthoptics, Aperture Rule (Base in)
Day 6: Variable Tranaglyphs, Computer orthoptics-Stereo, Accommodative Flippers (+/−1.50 D)
Day 7: Variable Vectograms (Clown), Computer exercise (Stereo), Brock string (in dextroversion and with rotation)
Day 8: Computer Orthoptics – Rotations, Transparent Eccentric Circles and Life saver card, Accommodative rock (VTS4)
Day 9: Brock String, Computer Exercises – Rotations, Eccentric circles at all gazes, Large transparent eccentric circles at 3 m, Bernelloscope (Base in)
Day 10: Brock String rotation, Computer Exercises – Rotations, Eccentric circles at all gazes, Large eccentric circles at 3 m, Aperture Rule (Base in)

Discussion

Acquired sixth nerve paresis is rare in young adults. The most common causes for non-traumatic sixth nerve paresis in children and adults include central nervous system mass lesions, demyelination and inflammation, vasculopathy, and multiple sclerosis.5, 6 Idiopathic presentations in adults can account for up to 22% of cases. Spontaneous recovery of 6th nerve paresis is common (in almost 71% of affected individuals) in traumatic sixth nerve palsy at 6 months after onset,7, 8, 9 and the angle of deviation is the most important determining the prognosis. In our case, idiopathic or presumably a viral etiology was the most likely etiology. We utilized the sequential management approach suggested by Caloroso and Rouse (1993). Few case reports,12, 13 have demonstrated the effectiveness of vision therapy in esotropia. Vision therapy improved the patient's range of fusion and thus significantly reduced the incidence of diplopia in both these patients. Saccadic peak velocities and latency are documented to be affected in sixth nerve palsies and hence saccadic training was thought to be constructive to improve saccades especially toward the paretic side. Though there is absence of quality data to suggest eye movement therapy may be helpful, from a physiological perspective we considered that this could be beneficial in preventing secondary contracture of the extraocular muscles. Also it has been well documented in literature that a high percentage of patients with a 6th nerve palsy show spontaneous remission that may take months. Thus, aggressive optometric treatment with prism, lenses, and vision therapy can help the patient be more comfortable during the time it takes for remission to occur, and also speed up the improvement in function. Though it could be argued that the natural history would allow for spontaneous resolving of symptoms even without active intervention, our case emphasizes the short course of vision therapy that could be of potential benefit and immediate relief to visually bothering symptoms of diplopia and asthenopia.

Conclusion

Vision therapy plays a significant role in improving fusional ranges, reduce asthenopic symptoms, and improve eye movements, thereby meeting the visual demands of the patient in idiopathic abducens nerve paresis. Thorough neurological investigations are required to rule out life threatening illness before commencing the therapy. Regular follow-ups and appropriate co-management are mandatory.

Conflicts of interest

The authors have no conflicts of interest to declare.
  10 in total

1.  Saccade dynamics in peripheral vs central sixth nerve palsies.

Authors:  Agnes M F Wong; Kylen McReelis; James A Sharpe
Journal:  Neurology       Date:  2006-05-09       Impact factor: 9.910

2.  The natural history of acute traumatic sixth nerve palsy or paresis.

Authors:  J M Holmes; P J Droste; R W Beck
Journal:  J AAPOS       Date:  1998-10       Impact factor: 1.220

3.  Aetiological patterns of ocular motor nerve palsies.

Authors:  V Menon; J Singh; P Prakash
Journal:  Indian J Ophthalmol       Date:  1984 Sep-Oct       Impact factor: 1.848

4.  Isolated third, fourth, and sixth cranial nerve palsies from presumed microvascular versus other causes: a prospective study.

Authors:  Madhura A Tamhankar; Valerie Biousse; Gui-Shuang Ying; Sashank Prasad; Prem S Subramanian; Michael S Lee; Eric Eggenberger; Heather E Moss; Stacy Pineles; Jeffrey Bennett; Benjamin Osborne; Nicholas J Volpe; Grant T Liu; Beau B Bruce; Nancy J Newman; Steven L Galetta; Laura J Balcer
Journal:  Ophthalmology       Date:  2013-06-06       Impact factor: 12.079

5.  Botulinum toxin treatment versus conservative management in acute traumatic sixth nerve palsy or paresis.

Authors:  J M Holmes; R W Beck; K E Kip; P J Droste; D A Leske
Journal:  J AAPOS       Date:  2000-06       Impact factor: 1.220

6.  Clinical features and natural history of acquired third, fourth, and sixth cranial nerve palsy.

Authors:  U-C Park; S-J Kim; J-M Hwang; Y S Yu
Journal:  Eye (Lond)       Date:  2007-02-09       Impact factor: 3.775

7.  Cause and prognosis of nontraumatic sixth nerve palsies in young adults.

Authors:  George B Peters; Sophie J Bakri; Gregory B Krohel
Journal:  Ophthalmology       Date:  2002-10       Impact factor: 12.079

8.  Incidence, associations, and evaluation of sixth nerve palsy using a population-based method.

Authors:  Sanjay V Patel; Srinivas Mutyala; David A Leske; David O Hodge; Jonathan M Holmes
Journal:  Ophthalmology       Date:  2004-02       Impact factor: 12.079

9.  Optometric management of binocular dysfunctions secondary to head trauma: case reports.

Authors:  A H Cohen
Journal:  J Am Optom Assoc       Date:  1992-08

10.  Isolated sixth-nerve palsies in younger adults.

Authors:  M L Moster; P J Savino; R C Sergott; T M Bosley; N J Schatz
Journal:  Arch Ophthalmol       Date:  1984-09
  10 in total

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