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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 28  |  Issue : 3  |  Page : 210-212

Retrograde trans-synaptic degeneration of visual pathway in an adult with head injury


Department of Ophthalmology, St. Joseph Eye and ENT Hospital, Kottayam, Kerala, India

Date of Web Publication2-May-2017

Correspondence Address:
Dr. Thomas Arun Varghese
Velenteth 35/1459, South Janatha Road, Palarivattom, Kochi - 682 025, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/kjo.kjo_35_17

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  Abstract 

A 41-year-old male with a history of head injury 16 years previously but no visual deficit, presented with reading difficulty. Examination showed disc pallor bilaterally, and perimetry showed the left homonymous hemianopsia. Optical coherence tomography showed a reduction of retinal nerve fiber layer temporally in the right eye and nasally in the left eye correlating with the field defect. Magnetic resonance imaging brain showed atrophy of the right half of chiasma and right optic tract, indicating retrograde degeneration of the right visual pathway.

Keywords: Retrograde degeneration, retrograde trans-synaptic degeneration, wallerian degeneration


How to cite this article:
Varghese TA, James A, Paul C. Retrograde trans-synaptic degeneration of visual pathway in an adult with head injury. Kerala J Ophthalmol 2016;28:210-2

How to cite this URL:
Varghese TA, James A, Paul C. Retrograde trans-synaptic degeneration of visual pathway in an adult with head injury. Kerala J Ophthalmol [serial online] 2016 [cited 2020 Apr 1];28:210-2. Available from: http://www.kjophthal.com/text.asp?2016/28/3/210/205433


  Introduction Top


Retrograde trans-synaptic degeneration (RTSD) was believed to happen only in congenital or childhood lesions. We present a case where this type of degeneration resulted from trauma sustained in adulthood.


  Case Report Top


A 41-year-old male teacher presented with the complaint of difficulty in reading small print for the past 6 months. He had sustained a head injury after falling off a train 16 years previously, for which he had intensive care treatment and recovered without any obvious deficit. Examination showed unaided visual acuity 6/6 both eyes (OU), corrected near vision N6 OU. Fundus examination showed pallor of the discs in OU [Figure 1] and [Figure 2].
Figure 1: The right eye fundus photo showing generalized retinal nerve fiber layer loss

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Figure 2: The left eye fundus photo showing retinal nerve fiber loss in nasal half

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Perimetry showed the left homonymous hemianopia [Figure 3] and [Figure 4] and optical coherence tomography (OCT) (OptoVue) of retinal nerve fiber layer (RNFL), reduction of temporal fibers in the right eye [Figure 5] and nasal fibers in the left eye [Figure 6], corresponding to the visual field defect. Magnetic resonance imaging (MRI) brain and orbit with contrast showed atrophy of the right half of chiasma [Figure 7] and right optic tract [Figure 8]. This is the first Indian report of RTSD in a patient with the insult acquired in adulthood.
Figure 3: Perimetry showing left hemianopia in left eye

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Figure 4: Perimetry showing left hemianopia in right eye

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Figure 5: Optical coherence tomography showing temporal retinal nerve fiber loss in the right eye

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Figure 6: Optical coherence tomography showing nasal retinal nerve fiber loss in the left eye

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Figure 7: Coronal magnetic resonance imaging showing atrophy of the right half of chiasma (yellow arrow)

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Figure 8: Coronal magnetic resonance imaging showing atrophy of the right optic tract (yellow arrow) and normal left optic tract (red arrow)

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  Discussion Top


RTSD was demonstrated in primates by Vanburen.[1] In humans, optic disc pallor and band atrophy have been described in humans with congenital occipital lesions by Hoyt et al.[2] Sachdev et al[3] made the first Indian report of RTSD in a 9-year-old child with symptoms at the age of 4 years. Observations in adults have been variable with Miller and Newman [4] reporting normal discs in a 57-year-old patient after a cerebrovascular accident. Mehta and Plant [5] showed RNFL thinning on OCT in congenital occipital lesions. Bridge et al.[6] for the first time demonstrated optic tract changes on MRI in patients with retrogeniculate lesions acquired in adulthood.

The finding of “band atrophy” or “bow – tie atrophy” in eyes with lesions of the nasal crossing fibers – as in chiasmal lesions – is well known. This is due to the loss of all fibers at nasal and temporal poles while elsewhere there is only partial loss. This will also result in loss of retinal ganglion cells (RGC) by  Wallerian degeneration More Details. In eyes with loss of noncrossing fibers due to occipital lobe lesions (ipsilateral eye in visual cortex lesion – for example, the right eye in a patient with right occipital cortex lesion and left homonymous hemianopia), there is thinning of all sectors except the nasal and temporal sectors. Corresponding RGCs are also lost over time.

The loss of RGCs in lesions acquired in adulthood in humans was first demonstrated by Jindahra et al.[7],[8] using OCT. This confirmed TSD in adult acquired lesions. We have used spectral domain OCT to demonstrate the loss of RGCs in this patient with lesion behind the lateral geniculate nucleus. Our findings agree with that of Jindahra et al. The above findings show that acquired unilateral damage to the occipital lobe resulting in homonymous hemianopia leads to nerve fiber layer thinning as measured by OCT. Previous equivocal reports could be because OCT is a more sensitive detector of RNFL loss than clinical examination.

The finding has significant implication for proposed rehabilitation strategies [9] in the patients with homonymous hemianopia as RGC loss indicating structural changes might be expected to reduce the potential for recovery.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Vanburen JM. Trans-synaptic retrograde degeneration in the visual system of primates. J Neurol Neurosurg Psychiatry 1963;26:402-9.  Back to cited text no. 1
    
2.
Hoyt WF, Rios-Montenegro EN, Behrens MM, Eckelhoff RJ. Homonymous hemioptic hypoplasia. Fundoscopic features in standard and red-free illumination in three patients with congenital hemiplegia. Br J Ophthalmol 1972;56:537-45.  Back to cited text no. 2
    
3.
Sachdev MS, Kumar H, Jain AK, Goulatia RK, Misra NK. Transsynaptic neuronal degeneration of optic nerves associated with bilateral occipital lesions. Indian J Ophthalmol 1990;38:151-2.  Back to cited text no. 3
[PUBMED]  [Full text]  
4.
Miller NR, Newman SA. Transsynaptic degeneration. Arch Ophthalmol 1981;99:1654.  Back to cited text no. 4
    
5.
Mehta JS, Plant GT. Optical coherence tomography (OCT) findings in congenital/long-standing homonymous hemianopia. Am J Ophthalmol 2005;140:727-9.  Back to cited text no. 5
    
6.
Bridge H, Jindahra P, Barbur J, Plant GT. Imaging reveals optic tract degeneration in hemianopia. Invest Ophthalmol Vis Sci 2011;52:382-8.  Back to cited text no. 6
    
7.
Jindahra P, Petrie A, Plant GT. Retrograde trans-synaptic retinal ganglion cell loss identified by optical coherence tomography. Brain 2009;132(Pt 3):628-34.  Back to cited text no. 7
    
8.
Jindahra P, Petrie A, Plant GT. The time course of retrograde trans-synaptic degeneration following occipital lobe damage in humans. Brain 2012;135(Pt 2):534-41.  Back to cited text no. 8
    
9.
Sabel BA, Kenkel S, Kasten E. Vision restoration therapy. Br J Ophthalmol 2005;89:522-4.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

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