Date post: | 15-Apr-2017 |
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OPTIC NEURITIS
Laya k pillai
OPTIC NERVE
• Forms innermost strata of the retina.
• Continuation of Axon From ganglion Cells (Second Order Neuron)
• Unmyelinated intra-retinally.
• Converge at optic disc (blind spot) & then acquires myelin.
• Exits through lamina cribrosa of the sclera.
• Optic Disc To Optic Chaisma
• 50mm in length
• Extraocular part is surrounded by meninges
• Saltatory Conduction Via the cell membrane
DEFINITION
• Includes inflammatory and demyelinating disorders of the optic nerve
ETIOLOGY• Idopathic
• Hereditary optic neuritis ( Lebers disease )
• Demyelinating disorders –
a) Multiple sclerosis (MC)
b) Devics disease
c) Schilder disease
• Parainfectious optic neuritis –
associated with measles , mumps, chicken pox or following
immunisation
• Infectious –
sinus related (ethmoiditis) , cat scratch fever , syphilis , lyme disease
, cryptococcal meningitis
• Autoimmune disorders associated with optic neuritis:
sarcoidosis, SLE, PAN, Guillain barre syndrome, wegeners
granulomatosis
• Toxic optic neuritis
PATHOLOGY
Perivascular infiltrate of inflammatory cells
Destruction of myelin
Removal of disintegrated myelin by phagocytic cells
Proliferative gliosis
Typical & Atypical ON
TYPICAL ATYPICAL
• Associated with demyelination Associated with causes other
than demyelination
• Particularly Multiple sclerosis eg. infectious
Clinical features
• Visual loss - typical
sudden, monocular, progressive and profound visual loss.
• Dark adaptation lowered
• Visual obscuration in bright light - typical
• Impairment of colour vision (dyschromatopsia)- always present
• Movement phosphenes and sound induced phosphenes – may be perceived
(visual flashing sensations brought about by side-to-side eye movement or sound)
• Uhthoff’s symptom- episodic transient obscuration of vision
• Pulfrich’s symptom – depth perception impaired
• Pain :
- mild dull eyeache more marked in retrobulbar neuritis than
papillitis.
- aggravated by ocular movements esp. in upward or downward
direction due to attatchment of some fibres of SR muscle to
duramater.
Signs
• Visual acuity markedly reduced
• Colour vision severly impaired (typically red saturation)
• Pupil shows ill sustained constriction to light MARCUS GUNN pupil – indicates relative afferent pupillary defect (RAPD ) detected by swinging flash light test
This is a common case in pupillary examination.
The swinging light test shows abnormal light response of the affected eye (initial dilatation followed by constriction). For example,
if the left eye were abnormal, both pupils constrict when the light is shown into the right eye. When the light is swung to the left eye, both pupils dilate. When the light is swung back to the right eye both pupils again constrict. This reaction indicates a defect in the afferent pupillary fibres from the left eye.
• Ophthalmoscopic features 1. Disc edema and physiological cup obliteration (2-3 D) 2. Retinal veins congested and tortous
3. Splinter hemorrhages and fine exudates may be seen on disc 4. Slit lamp examination may reveal inflammatory cells in vitreous 5. macular star formation – neuroretinits
6. In retobulbar neuritis fundus appears normal , ocassionally temporal pallor of disc may be seen
7. visual field defects : MC defect is a relative central or centrocaecal scotoma
8. Contrast sensitivity is impaired
9. Visually evoked response (VER) shows reduced amplitude and delay in transmission time
10. Fundus fluroscein angiography reveals mild to moderate leak in early phase which increases with time
Differenial diagnosis
Papillitis vs papilledema
Acute retrobulbar neuritis vs indirect optic neuropathy, cortical blindness
Diagnosis• The diagnosis of optic neuritis is clinical, based on the history and
physical findings.
• Investigations• Brain MRI• Serological tests: ESR, syphilis, antinuclear antibody (ANA),
antineutrophil cytoplasmic antibodies (ANCA)• CSF analysis (lumbar puncture) : Presence of oligoclonal band,
elevated IgG level suggest MS.
Brain MRI
• MRI of the brain and orbits with gadolinium contrast has become the cornerstone of the evaluation in patients with optic neuritis• To confirm the clinical diagnosis (look for additional plaques of
demyelination)• Offers very strong prognostic information about the risk of future
demyelinating events and MS • For treatment decision
A gadolinium-enhanced fat-saturated T1-weighted scan will show a bright enhancement of the inflamed optic nerve (upper left red arrow). Additionally, bright spots characteristic of multiple sclerosis may also be seen in the brain (lower right red arrow).
White matter lesions in brain MRI denote a higher risk of developing MS
TREATMENT
• Treat the undelying cause
• No effective treatment for idiopathic and hereditary optic neuritis and that associated with demyelinating disorders
• CORTICOSTEROID therapy may shorten the period of visual loss, but will not influence the ultimate level of visual recovery in patients with optic neuritis.
• Interferon therapy reduces the recurrences in patients with MS , costly with unknown long term benefits
OPTIC NEURITIS TREATMENT TRIAL (ONTT)
1. Oral prednisolone therapy alone is C/I in treatment of acute ON since it was associated with risk of new attacks of ON.
2. IV methylprednisolone – A pt presenting with AON should have brain MRI scan - if it show lesions supportive of multiple sclerosis regardless of severity of vision loss, each should receive immediate iv methyl prednisolone
RegimenIV methylprednisolone1g daily for 3 days followed by oral steroid as prednisone (1mg/kg/day) for 11 days and then tapered over 4 days
This therapy will delay conversion to clinical MS over the next 2 years.
Indiactions for IV methylprednisolone in AON with normal brain MRI scan
• Visual loss in both eyes simultaneously or subsequently within hours or days of each other.
• When the only good eye is affected
• When the slow progressive visual loss continues to occur
The most common side effects associated with Corticosteroids in the ONTT were :
• mood changes
• facial flushing
• sleep disturbances
• weight gain
• dyspepsia.