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Scientific article

Neuritis infectious optics.


Report of a pediatric case
Ferrero Rosanas a. - OC No. 8951 - Cavero L. Roig - ophthalmologist - Sierra Lorente - OC No. 17113

Optic neuritis is an inflammation of the optic nerve can cause a sudden loss of vision in the affected eye. This inflammation can be
the result of an infection, poisoning or may be caused by hereditary diseases. With the following article we make a review of the
etiology and symptoms that accompany infectious optic neuritis. We present a pediatric case deepen the visual examination should
be performed and additional tests that allow us to establish an appropriate differential diagnosis.

KEYWORDS

Optic neuritis, papilledema, defec- to relative


afferent pupillary (RAPD), scotoma
centrocecal.

INTRODUCTION

The term optical neuritis 1 It makes reference


to inflammatory conditions or demyelinating
optic nerve (NO). When it affects traocular
in- portion is called papillitis and is
characterized by inflammation of co optical
arranged. Instead, retrobulbar neuritis talk
about if the rear portion of NO which is
affected da, so that the fundus is in principle Figure 1. Neuritis optical infectious: lifting and blurring the edges of the papilla is observed. Absence of

standard. bleeding and signs of neuroretinitis.

(AV), impaired function pu- pillar and color CLINICAL CASE


vision. Cia apparent perimetric examination
The parainfectious optic neuritis 2 for the presence of centrocecal scotoma. Came to our office an 8-year decrease in AV
It is consecutive to a microorganism Cerebrospinal fluid (CSF) of these patients refers OD 10 days of evolution. The patient
infection. The most frequent cause is that of revealed elevated protein with pleocytosis has no medical history or had fever or
viral origin 3 ( parotiditis, chicken pox, etc.) and and neuroimaging studies are normal evils. malaise in the ultra- scams days. No
more rarely bacterial or otherwise. It occurs ophthalmological history or use graduation.
between 1 and 3 weeks un- since the To date visual behavior was normal and
infectious episode and generally affects asymptomatic MOS- lock. In the emergency
children. It may be unilateral, but almost department practice cranial and orbital
always it is a bilateral acute neuropathy da 4 papilla magnetic resonance imaging (MRI) and
elevation. The prognosis of infec- postin- neuritis in general analysis. All tests are normal.
terms of visual recovery is excellent,
although HA- bitual is to persist with papillary
pallor subtle defects in visual function.
It is characterized by reduced visual acuity

3. 4 September 440 Gazette Optics


It is oriented such as optic neuritis and
derived ophthalmology unit for diagnosis and
treatment.

In the first ophthalmologic review ca, the


uncorrected visual acuity (UCVA) of light
perception OD is 10 cm that does not
improve with pinhole. AVSC of OI is unity.
Retinoscopy gives: OD: +3.00 / OI: +2.00. In
exploring the pupillary function we detect one
DPAR OD. Color vision (11 sheets
pseudoiso- chromatic Ishihara) pue- not
assess the OD due to its low and the AV IO is
normal. When performing retinoscopy under
cyclo- plegia the value obtained is OD:

+ 5.50 / OI: 0.50 + 4.00 10º. Extrinsic ocular


motility is Normal and the patient complained
of pain on ocular motility. In the substantive
examination initial lifting eye and blurring of
the edges of the papilla in OD seen. No
bleeding or signs of neuroretinitis are evident
( Fig. 1).

Serology is requested 5 for toxo- plasma


gondii, Toxocara canis, bar- Tonella
henselae, borrelia bugdor- feri, EBV
(Epstein-Barr virus), VDRL (syphilis) and
FTA-ABS (treponemal antibody absorption
fluo- phosphors excited), being all normal
results. Determining ACE (angiotensin
converting enzyme) and PPD (purified protein
derivative) re- sultaron negative. Treat- ment
with corticosteroids (1 mg x kg weight) with
proton pump inhibitors orally pattern.

Figure 2. perimetry, at the initial stage of optic neuritis, reveals an altitudinal scotoma affecting mainly the lower hemifield and
macular area.

At 2 days UCVA OD allows you to count unit. Assessment of color vision OD reveals a progressive decrease in the dose of systemic
fingers at 80 cm (no improvement with teranomalía deu- and the OI remains normal. corticosteroids.
pinhole). AVSC of OI is unity. DPAR The biomicros- cópica exploration and
continues manifesting a mild response direct intraocular pressure are normal in both eyes. At 25 days, the OD is UCVA
reflection in the OD. Perimetry OD ( Fig. The evolution is progressive ophthalmoscopic 0.8 (no improvement with pinhole) and the OI
tion pro sively decreasing elevation and is 1. Opthalmoscopy found that papillary
fuzziness of the papillary edges. And fuzziness level of the nasal edge pallor tem-
2) reveals an altitudinal scotoma evidenced the temporal edge of the papilla ( Fig.porary industry persists. Perimetry has
predominantly in the lower and central normalized OD ( Fig. 5). From this moment the
involvement hemifield. Perimetry of OI is treat- ment is suspended corticosteroid.
normal.
3). In perimetry of the central scotoma OD it is
At 15 days of evolution concerns the pa- cient maintained with progressive resolution lower
improvement. UCVA OD is 0.2 (no scotoma ( Fig. 4). Fa- vorable before the onset
improvement tenopeico is-) and UCVA OI is of symptoms begins At 45 days UCVA is 1in AO.
Retinoscópicamente encon-

Gazette Optics September 440 35


discromatop- open with blue-yellow sia, or
cone dystrophy Stargardt disease arranged
chromatopsia red-green) angle 8.

5. perimetry . The impact of an injury on the


visual field depends largely uncompromised
area and its location on the assembly of the
visual pathway 9. Optic neuropathies are
probably the most frequent cause of central
scotoma or trocecal centered where the
functional loss is concentrated over the
macular area or the area papilo-macular
beam.

Ophthalmological examination will focus on


examination of segmental posterior to the
Figure 3. Improved fundus after 15 days of development, and where the temporal edge of the papilla is evident. eye. The anterior segment and intraocular
pressure does not tend to be affected by this
OD sections: +2.25 / OI: +2.00. Subjective consensual if we stimulate the other eye, disease.
examination gives OD: +1.00 / OI: +1.00. without anisocoria on. The contralateral eye
Ishihara test confirms that color vision is instead presents direct and consensual reflex.
normal in AO and the exploration of This is known as the vo relative afferent - posterior segment . For being a papilitis the
Funduscopic see that resolved the rise and pupillary defect (RAPD) or Marcus-Gunn optical disc is inflamed, characterized by
dad borrosi- papilla, while certain pallor pupil, and indicates the optical path pathology elevation and zándose borrosi- dad papillary
persists temporary dominance ( Fig. 6). pre geniculate. If there is no response to light edges. If it were retro- bulbar optic neuritis
but remains the consensual pupil speak appearance fundus would be within the
amauróti- ca. The RAPD is usually normal range.
proportional to the severity of the involvement
of NO 7.

DISCUSSION When the involvement is bilateral and if- The differential diagnosis of acute papillary
metric, there being no significant differences, visual loss with elevation in children should
Optometric examination 6 and logic we can not talk about DPAR, but we observe be established with the following entities:
ophthalmological will prove of great a slow, lazy pupi- lar response. Leber's disease, neuroretinitis, neoplastic
importance, not only as co method infiltration ca, toxic or nutritional neuropathy
diagnoses optic neuritis, but also to assess and papilledema 10.
its evolution through treatment efficacy. Four. color vision . Most axons carry no
informa- tion of the macular area and in it the
most abundant photoreceptors are cones.
Among the optometric examinations that we The duration of the inflammatory process, The Leber's optic neuropathy is a hereditary
perform, we highlight the following: color vision is altered with a clear eye optic neuropathy caused by a mutation of
discromatopsia affection, which in some mitochondrial DNA eleven. Forms affects
cases reaches not disappear completely. predominantly males and usually ma debut
1. Measurement of AV . Optical inflammation Involvement of color vision in optical between 15 and 35 years. It is characterized
causes a decrease in AV that can sometimes neuropathies follows the de- nominated by the appearance of a central visual
be severe. Köllner rule, according to which patients with painless loss of an eye, followed by a loss lar
primary disease predominate NO alterations the like in the contralateral eye with the
of the chromatic discrimination between course of the disease. With papillary
2. extrinsic motility . It is normal and in some red-green, while patients dEOS retinocoroi- elevation microangio- patía telangiectasia
cases may acompañar- of ocular pain. disorders show more often problems of often appears. None of the above
discrimination between blue and yellow characteristics occurred in our patient.
(there are exceptions to this rule as
3. pupillary reflexes . In a neutral unilateral glaucoma
optic ropatía the affected eye it shows a
decrease of direct pupillary reflex to light
stimulus, but maintaining response The neuroretinitis deposits associated
exudates at the posterior pole.

36 September 440 Gazette Optics


Scientific article

The most frequent cause paediatricians tría is


the cat-scratch disease produced by Bartonella
henselae 12. Other causes such as vi- rus,
borreliosis ( borrelia bugdorfe- ri) 13 or syphilis
(VDRL, FTA-abs.) 14 was- rum ruled out
serologically. The PPD was negative fifteen.

The neoplastic infiltration more frequent is


leukemia. NO is in- filtered in 13% of leu-
processes cémicos 16. In our patient's blood
test it was normal.

The Acute toxic neuropathy It is a bilateral


process with important discromatopsia,
scotoma cecal and history of exposure to
toxic Central. The most common are lead
poisoning or drugs. Our patient had no history
of exposure to any of these agents.

determined nutritional abnormalities tional 17 They


can cause neuropathies optical aunt. The
main causes are the deficits of vitamin B 1, B 6,

B 12 or folic acid. In our case no alteration


occurred tricional nu- state.

He papiledema 18 is the bilateral papillary


elevation edge fuzziness caused by
intracranial hyperten- sion. The pa- lifting
pillar is most evident in the upper and lower
poles of the disc, usually has no pulse of the
central retinal vein, hemorrhages peripapillary
and venous dilatation. The clinical picture
associated with headache, vomiting and
neurological symptoms 19.

Figure 4. central scotoma with progressive resolution lower altitudinal scotoma.

Treatment with corticosteroids is obtained in In our patient presented only a slight increase pediatric patients have not always easy to
most cases complete resolution of CUA- dro 2. Intó weight was normalized to remove the complete because of the difficulty to dif-
children should be controlled induction of medication. ferentiate acute or chronic processes to
systemic side effects (hirsutis- mo, weight define whether the disorder is congenital or
gain, insomnia, hypertension, full moon suffering PURCHASED Rido. Because of this
facies, etc.) and / or local level Ocular CONCLUSION exploration and resulting serology results as
(posterior subcapsular cataract, hypertension crucial not only to establish a good diagnosis
ocular, etc.). Infectious optic neuritis Infantiles useful is but to assess improvement after treat- ment.
one of the most frequent causes of visual
loss count neurological ori- gene.

In resistant cases, it may be required to Through anamnesis obtendre- mos important


immunosuppressants such as azathioprine. information for diagnosis, but In our case we set the final diagnosis by
elimination,

Gazette Optics September 440 37


Scientific article

as all required serology were negative and


clinical outcome was satisfactory.

It is common in op- tics in children neuropathies


most pa- sufficient concern bilateral involvement,
but this is not the case with our patient.

At the moment we choose not to prescribe bir


farsightedness, because you still shown patience
asymptomatic and this does not affect your
binocular vision.

BIBLIOGRAPHY

1. Vaphiades MS, Kline LB. Optic neuritis. Compr Ophthalmol Update 2007; 8

(2): 67-75; discussion 77-8.

2. Sanchez-Dalmau B. postvaccination and postinfectious disorders. Infectious

diseases. Crease J, Sanchez-Dalmau B. optical neuropathies: Diagnosis and

Treatment. Spanish Society of Ophthalmology, 2002. 9: 190-3.

3. Roussat B, P Gohier, Doummar D et al. Les neuropathies Optiques Aiguës

L'Enfant: Particularités Cliniques et thérapeutiques. À propos of 28 yeux 20

chez enfants. J Fr Ophthalmol 2001; 24: 36-44.

4. Chirapapisan N, Borchert MS. Optic neuritis Pediatric. J Med Assoc Thai

2008; 91 (3): 323-30.

5. Crease J, Sanchez-Dalmau B, C Roig, Rubio M. Protocols diagnostics optic

neuropathies. Crease J, Sanchez-Dalmau B. optical neuropathies: Diagnosis

and Treatment. Spanish Society of Ophthalmology, 2002; 14: 293-4.

6. Biarnés M, Marin J. Importance of detecting ischemic optic neuropathy.

Optical Gazette 2004; 382: 11-15.

7. Kardon R, Haupert C, Thompson HS. The Relationship Between static

perimetry and the relative afferent pupillary defect. Am J Ophthalmol 1993; 115: 351-6.

8. Hart WM. Color vision testing in Clinical Neuro-Ophthalmology. Tusa RJ,

Newman SA (eds.). Neuro-Ophthalmological disorders: diagnostic work-up and

management. New York: Marcel Dekker, 1995.

9. Harrington DO (ed.). The visual fields: a textbook and atlas of clinical

perimetry. 5th ed. St Louis: Mosby, 1981.

10. Llompart R. Findings and management anterior ischemic optic neuropathy

nonarteritic by nocturnal hypertension. Optical Gazette 2004; 387 11.

11. Ahmed E, Leber congenital amaurosis J. Loewenstein: disease, genetics

and therapy. Semin Ophthalmol 2008; 23 (1): 39-43.


Figure 5. Campimetry normalized at 25 days of development.
12. Suhler EB Lauer AK, Rosenbaum JT. Prevalence of serologic evidence of cat

scracht disease in Patients With neuroretinitis. Ophthalmology 2000; 107: 871-6.

13. Pfister HW, Wilske B, Weber K et al. Lyme borreliosis: basic science and

clinical aspects. Lancet 1994; 343: 1013-6.

14. Tramont EC. Treponema pallidum (syphilis). Mandell GL, Bennett JE, Dolin R

(eds). Principles and Practice of Infectious Diseases. 4th ed. New York:

Churchill Livingstone, 1996: p. 2117-33.

15. Stechschulte SU, Kim RY, Cunningham ET. Tuberculous neuroretinitis.

Neuroophthalmol J 1999; 19: 201-4.

16. Muñoz S, intraorbital Compression J. Prat. Crease J, Sánchez B. Optic

Neuropathies -Dalmau: Diagnosis and treatment. Spanish Society of

Ophthalmology, 2002; 11: 242, 253, 257.

17. Orssaud C, Roche O, Dufier JL. Nutritional neuropathies optic. J Neurol Sci

2007; 262 (1-2): 158-64.

18. Muñoz S, J Gascon, Reñé R, J. Crease Papilledema. Crease J,

Sanchez-Dalmau B optical neuropathies: Diagnosis and Treatment. Spanish

Society of Ophthalmology, 2002. 8: 157-171.

19. Shah M, Park HJ, Gohari AR, Bhatti MT. Loss of myelinated retinal nerve

fibers from chronic papilledema. J Neuroophthalmol 2008; 28 (3): 219-21.

Figure 6. After treatment has been resolved elevation and fuzziness of

the papilla, some pale predominantly temporal persist.

38 September 440 Gazette Optics

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