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ESPAÑOLA DE OFTALMOLOGÍA

www.elsevier.es/oftalmologia

Short communication

Anisocoria as initial manifestation of multiple

sclerosis. Use of 3 tesla magnetic resonance
imaging夽

A. Cerveró a,∗ , A. López-de-Eguileta a , Á. Cano-Abascal b ,

M.J. Sedano-Tous b , M. Drake-Pérez c , A. Casado a
a Departamento de Oftalmología, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Instituto de Investigación
Marqués de Valdecilla (IDIVAL), Santander, Spain
b Departamento de Neurología, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Instituto de Investigación

Marqués de Valdecilla (IDIVAL), Santander, Spain

c Departamento de Radiología, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Instituto de Investigación

Marqués de Valdecilla (IDIVAL), Santander, Spain

a r t i c l e i n f o a b s t r a c t

Article history: A 21-year-old woman seen in this clinic with non-reactive mydriasis in the right eye that
Received 25 November 2019 contracted with 1% pilocarpine. Cranial angio-CT and 1.5 T magnetic resonance imaging
Accepted 3 January 2020 (MRI) did not detect any disease. Given a subsequent limitation of adduction, supraduction,
Available online xxx and infarction of the right eye, a 3 T MRI was requested. This showed a lesion of the mid-
brain at the exit of the 3rd cranial nerve. After improvement, no new episodes were observed
Keywords: until 18 months later, when the patient presented with probable optic neuritis and systemic
Anisocoria symptoms. At this time the 1.5 T MRI detected infratentorial and supratentorial demyeli-
Third cranial nerve nating plaques. A subsequent lumbar puncture and clinic outcome confirmed the diagnosis
Multiple sclerosis of relapsing-remitting multiple sclerosis.
© 2020 Sociedad Española de Oftalmologı́a. Published by Elsevier España, S.L.U. All rights
reserved.

Anisocoria como manifestación inicial de esclerosis múltiple. Utilidad de

la resonancia magnética nuclear de 3 teslas

r e s u m e n

Palabras clave: Mujer de 21 años que presenta midriasis arreactiva en ojo derecho que contrae con el test
Anisocoria de pilocarpina al 1%. La angio-TC craneal y la resonancia magnética nuclear (RMN) de 1,5

夽
Please cite this article as: Cerveró A, López-de-Eguileta A, Cano-Abascal Á, Sedano-Tous MJ, Drake-Pérez M, Casado A. Anisocoria
como manifestación inicial de esclerosis múltiple. Utilidad de la resonancia magnética nuclear de 3 teslas. Arch Soc Esp Oftalmol. 2020.
https://doi.org/10.1016/j.oftal.2020.01.012
∗
Corresponding author.
E-mail address: casadorojo@hotmail.es (A. Cerveró).
2173-5794/© 2020 Sociedad Española de Oftalmologı́a. Published by Elsevier España, S.L.U. All rights reserved.

OFTALE-1631; No. of Pages 4

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Tercer par craneal T no detectaron anomalías. Ante una posterior limitación de la aducción, supraducción e
Esclerosis múltiple infraducción de dicho ojo, se solicitó una RMN de 3 T, que evidenció una lesión del mes-
encéfalo en la salida del tercer par craneal. Tras mejoría, no tuvo nuevos episodios hasta 18
meses después, cuando acudió con una probable neuritis óptica y síntomas sistémicos. En
este momento la RMN de 1,5 T detectó placas desmielinizantes infratentoriales y supraten-
toriales. La punción lumbar posterior y la evolución clínica confirmaron el diagnóstico de
esclerosis múltiple recurrente-remitente.
© 2020 Sociedad Española de Oftalmologı́a. Publicado por Elsevier España, S.L.U. Todos
los derechos reservados.

tration and tumor etiologies. Lumbar puncture and analytical

Introduction
Multiple sclerosis is a chronic disease of the central nervous
system caused by self-immune demyelinization that pro-
duces the loss of neurological functions. It is characterized by
inflammatory attacks against myelin and progressive axonal
degeneration that in time produces disseminated lesions.1
Multiple sclerosis gives rise to multiple signs. A case of multi-
ple sclerosis is presented having the first clinic expression of
anisocoria and subsequently 3rd cranial nerve pair paresis.
Clinic case report
Female, 21, without relevant personal antecedents, who vis-
ited the Emergency Dept. due to blurred vision in the right eye
(RE) with evolution of 48 h and anisocoria in the past 24 h.
Examination evidenced anisocoria in photopic conditions
in RE at the expense of areactive midriasis (Fig. 1A) without
relative afferent pupil defect and slight palpebral ptosis. The
patient did not refer previous traumatism or pharmacologi-
cal dilatation. Visual acuity was 20/20 (Snellen) in both eyes,
and ocular motility and ocular fundus examinations were
normal. Optical coherence tomography examination, which
included the retina nerve fiber layer (RNFL), macula and gan-
glion cell layer, did not show alterations. The pilocarpine test
was conducted without identifying pupil constriction 30 min
after administering 0.125% pilocarpine. However, miosis was
observed in the RE after the administration of 1% pilocarpine
(Fig. 1B). No other anomalies were observed in the neurologi-
cal examination. With the presumptive diagnostic of 3rd right
side cranial pair neuropathy with possible compressive eti-
ology, the patient was admitted and a cranial angio-CT and
nuclear magnetic resonance (NMR) were requested to identify
compressive vascular alterations without success.
After being in the hospital 72 h, the patient exhibited
ipsolateral upper eyelid ptosis with associated adduction,
supraduction and infraduction limitation in the RE (Fig. 1C).
These findings reinforced the hypotheses of right side cra-
nial pair compromise and accordingly a 3 T NMR with the
FIESTA sequence (fast imaging employing steady-state acquisition)
was requested. The NMR showed enhancement of midbrain
close to the right interpeduncular fossa corresponding to
the area of exit of the 3rd cranial pair, as well as incipient
compromise in the areas of entry of both trigeminal nerves
(Fig. 2A). Aneurysm was discarded as well as infectious, infil-
studies, including serology, autoantibodies and oligoclonal
bands in the cerebrospinal fluid produced normal results.
The visual field was also studied without showing any alter-
ation.
The patient was diagnosed with right side 3rd cranial pair
inflammatory neuropathy of unspecified origin. Three boluses
of intravenous methylprednisolone (1 g) were administered,
observing progressive improvement of symptoms, persistence
of diplopia in supra- and levoversion as well as of left eye
adduction limitation. Follow-ups by Ophthalmology and Neu-
rology did not evidence changes. Two months later, diplopia
was nonexistent for which reason botulinum toxin injection in
the left lateral rectus muscle was discarded. Six months later
an additional NMR was taken without finding changes.
After remaining 18 months asymptomatic, the patient
returned to the Emergency Dept. with diminished visual acu-
ity in the RE (best corrected visual acuity of 20/28 Snellen)
associated to slight pain during ocular movement in said
eye and dyschromatopsia. In addition, she referred hyposte-
sia feelings in the lower left limb and trunk in the past 2
weeks, associated to self-limited episodes of bilateral hemi-
facial hypoesthesia. Ocular fundus examination was normal
and optical coherence tomography did not reveal damages in
the RNFL or in the ganglion cell layer. Neurological exami-
nation showed preserved sensitivity in face and upper limbs,
slight hypopalestesia (diminished vibration sensitivity) in the
right lower limb and right trunk, as well as slight hyperalgesia
in the left lower limb and right trunk up to T4 level. Strength
was preserved in the 4 limbs, reflexes were normal, no dys-
metry could be observed and gait was normal.
The patient was diagnosed with retrobulbar optic neu-
ropathy and sensory alterations suggesting myelitis. A new
cranial-spinal 1.5 T NMR was taken which showed over 20
infra- and supra-tentorial demyelinizing plates, as well as
in the cervical and dorsal spinal column. Several of these
showed enhancement after contrast administration. In addi-
tion, the NMR showed compromise of the right optic nerve,
3rd right side cranial pair and bilateral 5th cranial pair (Fig. 2B).
Lumbar puncture showed the presence of 12 leukocytes and
oligoclonal bands. Visual evoked potentials and electroretino-
gram produced normal results as well as analytics, including
immunological profile and proteingram.
The diagnostic was recurrent-remitting multiple sclerosis.
Treatment was initiated with 5 boluses of methylpred-
nisolone (1 g intravenous) with improvement of symptoms.
Subsequently, maintenance treatment was established with
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Fig. 1 – ocular expressions. A) Anisocoria in photopic conditions. B) Constriction of RE pupil after administrating 1%
pilocarpine. C) right eyelid ptosis and RE limitation of adduction, supraduction and infraduction.

Fig. 2 – cerebral lesion shown in magnetic resonance. A) 3 tesla magnetic resonance with FIESTA sequence evidencing the
presence of enhancement in the anterior medial region of the right cerebral peduncle adjacent to the exit of the ipsilateral
3rd cranial pair (arrow). B) Cranio-medullary magnetic resonance with demyelinizing plates (supratentorial, infratentorial
and in the right medulla).
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fingolimod. No new symptoms of multiple sclerosis were
observed in 20 months follow-up.
Discussion
Multiple sclerosis is regarded as a simulating disease because
it can present with different clinical expressions, including
alteration of motor and sensory functions and visual, cognitive
and mental disorders. As regards ophthalmological diseases,
optic neuritis is the most frequent ocular expression. Other
ocular findings include ocular motility dysfunction due to
nystagmus, internuclear ophthalmoplegia and cranial nerve
palsy, particularly the 6th and 4th cranial pairs.2,3 Paresis of
the 3rd cranial pair as a sign of MS presentation is infrequent.
Overall, 8 articles documented 3rd cranial pair paresis as onset
of MS.4–8 In the majority of cases, compromise was unilat-
eral and though the literature also describes associations with
bilateral optic nerve compromise and internuclear ophthal-
moplegia. In 3 of said cases, 3rd cranial nerve compromise
was associated to pupil compromise.
In the present case, the first expression of multiple sclero-
sis was isolated anisocoria. In such a scenario it was difficult
to suspect demyelinizing etiology, even more so with normal
RNFL values. In some occasions, patients with multiple scle-
rosis without neuritis episodes can exhibit RNFL alterations.9
When the patient developed complete palsy of the 3rd cranial
pair, 3 T NMR was requested and this enabled the identifica-
tion of the inflammation plates in the fascicle of said cranial
pair.
A tesla (T) is a magnetic induction unit equivalent to 20,000
times the magnetic field of the Earth. NMR resolution is mea-
sured according to the teslas they exhibit. Lower resolution
NMR have 0.2 T and are still being used because it enables open
measurements. The NMR devices being used in usual clini-
cal practice have 1.5 T. The 3 T equipment is not so frequent
although it offers faster time, greater comfort, improved qual-
ity in diffusion techniques as well as improved contrast. Even
less frequently, some 7 T equipment are already in the mar-
ket, as well as 9.4 T NMR which has already been approved
after testing in humans. In the present case, we requested the
FIESTA sequence in the 3 T NMR (also available for 1.5 T NMR)
because it enables the visualization of cranial nerves at the
base of the skull and the differentiation of tumoral injuries
from inflammatory and demyelinization lesions.
Accordingly, it could be concluded that in the presence of
areactive midriasis that responds to the 1% pilocarpine test it
is essential to discard compressive courses such as aneurysm
(generally in the posterior communicating artery) by means
of angio-TC, NMR and arteriography.10 However it should be
noted that 3 T NMR with the FIESTA sequence enables the
observer to discard small lesions in the nucleus or the intra-
midbrain tract of the 3rd cranial nerve.
Conflict of interests
No conflict of interests was declared by the authors.
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