Download Acute postretinal blindness: ophthalmologic, neurologic

Veterinary Ophthalmology (2010) 13, 5, 307–314
Acute postretinal blindness: ophthalmologic, neurologic, and
magnetic resonance imaging findings in dogs and cats (seven cases)
Cristina Seruca,* Sergio Ródenas,† Marta Leiva,* Teresa Peña* and Sònia Añor‡
*ECVO, Servei d’Oftalmologia Veterinària, Departament de Medicina i Cirurgia Animals, Facultat de Veterinària, Universitat Autònoma de Barcelona,
Barcelona, Spain; †Southern Counties Veterinary Specialists LLP, Unit 6, Forest Corner Farm, Hangersley, Ringhood, Hampshire BH24 3JW, UK; and
‡Servei de Neurologia Veterinària, Departament de Medicina i Cirurgia Animals, Facultat de Veterinària, Universitat Autònoma de Barcelona, Barcelona,
Spain
Address communications to:
T. Peña
Tel.: +34 93 581 1387
Fax: +34 93 581 2006
e-mail: [email protected]
Abstract
Objective To describe the ophthalmologic, neurologic, and magnetic resonance
imaging (MRI) findings of seven animals with acute postretinal blindness as sole
neurologic deficit.
Methods Medical records were reviewed to identify dogs and cats with postretinal
blindness of acute presentation, that had a cranial MRI performed as part of the
diagnostic workup. Only animals lacking other neurologic signs at presentation were
included. Complete physical, ophthalmic, and neurologic examinations, routine
laboratory evaluations, thoracic radiographs, abdominal ultrasound,
electroretinography, and brain MRI were performed in all animals. Cerebrospinal
fluid analysis and postmortem histopathologic results were recorded when available.
Results Four dogs and three cats met the inclusion criteria. Lesions affecting the visual
pathways were observed on magnetic resonance (MR) images in six cases. Location,
extension, and MRI features were described. Neuroanatomic localization included:
olfactory region with involvement of the optic chiasm (n = 4), pituitary fossa with
involvement of the optic chiasm and optic tracts (n = 1), and optic nerves (n = 1). Of
all lesions detected, five were consistent with intracranial tumors (two meningiomas,
one pituitary tumor, two nasal tumors with intracranial extension), and one with
bilateral optic neuritis that was confirmed by cerebrospinal fluid analysis. Histologic
diagnosis was obtained in four cases and included one meningioma, one pituitary
carcinoma, one nasal osteosarcoma, and one nasal carcinoma.
Conclusions Central nervous system (CNS) disease should be considered in dogs and
cats with acute blindness, even when other neurologic deficits are absent. This study
emphasizes the relevance of MRI as a diagnostic tool for detection and
characterization of CNS lesions affecting the visual pathways.
Key Words: central nervous system, MRI, vision loss, visual pathways
INTRODUCTION
Blindness can be caused by bilateral lesions in four different
locations and by different mechanisms: lesions that produce
opacification of the clear ocular media, lesions that cause
failure of the retina to process the image, lesions that impede
transmission or relay of the message through the visual pathways, or lesions that cause failure of the final processing of
the image in the visual cortex.1,2
A systematic clinical approach should be performed in
cases of blindness. A thorough medical history and complete
Ó 2010 American College of Veterinary Ophthalmologists
physical and ophthalmic examinations are usually the first
steps. In addition, electroretinography (ERG) is frequently
used to assess retinal function. In cases of lack of significant
ocular lesions and normal ERG, blindness should be related
to a process located anywhere along the afferent visual pathway (postretinal blindness).1,2 Although routine diagnostic
procedures such as neurologic examination, routine laboratory examinations, and cerebrospinal fluid (CSF) analysis
can help to establish the most likely location and etiology of
CNS lesions in these cases, advanced imaging techniques are
necessary to confirm the exact location and reach a prompt
308 s e r u c a
ET AL.
presumptive diagnosis.1,2 In human beings, magnetic resonance imaging (MRI) is the current imaging modality of
choice for detection and characterization of most CNS
lesions affecting the visual pathways.3,4 However, little
information is available regarding MRI features of visual
pathway pathology in domestic animals.5–11
As a result of the intimate association of the visual
pathways with other intracranial structures, concurrent
neurologic deficits have been typically described in dogs and
cats with CNS lesions causing vision loss. To the best of our
knowledge, postretinal blindness as the only neurologic
deficit in domestic animals has been reported infrequently.9,12–15
The purpose of this study is to describe the ophthalmologic, neurologic and MRI findings of seven domestic animals (dogs and cats) with acute postretinal blindness as sole
neurologic deficit.
homogeneity, degree of contrast enhancement, presence of
mass effect, and miscellaneous features such as presence of
peritumoral edema, cyst formation, dilation of ventricles,
and presence of extracranial lesions.
Results of CSF analysis, serological tests, and polymerase
chain reaction (PCR) for several infectious diseases in blood
and CSF, and histopathologic studies were recorded when
available. CSF was collected from the cerebellomedullary
cistern. Total nucleated cell count (TNCC), total red blood
cell count (TRCC), differential nucleated cell count, and
total protein concentration were determined in all CSF samples. Histologic specimens were obtained postmortem, fixed
in 10% neutral-buffered formalin, embedded in paraffin,
sectioned at 5 lm, and stained with hematoxylin and eosin.
Histochemical and immunohistochemical stainings were
performed as dictated by the case. In these animals, presumptive and definitive diagnoses (histologically confirmed)
were correlated.
MATERIALS AND METHODS
Medical records from animals seen between January 2006
and December 2008 at the Veterinary Teaching Hospital of
the Autonomous University of Barcelona (VTH-UAB) were
reviewed. Dogs and cats with postretinal blindness of acute
presentation, and an MRI performed as part of the diagnostic workup were identified. Among these, only animals lacking other neurologic signs at the time of initial evaluation
were included in the study.
Each animal had complete physical, ophthalmic, and neurologic examinations. Ophthalmic examination included
assessment of the palpebral reflex, tests of vision (menace
response, cotton ball test, visual placement response, and
maze test), pupillary light and dazzle reflexes, Schirmer tear
test I, slit-lamp biomicroscopy, applanation tonometry, and
indirect ophthalmoscopy.
All animals had a complete blood cell count (CBC), complete serum biochemistry, urinalysis, thoracic radiographs,
abdominal ultrasound, short protocol ERG16, and cranial
MRI performed. MR images of the brain were obtained with
a 0.2 T permanent magnet (Esaote Vet-MRÒ unit, Esaote
Biomedica, Genova, Italy). The MRI protocol consisted of
sagittal, transverse and dorsal T2-weighted images (T2WI),
and precontrast and postcontrast T1-weighted images
(T1WI). Postcontrast T1WI were obtained immediately
after intravenous administration of gadolinium dimeglumine (DotaremÒ; Guerbet Sa, Madrid, Spain) at 0.2 mmol/
kg. Short tau inversion recovery (STIR) and fluid-attenuated
inversion recovery (FLAIR) images were obtained as
dictated by the case. The acquisition parameters were the
following: T1WI spin echo (SE), repetition time (TR) =
500 ms, and echo time (TE) = 20 ms; T2WI SE, TR/
TE = 2800/80 ms. Slice thickness ranged from 3 to 4 mm.
The following MRI characteristics were assessed: topographic location, axial origin (intra-axial, of nervous tissue
origin; extra-axial, originating in non-nervous tissue),
appearance (focal or multifocal), shape, signal intensity and
RESULTS
Seven animals (four dogs and three cats) of different breeds
and genders met the inclusion criteria (Table 1). The median age was 7.5 years for dogs (range 2–12 years) and
7.3 years for cats (range 3–10 years).
In all cases, the owners reported an acute onset of vision
deficiency with rapid progression to complete and permanent blindness. In no case, the initial vision deficiency was
related to scotopic/photopic conditions or to unfamiliar surroundings. Although blindness was the only sign reported in
all animals at presentation, two cases had a previous history
of systemic illness (Table 1; cat 1 and dog 5). Cat 1 had a
history of sneezing and nasal discharge of several months
duration that had improved with oral enrofloxacin (5 mg/kg
SID) and metronidazole (15 mg/kg BID). Dog 5 was
diagnosed with leishmaniasis 1 year prior to blindness onset
and was currently on treatment with allopurinol (10 mg/kg
BID PO). However, the patient was sero-negative to
Leishmania infantum at presentation for blindness. Apart
from these two patients, none of the other animals was
receiving any topical or systemic medication.
Physical examination was unremarkable in all animals
except for cat 3 (Table 1), that had upper respiratory noise
and reduced bilateral nostril airflow.
Complete blindness was confirmed in all patients by
ophthalmic examination. Anterior and posterior segment
evaluation failed to reveal any cause for the vision loss in 5/7
animals. In two patients (dogs 6 and 7), both optic nerve
heads appeared swollen, hyperemic, and edematous on
funduscopic examination. All animals had absent dazzle
reflex, complete or nearly complete afferent pupillary light
reflex deficits, and normal ERG (peak amplitude and latency
values for a and b waves within the reference range for our
laboratory). Based on the neuro-ophthalmic examination
and results of ERG, lesions were localized bilaterally in the
optic nerve, optic chiasm, or rostral part of the optic tracts.
Ó 2010 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 13, 307–314
DSH
Feline
Feline
Feline
Canine German
Shepherd
Canine Mixed
breed
Canine Mixed
breed
Canine French
Bulldog
1
2
3
4
5
6
7
Ó 2010 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 13, 307–314
2
8
12
8
10
9
3
Pituitary fossa
Nasal cavity with
intracranial
extension
M
M
M
Optic nerves
(intraorbital and
intracanalicular
part)
1st presentation:
unremarkable
2nd presentation:
Multifocal;
Gray matter and
subcortical white
matter of both
cerebral
hemispheres.
Olfactory region
(olfactory
peduncle)
Intra-axial
Extra-axial
Extra-axial
Extra-axial
Extra-axial
Extra-axial
Extra-axial
Signal intensity and
regularity
Irregular
–
Irregular
Regular
Irregular
Regular
ovoid
T1: Hypo/Isointense
T2: Hyperintense
T1: Isointense
T2: Iso/Hyperintense
Heterogeneous
T1: Isointense
T2: Hyperintense
Heterogeneous
T1: Isointense with
hypointense
area (cyst)
T2: Hyperintense
T1: Isointense
T2: Hyperintense/
Isointense
Heterogeneous
T1: Isointense
T2: Hyperintense
STIR: Hyperintense
Irregular/
T1: Isointense
Plaquelike T2: Iso/Hyperintense
Heterogeneous
Lesion localization Axial origen Shape
MN Nasal cavity with
intracranial
extension
M
Frontal lobe
FS
FS
Age
(year) Sex
Miscellaneous
features
–
No
Mild
peritumoral
edema
–
Mild
peritumoral
edema
Nonuniform
hyperintensity
within
both tympanic
bullae
Mild
Mild
peritumoral
edema
Marked Marked
peritumoral
edema
Marked Cystic
No
Mass
effect
Mild
No
Heterogeneous
Moderate
Homogeneous
Marked
Homogeneous
Marked
Homogeneous
Marked
Homogeneous
Mild
Homogeneous
Moderate
Homogeneous
Contrast
uptake
FS = spayed female; MN = neutered male; M = intact male; DSH = Domestic Shorthair; MRI = magnetic resonance imaging.
Persian
DSH
Breed
Patient Specie
Table 1. Signalment, MRI features, presumptive diagnosis, and histophatologic diagnosis in seven patients with acute postretinal blindness
Meningioma
Not performed
Nasal
osteosarcoma
Multifocal
Not performed
brain
disease
(presumptive
GME/EME)
Optic neuritis Not performed
(presumptive
GME)
Meningioma
Meningioma
Nasal tumor
Pituitary
carcinoma
Nasal carcinoma
Nasal tumor
Pituitary
tumor
Histopathologic
diagnosis
Presumptive
diagnosis
acute postretinal blindness 309
310 s e r u c a
ET AL.
Complete neurologic examination at the time of initial
evaluation failed to reveal any other neurologic deficits in all
cases.
The results of CBC, serum biochemistry profile, and urinalysis were within reference ranges in all animals, with the
exception of two cats, that had a moderate increase in serum
protein concentration. Cat 1 had a monoclonal gammopathy
(a2 globulin 2.11 g/dL, reference range [ref.] 0.4–0.9 g/dL),
and cat 3 had a polyclonal gammopathy (a2 globulin 2.70 g/
dL; b globulin 2.67 g/dL, ref. 0.9–1.9 g/dL). Negative
enzyme-linked immunosorbent assay results for feline
immunodeficiency and feline leukemia virus were obtained
in all cats. Thoracic radiographs and abdominal ultrasound
were unremarkable in all cases.
The clinically suspected lesions affecting the visual pathways were confirmed by MRI in 6/7 cases. The MRI study
of dog 7 was unremarkable at first, but showed multifocal
brain lesions not affecting the visual pathways at a second
presentation 2 years later. The MRI characteristics of the
different lesions are summarized in Table 1. The median
time from onset of blindness to performance of the first
MRI study was 1.3 days (range 0.5–3 days). Neuroanatomic
localization of the lesions included: frontal/olfactory lobe
region with involvement of the optic chiasm (4/7), pituitary
fossa with involvement of the optic chiasm and optic tracts
(1/7), optic nerves (1/7), and cortical gray matter and subcortical white matter of both cerebral hemispheres (1/7). Of
all these lesions, five were consistent with intracranial
tumors (two meningiomas, one pituitary tumor, and two
nasal tumors with intracranial extension), one with acute
bilateral optic neuritis, and one with multifocal brain
disease.
The two presumptive meningiomas were located on the
base of the skull, one affecting the frontal lobe (Fig. 1), and
the other the olfactory peduncle (dogs 4 and 5, respectively).
Involvement of the optic chiasm was observed in both of
them.
Two cats (cats 1 and 3) had irregular masses that originated in the nasal cavity and extended to the rostral brain,
affecting the optic chiasm (Fig. 2), and one cat (cat 2) had a
pituitary mass involving the optic chiasm and optic tracts
(Fig. 3).
Of the two dogs with optic nerve head inflammation on
funduscopic examination, only dog 6 had evident lesions
affecting the visual pathways in the MRI study. In this case, a
hyperintense signal in the intraorbital portion of both optic
nerves was observed on T2WI and STIR images. After
contrast administration, both optic nerves enhanced moderately, but homogeneously (Fig. 4). These findings were
suggestive of acute bilateral optic neuritis.
Cerebrospinal fluid analysis was performed in five animals, and was unremarkable in two. One cat with a pituitary
tumor (cat 2) had albuminocytologic dissociation (mild
increase in protein concentration [44 mg/dL; ref. <25 mg/
dL] with normal TNCC), and one dog with optic neuritis
(dog 6) had an elevated TNCC (24 TNCC/lL; ref.
(a)
(b)
(c)
Figure 1. Magnetic resonance (MR) images of a dog with a presumptive meningioma at the base of the skull involving the optic chiasm (dog
4). There is marked mass effect with deviation of midline structures
from left to right. The tumor (arrows) has an isointense, homogeneous
signal on transverse T1WI (a), and shows marked homogeneous
contrast enhancement on the tranverse (b) and sagittal (c) postcontrast
T1WI (arrows). Note a hypointense, well delineated structure
suggesting a cyst dorsal to the tumor (arrowheads).
<5 TNCC/lL), which consisted of a predominantly
lymphocytic population, and a mild increase in protein
concentration (43.2 mg/dL). In this dog, results for realtime PCR and reverse transcriptase PCR (RT-PCR) tests in
blood and CSF for canine distemper virus, Toxoplasma gondii,
Neospora caninum, and Ehrlichia canis, were negative. On the
basis of these findings, a presumptive diagnosis of the ocular
form of granulomatous meningoencephalitis (GME) was
made. CSF analysis of dog 7 at the second presentation
Ó 2010 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 13, 307–314
acute postretinal blindness 311
(a)
(a)
(b)
(b)
(c)
(c)
Figure 2. Magnetic resonance (MR) images of a cat with a nasal
carcinoma extending into the cranial cavity (cat 1). The lesion is
isointense and ill defined on transverse T1WI (a). The transverse
postcontrast T1WI (b) shows a contrast-enhancing mass at the level of
the optic chiasm (arrows). The sagittal postcontrast TIWI (c) shows an
irregular, contrast-enhancing mass originating in the nasal cavity and
extending to the rostral brain through the cribriform plate in a
plaque-like grow pattern (arrows).
revealed an elevated TNCC (39 TNCC/lL), consisting of a
predominantly eosinophilic cell population and a mild
increased in protein concentration (45.5 mg/dL). A serum
latex agglutination test for Cryptococcus neoformans, and realtime PCR and RT-PCR tests in blood and CSF for canine
distemper virus, Toxoplasma gondii, Neospora caninum and
Ehrlichia canis were performed with negative results. A fecal
flotation and a Baermann test performed to rule out
intestinal parasitic diseases were also negative. Differential
diagnoses at this time were idiopathic eosinophilic meningoencephalitis (EME) or GME.
In dog 7, although the results of MRI and CSF analysis
were unremarkable at first presentation, bilateral optic
neuritis was considered based on ophthalmic examination.
Figure 3. Magnetic resonance (MR) transverse images at the level of
the optic chiasm in a cat with a pituitary carcinoma (cat 2). The lesion
is isointense and ill defined on T1WI (a). Postcontrast T1WI (b) shows
a homogeneous, contrast-enhancing mass in the pituitary fossa (arrow).
The lesion (arrow) is hyperintense and heterogeneous on T2WI (c).
Mild peritumoral edema is present.
Serologic tests for Ehrlichia canis, Leishmania infantum, and
Toxoplasma gondii were performed by the referring veterinarian with negative results. Empiric treatment with prednisone
(1 mg/kg BID PO) was prescribed and visual improvement
was observed. Two years later, the dog re-presented for a
new episode of acute blindness. Ophthalmic examination
Ó 2010 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 13, 307–314
312 s e r u c a
ET AL.
(a)
(b)
Figure 4. Magnetic resonance (MR) transverse
images at the level of the frontoparietal lobe in a dog
with bilateral acute optic neuritis (dog 6). Part of the
intraorbital portion of both optic nerves is seen on
the T1WI (a) (arrows). The postcontrast T1WI (b)
shows mild contrast enhancement of both optic
nerves (arrows).
confirmed complete blindness and funduscopic evaluation
revealed moderate papillitis in both eyes. The results of
ERG were within the reference range. Complete neurologic
examination revealed this time behavioral abnormalities,
and signs of depression and disorientation.
Therapeutic options offered to patients with intracranial
tumors included surgical intervention (complete excision,
partial debulking or biopsy), radiation therapy, chemotherapy, and palliative therapy with glucocorticoids. Among
these patients, two cats were euthanized immediately after
diagnosis, and two dogs and one cat received palliative treatment with prednisone (0.5–1 mg/kg BID PO). Both dogs
with meningoencephalitis received immunosuppressive glucocorticoid therapy (1 mg/kg BID PO) for 2 months, with
subsequent tapering of the dose along time according to
clinical signs and results of CSF analysis.
A good response was observed in one case of meningoencephalitis (dog 7). At the time of publication, 3 years after
the first presentation, the dog had decreased vision in both
eyes and no other neurologic signs. The remaining four animals developed progressive neurologic signs with time. Of
these, three were euthanized and one died.
Definitive diagnoses were obtained by postmortem histopathologic examination in four cases (Table 1). Anatomic
location and diagnosis matched grossly with the ones performed during the animals’ life. Neoplasia was diagnosed in
all of them, and final diagnoses included one meningioma,
one pituitary carcinoma, one nasal osteosarcoma, and one
nasal carcinoma.
DISCUSSION
Vision loss with lack of significant ocular lesions and normal
ERG is indicative of a process located anywhere along the
afferent visual pathway (postretinal blindness). Although
routine diagnostic procedures, such as neurologic examination, routine laboratory evaluations, and CSF analysis might
be of help establishing the most likely localization and etiology of CNS lesions, advanced imaging techniques are necessary to confirm the exact location and achieve a presumptive
diagnosis.1,2 MRI is the diagnostic imaging modality of
choice in human medicine for most CNS diseases affecting
the visual pathways. MRI provides superior resolution of
retrobulbar and intracranial visual pathway lesions compared
to computed tomography (CT), and enables a focused examination of the entire visual pathway along its course, from the
inner aperture of the optic canal to the occipital lobe.3,4 Several reports describe the findings on standard and advanced
MRI images of diseases affecting the globe and visual pathways in humans, such as neoplasms, inflammatory/infectious
conditions, vascular, congenital and degenerative disorders.
Based upon their location, shape, invasiveness, signal intensity and homogeneity, and enhancement properties, it has
often been possible to predict the etiology or malignancy of
certain CNS lesions that cause visual deficits or complete
blindness as primary clinical sign.3,4,17–24 In the veterinary
literature, little information is available regarding the MRI
features of visual pathway lesions.5–11
In this study, lesions affecting the visual pathways were
confirmed at presentation by MRI in six of the seven
reported patients. In all of them, MRI enabled an accurate
and detailed description of the morphology of the lesions.
Lesion localization and extension was in accordance with
the neuro-ophthalmic dysfunction in all animals, and with
the anatomopathological results in patients in which a postmortem study was performed. In all these cases, the MRI
features of the lesions allowed differentiation between
neoplastic and inflammatory disorders, and identified the
tumoral and inflammatory secondary effects.
Based on similarities with the MR images of previously
reported cases,3,9,25–28 two masses involving the optic chiasm were considered meningiomas, and one of them was histopathologically confirmed. These tumors have been
previously described as extra-axial lesions, isointense on
T1WI and hyperintense or isointense on T2WI, which
enhance markedly and homogeneously after contrast administration. Mass effect is usually present and edema varies
widely from absent to extensive.29 A previous report of an
intracranial meningioma causing blindness as sole neurologic deficit was described in a cat.9 The tumor was located
in the rostral thalamus and extended to compress the optic
nerves and chiasm. MRI findings in this cat were similar to
the ones of the two cases here described.
The imaging findings of the pituitary tumor in this report
were similar to those described in cats and dogs by others.26,27,29 These tumors usually present as focal masses in
Ó 2010 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 13, 307–314
acute postretinal blindness 313
the region of the pituitary gland, they are isointense on
T1WI, and can present variable intensities on T2WI. Peritumoral edema is commonly absent to moderate. Contrast
enhancement ranges from minimal to strong, but it is usually
uniform, although heterogeneous enhancement can be
found in some cases.
Even though neuro-ophthalmic signs are frequently seen
in human beings with pituitary tumors, they are rare in animals.30–32 This difference has been attributed to the fact that
the pituitary stalk of domestic animals is directed caudoventrally rather than rostroventrally, as in human beings.30
According to previous studies, cats with pituitary tumors
had a significantly higher incidence of visual deficits than
dogs (35.7% and <10%, respectively).33,34 Individual differences in the orientation of the pituitary neoplasm or subtle
individual differences in hypothalamic/optic chiasm proximity have been proposed to explain the involvement of the
visual pathways in animals with pituitary tumors,14 and may
explain the visual deficits in the cat of this report.
The two nasal tumors of this report were irregular masses
that invaded the rostral brain lobes. They originated in the
caudal part of the nasal cavity, crossed the ethmoidal turbinates, and penetrated the cranial cavity, eventually reaching
the optic chiasm. The signal intensity and contrast uptake of
these tumors were similar to those previously described in
cats and dogs.27,35–37 The fact that blindness was the only
neurologic abnormality in these two cases is in contrast with
the neurologic findings commonly reported in small animals
with tumors of the nasal cavity that invade the brain.37,38
Although blindness as sole neurologic deficit was previously
reported in a dog with a nasal tumor,5,14 to the author’s
knowledge, these are the first reports of blindness as the only
neurologic sign in cats with nasal tumors and intracranial
extension.
Two cases of bilateral optic neuritis were seen in association with meningoencephalitis. For both of them, the diagnosis of optic neuritis was based on funduscopic
examination findings. An MRI study of the brain was performed in each case to look for subclinical brain lesions, such
as those related to meningoencephalitis or neoplasia. Hyperintensity on T2WI and STIR sequences and moderate contrast enhancement of both optic nerves were the only
abnormalities detected in one case. These MRI changes
were considered consistent with acute inflammation of the
optic nerves. In veterinary medicine, little information is
available about the MRI features of optic nerve pathology.6,9–11 In human beings, a hyperintense signal of the optic
nerves on T2WI is a nonspecific sign, as several lesions such
edema, demyelination and axonal loss, as well as chronic
gliosis can cause similar changes. However, contrast
enhancement reflects breakdown of the blood-brain barrier,
and therefore characterizes acute inflammation.4,17 In addition, analysis of the CSF in this patient revealed a lymphocytic pleocytosis. Potential causative infectious diseases were
ruled out by determination of serum/CSF antibody titers or
by means of infectious DNA detection by PCR. Based on
negative results of all these tests, a presumptive diagnosis of
ocular GME was made.
The MRI study and CSF analysis of the second optic
neuritis case were unremarkable at first presentation. At that
time, inflammatory/infectious diseases were considered the
most likely cause of optic neuritis. Because further ancillary
tests were declined by the owners, a definitive diagnosis
could not be reached. However, based on the fact that the
animal regained vision after receiving systemic corticosteroids, an inflammatory etiology for the optic neuritis was suspected. When the dog re-presented 2 years later, MRI of the
brain revealed multifocal lesions unrelated to the visual
pathways. These findings were thought to be consistent with
a multifocal CNS inflammatory or neoplastic disease. CSF
analysis revealed an eosinophilic pleocytosis. Although the
cell population was typical of that seen in parasitic, protozoal, mycotic, and immune-mediated meningoencephalitis,
other infectious agents were also investigated. After ruling
out infectious diseases, the main differential diagnosis was
idiopathic EME or GME. In this case, even though the MRI
findings were not in accordance with the neuro-ophthalmic
dysfunction, the imaging findings and the additional ancillary tests provided essential information to reach a diagnosis.
Despite the fact that both presentations of optic neuritis
could be caused by the same disease at different stages, the
possibility of different diseases causing the same or similar
clinical signs at different times should be also taken into
account.
Central nervous system disease should be considered in
dogs and cats with acute blindness, even when no other neurologic deficits are present. This study emphasizes the relevance of MRI as a diagnostic tool for detection and
characterization of CNS lesions involving the visual pathways. MRI provided essential information to reach a definitive diagnosis, to treat and to give a prognosis in seven
animals with acute postretinal blindness.
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