(Stroke. 1996;27:996-1001.)
© 1996 American Heart Association, Inc.
Neurological Manifestations of Acute Posterior Multifocal Placoid Pigment Epitheliopathy
Sinan Çomu, MD;
Thierry Verstraeten, MD;
Jeffrey S. Rinkoff, MD
Neil A. Busis, MD
From the Division of Child Neurology (S.Ç.) and Departments of
Ophthalmology (J.S.R.) and Neurology (N.A.B.), University of Pittsburgh School
of Medicine, and Retina Service (T.V.), Allegheny General Hospital,
Pittsburgh, Pa.
Correspondence to Sinan Çomu, MD, Children's Hospital of Pittsburgh, Division of Child Neurology, 3705 Fifth Ave, Pittsburgh, PA 15213-2583.
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Abstract
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Background Acute posterior multifocal placoid pigment
epitheliopathy
(APMPPE) is a chorioretinal disease that causes acute
visual
symptoms with characteristic fundus findings. Although this
entity
has been associated with a variety of neurological
complications,
it has received little attention in the neurological
literature.
We wanted to emphasize the spectrum of neurological
involvement,
in particular the occurrence and management of strokes in
patients
with APMPPE.
Case Descriptions We report three patients with APMPPE and
neurological disease. All three presented with marked visual
disturbances and headaches. One patient developed recurrent
strokes involving different vascular territories of the brain and
required immunosuppressive treatment for presumed cerebral vasculitis.
The other two patients had cerebrospinal fluid pleocytosis and
persistent headaches but recovered spontaneously. The review of the
literature demonstrates a particular pattern of neurological
complications in a subgroup of patients with APMPPE.
Conclusions APMPPE should be considered among the causes of
stroke and aseptic meningitis in young adults. The diagnosis is
critically dependent on a thorough ophthalmologic examination. Severe
neurological complications are difficult to predict at the onset of the
ophthalmologic disease. The patients should be monitored closely. If
investigations suggest cerebral vasculitis, immunosuppressive treatment
may be helpful to prevent recurrences.
Key Words: cerebral infarction meningitis ocular disease vasculitis vision disorders
 |
Introduction
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Acute posterior
multifocal placoid pigment epitheliopathy is
a chorioretinal disease
typically occurring in young adults
who present with binocular
visual blurring, metamorphopsia,
or scotomas.
1 2
Funduscopically, there are multiple circumscribed,
gray-white, flat
lesions at the level of the retinal pigment
epithelium (Fig 1

). The clinical course is self-limited with
return
of visual function over weeks to months. A third of these
patients have
a flulike illness at the onset. Systemic manifestations
are rare;
however, severe neurological involvement can cause
strokes and sudden
death (Table 1

).

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Figure 1. Color photograph of the left fundus at the time of
presentation. Note normal optic disk and yellow multifocal
patchy lesions.
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We report three patients with APMPPE and neurological complications who
were admitted to our neurology service since 1989. Although all three
presented similarly, only one developed strokes. On the basis
of the cumulative data from the reported cases, we suggest a strategy
for the workup and management.
 |
Case Reports
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Patient 1
A 23-year-old woman developed severe headaches and bilaterally
decreased
vision in May 1993. Initial ophthalmologic evaluation
revealed
visual acuity of 20/400 OD, 8/200 OS, and multiple creamy
yellow
patches involving the retinal pigment epithelium in both
posterior
poles (Figs 1

and 2

). Her past medical history
was significant
for poor dentition with loss of all permanent teeth at
an early
age. She had Native American ancestry on her paternal side.
There
were no other systemic findings, and an initial MRI of the brain
was
normal. The patient started treatment of 40 mg prednisone daily
for
presumed Vogt Koyanagi Harada disease. Subsequently, there
was some
subjective visual improvement, but her headaches persisted
intermittently.
Three weeks after her initial symptoms, while still
taking steroids,
she abruptly developed a severe headache followed by
unresponsiveness
and right-sided weakness. On admission, she was
stuporous with
dense right hemiplegia. Ophthalmologic examination at
this stage
revealed early pigmentation of the subretinal lesions in
both
eyes. CSF analysis showed 60x10
6 WBC/L
(90% lymphocytes), 20x10
6 RBC/L, protein of 0.45
g/L, and glucose of 3.2 mmol/L. Peripheral
WBC count was
22x10
9/L, and erythrocyte sedimentation rate was
30
mm/h. There were a few cellular casts in the initial urinalysis.
A
repeat MRI revealed bilateral parieto-occipital infarcts with
gyral
enhancement, left-sided basal ganglia signal changes with
an
enhancing putaminal lesion, and a nonenhancing lesion in
the splenium
of the corpus callosum. The occipital lesions later
underwent
hemorrhagic conversion (Fig 3A

through 3E). A cerebral
angiogram
was unremarkable, as was a chest radiograph and a
transthoracic
echocardiogram. APMPPE with associated
cerebral vasculitis was
diagnosed, and administration of
intravenous methylprednisolone,
250 mg QID, was started.
The patient improved gradually over
2 weeks. At discharge, she had
residual right hemianopsia, difficulty
in reading, and slight right
hemiparesis. Visual acuity had
improved to 20/40 OU, and mottled
pigmentation was present in
the posterior pole. Oral prednisone was
continued. Extensive
laboratory investigations (Table 2

)
did not reveal an etiology.
Serum adenovirus antibodies at the fourth
week of her illness
were positive at a titer of 1:128, but a single
measurement
could not prove an acute infection.

-Glutamyltransferase
and
alanine aminotransferase were initially slightly elevated at
176
U/L and 61 U/L, respectively. Human leukocyte antigen typing
was A11,
A26, B35, B44, Bw4, Bw6, Cw4, Cw5, DR14, DR15, DR52,
and DQ1.

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Figure 2. Top, Early frame of fluorescein
angiogram in the left eye. Note dark patchy lesions that block
background fluorescence. Bottom, Late frame of
fluorescein angiogram. Note intense staining of the lesions
described.
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Two months after the initial symptoms, the patient's visual acuity was
20/25 OU with pigment stippling in both maculae, and her right
hemianopsia had slightly improved. Shortly thereafter, she experienced
brief attacks of left arm and face dysesthesia. An electroencephalogram
was unremarkable. She received phenytoin for possible focal seizures.
The attacks continued but were somewhat less pronounced. A month later,
she had a right parietal stroke when her steroid tapering was at 40
mg/d (Fig 3F
). CSF revealed 32x106 WBC/L (90%
lymphocytes) and protein of 0.32 g/L. Cyclophosphamide (125 mg/d) was
added to her treatment. She again showed marked clinical improvement.
Prednisone was discontinued at 7 months because of side effects. Twelve
months after initial presentation, cyclophosphamide was
also discontinued. At 24-month follow-up, she was doing well
without medication.
Patient 2
A previously healthy 20-year-old man presented in
October 1989 complaining of 2 weeks of bilateral visual blurring, 1
week of black spots in the right eye, and 4 days of episodic right
retro-orbital headaches. His visual acuity was 20/200 OD and 1/200
OS. There were mild cellular infiltrates in the vitreous bilaterally
and multiple irregular-shaped placoid areas of pigment epithelial
graying in different stages of evolution, with the older lesions
displaying atrophic retinal pigment epithelium. Fluorescein
angiogram findings were diagnostic for APMPPE. Two weeks
later, his vision had decreased to 20/400 OU and his headaches had
intensified. Neurological examination was unremarkable. CSF
analysis showed 89x106 WBC/L (100%
mononuclear cells), 3x106 RBC/L, protein of 0.54
g/L, and glucose of 3 mmol/L. An unenhanced CT scan and a cerebral
angiogram were normal. Laboratory evaluation did not reveal an etiology
(Table 2
). Angiotensin-converting enzyme level was 143
U/L (normal, 44 to 125). The visual acuity improved spontaneously over
the next 3 months to a final level of 20/25 OD and 20/20 OS. Fundus
examination demonstrated areas of atrophy and hypertrophy
of the retinal pigment epithelium at the location of the previously
active lesions. His headaches also subsided without further
intervention.
Patient 3
A previously healthy 23-year-old man presented in
April 1989 with a 1-week history of severe headaches, difficulty in
focusing, and perception of black patches and white dots. The patient
also complained of slight fever, night sweats, chills, and nausea.
Ophthalmologic evaluation revealed a visual acuity of 20/50 OU,
multiple paracentral scotomas on Amsler grid visual-field testing,
mild inflammation in both anterior chambers with 1+ cells and flare,
and rare cells in the central vitreous of the left eye. Fundus
examination demonstrated multiple grayish-green placoid lesions at
the level of the retinal pigment epithelium, almost confluent in the
macula, with smaller scattered nonconfluent areas in the periphery.
Fluorescein angiogram findings further supported the
diagnosis of APMPPE. Two weeks later, his visual acuity was 20/60 OD
and 20/30 OS. Fundus examination showed pigment epithelial mottling in
the evolving lesions. Despite the improvement of his visual symptoms,
the headaches persisted. Neurological examination was unremarkable. A
cerebral angiogram and unenhanced CT scan were normal. CSF revealed
61x106 WBC/L (97% mononuclear cells),
17x106 RBC/L, protein of 0.46 g/L, and glucose of 3
mmol/L. The patient improved spontaneously without further
intervention. A brain MRI at the sixth week of the illness was
normal.
 |
Discussion
|
|---|
In 1968, Gass
1 reported three young women with
bilateral rapid
loss of central visual acuity secondary to multifocal
yellow-white
placoid lesions at the level of the pigment epithelium
and choroid
of the retina. Further reports revealed that this illness
affects
males and females equally, with striking preponderance for
young
adults.
2 Simultaneous onset in both eyes
is the rule; however,
involvement of the second eye can be delayed for
a few days
or even weeks. The lesions are mainly at the posterior pole
and
never anterior to the equator. The placoid lesions start to
fade
within a few days and by two weeks are replaced by areas
of partly
depigmented pigment epithelium with irregular pigment
clumping.
Fluorescein angiography demonstrates characteristic
hypofluorescent
lesions in the early phase of the angiogram followed by
late
hyperfluorescence of the same areas (Fig 2

, top and
bottom).
If the primary lesions do not involve the fovea, the prognosis
is
good, with nearly complete visual function returning over several
weeks.
Recurrences are infrequent and usually occur in the
first 6
months.
3 Occasionally, progressive disease can
lead to chorioretinal
atrophy and significant visual
loss.
4
Ocular histopathology of APMPPE is not available. The primary lesion
was originally considered to be at the pigment epithelium; however,
more recent evidence suggests that the lamina choriocapillaris is the
site mainly affected.5 Indocyanine green angiography
studies support choroidal hypoperfusion as a likely mechanism of injury
rather than primary pigment epitheliopathy.6 7 Choroidal
vasculitis has been proposed as the underlying pathological
process.8
The etiology of APMPPE is unknown. The frequent history of a preceding
flulike illness suggests a viral or parainfectious process. Isolated
cases were associated with adenovirus,9 Lyme
disease,10 11 systemic lupus
erythematosus,12 juvenile rheumatoid
arthritis,13 sarcoidosis,14
schistosomiasis,15 hepatitis B vaccination,16
thyroiditis,17 Crohn's disease,18 erythema
nodosum,19 and nephritis.20 HLA-B7 or DR2
antigens were reported in a group of patients21 and in two
familial occurrences.22 23 Despite lacking definite
associations, APMPPE appears to be a manifestation of various
infectious or autoimmune processes, analogous to aseptic
meningitis.
The differential diagnosis of the retinal findings include serpiginous
choroiditis, multiple evanescent white-dot syndrome, birdshot
chorioretinitis, acute retinal pigment epitheliitis, multifocal
choroiditis, and multifocal retinal metastasis.2 24
Certain systemic illnesses can involve both the brain and the eyes,
leading to the so-called uveoretinal-meningoencephalitis
syndromes. Specific entities include Vogt Koyanagi Harada disease,
sarcoidosis, Behçet's disease, systemic lupus
erythematosus, Crohn's disease, metastatic
malignancies, primary intraocular lymphoma, histoplasmosis,
toxoplasmosis, cytomegalovirus, and syphilis. Of these entities, Vogt
Koyanagi Harada disease is a primarily ophthalmologic disease that can
mimic APMPPE with initial funduscopic and angiographic
findings,25 and it has been suggested that these may
represent a continuum of a single disease.25
The common neurological complications of APMPPE are CSF
pleocytosis26 27 and headaches, which usually improve
spontaneously, as in two of our patients. However, some patients
develop transient hearing loss,28 optic
neuritis,3 meningoencephalitis,29 transient
focal deficits,26 and strokes30 31 32 33 due to
vasculitic changes.34 35 There are two reported cases of
death from large strokes.36 37 Of nine previously
described cases of strokes with APMPPE (Table 1
), five had angiographic
findings consistent with vasculitis. In one case, brain
histopathology revealed focal granulomatous inflammation of
medium-sized arteries.36 In another case, a muscle
biopsy was suggestive of vasculitis.33 In two previous
cases, angiography was normal, as in our first patient.
The pattern apparent from the reported patients with strokes is that
these are mostly young adults with evidence of inflammation in their
CSF. Cerebral vasculitis is the presumed mechanism of injury, although
angiographic evidence may be lacking. The onset of stroke is typically
concurrent with the ocular disease (in one case preceding it) or within
4 to 5 months. In one instance, meningoencephalitis29
developed 5 years after the onset of ocular disease. Infarcts involve
predominantly the posterior circulation and the basal ganglia. There
may be a biphasic course of the neurological illness,31
and the strokes can recur during the tapering of immunosuppressives.
This can be heralded by transient ischemic attacks, which may
have been the case in our first patient rather than the suspected focal
seizures.
APMPPE should be considered in young patients with unexplained strokes
or aseptic meningitis, particularly when associated with symptoms such
as scotomas or visual blurring. Although the diagnosis can be firmly
established with typical fundus and fluorescein angiography
findings, the lesions are difficult to identify with direct funduscopy.
Therefore, a thorough ophthalmologic evaluation is necessary in
suspected cases. Etiologic investigation for previously reported
associations may identify medically treatable cases and help with
prognostication. An initial brain MRI for patients without neurological
signs is not necessary. CSF analysis, MRI, and cerebral
angiogram should be undertaken if persistent headache, neck stiffness,
or transient ischemic attack is present. Meningeal biopsy
may be indicated if the workup is negative but the patient continues to
have ischemic attacks. Once cerebral vasculitis is diagnosed,
immunosuppressive treatment should be started. Although some patients
with cerebral vasculitis improved spontaneously, given the risk of
mortality and recurrent strokes, we advocate aggressive treatment.
Combination of steroids with cyclophosphamide or azathioprine is
reported to improve the outcome in primary cerebral
vasculitis.38 The immunosuppressive agents can be stopped
after 6 to 12 months, since there are no reported strokes after 5
months from the disease onset. It remains difficult to predict which
patients with CSF pleocytosis and headaches will evolve to have
strokes. We suggest that these patients be followed closely for
neurological deterioration rather than treated with low-dose
steroids.
 |
Selected Abbreviations and Acronyms
|
|---|
| APMPPE |
= |
acute posterior multifocal placoid pigment epitheliopathy |
| CSF |
= |
cerebrospinal fluid |
| OD |
= |
oculus dexter |
| OS |
= |
oculus sinister |
| OU |
= |
oculus unitas |
| RBC |
= |
red blood cell |
| WBC |
= |
white blood cell |
|
Received November 30, 1995;
revision received January 17, 1996;
accepted January 31, 1996.
 |
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