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CASE REPORT
Complete Ophthalmoplegia With Pupillary Involvement
as an Initial Clinical Presentation of Herpes Zoster Ophthalmicus
Tayson DeLengocky, DO
Christina M. Bui, MD
Complete oculomotor nerve palsy with pupillary involvement is a neuro-ophthalmologic emergency because it is
commonly caused by a compressive aneurysm at the junction
of the posterior communicating artery and the internal carotid
artery. If left untreated, this condition can be potentially
fatal within days. The present report describes a 45-yearold African American woman with human immunodeficiency virus who presented with complaint of new-onset
nonspecific headache, acute onset of complete oculomotor
nerve palsy, and a dilated pupil of the right eye. Results of
standard work-up for aneurysm and other etiologic factors
were negative. Ten days after presentation, papulovesicular
eruptions occurred over the V1 and V2 dermatomes,
revealing herpes zoster ophthalmicus. The present case may
be the first to identify a patient with complete ophthalmoplegia with pupil involvement as a pre-eruptive manifestation of herpes zoster. The literature on epidemiology, pathogenesis, clinical presentation, diagnosis, and current
treatment options for this rare form of shingles are reviewed.
J Am Osteopath Assoc. 2008;108:615-621
H
erpes zoster ophthalmicus is a rare form of shingles
that typically presents with prodromal symptoms followed by rash distribution along the V1 or V2 dermatomes.
Complete ophthalmoplegia associated with herpes zoster
ophthalmicus—either by the oculomotor, trochlear, or
abducens nerves—is even rarer.1 Only 16 incidents of complete ophthalmoplegia caused by this condition have been
reported in the medical literature.2 In those cases, complete
ophthalmoplegia was a late sequela of herpes zoster ophthalmicus and occurred approximately 2 months after the
onset of herpetic rash.2
In the current report, we describe a woman who presented to a medical center with a headache and ptosis of the
right eye and no skin lesions or rash. Physical examination
From South Texas Retina Consultants in Corpus Christi (Dr DeLengocky) and
private practice (Dr Bui) in McAllen, Tex.
E-mail: [email protected]
Submitted July 20, 2007; final revision received February 24, 2008; accepted
March 7, 2008.
DeLengocky and Bui • Case Report
and laboratory test results for aneurysm and other conditions were negative. However, 10 days after presentation, a
rash consistent with herpes zoster ophthalmicus occurred. The
available information on this condition—epidemiology,
pathogenesis, clinical presentation, diagnosis, and treatment
options—is reviewed.
Report of Case
A 45-year-old African American woman with human immunodeficiency virus (HIV) was admitted to the internal medicine
service at Interfaith Medical Center in Brooklyn, NY. She presented with new-onset headache on the right side and complete
ptosis of the right eye, for which the ophthalmology service was
consulted.
The patient’s medical history was significant for HIV
infection with a recent CD4 cell count of 8. She had chronic
anemia, schizophrenia, and herpes zoster, and she had Whipple
procedure for pancreatic cancer. She completed a review of systems and denied blurry vision, diplopia, eye pain, neck pain,
fever, and paresthesia. Family, social, and surgical history
were noncontributory. The patient had no known medication
allergies. Her medications and dietary supplements included
epoetin alfa, azithromycin, sulfamethoxazole and trimethoprim, omeprazole, olanzapine, fluconazole, and iron, multivitamins, and folic acid.
Physical examination at the bedside revealed that the
patient was alert and properly oriented (ie, to person, place, and
time). She was in no acute distress. Her blood pressure was
100/63 mm Hg; pulse, 80 beats per minute; respiration,
20 breaths per minute; and body temperature, 98⬚F.
On further examination, she had complete ptosis of the
right eye (OD) with normal periorbital and facial skin appearance (Figure 1). No rash was present, and the left eye (OS)
appeared normal. The patient had uncorrected near visual
acuity (20/200 OD, 20/100 OS). The pupils were anisocoric and
unequally reactive to light. In dim light, the pupils were 6 mm
OD and 4 mm OS. In bright light, they were 5.5 mm OD and
2 mm OS. The reaction of the pupil OD was sluggish, whereas
the pupil OS was brisk. There was no relative afferent pupillary reaction. Extraocular motility OD revealed absence of
adduction, infraduction, and supraduction. Extraocular motility
OS was full. Confrontational visual field appeared full in both
eyes. Globes were equally soft by palpation. Anterior and posterior segments were normal. The irises in both eyes were
JAOA • Vol 108 • No 10 • October 2008 • 615
CASE REPORT
A
B
C
D
E
normal. There were no cotton-wool spots or retinal hemorrhages.
Meningitis was suspected because of the patient’s initial
complaint of headache and her immunodeficient status. Results
from a computed tomography scan without contrast of head and
orbits were normal. A lumbar puncture was performed, and
analysis of cerebral spinal fluid (CSF) revealed clear fluid, no red
blood cells, no white blood cells, normal glucose level
(61 mg/dL), and normal gram stain and culture. Further tests
for opportunistic infections were done, but results from polymerase chain reaction (PCR) of CSF for tuberculosis, cryptococcus, cytomegalovirus, and venereal disease were all negative.
Blood cultures and direct antiglobulin were also normal. The
complete blood cell count was nonspecific for infections, and the
comprehensive metabolic profile was normal (Figure 2). However, her laboratory results revealed substantial hyponatremia.
616 • JAOA • Vol 108 • No 10 • October 2008
Figure 1. Clinical presentation of a 45-year-old African American
woman with human immunodeficiency virus who presented to a
medical center with complaint of new-onset headache on the right
side. The patient had (A) ptosis of the right eye, and (B) the right pupil
was dilated. The right eye (C) was noted to be slightly down and
out in primary gaze (exotropia and hypotropia), which is consistent
with the oculomotor palsy of the right eye. Further examination (D)
revealed absence of supraduction the right eye, and (E) full function of the right eye lateral rectus muscle and thus intact function of
the abducens nerve.
Because of the patient’s complete oculomotor nerve palsy
with pupillary involvement, further neuroimaging was
required to rule out a compressive lesion. Magnetic resonance
imaging of the brain with and without gadolinium dye were
normal (Figure 3). Because there was no obvious compressive lesion, a magnetic resonance angiography of the brain was
ordered and showed a 50% diameter reduction in the distal
right and left middle cerebral arteries (Figure 4). However,
no aneurysms were found. An internal right carotid cerebral
angiogram (Figure 5) showed a normal right internal carotid
artery, left vertebral artery, and basilar artery—the branches
of which were without demonstrable aneurysm, extravasations
of contrast, or mass affecting the arteries. Specifically, there was
no evidence of a posterior communicating artery aneurysm.
About 10 days after the initial presentation, papulovesicular rashes broke out over the right V1 and V2 dermatomes
(Figure 6). In light of the absence of compressive lesions,
aneurysm, lymphoma, cardiovascular risk factors, and
demyelinating process, the complete oculomotor nerve palsy
with dilated pupil was likely caused by herpes zoster. With this
classic clinical presentation of herpes zoster, intravenous acyclovir was recommended to the patient. She refused this treatment, so oral valacyclovir (1000 mg twice daily) was administered instead. The patient was observed for 2 additional
days before discharge to an outside assisted-living psychiatric facility.
Although the patient was lost to follow-up, her prognosis for recovery from the complete ophthalmoplegia as a
result of herpes zoster ophthalmicus is good. Research has
shown that improvement from complete ophthalmoplegia
following herpes zoster ophthalmicus can be seen within
2 months.2 Complete to near resolution generally occurs
within 18 months.2
Discussion
Herpes zoster (shingles) results from the reactivation of dormant varicella zoster (chicken pox) mostly in thoracic and
cranial sensory ganglia. This condition affects approximately
1 million people in the United States annually and causes significant morbidity.2-5 About 15% to 25% of all cases of herpes
zoster involve the trigeminal nerve, also known as herpes
DeLengocky and Bui • Case Report
CASE REPORT
䡲 Complete Blood Cell Count
▫ White blood cell count, 7400/␮L
▫ Hemoglobin, 12.3 g/dL
▫ Hematocrit, 37%
▫ Platelets, 82 ⫻ 109/L
▫ Neutrophils-segmented, 84.5%
▫ Neutrophils-band, ⬍10%
▫ Lymphocytes, 7.1%
▫ Monocytes, 8.2%
▫ Eosinophils, 0.1%
▫ Basophils, 0.1 %
䡲 Comprehensive Metabolic Profile
▫ Sodium, 133.2 mmol/L
▫ Potassium, 3.78 mmol/L
▫ Chloride, 102.5 mmol/L
▫ Bicarbonate, 26.3 mmol/L
▫ Blood urea nitrogen, 8 mg/dL
▫ Creatinine, 0.7 mg/dL
▫ Glucose, 101 mg/dL
▫ Calcium, 8.7 mg/dL
thermore, patients with HIV are 15 to 25 times more likely to
have herpes zoster.2-5
Pathogenesis
The varicella zoster virus is a double-stranded DNA virus
that causes two distinct clinical entities: primary varicella and
herpes zoster. Varicella zoster virus is transmitted via airborne
and direct contact.
During primary varicella infection, the virus invades the
cutaneous ends of sensory nerves and causes acute febrile
exanthamous illness. It then migrates to the dorsal root ganglia
of the spinal column and cranial nerve ganglia, where it
becomes latent. It typically remains dormant for decades unless
the immune system is compromised.6
Reactivation of the virus has been linked to patients with
cell-mediated immunity. The decline of varicella antibodies
occurs naturally in aging and can be induced by immunosuppressive conditions caused by illness or medication.
The reactivated virus in a sensory ganglion causes inflammation of the neuronal axons and results in shingles of the associated dermatome. Sensory nerves of the thoracic dermatomes
are most commonly affected, followed by cranial nerves.
Varicella zoster infection is more severe in patients who
▫ Aspartate aminotransferase, 51 U/L
▫ Alanine aminotransferase, 30 U/L
▫ Alkaline phosphate, 159 U/L
▫ Total bilirubin, 0.5 mg/dL
▫ Total protein, 6.4 g/dL
▫ Albumin, 2.5 g/dL
▫ Globulin, 3.9 g/dL
▫ Prothrombin time, 11.2 sec
▫ International normalized ratio, 0.83
Figure 2. Laboratory results for a 45-year-old African American woman
with human immunodeficiency virus presenting with ptosis and complaint of headache on the right side.
zoster ophthalmicus, of which 11% to 29% of patients present
with ophthalmoplegia.2-5
Epidemiology
About 99% of adults with a history of chicken pox and up to
90% of those without have serology that is positive for varicella
zoster.2-5 Age and immunoincomptence are the main risk factors. The lifetime risk of herpes zoster is estimated to be 10%
to 20%, though patients older than 85 years have an incidence
rate of 50%.2-5 Patients with immunodeficient conditions such
as HIV or AIDS, cancer, or autoimmune diseases show greater
prevalence of herpes zoster than the general population. FurDeLengocky and Bui • Case Report
Figure 3. Axial view of the brain and orbits as shown in a magnetic
resonance imaging scan without gadolinium contrast of a 45-year-old
African American woman with human immunodeficiency virus. The
patient presented with new-onset headache and ptosis of the right
eye. The scan did not reveal any obvious compressive lesion, which was
suspected to be the cause of the patient’s oculomotor nerve palsy.
JAOA • Vol 108 • No 10 • October 2008 • 617
CASE REPORT
Figure 4. Magnetic resonance angiography of the brain of a 45-yearold African American woman with human immunodeficiency virus
who presented with new-onset headache and ptosis of the right
eye. The image revealed a reduction in the distal right and left middle
cerebral arteries but no aneurysm.
are immunosuppressed, elderly, pregnant, or neonates. The
virus can cause a wide spectrum of disorders, including typical herpes zoster, recurrent herpes zoster, chronic disseminated herpes zoster, and visceral dissemination.
Several mechanisms of ophthalmoplegia as described in
the present report have been postulated:
▫ oculomotor nerve involvement caused by inflammation of the
trigeminal nerve spreading to the cavernous sinus or the
superior orbital suture7
▫ microinfarction of cranial nerves from occlusive vasculitis;
suggests the presence of chronic inflammatory cells infiltrating the long posterior ciliary vessels and nerves8
▫ meningeal inflammation at certain locations of cranial pathways9
▫ as described in autopsies, the pattern of onset and rate of
recovery point to a demyelinating process10,11
Figure 5. Right internal carotid angiogram of a 45-year-old African
American woman with human immunodeficiency virus who presented with new-onset headache and ptosis of the right eye. The
carotid artery, left vertebral artery, basilar artery, and its branches were
all normal with no evidence of aneurysm.
tophobia, or prickly or knife-like sensations in skin area of the
affected dermatome. These sensory changes are believed to be
the result of nerve fiber degeneration and usually precede
skin eruptions from a few hours to 1 week.
The acute stage is characterized by skin eruptions. The rash
progresses from erythematous macules to clusters of papules
and clear vesicles within 24 hours. It then evolves into pustules
within 1 week. These pustules will rupture and crust by day 10.
However, the lesions heal within 4 weeks, leaving hyper- or
hypopigmented scarring.
Figure 6. A rash consistent
with herpes zoster ophthalmicus occurred 10 days
after the patient, a 45-yearold African American
woman, presented to a
medical center with headache and oculomotor palsy.
Clinical Presentation
Herpes zoster usually evolves in three distinct stages: prodromal, acute, and chronic.4,5,12-15 Some patients may present
with overlapping stages.
In the prodromal stage, the patient may experience flu-like
symptoms, dysethesia, burning, itching, tingling, boring, pho618 • JAOA • Vol 108 • No 10 • October 2008
DeLengocky and Bui • Case Report
CASE REPORT
The chronic stage is most commonly manifested by postherpetic neuralgia (PHN) after the skin manifestations have
resolved. This condition occurs in 9% to 34% of all zoster
patients, though it affects 50% to 75% of elderly patients with
herpes zoster.16,17 It is the third most common cause of neuropathic pain after low back pain and diabetic neuropathy18
and has been described as constant deep pain, recurrent
shooting pain, and allodynia.16 It typically resolves within
2 months in 50% of patients and within 1 year in 70% to 80%
of patients.2
Herpes zoster ophthalmicus involves the ophthalmic division of the trigeminal nerve (Figure 7). The ophthalmic branch
is subdivided into frontal, nasosciliary, and lacrimal branches.
As the nasociliary branch innervates the globe and nose, a
lesion at the tip of the nose, commonly referred to as
Hutchinson’s sign, is a good clinical indicator of possible ocular
involvement. However, one-third of patients with ocular
involvement do not have Hutchinson’s sign.13
In herpes zoster ophthalmicus, numerous ocular structures5,19 can be involved:
䡲 Eyelids—Resolution of skin and adnexal inflammation can
leave cicatricial lagophthalmos.
䡲 Conjunctiva—Chemosis and circumcorneal injection usually
resolve within 1 week.
䡲 Episclera and Sclera—Inflammation causes localized dilation
of deep vessels and associated pain.
䡲 Cornea—Inflammation causes pseudodendrites and
decreases corneal sensitivity. Varicella DNA can still be
detected up to 34 days after rash onset.2
䡲 Anterior chamber reaction—Uveitis occurs in response to
viral antigens in the iris and ciliary body and is usually associated with increased intraocular pressure and sectoral iris
atrophy.2 Secondary glaucoma can be caused by inflammation of the uvea and the trabecular meshwork.
䡲 Cranial nerve—Palsy or paresis can be caused by one of the
mechanisms previously discussed.
䡲 Optic nerve—Neuritis may cause permanent visual loss.
䡲 Retina—Aggressive posterior inflammation can lead to acute
retinal necrosis or progressive outer retinal necrosis, which
have guarded visual prognosis.3,4,12,13,20-22
While herpes zoster ophthalmicus is generally a localized condition, systemic involvement is more serious. Severely
immunocompromised patients have a 40% risk of visceral
dissemination, which can affect the liver, lungs, and brain.13
Diagnosis
Myriad clinical conditions mimic the prodromal sensations
of herpes zoster ophthalmicus: trigeminal neuralgia, maxillary sinusitis, myocardial pain, and atypical facial pain.6 Also,
acneiform eruptions, candidiasis, cellulitis, contact dermatitis,
erysipelas, folliculitis, insect bites, lichen striatus, varicella,
and herpes simplex may mimic the skin lesions.23 The key
factor in the differential diagnosis of herpes zoster is that it
affects a specific dermatome.
With the recognition of the common signs and symptoms, herpes zoster can be easily recognized and accurately
diagnosed. Atypical presentations and other disseminated
forms require diagnostic work-up to prevent potentially life-
Supratrochlear n.
Supraorbital n.
Infratroclear n.
Ophthalmic area
Maxillary Area
Lacrimal n.
External nasal
branch n.
Mandibular Area
Figure 7. Illustration of branches of the ophthalmic nerve, one of three divisions of the trigeminal nerve, and dermatomal distribution. Up to 25%
of patients with herpes zoster have herpes zoster ophthalmicus, which is a type of herpes zoster that involves the trigeminal nerve.
DeLengocky and Bui • Case Report
JAOA • Vol 108 • No 10 • October 2008 • 619
CASE REPORT
threatening complications. Because varicella virus is labile,
viral culture has a low yield. Tzanck test, direct fluorescence
assay, and PCR are more capable of detecting the virus in
fluid and tissues.3,24 Furthermore, direct fluorescence assay
and PCR are more specific and sensitive and allow differentiation of herpes simplex from herpes zoster.
Treatment Options
The goal of therapy is to limit the severity of acute and chronic
pain, hasten the healing process, and reduce the chances of dissemination. Antiviral therapies in the form of acyclovir, valacyclovir hydrochloride, and famciclovir are approved by the
US Food and Drug Administration for the management of
herpes zoster, as follows:
▫ acyclovir, 800 mg orally five times daily for 7 to 10 days25
▫ famciclovir, 500 mg orally three times daily for 7 days26
▫ valacyclovir, 1000 mg orally three times daily for 7 days27
Antiviral therapy is substantially more effective if begun within
the first 72 hours of rash onset.25-27 It induces prompt resolution of skin lesions, diminishes viral shedding, lessens lesion
formation, and decreases corneal and uveal involvement. All
three medications are generally safe but may require dosage
adjustment for patients with renal insufficiency.25-27
The efficacy of antiviral therapy for PHN is still inconclusive. However, famciclovir and valcyclovir have proven
therapeutically equal or better than acyclovir in alleviating
symptoms. Generally, patients with PHN require treatment
during the acute phase of herpes zoster with antivirals or tricyclic antidepressants. These medications can significantly
reduce the incidence, severity, and duration of PHN.
Desipramine hydrochloride and nortriptyline hydrochloride
are the most commonly recommended tricyclic antidepressants for PHN.2-4,12,13,17,20,21 However, a full discussion of the
medical treatment of PHN is beyond the scope of the present
report.
A live attenuated herpes zoster vaccine for individuals
older than 60 years has recently been approved by the US
Food and Drug Administration.28 This vaccine has been shown
to reduce substantially the incidence of herpes zoster by 51.3%
and the occurrence of PHN by 66.5%.29,30 in addition to management of herpes zoster elsewhere in the body, specific ophthalmic care is warranted because herpes zoster ophthalmicus
can affect different layers and components of the eye:17,23
䡲 Skin, lashes, and conjunctiva—A cool and wet compress
and cleansing of the skin lesions followed by topical antibiotics (eg, neomycin, bacitracin, polymixin B) should be
applied to protect the ocular surface from keratitis and conjunctivitis. Systemic steroids can be added to control significant edema and pain while oral antivirals are used. Reducing
the soft tissue edema within the orbit helps prevent orbital
apex syndrome, which can cause catastrophic consequences
620 • JAOA • Vol 108 • No 10 • October 2008
as the second, third, fourth, sixth, and ophthalmic division
of the trigeminal nerves pass through the optic foramen and
superior orbital fissure at the apex of the orbit.
䡲 Cornea, sclera, and iris—Topical steroids (eg, 0.125%-1%
prednisolone) may be used between two and six times daily
under the care of an ophthalmologist for the treatment of
patients with keratitis, episcleritis, scleritis, or iritis. In addition, mydriatics and cycloplegics, such as cyclopentalate 1%
or homatropine 5% can be added for ocular pain and photophobia control. However, topical antivirals have proven
ineffective.
䡲 Optic disk—Prostaglandin inhibitors and pilocarpine are
contraindicated in managing secondary glaucoma caused
by herpes zoster because prostaglandin inhibitors induce
inflammation and pilocarpine may promote synechiae. Therefore, ␤-blockers, ␣-adrenergics, and carbonic anhydrase
inhibitors are the medications of choice.
䡲 Retina—Acute retinal necrosis requires intravenous acyclovir, foscarnet sodium, or both. Additional uses of oral
famicilovir or valacyclovir accompanied by systemic steroids
and anticoagulants have been used successfully to reduce
intraocular inflammation, vasculopathy, and neuropathy.
The suggested antiviral regimen for acute retinal necrosis
is 10 to 15 mg per kilogram of body weight twice a day for
2 weeks, followed by 1 g twice a day for 4 to 6 weeks.
Laser photocoagulation is also used to prevent retinal
detachment from retinal necrosis. Progressive outer retinal
necrosis requires the same treatment regimen recommended
for acute retinal necrosis. However, an intravitreal injection
of ganciclovir sodium and laser photocoagulation may also
be required to limit retinal damage.21
Conclusion
The present case is very unusual in that a 45-year-old woman’s
complete isolated unilateral oculomotor nerve palsy was a
pre-eruptive stage of herpes zoster ophthalmicus. The common
differential diagnoses for isolated oculomotor nerve palsies
involving the pupil include a posterior communicating artery
aneurysm; compressive lesion; ischemic microvascular disease, which is associated with diabetes mellitus and hypertension; tumor; or trauma. Uncal herniation, cavernous sinus
mass lesions, orbital lesions, herpes zoster, and leukemia are
less common causes. Onset of a oculomotor nerve palsy with
pupil involvement, especially associated with pain, warrants
magnetic resonance imaging, which produces high resolution images and can detect lesions smaller than 1 mm.31,32
However, because this imaging technique does not always
detect small aneurysms, further testing may be needed if there
is high clinical suspicion. Cerebral angiogram is still the “gold
standard” for aneurysm testing.
The recovery prognosis from external ophthalmoplegia of
the patient in the present report is good. Improvement from
complete ophthalmoplegia following herpes zoster can be
seen within 2 months, with complete to near resolution within
DeLengocky and Bui • Case Report
CASE REPORT
18 months.2 The patient’s sudden onset of oculomotor nerve
palsy with pupillary involvement 10 days before the cutaneous eruptions suggests herpes zoster as the etiologic cause
in the present case with an initial sign of pupil-involving oculomotor palsy. Oculomotor nerve ophthalmoplegia is a very
rare complication of herpes zoster ophthalmicus. In 16 reported
cases, ophthalmoplegia developed 2 months after herpes zoster
rash occurred.2
The case described in the present report may be the first
to identify a complete oculomotor nerve ophthalmoplegia
with pupil involvement as a pre-eruptive manifestation of
herpes zoster. Primary care physicians and neurologists must
be cognizant of the initial signs and symptoms of herpes zoster
ophthalmicus and refer these patients to an ophthalmologist
when ocular involvement is suspected.
Acknowledgment
We thank Vincent N. Tran, BS, graphic designer at Digital Canvas,
Inc, for the trigeminal dermatome graphic.
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