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 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.
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