This article is more than 5 years old. Information may no longer be current.
Patient has drooping face, incoherent speech
Click Here to Manage Email Alerts
A 72-year-old white male was referred by his ophthalmologist to the eye clinic for consultation. He complained of right-sided facial and mouth “droop” and that he was unable to close his right eye. After further questioning, the patient reported that the onset was sudden and painless. The patient’s wife said she first noticed the problem 10 days prior.
The patient had been diagnosed previously by the referring ophthalmologist with normal tension glaucoma and nuclear sclerotic cataracts 5 years earlier. Our patient’s ocular medications included timolol 0.5% (one drop in both eyes in the morning) and travoprost 0.004% (one drop in both eyes in the evening). There was no history of previous eye injuries or eye surgeries. The family history was negative for any pertinent ocular conditions.
Six months before our exam, the patient was found on the floor of his home with no memory of how it happened. He was treated initially in the hospital with intravenous acyclovir for suspected herpes encephalitis. The medication was stopped after 2 days when his symptoms resolved. He was seen by a neurologist 3 months later and was diagnosed with Lewy body dementia (which is seen commonly with Parkinsonism) due to memory loss and white matter changes noted on a CT scan of his brain. He is being treated currently with carbidopa-levodopa for Parkinson’s disease. He is allergic to no medications and denied any other systemic diseases including hypertension, diabetes, thyroid problems or dyslipidemia.
Image of the patient when he was asked to shut his eyes tightly. Note the absence of a Bell’s phenomenon of the right eye.
Lack of frontalis constriction on the patient’s right side when he was asked to raise his eyebrows.
Lack of levator anguli oris action on the right side of the patient’s mouth when he was asked to smile.
Laxity of the right side of the patient’s face. Note the absence of the nasolabial fold and down turning of the mouth on the patient’s right side.
Images: Turpin S
Entering corrected acuities were 20/100– OD and 20/25 OS with no improvement on pinhole. Extraocular motilities were full for each eye. Pupils were dilated from the visit earlier in the day. Confrontation fields in the right eye showed restriction in all sectors except inferior temporally. A small nasal defect was observed in the left eye. However, the patient did not fully understand the test instructions, reducing the reliability.
The anterior segment exam revealed mild, diffuse injection of the bulbar conjunctiva and areas of superficial punctate keratitis covering the entire cornea of the right eye. There was a mild nuclear sclerotic cataract in the right eye. Findings were unremarkable in the left eye except for mild nuclear sclerosis. Intraocular pressures were 7 mm Hg OD and 9 mm Hg OS measured with the iCare tonometer (Diaton). Tear break-up time was 4 seconds in each eye, and the Schirmer’s-2 test was 8 mm in the right eye and 6 mm in the left. Corneal sensitivity was tested with a cotton swab and rated as very poor.
Fundus examination revealed glaucomatous-appearing optic nerves with 0.9 cup-to-disc ratios in each eye. The macula was flat and dry, and the peripheral retina was flat and intact 360° in each eye. During auxiliary cranial nerve testing, the patient was unable to wrinkle the right side of his forehead or smile with the right side of his mouth. There was blunting of the nasolacrimal fold on the right side as compared to the left side. Examination of the right ear canal for herpetic lesions to rule out herpes zoster oticus (Ramsay-Hunt syndrome) was unremarkable.
When the patient was asked to close his eyes, the right eye remained open and did not properly elevate, while the left closed normally. We rated his Bell’s phenomenon as poor. The patient had trouble understanding directions throughout the exam. His speech was incoherent at times, making subjective testing difficult. Much of his ocular and medical testimony was obtained from his wife.
What’s your diagnosis?
See answer on next page.
Our patient’s symptoms were characteristic for the diagnosis of Bell’s palsy, which is caused by a lower motor neuron lesion. Alternatively, a stroke on the contralateral side of the brain from an upper motor neuron lesion can present with similar symptoms. Ipsilateral facial droop and speech difficulty are common signs for both conditions.
Vision care providers should be familiar with eye and facial signs that may aid in differentiating between the two. It is not likely that eyelid closure and frontalis function (furrowing of the forehead) would be affected in a patient who had suffered a stroke. Patients with Bell’s palsy will have a complete unilateral facial palsy but will not present with any other neurological signs such as extremity paralysis or arm drift.
Incidence
The incidence of Bell’s palsy is 11.5 to 40.2 per 100,000 for the general population (De Diego, et al.). The incidence of stroke in the U.S. is 3.35 to 15.6 times more common than that of Bell’s palsy (McCullough, et al.). In addition to the overall frequency of strokes, the situation is much more urgent and requires treatment within the first 3 to 4 hours. According to the Centers for Disease Control and Prevention, 113,103 individuals die from strokes annually, making it the fifth leading cause of death in the U.S. The importance of making the correct diagnosis is underscored by the seriousness of potential outcomes.
The pathophysiology of Bell’s palsy involves inflammation of cranial nerve (CN) VII (facial nerve). The most commonly accepted cause is infection by the herpes simplex virus (HSV-1). It can lie dormant in the peripheral ganglion of various nerves, including CN VII. HSV-1 DNA has been identified in endoneural fluid samples of patients with Bell’s palsy. This supports the theory of viral correlation and possible causation.
Management
The discoveries of the inflammatory and viral nature of the condition led to treatment strategies combining both corticosteroids and antivirals. Administration of oral steroids within 72 hours of onset has been shown to significantly increase the rate of recovery (Vakharia, et al.). Antiviral monotherapy is not recommended, and the results of antiviral treatment in combination with steroids are mixed. We presented this information to our patient and his wife, explaining that treatment may not be as effective because the onset in this particular case was likely at least 10 days earlier. He and his wife elected to attempt combination therapy because of his previous history of possible herpes encephalitis. We prescribed oral acyclovir 400 mg twice daily and oral prednisone 10 mg twice daily, both for 1 week.
Next, we addressed his risk for corneal exposure. Those patients who proceed to develop corneal damage despite appropriate conservative therapy need surgery to reanimate their paralyzed eyelids. The most vulnerable patient is one who manifests the “BAD” syndrome — that is, lacks the Bell’s phenomenon and has corneal Anesthesia and Dry eye. This patient was unable to close the involved right eye and was not observed to blink a single time during the exam. His Bell’s phenomenon was reduced when he attempted to close his eyes. Our testing also confirmed that he had corneal anesthesia and dry eye, putting him at high risk for exposure keratitis.
One treatment strategy involves inducing ptosis with either botulinum toxin injections into the levator of the non-closing eyelid or implantation of an eyelid weight. This way, the eyelid could still be lifted manually to examine the cornea and to apply the patient’s glaucoma medications. Both options were presented, and the patient elected to defer receiving botulinum toxin injections.
We chose to apply three strips of 3M surgical tape to the upper lid after cleaning the skin with Tincture of Benzoin. This was enough to induce a partial ptosis in primary gaze and close the eye when the patient tried to shut his eyes and the levator relaxed. Gel drop tear supplements were prescribed every 2 hours, with preservative-free ointment for overnight coverage. Scleral contact lenses have also been used to protect the ocular surface in cases of Bell’s palsy; however, we did not believe our patient was a good candidate. The patient was informed that without treatment, 100% of patients partially recover in 3 to 5 months, and 70% of those patients completely recover.
Follow-up visits
The patient returned to the clinic 1 week later for follow-up. The tape on the upper portion of his right lid had fallen off, but he already had slight recovery of orbicularis oculi function. He was able to close the right lid to the midline of the cornea. His cornea did not stain with sodium fluorescein, and his vision improved to 20/50–. We explained to the patient that he should finish his oral steroid and antiviral treatment. We continued the gel drops every 2 hours with preservative-free ointment at night. Botulinum toxin injections were not indicated based on the improvement of the epithelial health of his right cornea. He was scheduled for a 1-week follow-up to assess muscle function and corneal integrity.
On the patient’s third visit (2 weeks after his initial evaluation), his condition had improved greatly. He and his wife reported that he completed the oral antiviral and steroid treatment as directed. The visual acuity in his right eye improved to 20/25+, and he had no new visual complaints. The confrontation visual fields for the patient’s right eye improved slightly, as well, although significant glaucoma-related constriction remained. His corneal epithelium was intact and did not stain with sodium fluorescein. He was able to shut both his eyes tightly and displayed no residual lagophthalmos. The right side of his mouth did not turn up completely when he was asked to smile, but the majority of the muscle function had returned. The patient explained that he was now able to drink milk without it running down the right side of his face.
The scheduled use of the lubricating gel drops and ointment was discontinued, and the patient was advised to use the artificial tears as needed. He was advised to return to his referring ophthalmologist for continued management of his glaucoma and cataract.
- References:
- De Diego JI, et al. Otolaryngol Head Neck Surg. 1999;doi:10.1016/S0194-5998(99)70418-3.
- McCullough LD, et al. Nat Rev Neurol. 2014;doi:10.1038/nrneurol.2014.103.
- Leading Causes of Death. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/nchs/fastats/leading-causes-of-death.htm. Published 2016. Accessed May 29, 2016.
- Murakami S, et al. Ann Intern Med. 1996;124(1):27-30.
- Vakharia K, et al. Facial Plast Surg Clin North Am. 2016;doi:10.1016/j.fsc.2015.08.001.
- May M, Galetta S. The Facial Nerve. In: Tasman W, Jaeger E, eds. Duane’s Clinical Ophthalmology. Volume 2. Philadelphia, PA: Lippincott Williams and Wilkins; 2013:1-37.
- Portelinha J, et al. Saudi J Ophthalmol. 2015;doi:10.1016/j.sjopt.2014.09.009.
- For more information:
- Steven Turpin, BS, plans to graduate from Pacific University College of Optometry in 2017. He can be reached at turp1327@pacificu.edu.
- Leonid Skorin Jr., OD, DO, MS, FAAO, FAOCO, practices at the Mayo Clinic Health System in Albert Lea, Minn., and is a member of the Primary Care Optometry News Editorial Board. He can be reached at skorin.leonid@mayo.edu.
- Edited by Leo P. Semes, OD, FAAO, a professor of optometry, University of Alabama at Birmingham and a member of the Primary Care Optometry News Editorial Board. He may be reached at lsemes@uab.edu.
Disclosures: The authors report no relevant financial disclosures.