Unlike shingles, which usually manifests as a sensory neuropathy, RHS is distinguished by motor neuropathy.7 The patient usually reports weakness in the facial muscles on one side, leading to difficulty drinking water or puffing out the cheek and to drooling on one side of the face. A complaint of dryness in the ipsilateral eye may result from weakness or an inability to close the eyelid.
It is important to note that as in Bell’s palsy, RHS can be differentiated from stroke by the patient’s inability to wrinkle the forehead. The motor muscles of the forehead are innervated by both sides of the brain; in the case of stroke, only one side of the brain is affected, and movement of the forehead remains possible on the contralateral side. In facial nerve palsy, the nerve itself is affected; thus, no movement of the forehead is possible.13 Other common complaints in patients with facial nerve palsy include vertigo, hearing loss, and changes in facial sensation.
RHS was first described in 1907 as herpes zoster associated with Bell’s palsy by the neurologist J. Ramsay Hunt, for whom the condition is named.9,14 RHS is more common in men than women. It occurs most commonly in adults and is rare in children younger than 6.13,15
Diagnosis
In most cases, a diagnosis of RHS is made on a clinical basis.1 However, a polymerase chain reaction (PCR) assay can be performed on samples of tear fluid or submandibular saliva to detect the zoster virus.16,17 PCR can also be performed using exudates from the geniculate zone of the ear (a small area in the center of the auricle6,14), which is more sensitive than tears or blood.18,19 Findings from a complete blood count and the erythrocyte sedimentation rate can be used to differentiate between infectious and inflammatory causes.13
Head CT or MRI can be obtained to rule out any structural lesions. In one study, Kim et al20 examined MRI changes in patients with either Bell’s palsy or RHS. In both conditions, researchers were able to identify swelling of the labyrinthine segment of the facial nerve on temporal MRI scans.20 Although CT has not been shown to have any prognostic or diagnostic application, it can occasionally be used if decompression of the facial nerve is warranted.11
Treatment
Data used to support the use of corticosteroids for treatment of Bell’s palsy10,21,22 have been extrapolated to justify their use for treatment of RHS,23 and prednisolone is the most common choice.10 Steroids reduce the associated inflammation, resulting in decreased pain and neurologic symptoms. A daily dose for one to two weeks, followed by a slow taper, is the preferred prescribing method.10
The addition of acyclovir has been recommended to inhibit viral DNA replication9,23 (valacyclovir and famciclovir have also been mentioned12,18). If started within three days of symptom onset, acyclovir can help reduce pain and hasten resolution of symptoms.
In a large retrospective study, it was demonstrated that patients treated with prednisone at 1.0 mg/kg/d for five days, followed by a 10-day taper, combined with acyclovir, showed long-term improvement that was statistically significant.23 Complete facial recovery was reported in only 52% of patients, however. Risk factors for a poor prognosis include hypertension, diabetes mellitus, and advancing age.7
Artificial tears are also prescribed to keep the affected eye from becoming irritated and dry. The patient can be instructed to tape the eye closed at night.10
Early diagnosis and treatment (ie, within three days of symptom onset, and preferably with a combination of acyclovir and steroids23) is an important factor in a good prognosis.7,23 Because RHS-affected patients have only about a 50% chance of full recovery,23 proper follow-up care is extremely important. Follow-up visits are recommended at two weeks, six weeks, and three months.13 For optimal outcomes in patients with this neurologic diagnosis, referral to a neurologist is recommended for ongoing management. This practitioner is likely to detect subtle changes in patient presentation and can perform follow-up testing as needed.
THE CASE PATIENT
One week after the patient’s visit to the ED, he was contacted by hospital staff for a standard satisfaction and quality control survey. The patient (who had been treated with steroids and acyclovir, ibuprofen, and artificial tears) reported almost complete resolution of his pain; any mild pain, he said, was easily tolerated or could be resolved with OTC medication. He reported only minimal persistent facial weakness, stating that he was able to eat, drink, and speak normally.
The patient had not been seen by any health care provider for follow-up, but he agreed to make an appointment as soon as possible.