Week 3, Spring 2008

Today, I saw client with an interesting case history and pattern of test results. Also, first and foremost, she was a very sweet lady.

The client had previously visited our clinic due to auditory fullness and ear pain related to middle ear infections approximately one year ago. She was advised to seek medical attention at that time.

At the current visit, the patient described medical conditions including hypertension and rheumatoid arthritis. Medications used to lower blood pressure and used to manage inflammation and pain, secondary to rheumatoid arthritis, were taken regularly. The patient also reported “a cotton ball feeling” in her left ear and intermittent high frequency tinnitus lasting less than one minute. Her tinnitus was described as alternating between her ears. Head trauma from a car accident occurred in the 1980s. CAT scan results following the accident were normal, according to the client’s account.

Two episodes of true vertigo were reported. The first episode was approximately five to ten years ago and lasted at least two hours. The patient fell unconscious for a few minutes at work and was hospitalized. No conditions seemed to initiate or worsen the attacks. Meclizine was prescribed by the patient’s physician in order to manage future attacks, if needed. The second episode was also five to ten years ago and occurred at home. The patient reported a sensation, which she characterized as “spinning in bed and moving down a tunnel,” that lasted for approximately four to five hours. When she was hospitalized for the second episode, her physician reported that her blood pressure was extremely elevated. Continued use of Meclizine during attacks was the recommended course of treatment at that time.

Recent bouts of shingles, within the past few years, were noted as well. The first outbreak occurred eight or nine years ago. Symptoms included sores on the thoracic region up to the left side of the neck and head, including a sore on the left ear. A vision specialist was consulted, at that time, due to concerns about viral attacks on the optic nerve. A hearing evaluation was completed by the client’s ENT specialist following episodes of shingles; however, the client was not able to remember the exact results of that evaluation.

Residual numbness along the jawline has not remitted since the onset of shingles outbreaks. The client is currently undergoing evaluation for subcutaneous growths of unknown pathology around the shoulders and neck on her left side and will soon have an MRI.

Otoscopy revealed a subcutaneous node behind the left ear. Normal ear canals and clear, intact tympanic membranes were observed bilaterally. A normal (Type As) tympanogram from the right ear and a normal (Type A) tympanogram from the left ear were observed. Acoustic reflexes were tested ipsilaterally and contralaterally at 500, 1000, and 2000 Hz bilaterally. Normal ARTs were found with right ipsilateral and left contralateral stimulation. Absent ARTs were observed with left ipsilateral and right contralateral stimulation. Stimulation beyond 105 dB HL was not attempted due to tolerance problems and reports of associated nausea. Reflex decay did not occur in the left ear at 1000 Hz with contralateral stimulation. Right contralateral reflex decay could not be tested due to absent ARTs.

Normal hearing sensitivity in the right ear was observed. A unilateral, mild sloping to moderately-severe, high-frequency sensorineural hearing loss was documented in the left ear, beginning at 4000 Hz. Asymmetry of 10-35 dB HL between ears was found at all test frequencies with the most pronounced difference, of 35 dB HL, occurring at 6000 Hz. Significant asymmetries, of greater than 10 dB HL, were observed from 4000 to 8000 Hz.

Speech recognition thresholds were normal and in good agreement with pure tone averages bilaterally. However, a pronounced difference, of 15 dB HL, in SRT was noticed between ears, with the right SRT at 10 dB HL and the left SRT at 25 dB HL. Word recognition scores were excellent bilaterally with no outstanding ear differences.

The client had normal hearing sensitivity in her right ear, and a mild to moderately-severe high-frequency sensorineural hearing loss in her left ear. Significant asymmetries, of greater than 10 dB HL, were observed from 4000 to 8000 Hz. Case history information, including multiple bouts of shingles and an immunocompromised system, is highly suggestive of viral etiology. A viral insult on the vestibular branch of the VIII nerve also is suspected due to complaints of true vertigo. Reports of left-sided facial numbness and absent acoustic reflex thresholds on the probe side, ipsilateral to the shingles-effected side, were consistent with potential VII nerve involvement.

Results were discussed with the client, and a release of medical information was signed. Following client contact with her primary care physician, findings from the hearing evaluation performed at our clinic will be faxed to the appropriate medical facilities. The client was strongly encouraged to request an ENT consultation during or following a previously-scheduled MRI, which was intended to evaluate the nodes on her shoulder. Following neurootologic evaluation by a physician, the client was asked to return to our clinic every six months for follow-up hearing evaluations. In addition, a formal vestibular evaluation may also be warranted. Lastly, the client was advised to consult an ENT specialist immediately if sudden changes in her sensory perception occurred.

Because I am not a medical doctor, I couldn't make a specific conjecture about the origin of the patient's symptoms in my report in or in my discussions with her. However, in my blog, I will!

I think that this patient has Ramsay Hunt Syndrome (RHS). Varicella-zoster virus (VZV) reactivation causes zoster lesions in the auricle or oropharyngeal epithelium, as well as facial paralysis (FP) in patients with Ramsay Hunt syndrome(RHS). RHS is frequently complicated by disorders of the auditory nerve, such as hearing loss, tinnitus, and vertigo.

This article, Varicella-Zoster Virus Load and Cochleovestibular Symptoms in
Ramsay Hunt Syndrome by Fumio Ohtani, MD; Yasushi Furuta, MD; Hiroshi Aizawa, MD; Satoshi Fukuda, MD, compared two sets of patients with RHS.

Twenty-nine patients exhibited acute facial paralysis (FP) along with cochleovestibular symptoms (CVSs) and were categorized as group 1. Twenty-four of these patients also had zoster lesions on the skin or the oropharyngeal epithelium, and the remaining 5 patients did not have zoster lesions. In group 2, comprised of 27patients, cochleovestibular symptoms were absent. Those 27 patients also had acute FP and zoster lesions on the skin or oropharyngeal epithelium.

The study aimed to examine the association between varicella-zoster virus (VZV)reactivation and the onset of CVCs. They performed this analysis by analyzing saliva and blood samples. Results were somewhat inconclusive, but they did make some conjectures based on their findings.

They suspected that CVSs in RHS might be caused not only by the spread of inflammation to the cochleovestibular system through VZV reactivation in the geniculate ganglion, but also by reactivation of VZV in the spiral and/or vestibular ganglia themselves.

Importantly, prompt monitoring and treatment of clients with RHS is essential to appropriate care, as are necessary referrals.

http://search.ebscohost.com/login.aspx?direct=true&db=aph&AN=20255771&site=ehost-live

http://web.ebscohost.com.www.libproxy.wvu.edu/ehost/pdf?vid=39&hid=116&sid=5b7088be-e3c7-45f7-9df3-20ac14811b59%40sessionmgr108