Ear Development

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Ear development

The ear is a fascinating and complex appendage and organ. Formation is from structures called branchial arches. Branchial (from Greek branchia gills) arches are composed of endoderm on the internal aspect, by clefts composed of ectoderm on the external side with the central mesoderm containing the muscle, cartilage, vessels and nerves that will ultimately supply and establish the surrounding anatomic structures. Molecular signaling from the ectoderm leads the mesenchyme from the mesodermal (central) layer to eventually, if it works out as planned, to obliterate the clefts and and pouches. If clefts persist, they are given names, such as Type I branchial cleft cyst. When this signaling goes wrong, there are different degrees of anomalies, from absence of specific auricle components to microtia or even anotia if there is complete failure.

The ear begins to form the otic placode and vestibulocochlear ganglia at 3 weeks of gestation. The external canal then develops from the first branchial cleft at 4 weeks. By 28 weeks there is a fully open external canal. Failure to canalize can result in membranous or bony stenosis or atresia (from Latin a = no and Greek trēsisperforation, from tetrainein to pierce). Development of the auricle (external ear) begins at 5 weeks gestation with development of the auricular hillocks numbered from 1 through 6, derived from the first (mandibular) and second (hyoid) branchial arches. So the inner ear has already formed when the external ear begins.

The ear develops in a predictable manner, with various alterations in development resulting in predictable deformities when the process is interrupted. Knowledge of auricular development as well as normal external anatomy allows for precise evaluation of the ear and assists in selecting appropriate reconstructive techniques to optimize the complex 3-dimensional anatomical outcomes.

If you have a ear question, please do not hesitate to call me for an appointment. Office number is 989-839-6201, fax is 989-839-6202. Providers can page me through the Midland hospital operator. Patients can reach me by way of the patient portal.

Let me know how I can be of help to you.

Philip Harris, MD FARS
Ear Nose Throat and Cancer of the Head and Neck
Serving Gladwin, Clare, Midland and Alpena
Call for appointment and ask to see Dr. Harris

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Can an Audiogram Predict Cardiovascular Risk?

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Did you know a simple audiogram may help predict your heart disease risk?

In a study titled Audiometric testing as a predictor for Cardiovascular disease published in
Laryngoscope 119 Mar 2009 researchers hypothesized that low-frequency hearing loss is associated with underlying cardiovascular disease. Their conclusion? Audiogram patterns correlate strongly with cerebrovascular and peripheral arterial disease and may represent a screening test for those at risk. Patients with low-frequency hearing loss should be regarded as at risk for cardiovascular events, and appropriate referrals should be considered.

What commonly causes hearing loss?
We know that environmental noise and exposures, systemic disease, and family inheritance can lead to hearing loss. Years ago Dr. Schuknecht correlated audiometric patterns to hearing loss. He described classic character of presbycusis (age related hearing loss) seen on audiometric tests to cochlear pathology. The Schuknecht classification, as a general template for age-related hearing loss, has been validated through investigation. The presbycusis patterns include strial, cochlear conductive, sensory, and neural hearing losses.

Presbycusis is typically the result of degeneration within the cochlea, most commonly to outer hair cells but also to inner hair cells, spiral ganglion neurons, or the stria vascularis.

What is the Stria Vascularis?
The stria vascularis, in the lateral wall of the cochlea, is critical for establishing the endocochlear potential necessary for the propagation of auditory signals to the central nervous system. The stria vascularis is a capillary-rich structure fed by radial branches of the spiral modiolar artery. Arteries feeding the stria vascularis are terminal vessels with no anastomoses to supplement
flow or accommodate for spasm or occlusion. Additionally, the strial capillary network is relatively sparse at the apex when compared with the dense organization at the base. These anatomical features leave the apical cochlea exquisitely sensitive to ischemia. A reduction in endocochlear potential and clinically significant hearing loss occurs almost immediately after vascular occlusion
or anoxia. The vascular anatomy of the stria at the cochlear apex (low frequencies) establishes this area as a sensitive marker for systemic cardiovascular disease.

What next?
So that lowly audiogram may be a real help to you after all. You should seek out a trained audiologist (CCC-A designation) to evaluate you, especially if you have low frequency hearing loss and risk factors such as hypertension, diabetes mellitus, hyperlipidemia/cholesterolemia, age >75 years, and a history of smoking or prior events like myocardial infarction, diagnosis of coronary artery disease, stroke, transient ischemic attack, and claudication.

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Is Being Fat Killing Us?

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A new report addresses many novel and intriguing aspects of the relationship between cancer, cancer stem cells, and adipocytes (fat cells).

Fat (adipose) tissue has been suggested to play a direct role in resistance to cancer treatment. Obese (body mass index or BMI > 25) patients with leukemia have shown poor survival outcomes relative to non-obese patients (see 2010 ,M.A. Lichtman Oncologist, 15, pp. 1083–110). When one has cancer, traditionally there was weight loss. This was termed cachexia,a common and historically long-recognized hallmark of advanced cancer. Breakdown of adipose tissue through the action of pro-inflammatory cytokines leading to tissue atrophy occurs as part of cancer-induced cachexia. This dramatic metabolic disturbance was assumed to benefit the tumor at the expense of the normal tissue. These changes are only beginning to be more fully explored.

A recent mouse study found that leukemia cells utilized fat to hide away from the immune system. Numerous leukemia cells were found in gonadal addipose tissue (GAT), which is the largest visceral fat depot in mice, but not in subcutaneous fat deposits. The leukemia cells were located directly adjacent to adipocytes throughout the tissue. Even more worrisome, these phenotypically defined GAT-resident leukemic stem cells gave rise to leukemia at frequencies comparable to bone-marrow-derived leukemia stem cells. This established that adipose (fat) tissue can function as a reservoir for this cancer. As the mice’s leukemia progressed, atrophy of GAT was noted before the development of full-blown cachexia (weight loss).

Adipose tissue has previously been identified as an extra-medullary reservoir for normal hematopoietic stem cells (HSCs) and may promote tumor development.

As a cancer survivor and as a surgeon who treats head and neck cancer, I encourage you to be lean and fit. Maybe it will keep that cancer at bay or from recurring? You will feel and look better while fighting to keep away a disease that 50% of the population will get, cancer.

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Medullary Thyroid Cancer

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Medullary thyroid cancer (MTC) is a neoplasm of the thyroid that is rare and can occur in a sporadic form or in a hereditary form. It derives from neuroendocrine parafollicular or calcitonin cells. Approximately 75% of cases are sporadic. The remainder are hereditary owing to germline mutations activating the Rearranged during Transfection (RET) proto-oncogene. The hereditary form occur in multiple endocrine neoplasia type 2 (MEN2). These have district phenotypes resulting from a different RET gent mutation.
Although medullary thyroid cancer accounts represents 3% of all thyroid cancer, but is responsible for 14% of thyroid cancer–related deaths. MTC has a lower 10-year relative survival risk compared with patients with papillary and follicular carcinoma. When lymph nodes are involved, the prognosis decreases further.

We currently treat MTC by complete surgical excision, which includes at minimum a total thyroidectomy and central compartment neck dissection but may include varying levels of lateral neck dissection, depending on the patient presents.

In papillary thyroid cancer, radioactive iodine is utilized. For MTC, Radioactive iodine I-131 is not used. The parafollicular calcitonin cells do not actively take up iodine therefore treatment with radioactive iodine would be not effective. External beam radiation also is not helpful in this cancer. In fact it has been shown to be an independent predictor of decreased survival.

There are several identified predictors of survival for MTC. These include female sex, young age at the time of diagnosis, localized stage, well- or moderately differentiated histologic features, and absence of cervical lymph node involvement.

Oncologic drugs to treat MTC are limited. Vandetenib and Lenvatinib are approved kinase inhibitors for MTC that cannot be removed by surgery and is locally advanced or has metastasized.

After surgery, patients who have had MTC should be assessed regularly for presence of residual disease, localization of metastasis, and identification of progressive disease. Postoperative calcitonin and carcinoembryonic antigen levels should be monitored. If the postoperative calcitonin level exceeds 150 pg/ml, consider imaging such as computed tomography of the neck and chew, contrast enhanced magnetic resonance imaging (MRI), and ultrasound of the liver, bone scintigraphy, MRI of the bone, and positron emission tomography. Considering that metastatic MTC is not curable, management goals become priority. These include control of loco regional disease, palliate symptoms of hormonal excess (diarrhea), symptomatic metastases (bone pain, fracture), and life threatening bronchial obstruction or spinal cord compression.

Presented to you by Dr. Philip Harris

Should you have questions or care to schedule a patient to be seen, please call 989-839-6201

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Basal Cell Carcinoma

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Skin cancer in general is a very large topic and difficult to address in a blog. As a head and neck surgeon, I commonly see skin cancer on referral for surgical treatment.

I would reference the reader to two recent and good articles to review.

JNCCN May 2016 Basal Cell Skin Cancer, Version 1.2016, NCCN Clinical Practice Guidelines in Oncology  and

European Journal of Cancer November 2014 Surgical excision versus Mohs’ micrographic surgery for basal cell carcinoma of the face: A randomised clinical trial with 10 year follow-up

Basal cell carcinoma (BCC) is a common form of cancer. The incidence has increased over the past decades and is predicted to continue rising. The disease related mortality is very low due to the low rates of metastatic disease but morbidity can be high due to local tissue destruction, especially since most tumors occur in functional areas such as the head and neck.

Known risk factors for development of BCC are sunlight (relationship between sun exposure and BCC is complex, depending on timing, pattern, and amount of ultraviolet radiation), fair skin, red or blond hair, light eye color, and radiation treatment for other conditions, especially at a young age. BCC tends to occur in the head and neck area and within the treatment field of prior radiation therapy. BCCs that develop in the head and neck area are more likely to recur than those developing on the trunk and extremities. BCC located in the H-zone of the face, with positive excision margins in previous resections or with an aggressive histological growth pattern show higher recurrence rates. Compared with squamous cell carcinoma, BCCs are much less likely to metastasize

Workup begins with a history and physical examination. A skin biopsy may then be performed on a suspicious lesion. The biopsy needs to include deep reticular dermis if the lesion is suspected to be more than a superficial process.  Imaging studies may be considered when extensive disease such as bone involvement, perineural invasion, or deep soft tissue involvement is suspected. MRI has greater sensitivity for perineural disease.

Many therapeutic options are available today, standard surgical excision (SE) is still the most common form of treatment for BCCs and Mohs’ micrographic surgery (MMS), a specialized surgical technique where available. The difference between both treatments is the method of histological margin examination primarily. In standard SE, surgical margins are mostly examined on random vertical sections whereas in MMS, the specimen is flattened and sliced horizontally offering the possibility to examine 100% of the resection margins. Treatment of BCC is primarily surgical with radiation as an alternate and / or adjuvant treatment. Radiation is not the primary treatment choice. Superficial therapies for BCC have been explored (topicals, cryosurgery, and photodynamic therapy). Two hedgehog pathway inhibitors are approved by the FDA for systemic treatment of advanced and metastatic BCC. Recurrences are more common when tumors in high-risk locations are 6 mm or more in diameter and when tumors in moderate-risk locations are 10 mm or more in diameter. immunosuppression, such as organ transplantation and long-term use of psoralen and UV-A light (PUVA), increase the incidence of BCC. Tumors developing in sites of prior radiotherapy are high risk. Tumors with perineural involvement poses a greatly increased risk of recurrence. Associated risk factors for perineural spread include previous recurrent tumors, high-grade, larger lesion size, and infiltrating, morpheic, and basosquamous subtypes.

In most patients the removal is performed under local anesthesia.  Surgical excision is currently with a 4-5 mm clinically tumor free resection margin at a 90° angle into the subcutaneous fat (for well-circumscribed BCC lesions less than 2 cm in diameter, excision with 4-mm clinical margins should result in complete removal in more than 95% of cases). For Mohs micrognathic surgery, the tumor is excised with the same clinically tumor free resection margin at a 45° angle in order to obtain a bowl-shaped excision sample (the preferred surgical technique for high-risk BCC because it allows intraoperative analysis, of 100% of the excision margin). In the Netherland study noted above, the excisions were at previously recommended margins of 3 mm. The benefit of larger margins must always be carefully weighed against the disadvantage of larger defects. A larger defect worsens aesthetic outcome and may in some cases lead to reduced functionality. The costs of MMS are higher than costs of SE and should be reserved for high risk facial primary BCC and facial recurrent BCC for example. A high risk facial primary BCC would be defined as a BCC of at least 1 cm diameter either located in the H-zone of the face or being of an aggressive histological subtype. For these lesions, we consider MMS superior to SE.  Recurrences after surgical treatment can still occur up to and even after 10-years post treatment. In BCC treated with MMS, fewer tumors do recoccur during long-term follow-up.

A brief discussion of local treatments for the reader includes use of curettage and electrodesiccation, standard surgical excision followed by postoperative pathologic evaluation of margins, MOHS, cryosurgery, radiation, topical therapy and photodynamic therapy.

Curettage and electrodesiccation is the process of alternatively scraping away tumor tissue with a curette down to a firm layer of normal dermis and denaturing the area by electrodessication. Up to 3 cycles may be performed in a session. It is a fast and cost-effective technique for superficial lesions but does not allow histologic margin assessment. A skilled practitioner is required as it is highly operator dependent. If the subcutaneous layer is reached during the course of surgery, surgical excision should generally be performed instead.

Radiation therapy, as a primary treatment, results in higher recurrence rates than surgery, poorer cosmetic outcomes, and more postoperative complications.

Superficial therapies (cryotherapy, photodynamic therapy) should be reserved for patients for whom surgery or radiation therapy is contraindicated or impractical. Cure rates are lower with superficial therapies. A key limitation of cryotherapy is poorer cosmetic outcomes, operator dependent result, and lack of specimen for pathological assessment.

Recommendations for low risk BCC include curettage and electrodissection in areas without hair growth, standard excision with 4 mm margin, radiotherapy for nonsurgical candidates (generally limited to those over age 60 years due to risk of long term toxicity), and pursuit of Mohs if margins are positive after standard excision or re-resection based on pathology. High risk BCC are advised standard excision with wider margins, Mohs, or radiation therapy for non-surgical candidates. Adjuvant radiation therapy advised for large nerve or extensive perineural involvement and in case of positive margin. Hedgehog pathway inhibitors an be offered for systemic therapy after multidisciplinary consultation.

The subtypes encompassed by the term “aggressive growth pattern” including micronodular, infiltrative, sclerosing, and morpheaform (or desmoplastic) patterns are more likely to recur than nodular and superficial BCC.Non-aggressive subtypes include the keratotic variant, infundibulocystic variant, and fibroepithelioma of Pinkus.

All patients who have had skin cancer need continuous followup and monitoring.  30% to 50% of patients will develop another BCC within 5 years. Patients with a prior BCC are also at increased risk of developing SCC and cutaneous melanoma. Continued long-term surveillance is essential, as is education about the values of sun protection and regular self-examination of the skin.

Resources for you and your patients:

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Ear pulsing and Vertigo

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Ear complaints and balance problems can be very difficult to address, work-up, and treat. An unusual but possible cause to consider in your patients that present with a concur about vertigo concerns when exposed to noise, associated with ear fullness and / or conductive hearing loss is a disorder of the semicircular canals.

The semicircular canals are are three semicircular, interconnected tubes located inside each ear. When we say in the ear, we mean specifically housed inside the temporal bone.

There are three semicircular canals. These are the horizontal semicircular canal (also known as the lateral semicircular canal), the superior semicircular canal (also known as the anterior semicircular canal), and the posterior semicircular canal (also known as the inferior semicircular canal). The orientations of the canals cause a different canal to be stimulated by rotation of the head in different planes. The horizontal canal / lateral canal is stimulated when you turn your head to the left and right hand sides before crossing a road (transverse plane). The superior canal / anterior canal is stimulated when nodding your head (sagittal plane). The posterior canal / inferior canal is stimulated when you move your head to touch your shoulders (coronal plane). Each bony canal is fluid filled with motion sensors present at base of each canal in the dilated portion that opens into the utricle. The sensors in the dilated portion (ampullae) are motion sensitive. They are not gravity specific sensors. In the utricle and saccule there are gravity sensitive cells.

Semicircular canals require integrity of bone to function properly. Dehiscence or loss of bone covering, can affect function. Semicircular canal dehiscence (SCD) is an important entity that can present with symptoms of noise or pressure induced vertigo, autophony (unusually loud hearing your self speak), aural fullness and conductive hearing loss. SCD can have a varied presentation and mimic of other conditions.

In reviewing these cases, it is important to obtain a thorough history (ear fullness, what makes worse, for example exercise, voice louder in ear than usual, intermittent vertigo with noise, etc) and a careful examination to include supportive audiological testing and imaging (high-resolution CT images).

Semicircular canal dehiscence may occur in the superior, lateral or posterior canal. Your patient may experience vertigo, visual disturbance in which objects in the visual field appear to swing back and forth after exposure to noise or changes in pressure. Hearing loss with a conductive component can occur. The presence of autophony makes it difficult to separate from other ear disorders (otosclerosis, patulous eustachian tube, etc).

You can learn more about this topic by looking to this article:

American Journal of Otolaryngology
Vol 37 Issue 3
Christopher A. Schutt, John F. Kveton

If you have questions, please call. We are trained in 7 core areas over a 5 year residency after medical school: allergy, facial plastic and reconstructive surgery, head and neck, laryngology, otology, pediatric otolaryngology, and rhinology.

We are the only surgical specialty dedicated solely to this area.

MidMichigan Physicians Group
Midland / Gladwin / Bay City
Phone (989) 839-6201
Philip Harris MD FARS
OtoRhinoLaryngology-Head and Neck Surgery
General ENT, Cancer, Thyroid, Parathyroid, SInus

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Laryngopharyngeal Reflux

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What is LPR and why does it matter?

Laryngopharyngeal reflux (LPR) is retrograde movement of gastric contents (not just acid) into the larynx, pharynx, and upper aerodigestive tract. Patients may note hoarseness, throat clearing, cough, dysphagia (trouble swallowing), globus sensation, and postnasal drip. It becomes more important as a cause or contributing factor to diseases such as subglottic stenosis, laryngeal granuloma, asthma, and sinusitis; in children and adults. The symptoms do differ from gastroesophageal reflux disease (GERD). Patients do not have heartburn and regurgitation. They have nonspecific symptoms that can be thought to be due to other factors (allergy, smoking, environmental irritants, infection, or vocal abuse).

So how do you take the symptom data and glean from it that your patient may have LPR? Thankfully there are validated measures such as the reflux symptom index (RSI) and the reflux finding score (RFS) that can help. To assess and manage LPR, these questionnaires (RSI, RFS) along with physical exam, laryngeal examination, and further diagnostic studies are key.
However, in general otolaryngology practice, the diagnosis relies on empiric evaluation of symptomatology and physical examination for most cases. Completing questionnaires and / or performing laryngoscopy can be time and / or cost prohibited. It is encouraged to consider all these approaches and then pursue a clinical protocol to control cost as well as hopefully be able to remove prescribed agent for cost and health savings long-term once therapy has been successful.

Treatment is commonly use of empiric proton pump inhibitor (PPI) therapy. PPIs are commonly prescribed medications but have shown detrimental side effects (fractures, increased community-acquired pneumonia, renal damage, Clostridium difficile diarrhea, etc). These agents have also been shown to be less effective than expected in the treatment of LPR! Why would that occur? Possibly LPR is not only an acid issue but relates to gastric aspirate, such as pepsin.

The use of clinical protocols and care pathways in health care is popular. Clinical protocols do help standardize the delivery of care and reduce variability. This can improve quality of care. Care pathways have also been shown to reduce cost and improve documentation. A management protocol is particularly helpful in LPR management due to the high degree of uncertainty in diagnosis. LPR is most often diagnosed based on symptoms and exam findings as I discussed. Because most of the symptoms are non-specific, overdiagnosis may occur. Even 24-hour pH probe testing, which is the gold standard test, has low sensitivity.

Here is a protocol to consider. Evaluate patient, possible or probable LPR, eRx PPI such as esomeprazole or omeprazole at 20 mg po bid, counsel on diet and lifestyle modifications (weight loss, activity, fiber, possible need to see registered dietician). Give 3 month followup. At followup, evaluate better, partial response, or no response. If better, now titrate off PPI continue with diet and lifestyle modifications. If partial response, increase to 40 mg po bid and follow-up in 3 months (now 6 months). If no change, re-assess your diagnosis. At 6 month followup, if resolved, titrate off PPI and continue diet and lifestyle modifications. If not better, evaluate need for gastroenterology input.

You can learn more about this topic by looking to this article:
• Nikita Gupta, Ross W. Green, Uchechukwu C. Megwalu
• American Journal of Otolaryngology
• Vol 37 Issue 3

Other questions regarding eye, ear, nose, throat, head and neck cancer, sleep surgery, thyroid and parathyroid? Please do not hesitate to call. ENT is trained in 7 core areas over 5 years after medical school: allergy, facial plastic and reconstructive surgery, head and neck, laryngology, otology, pediatric otolaryngology, and rhinology. We are the only surgical specialty dedicated solely to the head and neck.

Philip Harris, M.D. FARS
MidMichigan Physicians Group
Midland / Gladwin / Bay City

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Primary Sjogren’s Syndrome

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What is PSS?

This chronic autoimmune disease is characterized by inflammation that affects exocrine glands (think salivary glands, lacrimal glands, etc) and leads to dryness phenomena. Commonly, patients who have primary sjogren’s syndrome (pSS) are very tired. The severity, degree of fatigue, is influenced by pain, depression, and sleep disturbances.

Fatigue is a hard and vague term. At times, we are all tired! We could define fatigue as an overwhelming sense of tiredness, lack of energy, feeling of exhaustion. In healthcare, we see this as a frequent feature of chronic inflammatory diseases, immunological diseases, cancer and neurological disorders. There are social (work, finances, etc) and genetic / molecular mechanisms that may aggravate fatigue. Certainly sickness behavior as it is called is seen in animals when infected in danger situations. The animal will exhibit sleepiness, depressive mood, social withdrawal, stop grooming, loose appetite and is an automated behavior thought to help protect the sick animal. People also exhibit these traits and can be due to chronic illness. Oxidative stress occurs with chronic inflammation. Heat shock proteins (HSPs) are proteins that protect under these conditions. These proteins can be intra and extracellular. They may play a role in signaling in chronic fatigue.

For pSS, there is no effective drug treatment. Could HSPs help us understand these two things, pSS and fatigue? pSS is associated with ocular / oral / and salivary gland symptoms. There may be focal sialoadenitis and anti-Ro/La antibodies (considered to be the most specific markers for pSS). Ocular dye tests (fluorescein stain for corneal surface and lissamine green for conjunctival surface) as well as Schirmer’s tear test can be done. Parotid sialography (to assess for diffuse sialectasis according to the scoring system of Rubin and Holt) as well as salivary scintigraphy according to the method proposed by Shall et al can be done. Hepatitis C must be excluded to diagnose pSS. Hepatitis C (HCV) may mimic the clinical, histological, and immunological features of pSS. Because HCV related sicca syndrome can meet criteria for pSS diagnosis, it must be excluded. Secondary Sjogren’s syndrome may be found with anticholingeric agents, antidepressants, antihypertensives, parasympatholytic drugs, neuroleptic agents, and past head and neck radiation treatment.

So in conclusion, fatigue is a natural phenomenon the body utilizes to help protect. It should be evaluated and if a disease process such as pSS is found, possible help can be given.

I hope you found this thought stimulating and helpful. ENT does not treat chronic fatigue of course as a specialty, but we do treat disorders of the head and neck, essentially what happens above your clavicle. If you have questions or concerns, we want to help. You can reach us at MidMichigan Health as noted below.

Philip Harris MD FARS

OtoRhinoLaryngology-Head and Neck Surgery
General ENT, Cancer, Thyroid, Parathyroid, Sinus
989-495-3166 (cell)
philipharrisent@aol.com

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Meniere’s disease: a primer

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For a more complete and thorough review, you are referenced to Lancet 372 2008

This disorder is a chronic illness that affects many people every year worldwide. It has been described since 1861! There are specific characteristics. Patients experience intermittent (not constant) episodes of vertigo lasting from minutes to hours, their hearing fluctuates (specifically sensorineural hearing), there is ringing of the ear(s) (tinnitus), and ear pressure sensation.

Even though there is currently no cure, more than 85% of those with Meniere’s are helped by either changes in lifestyle and medical treatment, or minimally invasive surgical procedures. Some of these procedures can be done in the office. Some do require more specialized surgery.

Such as intratympanic steroid therapy, intratympanic gentamicin therapy, and endolymphatic sac surgery. Vestibular neurectomy has a very high rate of vertigo control and is available for patients with good hearing who have failed all other treatments. Labyrinthectomy is undertaken as a last resort and is best reserved for patients with unilateral disease and deafness.

In 1927, scientist discovered the endolymphatic sac as the site of “outflow of endolymph” in guineapigs. This provided insight into the mechanics of endolymphatic flow in the inner ear. In 1967, scientists showed that blockage of the endolymphatic sac and duct causes obstruction of endolymphatic outflow, leading to hydrops of the inner ear.

Despite this knowledge, Meniere’s disease remains a difficult disease to diagnose! Patients may present to the emergency department in early stages with only cochlear symptoms such as hearing loss and pressure or fullness in the ear without true vertigo or even ringing in the ears. It is found more common in adults in their fourth and fifth decade. A strong positive family history can exist in patients with Meniere’s disease.

Meniere’s disease symptoms include intermittent episodes of vertigo lasting from minutes to hours (20 minutes to 12 hours), with fluctuating sensorineural hearing loss, tinnitus, and aural fullness. Most have one sideded symptoms,with the rate of bilateral disease to be as high as 50% after many years. It remains a clinical diagnosis; a diagnosis of exclusion. A detailed history and a complete physical examination are necessary. Any specific testing and imaging should be directed by knowledgeable planning to avoid expensive and unnecessary testing. Up-sloping low-frequency sensorineural hearing loss that fluctuates is noted on audiometric testing. A conductive loss can at times be seen.Symptoms can be aggravated by consumption of caffeine, chocolate, alcohol, and salt. Food allergies should be investigated, treated and avoided as much as possible. Salt intake should be maximum of 2 g per day, Diuretics such as a combination of hydrochlorothiazide and triamterene can be beneficial. Those allergic to sulpha could use acetazolamide or chlorthalidone. Steroids in the form of oral, intramuscular, intravenous, and intra-tympanic have been utilized in a beneficial manner for some. Destructive treatments can be used in patients with intractable vertigo. Gentamicin is one such agent, affecting both vestibular (balance) and cochlear (hearing) function. If the ear affected is a non-hearing hear, this may be a good option (ie, speech reception threshold worse than 50 db and speech discrimination score of less than 50%).

Pressure pulse treatment by the Meniett device may help some but the long-term efficacy is reportedly poor. Endolymphatic sac surgery is more invasive but considered an effective procedure for symptomatic Meniere’s disease. Vestibular nerve section is offered in specialized centers for intractable vertigo.

Non-surgical treatment can involve vestibular rehabilitation.

You can learn more about this topic by looking to this article:

H. Sajjadi, M.M. Paparella
Meniere’s disease
Lancet, 372 (2008), pp. 406–414
If you have questions regarding ear disease or nose, throat, cancer, sleep surgery, thyroid / parathyroid, please call. ENT is trained in 7 core areas over a 5 year residency after medical school: allergy, facial plastic and reconstructive surgery, head and neck, laryngology, otology, pediatric otolaryngology, and rhinology. We are the only surgical specialty dedicated solely to this area.
Philip Harris, M.D. FACS
MidMichigan Physicians Group
Midland / Gladwin / Bay City
Phone (989) 839-6201
www.midmichigan.org/mpg

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