Ambulatory Healthcare Pathways for Ear Disorders

Otitis Externa

1. Ear drops
   a. Domeboro® or Vosol® (acidifying and drying agent)
   b. Cortisporin Otic® Suspension
   c. Quinolone ear drops
2. Wick
   a. Rolled cotton
   b. Pope Otowick® (Xomed)
3. Canal cleaning:
   While otomicroscopy and suction are preferred, irrigation is acceptable. Assuming no tympanic membrane perforation exists, 1 or 2 irrigations is okay. If no success the ear canal must be manually cleaned with suction.

Otitis externa (a.k.a. swimmer’s ear) is found in individuals who swim frequently or extensively or in people who are chronic Q-tip® abusers. The pathogenesis is worth understanding. Normally, the external auditory canal is inhabited by a low concentration of Pseudomonas aeruginosa whose growth is inhibited by the ear canal’s slightly acidic pH. Those who scrape away the wax and epithelium with Q-tips® leave an open wound which exudes a high pH, becoming a favorable growth environment for bacteria. Alternatively, those whose ears are submersed in water for so long that the skin swells and loses its natural acidic protection can also develop a Pseudomonas aeruginosa perichondritis; i.e. otitis externa.

In North America, fungal infections are uncommon whereas in warm, humid environments such as the tropics they are more frequent. Treatment for otitis externa in North America is acidification. For this reason, virtually every eardrop available is buffered to an acid pH. Drying the ear is also beneficial and so hydrophilic compounds (i.e. drying agents such as alcohol) are frequently added. To whatever degree one believes that antibiotics and/or steroids would provide benefit, they too are added to some of the prescription eardrops.

The standard “swimmer’s ear” is treated with any one of a number of commercial eardrops. One, two, or three drops carefully placed in the external auditory canal two to four times a day will normally cure the illness in one, or at the most two, days. The inflamed ear canal is painful. Don’t be afraid to recommend aspirin or other analgesic. Heat, such as a heating pad, will also provide significant comfort.

If there is desquamated epithelium or other debris in the external auditory canal, the eardrops will not reach the ear canal’s skin surface. Therefore, this material should be removed. The easiest method is by irrigation. Otolaryngologists suction the ear canal under direct vision, often with the benefit of a microscope. With the ear canal cleaned, the eardrops now become efficacious. In some cases the ear canal is so edematous that it is swollen shut and the eardrops cannot get in. In these cases, a wick made from either a rolled wisp of cotton or the commercially available Merocel Otowick®, are necessary. A wick must be forcefully placed into the external canal, often causing a significant amount of pain. This cotton will then “wick” the eardrops into the canal.

Garden variety, run of the mill, otitis externa is easily treated with Domeboro® Otic or VoSol® Otic. If there appears to be a more advanced infection, particularly with a more significant bacterial component, polymyxin otic drops (e.g., Cortisporin Otic®) are popular and contain antibiotics and steroids. An occasional patient develops an allergic reaction to the antibiotic component of these drops. If the antibacterial properties wish to be continued, gentamicin or tobramycin ophthalmic drops can be safely administered to the external ear canal and have become popular as otic medicaments. The latest otic drops are the quinolones. Both Floxin Otic® and Cipro H.C. ® are excellent.

Diabetics are at risk for developing a Pseudomonas osteomyelitis of the temporal bone. This looks like otitis externa. The pain is greater and the disease is more severe. This is a fatal disease unless promptly diagnosed and aggressively treated.

Oral antibiotics are never given for otitis externa. For such to be effective, they would need to cover Pseudomonas. Penicillin, ampicillin, amoxicillin, erythromycin, cephalosporins, and sulfonamides do not. Therefore a quinolone or other anti pseudomonal antibiotics would be required.

The patient with a perforated eardrum and pus draining out the external auditory canal will have a reactive otitis externa. Antibiotic containing eardrops are normally administered, in part to treat the otitis externa and in part because they help treat the otitis media. In these cases, a quinolone eardrop (e.g. Floxin Otic® or Cipro H.C.® ) is preferred.

The inflammation of otitis externa virtually never extends off of the ear. If erythema extends beyond the auricle, the diagnosis is not otitis externa, but cellulitis, insect bite, or even parotitis.

The individual, who is a daily swimmer, may develop a chronic otitis externa. These are easily treated with non-antibiotic, non-steroid containing otic drops at the end of each swimming session. Domeboro® Otic and Vosol® Otic are the two most commonly prescribed.

Lastly, if pharmaceuticals are not available, either for financial reasons or one is on an outing away from pharmaceutical amenities, a home brew eardrop is one-part white table vinegar, one-part 70% isopropyl alcohol and one-part water. This is odiferous, but effective.

Cerumen Impaction

1. Irrigating an ear with a missing or diseased eardrum puts the middle ear and hearing at serious risk. In these situations, an ENT physician should be consulted to suction the wax under binocular microscopic vision. The PCP should never put a diseased ear at risk by irrigating or picking blindly.
2. Following irrigation, the ear canal is at risk for Pseudomonas proliferation and resultant otitis externa. This is easily prevented by placing 1 or 2 drops of Domeboro®, VoSol® or Cortisporin Otic® in the ear canal.
   
   For individuals who reaccumulate wax frequently, Domeboro®, 2 gtts a.u. twice weekly after showering is excellent treatment. Cerumen accumulates because of excess production or poor migration out of the external auditory canal. Ear canal skin is generated on the tympanic membrane and then migrates laterally out the ear canal. The Domeboro® Otic increases the migration rate, thereby improving cerumen removal.
3. Cerumen softeners
   a. Mineral oil or baby oil
   b. Cerumenex®
   c. Rubbing alcohol and white vinegar (mixed 50:50)

Cerumen production and impaction is a common problem, more frequent amongst some ethnic groups. The only real means available to the primary care physician to remove the wax is irrigation. This is an effective technique most of the time. In some cases, because the wax is too hard, it will not irrigate. The addition of cerumen softeners (either those commercially produced or plain mineral oil) will facilitate irrigation.

A number of different irrigation setups are available. The simplest is a 20 cc syringe with a 14-gauge angio catheter. Commercial irrigators are available. Some use a dental Waterpik. If compressed air is available, conventional ENT otic irrigation systems are used.

The base irrigant is water. Some add alcohol, some add hydrogen peroxide, some add vinegar, and some add a small amount of Burrow’s solution. The additives, as long as they are not harmful, are irrelevant. It is important that the water be body temperature. If the water is too hot or too cold, vestibular caloric stimulation occurs and patients will be dizzy. Those who become extremely dizzy may even vomit.

Following irrigation, it is wise to protect against otitis externa with a single application of any commercially available eardrop.

Irrigation with or without cerumen softeners will work most of the time. When irrigation fails to work, persistence rarely brings success, and often brings pain. Propitious ENT referral is then wise. An otolaryngologist will remove the wax under direct vision either with a loop and small cup forceps, often with a binocular microscope under 6x or 10x magnification.

There are some ears that should not be irrigated. These include those with chronic otitis media. If the eardrum is missing, irrigation will force the wax into the middle ear and will cause otitis media. It could also cause ossicular or round window damage and subsequent hearing loss.

Contraindications, therefore, are chronic ear disease or tympanic membrane perforation by history. If the patient has only a single hearing ear and this is the one filled with wax, then that patient should be taken care of by an otolaryngologist.

How to prevent recurrent cerumen accumulation is not a well-studied topic. If a patient requires cerumen disimpaction every two or more years, most are better off simply coming to their physician to have this done. If the accumulation is more frequent, or if they wish for definitive treatment, two options are recommended:

Option 1 is two or three drops of mineral oil self-administered into each ear canal once weekly. Some patients will use a small bulb syringe to flush their ear with warm water. If indeed they can keep the wax soft and successfully irrigate their ear, remove the wax, not hurt themselves, and not induce vertigo, this is a reasonable plan.

Option 2 is to prescribe a 60 cc bottle of Domeboro Otic® with instructions to place two drops into each ear once weekly after showering. Cerumen is produced by eccrine glands in the lateral portion of the external auditory canal. The accumulation is a balance between the wax production and the outward migration of the external auditory canal epithelium. The external auditory canal epithelium is generated on the tympanic membrane and then migrates laterally, exiting through the external auditory meatus. Domeboro® stimulates the epithelial migration and therefore facilitates natural removal. This is an effective technique, but requires a patient who is both compulsive and compliant.

A word about Q-tips. The standard ENT recommendation is to put “nothing smaller than your elbow in your ear canal”. This obviously excludes Q-tips. However, many individuals use Q-tips on a regular basis without encountering difficulty. The official recommendation is to not use them. The unofficial recommendation is to not use them, but if you do, to only use them once or twice a week, and to use them to gently swab the lateral half of the external auditory canal. At no time are they to be used on a once or twice daily basis and at no time are they to be used vigorously to scrub every last bit of wax and oil from the external auditory canal.

Auricular Hematoma

One might ask why auricular hematoma is included in the ENT Ambulatory Healthcare Pathways. With today’s ever improving athletic head gear it is decreasing in frequency. Nonetheless, it is a condition that requires early diagnosis and is easily treated by any interested physician.

The key is diagnosis. Invariably there is some inciting trauma such as a headlock applied during a wrestling match or some other shearing blow to the ear. The perichondrium is sheared from the underlying cartilage, bleeding results in the sub-perichondrial space, and a hematoma develops. The concerning issue is that the cartilage derives its blood supply from the perichondrium. With the perichondrium lifted off the cartilage, the cartilage loses its blood supply and over the next several days will die and change from a nicely shaped cartilage into an amorphous scar.

Treatment for auricular hematoma is twofold. Many of these individuals are on a medication which impairs coagulation. The use of aspirin, NSAIDs, warfarin (Coumadin®), Clopidegrel (Plavix®) or other anticoagulants should be discontinued if possible.

The auricular hematoma can often be drained by needle aspiration. This is easy to do and, as long as it does not reaccumulate, is all that is required. Infection is always a risk. The ear should therefore be swabbed with alcohol or Betadine®. A small amount of lidocaine with adrenaline should be injected into the epithelium and then using a 10 cc or 20 cc syringe with an 18-gauge needle, the hematoma should be evacuated. The ear should then be observed for a short period of time. If the hematoma does not reaccumulate, the patient is sent home and advised to remain at rest for 24 hours.

If one is skilled at applying a mastoid-type pressure dressing, this can be beneficial. If one is not so skilled, it is probably best to leave the ear unwrapped. If the hematoma reaccumulates, it can be needle aspirated 2 or 3 times. Needle aspiration will resolve the hematoma in the majority of cases but if it does not, incision and drainage is required.

To I & D a hematoma, choose an incision site where the blood will drain dependently, anesthetize the skin, and make a 5mm incision through the skin and perichondrium. Spread the wound open with a small hemostat. The hematoma can then be squeezed or expressed through the incision, or if a small sterile Frazier or neurosurgical suction tip is available, this can be used to evacuate the hematoma.

At this point most people would recommend a pressure dressing to cover the wound. Those that like drains will always place a drain. Those who are opposed to drains will rarely do so. The advantage of a drain is that it keeps the incision open and allows the wound to drain. Those who oppose drains argue that this predisposes to infection. If you chose to drain, all that is required is a small rubber band. If a drain is placed a dressing is required. In addition, if a drain is used, there is a sufficiently high risk of infection that oral antibiotics are required.

The organisms present are skin bacteria; therefore, an appropriate antibiotic such as cephalexin is recommended.

The dressing should be changed at 24 hours. Assuming no major oozing or bleeding, the drain can be removed at this time. The patient should have no residual cosmetic defect or damage to the ear.

Acute Otitis Media

1. Organism

   Streptococcus pneumonia Hemophilus influenzae Moraxella catarrhalis Streptococcus pyogenes (Grp. A) Staphylococcus aureus Viruses No microorganisms

   25-50% 15-30% 3-20% 2% 1% 45-70% 16-25%

   From: Pocketguide to Antimicrobial Therapy in Otolaryngology-Head & Neck Surgery, 12th Edition by David N.F. Fairbanks, M.D.

2. Antibiotics
   1. There is a high incidence of penicillin resistant Hemophilus in individuals exposed to antibiotics, e.g. day care center, etc. For these individuals, begin with second line drugs. For all others begin with first line therapy.
   2. 1^st line therapy
      1. Amoxicillin 500 mg p.o. tid x 7-10 days
   3. 2^nd line therapy
      1. Augmentin® (amoxicillin/clavulanate) 875 mg p.o. bid x 7-10 days
      2. Ceftin® (cefuroxime) 500 mg p.o. bid x 7-10 days
      3. Pediazole® (sulfisoxazole/erythromycin)
      4. Levo-gati-moxifloxacin oral (Levaquin)
   4. Penicillin allergic patients
      1. Macrolide x 7-10 days
      2. Septra DS® (sulfamethoxazole/trimethoprim) i p.o. bid x 7-10 days
      3. Erythromycin and Septra®

Otitis media is an incredibly common malady. The middle ear and mastoid are part of the upper respiratory tract system and are aerated through the eustachian tube. Secretions drain through the same tube. At birth and throughout early childhood the eustachian tube is short and often functions poorly. There appears to be growth periods or maturation periods for the eustachian tube and growth occurs around the age of four, again around the age of seven, and the last around puberty.

Illnesses and conditions predisposing to acute otitis media are upper respiratory tract viral infections, allergic rhinitis, chronic sinusitis, nasopharyngeal tumors, and congenital or anatomic eustachian tube abnormalities. The end result is the same. If the eustachian tube is dysfunctional, the ear fails to aerate, secretions are not drained, and infection ensues.

Virtually every child will have at least one ear infection by the age of 3 or 4. Those in day care environments, where the exchange of upper respiratory tract virus is an every day occurrence, may have 3-10 episodes of otitis media annually.

Although the same disease occurs in adolescents and adults, the frequency is considerably less. The signs, symptoms, diagnostic workup, and treatment are basically the same.

The following is a simplified treatment paradigm.

Acute otitis media is treated with antibiotics. Our recommendation is to begin simply. Amoxicillin is the first line drug of choice. If this fails, it can be presumed that the patient has a beta-lactamase producing bacteria and second line antibiotics are indicated. There are many who argue that the high frequency of beta-lactam resistant organisms warrants beginning therapy with second line drugs. I disagree. This practice promotes bacterial resistance, both for the individual and for the world. It wastes money and even in the short term has no proven benefit.

The use of ancillary treatments belongs to the art of medicine and is based upon other contributing illnesses. Antihistamines and decongestants, once considered the standard of care, are now thought to be of no benefit. Nose drops, both saline and decongestants, have no proven benefit. The only scientifically proven treatment for acute otitis media is antibiotics and follow-up.

If the otitis media fails to improve or if it should worsen, second and even third line antibiotics can be given. Assuming the infection resolves, all patients warrant follow-up to be certain that the residual fluid (serous otitis media a.k.a. chronic otitis media with effusion) fully resolves. Whether you have the patient follow-up at 2, 3 or 4 weeks, makes no difference—but you must follow to guarantee resolution of the fluid and restoration of hearing.

Recurrent or persistent acute otitis media is sometimes controlled with low dose prophylactic antibiotics. Myringotomies and middle ear ventilation tubes are also effective and may be used for cases of antibiotic failure or antibiotic intolerance.

Never, absolutely never, forget that the complications of acute or chronic otitis media can be fatal. These include acute and chronic mastoiditis, meningitis, brain abscess, suppurative labyrinthitis, sigmoid sinus thrombosis, facial paralysis, and other serious illnesses. Chronic untreated ear infections can also cause scarring and destruction of the middle ear ossicles and tympanic membrane and may impair sensorineural hearing. Patients can be left with a serious and permanent hearing impairment.

Lastly, the tympanic membrane can be difficult to visualize and otitis media difficult to diagnose. If one cannot see the ear drum or cannot see it sufficiently well to make a diagnosis with some certainty, consultation with a colleague is appropriate. It is far too easy to assume that the febrile, sick child whose ear canal is obstructed by wax or whose eardrum is reddened by screaming, has acute otitis media and to treat with a course of amoxicillin or “spectaculocillin.” Consultation with an otolaryngologist is not dishonorable.

Serous Otitis Media

1. Caveat: unilateral serous otitis media (a.k.a. chronic otitis media with effusion) in an adult requires one to rule out nasopharyngeal carcinoma.
2. Antibiotics
   1. 1^st line:
      1. Amoxicillin 500 mg p.o. qid x 7-10 days
      2. or if penicillin allergic
      3. Macrolide p.o. qid x 7-10 days
   2. 2^nd line:
      1. Augmentin® (amoxicillin/clavulanate) 875 mg p.o. bid x 7-10 days
      2. Pediazole® (sulfisoxazole/erythromycin)
      3. 3rd generation cephalosporin
3. Persistence is diagnosed by otoscopy or pneumotoscopy. Tympanometry is an unnecessary expense, but is accepted to assist in diagnosis.
4. Hearing loss documentation is by audiogram with or without tympanogram.
5. Myringotomy and tubes is safe, cheap and effective. Adenoidectomy may be indicated for the 2nd or 3rd set of tubes. Tonsillectomy is indicated for tonsillitis.

Serous otitis media (a.k.a. chronic otitis media with effusion) is a condition in which the middle ear is inadequately aerated and has abnormal fluid accumulation. This is generally felt to be secondary to eustachian tube dysfunction. Eustachian tube physiology is a function of age, growth, development, rhinitis, sinusitis, adenoid hypertrophy, upper respiratory tract infection, and a myriad of other problems. For example, individuals with cleft palate have abnormalities of their tensor tympani muscle leading to eustachian tube malfunction. As a result, virtually all cleft palate children have chronic otitis media. Nearly all cleft palate children and adults require middle ear ventilation tubes.

The treatment for serous otitis media is controversial. When we were younger, we practiced all sorts of complex treatment regimes. The older we get, and the more patients we see, the more we believe the illness is in the hands of “mother nature” and “father time”. The only thing that we as healthcare professionals can do to assist is to provide appropriate, safe antibiotics to treat and sometimes prevent infection.

We normally give “mother nature” three months to resolve a serous otitis media. During this time it is appropriate to give a minimum of one two-week course of antibiotics. Other treatments, be they topical, systemic, herbal, medicinal, or mystical are perfectly acceptable presuming they follow the Latin adage primum non nocere.

If at 3 months post diagnosis your examination reveals persistent fluid with a hearing loss, the individual should be recommended for myringotomy and tubes. Hearing impaired children, even those with minimal conductive hearing loss, have lifelong learning disabilities with documented decrements in language and verbal aptitudes.

If the fluid persists but there is no decrement in hearing and there is reason to wait, (e.g. we have come to the end of cold season, we are nearing the end of the seasonal allergy season, we are leaving day care centers), you can wait another four weeks. However, if it is clear that a drainage procedure will ultimately be required, it is better to recommend and perform the procedure early rather than late.

Chronic Otitis Media

1. Chronic otitis media includes cholesteatoma and chronically draining ears, typically with mastoid disease. These all require specialty consultation.
2. Antibiotics
   1. Amoxicillin 250–500 mg p.o. tid x 7–10 days
   2. Augmentin x 7–10 days
   3. Macrolide x 7–10 days
3. Ear drops
   1. Floxin Otic® (ofloxacin) 2 gtts qid
   2. Cipro HC® (ciprofloxacin) 2 gtts qid
   3. Many antibiotic eardrops are available. Current thinking is that the polymyxins and aminoglycosides are ototoxic and may cause sensorineural hearing loss in the presence of a tympanic membrane perforation. The quinolone drops are therefore the only safe topical antibiotic in the presence of a tympanic membrane perforation.
4. Audiogram. Assuming a correct diagnosis, an audiogram will be required when the ear is dry (not infected and draining). If you order an audiogram when the ear is infected, the audiogram will need to be repeated when the ear is dry.
5. The cost of not referring chronic otitis media is recurrent infection with ever diminishing hearing. Further risks are meningitis, facial paralysis, brain abscess, deafness and death.

Chronic otitis media is any inflammatory middle ear or mastoid malady. At a minimum this causes conductive hearing loss and recurrent infection. More commonly, it causes recurrent infection with ever increasing scarring to the middle ear and at its worst causes serious and even fatal complications such as meningitis, brain abscess, and death. This is a disease that requires specialty consultation.

If specialty consultation is not immediately available, oral antibiotics and antibiotic ear drops should be administered. When the ear is free of infection, an audiogram is appropriate and necessary.

Vertigo

Vertigo is so non-specific that it is a diagnostic dilemma, not a treatment dilemma. The 3 common labyrinthine causes are Ménière’s disease, viral labyrinthitis, and benign positional vertigo. The following excerpt is reproduced from the Clinical Manual of Otolaryngology-Head and Neck Surgery.

Vertigo is a feeling that the world is spinning around. People with extreme vertigo feel nauseous, often vomit, and talk about lying down and holding onto the carpet to keep from falling off the earth. Many patients complain of dizziness rather than of a true whirling sensation. A whirling sensation is usually associated with an identifiable labyrinthine etiology. The patient who complains of being dizzy may have a clear-cut and identifiable significant disorder, but often the diagnosis may remain obscure. Dizziness takes a long time to evaluate, and may require a complete history, physical, and laboratory examination. Time spent on the history will help direct the physician in decisions regarding testing and treatment. Failure to be thorough will result in a missed diagnosis. Physicians in different specialties have different experiences with vertigo. A triage officer at a Veterans Administration hospital, for example, may cite the leading causes of vertigo as cardiac arrhythmia and orthostatic hypotension. A neurologist might consider multiple sclerosis the most common cause, while a head and neck surgeon might believe that Ménière’s disease or vestibular neuronitis is most common. A general practitioner may believe most causes are idiopathic or functional. Each of these physicians reflects the nature of his or her own practice. The following outline describes my evaluation for each of my patients who complains of dizziness; it can be used as a guide for developing personal approaches. For differential diagnosis see the Diagnosis of Vertigo Pathway.

1. History
   1. Vertigo (what does the patient mean by dizziness?)
      1. Onset
      2. Intensity
      3. Duration
      4. Association with nausea and vomiting
      5. Feeling of faintness or loss of consciousness
   2. Hearing loss
   3. Tinnitus
   4. Feeling of fullness in ear
   5. History of ear pain, infection, surgery
   6. Recent illness
   7. Current medications
   8. Previous neurologic disorders (transient ischemic attack, stroke, multiple sclerosis, migraine headache)
2. Examination
   1. Hearing (tuning forks)
   2. Otoscopic
   3. Ophthalmic (to include extraocular movements, examination for nystagmus, and fundoscopic examination)
   4. Cranial nerves, with particular attention to nerves 3, 4, 5 (especially corneal reflex), 6, 7, 9, and l0
   5. Neck examination (to recognize carotid artery disease) and range of motion
   6. Blood pressure (to consider hypertension, hypotension, and orthostatic changes)
   7. Pulse (to diagnose arrhythmia)
   8. Neurologic (to exclude neurologic disease, especially multiple sclerosis and a cerebrovascular accident)
3. Laboratory tests
   1. Complete blood cell count (to rule out anemia)
   2. Electrolytes (to detect any imbalance)
   3. Calcium (to detect hypercalcemia)
   4. Tetraiodothyronine (T4) and TSH (to detect hypothyroidism)
   5. FTA-ABS or TPA (to rule out tertiary syphilis)
   6. Cholesterol and triglycerides (to detect hyperlipoproteinemia)
   7. Tests for diabetes and reactive hypoglycemia
   8. Electrocardiogram with rhythm strip (to diagnose any cardiac disease in elderly patients or with history suggestive of cardiac dysfunction)
   9. Audiogram and tympanogram (to evaluate hearing as well as evaluate type of loss) and BERA (to evaluate retrocochlear sensorineural hearing loss)
   10. Electronystagmogram (ENG; to evaluate labyrinthine function). This test measures gaze nystagmus, spontaneous nystagmus, positional nystagmus, and response to caloric irrigation. It is extremely useful to identify labyrinthine disease and also helps localize lesions to either the labyrinth, the acoustic nerve, or the central nervous system.
   11. MRI scan with gadolinium of the internal auditory canal indicated when acoustic neuroma, cerebellopontine angle tumor, multiple sclerosis, or other central problem suspected.
   12. X-rays of the cervical spine. The cervical spine is closely connected to the labyrinth via a vestibulospinal reflex arc. Cervical spine disease can cause vertigo and hence this must be evaluated.
4. Differential Diagnosis (see Diagnosis of Vertigo Pathway)
   This is not intended as an exhaustive differential plan, but rather to provide some insight into the different diseases that can cause vertigo. If the investigator is persistent a diagnosis can be made in over 90 percent of vertiginous patients.
   1. Ear
      1. Acute otitis media
      2. Serous otitis media
      3. Chronic otitis media
      4. Perilymph fistula
         (1) Trauma
         (2) Post-stapedectomy
         (3) Barotrauma (round window rupture)
      5. Labyrinthitis
         (1) Serous
         (2) Bacterial
         (3) Viral
         (4) Toxic
      6. Ménière’s disease
      7. Vestibular neuronitis
      8. Benign positional vertigo
      9. Acoustic neuroma or other cerebellopontine angle tumor
   2. Central nervous system
      1. Stroke (cerebrovascular accident)
      2. Transient ischemic attacks
      3. Multiple sclerosis
      4. Neurosyphilis
      5. Meningitis or encephalitis
      6. Migraine (posterior fossa)
   3. Neck
      1. Cervical arthritis
      2. Carotid artery stenosis
      3. Vertebral-basilar artery insufficiency
      4. Subclavian steal syndrome
      5. TMJ
   4. Metabolic disorders
      1. Hyper- or hypoglycemia
      2. Hyper- or hypothyroidism
      3. Electrolyte imbalance
      4. Hypercalcemia
      5. Anemia
      6. Polycythemia
      7. Leukemia
      8. Allergy
   5. Infections
      1. Influenza
      2. Herpes zoster
      3. Measles
      4. Mumps
      5. Other viral illnesses
   6. Drugs
      1. Streptomycin
      2. Kanamycin
      3. Gentamicin
      4. Diazepam
      5. Sedatives
      6. Opiates
      7. Alcohol
      8. Neuroleptics
      9. Aspirin
      10. Nicotine
      11. Caffeine
   7. Cardiac problems
      1. Arrhythmia
      2. Hypertension
      3. Hypotension
      4. Poor cardiac output

The treatment of vertigo often falls closer to the art than to the science of medicine. It sometimes seems that all the physician’s energy has been used in obtaining the history, conducting the laboratory examination, and reaching a reasonable diagnosis, and there is none left for creative therapy.

Specific causes of vertigo are treated. Bacterial labyrinthitis is a severe disease and must be treated with antibiotics, usually in the hospital. It is often considered a surgical emergency and an indication for labyrinthectomy to prevent spread of infection to the central nervous system. Although some physicians have very elaborate therapeutic regimens, a simple approach is equally effective.

Phenothiazines are the mainstay of treatment, and promethazine hydrochloride is as effective as any. For mild cases, 25 mg of promethazine can be taken orally every 6 hours. For some patients diazepam is useful alone or in combination with promethazine. For moderate intensity attacks, IV promethazine is indicated to stabilize the vertigo, after which oral or rectal suppositories can be used. Patients with severe cases frequently are dehydrated and need IV fluids. Promethazine is given IV frequently with diazepam. Alternatively, 0.5 mg to l.5 mg IV droperidol is effective in those patients unresponsive to diazepam. Promethazine should not be given in conjunction with the droperidol therapy. Hospitalization is often necessary. Intractable labyrinthine vertigo can be treated surgically, with cure rates approaching 90% to 95%.

Many patients will request medication to combat motion sickness and a number of medications are useful. The first choice of drugs for airsickness or seasickness is usually a non-prescription medicine such as Dramamine® (dimenhydrinate) or Antivert® (meclizine). These are effective and, although they cause some sleepiness, this tends to be mild. If the patient complains of motion sickness symptoms with very mild stimulation, such as flying in a modern jet or a long trip in a car, the cause may be psychologic. For these conditions, diazepam is effective, because it allays the patient’s anxiety and it is also an effective vestibular sedative.

The most difficult cases are those people with sensitive vestibular systems who wish occasionally to go boating in ocean waters where they are exposed to intense vestibular stimulation. Oral promethazine is effective in these situations; 25 mg can be taken the evening before boating, and should be repeated approximately l to l.5 hours before embarking. All of the phenothiazines have a long onset time; that is, they are not effective for at least 1 to 1.5 hours, and they also have a very long half-life. Therefore, the promethazine taken l2 hours earlier will still have some vestibular sedating effect when the patient embarks. Many patients do not like to take the evening dose of promethazine and simply begin with the first dose l.5 hours before going aboard. Unfortunately, such a dose will put most people to sleep. If it is possible to board the boat and sleep for the first several hours and allow their vestibular systems to adjust to the rocking of the boat while they are asleep, many patients will require little or no additional medicine. If any is needed, the original dose can be repeated every 6 hours. If it is important that the person be alert and functional at the beginning of the trip, it will be necessary to give some stimulant to counteract the sedative effects of the promethazine, such as 25 mg promethazine with 25 mg of ephedrine, both to be taken orally at least l.5 hours before boarding and not to be repeated more than once every 6 hours.

Another drug combination that has been popular with many sailors is 0.5 mg scopolamine with 2.5 to 10 mg of dextroamphetamine. This combination tends to be less sedating than promethazine and ephedrine. Another popular medication with many sailors is scopolamine supplied as a sticky patch to be placed on the skin behind the ear (Transderm-Scop®). The scopolamine is absorbed slowly and is reputed to be effective for periods of 2 to 3 days. Its side effects—which some find irritating—include a dry mouth and pupillary dilatation. For some, the side effects are not tolerable. It is, at the time of this writing, the most popular prescription treatment for motion sickness. It is contraindicated in the geriatric population.

Many times “on board physicians” are asked to treat motion sickness once it has occurred. In such circumstances, the previous recommendations are not effective. Promethazine given intramuscularly or as a rectal suppository is effective. If this fails, IV fluids combined with promethazine, diazepam, or droperidol can be required.

Individual head and neck surgeons organize their thoughts and their therapies regarding vertigo differently.

Vertigo is an incredibly complex and difficult illness. It cannot be evaluated in the usual 7-15 minute time slot, and in all fairness to the patient and the health provider, the patient should be scheduled or rescheduled for a long enough period to obtain a full history and perform a thorough examination.

To a cardiologist the most common cause of vertigo is arrhythmia; to an gerontologist the most common cause of vertigo is orthostatic hypotension; to a neurosurgeon all vertigo is a brain tumor until proven otherwise; to an infectious disease expert vertigo is neurosyphilis until ruled out; an endocrinologist will report hypothyroidism as the most common cause of vertigo; and to an otolaryngologist vertigo is a diagnostic challenge.

A good history, physical examination and laboratory assessment will point to the correct diagnosis.

Drugs, orthostasis, arrhythmias, dementias, neurologic illness, TIAs, carotid artery stenosis, and chemical imbalances of sodium, potassium, calcium or metabolic hormones, specifically thyroid, should be diagnosed.

The above aside, vertigo can be anything from a rather diffuse complaint of imbalance or unsteadiness to a very specific whirling vertigo in which the patient describes holding onto the rug to keep from falling off the earth. In severe cases, nausea and even vomiting can occur.

The three most common labyrinthine vestibulopathies are benign positional vertigo, viral vestibuloneuronitis, and Ménière’s disease.

Benign positional vertigo (BPV) is often, but not always, induced by head trauma. This can be minor or major. It classically presents as an acute onset dizziness brought on by tilting one’s head back and turning to the side. One can do this on the exam table using a technique called the “Dix-Hallpike maneuver”. This will induce the dizziness. The dizziness lasts for several minutes and diminishes with time. If the maneuver is immediately repeated, a similar response is elicited, although diminished in intensity. BPV, or BPPV (benign paroxysmal positional vertigo) as it is also called, continues for weeks to months. Some cases dissipate over several weeks, although many will take months and even longer to disappear.

Current recommendations are to diagnose benign positional vertigo by Dix Hallpike test or by electronystagmography (ENG) and then to perform otolith repositioning, a treatment described by Semont and separately by Epley. This maneuver works on the premise that there is floating debris in the posterior semi-circular canal. The maneuver consists of positioning the head in such a fashion that all the debris settles into the bottom of the canal. The head is then rotated in a series of maneuvers that trap the debris. The patient holds their head in this position for 24 hours. In 90 percent of patients, the vertigo is cured. For additional information visit Dr. Jeffrey Harris’ website http://drharris.ucsd.edu/Default.aspx?tabid=71.

Vestibuloneuronitis is felt to be a post-viral disease. It can occur concomitant with the viral infection or up to several weeks later as an autoimmune-like illness. Otologists are increasingly recommending steroids in the treatment of vestibuloneuronitis. In the acute phase, current recommendations are 100 mg of methylprednisolone (SoluMedrol®) IV push followed by 60 mg of oral prednisone daily for 1 week followed by a 1-week taper.

If a concomitant hearing loss is present, an audiogram should be obtained, steroids should be prescribed, and if the hearing loss has not returned or if the dizziness persists for longer than 6-weeks, an ENT referral is recommended.

The third diagnosis is Ménière’s disease. We begin with the caveat that not all that spins is Ménière’s. This is a diagnosis which has been used as a waste basket diagnosis and frequently over utilized. While Ménière’s is probably a multiplicity of illnesses with a similar end result, the classic Ménière’s is an acute onset illness with vertigo, decreased hearing, roaring tinnitus, and a feeling of aural fullness. Typically, the vertigo dissipates over several days, the hearing returns to normal, and the attack resolves. Ménière’s disease unfortunately is recurrent and episodes can occur frequently, regularly or irregularly.

There is an association between Ménière’s disease and allergic rhinitis. There is an association between Ménière’s disease and psychiatric illness with the usual discussions as to whether or not the psychiatric illness is causing the Ménière’s disease or whether the Ménière’s disease is causing the psychiatric illness. There are those that believe Ménière’s is a fluid or salt imbalance.

Another name for Ménière’s is labyrinthine hydrops. It is postulated that the efflux of endolymph is impaired. The endolymphatic fluid pressure increases with resultant symptoms.

Certainly, those with allergic rhinitis should be evaluated and treated. Those with psychiatric illness always benefit from psychiatric consultation. Endocrine and electrolyte imbalances must be diagnosed. Many otologists will recommend a trial of diuretics with potassium replacement. Vestibular sedatives diminish the symptoms.

Acoustic neuroma and other cerebellopontine angle tumors can present with symptoms mimicking the above illnesses. Their diagnosis is made by MRI.

Ménière's Disease

• Vertigo: attacks last hours to weeks
• Hearing loss +/- tinnitus: hearing loss fluctuates over time
• Aural fullness: aural fullness is a feeling of pressure in the ear

• Ear exam: audiogram
• Chemistry: electolytes include calcium, thyroid function tests, CBC

• Low salt diet
• Hydrochlorthiezide 25-50mg p.o. q day
• Potassium supplement 8-10 mq per day
• Phenothiazine or Diazepam for difficult attacks
• Surgery for progressive or incapacitating illness
• Repeat audiogram q 5 years and prn Sx change

• Difficulty in diagnosis
• Difficulty in treatment
• Progressive hearing loss
• Intractable vertigo

Sensorineural Hearing Loss

1. The use of steroids in sudden sensorineural hearing loss is controversial. Most ENT physicians will prescribe 2 weeks of oral prednisone. If this does not place the patient at some unusual risk, it certainly provides the maximum opportunity for recovery.
2. An audiogram is asymmetric (right versus left) if there is greater than a 30 dB summed difference in puretone thresholds or if there is a 20% or greater difference in speech discrimination.
3. Tumor concern is the issue. The greater the asymmetry, the greater the concern. Acoustic neuromas are generally slow growing tumors, so if the concern is low, retest at 12 months or sooner if there is further hearing deterioration. If the concern is greater, retest at 6 months. If there is real asymmetry, the evoked response audiograms are screening tools. MRI with contrast is the only definitive test.
4. Hearing aids are most appreciated with greater than 30 dB hearing loss with good discrimination. All hearing aids MUST be purchased with a full money back 30-day trial period. Only the user knows if he/she derives benefit.
5. MRI with gadolinium is the best examination for acoustic neuroma and other cerebellopontine angle (CPA) tumors. Special enhancing coils are typically used, so be sure to indicate suspicion for a CPA tumor.

Most sensorineural hearing losses are symmetric and insidious in onset. Most are a mixture of age (presbycusis) and noise exposure. Some are confounded by the companion tinnitus. Audiolometric testing is recommended. For those having communication difficulties, hearing aid evaluation is recommended. Three situations warrant special concern. The first is acute sensorineural hearing loss. The second is asymmetric sensorineural hearing loss and the third is sensorineural hearing loss with abnormalities of discrimination.

Acute sensorineural hearing loss is potentially an autoimmune disease. It is therefore treated with systemic steroids. The recommended dose is 60 mg of oral prednisone daily for 1 week, 40 mg daily for 1 week, and 20 mg daily for 1 week. If recovery is made, no further evaluation or treatment is required. If recovery is incomplete then the hearing loss is asymmetric and treated as per the ambulatory care pathway. Some, believing this is herpetic, will treat with high dose antiviral medication.

The issue with asymmetric hearing loss or asymmetric discrimination is that a small percentage of these represent the early symptoms of a cerebellopontine angle tumor. If the pure tone asymmetry is greater than 30 decibels or the difference in speech discrimination is more than 20%, cerebellopontine angle tumor is a concern. Evoked response audiometry (ABR or BAER) is an excellent, moderately priced test. ABR does not work for hearing losses exceeding 50 dB at 4000 Hz. For those with abnormal ABR or asymmetry with greater than 50 dB of hearing loss, MRI with gadolinium is recommended.

This then leaves the most common scenario which is asymmetry greater than 10 dB but less than 30 dB with reasonable discrimination scores. In other words, major asymmetry for threshold or discrimination requires ABR and possible MRI to rule out acoustic neuroma. Minor asymmetry can be followed with repeat audiograms at 6-12 month intervals with ABR and/or MRI if there is further change. Moderate asymmetries require clinical judgement. If concern exists obtain an ABR. If tumor suspicion is low, repeat the audiogram in 6 months and determine the need for work up by increasing hearing loss or asymmetrically deteriorating hearing.

Whether the primary care provider accepts this pathway or chooses a modified or different pathway, some rigorous organized thinking on this topic will benefit the patient, the physician, and the practice.

Tinnitus

Tinnitus or ringing is a noise perceived by the patient. The majority cannot be heard by the examiner and are therefore called subjective tinnitus. In an occasional case the noise, typically a low pitched vascular noise, can be heard by the examiner and this is called objective tinnitus. It is important when a patient complains of tinnitus to first determine if it is unilateral or bilateral and if it is high pitched or low pitched. The most concerning tinnitus is that which is low pitched, unilateral and which can be heard by the examiner. These are typically vascular lesions and can be cardiac murmurs, carotid bruits, vascular tumors — such as a glomus tympanicum. High pitched subjective tinnitus can be bilateral or unilateral. It is most commonly associated with sensorineural hearing loss, but other etiologies including neurologic, infectious and drug related causes are seen.

The evaluation of tinnitus begins with an audiogram. In those cases in which a sensorineural hearing loss is present and there is little concern for other etiology — the diagnosis is made i.e. sensorineural hearing loss causing tinnitus and attention is turned to treatment. Subjective tinnitus, otologic origin is now considered to be a central phenomenon. Early attempts with severe tinnitus to cut the acoustic nerve were rarely successful. Sophisticated PET scans and other information, suggests tinnitus is a central nervous system condition. The treatment is to counsel the patient. First and foremost this is not a symptom of other serious illness. Second, there is no easy treatment and the best advice is simply do not listen to the tinnitus. This is mind over matter. Most can do this and it is without question the best treatment.

The next line of treatment is to provide some degree of background noise, whether this is a radio, a television or a Radio Shack sleep machine, catalogue number 63-657, selling for approximately $40.00 is up to the patient. For those with significant hearing loss in which amplification may provide them benefit, hearing aids often reduce the tinnitus. For those patients in which the above fails to provide improvement, neuropathic pain medicines — typically antidepressants are recommended. It is not clear whether these work because they treat depression or because they in fact treat the tinnitus, but the fact of the matter is that anecdotal experience suggests that they are sometimes effective.

When all else fails, tinnitus maskers can be tried and there is new clinical research suggesting feedback with various frequency MP3 machines may provide some benefit. Patients are also referred to read the commentary “My Pets, the Spider and the Cricket” by Leon Morgenstern, a Los Angeles physician. This is present on Dr. Davidson’s website: http://drdavidson.ucsd.edu/MyPets/tabid/146/Default.aspx

For a more sophisticated review of tinnitus the reader is referred to the NEJM, "Current Concepts: Tinnitus", volume 347(12):904-910, September 2002. The authors are Lockwood AH, Salvi RJ and Burkard RF. The article is reproduced with permission of the NEJM for exclusive use on this website: http://www.NEJM.org/

Temporomandibular Joint Dysfunction (TMJ)

• Beware TMJ experts and clinics they can be expensive, long-term habits.
• The best treatment is stress reduction, decreased clenching, decreased bruxing, soft diet, hot or cold packs, nonsteroidals, TMJ physical therapy, stress reduction, Yoga, Botox injections and when all else fails neuropathic pain Meds.
• For some a conservative dental orthotic (night guard) is beneficial.

Some call this TMJ, some call it TMD (for temporomandibular dysfunction). This condition is ubiquitous. It is more common in women than men and it has been written that up to 75% of middle age women will have at least one symptom or sign of temporomandibular joint dysfunction at sometime in their life. For some this is an episodic, acute illness, for others, it is a more chronic malady, and for a few it is an obsession.

The epidemiology of TMJ is hotly debated. My opinion is that man’s recent evolution has decreased the size and the protrusion of the molar teeth. Whereas the TMJ is a non load-bearing joint, the resultant over closure now places a load on this joint and induces the TMJ syndrome. I divide the TMJ illnesses into extrinsic and intrinsic causes. The extrinsic causes are such illness as osteoarthritis, rheumatoid arthritis, septic arthritis, tumor, trauma, etc. The intrinsic causes are by far the most common and seem to be associated with malocclusion, bruxism, clenching, and stress. The pathogenesis of TMJ dysfunction is the same as the pathogenesis of a paraspinal muscle spasm. Something happens which either elicits pain or places the muscles of mastication into spasm. This in turn causes pain, pain causes spasm and a cycle is initiated. Until the cycle is broken or wears itself out, pain and dysfunction ensue.

In the evaluation, it is important to separate the various causes. If an individual has a severe malocclusion, this requires attention before resolution of the TMJ can be anticipated.

If the patient has a habit of clenching their teeth, chewing gum nervously, eating pencils, or grinding their teeth at night (a habit called bruxism), these practices need to be discontinued. Clenching can be consciously suppressed. Gum chewing should be easy to correct. Bruxism which occurs during sleep is more difficult, and is generally treated with an orthodontic appliance called a “night guard” or dental orthotic.

If the incipient cause is stress, be that neurosis, situational or otherwise, there is little use to prescriptions, appliances, consultations, etc., when what the individual needs is to focus on stress reduction.

Acute TMJ is treated first with cold packs. As symptoms of pain and spasm resolve, hot packs and nonsteroidal anti-inflammatory agents or other analgesics are recommended. Most importantly, the joint should be placed at rest. This is done by avoidance of hard, chewy foods and alimentation with either full liquids or at least, a very soft diet.

Chronic TMJ is often benefited by physical therapy. This may help in an acute exacerbation, but it certainly helps for chronic illness. For that illness which has become chronic, Botox injections into the muscles of mastication are recommended. In addition, neuropathic pain medication is often effective.

For some temporomandibular joint problems, consultation with a dentist to provide an orthotic is useful. I prefer orthotics which simply put the joint at rest and not those which disarticulate and radically reposition the temporomandibular joint.

There are individuals who have made a profession and a fortune out of TMJ. I sometimes wonder if in their treatments and medicaments create or exacerbate the illness. There are all manners of fancy treatments—joint repositioning orthotics, physical therapy, biofeedback, TENS (which is an electric stimulation), acupuncture, lots of dental visits, MRI, TMJ arthroscopy, and TMJ arthroscopic surgery.

There is a myriad of symptoms which temporomandibular joint dysfunction can cause. The primary care physician should be familiar with all of them.

Most patients present with ear pain. Only upon careful history can one discern that the pain is, in fact, in front of the ear, in the jaw joint and not in the ear, canal or on the ear itself.

Spasms in one of the muscles of mastication such as the masseter or temporalis will present with pain, often described as a headache. These located in the temple often undergo complex headache work ups, when in fact, they represent temporomandibular joint dysfunction. The jaw joint is very closely related to the ear. One of the tensors of the palate is innervated by the 5th cranial nerve and that muscle, the tensor tympani, also tightens the middle ear ossicles by pulling on the malleus. Spasms in this muscle, which is part of the reflex spasm to all of the 5th cranial nerve muscles, will cause decreased hearing, muffled hearing or a feeling of auricular fullness. There are some cases of vertigo which appear to be TMJ related and while it has been difficult to postulate the connection, it has been seen frequently enough that it must be remembered.

Facial Paralysis

1. Most prescribe steroids. The benefit is controversial. Conversely, 60 mg of prednisone for 7-10 days has only minor risks. Many also recommend antiviral therapy, such as acyclovir.
2. The prognosis is so poor for herpes zoster oticus cases that specialty consultation is required for patient satisfaction (that all possible was done) and for the PCP’s medicolegal protection.
3. Possible Lyme’s Disease in endemic areas.

One must begin with the statement that “not all that does not move is Bell’s.” Bell’s palsy, properly known as idiopathic facial paralysis, is by far the most common cause of facial paralysis, but it is a diagnosis of exclusion. Some of the causes of facial paralysis, such as trauma, are obvious. Others such as neoplasms commonly missed.

Certainly, a good ENT exam will include palpation of the parotid and an examination of the ear, looking for chronic otitis media or other abnormality. There are those that believe that most Bell’s palsy is caused by a herpes virus, and that the appropriate treatment is prednisone, usually 60 mg a day for 5-7 days, followed by 3 days of 40 mg and 3 days of 20 mg. Those who believe it is herpetic, will treat with acyclovir or one of the other antiviral medications.

A thorough head and neck exam, including cranial nerves is always required. Herpes zoster can present similarly, has a poor prognosis and must be treated aggressively with antiviral agents. Multiple cranial nerve involvement speaks for herpes infection and argues for antiviral therapy.

Trigeminal nerve defects, particularly the corneal division of the first branch, suggests a cerebellopontine angle tumor. It is very important to have documented the patient’s neurologic status at the time of initial presentation.

The most dangerous, immediate issue is corneal desiccation. In facial paralysis, the eyes do not close and particularly in individuals with a poor Bell’s phenomenon, the eye is at great risk for desiccation. If this is not picked up and treated immediately, the cornea can be lost and the patient left blind.

Tears Natural® or some other wetting agent can be prescribed for use throughout the day. The night time hours are the more difficult. The obvious solution would be to fill the eye with Lacrilube®. This unfortunately leaves one with a blurry vision and some patients do not care for it. Alternate therapy is complex. Some tape the eyelid shut. This is fine when it works, but, per chance the eye opens, and the tape or gauze comes in contact with the cornea, corneal abrasions may ensue. Other treatments involve creating moisture chambers. These involve taping a plastic material such as Saran Wrap® around the orbit in such a way that the eye’s own moisture is retained.

All patients with Bell’s palsy recover—it is only a matter of degree. Most improvement is made during the first three months, with the majority regaining 80% of facial nerve function. If a complete paralysis persists at 3 months, the patient did not have Bell’s palsy. An ENT referral and an evaluation for other causes is therefore required.

Lastly, Lyme’s disease can present with cranial nerve neuropathies. If there is reason to suspect the illness, a work up should begin.

Neuropathic Facial Pain

1. P Q R S T M
   1. P = Precipitating and palliating features
      (1) What brings it on?
      (2) What makes it go away?
   2. Q = Quality
      (1) Nociceptive: dull, sharp, aching, throbbing, gnawing
      (2) Neuropathic: burning, lancinating stinging
   3. R = Referral
      (1) Primary versus
      (2) Referred
   4. S = Severity
   5. T = Temporal relationships
      (1) Night
      (2) Day
      (3) Activity
   6. M = Medications
2. Quality-of-Life History?
   1. Depressed
   2. Anxiety
   3. Work or home related
   4. Sleep
3. Initiate Pharmacotherapy
   1. Titrate only one drug at a time
   2. Institute behaviorial medicine technologies, if appropriate
4. Use Pharmacologic Algorithm
   1. Tricyclic Antidepressants
      (1) If sleeping well, Nortriptyline (Pamelor) 10 mg qhs => 75 or 100 qhs
           or
      (2) Desipramine (Norpramin) 10 mg q am => 75 or 100 mg q am
      (3) If sleeping poorly, Doxepin (Sinequan) 10 mg qhs => 75 or 100 mg qhs
           or
      (4) Amitriptyline (Elavil) 10 mg qhs => 100 mg qhs
   2. Newer antidepressants-Venlafaxine – ½ of a 25 mg or 37.5 mg tab titrated in equal increments q 5-7 days to max dose of 150 mg /day (usual split as 75 mg BID)
   3. SSRIs (Selective Serotonin Reuptake Inhibitors) - SSRIs are generally not helpful in chronic pain
      (1) Sedating
      - Paroxetine (Paxil) 10-60 mg po q day- Paroxetine is used to combat tinnitus
      (2) Activiating
      - Sertraline (Zoloft) 50 to 200mg po q day
   4. Anticonvulsants
      (1) Gabapentin (Neurontin) 300 mg qhs, increase gradually on TID basis to 2000-3000 mg/day if needed
      (2) Topiramate (Topamax) 25 – 50 mg qd, incr. by 25 –50 mg/day q wk, max 1600 mg/d
      (3) Carbamazepine (Tegretol) 200 mg ½ tab BID and increase gradually to 600-800 mg/day
      (4) Phenytoin (Dilantin) 100 mg qhs and increase gradually to 200-300 mg/day
5. Combination therapy is sometimes useful. Little science is available regarding combination/doses.
6. Other therapies that may be useful in conjunction with pharmacotherapy
   1. Second opinion
   2. Physical/occupational therapy
   3. Psychological approaches (behaviorial, cognitive, relaxation)
   4. Vocational counseling
   5. Transcutaneous electrical nerve stimulation (TENS)
7. Always convey/impart hope, understanding, and compassion to every patient
8. Differential diagnosis for neuropathic facial pain
   • Neuropathic facial pain
   • Trigeminal neuralgia
   • Post herpetic neuralgia
   • Atypical facial pain
   • Post traumatic facial neuralgia
   • Cluster headache
   • Migraine/atypical migraine
   • Midfacial pain syndrome