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Headaches: Menieres vs Migraines

Headaches: Menieres vs Migraines

MENIERE’S

Subjective

 

  • Ménière’s disease affects about 1% of the population. Typically it presents as episodic vertigo, fluctuating hearing loss, tinnitus and aural fullness.
  • more common in industrialised countries
  • female preponderance and the typical age of onset is 30–50 years
  • Bilateral disease is not uncommon (15–20%), but both sides are seldom affected simultaneously except in patients with autoimmune disease.
  • Genetic predisposition has been reported in families with Ménière’s disease.
  • Factors such as diet, weather changes (low pressure fronts), emotional and physical stress, and urban living can precipitate attacks and make any symptoms worse. (1)

Endolymphatic hydrops are caused by either increased production of endolymph by the stria vascularis, or decreased absorption by the endolymphatic sac. (1)

 

  • Hearing deteriorates over time to about 50 db loss in 60–80% of patients.
  • Speech scores (understanding/clarity) drop with time to below 50% which is the minimal level at which a hearing device can be used.
  • Audiometry (pure tone audiograms) show variable configurations such as low frequency rising or high frequency falling patterns.
  • Vertiginous episodes vary between 6 and 11 per year (average 4),1 and decline with time.
  • Bilateral MD rarely presents with each ear
  • simultaneously but rather sequentially with the second ear
  • involvement occurring many years after the first (2)

 

A majority of patients with MD have migraine headaches as defined by the IHS. Sensitivity to visual motion, light and sound, head motion, smells, weather changes, or medication was present in 95% of all patients (2)

 

sensorineural hearing loss is the required symptom necessary for the diagnosis of Meniere’s disease, and pure-tone audiometry is still the only required test for suspected and confirmed patients. (2)

 

 

 

 

Objective

Otological problem characterised by episodic vertiginous spells, hearing loss, tinnitus and aural fullness

Middle aged adult presenting with rotational vertigo (with nausea and vomiting) lasting 30 minutes to hours, unilateral fluctuating hearing loss and tinnitus. (2)

Diagnosis of Ménière’s disease is mainly clinical, based on the history and audiometry.

Typical unilateral MD, the incidence of symptomatic and functional involvement of the contralateral ear increases almost linearly with the length of observation, resulting in bilaterality rate of almost 50 % at 30 years after onset of unilateral MD (3)

Definite Ménière’s disease (2)

  • Two or more definite spontaneous episodes of rotational vertigo for 20 minutes or longer
  • Audiometrically documented hearing loss (uni- or bilateral) on at least one occasion
  • Tinnitus or aural fullness in the affected ear
  • Other causes excluded such as vestibular schwannoma

Probable Ménière’s disease (2)

  • One definite episode of rotational vertigo
  • Audiometrically documented hearing loss (uni- or bilateral) on at least one occasion
  • Tinnitus or aural fullness in the affected ear
  • Other causes excluded
  • Ear examination is generally normal with no evidence of middle ear effusion or vascular lesions.
  • Hearing loss and hyperacusis are often present in Ménière’s ears, especially during, or around, the time of an attack.
  • Neck movements should be normal except in the acute or subacute stages of a Ménière’s episode when patients self-restrict movements to reduce dizziness or vertigo.
  • Saccadic, pursuit and optokinetic eye movements are usually normal with no dysconjugate movements or gaze-evoked nystagmus.
  • Spontaneous nystagmus observed after removing visual fixation by Frenzel glass or video goggles, post head shake nystagmus and positional nystagmus are all frequently present in the acute or subacute stages of an episode. Most, if not all, types of central nystagmus are enhanced with visual fixation and therefore can be readily seen with the naked eye. Frenzel’s glasses or video-electronystagmography remove visual fixation and enhance the detection of peripheral nystagmus which is commonly suppressed by visual fixation.
  • The vestibulo-spinal response is examined by asking patients to stand up unassisted and walk for several steps watching for any gross gait abnormalities or side stepping (abnormalities are more evident during an acute episode and less so during subacute and inactive stages of the disease).
  • Romberg’s sign is conducted with eyes open and eyes closed with the arms outstretched and observing postural sway and post stepping (Unterberger-Fukuda) rotation with eyes closed.
  • The vestibulo-cerebellar examination is conducted by observing the vestibulo-ocular visual suppression response.
  • The remainder of the neurological examination is usually normal in Ménière’s patients. Positive neurological findings on examination should direct the physician’s attention to the presence of central nervous system disease.

 

Management

Treatment options are limited and usually targeted towards reducing endolymphatic hydrops to stabilise the hearing loss and reduce the vertiginous episodes.

The most distressing symptom of an acute attack is the vertigo which should be treated symptomatically; 5 mg diazepam (Valium) with 2 mg glycopyrolate (Robinul) is very effective. Sublingual administration of 2 mg lorazepam (Ativan) is also very effective in controlling and shortening the duration of an attack.

First line treatment of MD often includes diet and lifestyle change. Although there is no strong evidence that diet and lifestyle changes affect the progress of MD, a few studies report that MD cases may improve with such changes (4).

 

Due to this postulated autoimmune association, anti- inflammatory medications such as steroids and immunosuppressants such as methotrexate are employed in treatment. Several studies reported a good response in approximately 20% of MD patients treated with oral prednisone, dexamethasone, and methylprednisolone (4)(5).

 

 

 

 

( 1) M A Hamid. Menieres Disease. Practical Neurology. Vol 9 issue 3.

(2) Yi Zhang,1,2 Bo Liu,1,2 Rui Wang,1,2 Ruo Jia,1,2 and Xin Gu. Characteristics of the Cochlear Symptoms and Functions in Meniere’s Disease.  Chin Med J (Engl). 2016 Oct 20; 129(20): 2445–2450.

 

(3) R. Gürkov I. Pyykö, J. Zou, and E. Kentala.  What is Menière’s disease? A contemporary re-evaluation of endolymphatic hydrops. J Neurol. 2016; 263: 71–81.

 

(4) Foster CA, Breeze RE. Endolymphatic hydrops in Meniere’s disease: cause, consequence, or epiphenomenon? Otol Neurotol. 2013;34(7):1210–1214.

 

(5) Lopez-Escamez JA, Carey J, Chung WH, Goebel JA, Magnusson M, Mandala M, Newman-Toker DE, Strupp M, Suzuki M, Trabalzini F, Bisdorff A. Diagnostic criteria for Meniere’s disease. J Vestib Res. 2015;25(1):1–7.

 

 

 

 

Vestibular Migraine

 

Vestibular migraine (previously called migrainous vertigo, migraine-associated vertigo, or migraine-associated dizziness) is a newly-described form of migraine with a population prevalence of roughly 1%.

 

SUBJECTIVE

 

  • A definite diagnosis of vestibular migraine requires =5 attacks with vestibular symptoms, a history of migraine headaches, and migraine-like symptoms with at least half the attacks.
  • Episode duration ranges from seconds to days.
  • Nystagmus, if present, may be peripheral, central, or mixed type. Headache is often absent. When headache does occur, it may begin before, during, or after the dizziness and may differ from the patient’s other typical migraine headaches.
  • Patients are likely to complain of nausea, vomiting, photophobia, phonophobia, and visual auras.
  • Patients with posttraumatic migrainous vertigo, which can occur with minor head trauma, often describe dizziness as spinning, rocking or to-and-fro oscillation sensations, floating, or drunkenness that in many ways makes it indistinguishable from vestibular migraine without prior trauma and also with postconcussive dizziness in general.
  • Severity of the head injury seems a poor predictor of whether a patient will develop migrainous vertigo.  It is related to basilar-type migraine, but episodes lack a second defining brainstem symptom such as diplopia, quadriparesis, or paresthesias.
  • An episode similar to prior spells with long illness duration, migraine features, no red-flags, and low vascular risk is sufficient for diagnosis without testing (1)

 

  • Unlike Meniere’s disease, the vertigo episodes may last for more than a day at a time. Other characteristic features include a family history of migraines, motion intolerance, and sensitivity to visual stimuli. Many people are mislabelled as having Meniere’s Disease when the attacks are actually migrainous. (2)

 

 

 

 

 

OBJECTIVE

  • There are no signs specifically characteristic or indicative of a to this particular condition or biomarkers, so diagnosis is currently based on clinical history and exclusion of alternative causes.
  • Vertigo is a common symptom in patients with migraines. It is reported that 27% of patients with migraines suffered vertigo compared with an incidence of 8% in patients with tension headaches. In addition, the vertigo episodes are often separate from the headaches. We can test for vertigo with various objective tests.

 

MANAGEMENT

  • There is evidence that education, prevention strategies and exercises can help migraines, sometimes dramatically.
  • It is very important for the physiotherapist to work closely with the patient and the physician especially as prevention is key to migraine management.
  • The most commonly used exercises are habituation exercises.
  • For acute attacks of tension-type headache and migraine, simple analgesics and nonsteroidal antiinflammatory drugs are commonly used.
  • Treatment involves dietary modifications and prophylactic therapies for migraine include calcium channel blockers, anticonvulsants, topiramate, tricyclic antidepressants, and beta-blockers.
  • Acute migraine-specific treatments such as ergotamine, dihydroergotamine,and the triptans may also be given.  (2,5) Abortive medications, such as the triptans, are usually not effective intreating the vertigo episodes. (2)
  • The general trend in studies is that treatment tends to be over a 4-6-month range. There has been documented success with migraine diets, prevention strategies (lifestyle and trigger management), eye exercises and a few other techniques (in addition to habituation exercises).
  • Some of these patients do well with some hands-on therapy as well, such as myofascial release.

 

  1.         Newman-Toker D, Edlow J. TiTrATE: A Novel Approach to Diagnosing Acute Dizziness and Vertigo. 2016;33(3):577–99.
  2.         Kutz JW. The dizzy patient. Med Clin North Am [Internet]. 2010;94(5):989–1002. Available from: http://dx.doi.org/10.1016/j.mcna.2010.05.011
  3.         Fife TD, Giza C. Posttraumatic vertigo and dizziness. Semin Neurol. 2013;33(3):238–43.
  4.         Acerra N, Finstad E, Van Ierssel J, Woodhouse S. Clinical Tidbits.
  5.         Lew HL, Lin P-H, Fuh J-L, Wang S-J, Clark DJ, Walker WC. Characteristics and Treatment of Headache After Traumatic Brain Injury. Am J Phys Med Rehabil [Internet]. 2006;85(7):619–27. Available from: http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage&an=00002060-200607000-00012

 

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