Vertigo – Medical and Surgical Treatment, March 1998 Article
MEDICAL AND SURGICAL TREATMENT OF VERTIGO
Michael J. LaRouere, M.D.
Michael D. Seidman, M.D.
Jack M. Kartush, M.D.
Vertigo is a term used to describe the hallucination of motion although the subject is stationary. The patient suffering from vertigo often uses the term “dizzy” to describe this sensation. However, it can also refer to such feelings as lightheadedness, unsteadiness, confusion, giddiness, or nausea.
It is the purpose of this chapter to discuss the medical and surgical treatments of vertigo. It is expected that the reader has a general knowledge of the anatomy and physiology of the vestibular system.
The prevalence of vertigo is difficult to ascertain. Disequilibrium has been found to be the first or second most common diagnosis in the short-stay hospital diagnosis related groups (DRG’s) with an average hospital stay of 4 days.1 The National Health Interview Survey Supplements on Aging has found that 18% of people over the age of 65 and 25% over the age of 75 have falls.2 When asked, “does dizziness prevent you from doing things you otherwise could do?” 34% of the population between 65- 74 answered yes increasing to 37% over the age of 75. This would place 12.5 million persons over the age of 65 as having serious dizzy complaints.2 National Ambulatory Medical Care Survey in 1981 found the most common presenting symptom in patients 75 years or older was dizziness.3 This information coupled with the fact that in 1980 it was estimated that 11% of the population was age 75 or older adds to the number at risk for vertiginous disorders. This number is expected to increase to nearly 21% by the year 2030.5
CAUSES OF VERTIGO
I.PERIPHERAL CAUSES OF VERTIGO
Vertigo is most commonly caused by disease of the peripheral vestibular system. Prosper Meniere (1861) expanded the work of Pierre Flourens and described an otogenic disorder, erroneously referred to as a triad, consisting of four symptoms: vertigo, tinnitus, fluctuating sensorineural hearing loss and aural fullness.6
Meniere’s disease usually begins between the ages of 20-60 years and is estimated to affect 2.4-4-8 million Americans.7 Typically the disease is unilateral, however up to 40% of patients develop symptoms in the opposite ear.19 Clinically, Meniere’s disease is characterized by the sudden onset of vertigo often accompanied by pallor diaphoresis, nausea and vomiting. The attacks are usually associated with tinnitus and/or aural fullness. The episodes may last from 20 minutes to several hours. Rarely, some patients may experience explosive attacks precipitating a fall. These drop attacks, termed Crisis of Tumarken or utricular crises, usually occur in the later stages of the disease.
More than a century has passed, there continues to be ambiguity as to the pathophysiology of this disorder. Schuknecht10 states that Meniere’s disease is a symptom complex caused by different diseases that share the same pathophysiology: endolymphatic hydrops. Hydrops, an increase in endolymphatic fluid, is thought to result from endolymphatic sac dysfunction (decreased resorptive capabilities) secondary to infection, congenital hypoplasia, trauma, inflammatory causes or an idiopathic etiology. Schuknecht classifies Meniere’s disease as an idiopathic endolymphatic hydrops. He has proposed a five step mechanism that leads to the development of Meniere’s disease. 1. Decreased endolymph resorption: This may be caused by labyrinthitis, trauma or hypoplasia. 2. Endolymphatic hydrops: occuring because of over accumulation of endolymph which distorts Reisner’s membrane. 3. Membrane rupture: Endolymph then mixes with perilymph which temporarily paralyzes the auditory and vestibular system. 4. Healing of ruptures: The breaks of Reisner’s membrane heal thus allowing the entire process to repeat itself. 5. Distortion and atrophy: With disease progression, permanent changes in the membranous labyrinth occur which cause persistent disequilibrium and/or hearing loss.12
Vestibular Neuronitis is characterized by the sudden onset of disabling vertigo often associated with nausea and vomiting without auditory symptoms. Typically the onset of symptoms occur after an upper respiratory tract infection. Vestibular neuronitis most often affects patients in the 3rd to 5th decades without a sex predilection. Vertiginous symptoms are often worse with head motion. Clinically, horizontal nystagmus toward the uninvolved ear may be detected during the acute phase. Caloric testing typically reveals a reduced response in the involved ear. Routine audiometry is usually normal. Recovery is generally expected within one to three months.
Histopathologic studies have suggested involvement of the superior vestibular nerve and vestibular ganglion often with little or no involvement of the actual endorgan. Infection has long been consider a causative factor in vestibular neuronitis.30 There has been little success in documenting a viral etiology, however, intracytoplasmic particles have been recently found in human vestibular ganglia. These are thought to be dormant forms of a virus and may, when activated, produce infection with resultant inner ear disease.29,33 Other causes such as occlusion of the anterior vestibular artery, cerebellar infarctions, and acute diabetic neuropathy have been implicated in the etiology of vestibular neuronitis.31 Toxic and allergic causes are also thought to play a role in the disease process.(ref)
It has been claimed that vestibular neuronitis affects only the vestibular portion of the VIIIth cranial nerve and that the cochlear portion is left unaffected. However, Rahko(ref) found that the involved ear has a 14-24 dB SPL threshold difference compared to the unaffected ear at 20 kHz implicating some degree of damage to the auditory system in patients with vestibular neuronitis.
Benign Positional Vertigo (BPV)
Benign positional vertigo (benign paroxysmal positional vertigo) was first described by Barany in 1921 as a brief violent vertiginous episode occurring within seconds after a change in head position. Usually the attacks resolve if the patient remains in that position.36 In 1981, the Research Committee for Peripheral Disorders in Japan proposed diagnostic criteria for BPV. These include: 1. Whirling vertigo induced by a specific head position or movement, 2. Characteristic burst of positioning nystagmus which is rotary in nature, fatiguable and occurs within seconds after position changes, 3. Exclusion of central nervous system disorders, cervical disorders and cochlear disorders associated with vertigo.38 The nystagmus is typically induced by turning the involved ear downward. Although the nystagmus is usually esotropic and torsional to the direction of the down turned ear, Stahle39 noted that the nystagmus pattern can vary. Calorics are normal in over 2/3 of the patients.(ref)
In many series, BPV is the most frequent cause of vertigo. BPV is most commonly seen in people over the age of 40 and females out number males 1.6:1.37 The process lasts for weeks to months with spontaneous recovery in 90%. It is possible that these episodes may recur.39 Longridge and Barber40 have demonstrated bilaterality in up to 15% of affected individuals. The etiology of BPV has been a source of controversy. Baloh37 studied 240 cases of BPV and found that the most common etiology was idiopathic (118/240), followed by post-traumatic (43/240), vial neurolabyrinthitis (37/240) and miscellaneous (42/240). The pathophysiology has been best documented by Schuknecht. He observed basophilic deposits in the cupula of the posterior semicircular canals in two patients with BPV.42 He proposed that otoconia are released from a degenerating utricular macula and settle on the cupula of the posterior canal, causing it to become heavier than the surrounding endolymph.43
A perilymphatic fistula is the result of an abnormal communication between the inner and middle ear spaces. It generally occurs as a result of stapedectomy, head trauma, barotrauma, chronic ear surgery, congenital anomalies, or spontaneously.(Seltzer and McCabe) Because the presenting symptomsare similar to other otologic disorders and the inability to formally diagnose a perilymph fistula, short of operative exploration, this disease continues to be a focal point for debate.
There are no definitive symptoms that will clearly point to a diagnosis of PLF, however, symptoms may be similar to those of Meniere’s disease or endolymphatic hydrops.49-50 Typically, a fluctuating unilateral sensorineural hearing loss occurs. Usually patients complain of associated tinnitus, aural fullness, and vertigo. One or more of these symptoms usually exists. Occasionally, Hennebert’s or Tullios sign are seen.54,55 In a symptomatic individual with a clear history of barotrauma, closed head injury or prior otologic surgery, the diagnosis is suspect.
Once the diagnosis of PLF is suspected, there are several tests that can be supportive. Only exploratory tympanotomy with direct observation can confirm the diagnosis and even this can be subject to error as local anesthetics may seep into the middle ear space, or minimal trauma on the promontory may cause microvascular disruption with release of vessel exudate. Noninvasive tests, such as the fistula test (positive and negative pressure applied to the tympanic membrane) can produce nystagmus and vertigo. Vertigo is most often seen during the application of negative pressure. Daspit56 coupled ENG testing and the fistula test adding more objective evidence as compared to the standard fistula test.56 Platform posturography testing has been recommended by Black59 with some success in diagnosing and a fistula. Recently Schweitzer60 has identified six “best amino acid markers” which differentiate perilymph from serum, plasma or CSF. These include Theonine, Asparginine, Arginine, Histidine, Valine and Glutamic acid.60
Trauma is a frequent cause of vertiginous symptoms. Any insult that disrupts the labyrinth or ossicular chain may lead to vertigo. Transverse temporal bone fractures, typically involve the otic capsule and cause labyrinthine dysfunction. Longitudinal temporal bone fractures less commonly cause vertigo but may do so either from head trauma itself, otic capsule injury or ossicular disruption. A concussive effect on the CNS may result in post-traumatic disequilibrium.
Acute and chronic infection may affect the middle or inner ears which may lead to a spectrum of clinical symptomatology. The occurrence of vertigo with acute suppurative otitis media, acute suppurative labyrinthitis and chronic suppurative otitis media with or without cholesteatoma has been well documented.(ref) Less commonly appreciated is the occurrence of vertigo in childhood related to eustachian tube dysfunction with resultant middle ear effusion. In a study of 27 children with dizziness, Blain62 found that five had serous otitis media or glue ear and, when treated appropriately, their dizziness resolved.
Involvement of the labyrinth secondary to infection may be caused by toxins, by actual bacterial invasion via emissary veins or by semicircular canal erosion.63 There exists a variety of viral causes of inner ear disease including mumps, measles, varicella zoster, cytomegalovirus and influenza B. Delayed onset vertigo may occur because of these viral disorders. For example, mumps causing a severe sensorineural hearing loss in childhood, may not affect the vestibular system until years later, perhaps due to delayed endolymphatic hydrops. While viruses are felt to be important etiologic agents, evidence is mostly circumstantial. At the present time only cytomegalovirus and the mumps virus have been cultured from the perilymph of affected ears.73,74
Immune-mediated attack upon the inner ear with resultant vertigo, sensorineural hearing loss, aural fullness and tinnitus has been an area of intensive research. It was first highlighted by McCabe in 197964 and elaborated by Hughes.65 Hughes states that autoimmune mediated inner ear disease is diagnosed by clinical findings, positive immunologic laboratory testing and positive treatment response.65 The typical patient is middle aged, female, and exhibits bilateral progressive sensorineural
hearing loss (may be asymmetric) with or without dizziness, aural fullness or tinnitus. Symptoms often progress over weeks to months although sudden hearing loss has been reported.67 Occasionally, the patient may have a systemic immune disease such as rheumatoid arthritis.64,65,66 Hughes65 examined 52 patients suspected of having autoimmune inner ear disease and found 7 to have Cogan’s syndrome, 4 with rheumatoid arthritis and 1 having systemic lupus erythematosus.65 Cogan’s syndrome is a rare disease characterized by non-syphilitic interstitial keratitis associated with tinnitus, vertigo and hearing loss.68 The etiology is uncertain but evidence suggests that immunologic or infectious causes are likely.69
II.CENTRAL CAUSES OF VERTIGO
The idea that vascular compression of cranial nerves may lead to clinically significant symptoms dates back to Dandy’s75 first description of trigeminal neuralgia secondary to a vascular loop. It is now well accepted that the cause of tic douloureux and hemifacial spasm is a loop of the anterior inferior cerebellar artery or nearby veins pulsating on the trigeminal or facial nerves respectively.76
More recently, vascular loops compressing the vestibulo- cochlear nerve have been considered a possible cause of hearing loss, vertigo and tinnitus.(ref) The symptoms oftem mimic cerebellopontine angle tumors. Examinations such as pneumo- computed tomography and magnetic resonance imaging (MRI) have, occasionally demonstrated prominent vascular loops penetrating into the internal auditory canal (IAC).77,78 Unilateral delays observed in auditory brainstem response (ABR) testing has also been correlated with compression of the VIIIth nerve complex by a vascular loop.Moeller16
Anatomic dissections indicate that approximately65% of specimens have vascular loops approaching the VIIth and VIIIth nerves.79,80 McCabe91 described eight patients with discrete spells of true vertigo who were previously diagnosed with Meniere’s disease or an unknown cause. All eight patients underwent vestibular nerve section and in each case a vascular loop extending far into the internal auditory canal with compression of the superior vestibular nerve was found. Janetta84 has suggested that patients with vascular loops are more apt to present with constant positional vertigo or disequilibrium with nausea. They generally do not have the typical hearing loss of Meniere’s disease and vestibular function testing is many times normal.84
Vascular insufficiency occurs in the vertebrobasilar system secondary to obstruction, stenosis or “steal” flow patterns. Ischemia is responsible for over 80% of central vestibular disturbances.85 The variable history and clinical findings associated with VBI occur because of the complexity and high numbers of sensory and motor pathways that are supplied by the posterior circulation. Carotid insufficiency secondary to stenosis may cause blood flow reversals in the posterior communicating artery with a resultant “steal phenomenon” from the vertebrobasilar system.85
Grad examined a series of 84 patients with posterior circulation problems and found that there was a high incidence of isolated episodes of vertigo associated with vertebrobasilar insufficiency. He also described a 42% incidence of unilateral caloric weakness, concluding that the vestibular labyrinth is selectively vulnerable to ischemia from disorders in the vertebrobasilar system.86 Visual dysfunction, drop attacks, unsteadiness and extremity weakness were the most common associated symptoms in patients with VBI.86
In Valvossori’s85 study of 200 patients with VBI, 87% complained of dizziness. He suggested that if computed tomographic dynamic exams were suspicious of flow aberrations, angiography should be obtained to confirm the flow abnormality.85
Multiple sclerosis is a demyelinating disorder that is characterized by a variety of neurological signs and symptoms which have a tendency towards remission and exacerbation. Typically, MS is a disease of young adult white females.
The etiology is unknown, however, based upon epidemiologic and virologic studies, it is suggested that MS may be caused by an abnormal immunologic response to prior viral exposure.89 Recent studies show wide discrepancies in the percentage of symptoms of vertigo or disequilibrium, ranging from 5% to 51%.92,93 A gaze induced horizontal nystagmus is thought to occur in up to 70% of patients with MS. Vertical nystagmus occurs in approximately one third of multiple sclerosis patients.(need reference)
Migraine was fist described by Hippocrates 25 centuries ago.96 It is a common disorder that affects approximately 25% of women, 20% of men and 2-5% of children.94,95 Typically, migraine is characterized by periodic headaches that are occasionally associated with nausea, vomiting and neurologic symptoms. In common migraine, absence of neurologic symptoms is the rule whereas in classical migraine an aura typically precedes the headaches.94,97,98 It is also well documented that neurologic symptoms termed “migraine equivalent” can occur in the interval between headaches.99 Of 200 patients with migraine examined by Kayan and Hood,100 53 complained of vertigo. Vertigo was noted as an aura in 8 patients, during the headache in 25 patients, after the headache in 1 patient, and between headaches in 19 patients.100
Bickerstaff was the first to describe basilar artery migraine. This was characterized by an aura of scotomata, transient blindness, vertigo, dysarthria, parasthesias, ataxia and tinnitus.
Cervical vertigo was first documented by Claude Bernard in 1858.107 Longet and Shift108,109 described gait disorders resembling cerebellar ataxia after severing cervical muscles in several animal species.108,109 There are several theories as to he etiology of cervical vertigo including inflammatory and degenerative changes in the cervical spine or neck musculature which can lead to altered neck proprioceptive input. These reflexes or impulses are important for cervical righting reflexes. Barre110 injected 1% procaine into deep cervical tissues and found not only vertigo, horizontal contralateral nystagmus, ipsilateral past pointing, and falling toward the injected side, but also observed tinnitus and an ipsilateral Horner’s Syndrome.110 Vascular insufficiency may be another cause of cervical vertigo. It is well known that turning the head leads to decrease flow in vertebral vessels,111 however, general cardiovascular causes such as atherosclerosis appear more important. Irritation of the cervical sympathetic system has also been implicated as a potential cause of cervical vertigo.110.112
III.MISCELLANEOUS CAUSES OF VERTIGO
There are multiple metabolic derangements that have been implicated as causative factors in inner ear disease According to Rubin117 there are five major organ systems responsible for inner ear homeostasis. These include the adrenal and pituitary glands, the hormonal and immune systems and the hypothalamus.117
The most frequent laboratory abnormality associated with vestibular dysfunction in hyperglycemia. Frequently dietary manipulation will lead to a beneficial response.118,119 Spencer120 reported on 1,400 patients with hearing loss and vertigo who were diagnosed with hyperlipidemia. Hypothyroidism has also been implied as a potential cause of neuro-otologic dysfunction.118
Many different drugs are known to produce vertigo including alcohol, Phenobarbital, Dilantin, Chlorpromazine, Adrenocorticotropic antagonists, Cholinomimetics, Cholinesterase inhibitors and Gammaaminobutyric acid agonists.121
It has also been suggested that food allergies or inhalant allergies may be a contributing factor in the development of endolymphatic hydrops. Shambaugh currently encourages dietary management of food allergens for relief of symptoms of Meniere’s Disease.122
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