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Vertigo is not a separate disease process, but a multisensory and sensorimotor syndrome with various etiologies and pathogeneses. It is among the commonest symptoms presented to doctors, with a lifetime prevalence of around 20% to 30%. Patients have often consulted multiple physicians before a diagnosis is made and therapy initiated. Selective literature research and review of the guidelines of the German Neurological Society. A careful history remains the cornerstone of diagnosis. Once the correct diagnosis is made, specific and effective treatments are available for most peripheral, central, and psychogenic forms of dizziness. Treatment may include medication, physiotherapy, and psychotherapy; a few limited cases may require surgical treatment. The treatment of choice for acute vestibular neuritis is the administration of corticosteroids. Menière's disease is treated with high-dose, long-term betahistine. A new approach to the management of downbeat and upbeat nystagmus, and of episodic ataxia type 2, involves the use of aminopyridines as potassium-channel blockers. Close multidisciplinary cooperation is essential in dizziness, and further multicenter studies are needed.
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Deutsches Ärzteblatt InternationalDtsch Arztebl Int 2008; 105(10): 173–80 173
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T
he term "dizziness" refers either to an unpleasant
disturbance of spatial orientation or to the erro-
neous perception of movement, which is more specifi-
cally called "vertigo." Vertigo involves a perceived
movement either of one's own body, such as swaying or
rotation, or of the environment, or both. Alongside head-
ache, dizziness and vertigo are among the more com-
mon symptoms with which patients present to physi-
cians in general, not just to neurologists. Their lifetime
prevalence is approximately 20% to 30% (1). Experi-
ence has shown that the affected persons often make an
odyssey of visits to physicians belonging to various
specialties, beginning with their family physicians and
proceeding through ENT specialists, neurologists, oph-
thalmologists, internists, and orthopedists, before the
correct diagnosis is made and the appropriate treatment
is begun. In other words, these patients often fall into the
cracks between medical specialties.
A patient's complaint of "dizziness" necessitates the
taking of a thorough history precisely because of the
many different meanings this term can have. Ancillary
testing is of secondary importance. The relative fre-
quencies of various syndromes presenting with dizzi-
ness and vertigo are listed in table 1. The important
criteria for distinguishing among them are as follows (2):
>The type of dizziness/vertigo: rotatory vertigo
resembles the sensation of being on a merry-go-
round (in vestibular neuritis and other disorders),
while postural vertigo resembles the sensation of
riding in a boat (e.g., in bilateral vestibulopathy).
Many patients use the term "dizziness" for
lightheadedness without any sensation of move-
ment (e.g., in drug intoxication).
>The duration of dizziness/vertigo: attacks may
last for seconds or minutes (as in vestibular
paroxysm) or hours (as in Menière's disease or
vestibular migraine). Persistent vertigo lasting
days or weeks is seen in vestibular neuritis,
among other conditions. Attacks of postural verti-
go lasting minutes to hours can be produced, for
example, by brainstem transient ischemic attacks.
>Precipitating and exacerbating factors of dizzi-
ness and vertigo: the symptoms arise at rest in
some conditions (e.g., vestibular neuritis); they
can also arise when the patient walks (as in bi-
lateral vestibulopathy) or be induced by turning
the head to the right or left (as in vestibular
paroxysm). Other possible precipitating factors
REVIEW ARTICLE
Diagnosis and Treatment
of Vertigo and Dizziness
Michael Strupp, Thomas Brandt
SUMMARY
Introduction: Vertigo is not a separate disease process, but
a multisensory and sensorimotor syndrome with various
etiologies and pathogeneses. It is among the commonest
symptoms presented to doctors, with a lifetime prevalence
of around 20% to 30%. Patients have often consulted
multiple physicians before a diagnosis is made and therapy
initiated.
Methods: Selective literature research and review of the
guidelines of the German Neurological Society.
Results: A careful history remains the cornerstone of
diagnosis. Once the correct diagnosis is made, specific and
effective treatments are available for most peripheral,
central, and psychogenic forms of dizziness. Treatment
may include medication, physiotherapy, and psychotherapy;
a few limited cases may require surgical treatment. The
treatment of choice for acute vestibular neuritis is the
administration of corticosteroids. Menière's disease is
treated with high-dose, long-term betahistine. A new
approach to the management of downbeat and upbeat
nystagmus, and of episodic ataxia type 2, involves the use
of aminopyridines as potassium-channel blockers. Close
multidisciplinary cooperation is essential in dizziness, and
further multicenter studies are needed.
Dtsch Arztebl Int 2008; 105(10): 173–80
DOI: 10.3238/arztebl.2008.0173
Key words: presenting complaint, vestibular disorder,
vertigo, dizziness, Menière’s disease, migraine
Neurologische Klinik der Universität München, Klinikum Großhadern:
Prof. Dr.med. Strupp, Prof. Dr. med. Dr. h.c. Brandt, FRCP
174 Deutsches Ärzteblatt InternationalDtsch Arztebl Int 2008; 105(10): 173–80
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include turning in bed (as in benign paroxysmal
positioning vertigo [BPPV]), coughing, pressing,
and loud tones of a particular frequency (Tullio's
phenomenon, seen in perilymph fistula), as well
as certain social or environmental conditions
(e.g., phobic postural vertigo).
>The accompanying symptoms, if present, may
arise from the inner ear – e.g., attacks of intense
tinnitus, hearing impairment, and a pressure sen-
sation in the ear, which are typical of Menière's
disease. Diplopia, sensory disturbances, dyspha-
gia, dysarthria, and paralysis of arms and legs are
symptoms of central origin that usually arise in
the brainstem. Headache or a history of migraine
may point to the diagnosis of vestibular migraine
but can also be caused by brainstem ischemia or
posterior fossa hemorrhage.
General principles of treatment
The treatment of dizziness and vertigo (2) may include
medication, physical therapy, and psychotherapy; a few
limited cases may require surgical treatment . Before the
treatment is begun, the patient should be told that the
prognosis is generally good: many of these conditions
have a favorable spontaneous course, both because
peripheral vestibular dysfunction tends to improve and
because there is central vestibular compensation for
asymmetrical peripheral vestibular tone. Moreover,
most of these conditions can be treated successfully.
In this review article, the authors summarize the diag-
nosis and treatment of dizziness, vertigo, and
dysequilibrium. The information presented here was
drawn from a selective review of the literature and from
the guidelines of the German Neurological Society.
The common types of dizziness and vertigo
and their treatment
Peripheral vestibular vertigo
A functional classification of peripheral vestibular
disorders divides them into three main types, which
can be distinguished on the basis of their typical
symptoms and signs (table 2):
>Chronic, bilateral dysfunction of the vestibular
nerve or the peripheral vestibular organs;
>Acute, unilateral vestibular dysfunction;
>Paroxysmal pathological excitation or inhibition
of the vestibular nerve or vestibular organs.
In the following sections, we will present the charac-
teristic history, clinical findings, and treatment of these
three common types of peripheral vestibular vertigo.
Benign paroxysmal positioning vertigo (BPPV)
This is the most common type of vertigo; it mainly
affects older patients (table 1) and has a lifetime preva-
lence of 2.4% (1). It is characterized by brief attacks of
rotational vertigo, accompanied by vertical positioning
nystagmus that rotates toward the lower of the two ears
and beats toward the forehead. The attacks are
precipitated by reclination of the head, or by lateral
positioning of the head or body, with the affected ear
downward. After a change in position of one of these
types, rotational vertigo and nystagmus arise after a
latency of a few seconds and then take a characteristic
crescendo-decrescendo course, lasting a total of 30 to 60
seconds. The nystagmus corresponds to a so-called am-
pullofugal excitation of the affected posterior vertical
semicircular canal of the affected (lower) ear.
More than 90% of cases are idiopathic; the remain-
ing, symptomatic cases are most commonly due to
head trauma, vestibular neuritis, or Menière's disease
(3). BPPV also arises with greater than usual frequen-
cy after prolonged bed rest necessitated by other
diseases, or after surgery. BPPV of the horizontal
semicircular canal is rare and is precipitated by rota-
tion of the head in the recumbent position. BPPV is
called "benign" because it usually resolves sponta-
neously within a few weeks or months; in some cases,
however, it can last for years. If left untreated, it per-
sists in about 30% of patients.
The canalolithiasis hypothesis explains all of the
manifestations of positioning vertigo and nystagmus
(4). According to this hypothesis, the condition is due
to the presence of agglomerates of many otoconia that
nearly fill the lumen of the semicircular canal and are
freely mobile within it, instead of the small pieces of
particulate matter that adhere firmly to the cupula (so-
called cupulolithiasis).
BPPV is treated with positioning maneuvers: rapid
repositioning of the head can move the otoconial ag-
glomerate out of the semicircular canal so that it can
no longer cause positioning vertigo. The treatments of
choice are the Semont (5) and Epley maneuvers. For
the Semont maneuver, see figure 1; the Epley maneuver
TABLE 1
The relative frequencies of different dizziness and
vertigo syndromes
Diagnosis Number of Percent
patients
Benign paroxysmal
positioning vertigo 1336 18.6
Phobic postural vertigo 1127 15.6
Central vestibular vertigo 893 12.4
Basilar/vestibular migraine 738 10.2
Menière's disease 677 9.4
Vestibular neuritis 531 7.4
Bilateral vestibulopathy 367 5.1
Vestibular paroxysmia 284 3.9
Psychogenic dizziness 228 3.2
Perilymph fistula 44 0.6
Dizziness syndromes
of unclear etiology 239 3.3
Other 741 10.3
Overall 7205
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involves rotation of the patient in the recumbent posi-
tion with the head hanging down. Most patients can
perform these maneuvers themselves after brief train-
ing. The two are equally effective, and the cure rate is
more than 95% within a few days, as shown by multi-
ple controlled studies and meta-analyses (6). The rate
of recurrence of BPPV is about 15% to 30% per year.
The symptoms eventually recur at some time after ef-
fective treatment in about 50% of patients (7) but can
then be treated effectively a second time in the same
manner.
Vestibular neuritis
The clinical syndrome of vestibular neuritis is charac-
terized by the following (figure 2):
>Persistent rotational vertigo with a pathological
inclination of the visual vertical axis toward the
side of the affected labyrinth
>Spontaneous, horizontally rotating nystagmus
toward the unaffected side, producing apparent
movement of the environment ("oscillopsia")
>Gait deviation and falling tendency toward the
affected side
>Nausea and vomiting
>Unilateral dysfunction of the horizontal semi-
circular canal, as revealed by the Halmagyi-
Curthoys head impulse test (8) for the function of
the vestibulo-ocular reflex, as well as by caloric
testing.
A viral and/or autoimmune etiology for vestibular
neuritis is probable but has not yet been proven. Au-
topsy studies have revealed inflammatory degen-
eration of the vestibular nerve, the presence of viral
DNA from herpes simplex virus type I, and the so-
called "latency-associated transcript" (LAT) in vestib-
ular ganglion cells (9). The treatment is symptomatic,
causal, and physiotherapeutic:
>Symptomatic treatment: antivertiginous medica-
tions, such as 100 to 300 mg of dimenhydrinate,
should be given only in the first three days and
only if necessary to treat severe nausea and vom-
iting, because they delay the development of cen-
tral compensation mechanisms.
>"Causal" treatment: a four-armed, placebo-
controlled trial was performed, based on the as-
sumption that vestibular neuritis is caused by the
reactivation of a latent herpes simplex virus type
1 infection. The trial revealed that monotherapy
with a glucocorticoid-methylprednisolone at an
initial dose of 100 mg daily, reduced in 20-mg
steps every four days, significantly improved the
recovery of peripheral vestibular function. The
administration of valacyclovir alone had no
effect, nor did its administration in combination
with the glucocorticoid have any additional effect
(10).
>Physical therapy: a further principle of treatment is
the promotion of central compensation by physical
therapy. Equilibrium training significantly lessens
the time required for vestibulospinal compensation
and postural regulation to develop (11). Voluntary
eye movements and fixation are exercised in order
to improve impaired visual fixation; furthermore,
active head movements are exercised to realign the
vestibular reflex, as well as balance tasks, goal-
directed movements, and walking to improve ves-
tibulospinal postural regulation and goal-directed
motor function. Patients should exercise for
30 minutes three times a day.
Menière's disease
This condition is probably due to labyrinthine endo-
lymphatic hydrops with periodic rupturing of the
membrane that separates the endolymphatic and
TABLE 2
The presenting manifestations and causes of peripheral vestibular types of vertigo
Type of disorder Presenting manifestations Examples and causes
Chronic, bilateral peripheral Oscillopsia on head movement (loss of Bilateral vestibulopathy due to (e.g.):
vestibular dysfunction the vestibulo-ocular reflex) – ototoxic substances (aminoglycosides)
Unsteadiness of stance and gait, worsening in – bilateral Menière's disease
darkness and on uneven ground (because of – meningitis
the partial or total removal of visual – bilateral acoustic neuromas
or somatosensory cues) ( = neurofibromatosis type 2)
Impairment of spatial memory
Acute/subacute unilateral Rotatory vertigo (lasting a few days to weeks) Vestibular neuritis due to reactivation of a latent
vestibular dysfunction Oscillopsia due to spontaneous nystagmus herpes simplex virus type 1 infection
(labyrinth and/or vestibular Tendency to fall to a particular side
nerve) with asymmetrical Nausea
vestibular tone
Inappropriate unilateral Attacks of rotational or swaying vertigo Benign peripheral paroxysmal positioning vertigo
paroxysmal excitation or that (depending on their cause) due to canalolilthiasis
loss of function of the peripheral may or may not be externally precipitated, Menière's disease due to rupture of the
vestibular system are of varying duration, and are accompanied endolymphatic membrane
by various other symptoms Vestibular paroxysm due to neurovascular
contact
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perilymphatic spaces. These ruptures precipitate the
paroxysmal attacks that last a few minutes to hours
(12). The ultimate etiology is impaired resorption in
the endolymphatic sac due to perisaccular fibrosis or
to obliteration of the endolymphatic duct. Attacks are
produced when rupture of the endolymphatic tube
causes calcium-induced depolarization of the
vestibulocochlear nerve. A classic Menière's attack
consists of rotatory vertigo, tinnitus, hearing impair-
ment, and pressure sensation in one ear. The lifetime
prevalence of this condition is approximately 0.5%
(1). It usually begins on one side, and the frequency of
attacks is highly variable. Menière's disease becomes
bilateral in 50% of cases (13) and is the second most
common cause of bilateral vestibulopathy.
Its treatment is based on two principles:
>Treatment of individual attacks: vertigo and nau-
sea can be improved with antivertiginous medica-
tions just as in the treatment of other types of acute
labyrinthine dysfunction. For example, 100 mg
dimenhydrate suppositories can be used.
>Attack prophylaxis: this type of treatment is aimed
at improving the underlying endolymphatic hydrops.
Despite the high prevalence of Menière's disease
and the large number of clinical studies that have
been performed, there is still no treatment of this type
that has been conclusively shown to be effective.
The spectrum of recommendations ranges from
a sodium-free diet to diuretics, transtympanic
gentamicin instillation (20 to 40 mg given repeatedly,
at intervals of several weeks, until symptoms
improve), betahistine, and surgical procedures
(12). Abeneficial effect on the frequency of attacks
has been reported for transtympanic gentamicin (6)
and for the prolonged high-dose administration of
betahistine hydrochloride (48 mg tid for 12
months). The latter dose of betahistine hydrochloride
is currently recommended on the basis of a recently
reported observational treatment study in 112 patients
who were treated for at least 12 months at doses of
16, 24, or 48 mg tid (14). The highest dose led to a
statistically significantly greater reduction of attack
Figure 1: The treatment of benign paroxysmal positioning vertigo (BPPV) with the Semont maneuver. The illustration shows the treatment of
BPPV due to canalolithiasis of the right posterior semicircular canal.
a) In the initial, sitting position, the head is turned 45° to the side of the unaffected ("healthy") ear.
b) The patient is laid on the right side, i.e., on the side of the affected ear, while the head is kept in 45° of rotation to the other side.
This induces movement of the particulate matter in the posterior semicircular canal by gravity, leading to rotatory nystagmus toward the
lower ear that extinguishes after a brief interval. The patient should maintain this position for about one minute.
c) While the head is still kept in 45° of rotation toward the side of the healthy ear, the patient is rapidly swung over to the side of the
unaffected ear,so that the nose now points downward. The particulate matter in the semicircular canal now moves toward the exit from
the canal. This position,too, should be maintained for at least one minute.
d) The patient returns slowly to the initial, sitting position. The particulate matter settles in the utricular space, where it can no longer induce
rotatory vertigo. This sequence (a–d) should be performed three times in a row three times per day,in the morning, at noon, and at night.
Most patients are free of symptoms after doing this for three days.
a
b
c
d
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frequency and was well tolerated. These findings
provided the motivation for a multicenter, controlled
dose-finding study that is currently in progress (Eu-
draCT number 2005-000752-32; BMBF177zfyGT).
Central vestibular syndromes
Central vestibular syndromes are mainly caused by
lesions of the vestibular pathways, which arise in the
vestibular nuclei in the caudal portion of the brain-
stem and proceed to the cerebellum, thalamus, and
vestibular cortex, or by damage to the vestibulocere-
bellum. Pathological excitation is a rare cause, as
occurs, for example, in the paroxysmal brainstem
attacks with ataxia that can be produced by multiple
sclerosis or vestibular epilepsy. The common causes
of central vestibular vertigo include vestibular mi-
graine and ischemic lesions in the brainstem. Further-
more, central vestibular disturbances arise in the
setting of certain ocular motor disorders such as
downbeat and upbeat nystagmus, as attacks in episod-
ic ataxia type 2, and in vestibular migraine. These
individual disorders, and the treatment of each, will be
discussed in the following sections.
Downbeat and upbeat nystagmus
Two types of vertically beating central nystagmus are of
special importance: downbeat nystagmus (DBN) and
upbeat nystagmus (UBN), each named after the direc-
tion of the rapid, beating phase. DBN is the most com-
mon type of acquired, persistent nystagmus (15). Both
types manifest themselves above all with swaying nys-
tagmus and unsteadiness of gait and only secondarily
with oscillopsia, i.e., apparent movement of the envi-
ronment due to oscillation of the retinal image. In
distinction to spontaneous nystagmus such as in vestib-
ular neurits, DBN and UBN are types of fixation nys-
tagmus, i.e., their intensity increases with visual fixa-
tion. Both DBN and UBN always indicate the presence
of a central disturbance and possess special localizing
significance. DBN is usually due to bilateral dysfunc-
tion of the flocculus (16); its three common causes are
cerebellar atrophy, ischemia, and Arnold-Chiari malfor-
mation (15). UBN – which, unlike DBN, generally per-
sists for no more than a few weeks – can be caused by
paramedian medullary or pontomesenchephalic lesions,
e.g., brainstem infarct or hemorrhage.
A randomized, placebo-controlled study of DBN has
shown that the potassium-channel blockers 3,4-
diaminopyridine (17) (figure 3) and 4-aminopyridine
can significantly improve this type of nystagmus (18).
The dosage is 5 to 10 mg tid; follow-up ECG is neces-
sary. The effectiveness of this treatment has since been
confirmed by multiple studies. 4-Aminopyridine seems
to be effective against UBN as well, but this has been
documented to date only in a single case study (20).
Episodic ataxia type 2
The familial episodic ataxias are rare genetic dis-
eases of autosomal dominant transmission. There are
at least two well-defined varieties. Type 2 (EA 2) is
characterized by recurrent attacks of dizziness and
ataxia that are precipitated by physical activity, stress,
or alcohol and usually last for hours. In between
attacks, more than 90% of patients have marked cen-
tral ocular motor disturbances, often DBN. EA 2 is
caused by mutations in the CACNA1A gene (PQ cal-
cium channel gene). Most patients can be treated suc-
cessfully with acetazolamide. If this treatment is inef-
fective, or if adverse effects such as kidney stones
develop, patients with EA 2 can also be treated with
4-aminopyridine (5 mg tid) (21).
Aminopyridines are thus an effective treatment for
DBN, UBN, and EA 2 which is well tolerated at the low
dose that is generally used. These studies have also led
to the development of a new principle of treatment; ac-
tivation of cerebellar Purkinje cells through potassium-
channel blockade enhances the cerebellar inhibitory in-
fluence on the vestibular and cerebellar nuclei.
Vestibular migraine or migraine with vestibular aura
Vestibular migraine is characterized by recurrent
attacks that last minutes to hours and usually consist
of rotatory vertigo (22, 23). It is the most common
cause of spontaneously occurring attacks of vertigo
(table 1). Its lifetime prevalence is 0.98% (1). In more
than 60% of patients, these attacks are associated with
headache and/or photophobia or phonophobia; the re-
maining patients have attacks of vertigo alone. Most
The symptoms and clinical findings in right vestibular neuritis.
The rotatory vertigo often arises acutely and lasts from several days
to a few weeks. Clinical examination is performed with Frenzel’s
goggles that are lit from within and contain magnifying lenses
(+16 diopters). These goggles prevent the suppression of spontaneous
nystagmus by visual fixation and make the patient's eye movements
easier to observe. Spontaneous nystagmus away from the affected
side is seen, along with a falling tendency, ocular tilt, and deviation of
the subjective visual vertical axis toward the affected side.
FIGURE 2
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patients also have migraine attacks with or without an
aura; this fact makes the condition easier to diagnose.
In some patients, the diagnosis can be made only on
the basis of a positive response to the treatment of the
individual attacks with medication and to pharmaco-
logical prophylaxis. The prophylactic treatment of
vestibular migraine is analogous to that of migraine
with aura and consists of the administration of beta-
blockers, valproic acid, and topiramate. No random-
ized, controlled studies on the efficacy of medications
for vestibular migraine have yet been published.
Phobic postural vertigo
Phobic postural vertigo is the second most common
diagnosis in a specialized neurological ambulatory
clinic for dizziness and vertigo. This disorder is not
found in the diagnostic repertoire of most neurologists
and ENT specialists. Patients with phobic postural
vertigo usually complain of swaying vertigo, light-
headedness, and gait unsteadiness that are continually
present but fluctuate in severity. These symptoms are
often accompanied by anxiety and are situationally
dependent. The precipitating factor may be the pres-
ence of a large crowd, or waiting in the check-out line
at a store; often, avoidance behavior results (2). The
symptoms typically improve when the patient partici-
pates in sports or has had a small amount of alcohol to
drink. The affected patients often have an obsessive-
compulsive personality, in the sense of "accentuated"
personality traits, with a marked tendency toward
introspection and a need to "have everything under
control." The central problem in phobic postural ver-
tigo is the patient's attempt to establish conscious con-
trol over body equilibrium, which leads to a "spiral of
self-observation." When this happens, the body's own
movements may be perceived as movements of the
outside world. The main features of this disorder and
its treatment are summarized in the box. The clinical
neurological examination and ancillary tests reveal no
relevant pathological findings.
These patients can be treated with three or four of
the following measures: Athorough diagnostic assess-
ment serves to reassure the patient that the symptoms
are not caused by an organic disorder. Psycho-educative
explanation informs the patient about the underlying
mechanism of excessive self-observation. Desensi-
tization can be performed by repeated exposure to the
precipitating situation(s) and by regular participation
Mean peak slow phase velocities (PSPV) of DBN measured by 2-D recordings of eye movements. The two graphs on the left show the original
data of mean PSVP of each subject: (a) Control versus 3,4-DAP, (c) control versus placebo.The two graphs in the middle give the box plot charts
with the mean, median, and the 50% percentile as well as the range for control versus 3,4-DAP (b) and control versus placebo (d).3,4-DAP
reduced mean PSPV of DBN from 7.2 ± 4.2 deg/s (mean ± SD) before treatment to 3.1 ± 2.5 deg/s 30 min after ingestion of the 3,4-DAP
(n = 17, p < 0.001, two-way ANOVA). The inset (e) shows an original recording of the vertical eye position before (upper trace) and 30 min after
ingestion of the drug (lower trace).
From: Strupp M, Schuler O,Krafczyk A, Jahn K, Schautzer F, Buttner U, Brandt T:Treatment of downbeat nystagmus with 3,4-diaminopyridine: a
placebo-controlled study. Neurology 2003; 61:165-70, with the kind permission of Lippincott Williams and Wilkins.
FIGURE 3
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MEDICINE
in sports; these activities strengthen the patient's con-
fidence in his or her own balancing ability. Finally, if
the symptoms persist, pharmacotherapy with a selec-
tive serotonin reuptake inhibitor and/or cognitive be-
havioral therapy can be initiated (24). Combined
therapy according to this approach leads to marked
improvement in more than 70% of patients, even if the
disorder has been present for many years (25).
Conflict of interest statement
Professor Strupp has received lecture fees from the following companies in
Germany: Solvay Pharmaceuticals (Hanover), Hennig-Pharma (Flörsheim),
Schwarz Pharma (Monheim), and Serono (Unterschleissheim). Professor Brandt
has received lecture fees from Solvay Pharmaceuticals (Hanover).
Manuscript received on 27 August 2007 2007; revised version accepted on
19 November 2007.
Translated from the original German by Ethan Taub, M.D.
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13. Takumida M, Kakigi A, Takeda T, Anniko M: Meniere's disease: a
long-term follow-up study of bilateral hearing levels. Acta Oto-
laryngol 2006; 126: 921–5.
14. Strupp M, Huppert D,Frenzel C, Wagner J, Zingler VC, Mansmann
U, Brandt T: Long-term prophylactic treatment of attacks of verti-
go in Menière's disease-comparison of a high with a low dosage
of betahistine in an open trial. Acta Otolaryngol (Stockh) 2008.
In press.
15. Wagner JN, Glaser M, Brandt T, Strupp M: Downbeat nystagmus:
Aetiology and comorbidity in 117 patients. J Neurol Neurosurg
Psychiatry 2007 Sep 14 (Epub ahead of print).
16. Kalla R, Deutschlander A, Hufner K et al.: Detection of floccular
hypometabolism in downbeat nystagmus by fMRI. Neurology
2006; 66: 281–3.
17. Strupp M, Schuler O,Krafczyk S et al.: Treatment of downbeat
nystagmus with 3,4-diaminopyridine: a placebo-controlled study.
Neurology 2003; 61: 165–70.
18. Kalla R, Glasauer S,Buttner U, Brandt T, Strupp M:4-Aminopyri-
dine restores vertical and horizontal neural integrator function in
downbeat nystagmus. Brain 2007; 130: 2441–51.
19. Sprenger A,Rambold H, Sander T et al.:Treatment of the gravity
dependence of downbeat nystagmus with 3,4-diaminopyridine.
Neurology 2006; 67: 905–7.
20. Glasauer S, Kalla R,Buttner U, Strupp M, Brandt T: 4-aminopyri-
dine restores visual ocular motor function in upbeat nystagmus.
J Neurol Neurosurg Psychiatry 2005; 76: 451–3.
21. Strupp M, Kalla R,Dichgans M, Freilinger T, Glasauer S,Brandt T:
BOX
Phobic postural vertigo: the second
most common cause of vertigo
CClliinniiccaall ffeeaattuurreess
>The patient has postural vertigo with unsteadiness of
stance and gait; the neurological examination and
ancillary tests are generally unremarkable
>Fluctuating unsteadiness of stance and gait with
attacks of fear of falling, but without an actual fall
>Anxiety and autonomic disturbances sometimes occur
during or just after the attacks
>The attacks are precipitated or exacerbated by typical
situations, e.g., crowds,empty spaces, driving
>The symptoms often improve during sporting activity or
after the consumption of a small amount of alcohol
>Increasingly severe avoidance behavior is common
The patient's personality is usually of an obsessive-
compulsive or reactive-depressive type. At the onset of
the disorder,there is often a vestibular disturbance (25%)
or a situation giving rise to particular stress (70%).
TTrreeaattmmeenntt
>A thorough diagnostic assessment to allay the patient's
fear of having a serious organic disease
>Psycho-educative therapy to inform the patient about
the pathological mechanism and the precipitating
factors and situations
>Desensitization by self-exposure, i.e., the deliberate
seeking out of situations that precipitate vertigo. Light
sporting activities are also helpful.
>If the symptoms persist, pharmacotherapy, e.g., with
selective serotonin reuptake inhibitors, and/or cognitive
behavioral therapy are indicated
Treatment markedly improves symptoms in about 70% of patients (25)
180 Deutsches Ärzteblatt InternationalDtsch Arztebl Int 2008; 105(10): 173–80
MEDICINE
Treatment of episodic ataxia type 2 with the potassium channel
blocker 4-aminopyridine. Neurology 2004; 62: 1623–5.
22. Neuhauser H, Leopold M,von Brevern M, Arnold G,Lempert T:
The interrelations of migraine, vertigo, and migrainous vertigo.
Neurology 2001; 56: 436–41.
23. Dieterich M, Brandt T: Episodic vertigo related to migraine (90
cases): vestibular migraine? J Neurol 1999; 246: 883–92.
24. Holmberg J, Karlberg M,Harlacher U, Magnusson M: One-year
follow-up of cognitive behavioral therapy for phobic postural
vertigo. J Neurol 2007; 254: 1189–92.
25. Huppert D, Strupp M,Rettinger N, Hecht J, Brandt T: Phobic
postural vertigo-a long-term follow-up (5 to 15 years) of 106
patients. J Neurol 2005; 252: 564–9.
Corresponding author
Prof. Dr. med. Michael Strupp
Neurologische Klinik der Universität München Klinikum Großhadern
Marchioninistr.15
81377 München, Germany
Michael.Strupp@med.uni-muenchen.de
... Dizziness is a common, non-specific symptom and is among one of the most frequent medical complaints [1]. Defined as disorientation that produces a disturbed postural awareness, dizziness has been attributed to neurologic, vestibular, psychosomatic, and cervical spine dysfunction [2,3]. Of these etiologies, this systematic review is concerned specifically with dizziness related to cervical spine dysfunction. ...
... Participants must be military-aged adult humans (18-45 years old) with traumatic CGD, defined as dizziness that is temporally associated with neck pain and injury after other causes of dizziness (such as central or peripheral vestibular pathologies) have been excluded [29]. This review will include all studies examining at least one of the following interventions: (1) education (i.e., patient education, postural or ergonomic information, brochures), (2) exercise (i.e., cervical or scapular retraction, stabilization or strengthening, proprioceptive or kinesthetic retraining), (3) manual therapy (i.e., mobilization, manipulation, Mulligan or Maitland techniques, massage, myofascial release, suboccipital release), (4) vestibular rehabilitation (i.e., gaze stabilization, habituation), and (5) modalities (i.e., dry needling, acupuncture). Comparison interventions may include placebo, usual care, higher versus lower intervention dosage, or different types of interventions applied with similar dosage. ...
... Antonio-Fort Sam Houston, TX 78234, USA. 2 ...
Article
Full-text available
Background: Traumatic cervicogenic dizziness is dizziness that is temporally associated with neck pain and injury after other causes of dizziness have been excluded. It can lead to activity limitations and participation restrictions that may include lost duty or work days. The objective of this systematic review is to determine which interventions are most effective in decreasing dizziness or vertigo and neck pain in military-aged adults with traumatic cervicogenic dizziness. Methods: The literature will be systematically searched using the following online databases: MEDLINE, EMBASE, The Cochrane Library (Cochrane Database of Systematic Reviews, CENTRAL, Cochrane Methodology Register), CINAHL, SCOPUS, Web of Science, and J-STAGE. The review will include randomized controlled trials (RCTs), including cluster RCTs and controlled (non-randomized) clinical trials or cluster trials, and observational studies (including prospective and retrospective comparative cohort and case-control or nested case-control studies) and determine the effectiveness of physical therapy interventions for the treatment of traumatic cervicogenic dizziness in military-aged adults. Assessment of methodological quality will be performed by two independent, blinded reviewers using the PEDro scale. The level of evidence will be determined using the GRADE scale. The primary outcome measures will be change in dizziness and neck pain and disability from baseline to the last available follow-up, measured using the Dizziness Handicap Inventory and Neck Disability Index. Other relevant outcome measures will include self-reported change in symptoms, time to return to duty or work, and quality of life. Discussion: This systematic review will identify, evaluate, and integrate the evidence on the effectiveness of physical therapy interventions for cervicogenic dizziness in a military-aged population. We anticipate our findings may inform individual treatment and future research. Clinical recommendations generated from this systematic review may inform military physical therapy treatment of individuals with cervicogenic dizziness. Systematic review registration: In accordance with the guidelines, our systematic review protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO) on 21 January 2020 (registration number CRD42020150853). In the event of protocol amendments, the date of each amendment will be accompanied by a description of the change and the rationale.
... Since dizziness and vertigo are caused by various disorders including peripheral or central vestibular diseases, psychiatric disorders, and systemic illnesses, it would be important to identify the underlying causes and their proportion according to age and sex not only for diagnosing and treating individual patient but also for establishing public health strategy. The etiologic distribution of dizziness/vertigo has been reported in Germany [4,5]. Etiologic distribution, however, may be dissimilar among different ethnic groups and can be dependent upon the clinical settings (acute vs. referral-based) or the physicians in charge (otolaryngologists vs. neurologists vs. others). ...
... Diagnostic terms were unified and entered into the registry that consisted of the main and sub-categories. The main category included the disorders responsible for dizziness/ vertigo according to the International Classification of Vestibular Disorders (ICVD-I) layer 3 and the disorders adopted in the previous study [4,6], while the sub-category included the specific diagnosis or subtypes of the diseases. ...
... The etiologic distribution observed in this study is similar to that reported in Germany [4]. This indicates no significant differences in the proportion of diseases causing dizziness and vertigo across different ethnic groups. ...
Article
This study aimed to determine the etiologic distribution of dizziness and vertigo in a referral-based dizziness clinic in South Korea. We analyzed the diagnoses of 21,166 consecutive dizzy patients (12,691 women, mean age = 57.9 ± 15.7, age range = 3–97) seen from 2003 to 2019 using a registry and medical records. Overall, dizziness and vertigo were more common in women (60.0%, CI 0.59–0.61) than in men without a difference in age (57.7 ± 15.5 vs. 58.1 ± 16.1, p = 0.094). Benign paroxysmal positional vertigo (BPPV, 24.1%) was the most common cause of dizziness/vertigo, followed by psychiatric or persistent postural perceptual dizziness (20.8%), vascular disorders (12.9%), vestibular migraine (10.2%), Meniere’s disease (7.2%), and vestibular neuritis (5.4%). These six disorders comprised more than 80% of all disorders. The etiology could not be determined in 5.0%, and more than one etiology was found in 14.1%. Vestibular migraine was the most common disorder in children and adolescents (< 19 years), psychiatric or persistent postural perceptual dizziness (26.3%) in the adults (19–64 years), and BPPV (28.2%) in the elderly (≥ 65 years). This etiologic distribution is similar to that reported in another country, and indicates no significant differences in the proportion of diseases causing dizziness and vertigo across different ethnic groups. This study provides valuable information to establish healthcare policy for dizziness and vertigo.
... Vertigo and dizziness, belonging to the most frequent symptoms with an estimated lifetime prevalence of 17-30% [1], cover diseases and conditions of various origin [2,3]. In a narrower sense, vertigo refers to peripheral or central vestibular diseases with a lifetime prevalence of up to 10% [1,4] and a yearly incidence of 1.4% [4]. ...
... In a narrower sense, vertigo refers to peripheral or central vestibular diseases with a lifetime prevalence of up to 10% [1,4] and a yearly incidence of 1.4% [4]. The most prevalent types of peripheral vestibular vertigo are benign paroxysmal positional vertigo (BPPV), Meniere's disease (MD), vestibular neuritis and bilateral vestibulopathy; vestibular migraine is one of the most common examples of central vestibular vertigo [3,5]. ...
Article
Full-text available
Background: Vertigo, a highly prevalent disease, imposes a rising burden on the health care system, exacerbated by the ageing of the population; and further, contributes to a wide span of indirect burden due to reduced capacity to work or need of assistance in activities of daily living. The aim of this review was to summarise the evidence on the economic burden of vertigo. Methods: All original studies published between 2008 and 2018 about the economic evaluation of peripheral or central vestibular vertigo in developed countries were considered eligible, unrestricted to setting, health care provider, or study type. Results: The electronic search in three databases identified 154 studies from which 16 qualified for inclusion. All studies presented partial economic evaluation referring to a variety of vestibular vertigo including unspecified vertigo. Nine studies presented monetised cost results and seven studies reported health care utilization. Direct costs derived mainly from repeated and not well-targeted consultations at all levels of health care, excessive use of diagnostic imaging, and/or of emergency care. Considerable societal burden was caused by decreased productivity, mainly due to work absenteeism. Conclusion: To the best of our knowledge, this is the first systematic review of the existing evidence of the economic burden of vertigo. The lack of conclusive evidence revealed apparent targets of future research. First, studies of diagnostics and therapies for vestibular disease should include cost-effectiveness considerations. Population-based studies of health services utilization should include simple vestibular assessments to get more reliable estimates of the burden of disease and associated costs on the level of the general population. Further, clinical and population-based registries that include patients with vestibular disease, should consider collecting long-term data of societal burden. Primary data collection should increasingly include assessment of health care utilization e.g. by linking their diagnoses and outcomes to routine data from health insurances.
... Although the large majority of patients with vertigo are due to benign and peripheral causes, which are mostly non-life-threatening, a small percentage has serious central pathologies. 5 The symptoms originating from pathology in the cerebellum or brain stem are classified into the central type whereas symptoms arising in the inner ear or from the vestibular nerve are classified as peripheral vertigo. 6 A central cause is suspected if the history and physical examination rule out the peripheral cause or if the patient presents with additional neurological complaints of weakness, dysarthria, sensory changes, ataxia, or confusion. ...
Article
Full-text available
Background: Dizziness is a common symptom affecting about 30% of people over the age of 65years. In this study, we tried to determine the usefulness of MRI in evaluating the causes of vertigo presenting in ENT outpatient clinics. Materials and methods: We retrospectively analyzed 98 vertigo patients, who came or were referred to outpatient clinics of Otorhinolaryngology Department of Manipal College of Medical Sciences, Pokhara, Nepal. MR imaging of the head and cervical spine was performed in all patients with exception of those with vertigo secondary to trauma, drugs, cardiovascular, or patients in whom MRI was contraindicated. Demographics, comorbidities, and MRI findings were evaluated. Results: There were 98 patients fulfilling the study criteria in our study. There were 41 males (41.84%) and 57 females (58.26%) with M: F ratio of 0.70. The mean age of the patients included in the study was 52.16±14.524 years (21-84 years). Systemic arterial hypertension was the only parameter showing statistically significant against normal and abnormal MRI findings (p-value =0.017) in patients presenting with vertigo. Cervical findings (Prolapsed Disc and Canal stenosis) were the commonest positive findings in MRI (n=27, 27.6%) followed by White matter lesions in the brain (18, 18.4%) and cerebral infarcts (n=12, 12.2%). Conclusion: The utility of MRI may not be high in patients with acutely isolated vertigo however MRI has indicated if it suggests central cause with neurological signs and symptoms, risk factors of the cerebral vascular accident, treatment-resistant cases or cases with diagnostic uncertainty. Abnormalities in MRI are common in patients with co-existing dizziness and systemic arterial hypertension.
... In neurological ER services, VD accounts for > 10% of patients and is the third most common leading symptom after headache (20%) and motor deficit (13%) [27], respectively, after cerebrovascular disorders (28%) and headache (22%) [5]. VD may present as acute vestibular syndrome (AVS) in unilateral vestibular dysfunction (peripheral or central), but other diagnoses have to be kept in mind from benign paroxysmal positional vertigo (BPPV) to anxiety related dizziness [29]. Patients presenting to the ER are diverse with regard to presenting symptoms, underlying pathologies, pre-existing conditions, age and socioeconomic background [10,30,32,34]. ...
Article
Full-text available
Distinguishing between serious (e.g., stroke) and benign (e.g., benign paroxysmal positional vertigo, BPPV) disorders remains challenging in emergency consultations for vertigo and dizziness (VD). A number of clues from patient history and clinical examination, including several diagnostic index tests have been reported recently. The objective of the present study was to analyze frequency and distribution patterns of specific vestibular and non-vestibular diagnoses in an interdisciplinary university emergency room (ER), including data on daytime and season of presentation. A retrospective chart analysis of all patients seen in a one-year period was performed. In the ER 4.23% of all patients presented with VD (818 out of 19,345). The most frequent-specific diagnoses were BPPV (19.9%), stroke/transient ischemic attack (12.5%), acute unilateral vestibulopathy/vestibular neuritis (UVH; 8.3%), and functional VD (8.3%). Irrespective of the diagnosis, the majority of patients presented to the ER between 8 a.m. and 4 p.m. There are, however, seasonal differences. BPPV was most prevalent in December/January and rare in September. UVH was most often seen in October/November; absolute and relative numbers were lowest in August. Finally, functional/psychogenic VD was common in summer and autumn with highest numbers in September/October and lowest numbers in March. In summary, daytime of presentation did not distinguish between diagnoses as most patients presented during normal working hours. Seasonal presentation revealed interesting fluctuations. The UVH peak in autumn supports the viral origin of the condition (vestibular neuritis). The BPPV peak in winter might be related to reduced physical activity and low vitamin D. However, it is likely that multiple factors contribute to the fluctuations that have to be disentangled in further studies.
... 74 Vestibular specialists, however, have long considered migraine to be a common cause of dizziness in specialty clinics, and survey research indicates that it is also common in the general population. 77,78 The slow adoption of migraine as a common cause of vestibular/auditory symptoms might relate to the previous use of other diagnostic labels, such as benign recurrent vertigo and vestibular Ménière's diseasewhich are now considered VM. 79 Migraine with brainstem Table 6. ...
Article
Objective Ménière’s disease (MD) is a clinical condition defined by spontaneous vertigo attacks (each lasting 20 minutes to 12 hours) with documented low- to midfrequency sensorineural hearing loss in the affected ear before, during, or after one of the episodes of vertigo. It also presents with fluctuating aural symptoms (hearing loss, tinnitus, or ear fullness) in the affected ear. The underlying etiology of MD is not completely clear, yet it has been associated with inner ear fluid (endolymph) volume increases, culminating in episodic ear symptoms (vertigo, fluctuating hearing loss, tinnitus, and aural fullness). Physical examination findings are often unremarkable, and audiometric testing may or may not show low- to midfrequency sensorineural hearing loss. Conventional imaging, if performed, is also typically normal. The goals of MD treatment are to prevent or reduce vertigo severity and frequency; relieve or prevent hearing loss, tinnitus, and aural fullness; and improve quality of life. Treatment approaches to MD are many and typically include modifications of lifestyle factors (eg, diet) and medical, surgical, or a combination of therapies. Purpose The primary purpose of this clinical practice guideline is to improve the quality of the diagnostic workup and treatment outcomes of MD. To achieve this purpose, the goals of this guideline are to use the best available published scientific and/or clinical evidence to enhance diagnostic accuracy and appropriate therapeutic interventions (medical and surgical) while reducing unindicated diagnostic testing and/or imaging.
... 74 Vestibular specialists, however, have long considered migraine to be a common cause of dizziness in specialty clinics, and survey research indicates that it is also common in the general population. 77,78 The slow adoption of migraine as a common cause of vestibular/auditory symptoms might relate to the previous use of other diagnostic labels, such as benign recurrent vertigo and vestibular Ménière's diseasewhich are now considered VM. 79 Migraine with brainstem Table 6. ...
Article
Objective Ménière’s disease (MD) is a clinical condition defined by spontaneous vertigo attacks (each lasting 20 minutes to 12 hours) with documented low- to midfrequency sensorineural hearing loss in the affected ear before, during, or after one of the episodes of vertigo. It also presents with fluctuating aural symptoms (hearing loss, tinnitus, or ear fullness) in the affected ear. The underlying etiology of MD is not completely clear, yet it has been associated with inner ear fluid volume increases, culminating in episodic ear symptoms (vertigo, fluctuating hearing loss, tinnitus, and aural fullness). Physical examination findings are often unremarkable, and audiometric testing may or may not show low- to midfrequency sensorineural hearing loss. Imaging, if performed, is also typically normal. The goals of MD treatment are to prevent or reduce vertigo severity and frequency; relieve or prevent hearing loss, tinnitus, and aural fullness; and improve quality of life. Treatment approaches to MD are many, and approaches typically include modifications of lifestyle factors (eg, diet) and medical, surgical, or a combination of therapies. Purpose The primary purpose of this clinical practice guideline is to improve the quality of the diagnostic workup and treatment outcomes of MD. To achieve this purpose, the goals of this guideline are to use the best available published scientific and/or clinical evidence to enhance diagnostic accuracy and appropriate therapeutic interventions (medical and surgical) while reducing unindicated diagnostic testing and/or imaging.
... Učestalost vrtoglavica u općoj populaciji vrlo je velika. Životna prevalencija vrtoglavica u općoj populaciji Republike Njemačke na razini je 20 -30%, 1 dok je godišnja prevalencija 22,9%, a incidencija (pojava prve epizode bolesti) 3,1%. 2 Među sveukupnim uzrocima vrtoglavica funkcionalni vestibularni poremećaji (FVP) ističu se svojom zastupljenošću i drugi su najčešći uzrok vrtoglavica u odrasloj populaciji, odmah iza BPPV-a, a u pojedinim dobnim skupinama, kao što su adolescentska dob i ona od 30 do 50 godina, čak i najčešći. 3 Usto, oni su najčešći oblik kroničnih vrtoglavica, za kojima slijede bilateralne vestibulopatije, ali s mnogo manjim udjelom od oko 5%. 4 Prevalencija FVP-a kao primarnog uzroka vrtoglavica iznosi oko 10% u neurootološkim centrima. ...
Article
Full-text available
Functional dizziness is noted for its frequency and is the second most common cause of dizziness in the general population, most prevalent in the age group of 30–50 years. The classic diagnostic process is aimed at finding a medical or surgical diagnosis, and in case it is not found, it is said to be caused by a “psychogenic” disease. In recent decades, using a new, integrative way of thinking, there has been a discovery of functional vestibular disorders. They have always been overcome by acute or back vestibular disease due to poor readout of the postural system. The reason for this lies in a close connection to the brain of nerve projections responsible for controlling motion and position of the body in space with those responsible for danger and fear. The Nomenclature and Classification Committee of Barany’s Vestibular Disorders recently established diagnostic criteria for persistent postural-perceptive dizziness (PPPD). This is the most common functional vestibular disorder, which includes the previously established: persistent postural dizziness, visual and chronic subjective dizziness. The dominant symptom of PPPD is non-rotatory dizziness that lasts for at least three months continuously and is always associated with the condition of the body. The hypersensitivity to moving stimuli occurs, including the movements of large visual objects or complex visual stimuli in a wide field of vision and the difficulty of performing precision visual actions. For mild and moderate interferences it is advisable to conduct vestibular rehabilitation, as most patients have provocative factors related to vision and movement. Individually tailored exercises are used to reduce susceptibility to provocative movements, and conditioning exercises are very useful for repairing disturbed body posture. Pharmacotherapeutic treatment with selective serotonin or serotonin and norepinephrine reuptake inhibitors is also indicated. Good results are achieved by the use of cognitive-behavioural psychotherapy, changing of negative automatic thoughts, refocusing attention, re-allocation, systematic and gradual exposure or exposure at once, biofeedback etc. The prognosis of the disease is better in patients without comorbidity, while in those with comorbidity it is significantly worse.
Article
Introduction: Vertigo appears as a result of a sudden neural activity imbalance of the vestibular system. The vertigo prevalence is higher in patients over 60 years of age compared to patients under 40 years of age. Objectives: The purpose of this study was to analyze the effect of craniosacral osteopathy on dizziness and balance in individuals who have peripheral vestibular pathology. Methods: A total of 30 individuals, aged 24-50 years, participated in this study. Twenty-four of the participants were female (80%) and 6 were male (20%). The participants were separated into 2 groups, with 15 patients included in the cranial osteopathy treatment group (study group) and 15 patients included in the group that used dimenhydrinate (control group). The individuals were evaluated in terms of dizziness and balance. A visual analog scale was used to evaluate dizziness. Balance was evaluated using the Berg balance scale and the Activities-Specific Balance Confidence scale. The craniosacral treatment program was applied once per week for 6 sessions. All of the individuals included in this study were evaluated 3 times, i.e., prior to treatment, on the third week of treatment, and on the sixth week of treatment. Results: Significant improvement was noted within each group in terms of dizziness and balance (p < 0.05). When the groups were compared with each other, it was observed that craniosacral osteopathy was more effective than dimenhydrinate treatment for dizziness and balance (p < 0.05). Conclusion: Craniosacral osteopathy is an effective treatment choice in individuals who have chronic peripheral vestibular pathology. In individuals who have resistant and chronic vestibular pathology, craniosacral osteopathy should be evaluated among the treatment choices.
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The review analyses the diseases and conditions caused by acute and chronic stress. The authors describe the pathogenesis of stress-induced disorders from the perspective of imbalance between stress-realizing and stress-limiting systems (sympathetic and parasympathetic nervous systems). The effects of acute and chronic stress on the cardiovascular, respiratory, and immune systems, the contribution of stress to the pathogenesis of skin diseases, the gastrointestinal tract, post-stroke disorders, headaches, and dizziness are considered. The authors highlight the role of gamma-aminobutyric acid (GABA) as the main mediator of stress-limiting systems in protecting the nervous system and target organs from the damaging effects of acute and chronic stress. The authors recommend aminophenylbutyric acid hydrochloride, an analogue of GABA, as a drug with protective effect on organs and systems that are exposed to the negative effects of acute and chronic stress. Aminophenylbutyric acid hydrochloride (anvifen) is successfully used in both adults and children, has good tolerance, has no significant drug interactions and side-effects.
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Animal experiments have shown that central vestibular compensation of unilateral peripheral vestibular lesions can be improved by vestibular exercises. There are, however, no equivalent clinical studies on the efficacy of such specific physiotherapy on acute unilateral peripheral vestibular lesions in humans. To quantify the differential effects of specific vestibular exercises on central compensation in patients with an acute/subacute unilateral vestibular lesion (vestibular neuritis), we determined the time course of recovery of 1) the ocular torsion (OT) for the vestibulo-ocular system, 2) the subjective visual vertical (SVV) for perception, and 3) the total sway path (SP) values for postural control in 19 patients with and 20 patients without vestibular exercises. All patients had a persisting peripheral vestibular deficit for at least 30 days (statistical end point). Although normalization of OT and SVV was similar in the control and physiotherapy groups, the total SP values on day 30 after symptom onset differed significantly: 3.2 +/- 1.9 m/min in the physiotherapy group and 16.9 +/- 6.1 m/min in the control group (ANOVA, p < 0.001). This prospective clinical study suggests that specific vestibular exercises improve vestibulospinal compensation in patients with acute peripheral vestibular lesions.
Chapter
Background Framing answerable clinical questions and general approach to search evidenceCritical review of the evidence for each questionConclusion Acknowledgement
Article
Herpes simplex virus type 1 (HSV-1) enters sensory neurons and can remain latent there until reactivation. During latency restricted HSV-1 gene expression takes place in the form of latency-associated transcripts (LAT). LAT has been demonstrated to be important not only for latency but also for reactivation, which may cause cranial nerve disorders. Tissue sections of the trigeminal ganglia (TG), geniculate ganglia (GG), and the vestibular ganglia (VG) from seven subjects were examined for the presence of LAT using the in situ hybridization technique. LAT was found on both sides in all TG (100%), on both sides of five subjects (70%) in the GG, and in none of the VG. Using a second more sensitive detection method (RT-PCR), we found LAT in the VG of seven of ten other persons (70%). This is the first study to demonstrate viral latency in the VG, a finding that supports the hypothesis that vestibular neuritis is caused by HSV-1 reactivation. The distribution of LAT in the cranial nerve ganglia indicates that primary infection occurs in the TG and GG and subsequently spreads along the faciovestibular anastomosis to the VG.
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One hundred and six patients diagnosed between 1987 and 1998 to have somatoform phobic postural vertigo were examined in a follow–up study with a selfevaluating questionnaire. The improvement rate after a mean follow–up time of 8.5 years (5 to 15.9 years) was 75% (27% of the patients reported a complete remission). While the majority of these patients experienced improvement or remission during the first year after assessment of diagnosis and a short–term psychotherapeutic approach, some patients also had considerable improvement even after two or more years. There was a negative correlation between the duration of the condition before assessment of the diagnosis and the improvement/regression rate. The improvement/regression rate was independent of gender, age, preceding vestibular or nonvestibular organic disorders, and the various medical, physical, or psychotherapeutic interventions. Transient relapses occurred in 47% of the improved patients once or repeatedly. The probability of developing a relapse remained constant throughout the entire follow–up. None of the patients required a revision of the initial diagnosis on the basis of the questionnaire.
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Unilateral loss of horizontal semicircular canal function, termed canal paresis, is an important finding in dizzy patients. To our knowledge, apart from head-shaking nystagmus, no clinical sign of canal paresis has yet been described and the term derives from the characteristic finding on caloric tests: little or no nystagmus evoked by either hot or cold irrigation of the affected ear. We describe a simple and reliable clinical sign of total unilateral loss of horizontal semicircular canal function: one large or several small oppositely directed, compensatory, refixation saccades elicited by rapid horizontal head rotation toward the lesioned side. Using magnetic search coils to measure head and eye movement, we have validated this sign in 12 patients who had undergone unilateral vestibular neurectomy.
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Theoretical evidence is presented that all the typical features of BPPV (benign paroxysmal positioning vertigo) cannot be explained by cupulolithiasis in that otoconial debris become settled on the cupula of the posterior semicircular canal. A free floating clot of inorganic particles (heavier than endolymph) in the ampullofugal branch of the posterior semicircular canal is more likely to cause the syndrome. The clot always gravitates to the most dependent part of the canal as soon as the patient's head is moved in a way that alters the angle between the canal's plane and the gravity vector. As compared to a plunger (depending on the direction it moves) the clot produces push or pull forces on the cupula, thereby eliciting the BPPV attack. This clot-induced endolymph flow mechanism is compatible with all features of BPPV such as latency, limited duration, fatigability, change in direction of the induced nystagmus, and the efficacy of physical therapy in both posterior and horizontal semicircular canal BPPV. The floating clot is only activated by changes in position of the head relative to the gravitational vector (positioning vertigo) but not by prolonged static positions of the head (positional vertigo), which fits clinical experience. Therefore, canalolithiasis rather than cupulolithiasis provides a better definition of the underlying mechanism in BPPV.
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Betahistine is used for treatment of several vestibular disorders. Despite the accepted use of this histamine-like substance, its mechanism of action is not well understood. The purpose of this study was to assess the possibility that one of the activities of betahistine is increasing blood flow in the peripheral vestibular end organs. Using a novel surgical approach, we identified the posterior semicircular canal ampulla of guinea pigs and placed a laser Doppler probe in position to obtain blood flow measurements from the posterior semicircular canal ampulla. Blood pressure, heart rate, and vestibular blood flow were continuously recorded. Concentration-response curves were obtained for betahistine (2.5, 5, 7.5, and 10 mg/kg) and control-vehicle (0.15 mol/L NaCl) infusions. A separate group of subjects was pretreated with the competitive selective H3 agonist, thioperimide maleate, before betahistine treatment. Increases in vestibular blood flow and decreases in blood pressure were observed in response to betahistine infusions. Pretreatment with thioperamide maleate abolished these changes at low doses of betahistine and attenuated the responses at higher doses of betahistine. These results show that betahistine administration induces increases in vestibular blood flow. These findings support the potential use of betahistine for treatment of vestibular disorders, which may be caused by compromised circulation.
Article
A retrospective study was conducted on 90 patients with episodic vertigo that could be related to migraine as the most probable pathomechanism. Since the majority of the patients did not fulfill the criteria of the International Headache Society (IHS) for basilar migraine, the diagnosis was substantiated by disease course, medical efficacy in treating (ergotamines) and preventing (metoprolol, flunarizine) attacks, ocular motor abnormalities in the symptom-free interval, and careful exclusion of the most relevant differential diagnoses, such as transient ischemic attacks, Menière's disease, and vestibular paroxysmia. The following clinical features were elaborated. The initial manifestation could occur at any time throughout life, with a peak in the fourth decade in men and a "plateau" between the third and fifth decades in women. The duration of rotational (78%) and/or to-and-fro vertigo (38%) could last from a few seconds to several hours or, less frequently, even days; duration of a few minutes or of several hours was most frequent. Monosymptomatic audiovestibular attacks (78%) occurred as vertigo associated with auditory symptoms in only 16%. Vertigo was not associated with headache in 32% of the patients. In the symptom-free interval 66% of the patients showed mild central ocular motor signs such as vertical (48%) and/or horizontal (22%) saccadic pursuit, gaze-evoked nystagmus (27%), moderate positional nystagmus (11%), and spontaneous nystagmus (11%). Combinations with other forms of migraine were found in 52%. Thus, migraine is a relevant differential diagnosis for episodic vertigo. According to the criteria of the IHS, only 7.8% of these patients would be diagnosed as having basilar migraine. However, to ensure that at least those presenting with monosymptomatic episodic vertigo (78% in our study) receive effective treatment, we propose the use of the more appropriate term "vestibular migraine."
Article
Benign paroxysmal positional vertigo (BPPV) originating from the posterior semicircular canal (pSCC) is a common vestibular disorder that is easy to diagnose and usually easy to treat. The majority of patients with BPPV have no known inner ear disease; they have "primary" or "idiopathic" BPPV. However, a minority does have objective evidence of an inner ear disease on the same side as the BPPV and this group has "secondary" or "symptomatic" BPPV. Previous publications differ on the prevalence of secondary BPPV and about the types of inner ear diseases capable of causing it. In order to determine what proportion of patients have secondary as opposed to primary BPPV and which inner ear diseases are capable of causing secondary BPPV, we searched our database for the 10-year period from 1988 to 1997 and found a total of 2847 patients with BPPV. Of these, 81 (3%) had definite pSCC-BPPV secondary to an ipsilateral inner ear disease. Sixteen had Menière's disease, 24 had an acute unilateral peripheral vestibulopathy, 12 had a chronic unilateral peripheral vestibulopathy, 21 had chronic bilateral peripheral vestibulopathy and 8 had unilateral sensorineural hearing loss. It seems that any inner ear disease that detaches otoconia and yet does not totally destroy pSCC function can cause BPPV and that a case can be made for audiometry and caloric testing in all patients with BPPV.