Deutsches Ärzteblatt InternationalDtsch Arztebl Int 2008; 105(10): 173–80 173
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
Diagnosis and Treatment
of Vertigo and Dizziness
Michael Strupp, Thomas Brandt
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
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
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
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-
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
The relative frequencies of different dizziness and
Diagnosis Number of Percent
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
of unclear etiology 239 3.3
Other 741 10.3
Deutsches Ärzteblatt InternationalDtsch Arztebl Int 2008; 105(10): 173–80 175
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
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
>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
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
>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.
This condition is probably due to labyrinthine endo-
lymphatic hydrops with periodic rupturing of the
membrane that separates the endolymphatic and
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
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
176 Deutsches Ärzteblatt InternationalDtsch Arztebl Int 2008; 105(10): 173–80
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.
Deutsches Ärzteblatt InternationalDtsch Arztebl Int 2008; 105(10): 173–80 177
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.
178 Deutsches Ärzteblatt InternationalDtsch Arztebl Int 2008; 105(10): 173–80
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.
Deutsches Ärzteblatt InternationalDtsch Arztebl Int 2008; 105(10): 173–80 179
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.
1. Neuhauser HK: Epidemiology of vertigo.Curr Opin Neurol 2007;
2. Brandt T, Dieterich M,Strupp M: Vertigo – Leitsymptom Schwin-
del. Darmstadt. Steinkopff 2003.
3. Karlberg M, Hall K,Quickert N, Hinson J, Halmagyi GM:What in-
ner ear diseases cause benign paroxysmal positional vertigo?
Acta Otolaryngol 2000; 120: 380–5.
4. Brandt T, Steddin S:Current view of the mechanism of benign
paroxysmal positioning vertigo: cupulolithiasis or canalolithiasis?
J Vestib Res 1993; 3: 373–82.
5. Semont A,Freyss G, Vitte E:Curing the BPPV with a liberatory
maneuver.Adv Otorhinolaryngol 1988; 42: 290–3.
6. Strupp M, Cnyrim C,Brandt T: Vertigo and dizziness:Treatment of
benign paroxysmal positioning vertigo, vestibular neuritis and
Menère's disease. In: Candelise L (ed.):Evidence-based Neurolo-
gy – management of neurological disorders. Oxford: Blackwell
Publishing 2007, 59–69.
7. Brandt T, Huppert D,Hecht J, Karch C, Strupp M:Benign paroxys-
mal positioning vertigo: a long-term follow-up (6-17 years) of 125
patients. Acta Otolaryngol 2006; 126: 160–3.
8. Halmagyi GM, Curthoys IS:A clinical sign of canal paresis. Arch
Neurol 1988; 45: 737–39.
9. Theil D,Arbusow V,Derfuss T et al.: Prevalence of HSV-1 LAT in
human trigeminal, geniculate, and vestibular ganglia and its implica-
tion for cranial nerve syndromes. Brain Pathol 2001; 11: 408–13.
10. Strupp M, Zingler VC, Arbusow V et al.:Methylprednisolone,
valacyclovir,or the combination for vestibular neuritis. N Engl J
Med 2004; 351: 354–61.
11. Strupp M,Arbusow V, Maag KP, Gall C, Brandt T:Vestibular exer-
cises improve central vestibulospinal compensation after vestibu-
lar neuritis. Neurology 1998; 51: 838–44.
12. Minor LB, Schessel DA,Carey JP: Meniere's disease. Curr Opin
Neurol 2004; 17: 9–16.
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.
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:
Phobic postural vertigo: the second
most common cause of vertigo
>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%).
>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
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.
Prof. Dr. med. Michael Strupp
Neurologische Klinik der Universität München Klinikum Großhadern
81377 München, Germany