AUDIOLOGICAL MEDICINE 2005; 3(1): 4–6

Definition and Classification of Paroxysmal Positional Vertigo

BEATRICE GIANNONI, PAOLO VANNUCCHI AND PAOLO PAGNINI

From the Department of Surgical Otoneuro-Ophthalmological Sciences, Section of Audiology, University of Florence, Italy

Giannoni B, Vannucchi P, Pagnini P. Definition and Classification of Paroxysmal Positional Vertigo.

Audiological Medicine 2005; 3(1): 4–6.
The aim of the present paper is to focus on the classification of one of the most frequent peripheral
vestibular pathologies: benign paroxysmal positional vertigo (BPPV) or paroxysmal positional vertigo
(PPV). Having discussed some aspects of the terminology of PPV, the authors describe its natural course
and evolution. Three different types of classification are proposed basing the first on the pathogenesis of
PPV, the second on aetiological factors and the third on the topographical localization of otoconial debris
in the labyrinth. Key words: benign paroxysmal positional vertigo, classification.
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DEFINITION localized to different sites. The nystagmus can also

Paroxysmal positional vertigo (PPV) can be defined as a
‘labyrinthine disorder with a high prevalence, character-
ized by objective, brief and paroxysmal vertiginous
attacks caused by movements of the head in the horizontal
or in the vertical plane’. The crises are repetitive and
usually clustered in a limited period of time that we can
For personal use only.
present in an ‘atypical’ form, which necessitates a
differential diagnosis with other peripheral and central
vestibular pathologies.
In the literature PPV is also called ‘benign PPV’. In our
opinion, the use of the adjective ‘benign’ is not justifiable
by the nature of the symptomatology of the disease which

define as the ‘active phase’ of the disease; after an
unpredictable silent interval, the ‘inactive phase’, PPV
has a tendency to recur. Although PPV can occur at any
age, it is rarer in the two first decades of life and more
frequent in adults and the elderly.
This disease has a multifactorial aetiology but no cause
can be detected in over 50% of patients. Thus, PPV is
fundamentally considered as idiopathic in origin. The
pathogenesis of PPV is otherwise almost certain and
identifiable in the detachment and dislocation of an
otolithic mass into the semicircular canals. The term
‘canalolithiasis’ indicates the presence of otoconial debris
(canaliths) in the canal lumen which is free to move in the
endolymph. Since this pathology can involve various
areas of the labyrinth (semicircular canals, common crus,
ampullae) the better term to identify the pathogenetic
mechanism of PPV is ‘labyrintholithiasis’. Although the
term cupulolithiasis is often used in the literature as a
synonym of PPV, it is, in our opinion, incorrect and is
better reserved for the case of suspected adherence of the
debris to the cupula, thus indicating another possible
pathogenetic mechanism of PPV. Lithiasis usually
involves only one labyrinth and predominantly affects the
vertical semicircular canals, in particular the posterior
one, as opposed to the lateral canal.
Paroxysmal positional nystagmus, detectable only
during the active phase, is the pathognomonic sign of
PPV. Nystagmus has a ‘paradigmatic’ morphology
according to the involved canal; it is possible to observe
some variants that are attributable to the canaliths being
is often characterized by violent vertiginous crises with
serious vagal complications; it is not supported either by
the duration of the symptomatic period, which can last for
months. The term ‘benign’ should be reserved only for
paroxysmal positional nystagmus when present in typical
form, and not to the whole pathology.
PPV can be considered a ‘syndrome’ (1), since it
constitutes the sequelae of different inner ear illnesses; on
the other hand we can also consider PPV as a ‘disease’ (2)
since it is a morbid condition for which at least two of the
three fundamental nosological aspects of aetiology,
pathogenesis and symptomatology are known.
The prevalence of PPV in the general population is
high; according to the definition of vertigo as an illusion
of movement, PPV is the most frequent cause of acute
vertigo in man.
NATURAL COURSE
The disease is characterized by an ‘active phase’ in which
the patient suffers from paroxysmal and repeatable
vertiginous attacks; especially in the case of prolonged
illness, the symptoms may progressively attenuate, losing
their paroxysmal features. The active phase generally
lasts for days or weeks, although it can spontaneously
resolve within 24 hours. On the other hand there are some
untreatable cases presenting with a chronic vertigo and
persistent peripheral positional nystagmus which can
continue for many months and are resistant to therapy.
It is typical of PPV also to have a period in which there
is no evidence of vertigo or paroxysmal nystagmus; this

# 2005 Taylor & Francis. ISSN 1651-386X

DOI 10.1080/16513860510029436 AUDIOLOGICAL MEDICINE 2005

phase can be defined as the ‘inactive phase’. Not always
during this period is there a complete absence of symp-
toms: a vague vertiginous-postural disturbance, a sense
of insecurity, or brief sensation of vertigo may persist.
The causes of such residual disturbances are not fully
understood; they may be due to an alteration of the
cupula-endolymph mechanics or to utricular-saccular
dysfunction and, in some patients, a psycho-pathological
mechanism can be active.
The inactive phase of PPV can last for life; more
frequently a new active phase recurs after an unpredict-
able period of time. The nature of recurrences is not well
characterized, owing to the lack of epidemiological
studies which follow a large number of patients for many
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years. The prevalence of recurrences appears to be greater
in forms without a defined aetiology compared to post-
traumatic forms.
CLASSIFICATION
Pathogenetic classification
In our opinion the principal classification of PPV should
be based on the pathogenesis of onset.
For personal use only.
Primary otolithic PPV. Primary forms are caused by
otolithic detachment, and begin without any previous
or contemporary labyrinthine pathologies. In these
patients a ‘non-positional’ nystagmus is not observed.
Caloric tests often provide symmetrical responses, except
in cases of horizontal canal PPV in which a unilateral
pseudo-areflexia is caused by debris that prevents the
hydrodynamic movements of endolymph in the canal
subsequent to thermal stimulation. Primary forms of
PPV are almost always idiopathic; sometimes they can
be of traumatic origin, when the trauma causes an inertial
otolithic detachment without labyrinthine failure.
Secondary labyrinthine PPV. This is diagnosed when
documented labyrinthine pathology leads to otolithic
detachment as a result of the labyrinthine damage being
due to various aetiological factors. Usually, these patients
have symptomatology and signs that are initially char-
acterized by vertigo and non-positional nystagmus, while
PPV develops successively; these cases often present a
vestibular caloric deficit. Such a vestibular deficit may be
complete, as in the Lyndsay-Hemenway syndrome (3),
characterized by a horizontal canal areflexia and by a
normal function of the posterior semicircular canal and of
the utricular macula, or partial, e.g. in the initial phase of
Ménière’s disease.
We can consider secondary labyrinthine PPV also in
those forms for which a sudden hypoacusis is docu-
mented, and for this a damage of the internal ear is
presumed, and there is no detectable unilateral vestibular
failure.
Definition of paroxysmal positional vertigo 5
Aetiological classification
Another important classification is based on the aetio-
logical agent.
Idiopathic PPV. This refers to the form of the disease
that develops in otherwise healthy patients, without
spontaneous clinical signs, evoked or provoked, of
labyrinthine dysfunction, or without regional or systemic
disorders associated or predisposition to peripheral
labyrinthine pathologies.
PPV of presumed etiology. This manifests in patients
with pathological conditions likely to provoke otoconial
detachment. The causes of PPV of presumed origin
include Ménière’s disease, chronic otitis media, haematic
hyperviscosity and prolonged bedrest (4). These forms of
PPV could be further subdivided into probable and
possible forms, for example:
 PPV occurring in a patient with hypertension, cardio-
pathy or ischaemic cerebropathy has an aetiology of
probable vascular nature.
 PPV appearing contemporarily with, or subsequent to,
influenza can be considered of possible viral origin.
PPV of known aetiology. It can be diagnosed in patients
with head trauma, provided that a narrow temporal rela-
tionship exists between the traumatic event and the onset
of PPV. Cranial trauma, whiplash injuries and iatrogenic
trauma after middle-ear surgery represent events likely to
provoke otoconial detachment.
We can consider of certain aetiology also those forms
in which there is definite clinical evidence of PPV
occurring contemporary with herpes zoster oticus or
epidemic parotitis or where there is documented sero-
logical evidence, such as for cytomegalovirus infections.
Topographical classification
PPV can be also classified according to the position of the
otoconial debris in the labyrinth. This classification
considers the uni- or bi-lateral nature of the disease, the
canal involved and the position of the otoconia in the
canal.
CANALOLITHIASIS
Vertical semicircular canals
Superior
 Ampullar hemicanal
 Non-ampullar hemicanal
Posterior
 Ampullar hemicanal
 Non-ampullar hemicanal
AUDIOLOGICAL MEDICINE 2005
 6 B. Giannoni et al.
Common crus
Horizontal semicircular canal
 Ampullar hemicanal
 Non-ampullar hemicanal
CUPULOLITHIASIS
 Cupula of the posterior semicircular canal
 Cupula of the superior semicircular canal
 Cupula of the horizontal semicircular canal
The most frequent form of PPV involves the posterior
semicircular canal where the canaliths probably locate in
the ampullary hemicanal (the lowermost part of the canal
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in the upright position). This causes the classic torsional
nystagmus seen in the Dix-Hallpike position, beating
counter-clockwise-up and clockwise-up, respectively for
the right and left posterior semicircular canal. If the cana-
liths move to the part of the canal distal to the ampulla (the
superior part of the canal), or into the common crus, the
diagnostic manoeuvres cause an ‘unexpected nystagmus’
beating clockwise-down for right positioning or, for
example, in a purely torsional direction.
If otoconial debris is in the non-ampullar part of the
For personal use only.
horizontal semicircular canal, rotations of the head on the
horizontal plane, with the patient supine, lead to the onset
of geotropic nystagmus (5); the apogeotropic variant is
due to otoconia in the ampullar part of the hemicanal (6).
Based on current knowledge, some of the forms listed
in the preceding topographical classification are only
hypothetical, even if it is entirely likely that they do exist.
More than one variant of PPV may be observed in
the same patient, either in the same session, following
diagnostic or therapeutic manoeuvres, or during sub-
sequent examinations. Transformation of one form of
AUDIOLOGICAL MEDICINE 2005
nystagmus into another is commonly observed; a poste-
rior canal nystagmus can transform into an apogeotropic
nystagmus and even a clockwise nystagmus can become
counter-clockwise. Likewise, PPV may contemporarily
involve more than one canal (pluricanal forms), either on
the same side (unilateral forms) or on opposite sides
(bilateral forms). Finally, in some cases, the otolithic
debris can adhere to one of the three cupulae of one or
both sides.
REFERENCES
1. Baloh RW. Benign positional vertigo. In: Baloh RW,
Halmagyi GM, editors. Disorders of the vestibular system.
New York: Oxford University Press; 1996. p. 328–39.
2. Ralli G, Lamberti A, Nola G, De Rosa A, De Vincentiis I. La
videooculografia nella vertigine parossistica posizionale
benigna. Valsalva 1997; 4: 177–93.
3. Lindsay JR, Hemenway WG. Postural vertigo due to unilat-
eral sudden partial loss of vestibular function. Ann Otol
Laryngol 1956; 65: 692–708.
4. Gyo K. Benign paroxysmal positional vertigo as a compli-
cation of post-operative bedrest. Laryngoscope 1998; 98:
3322–5.
5. Pagnini P, Nuti D, Vannucchi P. Benign paroxysmal vertigo
of the horizontal canal. ORL J Otorhinolaryngol Relat Spec
1989; 51: 161–5.
6. Nuti D, Vannucchi P, Pagnini P. Benign paroxysmal
positional vertigo of the horizontal canal: a form of canalo-
lithiasis with variable clinical features. J Vestib Res 1996; 6:
173–84.
Address for correspondence:
B. Giannoni
Department of Surgical Otoneuro-Ophtalmological Sciences
Section of Audiology
University of Florence
Italy
E-mail: audiologia@med.unifi.it