Buttner U, Helmchen Ch, Brandt Th. Diagnostic criteria for central 6ersus peripheral positioning nystagmus and 6ertigo.
Acta Otolaryngol (Stockholm) 1999; 119: 15.
Head positioning can lead to pathological nystagmus and vertigo. In most instances the cause is a peripheral vestibular
disorder, as in benign paroxysmal positioning vertigo (BPPV). Central lesions can lead to positional nystagmus (central
PN) or to paroxysmal positioning nystagmus and vertigo (central PPV). Lesions in central PPV are often found
dorsolateral to the fourth ventricle or in the dorsal vermis. This localization, together with other clinical features
(associated cerebellar and oculomotor signs), generally allows one to easily distinguish central PPV from BPPV. However,
in individual cases this may prove difficult, since the two syndromes share many features. Even if only BPPV as a
peripheral lesion is considered, differentiation based on such features as latency, course, and duration of nystagmus during
an attack, fatigability, vertigo, vomiting, and time period during which nystagmus bouts occur, may be impossible. Only
the direction of nystagmus during an attack can allow differentiation. Key words: central positioning nystagmus, central
positioning 6ertigo, paroxysmal nystagmus, paroxysmal 6ertigo.
INTRODUCTION
A specific change in head position can, under pathological conditions, cause nystagmus that outlasts the
head movement. It is necessary to distinguish between positioning and positional nystagmus: the
former term implies that the actual head movement is
the cause, whereas the term positional indicates
that the new head position (which has a different
otolith input) causes the nystagmus. Basically, three
types of peripheral or central positional/positioning
nystagmus (PN) have been distinguished (1): (i) In
cases of PN I, or central positional nystagmus (central PN), the nystagmus lasts as long as the head
remains in the precipitating position. It is usually of
central origin (2) and not combined with vertigo. (ii)
PN II, or benign paroxysmal positioning vertigo
(BPPV), is caused by a peripheral canal disorder;
vertigo is a dominant feature. (iii) PN III or central
positioning nystagmus and vertigo (central PPV) is
caused by a central lesion and consists of short-lasting nystagmus combined with vertigo. This disorder
has also been called pseudo-BPPN (3).
The absence of vertigo and the presence of sustained nystagmus during the precipitating head position for central PN usually allows one to easily
distinguish BPPV and central PPV. However, it is not
as easy to distinguish between BPPV and central PPV
with paroxysmal nystagmus and vertigo present.
BPPV was first described by Barany in 1921 (4).
The term itself was introduced by Dix and Hallpike
in 1952 (5). In the past, widely accepted criteria were
developed for the diagnosis of BPPV. Since in most
instances the posterior canal (PC) is affected, a head
movement in the PC plane from the erect sitting
1999 Scandinavian University Press. ISSN 0001-6489
U. Buttner et al.
such differentiation, however: in a peripheral disorder, the resulting nystagmus always beats in the
direction of the expected eye movements if the affected semicircular canal is optimally stimulated.
Thus, the nystagmus in h-BPPV always beats horizontally and is elicited by stimulation in the horizontal
plane. This does not have to be the case for central
paroxysmal PN (central PPV).
MAIN FEATURES OF PERIPHERAL AND
CENTRAL PAROXYSMAL PN AND VERTIGO
Latency
In cases of posterior canal BPPV (p-BPPV), the
latency is 215 sec and decreases with increasing
speed of the positioning manoeuvre (12). In h-BPPV
there can be virtually no latency (13). In patients with
central PPV either no latency (14, 15) or latencies up
to 35 sec (16) have been encountered. In experimental lesions of the dorsal vermis (nodulus), latencies can
vary between 0 and 50 sec (17, 18).
Duration of an attack
P-BPPV typically lasts between 5 and 30 sec (12). In
the static position some continuous subtle nystagmus
can be present; this has been reported in 40% of these
patients (8). H-BPPV usually lasts about 1 min and
thus longer than p-BPPV (10).
In patients with central PPV the attack can last
from a few seconds (5 6 sec (19); 15 sec (14)) up to
1 min (20). In experimental lesions of the dorsal
vermis, the duration of central PPV is 30 180 sec
(18).
Direction of nystagmus
The posterior canal (p-BPPV) is most often affected in
BPPV. During the investigation, the head of the
sitting patient is turned 45 to bring the PC into the
plane of stimulation before the body is tilted to the
side. This leads to ampullofugal movements of the
particles within the PC and as a result to activation of
the superior oblique muscle of the ipsilateral eye and
the inferior rectus muscle of the contralateral eye.
The induced nystagmus consists of vertical and
torsional components which rotate around an axis
perpendicular to the PC. The fast phase has an
upward component and beats torsionally toward the
undermost ear (geotropic). This latter component
becomes more pronounced when the patient looks in
the direction of the uppermost ear (21). Although
bilateral p-BPPV may not be uncommon (22), the
improper positioning of the patient often leads to this
false diagnosis. Only when proper positioning is ensured does nystagmus to the undermost ear
(geotropic) during left and right positioning manoeu-
U. Buttner et al.
Table I. Clinical features of peripheral benign paroxysmal positioning 6ertigo/nystagmus (BPPV) and central
paroxysmal positioning 6ertigo/nystagmus (central PPV)
Features
BPPV
Central PPV
05 sec
5B60 sec
Pure vertical; pure torsional, not
attributable to the stimulated canal
plane
Fatigability
Course of nystagmus and vertigo
in an attack
Vertigo
Nausea and vomiting
Normal
Possible
Crescendodecrescendo possible
Typical
Frequent on single precipitating
manoeuvres (not necessarily associated
with strong nystagmus intensities)
Spontaneous recovery within weeks
possible
None possible, often cerebellar and
other oculomotor signs
Normal; lesions of the dorsal vermis
and/or dorsolateral to the fourth
ventricle
REFERENCES
1. Harrison MS, Ozsahinoglu C. Positional vertigo: aetiology and clinical significance. Brain 1972; 95: 36972.
2. Nylen CO. The oto-neurological diagnosis of tumours
of the brain. Acta Otolaryngol Suppl (Stockh) 1939;
33: 1 151.
3. Sakata E, Ohtsu K, Shimura H, Sakai S. Positional
nystagmus of benign paroxysmal type (BPPN) due to
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.