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Cortical matching of visual and vestibular 3D coordinate maps.

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There were 63 females and 48 males (ratio 1.3:1), with a
mean age of 53.5 years and mean age o f onset of 39.9 years.
Because of the lack of relapses and therefore the absence of a
second genuine attack, no patients could be classified as having either CDMS or LSPMS. Forty-one patients (36.9%)
were designated as having LSDMS, and 51 were considered
to have CPMS (45.9%). Nineteen patients (17.1%) did not
satisfy the criteria for any of the Poser groups and were
therefore designated as suspected cases, 3 patients being excluded from the classification because of onset of symptoms
after the age of 59 years.
By comparison with these data, the recent Northern Ireland epidemiological study (12.5% of patients had PPMS)
provided the following proportions in the Poser groups [5]:
CDMS (64%), CPMS (15%), LSDMS (8%), LSPMS (1%).
Suspected cases represented 12% o f these cases.
The Poser criteria provide an excellent and widely accepted standard in MS diagnosis. However, the definition of
"attacks" and the absence of these in the clinical course of
patients with PPMS strictly limits the diagnostic categories
available for classification of such patients, a significant proportion not satisfying any of the Poser categories. The age
limits in the Poser criteria increase the potential for exclusion
of PPMS patients who tend to have a significantly later age
of onset than those with relapsing-remitting or secondary
progressive disease. Overall, these results indicate a need for
re-evaluation of the diagnostic criteria with regard to PPMS
to allow the valid assessment and comparison of epidemiological and scientific data and to permit appropriate, inclusive recruitment of patients for therapeutic trials.
*Northern IreLand Neurology Service, Royal Victoria Hospital,
Be&; And fDepartment o f Medicine, The Queen >
University of Belfast, Be& Northern Ireland
1. Poser CM, Paty DW, Scheinberg L, et al. New diagnostic criteria for multiple sclerosis: guidelines for research protocols. Ann
Neurol 1983;13:227-231
2. Thompson AJ, Polrnan CH, Miller DH, et al. Primary progressive multiple sclerosis. Brain 1997;120:1085-1096
3. Hillert J, Gronning M, Nyland H, et al. An irnmunogenetic heterogeneity in multiple sclerosis. J Neurol Neurosurg Psychiatry
4. Revesz T, Kidd D, Thompson AJ, et al. A comparison of the
pathology o f primary and secondary progressive multiple sclerosis. Brain 1994;117:759-765
5. Hawkins SA, McDonnell GV. Changing epidemiology o f multiple sclerosis (MS) in Northern Ireland (NI). Neurology 1997;
48:A429 (Abstract)
Cortical Matching of Visual and Vestibular 3D
Coordinate Maps
Thomas Brandt, M D
Tilts of subjective visual vertical (SVV) [I] and room tilt
illusions [2, 31 (transient 180" upside-down vision or apparent 90" tilts of the visual scene) are vestibuIar signs that in-
dicate spatial disorientation. Are both phenomena the same,
their net tilt angles differing only in size? There is evidence
that they are different and that room tilt illusions may be the
perceptual result of a transient erroneous cortical mismatch
o f the visual and vestibular coordinate maps.
Spatial orientation is based on visual-vestibular interaction
[4,51. Both senses provide us with visual cues about vertical
orientation in a three-dimensional (3D) coordinate system.
These are the three major planes of action of the vestibular
system: the frontal roll plane, the sagittal pitch plane, and
the horizontal yaw plane. Because two different verticalsvisual and vestibular-cannot be perceived at the same time,
there must be a cortical mechanism that integrates visualvestibular input (by aligning the pair of axes) to determine
the current percept of a unique verticality.
Both SW tilts and room tilt illusions involve "graviceptive" pathways that extend from the otoliths and the vertical
semicircular canals through the vestibular nuclei and the
thalamus to the parietoinsular vestibular cortex. Directionspecific S W tilts are the most sensitive sign of an acute unilateral brainstem lesion; they have been reported in lesions of
all these structures [I]. Room tilt illusions have also been
reported to occur with brainstem lesions as a manifestation
of a dynamic mismatch between inappropriate otolithic input and correct visual input [3]. Why are S W tilt and room
tilt illusions different phenomena?
S W tilts are usually stable signs and recovery occurs
gradually, within days to weeks; room tilt illusions are
paroxysmal or transient phenomena.
S W tilts manifest as a continuum of angle of tilt up to
about 30" as a maximum; room tilt illusions occur in 90"
steps as a lateral tilt or as 180" tilt with upside-down vision.
S W tiIts are not usually associated with the perception of
room tilt.
S W tilt is a sensitive measure (in degrees) of a graviceptive vestibular tone imbalance when determined without additional visual cues of orientation [ 11. Because patients with
significant tilts of the S W do not usually complain spontaneously about an apparent tilt of the visual scene (room tilt),
this deviation must be largely compensated for by the cortical match o f visual-vestibular coordinates. This matching of
separate sensory 3D coordinate maps is a continuous and
robust process that must tolerate slight incongruencies between expected and actually received sensory inputs. Furthermore, it must be plastic to compensate for an acquired vestibular tone imbalance (eg, unilateral labyrinthine loss) or to
adapt to unusual environments (microgravity).
In brief, room tilt illusions are transient mismatches of the
cortical visual and vestibular 3D coordinate maps that consequently occur in 90" or 180" steps as the erroneous result
of the attempt to match the pair of axes in acute vestibular
tone imbalances. Perceived tilt in one plane causes the afflicted person to attribute upright to horizontal or even
down. The visual scene, however, which itself contains empirical spatial cues for upright, will then in turn "dominate
Annals of Neurolow
Vol 42
No 6
December 1997 983
Department of Neurology, University of Munich, Klinikum
Groflhadern, Munich, Germany
1. Brandt T, Dieterich M. Vestibular syndromes in the roll plane:
topographic diagnosis from brainstem to cortex. Ann Neurol
2. Ropper AH. Illusions of tilting of the visual environment: report
of 5 cases. J Clin Neuroophthalmol 1983;3:147-151
3. Tiliket C, Ventre-Dominey J, Vighetto A, Grochowicki M.
Room tilt illusion: a central otolith dysfunction. Arch Neurol
4. Dichgans J, Brandt T. Visual-vestibular interaction: effects on
self-morion perception and postural control. In: Held R, Leibowitz HW, Teuber H-L, eds. Handbook of sensoty physiology.
Vol 8. Springer, Heidelberg, 1978:755- 804
5. Dichgans J, Held R, Young LR, Brandt T. Moving visual scenes
influence the apparent direction of gravity. Science 1972;178:
1217-1 2 19
Multiple Sclerosis and Retroviruses
Michel Brahic, MD, PhD,
and Jean-Francois Bureau, MD, PhD
Fig. Schematic representation of the head ,as a cube with the
cortical matching o f the vestibular and the visual 30 coordinate maps. The three major planes of action of the vestibular
system are the fiontal roll, the horizontal yaw, and the sagittal
pitch about the x, y, and z axes, respectiwly. (Top) Visual
scene matched with the vestibular coordinates. (Middle) Room
tilt illusion with 180" tilted visual scene in the pitch plane
(upside-down vision). (Bottom) Room tilt illusion with 90"
tilt in the roll plane.
and correct" spatial orientation. Vision will tell the vestibular
system where upright is. Therefore, room tilt illusions are
transient: you cannot perceive two verticals at once.
Annals of Neurology
Vol 42
No 6
December 1997
During the past 20 years, some dozen claims to have isolated
a virus causing multiple sclerosis (MS) have appeared in the
literature. Unfortunately none has stood the test of time.
Perron and colleagues [I], following up on some controversial work published 8 years ago, recently described a retroviral sequence isolated from MS material. In their older work,
the researchers reported the presence of a weak peak of reverse transcriptase (RTase) activity in sucrose gradients
loaded with the supernatant of cultures of leptomeningeal
cells obtained from the cerebrospinal fluid of an MS patient.
In their recent paper, Perron and co-workers [ l ] used polymerase chain reaction to amplify from the peak of RTase
activity a cDNA sequence that corresponds to that of a pol
gene. This sequence, which they call MSRV, and seven others that the group deposited in GenBank, are closely related
to ERV9, a well-characterized human endogenous retrovirus.
Perron and associates emphasize the novelty of MSRV and
the fact that it was repeatedly isolated from MS tissues and
not from controls. In fact, as shown in the Figure, which we
prepared by searching GenBank, MSRV belongs to a group
of very closely related pol sequences, among which are four
human genomic sequences and RT11, a sequence described
by our group in 1995 [2]. RT11 was found, together with
five other previously unreported pol-related sequences, in
cDNA prepared from MS as weil as from control brain tissue. The divergence between these different sequences is very
small and not greater than that between the sequence of
MSRV as published by Perron and co-workers [l] and as
deposited in GenBank! As far as the association with MS is
concerned-an association suggested repeatedly by the authors, including in the title of their article-we want to emphasize that, although R T l l and other closely related sequences are indeed expressed in some MS brain, they are also
expressed in control brain and in nonneural tissues [2]. In
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visual, matching, maps, cortical, vestibular, coordinated
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