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Detection of silent cerebellar lesions by increasing the inertial load of the moving hand.

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Detection of Silent Cerebellar Lesions
by Increasing the Inertial Load
of the Moving Hand
M. Manto, MD," E. Godaux, MD,? and J. Jacquy, M D "
I n a previous study, we analyzed the hypermetria of wrist flexion movements in patients with a cerebellar syndrome.
We found that hypermetria augmented when the inertial load of the moving hand was artificially increased. I n the
present study, we applied the same protocol to patients with an apparently normal neurological examination, in spite
of a cerebellar lesion documented by magnetic resonance imaging. I n all of these patients, the addition of a mass to
the moving hand caused the appearance of a hypermetria. This lack of adaptation of fast and accurate movements to
an increased inertia thus appears as a new diagnostic tool enabling the detection of silent cerebellar lesions.
Manto M, Godaux E, Jacquy J. Detection of silent cerebellar lesions by increasing the inertial
load of the moving hand. Ann Neurol 1995;37;344-350
From his everyday practice, every neurologist knows
that the deficits caused by a brain infarction can be
followed by a substantial recovery and that a slowly
developing lesion can remain astonishingly asymptomatic during a long time. For instance, patients with infarction in the territory of the superior cerebellar artery
were repeatedly reported to improve spontaneously
without sequelae [l-41. It remains to establish
whether this apparently complete recovery is due to a
large brain plasticity in response to injury or to the
fact that usual clinical testing does not explore all the
functions of the injured area.
To address this question, we selected patients with
a normal neurological examination in spite of a cerebellar lesion documented by magnetic resonance imaging
(MRI). Then, we analyzed their fast and accurate
movements and the associated electromyographic
(EMG) patterns when the inertial load was artificially
increased. Indeed, in a previous study, we showed that
hypermetria, a classic cerebellar symptom [ S , 61, was
worsened by addition of mass to the moving limb 171.
W e applied the same paradigm to our asymptomatic
patients to see whether it would unravel a hypermetria
not detected by standard testing.
Patients and Methods
The methodology was exactly the same as that used in a
previous study [ 7 ] . In brief, each patient was asked to make
fast and accurate goal-directed wrist movements with their
fingers extended. In response to a go signal, a horizontal
From the ?Department of Neurophysiology, Faculty of Medicine,
University of Mons, Mons, and *Department of Neurology, HBpital
Civil de Charleroi, Charleroi, Belgium.
wrist flexion had to be made toward an aimed target located
either 15 or 50 degrees from the start position (see Fig 1 of
E71). Movements were made before and after alteration of
the mechanical state of the hand by fixing weights of 200 or
500 gm at the level of the metacarpophalangeal joints. In
each of the three mechanical states, subjects performed some
practice trials before data were collected. Moreover, the effect of the 200-gm load was always investigated before that
of the 500-gm load.
Patients
Recordings were carried out on 8 patients with a cerebellar
lesion and presenting a normal neurological profile upon examination (Table 1).Recordings performed on these patients
were compared with those obtained on 11 healthy subjects
in a previous study [7]. The mean age of that control group
was 46 years, with a range from 16 to 81 years. The mean
age of the patients of this study was 54 years, with a range
from 23 to 73 years. The patient's informed consent was
obtained following full explanation of the experimental procedures.
Motion Recording
Computerized motion analysis in three dimensions was made
with a Selspot I1 system (Selcom).One infrared light-emitting
diode (LED) was attached to the forefinger. Two cameras,
each fitted with a photodetector unit, recorded the twodimensional positioning of the LED. Sampling rate was 300
times per second and the resolution was 0.25 mm. Threedimensional positioning was computed using the two-axes
camera recordings.
Received Juri 6, 1994, and in revised form Sep 1. Accepted for
publication Oct 6, 1994.
Address correspondence to Prof Godaux, University of Mom, 20
Place du Parc, 7000 Mons, Belgium.
344 Copyright 0 1995 by the American Neurological Association
Table I. Clinical Data for Patients with Cerebellar Lesion
Patient
Age (yr)
Sex
Length of Illness
Diagnosis
R.C.
45
M
2 Yr
Z.S.
73
P.S.
68
M
M
20 yr
5 Yr
D.G.
D.M.
M.M.
47
63
23
M
M
F
4 month
20 month
Unknown
B.J.
68
M
4 Yr
C.G.
45
M
Unknown
Occlusion of the right superior
cerebellar artery
Left cerebellar ischemia
Occlusion of the right superior
cerebellar artery
Bilateral cerebellar ischemia
Right cerebellar ischemia
Arachnoidal cyst
Bilateral cerebellar ischemia
Cerebellar idiopathic atrophy
Electromyographic Activity: Recording and Averaging
The activity of the flexor carpi radialis (agonist muscle) and
of the extensor carpi radialis (antagonist muscle) was recorded by surface electrodes. EMG signals were differentially
amplified, filtered ( x 2,000, 30-8,000 Hz), and full-wave
rectified. Twelve observations were made on both muscles
of each subject in six different experimental protocols (amplitude = 15 o r 50 degrees; additional mass = 0 or 200 or
500 gm). Those 12 observations were then averaged (Pathfinder I, Nicolet Instrument Co, Madison, WI) after aligning
them to the moment when the finger crossed a light beam
received by a photoelectric cell located 7 and 4 degrees away
from the initial position for the 50- and the 15-degree amplitude movements, respectively.
EMG activities were quantified according to the method
described by Gottlieb and colleagues [8]. The rectified envelope of the agonist EMG activity was integrated over the
interval from the onset to the first return to zero of the
acceleration (integrated agonist activity over the acceleration
phase of the movement). The antagonist EMG was integrated
from the onset to the second zero-crossing of the acceleration
(integrated antagonist activity over the deceleration phase of
the movement).
A mean of integrated EMG activities developed by different subjects is meaningless, as the EMG activity related to a
particular movement varies from subject to subject as a function of electrode position, muscle mass, diameter of the muscle fibers, and thickness of the superficial fat layer. Because
we wanted to compare the change in EMG activities associated with the addition of extra masses to the moving limb
in two different groups (healthy subjects and patients), we
considered, for each subject, the integrated EMG activities
recorded with no load as a reference value (100% value) and
expressed the integrated EMG activities recorded with extra
loads (200 or 500 gm) in percentages of those basal activities.
The mean ( 2 SD) of those relative values is not prone to
interindividual variations as would be the raw values of integrated EMG activities.
Statistical Analysis
In the basal state, the movement amplitudes and the onset
latencies of antagonist activity were compared in both groups
(patients versus normal) by the Student t test. When the
inertia was artificially modified, the movement amplitudes
and the onset latencies of antagonist activities were compared
by repeated-measure analysis of variance (contrast method).
That method was used to assess the difference between both
groups (normal versus patients) and to detect if an eventual
intergroup difference was due or accentuated by addition of
extra masses (group by mass interaction).
The Friedman test was used to evaluate the statistical significance of alterations of the integrated EMG activities compared with those observed in the basal state.
Results
Hypemetria Associated with Increased Inertia of the
Limb: A Case Report
We will first report a typical observation made on a
patient with a clinically asymptomatic cyst located in
the left part of the posterior fossa. In that particular
case, the movements performed by the left wrist (limb
ipsilateral with respect to the cyst) and the associated
EMG activities were compared with those performed
by the right (contralateral) wrist.
A 23-year-old woman who had been suffering from
a classic migraine for 5 years noticed the appearance
of headache with which she was not familiar. This headache, which lasted for 1 to 3 days, was untractable,
triggered by a neck flexion, and accompanied by a vertigo. Three months after the beginning of this new
symptomatology, the patient took medical advice. The
neurological examination was then quite normal but an
MRI of the brain showed a subarachnoidal cyst compressing the left hemicerebellum (Fig 1).
Figures 2A and 3A show the movement of the index
and the associated EMG activities when the patient
flexed her right (Fig 2A) or her left (Fig 3A) wrist
towards a target located at 15 degrees from the start
position. The kinematic and EMG features of these
movements, performed in the basal state, were normal.
Neither the left nor the right index overshot the aimed
target. The latency of the onset of the antagonist activity either on the right side (20 msec) or on the left
side (21 msec) was not increased.
When a weight of 500 gm was affixed t o the right
hand (Fig 2B), the activity of the agonist was increased
Manto et al: Silent Cerebellar Lesions
345
Fig I . Magnetic resonance imaging IMRI) (spin echo: echo time,
25 msec; repetition time, 480 msec) of the brain of Patient
M.M. showing a subarachnoida( cyst compressing the left hemicerebellum. (A)MRI in the horizontal plane. (B) MRI in a
parasagittal plane passing through the left hemicerebellum.
A
2o
r
B
no load
*O
+ 500 grn
r
A
B
2o
no load
r
20 -
gl5-
9
0
4 10-
1
9
-
I
Q
0
-
1
5
9
5 0-
______._.__...
' W r(
e.J.
20 msec
u
100 msec
20 msec
u
100 msec
Fig 2. Kinematic and electromyographic (EMG)features of fast
and accuratejexion movements made by the right wrist of a patient with a subarachnoidal cyst compressing her lejt hemicerebellum (see Fig 11. The movements were performed in two mechanical states of the moving hand, no overload in A. addition of an
extra load of 500 gm in B . Each top panel corresponds t o the superimposition of the individual records of position for I2 jexion
movements (target distance. 15 degrees). The middle and bottom
panels correspond to the averagrs of the full-rectified EMG artivitiej. associated with these 12 movements. E M G AGO and EMG
A N T A are agonist EMG activities (flexor carpi radialis) and
antagonist EMG acthities (extensor carpi radialis), respectively.
346 Annals of Neurology
Vol 37
No 3 March 1995
CYI
I ,
21 msec
I 5
I
100 msec
&
20 msec
-
100 msec
F i g 3. Kinematic and electromyographic (EMG)features of fast
and accurate flexion movements made by the left wrist of a patient with a subarachnoidal cyst compressing her lejt hemicerebellum (lee F ig J i . (Ai Movement, EMG agonist (AGOi activity,
and EMG antagonist ( A N T A ) actitity for flexions made without any extra load. See Figure 2 for details. (B) Movement,
EMG agonist activity, and EMG antagonist activity Jor
jexions made after addition of an extra load of 500 gm. See
Figare 2 for details.
(to launch the hand at high speed in spite of the added
inertia), as well as the activity of the antagonist (to
brake the launched extra mass). As a result, no hypermetria occurred (compare the top traces of Fig 2A and
B).
By contrast, when a mass of 500 gm was affixed to
the left hand (Fig 3B), the activity of the agonist still
increased but not that of the antagonist (compare the
bottom EMG traces of Fig 3). Consequently, the patient's left finger overshot the aimed target (top trace
of Fig 3B). Therefore, an otherwise asymptomatic lesion of a hemicerebellum was unmasked by the appearance of a hypermetria when the inertia of the hand
controlled by the pathological hemicerebellum was artificially increased.
Analysis of a Group of Patients
The typical observation detailed in the previous section
was confirmed by comparing similar tests performed
on a group of patients presenting a silent cerebellar
lesion, with results observed in a control group already
described in this journal [7]. When the lesion was bilateral, the side (left or right) of the investigated wrist
did not matter. When the lesion was unilateral, we
only considered the limb on the side of the lesion.
For instance, for the patient described in the preceding
section, only the flexions of her left wrist were included in the present intergroup comparison.
The cerebellar lesion exhibited by the 8 patients under study was bilateral in 3 cases and unilateral in 5
cases (see Table 1). When the lesion was ischemic, the
data were recorded from 4 months to 20 years after
the stroke (see Table 1).
In the basal state (without any extra load) the kinematic and EMG features of the movements performed
by these patients were normal. Patients did not overshoot the target more than did the healthy subjects.
When the aimed amplitude was 15 degrees, the mean
amplitude of the movements in the control group (16.5
+ 1.4 degrees) was not significantly different from that
observed in the group of patients (16.5 0.6 degrees)
(Student test, p = 0.950). When the aimed amplitude
was 50 degrees, the mean amplitude of the movements
in the control group (52.3 .t 1.9 degrees) was not
*
significantly different from that observed in the group
of patients (52.2 rt 0.6 degrees) (Student test, p =
0.994). The associated EMG patterns were not altered
by the lesion. When the aimed amplitude was 15 degrees, the mean latency of the onset of antagonist activity (with respect to the onset of agonist) did not significantly differ in the reference group (47 rt 14 msec)
compared with the group of patients (39 -+ 12 msec)
(Student test, p = 0.183). Similarly, when the aimed
amplitude was 50 degrees, the mean latency of the onset
of antagonist did not significantly differ in the healthy
group (42 ? 15 msec) compared with the group of
patients (37 -+ 15 msec) (Student test, p = 0.341).
By contrast, overloading of the fingers caused the
appearance of a hypermetria in patients. Table 2 lists
the amplitudes of the movements carried out by both
groups (healthy subjects versus patients) in six experimental protocols (15 or 50 degrees; no overload or
200 or 500 gm). The repeated-measure analysis of variance showed a group (healthy subjects versus those
with cerebellar lesion) difference ( p < 0.001) that was
mass dependent (group by mass interaction; p <
0.005).
The appearance of this hypermetria was not due to
an increased latency of the onset of antagonist activity.
Table 3 lists those latencies in the six combinations of
experimental conditions. The repeated-measure analysis of variance showed no group (healthy versus with
cerebellar lesion) difference ( p = 0.325). When the
patients performed movements of 50 degrees aimed
amplitude, the onset latency of antagonist EMG activity seemed to increase with increasing inertial load (see
the bottom line of Table 3), but this trend was not
confirmed by the repeated-measure analysis of variance
( p = 0.388). In the other cases (healthy group, aimed
amplitude, 15 degrees; healthy group, aimed amplitude, 50 degrees; with cerebellar lesion group, aimed
amplitude, 15 degrees) the onset latency of antagonist
activity did not seem to be influenced by the inertial
load. This was confirmed by the repeated-measure
analysis of variance ( p = 0.570, p = 0.924, and p =
0.185, respectively).
The hypermetria revealed by an artificial increase of
the inertia of the moving hand was actually due to the
Table 2. Movement Amplitudes
~
Group
Aimed
Amplitude
(degrees)
Inertial Load"
No Load
+ 200gm
+
Healthy subjects
Healthy subjects
Cerebellar lesion
Cerebellar lesion
15
50
15
50
16.5
52.3
16.5
52.2
16.0
51.4
17.3
53.5
15.8
51.3
18.6
54.7
?
?
2
?
1.4
1.9
0.6
0.6
?
?
2
?
0.5
0.8
0.7
0.5
500gm
&
0.6
?
0.8
?
0.3
0.6
?
"Values are means 2 SD. These values are expressed in degrees.
Manto et al: Silent Cerebellar Lesions
347
Table 3. Onset Latencies of Antagonist Electromyographic Activity
Group
Aimed
Amplitude
(degrees)
No Load
+ 200gm
+ 500gm
Healthy subjects
Healthy subjects
Cerebellar lesion
Cerebellar lesion
15
50
15
50
47 t 14
42 2 15
39 t 12
37 2 15
44 t 15
40 t 19
45 t 8
40 2 14
42 .+. 13
39 2 19
"Values are means
%
Inertial Loadd
30 t 15
47 t 9
SD. Onset latencies are expressed in milliseconds and are measured from the onset of agonisr electromyographic activity.
inability of the patients to increase the intensity of the
activity of the antagonist muscle. Figure 4 plots the integrated EMG activities recorded in the control group
and in the patient group as a function of the mechanical state of the hand. As explained in Materials and
Methods, EMG activities were expressed as percentages of the corresponding basal EMG activities, to
suppress interindividual variations ( k SD). The integrated agonist EMG activity increased when an extra
load (either 200 or 500 gm) was added in the control
group as well as in the patient group (Friedman test,
# < 0.001). The integrated antagonist EMG activity
also increased when an extra load (either 200 or 500
gm) was added in the control group as well as in the
patient group (Friedman test, p < 0.001). However,
the increase of the antagonist EMG activity was much
larger in the control group than in the patient group
(compare bottom of Fig 4 A and B). Indeed, the repeated-measure analysis of variance on the EMG activities measured when extra loads were applied
showed no intergroup difference for the agonist activity (group effect; significance of F , p = 0.279) but
revealed a difference in the antagonist activity (group
effect; significance of F , p < 0.001). Furthermore,
the intergroup difference with respect to the antagonist activity became more severe when inertia was
increased (interaction group by mass; significance of
F , p = 0.011).
Discussion
The two major findings of this study can be summarized as follows: (1) By adding a mass to the moving
hand, it is possible to unmask a hypermetria in patients
with an apparently normal neurological examination in
spite of a cerebellar lesion. (2) This hypermetria is associated with an inability to scale appropriately the amplitude of the antagonist muscle and not with a delayed
onset of the antagonist activity.
During the task of reaching a target as fast and accurately as possible, the movement is controlled by a
triphasic pattern of EMG activity {9-17). A burst of
activity in the agonist is followed by a burst in the
antagonist, followed by another burst in the agonist.
348 Annals of Neurology Vol 37 No 3 March 1995
A
HEALTHY
SUBJECTS
PATIENTS WITH
CEREBELLAR LESION
integrated
agonist
140r
no
load
+ZOO
+500
gm
gm
integrated
agonist
EMG
no
load
+ZOO
gm
+500
gm
aimed amplitudes
0 50degrees
160
"I50
[
integrated
antagonist
EMG
integrated
antagonist
140
no
load
+ZOO
gm
inertial load
+ 500
gm
no
load
+ZOO
gm
+500
gm
inertial load
Fig 4. Integrated agonist electromyographic (EMG) activity
(over the acceleration phase of the movement)and integrated antagonist EMG activity (over the deceleration phase of the movement) associated with fast and accurate flexions of the wrist carried out by healthy subjects (A) or patients with a cerebellar
lesion (3)under three different mechanical states of the moving
hand (no extra load, addition of 200 gm, addition of SO0 gmj.
Values are expressed in percentages of the EMG activities recorded in the basal state. Filled circles show EMG recorded
when subjects were asked to make SO-degree flexion movements;
open circles refer t o 15-degreeflexion movements.
The role of the first burst of activity in the agonist
muscle is to launch the movement. The role of the
burst of activity in the antagonist is to brake the movement. When a patient suffering from a cerebellar disease has to make such a type of movement, he often
overshoots the aimed target (a symptom called hypermetria). A priori, hypermetria might be due either to
a delayed braking function or to a too weak braking
function or to both of them. The underlying defect
in the hypermetria of the movements performed by
cerebellar patients has been repeatedly found to be an
increase in the latency of the onset of antagonist activity [18-22). These findings have led to the current
general concept that the role of the lateral cerebellum
in programming ballistic movements is restricted to the
timing of agonist-antagonist activities (see 1231 for a
review of the genesis of the current concepts in cerebellar pathophysiology). However, in a previous study,
we found that, when a weight was added to the moving
limb, the cerebellar hypermetria was worsened and
that the underlying deficiency was the inability of the
cerebellum to increase the intensity of the braking activity of the antagonist muscle 171.We have suggested
that the lateral cerebellum might compute the muscle
activity needed for the braking action of the antagonist
muscle, including the onset time and the amplitude,
based on the initial position of the limb, the position
of the target, and the inertia to be overcome. As summarized by Gilman [231: “the cerebellum has been
deduced to be responsible for much more than a simple timing function.” The findings of the present study
strengthen this conclusion, since we observed in particular circumstances a cerebellar hypermetria due solely
to an inadequate amplitude of the activity of the braking antagonist muscle. Moreover, the fact that the patients expected the change in inertial load and still
could not compensate for it makes the results stronger.
We describe here a procedure to unravel silent cerebellar lesions. However, to be useful, the test must be
performed in a laboratory of clinical neurophysiology.
Indeed, adding 500 gm to the hand of these patients
with asymptomatic cerebellar lesions produces a significant but small hypermetria (the overshoot was
about 2 degrees larger than that observed in the control subjects for the 50-degree amplitude movements).
Such an overshoot will not be visible to the naked eye
of the examiner. T o detect it, it is necessary to perform
quantitative measurements. Moreover, the changes in
antagonist EMG activities associated with the changes
in inertial load seem more reliable than the changes in
movement amplitudes in the differentiation of lesioned
patients from healthy subjects (compare the bottom
diagrams of Fig 4 with the values of Table 2).
However, to date, it is impossible to assess the specificity and the sensitivity of our test since our group of
patients was small and since our test has not yet been
applied to a large group of individuals picked at
random.
To appreciate the usefulness of the test presented
here, it is important to know whether our patients were
really totally asymptomatic. The patients explored here
were described to have silent lesions because they had
a normal clinical examination and did not have any
complaint in their everyday motor behavior. Interestingly, one of them who was a manual worker noticed
that he had become clumsy only when he handled
heavy loads at work. Of course, usual patients rarely
encounter inertial loads of 500 gm in the normal daily
activity, but during the laboratory testing, all the patients perceived their problem without being able to
compensate for it. There was thus a good correlation
between our objective measurements and the subjective perceptions of the patients.
In this study we describe a protocol enabling one to
unmask asymptomatic cerebellar lesions. Such procedures are potentially useful in neurology. For instance,
the diagnosis of multiple sclerosis (MS) is based on the
demonstration of multiple lesions in the central nervous system. In front of a patient with an isolated neurological sign, detection of a second silent lesion is
crucial to establish the diagnosis. Laboratory procedures such as the evoked potentials [24-27) and MRI
{28, 293 have made possible the detection of clinically
unsuspected lesions. The study of the adaptation of
fast and accurate movements to an increased inertia
might also be viewed as a new diagnostic tool to detect
silent lesions.
This study was supported by a grant from the Philippe and Therese
Lefebvre’s Fund.
We are grateful to Christiane Busson for secretarial assistance and
to Bernard Foucart for taking care of the electronic equipment.
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Cerebellar Lesions
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