One of the more frequent alterations of the pyramidal system is the
capsular stroke. Vascular accidents of the internal capsule produce, because of the
interruption of the corticospinal and corticobulbar fascicles, a paralysis in the
contralateral superior and inferior limb and in the inferior contralateral facial muscles.
The progress of the capsular stroke is normally positive, though the initial absence of
movement in the contralateral limbs, but there is an increased difficulty in the
recuperation of the more distal parts of both limbs (Arboix et al., 1990; Elcano et al.,
1989). It is also common the persistent difficulty in the performance of precise
movements, as well as the presence of associated movements (Young & Young, 1998).
Recent Positron Emission Tomography (PET) studies (Chollet et al.,
1991; Weiller et al., 1992; Weiller et al., 1993) has revealed bilateral activation of
motor cortices after functional recovery, during recovered-fingers movement. This
bilateral activation is related to associated-involuntary movements (Weiller et al., 1993)
of normal fingers.
Cortical potentials related to voluntary movement may help to elucidate
the neural mechanisms participating in associated-movement preparation. These cortical
potentials are generally defined as movement-related potentials (MRPs) and reflect a
preparatory activity that is related to the specific movement being executed (Shibasaki
& Ikeda, 1996). MRPs associated with hand or finger movements begin with a long phase
of rising negativity (Hallet, 1994). The later part of this rising negativity, starting
about 400 msec before the onset of movement, is called the negative slope (NS).
NS becomes steeper especially at the centroparietal region contralateral to the
movement side and peaks about 90 msec before the onset of EMG activity. Sometimes the
NS is followed by the motor potential (MP), which begins before movement, peaks
after movement beginning, and produces the main negativity. The initial slope of the MP
(isMP) occurs after the peak of NS and before the onset of EMG activity. This
initial slope has a discrete and focal topography and appears over the contralateral
primary motor cortex representing its activation (for a review see (Barret et al., 1985;
Barret at al., 1986).
To our interest, erroneous bilateral cortical predominance observed in
mirror movements (similar to that described after motor recovery in capsular infarction)
is well represented by MRPs recording, indicating an abnormal bilateral NS
(Shibasaki & Nagae, 1984) and MP (Cohen et al., 1991).
Therefore, we expect that MRPs (NS-MP) will reflect a bilateral
activation of motor cortices during self-paced, recovered-hand movements, in a patient
with capsular stroke.
Patient and Methods
64 years old female (patient M.P) with a history of hypertensive
illness, is admitted to San Carlos University Hospital, with an acute episode, that
consist in a speech disorder associated to a motor deficit in the right hemibody without
lost of consciousness. Neurological examination reveals a moderate disartria, right
central facial paresis and a predominantly crural right hemiparesis. There are no sensory
alterations. The rest of the physical and neurological examinations were within normal
limits. Diagnose was a pure motor hemiparesis.
The MRI (T2 images), two weeks after the acute episode, reveals few
high intensity images in the posterior area of the left internal capsule (see Figure 1).
After the acute episode, the patient attended to a rehabilitation
program with a completed recuperation after three months.
11 moths after the acute episode, patient M.P was asked to make
self-paced, brisk abduction movements of the right (recovered) and left (normal) hands at
an irregular rate of approximately one movement every 4 seconds, while her eyes fixated at
a point 1.7 m away. M.P completed 150 to 180 movements, divided into blocks of 30 to 50
movements for each hand in a single recording session.
Cerebral evoked potentials were recorded from C3, Cz, C4 Ag/AgCl
electrodes on the scalp according to the international 10/20 system. Eyes movements were
monitored by an electrode, placed infraorbitally, referenced to linked ear electrodes
A1/A2. An unrectified EMG was recorded from an electrode placed over the belly of the
common extensor digitorum muscle of each hand, referenced to an inactive electrode placed
on the dorsum of the ipsilateral hand. The bandpass was 0.3-70 Hz and the impedances <5
k Ohms for all electrodes. EEG recordings were performed in a quiet, dimly lighted room.
M.P was resting comfortably in an armchair with her hands extended naturally in a pronated
position on a pillow. She was requested to assume a relaxed posture in order to minimised
head and eye movements.
We analysed the latency of the movement related cortical potentials
over C3, C4 and Cz electrodes, measuring the Negative Shift Peak and Motor potential peak
and reaction time measuring EMG onset of voluntary hand movement. The latencies of the
movement-related potentials were measured manually using the computer, following the
criteria previously defined by Tarkka and Hallet (1991).
Data were analysed off-line by means of a polygraph interface (ATI
Nautilus 5.28). To this effect, cerebral, EMG, and EOG channels were aligned by the onset
of the initial negative deflection of the compound muscle action potential. An interval of
1,500 milliseconds, 1000 backwards and 500 forwards from EMG onset, was then analysed.
Trials containing substantial artefacts or contaminated by eye movements were excluded
from subsequent analysis.
The main result observed in the EMG register is the continuous presence
of associated movements in the left hand during the performance of the self-paced right
hand (recovered hand) movements (Figure 2). However, left hand movements were not
associated to any abnormal movement.
The onset of the EMG in the right hand appears at 209 msec and at 187,3
msec in the left hand. The associated movement that appears in the left hand when a
movement in the right hand appears at 692 msec.
Figure 3 show MRPs recorded from scalp electrodes C3, Cz and C4.
Approximately 400 msec before EMG onset the waveforms became steeper (NS) and reach
a peak about 50 msec before EMG onset, with larger amplitude over contralateral electrodes
for left hand normal movement.
In opposite to left hand movement, MP has a clear bilateral
distribution during right movements. This component begins close to EMG onset and peaks
about 170 msec after. MRPs associated to left hand movement present a clearly diminished
amplitude over C3 electrode; while both right and left hand movements, elicitates a MP
component of maximum amplitude over C4. Moreover, right hand movement elicitates an
abnormal high-amplitude MS component over C4, with a significative delay (40 msec)
compared to left hand MS. This left-to-right MS delay is also observable over Cz.
Results above presented confirm two previously well defined evidences:
1.Neural reorganization necessary to overcome some motor deficits, may consequently cause
a bilateral activation of motor cortices during recovered-limb movements; and 2. This
bilateral cortical activation may produce, as a consequence, associated movements in
The bilaterality of the NS y MP components is a normal
observation in the mirror movements (Shibasaki & Nagae, 1984). This pathology is
characterised, like in other patients with a capsular infarction, by the presence of
involuntary associated abnormal movements (Schott & Wyke, 1981). But this is not the
only similarity in both diseases. When we considered Weiller y Chollet results (Chollet et
al., 1991; Weiller et al., 1992; Weiller et al., 1993), the onset of bilateral activity
(that includes premotor areas and caudate nuclei) and associated movements, is a
consequence of a desinhibition process. This implies that there is a functional inhibition
in these areas under normal conditions, which is determined under by contralateral
structures (Weiller et al., 1992), mainly between homotopic regions. For these authors,
the decreased of the natural process of transhemispheric inhibition (mostly transcallosal)
could be a valid explanation.
This hypothesis is narrowly related to Daneks and the mirror
movements. As Danek et al. (Danek et al., 1992) pointed out, a bilateral distribution of
descending motor pathways can not sufficiently explain mirror movements, as far as some
neurones in the unlesioned primary motor cortex address hand muscles bilaterally, both in
monkeys (Tarkka et al., 1990) and humans (Fries et al., 1991). Accepting this latent
bilaterality of motor commands as normal, some authors (Cohen et al., 1991; Danek et al.,
1992) postulated an «inhibition theory» of mirror movements. This theory claims that
commands from the motor cortex that would excite ipsilateral muscles via ipsilateral
pathways normally are suppressed by the opposite, not primarily active, motor cortex
(Shibasaki & Kato, 1975). Such inhibition, is thought to be exerted by
cortico-cortical fibers crossing the corpus callosum. When this callosal fiber system
fails, as occurs in the agenesis of corpus callosum, mirror or associated movements
Recently, Ortiz et al (In press), have been able to probe that certain
associated movements that appears in Alzheimers disease (similar to the alterations
that appears in the capsular infarctions) are narrowly related with a significant
decreased in the volume of anterior areas of the corpus callosum. We can conclude,
therefore, that there is a constellation of motor disturbances (mirror movements,
associated movements in striato-capsular infarction and Alzheimers disease) that are
characterised by an abnormal bilateration of the neural activity, that could be explained
because of the disappearance of the natural process of the active inhibition, that is
originated either because a callosal alteration or because of an abnormal reorganization
of the pyramidal system.