close

Вход

Забыли?

вход по аккаунту

?

Correlation of phasic muscle strength and corticomotoneuron conduction time in multiple sclerosis.

код для вставкиСкачать
ORIGINAL ARTICLES
Correlation of Phasic Muscle Strength
and Corticomotoneuron Conduction Time
in Multiple Sclerosis
W. van der Kamp, MD, A. Maertens de Noordhout, MD, P. D. Thompson, FRACP, J. C. Rothwell, PhD,
B. L. Day, DPh1, and C. D. Marsden, DSc
Central motor conduction times for the adductor pollicis muscle, the twitch force of that muscle to scalp magnetic
motor cortex stimulation, and the maximum force of phasic voluntary contraction of the same muscle were measured
in 15 patients with multiple sclerosis. Two tests of manual dexterity of the same hand also were studied: the Purdue
pegboard test, and the maximal frequency of a scissors movement of the thumb and index finger. The patients had
normal strength or minimal weakness of the intrinsic muscles of the hand on clinical examination. The mean central
motor conduction times for the adductor pollicis muscle for the patients were longer than normal, the peak twitch
force of the adductor pollicis muscle evoked by cortical stimulation and the maximum force of a phasic voluntary
contraction of the adductor pollicis muscle were smaller than normal. There were strong correlations between all these
measures. Central motor conduction time in the patients was inversely correlated with voluntary phasic force and the
twitch force after cortical stimulation. That is, the longer the central motor conduction time, the weaker the force.
Prolonged central motor conduction time is likely to be accompanied by conduction block in corticomotoneuron
pathways. The correlation of central motor conduction time with voluntary phasic force and the twitch force most
likely reflects the degree of conduction block and temporal dispersion rather than delay in conduction per se. These
results indicate that objective assessments of phasic muscle strength may reveal correlations with central motor
conduction time that are not evident on conventional clinical examination which assesses tonic muscle contraction
strength. There also was some correlation of central motor conduction time, twitch force, and voluntary phasic force
with the performance of tests of manual dexterity. Since the voluntary phasic strength and twitch force to cortical
stimulation were similarly weakened, the findings would also be consistent with the cortical stimulus and voluntary
contraction using the same descending motor tracts.
van der Kamp W, Maertens de Noordhout A, Thompson PD, Rothwell JC, Day BL, Marsden CD.
Correlation of phasic muscle strength and corticomotoneuron conduction time
in multiple sclerosis. Ann Neurol 1991;29:6-12
Conduction time in central motor pathways (CMCT)
estimated by using the techniques of electrical and
magnetic scalp stimulation of the motor cortex {l, 2)
may be prolonged in patients with multiple sclerosis
(MS) 13-10]. It has emerged from these studies that a
high proportion (up to 90%) of patients with obvious
clinical signs of an upper motor neuron syndrome exhibit prolongation of CMCT {S- lo}. Conventional
clinical assessment of muscle strength in the upper
limbs, however, has not revealed a clear correlation
between weakness and the extent of CMCT delay [6,
8-10]. Additionally, prolongation of CMCT to upper
limb muscles that are neither weak nor spastic may be
found in up to 50% of patients with MS or suspected
MS 16, 8-10). In the study of Hess and co-workers
[S], brisk tendon reflexes of finger flexor muscles were
found to correlate with CMCT delay to the abductor
digiti minimi, whereas impaired fine finger movements
and weakness of that muscle were only weakly correlated. Ingram and colleagues f91 found that the maximal isometric strength in upper limbs (assessed clinically) was normal in 78 of 80 muscles examined, yet
CMCT was abnormal in half of these muscles. Tendon
reflexes did not correlate with CMCT in the upper
limb. In contrast, correlations of the absolute latency
of responses in leg muscles to cortical stimulation and
the Kurtzke disability rating based on ambulatory
function { 7 ] ,and of CMCT with the Kurtzke and Ambulatory Index scales and extensor plantar reflexes
have been described [9].
From the MRC Human Movement and Balance Unit, Institute of
Neurology, The National Hospital for Nervous Diseases, London,
Address correspondence to Prof Marsden, University Department
of Clinical Neurology, The National Hospital for Nervous Diseases,
Queen Square, London W C l N 3BG, UK.
UK.
Received May 25, 1990. Accepted for publication Jun 25, 1990.
6 Copyright 0 1991 by the American Neurological Association
A question that remains unanswered by these studies is what, if any, aspects of voluntary motor performance in the upper limb are correlated with conduction in central motor pathways. The purpose of the
present study was to investigate whether quantitative
assessments of hand function in patients with MS correlate with abnormalities in CMCT.
Patients and Methods
Four male and 11 female patients with MS, mean age 44
years (range, 29-57 years) with an average disease duration
of 9.5 years (range, 1-20 years) were studied. All but one
had a definite diagnosis of MS according to the criteria of
McAlpine [l 11 or a laboratory supported diagnosis by using
the criteria of Poser and colleagues [12). The remaining patient was classified as having possible MS. The patients were
chosen on the basis of normal strength (n = 12) or minimal
weakness (n
3) of the intrinsic muscles of one hand in the
limb studied with minor or insignhcant objective or subjective functional impairment. Muscle tone was abnormal in 3
patients, and tendon reflexes were exaggerated in 10. Patients with sensory loss or cerebellar deficits affecting the
upper limbs were not included in the study.
Fifteen healthy volunteers, 8 men and 7 women, mean age
33 years (range, 23-60 years) were studied as control subjects. All patients with MS and normal control subjects gave
informed consent to the procedures performed. The protocol had been approved by the local ethical committee.
Stimulation of the motor cortex and over the spinous process of C-7 was performed with a Novametrix 200 magnetic
stimulator by using the maximum stimulating intensity of the
device (100% of output). Muscle responses were obtained
from surface electrodes placed over the adductor pollicis
muscle while the subject exerted a gentle background voluntary contraction (about 59% maximum) of the muscle. The
signals were preamplified (Devices 3160),amplified (Devices
3120), and rectified before being stored on disk for later
analysis. The larency to onset of electromyographic (EMG)
responses was measured after spinal and cortical stimulation,
and the CMCT was estimated by subtracting the latency of
the adductor pollicis EMG response to stimulation over C-7
from that obtained when stimulating the motor cortex 13, 4,
6, 8-10].
Force measurements were made in the following way:
Subjects were comfortably seated on a chair with their right
forearm and wrist extended in front of them and their arm
and hand resting on a table. To measure the twitch force of
the thumb adductor, the forearm was supinated and the
thumb attached to a stiff force transducer by a wire loop
around the proximal phalanx. The supinated forearm was
immobilized by a strap attached to the table top so as to
prevent extraneous movement of the arm contributing to the
thumb twitch. Subjects were then asked to make 10 brisk,
maximum voluntary adduction movements of the thumb
against the force transducer. Measurements were made from
the strongest of the phasic contractions. Twitch force also
was measured after magnetic cortical, magnetic spinal, and
supramaximal electrical peripheral ulnar nerve stimulation (at
the wrist), and the rate of change of force was obtained by
differentiating the twitch forces.
Manual dexterity was assessed by measuring the time
taken to place 10 pegs in a pegboard (Purdue pegboard test
1131)and by measuring the maximal frequency of rapid alternating movements of the thumb and index finger. The latter
was obtained by asking the patient to open and close a pair of
scissors between the index finger and thumb as rapidly as
possible for 15 seconds. The movements were detected by a
potentiometer attached to the scissors and recorded on the
computer for later counting.
Statistical analyses were performed by using two-tailed
Mann-Whitney tests and Spearman's rank order of correlation. Associations between the abnormal clinical signs (rated
from 0 I = none] to 3 { = severe]) and CMCT were performed by using x2 tests.
Results
Central Motor Conhction
Times
The estimates of CMCT for the adductor pollicis muscle in the group of patients with MS and the normal
values are shown in Figure 1. T h e mean (k 1 SEM)
CMCT for this muscle in normal subjects was 6.7 +0.1 msec with a range of 5.0 to 7.6 msec and an upper
2.5 SD). I n the group
normal limit of 8 msec (mean
of patients with MS, the mean CMCT was significantly
2.1 msec ( p < 0.001) despite the
prolonged to 15.2
absence of or only minimal clinical signs of an upper
motor neuron lesion in the arms. The spread of CMCT
values in the patients with MS, ranging from 7.4 to 35
+
*
msec, also was greater than seen in normal subjects
(see Fig 1). S i x of the 15 patients with MS had CMCT
values of 8 msec or less.
40
f
L
30
20
10
~
I
**
N
MS
Fig 1. Central motor conduction times (CMCT)for adductor
pollicis muscle afrer scalp magnetic stimulation of the motor cortex in 15 normal subjects (N)
and 15 patients with multiple
sclerms (May).
Brain stzmulation wa1 performed at the m x a m d
output of the stimukator during a gentle background (5% OJ'
maximum) voluntary contraction. Horizontal dashed Iines represent n o m l mean & 2 SD.
van der Kamp et al: Phasic Muscle Strength in Multiple Sclerosis 7
CORTICAL STlMULATlON
Twitch Force
Adductor Pollicis EMG
113N
500ms
Force
Adductor Pollicis EMG
1sec
1sec
I
1OOms
Fig 2. Peak twitch force and electromyographic (EMG) responses
in adductor pollicis a&er scalp magnetic stimulation of the motor
cortex (@t two columns, re.ipectively),and the force and rectified
E M G activity during a phasic maximum soluntary thumb adduction movement (two right columns, respectively)from 3 patients with multiple sclemis (upper three rows) and a normul
subject {lower row). Results of these single trials are superimposed
(three trials superimposed). Magnetic brain stimulation (giz,enat
the beginning of the tracesj was at 100% of the ozdtput of the
stimulator. The EMG responses to magnetic brain stimukztion
in the patients were delayed and smaller in size than normal.
The twitch force evoked by the cortical stimulus and the peak
voluntay phasic voluntary twitch force also were smaller than
normal.
Muscle Force
A series of responses from 3 patients with MS and one
normal subject are shown in Figure 2, and the results
of the force measurements are summarized in Figure
3. The mean peak force of the strongest phasic voluntary contraction in the group of patients with MS was
less than that of normal subjects ( p = 0.01). The mean
peak twitch force of adductor pollicis generated by
magnetic stimulation of the cortex also was less than
that recorded in normal subjects ( p < 0.001).The rate
of rise of force was greater in the normal subjects. This
8 Annals of Neurology
VOLUNTARY CONTRACTION
Vol 29 No 1 January 1991
was the case for both phasic voluntary contraction ( p
= 0.01) and the twitch force evoked by the cortical
stimulus ( p < 0.01) (see Fig 3). The time from the
onset of muscle contraction to peak force after cortical
stimulation also was prolonged (normal subjects 177
& 5 msec; patients with MS, 236 2 11 msec; p < 0.01
{mean f 1 SEMI). There was no difference between
the mean peak twitch force of adductor pollicis muscle
after ulnar or spinal stimulation in either group of patients ( p > 0.05) (see Fig 3).
The mean peak twitch force after cortical stimulation in the group of patients with MS correlated with
the peak force of the strongest phasic contraction ( p <
0.01) (Fig 4A).
Manual Dexterity Tests
The mean ( + 1 SEM) time taken by normal subjects
to complete the pegboard test was 15 2 1 second. The
patient with MS took significantly longer to complete
this test (63 5 20 seconds) ( p < 0.001). Similarly, the
mean ( 2 1 SEM) frequency of the scissor movement
was slower in the group of patients with MS (3.9 2
0.3 Hz) compared with the normal subjects (5.8 k 0.2
Hz) ( p < 0.001).
**
T
0
VOL
CORTEX
ULNAR
120
80
40
160
200
C7
Vduntmy Force (N)
MULTIPLE SCLEROSIS
im r
-iI
I
O
A
NOAMALSUPJECTS
-z
**
150
500
0
b
k
0
F
-5
c
'
0
VOL
CORTEX
Fig 3. Twitchforce (Force)and the rate of change of twitch force
(dForcej in adductor pollicis during maximum voluntary phasic
contraction (vol),in response t o motor cortical magnetic stimulation (cortex),electrical ulnar nerve stimulation at the wrist (ulnar), and stimulation over the spinal column (C7) in 15 patients with multiple sclerosis (MS) (solid bars) and 15 normal
subjects (hatched bars). Mean ? 1 SEM are shown. The
strength of voluntay contraction was weaker in the group of
patients with MS as was the twitch force evoked by cortical
stimulation. The twitch force to stirnulation of the peripheral
nerves was the same in both groups. The rate ofri.re of the fvrce
also was greater in the normal subjects. Note that the patients
with MS were selected because they exhibited minimal or no signs
of an upper motor neuron syndrome in the upper limbs and had
normalstrength or only minimal weakness of the intrinsic hand
muscles on conventional clinical testing (see text for further clinical details). ""p < 0.01, **'p < 0.001.
Cowelations of Muscle Force and CMCT
In the group of patients with MS, there was an inverse
correlation between the CMCT and (1) the maximum
phasic voluntary force ( p < 0.001) (Fig 4B), (2) the
peak rate of change of the maximum phasic voluntary
force ( p < 0.05), ( 3 ) the maximal twitch force evoked
by the cortical stimulus ( p < 0.01) (Fig 4C), and (4)
the peak rate of change of the cortical twitch force ( p
< 0.05). Therefore, prolongation of CMCT was associated with a similar effect o n the recruitment of spinal
motoneurons by both the cortical stimulus and a phasic
voluntary contraction. There was no correlation between the CMCT and the twitch force generated by
ulnar nerve stimulation at the wrist or spinal stimulation ( p < 0.05).
6
75-
50.
so*4
25
*
*
30
35
CMCT (ma)
B
40
1
t
0
0
5
10
15
20
25
40
CMCT (ms)
C
Fig 4. (A)Peak force of maximum phasic voluntary contraction
of d u c t o r pollicis plotted again.it peak twitch force in that
muscle to scalp magnetic stimulation ofthe motor cortex in 15
patients with multiple sclerosis (MS) (solid diamonds) and I5
normalsubjects (circles). The twitch force and the maximal
phasicforce were smaller than normal in most of the group of
patients with MS. The size ofthe evoked muscle twitch correlated
with the strength o f phasic voluntary contraction (patients,
S p e a m n rank order = 0.79, p < 0.01; normalsubjectsSpearman rank order = 0.5094, p > 0.03). (B) Peak phasic maximum voluntary contractionforceplotted against central motor
conduction times (CMCT)for adductor pollicis. Symbols as for
(Aj. In the patients with MS there wa.r an inverse correlation
betweea the CMCT and the twitch force (Spearman rank order
= - 0.91, p < 0.001). (C) Peak twitch force in adductor
pollicis evoked by scalp magnetic stimulation of the motor cortex
plotted against CMCT for that muscle. As with the peak voluntary contraction, in the patients with MS, the longer the
CMCT, the smaller the twitch force (Spearman rank order =
- 0.84, p < 0.01).
van der Kamp et al: Phasic Muscle Strength in Multiple Sclerosis 9
Correlation of Manual Dexterity Tests
with CMCT and Twitch Force
A signlficant correlation was found in the group of
patients with MS between CMCT and the time to
complete the pegboard test ( p < 0.01) but not the
frequency of scissor movement ( p > 0.05). The frequency of scissor movements was correlated with both
the cortical twitch force and the voluntary twitch force
( p < 0.01). In contrast, the pegboard tests were not
correlated with twitch force evoked by cortical stimulation or the maximal phasic voluntary twitch force ( p >
0.05).
Correlation of ClinicaL Signs with CMCT
The presence or absence of abnormal CMCT did not
correlate with brisk tendon reflexes (x2 = 5.1), increased muscle tone (x2 = 2.5), or muscle weakness
(x2 = 0.8) ( p > 0.05 for all clinical signs).
Discussion
The novel feature of the present results is the finding
of a correlation between changes in CMCT and several
aspects of motor performance in an intrinsic hand muscle of patients with MS. Patients whose objective tests
of phasic voluntary strength were weaker than normal,
and who performed poorly in the pegboard test of
manual dexterity, also tended to have prolonged
CMCT.
Abnormalities in CMCT probably reflect conduction defects in the large diameter corticomotoneuronal
fibers of the corticospinal tract [GI. Prolonged CMCT
in MS is due in part to demyelination causing slowed
conduction in corticomotoneuron fibers. The effect of
slowed conduction due to demyelination on function is
well established in peripheral nerves, as for example
in inflammatory demyelinating neuropathies, where
slowed conduction alone may not compromise function. If slowed conduction is associated with conduction block in some affected peripheral nerve fibers,
there will be a decrease in the size of the transmitted
compound muscle action potential and weakness. The
same principles apply in the central nervous system {b}
but with added complicating factors in the corticomotoneuron pathway. Stimulation of the motor cortex, by
either the electrical or magnetic methods, generates
not a single action potential as is the case in peripheral
nerves but a series of descending volleys (D and I
waves) at very short intervals of approximately 500 Hz
{14}. Motoneurons may fire at the time of arrival of
the first (D) wave or subsequent (I) waves, depending
on their strengths and summation. Accordingly, conduction block alone may delay CMCT by 2 to 6 msec,
without any delay in conduction itself [b]. Additionally, temporal dispersion of volleys in the many corticomotoneuron fibers that input onto an individual
10 Annals of Neurology
Vol 29 No 1 January 1991
anterior horn cell will interfere with the generation of
a summated excitatory postsynaptic potential in that
cell. Temporal dispersion of the descending volleys
would be expected to alter the time course of the
compound EPSP in each anterior horn cell and could
well delay the instant at which it discharges. Delays in
CMCT probably reflect variable combinations of
slowed conduction, conduction block, and temporal
dispersion; the longer the delay, the greater the contribution of slowed conduction, but so too is the likelihood of increasing conduction block and temporal dispersion. Thus, CMCT delay may well be a measure not
only of conduction time but also of conduction block
and temporal dispersion in descending corticomotoneuron fibers. We suggest that this is the reason why
we have found such strong correlations be: ween
CMCT and twitch force and maximal phasic voluntary
force for adductor pollicis in patients with MS. Of
course, it would be better to have a direct measure of
conduction block in corticomotoneuron fibers, such as
the absolute size of the compound muscle action potential as used in peripheral nerve conduction studies.
The complicating issue of multiple descending volleys
in corticomotoneuron pathways producing polyphasic
EMG responses, however, makes the interpretation of
the evoked muscle action potential difficult 114, 151.
Instead, we suggest that the measurement of resulting
evoked twitch force is the best measure of synchronous muscle activation and hence of conduction block
and temporal dispersion in corticomotoneuron pathways.
Having established in this study a close correlation
between CMCT in patients with MS and evoked muscle twitch force, as well as with maximum phasic voluntary contraction force of adductor pollicis, why is there
no such relation of CMCT with conventional tests
of muscle power (which estimate isometric muscle
strength), and why are there inconsistent correlations
with spastic muscle tone and hyperreflexia? Others
have found weak correlations between CMCT, hyperreflexia, and spasticity [8, 91; we could not find an
association in the group of patients with MS chosen in
this study. We suggest that the lack of strong correlation of CMCT with isometric force, hyperreflexia, and
spasticity is because the major function of the fast conducting corticomotoneuron pathway in humans is to
generate rapid phasic muscle action, particularly of the
hand and arm.
There is good evidence from primate experiments
that the large diameter component of the corticospinal
tract is necessary for performance in the task we chose
to study here. In monkeys, lesions of the pyramidal
tract produce little obvious motor deficits, and maximal strength tested clinically is virtually unaffected
[lb]. There are only two persisting deficits. First, there
is a decline in fine manipulative skills [16-181. The
importance of the pyramidal tract in the latter is reinforced by recordings from large pyramidal cells in the
motor cortex. The discharge of these cells was greater
when the animal performed independent finger movements than when exerting power grip E19, 201. The
second deficit is a reduction in the speed of phasic
voluntary contraction. The role of the large diameter
component of the pyramidal tract in the latter is supported in the present study by the correlation of
CMCT with phasic twitch force evoked by cortical
stimulation and a phasic voluntary contraction. Because it is believed that the early latency responses to
brain stimulation are conducted by the largest diameter fibers of the corticospinal tract, the deficits observed in this study are likely to be due, at least in part,
to involvement of the corticospinal system. The difficulties in previous studies of identifying a correlation
between CMCT and muscle strength on clinical examination may be related to the fact that clinical assessments of strength rely on tonic muscle activation.
Tonic and phasic muscle activity may use different
descending inputs, at least in the monkey [19-21],
and obscure any correlation.
As previously argued, we believe that it is conduction block and the resulting failure to transmit rapid
trains of impulses and temporal dispersion in corticomotoneuron fibers that is most important in producing
phasic muscle weakness and lack of manipulative skills.
Failure to transmit impulses through a demyelinated
segment of nerve occurs with frequencies greater than
approximately 50 Ht [22, 231. Such frequencies of
discharge in pyramidal tract neurons probably are exceeded at the onset of a phasic voluntary contraction
[20, 21). If blocking occurred, there would be a delayed and reduced build-up of force in the muscle. The
same explanation applies to the relatively small muscle
twitch evoked by cortical stimulation in the patients
with MS. A single cortical shock produces multiple
descending volleys at maximum frequencies of approximately 500 Hz [ 141. Such volleys are very effective in
producing rapid recruitment of motoneuron firing in
normal subjects; however, in patients with MS, conduction block of later impulses in the train would lead
to a small twitch and a slow rate of rise of force.
Although it is possible to explain the present results
solely on the basis of corticospinal tract involvement,
other factors also may be involved. Demyelination may
affect other long spinal tracts in addition to the corticospinal tract. To achieve a maximum rate of rise in muscle strength, an optimal descending input in all pathways may be necessary. A defect in any of these other
pathways also could contribute to a reduction in phasic
strength. Berardelli and colleagues [lo] have reported
a correlation between abnormal muscle responses to
brain stimulation and somatosensory evoked potential
latencies. If slowing of conduction in central sensory
pathways produces subtle sensory deficits, these also
may contribute to poor performance in the functional
tests of manual dexterity.
In conclusion, these results give some insight into
the role of the fast conducting corticomotoneuron pyramidal pathway in humans. The correlation in the
patients of adductor pollicis twitch force evoked by
motor cortex stimulation with maximum phasic voluntary force, and with a test of manual dexterity (the
pegboard test) involving phasic contraction of the adductor pollicis, both point to the preeminent role of
the pyramidal pathway in controlling fast fractionated
finger (thumb) movement.
We are grateful to Mr H.C. Bertoya and Mr R. Bedlington for their
invaluable technical assistance, to Mr Zwinderman for assistance
with statistical analysis, and to R.A.C. Roos, PhD, for kind advice.
References
1. Merton PA, Morton HB. Stimulation of the cerebral cortex in
the intact human subject. Nature 1980;285:227
2. Barker AT, Jalinous R, Freeston IL. Non-invasive magnetic
stimulation of the human motor cortex. Lancet 1385;2:11061107
3. Cowan JMA, Dick JPR, Day BL, et al. Abnormalities in central
motor conduction pathways in multiple sclerosis. Lancet
1984;2:304-307
4. Zvfills KR, Murray NMF. Corticospinal tract conduction time in
multiple sclerosis. Ann Neurol 1985;18:601-605
5. Snooks SJ, Swash M. Motor conducrion velocity in the human
spinal cord: slowed conduction in multiple sclerosis and radiation myelopathy. J Neurol Neurosurg Psychatry 1985;48:
1135-1139
6.Thompson PD, Day BL, Rothwell JC, er al. The interpretation
of electromyographc responses to electrical stimulation of the
motor cortex in diseases of the upper motor neurone. J Neurol
Sci 1987;80:91-110
7. Barker AT, Freeston IL, Jalinous R, Jarrat JA. Magnetic stimulation of the human brain and peripheral nervous system: an
introduction and the results of an initial clinical evaluation.
Neurosurgery 1987;ZO:100-109
a. Hess CW, Mills KR, Murray NMF, Schriefer T N . Magnetic
brain stimulation: central motor conduction studies in multiple
sclerosis. Ann Neurol 198?;22:744-752
9. Ingram DA, Thompson AJ, Swash M. Central motor conduction in multiple sclerosis: evaluation of abnormdties revealed
by transcutaneous magnetic stimulation of the brain. J Neurol
Neurosurg Psychiatry 1988;51:487-494
10. Berardclli A, Inghilleri, Cruccu G, et al. Stimulation of motor
tracts in multiple scierosis. J Neurol Neurosurg Psychiatry
1988;51:677-683
11. McAlpine D. Course and prognosis. In: McAlpine D, Lumsden
CE, Acheson DA, eds. Multiple sclerosis: a reappraisal. Edinburgh: Churchill Livingstone, 1972202
12. Poser CM, Paty DW, Scheinberg L, et al. New diagnostic criteria for multiple sclerosis: guidelines for research protocols. Ann
Neurol 1983;13:227-231
13. Costa LD, Vaughan HG, Levita E, Farber N. “Purdue” pegboard test as a predictor of the presence and laterality of cerebral lesions. J Consult Clin Psycho1 1963;27:133-137
14. Day BL, Rothwell JC, Thompson PD, et al. Motor cortex stimulation in intact man. 11. Multiple descending volleys. Brain
1987;110:1191-1209
van der Kamp et
al: Phasic Muscle Strength
in Multiple Sclerosis
11
15. Rothwell JC, Thompson PD, D a y BL, et al. Motor cortex stimulation in intact man 1. General Characteristics of EMG responses in different muscles. Brain 1987;110:1173-1190
16. Lawrence DG, Kuypers HGJM. The functional organisation of
the nervous system in the monkey. I. The effects of bilateral
pyramidal lesions. Brain 1968;91:1-14
17. Hepp-Reymond MC, Wiesendanger M. Unilateral pyramidotomy in monkeys: effect on force and speed of a conditioned
precision grip. Exp Brain Res 1972;36:117-131
18. Hepp-Reymond MC, Trouche E, Wiesendanger M. Effects of
unilateral and bilateral pyramidotomy on a conditioned rapid
precision grip in monkeys (Macaca fascicularis). Exp Brain Res
1974;211519-52 7
12 Annals of Neurology Vol 29 No 1 January 1991
19. Lemon RN, htantel GWH, Muir RB. Corticospinal facilitation
of hand muscles. J Physiol (Lond) 1986;381:497-527
20. Evarts EV. Relation of pyramidal tract activity to force exerted
during voluntary movement. J Neurophysiol 1968;31:14-27
21. Cheney PD, Fetz EE. Functional classes of primate corticomotoneuronal cells and their relation to active force. J Neurophysiol
1980;44:773-791
22. McDonald WI, Sears TA. The effect of experimental demyelination on conduction in the central nervous system. Brain
1970;93:583-598
23. Kaji R, Suzumura A, Sumuer AJ. Physiologicalconsequences of
antiserum mediated experimental demyelination in CNS. Brain
1986;111:67 5-694
Документ
Категория
Без категории
Просмотров
1
Размер файла
623 Кб
Теги
correlation, muscle, times, strength, corticomotoneuron, sclerosis, multiple, phasic, conducting
1/--страниц
Пожаловаться на содержимое документа