views heviews
The pyramidal tract
Robert A. Davidoff, MD
Many neurologists have been taught that the pyramidal
tract (PT) is the major, if not the only, neuronal system
that mediates voluntary movements. According to the
traditional concept, the PT originates from the pre-
central motor cortex, consists of rapidly conducting
myelinated fibers that make contact with spinal
motoneurons, and is concerned with voluntary skilled
movements.’-3Implicit in this formulation is the notion
that the PT provides the pathway for the highest level
of central nervous system control over voluntary motor
functions. Furthermore, classic neurologic dicta stipu-
late that a PT lesion invariably produces the “pyram-
idal tract syndrome”-hyperreflexia and spasticity,
Babinski sign, and paralysis of voluntary movements.
However, because much novel information is available
concerning PT f u n c t i ~ n , ~many
- l ~ of these “classic”
concepts have been modified. This survey presents and
evaluates contemporary evidence regarding the form
and function of the PT.
What is the PT? Strictly speaking, it consists of
those descending fibers that originate in the cerebral
cortex and extend longitudinally through the bulbar
pyramid. The PT does not consist of a homogeneous
population of neurons. Although it was once thought
that all fibers constituting the tract extended from the
cerebral cortex to the spinal cord, it is now known
that only about of PT fibers, those constituting the
corticospinal tract itself, actually terminate in the spi-
nal cord.4 Many PT axons terminate in, or send collat-
eral branches to, a number of supraspinal structures
(eg, striatum, sensory and motor nuclei of the
thalamus, red nucleus, pontine nuclei, midbrain and
bulbar reticular formation, inferior olive, dorsal col-
umn nuclei, trigeminal n ~ c l e i ) . ~Some
Jl of these su-
praspinal cell groups (eg, red nucleus, reticular forma-
tion) in turn project to the spinal cord. Despite the
commonly held concept that the PT is the largest
motor pathway in the brain, many PT fibers termi-
nate in structures that are generally considered sen-
sory in function (eg, thalamus, dorsal column nuclei,
trigeminal nuclei). One must conclude that the PT
consists of several subsystems with various fiber
types and with different cortical origins, termina-
tions, and functions.
~ ~~
From the Departmentof Neurology, University of Miami School of Medicine, and the NeurophysiologyLaboratory, Veterans AdministrationMedical Center,Miami,
FL.
Supported in part by USPHS grant NS 17577 and Veterans Administration Medical Center Funds (MRIS 1769).
Portions of this material appeared in Neurology and Neurosurgery Update Series, 1979;Z:lesson9; Reprinted with permission of the ContinuingEducation Center,
Princeton, NJ.
Received June 29,1989. Accepted for publication in final form July 28,1989.
Address correspondence and reprint requests to Dr. Robert A. Davidoff, Department of Neurology (D4-5), PO Box 016960,University of Miami School of Medicine,
Miami, FL 33101.
332 NEUROLOGY 40 February 1990
NEUROLOGY 1990;40:332-339
Origin of the pyramidal tract. There is a curious
desire by clinical neurologists to retain the misconcep-
tion that the PT originates exclusively from the Betz
cells of the “classic” motor strip (Brodmann’s area 4,
primary motor cortex; MI),12 although it has been
known for many years that the gigantopyramidal cells
of Betz account for only about 3 to 4% of the total
number of fibers in the PT.I3A variety of experimental
techniques has been used to determine the cortical re-
gions that give rise to the PT in the m ~ n k e y . lThese
~-~~
studies indicate that the MI and the rostrally adjoining
premotor and supplementary motor areas (Brodmann’s
area 6) give rise to about 60% of the PT fibers. The
remaining fibers arise mainly from the postcentral
gyrus and parietal cortex (areas 3,1,2,5, and 7). Because
of obvious experimental constraints, the origin of the
PT cannot be determined with any degree of precision
in humans. The present consensus, however, is that
there is a more constricted origin of the PT in humans
than in and that approximately 60% of PT
axons arise from area 4.28The remainder come from
area 629and from the parietal lobe.14
Other corticofugal systems arise from these same
cortical areas and descend with PT fibers through the
corona radiata and internal capsule to reach subcortical
structures that include the striatum, thalamus, hypo-
thalamus, red nucleus, midbrain tegmentum, and pon-
tine nuclei. From some of the locations (eg,rednucleus),
axons descend to the spinal cord to terminate in the
same regions as PT axons.
According to the classic view, MI contains a strict
somatotopic representation of body parts, and a given
point on the cortical surface projects to a specific
motoneuron nucleus in the spinal cord. This view has
been derived from the results of experiments in which
electrical stimulation of the surface of the precentral
gyms was used to evoke contractions of localized groups
of muscles of the opposite extremities, trunk, and
The results of such studies have been sum-
marized by depicting the contralateral body parts on
the surface of the motor strip as a distorted map-a so-
called h o m u n c u l u ~ . ~ ~
Recent investigations, using the technique of micro-
stimulation of both the cortical surface and the depth of
MI, have demonstrated several major departures from
the classic view. There is now evidence supporting the
notion of multiple representations of different body
parts in M1.33.34In other words, 2 or more vertical
aggregates or clusters of cortical neurons may project to
a single spinal motoneuron pool that controls an indi-
vidual m ~ s c l e . These
~ ~ - ~vertical
~ aggregates can be lo-
cated in separate positions in the motor strip, although
they are found in the same general area. A single aggre-
gate or cluster of cortical neurons projecting to
motoneurons innervating a single muscle was originally
thought to be concentrated in a small finite volume of
cortex with a columnar shape,3sbut it is now thought
that an aggregate for a given motoneuron may be large
(several mm in diameter), and commonly overlaps ag-
gregates projecting to motoneurons innervating syn-
e r gi s t i c a n d even a n t ago n i s t i c muscles .33,35
Furthermore, there is extensive linking of cortical
pyramidal cells by recurrent axon collaterals that
spread widely to synapse on other pyramidal cells and
on excitatory and inhibitory interneurons.
Individual cortico-motoneuronal fibers branch ex-
tensively in the spinal cord. Collaterals or branches of
such fibers can synapse on several spinal motoneuron
nuclei that may have different functions and that may
even be located at different spinal l e v e l ~ . ~Further-
~-~l
more, it appears that spinal motoneurons receive syn-
apses from more than 1corticospinal neuron.35~42.43
Each cortical aggregate consists of a variety of
pyramidal neurons ranging greatly in perikaryon size
and in axon diameter.25r44 Thus, the spectrum of diame-
ters of human PT axons in the medulla varies from
greater than 20 ym to less than one pm. Although about
60 to 95% are myelinated, 90% of the fibers are smaller
than 4 pm.45,46 These data indicate that most PT axons
conduct at a slow rate and would require several hun-
dred msec to conduct impulses from the cerebral cortex
to the lumbar enlargement. Only a very small minority
of PT neurons can conduct rapidly.
Course of the pyramidal tract. Most textbooks re-
iterate the conclusions reached by C h a r ~ o and t ~ ~De-
jerine48 that corticospinal fibers occupy the anterior
half of the posterior limb of the internal capsule. How-
ever, data from stereotaxic stimulation studies in hu-
m a n ~and ~ from
~ , case
~ ~ reports of patients with isolated
internal capsule i n f a r c t ~ ~arel r ~in
~ apparent conflict
with this notion, and indicate that both corticospinal
and corticobulbar fibers lie in a compact bundle in the
posterior part of the posterior limb. The controversy
about location probably arose because the PT does not
maintain a fixed position in the internal capsule. There
is a.shift from anterior to posterior in its rostrocaudal
course in the internal capsule.53
Presumably because the tract is phylogenetically re-
cent, the corticospinal portion of the PT is subject to
considerable individual variation in its anatomic orga-
n i z a t i ~ n . ~In* -general,
~~ however, between 75 and 90%
of corticospinal fibers cross the midline of the medulla,
and 3 separate corticospinal tracts are formed on each
side.55The largest is, of course, the crossed lateral corti-
cospinal tract that extends caudally in the dorsolateral
fasciculus to the last sacral ~ e g m e n t . ' The
~ . ~ ~fibers of
this tract terminate in the dorsal horn, the intermediate
zone, and the ventral horn of the spinal ~ord.8J8J9,~6,57
The anterior or ventral corticospinal tract consists of
fibers that do not cross in the medullary decussation. It
occupies an oval area in the spinal cord adjacent to the
anterior median fissure and extends caudally only to the
upper thoracic ~ o r d .The * ~ ~that form it decus-
~ ~fibers
sate at various levels of the cervical cord through the
anterior white commissure to terminate largely upon
contralateral motoneurons located in the medial por-
tion of the ventral horn. These motoneurons primarily
innervate the musculature of the neck, trunk, and prox-
imal upper extremities. There is also an uncrossed lat-
eral corticospinal tract58s59which varies in size from
individual to individual. It may consist of only a few
isolated fibers or it may be a compact, well-delineated
tract. The fibers composing it descend in the lateral
funiculus and are located ventrally to the lateral cortico-
spinal tract. Their function is not known.
Effects on the spinal cord. Corticospinal fibers end
in most parts of the gray matter of the spinal
~ ~ r d . Fibers
~ , ~from~ ,the~ sensory
~ , ~ cortex~ of the pari-
etal lobe tend to project to the more dorsal regions of the
cord and to terminate largely in the dorsal horn.24,26~57~61
Fibers from the precentral gyrus have a more extensive
termination in the intermediate zone between the dor-
sal and ventral horns and in the ventrolateral part of the
ventral horn?Jn~2e,60 While there is a preferential distri-
bution of fibers from motor and sensory cortical regions,
complete segregation does not exist. In primates, corti-
cospinal fibers end directly on alpha motoneurons that
supply extrafusal muscle fibers,21,24,27 on gamma
(fusimotor) motoneurons that supply the intrafusal fi-
bers of muscle s p i n d l e ~ , 6and
~ , ~ on~ various types of
interneurons and sensory relay cells. Generally, the
tightest and most direct links with alpha motoneurons
are formed by corticospinal neurons with large cell
bodies and rapidly conducting axons in the precentral
gyrus.37
Although stimulation of the cerebral cortex produces
monosynaptic excitatory postsynaptic potentials
(EPSPs) in many alpha motoneurons, this facilitatory
action is predominantly to the motoneurons supplying
the distal musculature of the l i m b ~ ~ ~inqfact, - ~ ~ some
;
motoneurons to proximal muscles receive no direct in-
nervation from PT fibers. Judging from the brief la-
tency of the synaptic action evoked by MI stimulation,
it appears that the largest PT fibers are the ones respon-
sible for these monosynaptic excitatory effects. There
are, however, only a very few large PT fibers; and there-
fore, although the corticospinal system can influence
alpha motoneurons quickly, it does so relatively weakly.
The effects of the small PT axons on alpha moto-
neurons and on other spinal neurons are not well under-
stood.
Static and dynamic gamma motoneurons can be acti-
vated via the PT by the same cortical stimuli that
facilitate alpha m o t o n e ~ r o n s . 6In~general,
~ ~ ~ alpha and
gamma motoneurons supplying the same muscle are
activated t~gether~~-so-called coactivation. Coactiva-
February 1990 NEUROLOGY 40 333
tion of alpha and gamma motoneurons by the PT causes
contraction of both extrafusal and intrafusal muscle
fibers. Intrafusal muscle contraction optimizes the sen-
sitivity of the sensory endings of the muscle spindle so
that they remain sensitive to changes in muscle length
even under conditions of muscle shortening.
Much of the PT control over spinal output is medi-
ated via interneurons intercalated in reflex pathways
that in turn terminate on alpha and gamma moto-
neurons. In this way MI can influence complex patterns
of muscle contraction via the control of “hard-wired”
reflexes organized in the spinal cord. One set of inter-
neurons affected by PT volleys is located directly in
reflex pathways between primary afferent fibers from
muscle and skin and alpha m o t o n e u r o n ~Excitation
.~~
of such interneurons by volleys in PT fibers can result in
either facilitation or inhibition of specific segmental
spinal reflexes. A 2nd set of interneurons excited by the
PT is located in pathways that produce presynaptic
inhibition. Presynaptic inhibition activated by MI is
exerted mainly on the terminals of primary afferent
fibers from Golgi tendon organs, the secondary endings
of muscle spindles, and certain cutaneous receptors that
mediate touch and p r e s ~ u r e .This
~ ~ *type
~ ~ of inhibition
reduces the amount of excitation fed by the affected
afferent fibers into reflex pathways. The PT does not
act upon the afferents from primary endings of spindles
in this way.
PT fibers also affect spinal motor mechanisms by
indirect means. For example, collaterals of PT axons
make mono- and disynaptic connections with red nu-
cleus neuron~.~O*~~ Rubrospinal axons then act on the
spinal segment in a manner similar to that of PT fibers72
and, in general, the 2 systems facilitate the effects of
each other.
Another population of PT axons passes bilaterally to
the medial bulbar reticular formation. This site, in turn,
projects to the medial groups of motoneurons in the
ventral horn that innervate the muscles of the trunk
and proximal limbs. This bilateral pathway may be used
to mobilize the postural mechanisms needed to support
the manipulative activity of the distal musculature that
is more directly connected to the PT.
In summary, the effects exerted by PT axons on the
motor outflow of the spinal segment are complex. It is
obvious that the PT can directly influence the “final
commonpath” to muscle, particularly to the distal mus-
culature used for fine movements, but PT fibers can also
indirectly activate spinal mechanisms through other
descending systems, and the discharge of PT fibers can
interact with afferent information originating in pe-
ripheral sensory receptors of many types and with ac-
tivity in a variety of reflex arcs.
PT and movement. The classic concepts73that the
movement originates and commences in MI and that
the PT represents the highest level of motor control is
now thought to be i n ~ o r r e c t . ~ItJ ~is clear that the
transient PT neuron discharges preceding and accom-
panying muscle contraction and movement occur in
response either to self-initiated signals in regions of the
CNS other than MI (see below) or to external cues. The
334 NEUROLOGY 40 February lDO0
modulation of PT neuron firing is determined largely by
the 3 major types of information that MI receives and
processes: central motor programs, internal feedback,
and external sensory feedback.74
Many types of movement (eg, reaching to grasp an
object) involve initial high velocity movements and
then final adjustments made on the basis of feedba~k.’~
In this type of movement, the initial phase of PT neu-
ron discharge and the ensuing muscle contractions are
based on centrally programmed “open loop” control
without reflex influences or sensory f e e d b a ~ k .Open
~~.~~
loop control is particularly important when the move-
ment is large; it confers the advantage of speed of ad-
justment. In addition, feedback would not function ef-
fectively during a rapid, large movement. External
proprioceptive and cutaneous feedback (“closed loop”
control) from peripheral sensory receptors is used to
correct small errors during the later more precise and
slower phases of the movement. In contrast, peripheral
feedback may control much of the PT output at the
initiation of small, low velocity movements.
Centrally programmed movement. The intended
(centrally programmed, open loop) components of PT
neuron firing are directed in large part by the storage
and distribution of information through multiple CNS
region^.^^!^^ The result is the generation of appropriate
patterns of activity in precentral neurons. The path-
ways that give rise to the PT discharges underlying
centrally programmed movements include corticocor-
tical inputs from premotor and supplementary motor
areas80*81(which acquire corticocortical projections
from the prefrontal and posterior parietal association
cortex and cerebellar and basal ganglia projections re-
layed via the thalamuss2qe3)and thalamocortical inputs
from the lateral cerebellum (which receives projections
from large areas of the cerebral cortex, including associ-
ation cortex).84.85
Internal feedback. Collaterals of PT neurons con-
stantly inform the cerebellum and other subcortical
structures about control signals descending to the spi-
nal cord to initiate movement. In turn, internal feed-
back information is continuously fed back to MI and
furnishes MI with a provisional estimate of the position
and movement of a limb before real sensory information
from the periphery is available and even before the
movement itself has actually occurred. This mechanism
allows the rapid correction of errors without waiting for
external feedback from peripheral sensory receptors on
how the movement is progre~sing.~~
External sensory feedback. PT neurons in MI (par-
ticularly those synapsing on motoneurons innervating
distal limb muscles) receive a powerful topographically
organized afferent input from sensory receptors in the
periphery.86-88This input is similar to that arriving at
the sensory cortexegand is quite effective in altering PT
activity. Although controversial, it is believed that the
peripheral input to MI is funneled 2 ways: the 1st is a
path that involves a direct input to MI from the
thalamus (from nucleus ventralis posterior lateralis
pars oralis, VPL,)90-92;the 2nd involves corticocortical
inputs from the somatosensory c o r t e ~ . 9It ~ -appears
~~
that the dorsal columns play the major role in transfer-
ring peripheral inputs to MI via both pathways.96
PT neurons are particularly influenced by joint
movement, but some are excited by activation of muscle
spindles, and a smaller number respond to cutaneous
inputs from small, fixed, restricted zones located in the
contralateral periphery.86-88 The majority of precentral
cells that project to the motoneurons innervating a
particular muscle receive their input from sensory re-
ceptors in joints and muscles that would be excited by
the contractions of that muscle (ie, the afferent input
zone and the motor output region approximately coin-
~ i d e ) .In~addition,
~ , ~ ~ they receive input from skin areas
most likely to be stimulated by contacts produced by
movement of the r n u ~ c l eThis
. ~ ~is~particularly
~~ true of
neurons concerned with the control of finger move-
ments that may receive a large source of their input
from cutaneous receptors located in the skin of the
digits.92It thus appears that afferent inputs to MI pro-
vide feedback information associated with the con-
traction of a particular muscle or a synergistic group of
muscles.
The feedback coupling of peripheral afferent input to
MI efferent output via the PT could function in several
interrelated ways:
1. Such coupling could provide the substrate for
transcortical long-loop stretch reflexes activated by
limb displacement and muscle stretch.42J00J01 It is hy-
pothesized that these reflexes play an important role in
adjusting motor cortex neuronal output and in regulat-
ing skilled voluntary movement automatically and con-
tinuously by compensating for sudden unexpected load
changes that would interfere with the m ~ v e m e n t In .~
other words, after a movement is initiated and in pro-
gress, the rate of PT neuron discharge is determined, in
part, by afferent inputs from the periphery signaling
mismatches between the actual and intended limb posi-
. ~ ~a change in PT firing would reestablish the
t i ~ nSuch
trajectory of a movement against external perturba-
tions. Since there is a lag involved in such circuits and a
reduction of sensory input during rapid movements, it
is unlikely that such transcortical reflexes play a role in
very rapid ballistic movements, but they appear very
important in slower, precisely controlled, small move-
ments and in postural s t a b i l i ~ a t i o n . ~ ~ J ~ ~
2. Input-output coupling may be employed during
active tactile exploration of extrapersonal space by the
hand-a situation where movement itself is an impor-
tant generator of afferent feedba~k.9~JO~ In this regard,
lesions of the dorsal columns impair digital control and
precise coordination of wrist and f i n g e r ~ . ' ~ ~ J ~ ~
3. 'Such coupling may provide a basis for initiating
both grasp reflexes and contactual orienting reflexes
such as the tactile placing r e ~ p o n s e . ~ ~ J ~ ~
Neuron discharges associated with movement. It
is possible to record the action potentials of individual
PT neurons in conscious monkeys able to move their
forelimbs freely. When combined with recordings of
EMG activity in various muscles and with observations
of the behavior of the animals, this advance has made it
possible to analyze, in functional terms, the efferent
signals transmitted from MI to the spinal cord. Some of
the investigations have demonstrated the following
points:
1. Most PT neurons are spontaneously active during
rest. Before movement occurs, many PT neurons in the
precentral gyrus change their firing rate.102J06In fact,
PT cells can discharge during the time when the animal
is "getting set" to move a limb. The occurrence of PT
activity prior to movement indicates that this PT dis-
charge cannot be determined solely by sensory feedback
from the periphery.
2. When the animal moves its arm, the activity of the
contralateral PT units changes.lo7Most of the neurons
show their full range of firing frequency during small
movements and show more modulation in their dis-
charge pattern when the monkey makes small precise
independent finger movements than when it makes
coarse, powerful movements.lo8
3. Many PT neurons that project directly to alpha
motoneurons show a clear relationship between dis-
charge rate and the amount of muscular activity respon-
sible for exerting the force generated during a given
- ~ ~ ~ number of PT cells show
m ~ v e m e n t . ' ~A~smaller
changes in discharge frequency related to the positional
aspects of movement.10g
4. The activity of most PT neurons is related to a
particular pattern of muscular c o n t r a ~ t i o n ' ~ ~ J ~ ~ J ~
rather than to the amount of joint displacement or to
the position of the joint. In addition, PT neurons do not
appear to control each muscle separately since the firing
rate of most PT neurons can be correlated with the
activity of several muscles.l12 It appears that the infor-
mation conveyed from MI to the spinal cord by PT
fibers concerns contraction of specific related muscles
rather than the final position of the limb at the end of a
movement.
On the basis of the above information concerning PT
activity, muscular contraction, and limb movement, it
is easy to conceive of the PT output as a command
signal from MI specifying which groups of muscles
should contract to produce a particular movement and
the force that should be developed in those muscles to
achieve the movement. It also appears that MI neurons
are specialized for the control of fine accurate move-
ments. However, conclusions regarding PT activity
must be limited by the fact that almost all observations
made on identified PT neurons involve cells with
rapidly conducting axons. We have little information
on the discharges of the vast majority of PT elements
contributing slowly conducting axons to the PT.
Cortical effects on sensory transmission. From
the anatomic evidence already outlined, it is apparent
that the PT also serves functions other than motor.
And, indeed, recent physiologic studies indicate that
the PT contains many fibers of cortical origin that
affect sensory input and somatosensory transmission at
each synaptic relay at both spinal and subcortical levels.
In the spinal cord, activity in fibers descending
mainly, but not exclusively, from the parietal lobe can
control the transmission of sensory information arriv-
February 1990 NEUROLOGY 40 336
ing from the periphery. PT volleys can presynaptically
inhibit the influx of certain types of afferent informa-
tion into the spinal cord. When this occurs, impulses
sent by sensory receptors into the nervous system are
inhibited bv PT fibers at the earliest possible locus-
before the impulses can excite sensory relay neurons.
The PT also exerts postsynaptic facilitatory and inhibi-
tory control over sensory relay cells located in the dorsal
horn115that are involved in the transmission of somes-
thetic and proprioceptive information to dorsal column
nuclei and the thalamus. Similar controls are exerted by
the PT on sensory relay neurons located at supraspinal
level^.^ For example,the PT decreases the output of the
dorsal column nuclei through the medial 1 e m n i ~ c u s “ ~ J ~PT~ section experiments:
and depresses the responsiveness of thalamic and cor-
tical neurons to natural ~ t i m u l i , ~before
~ J l ~ and during necessary for skill and precision in movement and for
high velocity voluntary limb movements, when there is
a greatly increased barrage of sensory information en-
tering the CNS. In contrast, there is enhancement of
MI neuronal responses to kinesthetic stimuli during
accurate positioning and controlled fine movement.77
It thus appears that the cortex, actingvia the PT, can
modify the amount and even type of sensory informa-
tion ascending to it. It is assumed that such corticofugal
mechanisms allow the brain to select its own input; it
can suppress unimportant or unwanted signals or it can
augment transmission of desired sensory data through a
given pathway. This is still a very novel idea, and its
relationship to the deficits produced by neurologic le-
sions involving the PT has yet to be determined.
Lesions of the pyramidal tract. It has been gener-
ally accepted that the pyramidal tract syndrome of clin-
ical neurology is characterized by a spastic hemiplegia
with impairment of skilled voluntary movements, in-
creased deep tendon reflexes and resistance to passive
manipulation of the limbs (“muscle tone”), and a
Babinski sign. However, surgical section of the PT in
the cerebral peduncle in humans is reported to produce
only a modest impairment of voluntary movements and
no s p a s t i ~ i t y . There
~ ~ ~ - are
~ ~ cases
~ of vascular brain-
stem lesions that involve the PT122-128; the result of such addition, the rubrospinal tracts are sectioned. Section
lesions has been a hypotonic hemiplegia which, after a
few weeks, changed into a spastic paresis with increased
reflexes and a Babinski sign. In all reported cases, how-
ever, the lesion extended beyond the bulbar pyramids.
When the PT is surgically sectioned in the medulla or
in the peduncle of experimental primates, surprisingly
little permanent disability is produced.129The common
conclusion of a variety of studies is that during the 1st
few months there is an impressive recovery of manual
ski11.129-131Although well-coordinated, strong move-
ments return, certain deficits in the function of the
upper extremity are apparent in monkeys during careful
testing. These include slowness of movement, easy
fatigability and, in particular, difficulty with indepen-
dent movements of the digits of the hand for skilled
discrete a c t i v i t i e ~ .Despite
~ ~ ~ - these
~ ~ ~ deficits, monkeys
with such lesions can be trained to perform difficult and
precise motor a ~ t s . In ~ other
~ ~ Jwords,
~ ~ there is some
limitation in voluntary movements, but this is only
modest in degree and can be compensated for. A con-
336 NEUROLOGY 40 February 1990
stant deficit followingpyramidotomy is a defect in con-
tactual orienting responses of the hand and placing
reactions of the foot.78J31J35 These latter responses are
reflex in origin.
In addition, most workers report an enduring hypo-
tonia of the affected limbs.24~78~128~’31~136-138This is mani-
fested by decreased resistance to passive manipulation
of the limbs. Myotatic reflexes, however, are usually
normal. The persistent decrease in the tone of the limbs
has been attributed to a depression of the afferent re-
sponse of the muscle spindle to stretch as a result of a
decreased fusimotor drive.139
Several conclusions can be drawn from the results of
1. An intact corticospinal component of the PT is
the production of independent and individual finger
movements.
2. An intact corticospinal tract is not needed to pro-
vide “voluntary” movements, but it is necessary for
speed and agility during these movements.
3. A lesion confined to the corticospinal component
of the PT does not produce an enduring paresis or
spasticity.
The deficits produced by pyramidotomy or pedun-
culotomy are not equivalent to those produced by cap-
sular hemiplegias in humans. Capsular hemiplegia
invariably results from a lesion that sections not only
PT axons, but also a variety of other corticofugal fibers
(eg, corticostriate, corticothalamic, corticopontine, and
others). Furthermore, experimental pyramidotomy in-
terrupts the PT only after descending axons have given
rise to many collateral branches. The proximal portions
of the neurons remain and are presumably functional.
Suprabulbar collaterals can feed information from MI
into descending pathways other than the corticospinal
t r a c t , a n d t h i s information can reach spinal
motoneurons via these pathways. The importance of
this latter point is emphasized by the fact that pyram-
idotomized monkeys, with very little loss of limb move-
ment, are unable to use their distal forelimbs if, in
of the rubrospinal tract in an otherwise intact monkey
produces little, if any neurologic deficit.140
In summary, capsular lesions and pyramidal section
are 2 very distinct and different pathologic processes
and the abnormalities in function produced by one can-
not be easily compared with the deficits produced by the
other because neither lesion gives rise to a “pure” dis-
ruption of the PT. Whether the term “pyramidal tract
syndrome” is a misnomer cannot be determined at pres-
ent since there is no method to preferentially destroy
PT neurons at their origin without producing lesions in
other corticofugal pathways as well.
Function of the pyramidal tract. Because the PT is
such a conspicuous structure and its gross appearance
so easily defined, one feels that it should be possible to
ascribe to it a unified function. It is clear, however, from
the wealth of new information concerning the micro-
physiology and anatomy of the PT reviewed above, that
the PT is a heterogeneous structure arising from func-
tionally dissimilar cortical areas and that it consists of
different types of fibers distributed to a variety of spinal
and supraspinal loci. A comprehensive statement about
its function cannot yet be made. However, some hy-
potheses concerning its role in CNS integration can be
formulated.
First, we can regard the PT as an internuncial path-
way intercalated between subcortical structures (eg,
basal ganglia, cerebellum), cortical areas (eg, premotor
cortex, association cortex), and afferent inputs from
peripheral sensory receptors and spinal motoneurons.
As such, it occupies a central position as the site of
convergence for several dispersed sets of neurons-a
summing point that could feed information by means of
direct and secure monosynaptic connections to the spi-
nal cord. This view would, of course, downgrade the PT
and MI from the position of structures initiating and
commanding movement to a lower level in the hierarchy
of the brain. In addition, spinal inputs are also relayed
from the motor cortex through red nucleus and other
subcortical structures that operate in parallel to the PT
inputs to the spinal cord.
Second, the classic notion that the corticospinal por-
tion of the PT is necessary for the production of voli-
tional movement is no longer tenable because it is
obvious that animals and humans can move quite well
following section of corticospinal fibers. On the other
hand, the idea that the corticospinal tract is particularly
important in the control of the fingers for discrete fine
movements appears to be correct. However, corticospi-
nal fibers alone may not be sufficient to produce these
fine movements; a number of indirect corticofugalpath-
ways must also function to produce voluntary move-
ment.
Third, the PT provides a pathway for corticofugal
regulation of various sensory relays. This control of
sensory inflow into central structures could influence
the type and amount of somesthetic and proprioceptive
information carried to the sensory receiving cortex and
to the association cortex. This type of control could be
important during those interactions between motor
output and afferent input that occur during active sen-
sory exploration of the environment. In this regard, it
appears that the PT forms the efferent limb of various
contactual orienting reflexes in which the hand actively
moves toward a touch stimulus to bring the stimulating
object into more intimate contact with itself.
Acknowledgment
I wish to thank Dr. Sid Gilman for critically reading an earlier draft of
this paper.
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 The pyramidal tract
Robert A. Davidoff, MD
Neurology 1990;40;332
DOI 10.1212/WNL.40.2.332

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