Download Pyramidal (Voluntary Motor) System

Pyramidal
(Voluntary Motor)
System
Dr. G. R. Leichnetz
In general terms, it takes a chain of two neurons from the motor
cortex to a voluntary skeletal muscle on the opposite side of the
body:
Upper Motor Neuron and Lower Motor Neuron
UPPER MOTOR NEURONCorticospinal tract
LOWER MOTOR NEURONAlpha motor neuron in ventral
horn of spinal cord through
peripheral nerve to the muscle
BASIC PATTERN OF
THE VOLUNTARY
MOTOR SYSTEM
The primary motor
(M1) cortex is located
in the precentral gyrus,
which extends onto the
medial aspect of the
hemisphere into the
rostral part of the
paracentral lobule (leg
representation).
Lower
extremity
Upper extremity
Origin of
Corticospinal
Tract (body)
Paracentral
lobule
Head
Origin of
Corticobulbar
Tract (head)
Motor Homunculus
Precentral
Gyrus
A representation of
the body’s
musculature is
somatotopicallyorganized on the
precentral gyrus
and paracentral
lobule, known as the
motor homunculus.
The corticospinal tract
originates from the
dorsolateral precentral
gyrus (arm/hand
region) and rostral
paracentral lobule (leg).
The corticobulbar tract
originates from the
ventrolateral precentral
gyrus (head).
Voluntary movements are initiated in the primary motor
(M1) cortex. Planning/programming of movements occurs
in the “ premotor” supplementary motor (M2) cortex,
which then projects to the M1 cortex for execution of
movement.
M2
Kandel
M1
Corticospinal Tract
Giant pyramidal neurons (Betz
cells) in lamina V of the primary
motor cortex are the cells of origin
of the pyramidal (corticospinal)
tract. Their long axons terminate in
the contralateral spinal cord.
Motor cortex,
layer V
Crus cerebri,
midbrain
Basilar pons
Medullary
pyramid
Pyramidal decussation
Lateral
corticospinal
tract
Anterior
corticospinal
tract
The corticospinal
(pyramidal) tract axons
(upper motor neurons)
originate in lamina V of
the motor cortex and
descend thru the internal
capsule and brainstem
(crus cerebri, basilar pons,
medullary pyramid) to the
caudal medulla where 90%
or more cross in the
pyramidal decussation to
the opposite side of the
spinal cord (then called the
lateral corticospinal tract).
A few corticospinals remain on
the same side (ant. corticospinal
tract) but cross at the level of
termination.
Most corticospinal fibers terminate on “interneurons” in
lamina VII of the intermediate zone of the contralateral
spinal cord. Only about 10% actually terminate directly on
large motor neurons of lamina IX of the anterior horn.
+
Modified from: House, Pansky & Siegel
Excitatory corticospinal fibers
drive inhibitory interneurons;
hence, if the tract is cut, it
produces spasticity.
Corticospinal fibers terminate primarily
in lateral part of the intermediate zone
and ventral horn on motor neurons
concerned with control over distal muscles
of the upper & lower extremities for
independent fractionated movements.
The lateral corticospinal tract is somatotopically-organized
and is the largest tract in the dorsolateral quadrant of the
lateral funiculus, with sacral most lateral and cervical
most medial.
Lateral corticospinal tract
C
Kahn et al, Correlative Neurosurgery
Corticobulbar Tract
The corticobulbar tract projects to cranial nerve motor
nuclei in the brainstem that innervate voluntary muscle in
the head (GSE, derived from somites, and SVE, derived
from visceral arch mesoderm, branchiomeric)
Corticobulbars
Cranial nerve
motor nuclei
(GSE, SVE)
Motor Nuclei of the Brainstem:
III, IV, VI, and XII are GSE.
V, VII, nuc. ambiguus are SVE.
The corticobulbar tract originates from lamina V large
pyramidal neurons in the head region of the motor
cortex (ventrolateral precentral gyrus), and descends
into the brainstem, projecting bilaterally (ie. crossed and
uncrossed) to all cranial nerve motor nuclei.
Cranial nerve
motor nuclei
(GSE, SVE)
Like corticospinals, while
some go directly to lower
motor neurons within the
motor nuclei, most
corticobulbars terminate
on interneurons in the
reticular formation near
cranial nerve motor nuclei.
Since corticobulbars project bilaterally to cranial nerve
motor nuclei, how does the clinician diagnose a
unilateral corticobulbar tract lesion?
since there would be no profound paralysis in head
muscles because the other side (intact contralateral
corticobulbar tract) would still innervate the nucleus.
Diagnosis of a corticobulbar tract lesion is facilitated by
the unique corticobulbar innervation of the facial
nucleus.
The facial nucleus in the pontine tegmentum receives a
unique corticobulbar innervation.
Facial
nucleus
Haines
The lower half of the facial nucleus (innervating the lower face)
only receives crossed corticobulbar innervation, so a lesion of the
corticobulbar tract results in a contralateral paralysis of the
lower face.
Corticobulbar
tract lesion
The upper half of the facial nucleus
innervates the muscles of the upper face;
lower half to muscles of the lower face
The hypoglossal nucleus in the caudal medulla also receives a
predominantly crossed corticobulbar innervation, so that a lesion of
the corticobulbar tract may also result in a contralateral paralysis of
the tongue (tongue deviated toward the opposite side).
Haines
Corticobulbar
tract lesion
Hypoglossal
nerve lesion
Corticobulbar
innervation of the
hypoglossal nucleus
is primarily crossed.
Corticobulbar tract
lesion (UMN lesion)
leads to
contralateral
paralysis of tongue;
tongue deviated
contralaterally.
Hypoglossal nucleus
or XIIth nerve
lesion (LMN lesion)
leads to ipsilateral
paralysis of tongue;
tongue deviated
ipsilaterally.
Tongue deviates toward
the paralyzed side
Control of Voluntary Eye Movement
Head
Voluntary rapid eye movements (“saccades”)
are initiated in the frontal eye field
Corticobulbar fibers
related to the control of
voluntary eye movement
are not located in the head
area of the precentral
gyrus, but originate in the
frontal eye field (FEF) in
the caudal part of the
middle frontal gyrus.
They project to
interneurons in
pre-oculomotor centers in
the brainstem reticular
formation near the
brainstem extraocular
motor nuclei (III, IV, VI).
Mid-Sagittal Brainstem Section Showing the Preoculomotor
Centers for Vertical and Horizontal Saccades
Vertical Eye
Movements
(riMLF, INC)
Trochlear
nucleus
Abducens
nucleus
Midbrain
Reticular
Formation
Oculomotor
nucleus
Horizontal Eye
Movements (PPRF)
Pontine
Reticular
Formation
Corticobulbars from the FEF
project to pre-oculomotor centers
in brainstem reticular formation
near extraocular motor nuclei.
Clinical Applications
Contrasting Upper Motor Neuron vs. Lower
Motor Neuron Lesions
Upper Motor Neuron: lesions of the pyramidal tract
(corticospinal) results in spasticity, hyperreflexia,
hypertonia, and positive Babinski sign
Lower Motor Neuron: lesions of cell bodies of motor
neurons (in cranial nerve motor nuclei or ventral
horn of spinal cord) or their axons in nerves to the
muscle (“final common pathway”) results in
flaccidity, hyporeflexia, hypotonia, with atrophy
Siegel and Sapru, Essential Neuroscience
In an adult, a positive Babinski sign
(plantar reflex) indicates a lesion of
the pyramidal (corticospinal) tract.
Hoffman Sign- also known
as the “finger flexor reflex”
Considered the upper limb
equivalent of the Babinski’s
sign, because, like the
Babinski, it indicates upper
motor neuron dysfunction
(verifies presence or absence
of problems in the
corticospinal tract)
Tapping the nail or flicking
the terminal phalanx of the
third or fourth finger. A
positive response is seen
with flexion/adduction of the
terminal phalanx of the
thumb.
Occlusion of branches of the middle cerebral artery to the lateral
aspect of the brain produces a vascular lesion in the precentral gyrus
and Broca’s motor speech area.
Lesion of the corticobulbar tract may
result in contralateral paralysis of the
tongue (tongue deviates to opposite
side).
Arm
Contralateral
monoplegia of
the upper
extremity
Head
Broca’s
area
Lesion of the corticobulbar tract
results in contralateral paralysis
of the lower face.
House, Pansky & Siegel
Expressive aphasia (Broca’s)
Occlusion of branches of the middle cerebral artery to the genu and
posterior limb of the internal capsule, affecting corticobulbar &
corticospinal tracts, results in a capsular hemiplegia.
Lesion of the corticobulbar tract
(genu) results in contralateral
paralysis of the tongue.
Lesion of corticospinal tract (post.
limb) results in contralateral
hemiplegia.
Lesion of the corticobulbar tract
(genu) results in a contralateral
paralysis of the lower face.
House, Pansky & Siegel
Weber’s Syndrome: Alternating Oculomotor Hemiplegia
(“alternating”= ipsilateral cranial nerve deficit, contralateral hemiplegia)
Occlusion of branches of the post. cerebral artery to the crus cerebri
(lesion of corticospinal and corticobulbar tracts) and oculomotor
(IIIrd) nerve.
Ipsilateral:
Exotropia
Ptosis
Pupillary dilation
(mydriasis)
Contralateral:
Hemiplegia
CS
CB
House, Pansky & Siegel
Alternating Abducent Hemiplegia
Occlusion of branches of the basilar artery to the basilar pons,
produces lesion of the pyramidal tract and abducens (VIth) nerve.
Corticospinal tract lesion:
contralateral hemiplegia
Abducens nerve (VI) lesion:
ipsilateral paralysis of lateral
rectus
“esotropia”- internal deviation
of the eye
House, Pansky & Siegel
Alternating Hypoglossal Hemiplegia
Occlusion of branches of the anterior spinal artery to the
ventromedial medulla, produces lesion of the pyramidal tract,
hypoglossal (XIIth) nerve, and medial lemniscus.
Corticospinal tract lesion:
contralateral hemiplegia
House, Pansky & Siegel
Hypoglossal nerve (XII) lesion:
ipsilateral paralysis of tongue
Amyotrophic Lateral
Sclerosis (ALS)
(Lou Gehrig’s Disease)
Affects both upper and
lower motor neurons
Demyelinization (sclerosis) of
the lateral corticospinal tract.
Twitches (fasciculations),
uncontrolled small discharges,
and atrophy occur in muscle
groups as motor neurons in the
brainstem and spinal cord
degenerate. Slurred speech,
difficulty swallowing.
No sensory impairment.
No cognitive or memory
impairment.
Brown-Sequard Syndrome
(Spinal Cord Hemisection)
Produces
ipsilateral spastic
paralysis (lateral
corticospinal tract
lesion) with
ipsilateral loss of
conscious
proprioception
(dorsal column
lesion), and
FG
CST
LSTT
contralateral loss
of pain and temp.
(lateral
spinothalamic tract
lesion)
Poliomyelitis
The virus attacks motor
neurons of the ventral
horn of the spinal cord.
Death of spinal cord
motor neurons produces
a lower motor neuron
lesion, resulting in
flaccid paralysis of the
extremities, with
hypotonia, hyporeflexia,
and atrophy.