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Motor Areas Pyramidal System
Figure 13.11
3
organization of motor subsystems
Introduction
• Basal ganglia motor
related signals to the
motor cortex are
inhibitory
• Cerebellar motor related
signals to the motor
cortex are excitatory
• Balance of these systems
allows for smooth,
coordinated movement
Motor system includes
• Tracts
eg. Corticospinal (pyramidal)
(Skillful voluntary movement)
Corticobulbar and Bulbospinal (Extrapyramidal)
• Basal Ganglia (regulator)
• Cerebellum (regulator)
Cerebral
Cortex
Cerebral
Cortex
CEREBRAL
CORTEX
BASAL GANGLIA
Corticospinal tracts
THALAMIUS
Corticobulbar tracts
BRAIN STEM
CEREBELLUM
Bulbospinal tracts
SENSORY INPUT
SPINAL CORD
FINAL COMMON PATH
Major Motor Pathways
1. Corticospinal (cortex to spinal cord)
a) Lateral – distal limb muscles (fine manipulations).
b) Ventral – trunk and upper leg muscles
(posture / locomotion).
2. Corticobulbar (cortex to pons, 5th, 7th, 10th and 12th cranial
nerves) – control of face and tongue muscles; upper face both
contralateral, lower face contralateral
3. Ventromedial (brain stem to spinal cord) – trunk and proximal
limb muscles (posture, sneezing, breathing, muscle tone)
4. Rubrospinal (red nucleus to spinal cord) – modulation of
motor movement (limb movement independent of trunk
movement)
Components of motor neurons
•
Upper motor neuron (corticospinal &
corticobulbar).
Starts from motor cortex and ends in
1. Cranial nerve nucleus (corticobulbar).
2. Anterior horn of spinal cord in opposite
side(corticospinal tracts).
•
Lower Motor Neuron
Starts from anterior horn of spinal cord and ends in
appropriate muscle of the same side.
eg. All peripheral motor nerves.
MOTOR TRACTS & LOWER MOTOR NEURON
MOTOR CORTEX
MIDBRAIN &
RED NUCLEUS
(Rubrospinal Tract)
UPPER MOTOR NEURON
(Corticospinal Tracts)
VESTIBULAR NUCLEI
(Vestibulospinal Tract)
PONS & MEDULLA
RETICULAR FORMATION
(Reticulospinal Tracts)
LOWER (ALPHA) MOTOR NEURON
THE FINAL COMMON PATHWAY
SKELETAL
MUSCLE
Somatic Motor System
Interactions of the sensory and
motor systems enable voluntary
movement.
Steps in Motor Action
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Levels of motor control
• Cerebral cortex
• Brain stem
• Spinal cord and cranial motor nuclei
Cortical Motor Areas
Includes
1.
Primary Motor Cortex (M-I)
2.
Supplementary Motor Area (M-II)
3.
Premotor Cortex (PMC)
4.
Frontal Eye Field Area
5.
Broca’s Area for speech
Motor cortex
• Primary motor cortex ( M1)
• Premotor area (PMA)
• Supplementary motor area (SMA)
Note: All the three projects directly to the spinal
cord via corticospinal tract.
• Premotor and supplementary motor cortex also
project to primary motor cortex and is involved
in coordinating & planning complex sequences
of movement (motor learning).
Primary Motor Cortex (M-I)
Location :Immediately anterior to the central sulcus and extends
to the medial surface of hemisphere also known as
Broadmann’s area 4.
Description:
Body is represented as up side down and stretched on
the medial surface where pelvic and leg muscles are
represented. Hand and mouth has a greater area of
representation and is large because of frequently used
(skill).

Body map: human body spatially represented
• Where on cortex; upside down
Primary Motor Cortex (M-I)
controls the musculature of the opposite side of the body.
Face area is bilaterally represented.
Functions:Is used in execution of skilled movements and the direction,
force and velocity of movements.
Lesions:Ability to control fine movements is lost.
Ablation of M-I alone cause hypotonia not spasticity.
Supplementary Motor Area (M-II)
Location:
Found in lateral and medial aspect of the
Frontal lobe.
Function:
It works together with premotor cortex.
Involved in programming of motor sequences.
Lesions:
Reduces ability in performing complex activity.
Premotor Cortex (PMC)
Location:
Broadmann’s area 6. It lies immediately anterior to
primary motor cortex. It is more extensive than primary
motor cortex (about 6 times)
Functions:
It works with the help of basal ganglia, thalamus,
primary motor cortex, posterior parietal cortex. It plays
role in planning and anticipation of a specific motor
act.
Lesion:
Its lesion do not cause paralysis but only
Slowing of the complex limb movement.
Lesion may result in loss of short-term or
Working memory.
White matter of the spinal cord




Ascending pathways:
Sensory information by multi-neuron chains from
body up to more rostral regions of CNS
• Dorsal column
• Spinothalamic tracts
• Spinocerebellar tracts
Descending pathways:
Motor instructions from brain to more caudal
regions of the CNS.
• Pyramidal (corticospinal) most important to
know.
• All others (“extrapyramidal”).
Functions of pyramidal tract
Controls primarily distal muscles which are finely
controlling the skilled movements of thumb & fingers
on the opposite side.
eg. Painting, writing, picking up of a small object etc.
Effect of lesion: loss of distal motor function in opposite
side.
Pure corticospinal tract lesion cause hypotonia instead
of spasticity.
The reason is that pure pyramidal tract lesion is
very rare, and spasticity is due to loss of inhibitory
control of extrapyramidal tract.
Some Descending Pathways
Synapse with ventral
(anterior) horn interneurons
Pyramidal tracts:
Lateral corticospinal – cross in
pyramids of medulla; voluntary motor
to limb muscles
Ventral (anterior) corticospinal – cross
at spinal cord; voluntary to axial
muscles (Trunk and upper leg
muscles).
“Extrapyramidal” tracts: one
example
Somatic Motor Clinical signs
Position sense test
Clonus
Babinski sign
Enhanced deep tendon responses
Spasticity
Clasp knife response
Position sense
With the client’s eyes closed, the clinician manipulates the client’s
right thumb. He is asked to point his left thumb in the same direction
as his right thumb. The clinician switches sides and he is no longer
able to perform the task.
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Clonus
A series of fast, involuntary contractions
symptomatic of damage to upper motor neurons.
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Babinski reflex
An extension of the great toe, sometimes with fanning of the
other toes, in response to stroking of the sole of the foot. It is a
normal reflex in infants, but it is usually associated with a
disturbance of the pyramidal tract in children and adults.
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Enhanced Deep Tendon Reflexes
An unusually vigorous patellar tendon reflex may be observed
following upper motor neuron damage, often in conjunction with
heightened muscle tone (spasticity) and clonus.
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-Spasticity (hypertonia) is a feature of altered muscle
performance,occurring in disorders of the central nervous
system which give rise to the Upper Motor Neuron Syndrome
(UMNS ).
- It can be defined as increased resistance to
passive stretch.
-Patients complain of stiffness & inability to relax
-Muscles become permanently "tight" or spastic.
When there is a loss of descending inhibition from the brain to
BRAIN STEM EXCITATORY CENTERS,vestibulospinal &reticulospinal
EXCITATORY signals cause muscles to become overactive, & spastic .
- The condition can interfere with walking, movement, or speech.
Spasticity
The man exhibits spasticity of the right side, while the woman
exhibits spasticity of the left side.
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Clasp knife response
Initially there is great resistance to extension of the joint, followed by a
gradual “melting” of the resistance as continued, steady pressure is
applied.
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Features of upper motor neurone disease
1) Paralysis affect movement rather than muscles.
2) No remarkable muscle wasting, but disuse atrophy
3) Spasticity ( hypertonia ) , frequently called
“ clasp-knife spasticity ”
4) Clonus Repetitive jerky motions (clonus), especially
when limb moved & stretched suddenly
5) exaggerated tendon jerks
6) Extensor plantar reflex = Babinski sign ( dorsiflexion
of the big toe and fanning out of the other toes )
7) Absent abdominal reflexes
Features of lower motor neurone disease
1) Weakness and decreased muscle tone (Flaccid
paralysis)
2) Remarkable muscle wasting.
3) Absent tendon jerks.
4) Negative extensor plantar reflex (Babinski sign).
5) Present abdominal reflexes.