Transcript Central Control of Motor Function

VMED 5171/NS28/GMS
Central Control of
Motor Function
Student Preparation
Textbook of Medical Physiology
Guyton and Hall, Ch. 55, 56
Neuroscience
Bear et al., Ch. 14
Overview
• Cerebral (association) cortex - generates the
impulse to act, the design and the planning
of movement.
• Basal ganglia and thalamus - provide the
gross motor “programs.’
• Motor cortex, brain stem and spinal cord
interact to maintain posture and movement
execution.
• Cerebellum - maintains equilibrium and
smooth coordination of movement.
Descending Motor Control
• Higher centers are required for:
– initiation of voluntary movement
– regulation of the rate, forcefulness, and
smoothness of movement
• Descending tracts - control motor function
• Ascending tracts - sensory function for
planning and feedback.
Hierarchy of Motor Control
LEVEL
FUNCTION
STRUCTURES
high
strategy
association areas of
neocortex, basal ganglia
middle
tactics
motor cortex, cerebellum
low
execution
brain stem, spinal cord
Example of the Role of Central
Control of Motor Function
How Does the Brain
Communicate With the Motor
Neurons of the Spinal Cord?
Two Major Groups of
Descending Pathways
• Lateral pathways – involved in voluntary
movement of the distal musculature; under
direct cortical control.
• Ventromedial pathways – involved in the
control of posture and locomotion; under
brain stem control.
Descending Tracts In Spinal Cord
Lateral
pathways
Ventromedial
pathways
Lateral Pathways:
Corticospinal tract
Rubrospinal tract
Ventromedial Pathways:
Vestibulospinal tract
Tectospinal tract
Ventromedial Pathways:
Pontine (medial) reticulospinal tract
Medullary (lateral) reticulospinal tract
Summary of the
major descending
spinal tracts and
their points of
origin
corticospinal tract
reticulospinal tracts
rubrospinal
tract
tectospinal,
vestibulospinal
tracts
Central Motor Control Systems
• Pyramidal system (corticospinal tract)
[lateral pathways]
• Extrapyramidal system (everything
else: basal ganglia, cerebellum, brain
stem) [ventromedial pathways]
Cerebral Cortex
• Primary motor cortex - discrete purposeful
movements
• Premotor area - patterns of movement
• Supplemental motor area - bilateral
movements, fixation movements
Human area 4 = M1 =
primary motor cortex
Human area 6 =
premotor area (PMA) and
supplemental motor
area (SMA) = premotor
cortex
Corticospinal Tract
(Pyramidal Tract)
• Arises from primary motor cortex (30%),
premotor cortex and supplementary motor area
(30%), and somatic sensory areas of cortex (40%).
• Projects from cerebral cortex to spinal cord
without interruption.
• Synapses with:
– motor neurons controlling distal muscles (alpha and
gamma motor neurons)
– interneurons controlling motor neurons
Pathway of Pyramidal Axons
• CST axons are grouped together and form
the medullary pyramids.
– CST also called the pyramidal tract
• Most CST axons decussate at the junction
between medulla and spinal cord. These
axons form the lateral corticospinal tract.
• Lateral CST innervates contralateral (to
cortex) interneurons and motor neurons
supplying distal limb muscles.
Pathway of Pyramidal Axons
• Some axons descend without decussation in
ventral columns to form the medial (ventral)
corticospinal tract. Most of these fibers
cross to the opposite side of the cord in
thoracic or cervical areas of cord.
• Involved in control by supplementary motor
area of bilateral postural movements and
motor neurons supplying trunk and
proximal limb muscles.
Other CST Targets
• Feedback signals from the cortex to inhibit
adjacent motor cortex areas to “sharpen” the
boundaries of excitatory output.
• Fibers to caudate nucleus and putamen of BG.
• Fibers to red nucleus – rubrospinal tract.
• Fibers to the reticular substance and
vestibular nuclei – reticulospinal and
vestibulospinal tracts, reticulocerebellar and
vestibulocerebellar tracts.
Other CST Targets cont.
• Fibers to the pontine nuclei –
pontocerebellar tract.
• Fibers to the inferior olivary nuclei –
olivocerebellar tract.
So, descending information in CST also
results in activation of the basal ganglia,
cerebellum, and brain stem.
Inputs to Motor Cortex
• Subcortical fibers from other cortical areas:
somatosensory, frontal, auditory, visual.
• Subcortical fibers from contralateral cortex
through the corpus callosum.
• Somatosensory fibers from thalamic ventrobasal
complex.
• Fibers from thalamic VL and ventroanterior nuclei
– from cerebellum and basal ganglia.
• Fibers from thalamic intralaminar nuclei – arousal.
CST Lesions
• Common causes of CST lesions include:
– stroke
– tumors
– trauma
• Upper motor neuron (UMN) disease
• Lesions to motor cortex will affect limb
muscles contralateral to lesion. Why?
CST Lesions – Positive Signs
• Abnormal responses to stimuli
(hyperreflexia) or motor behaviors that
emerge as a result of the lesion.
• Primarily due to withdrawal of inhibitory
influences or to interneuron connection
defects.
CST Lesions – Negative Signs
• Loss of the function normally controlled by CST
(paralysis), resulting in the inability to initiate fine
voluntary movements, or a loss of fractionation
(the inability to control individual muscles
independently.)
• Primarily due to a loss of connections of CST
neurons onto alpha motor neurons.
• Examples: hypotonia (decreased muscle tone),
weakness, diminution of movement (paresis).
CST Conclusion
• Direct activation of alpha, gamma motor
neurons and interneurons.
• Background tonic signals to motor areas of
cord.
Brain Stem Motor Centers
• Pontine reticular nuclei – excite antigravity muscles
(muscles of the vertebral column and limb extensor
muscles) – pontine reticulospinal tract.
• Medullary reticular nuclei – inhibit antigravity
muscles – medullary reticulospinal tract.
Pontine & medullary systems balance each other.
• Vestibular nuclei – supplement the excitatory function
of the pontine system by integrating vestibular
information – lateral and medial vestibulospinal tracts.
Basal Ganglia and Cerebellum
The basal ganglia and cerebellum are large
collections of nuclei that modify movement on
a minute-to-minute basis. The motor cortex
sends information to both, and both structures
send information back via the thalamus.
Output of the cerebellum is excitatory and
inhibitory, while the basal ganglia are
inhibitory. The balance between these two
systems allows for smooth, coordinated
movement, and a disturbance in either system
will show up as movement disorders.
Basal Ganglia (Basal Nuclei)
• Nuclei deep to the cerebrum
• Important in posture and planning and
coordination of motor action (via dopamine)
• Loss of actions results in muscle tremors
(Parkinson’s disease)
• Striatum [caudate, putamen], globus pallidus,
substantia nigra, subthalamic nucleus
Basal Ganglia
• Most afferents come from the cerebrum,
most efferents go to the cerebrum
• Connected to the motor area of the cortex
and to the thalamus
• No direct connection to alpha motor
neurons
Feedback loop from
the cortex, to the
basal ganglia, to the
thalamus (VLo), to
cortical area 6 (SMA)
Putamen Pathway For Execution
of Learned Patterns of Movement
X
Caudate Pathway For Cognitive
Planning of Motor Patterns
X
Corpus Striatum
(caudate nucleus and putamen)
• Afferents - premotor and
supplemental motor areas
of cortex, somatosensory
cortex, substantia nigra
• Efferents - globus pallidus,
eventually back to cortex
• Gross movement initiation,
visual limb placement
Globus Pallidus
• Afferents –from the
striatum, subthalamus
• Efferents – to substantia
nigra, subthalamus,
thalamus, RF
• Motor relay, tonic
background contractions
Neurotransmitters
• Dopamine (-):
substantia nigra to
caudate nucleus
• ACh (+): from cortex
to putamen and
caudate
• GABA (-): from
caudate and putamen
to globus pallidus and
substantia nigra
Neurotransmitters
• Norepinephrine,
serotonin, enkephalin,
glutamate also serve as
transmitters.
Neurotransmitters
Diseases
• Parkinson’s disease (paralysis agitans) –
widespread destruction of substantia nigra
and or globus pallidus. Characterized by
rigidity, tremor at rest, and akinesia.
• Loss of dopamine secreting neurons in
substantia nigra; excessive ACh activity in
the striatum from cortex.
• Treat by replacing dopamine (L-DOPA)
and/or by blocking ACh from cortex.
Diseases
• Chorea (Huntington’s disease) – associated
with degeneration of striatum. Irregular
pattern of involuntary movement of muscle
groups (chorea = dance). Progresses to
rigidity and dementia, death.
• Unopposed DA release by substantia nigra.
• Results from loss of GABA containing
neurons and therefore the loss of inhibitory
input to globus pallidus.
Diseases
• Ballism – violent flailing movements.
• Caused by destruction of subthalamic nuclei
or its connections.
• Hemi-ballism – unilateral.
• Athetosis – writhing movements of hand,
arm, neck, or face.
• Caused by lesions in the globus pallidus.
Diseases
• Black walnut toxicosis in horses – produces
laminitis and liquefactive necrosis of the
substantia nigra and globus pallidus. Can result
from as little as 5% in shavings used as
bedding. Treated by removing bedding.
• Yellow star thistle poisoning in horses
(nigropallidal encephalomalacia) – necrosis of
substantia nigra and globus pallidus. No tx.
Cerebellum (Little Brain)
The cerebellum contributes to smooth
coordination of motor activity. With a huge
sensory input, the cerebellum rapidly
processes information on instantaneous
body position and makes corrective
adjustments of planned motor activity. The
cerebellum operates through numerous
reciprocal connections which “follow-up”
motor activity in a servomechanism fashion.
Sensory Homunculi of the CBL
Cerebellar Function
• In voluntary movement
– corrects motor irregularities
– compares motor “central” intentions to
“peripheral performance”
– controls ballistic movements
• In posture and equilibrium
– cooperation with spinal cord, cortex and
reticular formation
• Primarily inhibitory function
Cerebellar Inputs and Outputs
• The cerebellum operates in 3’s:
– there are 3 routes in and out of the cerebellum
– there are 3 main inputs
– there are 3 main outputs from 3 deep nuclei.
• The 3 routes are the peduncles, or “stalks” the rostral, middle and caudal cerebellar
peduncles.
Cerebellar Inputs and Outputs
• The 3 inputs are:
– mossy fibers from the spinocerebellar pathways
and
– mossy fibers from the pons, carrying
information from the contralateral cortex
– climbing fibers from the inferior olive
Cerebellar Afferent Pathways
mossy fibers
climbing fibers
Cerebellar Inputs and Outputs
• The 3 deep nuclei are:
– (1) fastigial - concerned with balance; sends
information mainly to the vestibular and
reticular nuclei
– (2) dentate and (3) interposed - both concerned
with voluntary movement; send axons mainly
to the thalamus and red nucleus
• All 3 receive inputs from sensory afferent
tracts and from the cerebellar cortex.
Cerebellar Efferent Pathways
• To medullary and pontine regions of the brain
stem – posture and equilibrium
• To thalamus (VL & VA), to cortex, to
thalamus (midline), to basal ganglia, red
nucleus, & reticular formation – coordination
between agonists and antagonists
• To thalamus (VL & VA) to cortex –
coordination of sequential motor actions
Cerebellar Circuits
Cerebellar Circuits
• Inputs to the cerebellar cortex (mossy and
climbing fibers) excite the deep nuclei cells as
they enter.
• The output of the CBL cortex (Purkinje cell
axons) inhibits the deep nuclei cells.
• Climbing fibers excite Purkinje cell dendrites.
• Mossy fibers excite granule cells, whose axons
(parallel fibers) excite Purkinje cell dendrites.
• Deep nuclei cells and Purkinje cells fire tonically.
Cerebellar Circuits
Feedback loop from
the cortex, to the
cerebellum, to the
thalamus (VLc), to
cortical area 4 (PMA)
Diseases
• Cerebellar lesions – intention tremor.
• Hereditary cerebellar degeneration
(abiotrophy): Kerry blue terrier, rough-coated
collie, Gordon setter, Arabian horses,
Holstein-Friesian cattle, Yorkshire swine –
loss of Purkinje cells.
• Cerebellar hypoplasia – perinatal infection by
feline parvovirus – kills granule cells, P-cells.
Decortication Lesion (A)
• Hypermetria
• Spasticity/hyperreflexia
• Hemiparesis
Decerebration Lesion (B)
•
•
•
•
•
Lose cortex, thalamus
Leaves subthalamus
Hyperactive reticular formation
Extensor rigidity
Hyperexcited gamma and alpha motor
neurons
• Unopposed vestibular facilitation
• Flexor hypertonus
Cerebellar Lesion
•
•
•
•
•
Hypotonia
Ataxia
Nystagmus
Intention tremor
Dysmetrias
Over-Simplified Summary
• Motor cortex – initiation of movements
• Brain stem centers – balance of excitation and
inhibition of antigravity muscles; integration of
vestibular information
• Basal ganglia – posture and planning and
coordination of motor action
• Cerebellum – equilibrium; coordination of motor
action based on sensory information and feedback
Hierarchy of Motor Control
LEVEL
FUNCTION
STRUCTURES
high
strategy
association areas of
neocortex, basal ganglia
middle
tactics
motor cortex, cerebellum
low
execution
brain stem, spinal cord