MOTOR SYSTEMS
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Muscles and Joints
Muscles
Moving
The Spinal Cord
Spinal Reflexes
Reciprocal Control of Opposing Muscles
Polysynaptic Adaptations and Reflexes
The Motor Cortex
The Basal Ganglia
Limbic System
The Cerebellum
Cranial Nerves
Muscle groups are complex; attach bone to
bone via tendons and ligaments
A muscle group has many fibers
The Neuromuscular junction (NMJ): The
receptive portion of muscle-the motor end-plate
The NMJ ( sometimes called the motor
end-plate)
nACHr
End-plate potential
• Larger
• Longer
• Leads to Ca+ influx in sarcolema of muscle
– Ca+ causes muscle contraction
Disease of the NMJ?
MG
MG
muscle fibers encase myofibrils. The casing
is called the sarcolema
Muscle group
myofibril
Muscle fiber
End-plate potential causes ca+ influx into
sarcolemma
Myofibrils in turn contain
“Actin and Myosin” filaments
When the NMJ is activated Actin-myosin interact
to shorten the length of a muscle fiber
Sliding filament model of muscular
contraction
Muscle shortens=work
Cortical vs Spinal control of behavior
• Goal-directed
• Reflexive
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• Simple
• Automatic
• inplastic
Complex
Higher levels of control
Plastic
Numerous reflexive
behaviors are involved
Spinal reflex ARCs
• Monosynaptic
– stretch
• Polysynaptic
– Withdrawal
– Antagonist muscle groups
– Synergistic muscle groups
– Polysegmental relexes
– Cross-spinal reflexes
A “monosynaptic” spinal reflex arc- the
Stretch reflex
The stretch reflex involves neuromuscular
“spindles”
Stretch reflex regulates muscle tension in
every muscle group
The polysynaptic part of stretch reflexes:
inhibition of Antagonist muscles
Spinal inhibition of antagonist muscles require
inhibitory interneurons
The “withdrawal reflex arc” a polysynaptic
spinal reflex
Also involves interneurons
And may involve more than one spinal cord
segment
And/or Cross spinal reflex arcs
The Goli tendon organ (GTO) reflex
Neural activity of spinal neurons
related to whole muscle group activity
Lower motor neurons “the final common
pathway”
Goal-Directed Behavior and Reflexive
Behavior
Goal-Directed
Reflex
Relatively Complex
Relatively Simple
Consciousness? Intention
Automatic
Plastic
Relatively Inplastic
Requires Cortex
Cortex not required
Learning /experiences are major
influence
Genetics are major influence
Goal-Directed Behaviors Require:
• Goal selection and prioritization
• Resistance to distracters
-Cross-modal Sensory integration
– Perception of target
– Awareness of location of movable body part
– Ability to aim movement of body part
– Ability to detect errors and re-adjust, (use feedback)
– Ability to use feedback to control movement of
body part
Sensory-Motor Integration in the frontal
lobes
THE DLPFC: “The conductor”
Integrates cross modal input- may initiate goal-directed behaviors
Lesions of the dorsolateral frontal areas results
in a number of “executive” motor
impairments. These include perseveration,
incoordination, motor impersistence, apraxias
and hypokinesia.
The premotor and supplementary motor
ctx: “The sections”
Stimulation= complex sequences of behavior (aimless behavior)
Damage to the secondary Motor
Cortex?
• Ideomotor Apraxia
• This apraxia is associated with great difficulty in the sequencing and
execution of movements. A common test of apraxia is to request the
patient to demonstrate the use of a tool or household implement (e.g.,
"Show me how to cut with scissors"). Difficulties are apparent when the
patient moves the hand randomly in space or uses the hand as the object
itself, such as using the forefinger and middle finger as blades of the
scissors. They have additional trouble sequencing the correct series of
movements and make errors in orienting their limbs in space consistent
with the desired action. Imitation of the movements of others will usually
improve performance but it is still usually defective.
• Memories for skilled acts are probably stored in the angular gyrus of the
parietal lobe in the left hemisphere.
The primary motor cortex; “the
instrument”
Stimulation = relatively simple fragments of behavior
TWO MAJOR DESCENDING PATHWAYS FROM THE
PRIMARY MOTOR CORTEX: The Dorsolateral pathway
And the VM Path.
• The VM pathway does not
discretely decussate, but
does branch and innervate
contra lateral segments in
the spinal cord.
DL vs VM descending motor paths
• Dorsolateral
• Ventromedial
• Decussates at medullary
pyramids
• Distal muscle groups
• More direct
• More volitional control
• Higher resolution of
control
• Does not cross
• Medial muscle groups
• Gives off spinal
collaterals
• Yoking
• Lower resolution of
control
Other Motor Pathways
• In addition there are other motor paths that
have relays in the brainstem
• These other paths innervate nuclei of the RAS,
cranial nerve nuclei, etc…
Descending paths get additional inputs
Both pathways terminate in spinal cord
segments
According to part of the body they control
On lower motor neurons
(alpha motor neurons)
Amyotropic lateral sclerosis (ALS)
disease of the alpha motor neurons
ALS
Alpha motor neurons project to form part
of spinal nerve pairs
Terminate on muscle fibers
At each spinal segment
BASAL GANGLIA
• Nigro-striatal Pathway
• Striato-Pallidal pathway
Basal Ganglia
• Neostriatum
– Caudate (kaw-date) nucleus and putamen (pew-TAY-men)
• Globus Pallidus ( GLOB-us PAL-i-dos)
• Substantia nigra (included by functional
relationship)
• Subthalamus
• others
not anatomical
Basal ganglia- Complex ccts
The basal ganglia are involved in motor regulation, but are only one
component of the control of behavior. The way in which the basal ganglia
controls movement is complicated and not completely understood, but at his
time may be fairly described as the gate-keeper of movement. Disorders of
the basal ganglia can either lead to too much behavior or too little behavior.
Basal Ganglia-Neostriatum
( composed of the caudate nucleus and the Putamen)
The Nigro-striatal pathway- the
behavioral “grease” system
The Globus Pallidus ( the striato-pallidal
circuit= the behavioral “brakes” system)
Basal Ganglia Syndromes
too much or too little behavior
• Damage to the Nigro-striatal pathway
– Parkinsons
(not enough behavior)
– http://video.google.com/videosearch?hl=en&rls=GGIC,GGIC:200701,GGIC:en&um=1&q=parkinsons&ndsp=20&ie=UTF-8&sa=N&tab=iv#
– http://video.google.com/videosearch?hl=en&rls=GGIC,GGIC:200701,GGIC:en&um=1&q=parkinsons&ndsp=20&ie=UTF-8&sa=N&tab=iv#
Basal Ganglia syndromes
• Strato-Pallidal Pathway- too much behavior
– Huntingtons
– Tourettes’
– Balisms
– Others
• Huntington's Chorea is principally
characterized by hyperkinesias - abnormal,
purposeless, involuntary motor movements
that can occur spontaneously or only when
the patient is trying to do something. These
movements may be repetitive or nonrepetitive.
Tourettes Syndrome
• TS usually becomes apparent in children
between ages 2 to 15, with approximately
50% of patients affected by age 7. The age of
symptom onset is typically before the age of
18. TS is more frequent in males than females
by a ratio of about 3 or 4 to 1. The disorder is
thought to affect 0.1% to 1.0% of individuals
in the general population.
Tourettes
• Motor tics
Initially, patients develop sudden, rapid, recurrent, involuntary movements
(motor tics), particularly of the head and facial area. At symptom onset,
motor tics usually consist of abrupt, brief, isolated movements known as
simple motor tics, such as repeated eye blinking or facial twitching. Simple
motor tics may also include repeated neck stretching, head jerking, or
shoulder shrugging. Less commonly, motor tics are more "coordinated," with
distinct movements involving several muscle groups, such as repetitive
squatting, skipping, or hopping. These tics, referred to as complex motor
tics, may also include repetitive touching of others, deep knee bending,
jumping, smelling of objects, hand gesturing, head shaking, leg kicking, or
turning in a circle. In addition to affecting the head and facial area, motor
tics also affect other parts of the body, such as the shoulders, torso, arms,
and legs. The anatomical locations of motor tics may change over time.
Rarely, motor tics evolve to include behaviors that may result in self-injury,
such as excessive scratching and lip biting.
Vocal tics
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Vocal tics are sudden, involuntary, recurrent, often relatively loud
vocalizations. Vocal tics usually begin as single, simple sounds that may
eventually progress to involve more complex phrases and vocalizations.
For example, patients may initially develop simple vocal tics, including
grunting, throat clearing, sighing, barking, hissing, sniffing, tongue
clicking, or snorting. Complex vocal tics may involve repeating certain
phrases or words out of context, one's own words or sounds (palilalia), or
the last words or phrases spoken by others (echolalia). Rarely, there may
be involuntary, explosive cursing or compulsive utterance of obscene
words or phrases (coprolalia).
LIMBIC STRUCTURES
• AMYGDALA
HIPPOCAMPUS
SEPTUM
AFFECTIVE IMPUSLES
• The 4-F’s, but different