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Control of Movement
It’s purpose:
 Self-propagation, self-protection
 Species propagation, species-protection
 Biodiversity-propagation, biodiversity-protection
 Involuntary
 Rhythmic movements
 Voluntary
Need for more complex movements -> more complex nervous tissue (induces development of
sensory organs, memory formation and planning)
More complex nervous tissue -> more complex movement
Learning -> more complex structures and functions -> planning movements -> more efficient
Speed, force, dimension, complexity determined by:
 State of development of nervous system
 Biomechanical properties
State of development
 More advance nervous system -> more complex movement
 Simple – 2 neuronal system of sea angel
 Complex – mammals (some species can walk right after birth)
 Humans – 1 year for walking (Toddlers can’t walk, because there isn’t a strong enough
skeleton-muscular and neuronal system.)
Biomechanical properties
 206 bones, 200-300 muscles
 Different joints for different movement
 Muscle binds to bones via collagen, surrounded by protective tissue
 Muscle cell membrane – Sarcolemma
 Myofibrils – Thin filaments (actin), Thick filaments (myozin) -> create stipes
 Functional structure: sarcomere
 Troponin (attached to tropomyosin), tropomyosin, torponin C (binds Ca2+ ions)
Excitation -> contraction
 One motor unit can innervate hundreds of muscle fibers
 Different motor units are intermingled
 Ca2+ is stored and then released from the sarcoplasmatic reticulum -> troponin C
Motor unit types
 Slow (red muscle) – slower contraction, low force, fatigue resistant
 Fast, fatigue resistant – fast contraction, medium force
 Fast, fatigable – fast contraction, high force
AP -> muscle response
 More AP -> more response and the amplitude will increase until reaching the plateau
 At first: summation -> incomplete tetanus -> tetanus (the responses melt together)
 It takes time to remove the Ca2+ and by rapidly stimulating the muscle, there is no time to
remove it entirely thus increasing the
 Tetanus can be caused by bacteria
 We can suddenly change the contraction by
missing or adding an impulse
 Golgi – protects the muscle, inhibits the
 Muscle spindle – parallel to the extrafusal
Human gait
 Phasic component: without central regulation,
rhythmic alternating contractions, functional
at birth
 Tonic component: postural muscles, immature
at birth
Spinal cord injury, Decerebration, Decortication
Spinal cord - reflexes
Brainstem – breathing, eye movements walking -> rigidity
Diencephalon – eating, drinking
Basal ganglia – initiation of movement
Cerebral cortex – speech, hand/finger movements
Central (motor) pattern generator (CPG/MPG): rhythmic output
 Generated by: endogen oscillating neurons, network activity of non-oscillating neurons
Clione – 2 neuron system
 Half-center oscillator: 2 neuron reciprocal innervation -> rhythms (contraction and
Partially inactivated voltage-dependent Na and Ca channels -> hyperpolarisation ->
activation -> it’s easier to depolarise it -> AP -> inhibit the other cell -> hyperpolarisation
 Different inputs cause different outputs -> reaction depends on the neurotransmitter
 Sensory information -> trigger neurons -> rhythmic activity
 Gating neurons: determines the duration ode the activity
 Short activation of trigger neurons -> long-lasting activation of gating neurons -> long
lasting activation of CPGs and motoneurons
Lamprey – command system of vertebrates
 In CPG - excitatory and inhibitory interneurons, reciprocal inhibition with the other half
 Stretch receptors will feed-back to CPG
 Excitatory reticulospinalis neurons -> induce plateau potentials in pattern-generating
 NMDA -> Ca2+ level increases
Stimulating the dorsal root -> rhythmic burst activity of CPGs
Skin -> interneuron of ipsilater side -> modify the motor program (neuron firing)
Movement initiation – basal ganglia
 Pallidum inhibits other motor centers -> if we want to do
something we need disinhibition
 Substantia nigra (dopaminergic) – activation of the
neurons -> if it’s not working properly (Parkinson) it’s
difficult to start and stop the movement
 Too much dopamine -> can’t control the movement
Posture and balance
 Sensory, vestibular and visual input -> muscle
Proprioception – sense of position and movement
 Compensatory reflexes – stretch reflex
 Phasic and tonic components, reciprocal
 Adjustable sensitivity – fuzimotor fiber
 Modified by presynaptic inhibition
Nociceptive reflex – pain induced reflexes
 Multisensor convergence
 Contralateral inhibition
Moving platform
 Triggers the ankle strategy – feed-back mechanism
If the movement is small, we can analyze it
Forward movement – backward sway -> activation of quadriceps, abdominal muscles
Tilted platform
 Triggers hip strategy – feed-back mechanism
 Forward tilting – forward sway -> paraspinal, ham string, triceps surae muscle activation,
Feed-back if unexpected postural disturbance occurs, feed forward if expected -> preventing
Vestibulocervical an vestibulospinal reflexes stabilize head and body posture
Romberg test
 No visual input -> proprioceptive and vestibular sensors only
 Won’t be able to maintain balance
 Can be use to test proprioceptive and vestibular damage
Medial posture system
 Proprioceptive, vestibular and visual information -> motor response
 Innervates axial muscles and proximal part of limbs
 Vestibular nuclei – connection with cerebellum, receives sensory information from the
 Medial longitudinal fascicle > superior vestibular nucleus -> motor nuclei of the eye
 Lateral vestibular nucleus -> spinal cord -> ipsilater extensor muscle of the limbs
Lateral voluntary system
 Corticospinal pathway
 Rubrospinal pathway
Cortical areas involved in motor control
 Stimulation induce or alters movements
 Area 4, 6 (Brodman) (and 1,2,3,5,7,24)
 Communicate with other motor structures and receive subcortical and cortical afferents
Somatotopic representation – the size of the area shows how fine the movement of that body
part is in the cortex
Primary motor cortex
 Agranular – layer 4 is small or absent, no internal granular layer
 Pyramid cells are dominant
Plasticity of motor cortex
 Occurs: Denervation, stroke, intensive use of muscles
 After denervation, many function can be regained, but need training
Planning, voluntary movements
 Complex hand movements bilateral activation: sensorimotory, supplementar motor,
ventrolateral premotor areas
Contralateral: Dorsolateral premotor, medial cortical areas
M1 neurons regulate the dynamics of movement – discharged neuron number correlate with the
force exerted
Discharged neuron number is correlated with the direction
Processing the visual input
 More visual input -> delay time increases
 Children can’t respond that fast -> not able to process the speed of the cars
If we have to think about the movement, it activates the same areas as during actual movement
Lesion of supplementer area
 Can’t coordinate bimanual movements
 If supplement is active -> inhibits the other side
 If it’s injured, it can’t -> it will be the same movement
Premotor neuron encodes the goal of the movement