Motor Control Flashcards

1
Q

hierarchical organisation

A
  • high order areas of hierarchy are involved in more complex tasks (programming and deciding on movements, coordinating muscle activity)
  • lower level areas of hierarchy perform lower level tasks (execution of movement)
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2
Q

functional segregation

A

motor system organised in a number of different areas that control different aspects of movement

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3
Q

motor system hierarchy

A

motor cortex receives info from other cortical areas and sends commands to brainstem and thalamus

cerebellum and basal ganglia adjust the commands received from other parts of the motor control system

brainstem passes commands from cortex to spinal cord

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4
Q

major descending tracts

A
pyramidal tracts (pass through pyramids of the medulla) - voluntary movements of body and face
extrapyramidal tracts (do not pass through pyramids of medulla)- involuntary movements for balance, posture and locomotion
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5
Q

pyramidal tracts

A

UMN in motor cortex directly innervate LMN in anterior horn of spinal cord:

  • corticospinal
  • corticobulbar
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6
Q

extrapyramidal tracts

A

UMN in brainstem do not directly innervate LMN, interneurones innervate muscle groups:

  • vestibulospinal
  • tectospinal
  • reticulospinal
  • rubrospinal
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7
Q

corticospinal tract

A

UMN cell bodies in primary motor cortex
axon fibres go through internal capsule to form medullary pyramid on ventral surface of brainstem
at the level of the medulla:
- 90% of fibres decussate to form lateral corticospinal tract
- these fibres synapse with LMN in the anterior horn of the spinal cord to innervate limb muscles
- 10% of fibres do not cross and from the anterior corticospinal tract
- these fibres cross over and then synapse with LMN in the anterior horn of the spinal cord to innervate the trunk muscles

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8
Q

corticobulbar tract

A

UMN cell bodies in primary motor cortex
axon fibres go alongside corticospinal tract to brainstem

These axons will depart the tract and synapse directly with the contralateral lower motor neurons for Cranial Nerves V, VII, XI, and XII at their corresponding levels of the Pons and medulla

Some of the upper motor neurons branch into two fibers which synapse with both the ipsilateral and contralateral motor nuclei

These include cranial nerves V, which controls the muscles for chewing, XI, which controls the muscles of the neck, and the part of VII that innervates the muscles in the upper half of the face

This means the muscles innervated by these nerves receive motor signals from the motor cortex from both hemispheres of the brain

The upper motor neurons of cranial nerve VII that control the lower half of the face, and cranial nerve XII, which control tongue movement, crossover in the brainstem without branching and only synapse with the contralateral nuclei

So the muscles innervated by these cranial nerves only receive motor information from the contralateral cerebral cortex

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9
Q

vestibulospinal tract

A

From the vestibular nuclei
Stabilise head during body movements, or as head moves
Coordinate head movements with eye movements to keep vision fixed
Mediate postural adjustments

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10
Q

reticulospinal tract

A

Most primitive descending tract
Large proportion from medulla and pons
Changes in muscles tone associated with voluntary movement
Postural stability

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11
Q

tectospinal tract

A

From superior colliculus of midbrain(visual system)

Orientation of the head and neck during eye movements

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12
Q

rubrospinal tract

A

From red nucleus of midbrain
In humans mainly taken over by corticospinal tract , active in primitive species.
Innervate lower motor neurons of flexors of the upper limb

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13
Q

upper motor neuron lesion

A

Negative signs:
Loss of voluntary motor function
Paresis: graded weakness of movements
Paralysis (-plegia): complete loss of voluntary muscle activity

Positive signs:
Increased abnormal motor function due to loss of inhibitory descending inputs
Spasticity: increased muscle tone
Hyper-reflexia: exaggerated reflexes
Clonus: abnormal oscillatory muscle contraction
Babinski’s sign

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14
Q

apraxia

A

consequence of UMN lesion

  • a disorder of skilled movement
  • patients not paralyzed but have lost information about how to perform skilled movements
  • lesion of inferior parietal lobe/ frontal lobe (premotor cortex, supplementary motor area)
  • any disease of these areas can cause apraxia, most commonly stroke and dementia
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15
Q

lower motor neuron lesion

A

Weakness
Hypotonia (reduced muscle tone)
hyporeflexia (reduced reflexes)
Muscle atrophy
Fasciculations: damaged motor units produce spontaneous action potentials, resulting in a visible twitch at the NMJ
Fibrillations: spontaneous twitching of individual muscle fibres; recorded during needle electromyography examination Smaller AP fasciculations not visible to naked eye

signs found in cranial nerve nuclei if LMN of CORTICOBULBAR
signs found in spinal cord if LMN of CORTICOSPINAL

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16
Q

motor neuron disease (MND)

A

(also known as amyotrophic lateral sclerosis (ALS))

progressive neurodegenerative spectrum of disorders of the motor system that can affect both UMN and LMN

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17
Q

MND UMN signs

A
Spasticity (increased tone of limbs and tongue)
Brisk limbs and jaw reflexes 
Babinski’s sign
Loss of dexterity
Dysarthria (difficulty speaking)
Dysphagia (difficulty swallowing)
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18
Q

MND LMN signs

A
Weakness
Muscle wasting
Tongue fasciculations and wasting
Nasal speech
Dysphagia
19
Q

basal ganglia structure

A
Caudate nucleus
Lentiform nucleus (putamen + external globus pallidus) – together caudate and putamen are known as the striatum
Thalamus
Nucleus accumbens
Subthalamic nuclei
Amygdala
Anterior commisure
Substantia nigra (midbrain)
Ventral pallidum, claustrum, nucleus basalis (of Meynert)
20
Q

basal ganglia function

A

Decision to move
Elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)
Moderating and coordinating movement (suppressing unwanted movements)
Performing movements in order

21
Q

basal ganglia circuitry problems

A

Parkinson’s -Degeneration of the dopaminergic neurons that originate in the substantia nigra and project to the striatum

Huntington’s disease- Degeneration of GABAergic neurons in the striatum, caudate and then putamen

Ballism-Usually from stroke affecting the subthalamic nucleus.

22
Q

parkinsons

A

Bradykinesia - slowness of (small) movements (doing up buttons, handling a knife) Hard for dexterous movements
Hypomimic face - expressionless, mask-like (absence of movements that normally animate the face)
Akinesia - difficulty in the initiation of movements because cannot initiate movements internally
Rigidity - muscle tone increase, causing resistance to externally imposed joint movements
Tremor at rest - 4-7 Hz, starts in one hand (“pill-rolling tremor”); with time spreads to other parts of the body

23
Q

huntingtons

A

Choreic movements (chorea - dance)
rapid jerky involuntary movements of the body; hands and face affected first; then legs and rest of body
Speech impairment
Difficulty swallowing
Unsteady gait
Later stages, cognitive decline and dementia
Gabaergic neurons-loss of inhibitory functions
Genetic neurodegenerative disorder , Chromosome 4, autosomal dominant , CAG repeat

24
Q

ballism

A

Sudden uncontrolled flinging of the extremities
Symptoms occur contralaterally.
Rotatory movement of limbs-opposite side of body usually from stroke that affects subthalamic nucleus

25
Q

cerebellum

A

Located in posterior cranial fossa covered by a layer of dura.
Separated from cerebrum above by tentorium cerebelli
Coordinator and predictor of movement
Takes signals down, compare what CNS receiving and outputting-Coordinate movements and make them fluid.
Pons connect 2 cerebellum lobes
Cerebral peduncles in the anterior inferior view-large motor tracts down to the pyramids where many fibers cross over

26
Q

vestibulocerebellum

A

Regulation of gait, posture and equilibrium
Relate to ataxis – poor coordination with walking and falling
Coordination of head movements with eye movements
Damage (tumour) causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)

27
Q

spinocerebellum

A

Coordination of speech
Adjustment of muscle tone
Coordination of limb movements
Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)

28
Q

cerebrocerebellum

A

Coordination of skilled movements
Cognitive function, attention, processing of language
Lateral side- coordinate skilled movemnts
Emotional control
Damage affects mainly arms/skilled coordinated movements (tremor) and speech

29
Q

main signs of cerebellar dysfunction

A

apparent only on movement:
- Ataxia
General impairments in movement coordination and accuracy. Disturbances of posture or gait: wide-based, staggering (“drunken”) gait
- Dysmetria
Inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)
- Intention tremor
Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)
- Dysdiadochokinesia
Inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms)
- Scanning speech
Staccato, due to impaired coordination of speech muscles

30
Q

alpha motor neurons

A

Lower motor neurons of the brainstem and spinal cord
Innervate extrafusal muscle fibres of skeletal muscles- the contractile elements
Intrafusal-contain the sensory elements for stretch- status of muscle for reflex
Anterior horn cells active grey matter, which when activated cause contraction
Motor neuron poll contains all the alpha motor neuron innervating a single muscle

31
Q

motor unit

A

a single motor neuron together with all the muscle fibres that it innervates. It is the smallest functional unit with which to produce force.
2 neurons in the horn, in birth the motor neurons may overlap with muscle. In development a single neuron will win out for muscle fibre innervation.
The lower the number-the higher the resolution and precise control and smaller increases in grain.

32
Q

motor unit classification

A

classified by:

  • Amount of tension generated
  • Speed of contraction
  • Fatiguability
33
Q

motor unit types

A
Slow (S, type I)- 
•smallest diameter cell bodies
•small dendritic trees
•thinnest axons
•slowest conduction velocity
Fast, fatigue resistant (FR, type IIA)- 
•larger diameter cell bodies
•larger dendritic trees
•thicker axons
•faster conduction velocity
Fast, fatigable (FF, type IIB)-
•larger diameter cell bodies
•larger dendritic trees
•thicker axons
•faster conduction velocity
34
Q

regulation of muscle force

A

done in four ways:

  • recruitment
  • rate coding
  • neurotrophic factors
  • cross innervation
35
Q

recruitment

A
  • Recruited in order, governed by size principle.
  • Smaller units first-usually type I, as more forced need more units and different type of units
  • Allows for fine control when low levels of forced needed.
  • Typical ramp up and ramp down contraction
36
Q

rate coding

A
  • Motor unit fire at a range of frequencies, Type 1 at a lower frequency
  • As Hz’s increase, forced produced increase
  • Summation occurs when units fire at frequency to allow muscle relax between arriving action potentials- hence slower muscle in constant usage.
37
Q

neurotrophic factors

A
  • growth factor to prevent neuronal death and promote neuronal growth post injury
  • Motor neurones provide more than action potential
38
Q

cross innervation

A
  • If a fast twitch muscle and a slow muscle are cross innervated, the soleus (calf muscle) becomes fast and the FDL becomes slow.
  • this shows that the motor neuron has some effect on the properties of the muscle fibres it innervates.
39
Q

plasticity

A
  • Type IIB to Type IIA - Training
  • Type I to type II - Severe deconditioning or spinal cord injury, Microgravity during spaceflight results in shift from slow to fast muscle fibre types and atrophy
  • Loss of Type I and II fibres – preferential loss of type II with ageing. Larger proportion of type I fibres in aged muscle- evident by slower contraction times
40
Q

reflex

A
  • An automatic response to a stimulus that involves a nerve impulse passing inward from a receptor to a nerve centre and then outward to an effector (as a muscle or gland) without reaching the level of consciousness.
  • Integrated in the CNS then back to muscle
  • An involuntary coordinated pattern of muscle contraction and relaxation elicited by peripheral stimuli
  • the magnitude and timing of reflex are determined respectively by the intensity and onset of the stimulus
  • Reflexes differ from voluntary movements in that once they are released, they can’t be stopped.

Monosynaptic reflex. Sensory -> Afferent -> Dorsal root ganglia -> Lower motor neurone -> Muscle(to antagonist)

41
Q

Jendrassik maneuver

A

alter reflex amplitude by removing inhibition by upper CNS and neurons exert on the reflexes.
Removes descending inhibition eg when the patellar tendon is tapped.
•Higher centres of the CNS exert inhibitory and excitatory regulation on the stretch reflex
•Inhibitory control dominate in normal
•Decerebration reveals excitatory control from supraspinal areas
•Rigidity and spasticity can result from brain damage giving over-active or tonic stretch reflex.
•Separates cerebral cortex from lower- greater reflex response and goes into a phasic & tonic.

42
Q

hyper-reflexia

A

Overactive reflexes
Loss of descending inhibition
Associated with upper motor neuron lesion-loss of voluntary pathway

43
Q

clonus

A

Involuntary and rhythmic muscle contractions
Loss of descending inhibition
Associated with upper motor neuron lesions

44
Q

Babinski sign

A

When sole stimulated with blunt instrument the big toe- outside of sole and balls of feet stroked outside to inside
Curls downwards – normal-Especially big toe
Curls upwards – abnormal in adults. This is a positive Babinski sign. Associated with upper motor neuron lesions
Note: Toe curls upwards in infants – this is normal.