B&B Motor control Flashcards

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1
Q

Describe low, middle and high motor control hierarchy

A

High : Strategy
(what is the goal of movement?)
Association of neocortex, basal ganglia and cerebellum

Medium: Tactics
(Muscle contractions required to achieve the strategic goal)
Motor cortex, cerebellum.

Low: Execution
(Activation of motor neuron and interneuron pools that generate the movement)
Brain stem, spinal cord

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2
Q

What does the Cerebral neocortex provide

A

information about body positioning in egocentric space

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3
Q

Why can ballistic movements not be altered once initiated?

A

No sensory feedback

But there is sensory information before the movement is initiated or during the movement.

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4
Q

Sensorimotor transformation = sensory stimuli being converted into motor commands.
It depends on 2 things. What are these?

A
  1. Extrinsic information about the world around us – spatial location of a target.
  2. Intrinsic information about our body – kinematic and kinetic information
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5
Q

Give some examples of kinematic and kinetic information

A
Kinematic = Position, velocity and acceleration of the hand. Joint angle. Lengths of muscles
Kinetic = The forces generated or experienced by the body.
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6
Q

How do sensorimotor transformations generate movement to a desired location?

A

1) Target is localised in egocentric space (relative to the head)
2) Plan of movement (path and trajectory) and initial location of endpoint and endpoint trajectory.
3) Inverse kinematic transformation. The joint trajectories to achieve the hand path are determined.
4) Inverse dynamic transformation. Joint torques or muscle activities to achieve joint trajectory are determined

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7
Q

What is the motor response?

A

Stimulation of the primary motor cortex

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8
Q

Neural circuits compute sensorimotor transformations = internal models
Internal models can take 2 forms. What are these?

A

Forward model

Inverse model

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9
Q

Describe the forward model

A

1 of 2 internal models
The internal model that represents the relationships between actions and their consequences (the predicted behaviour)
Estimates future sensory inputs based on motor outputs.
Anticipates how the motor system will change as a result of the motor command

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10
Q

Describe the inverse model

A

1 of 2 internal models
the internal model that calculates motor outputs from sensory outputs (the desired behaviour)
Determines the motor commands that are needed to produce the movements necessary to achieve the desired consequence.

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11
Q

What is the speed accuracy trade off?

A

A limited ability to move rapidly and accurately at the same time
Subject is required to hit a target perpendicular to the direction in which they move
Each subject starts from three different positions.
Each subject is required to complete the movement within three different times (140,170 or 200ms).

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12
Q

Describe feedforward vs feedback control

A

Feedforward control is used to reduce the effects of measurable disturbances
Feedforward controller generates a motor command based on the desired state.
The movement is not monitored for errors ie. there is no sensory feedback.

while feedback trim compensates for inaccuracies in the process model, measurement error, and unmeasured disturbances.

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13
Q

What is propioception?

A

Perception or awareness of body position and movement
Patients who have lost proprioception have difficulty controlling the dynamic properties of their limbs. They make clumsy, uncoordinated and inaccurate movements.

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14
Q

How is locomotion controlled?

A

Locomotion – using rhythmic and alternating movements of the body or appendages.
eg swimming
Locomotion is controlled automatically at relatively low levels of the CNS without the intervention by higher centres

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15
Q

Flexors and extensors inhibit each other reciprocally, what does this give rise to?

A

Alternating stepping movements

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16
Q

The motor output for locomotion is produced primarily by the WHAT?

A

Neuronal system in the spinal cord

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17
Q

Flexors and extensors inhibit each other reciprocally, giving rise to alternating stepping movements
It is divided into 4 phases, what are these?

A
  • Flexion (F)
  • First Extension (E1)
  • Second extension (E2)
  • Third extension (E3)
18
Q

Describe F, E1, E2, E3

A

-Flexion (F)
-First Extension (E1)
Occur in the swing phase when the foot is off the ground.

-Second extension (E2)
-Third extension (E3)
Occur during stance when the foot makes contact with the ground.

19
Q

Describe the stumbling corrective reaction

A

Sensory receptors in the skin influence walking by detecting obstacles and adjusting stepping to avoid them
In cats: Mild mechanical stimulus applied to dorsal part of the paw in swing phase
Excitation of flexor motor neurons and inhibition of extensor motor neurons.
Rapid flexion of the paw away from stimulus and elevation of the leg to step over object

20
Q

Describe spinal preparations (acute spinal)

A

Different preparations are used to study the neuronal control of stepping
Spinal preparation = spinal cord transected at the lower thoracic level.

  1. Acute spinal preparations – adrenergic drugs such as L-DOPA or nialamide are administered immediately after the transection.
  2. Elevation of norepinephrine in the spinal cord.
  3. Spontaneous generation of locomotor activity 30minutes after administration
21
Q

Describe spinal preparations (chronic spinal) in cats

A

Different preparations are used to study the neuronal control of stepping
Spinal preparation = spinal cord transected at the lower thoracic level.

  1. Chronic spinal preparations – transection of the spinal cord, studied for weeks or months.
  2. Locomotor activity can return within a few weeks of cord transection.
  3. Locomotor function returns spontaneously in kittens.
  4. Daily training is required to restore function in adult cats.
22
Q

What are the 3 descending spinal tracts?

A
  1. Corticospinal pathways
  2. Medial pathways
  3. Lateral pathways
23
Q

Describe the corticospinal tract

A

Functions:
Control of voluntary, discrete and skilled movement.
Distal limbs

Pathway:
Arises from motor and sensory cortices.
Pass through internal capsule. 
Enter crus cerebri of the midbrain.
Ventral portion of the pons.
Medulla oblongata (two prominent columns on dorsal surface = pyramids AKA pyramidal tracts).
Fibres decussate:
Lateral corticospinal tract (75%-90%)
24
Q

Describe Hereditary spastic paraparesis

A

Background:

Inherited degenerative disorder.

Autosomal dominant.

Progressive weakness of the legs.

Increased muscle tone.

Marked stiffness in gait.

Cause:

Degeneration of lateral corticospinal tract.

Chiefly affects thoracic spinal cord

Spastic paraparesis.

25
Q

Injury to spinal cord results in WHAT?

A

Loss of sensation
Loss of movements
Loss of autonomic function

26
Q

Describe Rehabilitative training after spinal cord injury

A

Repetitive weight supported stepping on a treadmill
Partial support of body weight is essential as it reduced the requirements for supraspinal control of posture and balance

27
Q

The basal ganglia is composed of 4 principle nuclei. What are these?

A
  1. Striatum
    • Caudate
    • Putamen
  2. Globus pallidus
    • Internal (GPi)
    • External (GPe)
  3. Substantia nigra
  4. Subthalamic nucleus (STN)
28
Q

What are the functions of the basal ganglia?

A

Production of movement

  • Voluntary behaviour and movements.
  • Inhibiting inappropriate involuntary movements

Extensive connections with frontal cortex indicate involvement in:
Memory, cognition, emotion.

29
Q

Describe Parkinson’s disease

A

Idiopathic
Loss of cells in the substantia nigra
Lower dopamine levels
Tremor at rest and shuffling gait
By the time motor symptoms appear, 60% of dopamine neurones are lost
Reduced drive of direct pathway to the GPi.
Excessive GABA inhibition of the thalamus.
Reduced cortical and striatal (putamen) stimulation

30
Q

What are histological hallmark’s of Parkinson’s

A

Fibrillar aggregates = lewy bodies

31
Q

What medications are there to help with Parkinson’s?

A

No cure
Levadopa
Ingested
Converted to dopamine
Often combined with other medication such as benserazide
Additional medications stop levodopa being broken down in the bloodstream before it gets to the brain
Also reduce side effects of levadopa which include tiredness, dizziness, feeling sick

Deep brain stimulation
Surgically implanting a pulse generator (similar to a heart pacemaker) into the brain

32
Q

Why is Levadopa less effective as more cells are lost?

A

Need dopaminergic neurones to release dopamine

Long-term use of levodopa is linked to:
uncontrollable, jerky muscle movements (dyskinesias).
“on-off” effects, where the person rapidly switches between being able to move (on) and being immobile (off).

33
Q

Describe Huntington’s disease

A

Neurodegenerative condition.
Autosomal dominant – trinucleotide repeat.
Incidence 1 in 10,000-12,000.
Selective loss of medium spiny neurons in striatum

34
Q

What are some Huntington’s disease therapies

A

Mood disturbances = anti- psychotic
Depression = anti- depressants
Impulsiveness and aggression = anti - epileptics (valproate)
Dystonia, myoclonus (muscle spasm) =anti - spasticity or anti - parkinsons
Chorea (unpredictable movements) = Dopamine blocking agents
Cell transplantation

35
Q

What are the general functions for the cerebellum?

A

Regulation of voluntary movement

Posture, balance, motor co-ordination and speech

36
Q

The cerebellum consists of 3 lobes. What are these?

A

Anterior
Posterior
Flocculonodular

37
Q

Describe the flocculonodular lobe of the cerebellum

A
  • Made up of nodulus and flocculus.
    Most primitive part – appearing first in fish.
    Balance of the head and eyes
38
Q

Describe the anterior and posterior lobe of the cerebellum

A

Anterior
= birds and reptiles
= muscle tone

Posterior
= most modern
= co-ordination of movement

39
Q

What happens if there is damage to the cerebellum?

A

Hypotonia (low level of muscle tone).

Ataxia (lack of co-ordination – voluntary movement).

Action or intention tremors (tremor at the end of a movement)

40
Q

Describe hereditary ataxias

A

Friedreich Ataxia
Most common of the inherited ataxias.

Autosomal recessive (expansion of GAA trinucleotide repeat in intron one of the FRDA gene).

Lowered protein fraxin.

Iron accumulation in mitochondria leads to excess production of free radicals.

Fibre loss in dorsal columns and spinocerebellar tracts.

Cellular damage and death.