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Year 2- Neuroscience > Motor Control > Flashcards

Motor Control Flashcards

1
Q

Describe the broad principles of motor control

A

Hierarchical organisation

  • high order areas of hierarchy are involved in more complex tasks (programme and decide on movements, coordinate muscle activity)
  • lower level areas of hierarchy perform lower level tasks (execution of movement)

Functional segregation

  • Motor system organised in a number of different areas that control different aspects of movement
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2
Q

Describe and Draw out the Motor system Hierachy

A
  • different parts of the brain interact with each other in order to bring out voluntary or involuntary movement
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3
Q

what are the major descending paths?

Describe their paths and functions

A

Pyramidal tracts: pass through the pyramids of the medulla
• Corticospinal
• Corticobulbar
• Path: Motor cortex to spinal cord or cranial nerve nuclei in brainstem
• Function: Voluntary movements of body and face

Extrapyramidal tracts: do not pass through the pyramids of the medulla
• Vestibulospinal
• Tectospinal
• Reticulospinal
• Rubrospinal
• Path: Brainstem nuclei to spinal cord
• Function: involuntary (automatic) movements for balance, posture and locomotion

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4
Q

What is the location and function of the primary motor cortex?

A
  • located in precentral gyrus; anterior to the central sulcus

Function:

  • controls fine, discrete, precise voluntary movements.
  • provides descending signals to execute movements.
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5
Q

What is the location and function of the premotor area?

A
  • located anterior to primary motor cortex
  • involved in planning movements
  • regulates externally cued movements
    e. g. seeing an apple and reaching out for it
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6
Q

What is the location and function of the supplementary motor area?

A
  • located anterior and medial to primary motor cortex
  • involved in planning complex movements (e.g. internally cued, speech)
  • becomes active prior to voluntary movemen
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7
Q

Describe and draw out the pathway of the corticispinal tract

A
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8
Q

Draw out the homunculus using somatotopy for MOTOR control

A
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9
Q

Describe the corticobulbar tract

A
  • upper motor neurones in the primary motor cortex
  • synapse with brainstem nuclei
  • principal motor pathway for voluntary movement of face (and neck).
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10
Q

What are the extrapyramidal tracts? Give functions

A

-Vestibulospinal

  • Stabilise head during body movements, or as head moves
  • Coordinate head movements with eye movements
  • Mediate postural adjustments.
  • LMN synapse in vestibular nuclei

Reticulospinal

  • Most primitive descending tract - from medulla and pons (has reticular formation in both where it arises from)
  • Changes in muscles tone associated with voluntary movement
  • Postural stability

Tectospinal

  • From superior colliculus of midbrain
  • Orientation of the head and neck during eye movements

Rubrospinal

  • From red nucleus of midbrain
  • In humans mainly taken over by corticospinal tract
  • Innervate lower motor neurons of flexors of the upper limb.
  • Starts functioning properly if there’s lesions in corticospinal tract
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11
Q

What are the NEGATIVE and positive signs of an 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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12
Q

What is apraxia?

A

A disorder of skilled movement. Patients are not paretic but have lost information about how to perform skilled movements

UMN lesions

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13
Q

what causes apraxia

A
  • lesion of inferior parietal lobe, the frontal lobe (premotor cortex, supplementary motor area - SMA)
  • stroke and dementia are the most common causes
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14
Q

what are the signs of a 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
  • Fibrillations: spontaneous twitching of individual muscle fibres; recorded during needle electromyography examination
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15
Q

what is Motor neurone disease? (MND)

A
  • Progressive neurodegenerative disorder of the motor system
  • Spectrum of disorders
  • Also known as Amyotrophic Lateral Sclerosis (ALS)
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16
Q

What are the Upper motor neuron signs of MND

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)
17
Q

What are the lower motor neurone signs of MND

A
  • Weakness
  • Muscle wasting
  • Tongue fasciculations and wasting
  • Nasal speech
  • Dysphagia
18
Q

Describe the structure of the basal ganglia

A
  • Caudate nucleus:
  • Lentiform nucleus (putamen + external globus pallidus) - together caudate and putamen are known as the striatum
  • Nucleus accumbens
  • Subthalamic nuclei
  • Substantia nigra (midbrain)
  • Ventral pallidum, claustrum, nucleus basalis (of Meynert)
19
Q

What is the function of the Basal ganglia?

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
  • Perception
20
Q

Label this diagram

A
21
Q

Draw out the basal ganglia circuitry and what affected pathways can cause some diseases

A
22
Q

What causes parkinsons disease

A

Degeneration of the dopaminergic neurones that originate in the substantia nigra and project to the striatum

23
Q

What are the signs of Parkinsons disease

A

• Bradykinesia - slowness of (small) movements (doing up buttons, handling a knife).

• Tremor at rest - 4-7 Hz, starts in one hand (“pill-rolling tremor”); with time spreads to other parts of the body.

  • Rigidity - muscle tone increase, causing resistance to externally imposed joint 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

24
Q

what causes Huntingtons disease?

A

Genetic neurodegenerative disorder

  • Chromosome 4, autosomal dominant
  • CAG repeat.

This leads to degeneration of GABAergic neurons in the striatum, caudate and then putamen

25
Q

What are the signs of Huntingtons disease

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
26
Q

what is balliism and what causes it?

A

Stroke in subthalamic nucleus.

There’s sudden uncontrolled flinigng of extremities

Symptoms occur contralaterally.

27
Q

What is the location and function of the cerebellum?

A
  • Located in posterior cranial fossa
  • Separated from cerebrum above by tentorium cerebelli
  • Coordinator and predictor of movement- takes information frpom joints/receptors and help to coordinate movement.
28
Q

What are some functional regions of the cerebellum?

A
  • vestibulocerebellum
  • spinocerebellum
  • cerebrocerebellum
29
Q

Describe function of the vestibulocerebellum

what happens when it is damaged?

A
  • Regulation of gait, posture and equilibrium
  • 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)

30
Q

Describe function of the spinocerebellum and describe what happens when it’s damaged

A
  • Coordination of speech
  • Adjustment of muscle tone
  • Coordination of limb movements

Damage:

Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)

31
Q

Describe function of the cerebrocerebellum, describe the effects when damaged

A

Function:

  • Coordination of skilled movements
  • Cognitive function, attention,
  • Processing of language
  • Emotional control

Damage: affects mainly arms/skilled coordinated movements (tremor) and speech

32
Q

What are the Main signs of Cerebellar dysfunction

A

it is APPARENT ONLY ON movement.

Signs are:

Ataxia
> 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

33
Q

In a UMN lesion, why are abdominal reflexes (superficial reflexes) absent while the other reflexes (deep tendon reflexes) are brisk?

A

This is the hallmark of a pure corticospinal tract lesion.

Stroking the skin of the abdomen causes the abdominal wall muscles to contract, sometimes pulling the umbilicus towards the stimulus. These reflex contractions are often absent in upper motor neurone disorders.

Another example is the cremasteric reflex

34
Q

Explain the physiology behind the fasciculation seen in a LMN lesion

A

There is denervation then reinnervation to the denervated muscle fibres,

The resulting new motor unit is larger and less stable and prone to ectopic generation of electrical stimuli in the distal axon that cause contraction of the muscle fibres.

Year 2- Neuroscience (13 decks)

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