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Flashcards in SPR L22 Pathophysiology of Motor Control Deck (11):

Learning Outcomes

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Physiology of motor control: overview

Give an overview

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Physiology of motor control: voluntary control

  1. Where is the motor cortex?
  2. What does the RIGHT side of the cortex control?
  3. What are the descending motor pathways? (tracts)
  4. What are the spinal motorneurones?



  1. Pre-central gyrus, frontal lobe
  2. LEFT side body
  3. (upper motor neurones)





​4. (lower motor neurones)

alpha : control movements

gamma: set tone


Physiology of motor control: reflexes and tone


  • muscle spindles detect stretch
  • monosynaptic reflex arc via an alpha motoneurone  
    • contraction stretched muscle
  • relay via inhibitory neurones
    • inhibition antagonist muscle
  • gamma motorneurone controls spindle contraction
    • helps set ‘passive’ muscle tone


Pathophysiology of motor control: nerve roots or peripheral nerve damage

What happens in a Lower motor neurone defect?

Loss of a- and g-motoneurone control

  • muscle weakness
  • reduced tone (flaccid paralysis)
  • loss of reflexes
  • muscle wasting

Denervation induced hypersensitivity to acetylcholine

  • muscle fasciculation


Pathophysiology of motor control: damage to the descending motor pathways

What happens in an Upper motor neurone defect/ pyramidal lesion?

Loss of voluntary motor control

  • muscle weakness
  • loss of skilled movement

Disinhibition of a- and g-motor neurones

  • increased tone develops (spastic paralysis)
  • increased reflexes
  • no wasting

Upgoing plantars (Babinski +ve)


Pathophysiology of motor control: patterns of upper motor loss

What will the following give rise to?

  1. Corticospinal damage above decussation in medulla (eg stroke involving internal capsule)?
  2. Bilateral spinal cord damage?
  3. Unilateral spinal cord damage?

  1. Contralateral hemiplegia, Upper limb: flexors dominant, Lower limb: extensors dominant
  2. Cervical region: quadraplegia, Below cervical cord: paraplegia.

  3. Ipsilateral weakness below lesion


Pathophysiology of motor control: cranial motor nerves

What will pathology of the following give rise to?

  1. Extraocular muscles (III,IV and VI)
  2. CN VII


  1. Diplopia and squinting
  2. Facial nerve palsy (VII)

    UMN lesion: contralateral weakness lower half of face

    LMN lesion: ipsilateral weakness of all muscles of facial expression 


Pathophysiology of motor control: cranial motor nerves

What are the following?

  1. Bulbar Palsy
    1. Give symtoms
  2. Pseudobulbar palsy

    1. Give symtoms


  1. Bilateral damage to LMN in cranial nerves in brainstem: IXth, Xth, XIth and XIIth nerves

    1. depressed gag reflex



      limited head movement, shoulder shrug

      flaccid paralysis tongue

  2. Bilateral supranuclear (UMN) lesions affecting lower cranial nerves 

    1. gag reflex preserved

      dysphagia/dysphonia/neck shoulder weakness

      slow, spastic tongue

      enhanced jaw jerk (motor n. V)


Cerebellum: physiology and pathophysiology

  1. What are the cerebellar inputs?
  2. And the outputs?
  3. What are the functions of the cerebellum?
  4. What are the symptoms of pathophysiology of the cerebellum?

  1. Vestibular apparatus

    Peripheral sensory receptors

    Visual and auditory systems

    Motor cortex

  2. Motor cortex

    Brainstem motor areas

  3. Balance and gait

    Corrective motor feedback

  4. Loss of balance, falling towards side of lesion

    Broad based, unsteady (ataxic) gait

    Intention tremor with past-pointing


    Nystagmus (fast component towards lesion)

    Dysarthria (scanning speech)

    Reduced tone and reflexes (pendular reflexes)


Basal ganglia (extrapyramidal system): physiology and pathophysiology

  1. What are the inputs?
  2. What are the outputs?
  3. What are the functions?
  4. What are the signs and symptoms of pathology of the basal ganglia (extrapyramidal system)?

  1. Motor and other areas of cortex

    Thalamus (sensory relay)

    Substantia nigra

  2. Motor cortex (via thalamus)

  3. Initiation of movement

    Control of body posture and tone

  4. Reduced neurotransmitter levels (dopamine in Parkinson’s disease)

    Reduced voluntary movement (akinesia)

    Slow movement (bradykinesia)

    Increased tone (cog wheel or lead pipe)

    Involuntary movements (dyskinesia) - resting tremor (decreases with action), chorea, hemiballismus

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