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BRS2 Term 1 > Motor control > Flashcards

Motor control Flashcards

1
Q

What are the pyramidal tracts? (examples, pathway, function)

A
  • corticospinal and corticobulbar tracts
  • cell bodies of upper motor neurons in motor cortex
  • -> pass through the medullary pyramids on ventral surface of brainstem
  • -> lower motor neurons in anterior horn of spinal cord OR cranial nerve nuclei (LMNs of corticobulbar) in brainstem
  • voluntary movements of body and face
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2
Q

What are the extrapyramidal tracts? (examples, pathway, function)

A
  • vestibulospinal, tectospinal, reticulospinal, rubrospinal
  • do not start in cerebral cortex
  • upper motor neurons in nuclei in brainstem–> axons travel down spinal cord
  • -> many synapse with interneurons to indirectly modulate movement
  • coordinate involuntary movements for balance, posture and locomotion
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3
Q

Where is the primary motor cortex?

A

located in precentral gyrus, anterior to central sulcus

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4
Q

What is the premotor area?

A
  • located anterior to primary motor cortex
  • involved in planning movements
  • regulates externally cued movements e.g. reaching for an object
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5
Q

What is the supplementary motor area?

A
  • located anterior to primary motor cortex and medial to premotor area
  • involved in planning complex movements e.g. internally cued speech
  • becomes active prior to voluntary movements
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6
Q

What is the difference between the anterior and lateral corticospinal tracts?

A
  • lateral corticospinal tract: crossed over fibres (85-90%), responsible for limb muscles
  • anterior corticospinal tract: uncrossed fibres (10-15%), innervate axial/trunk muscles
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7
Q

What is the function of the vestibulospinal tract?

A
  • stabilise head during body movements or head movements
  • coordinate head movements with eye movements
  • mediate postural adjustments
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8
Q

What is the function of the reticulospinal tract?

A
  • originates from medulla and pons

- postural stability and changes in muscle tone

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9
Q

What is the function of the tectospinal tract?

A
  • arises from superior colliculus of midbrain

- orientation of head and neck during eye movements

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10
Q

What is the function of the rubrospinal tract?

A
  • from red nucleus in midbrain

- mainly taken over by corticospinal tract in humans

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11
Q

What are the negative signs of upper motor neuron lesions?

A

loss of voluntary motor function

  • paresis: graded weakness of movements
  • paralysis (plegia): complete loss of voluntary muscle activity
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12
Q

What are the positive signs of upper motor neuron lesions?

A

increased abnormal motor function due to loss of inhibitory descending inputs
- spasticity: increased muscle tone (stiff muscles)
- hyperreflexia: exaggerated reflexes
- clonus: abnormal oscillatory muscle contraction
Babinski’s sign

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13
Q

What is apraxia?

A
  • disorder of skilled movement
  • not paretic, but lost information about how to perform skilled movements
  • stroke and dementia most common causes
  • lesion of inferior parietal lobe, or frontal lobe (premotor cortex, supplementary motor area/SMA)
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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- size and briskness)
  • muscle atrophy
  • fasciculation: damaged motor units produce spontaneous action potentials–> visible twitch
  • fibrillations: smaller spontaneous twitching of individual muscle fibres recorded during needle electromyography (invisible to naked eye)

*opposite to upper motor neuron lesion

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15
Q

What is motor neuron disease (MND)/ amyotrophic lateral sclerosis (ALS)?

A
  • progressive neurodegenerative disorder of motor system
  • affects upper motor neurons, lower motor neurons in brainstem (issues w/ voluntary contraction of tongue)
  • issues w/ intercostal muscles and voluntary contraction of upper and lower limb muscles
  • no cure
  • eventually results in death due to lack of respiratory muscle function
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16
Q

What are the upper motor neuron signs of motor neuron disease (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)
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17
Q

What are the lower motor neuron signs of MND?

A
  • muscle weakness
  • muscle wasting
  • tongue fasciculations and wasting
  • nasal speech
  • dysphagia
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18
Q

What are the functions of the basal ganglia?

A
  • decision to move
  • elaborating associated movements e.g. arms swinging when walking, changing facial expression to match emotions
  • moderating and coordinating movements (and suppressing unwanted movements)
  • performing movements in order
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19
Q

What is Parkinson’s disease?

A
  • degeneration of dopaminergic neurons that originate in the substantial nigra and project to the striatum
  • bradykinesia: slow small movements e.g. doing up buttons
  • hypomimic face: expressionless
  • akinesia: difficult in initiation of movements, as cannot generate movements internally
  • rigidity: inc. muscle tone, causing resistance to externally imposed joint movements
  • tremor at rest (4-7Hz): starts in one hand but spreads to other parts of body- ‘pill rolling tremor’
20
Q

What is Huntington’s disease?

A
  • degeneration of GABAergic neurons in the striatum, caudate and then putamen
  • choreic (dance-like) movements: rapid, jerky involuntary movements of body–> hands and face first, then legs an rest of body
  • speech impairment
  • dysphagia
  • unsteady gait
  • later stages, cognitive decline and dementia
21
Q

What is ballism?

A
  • sudden uncontrolled flinging of limbs
  • usually from stroke affecting subthalamic nucleus
  • symptoms occur contra laterally
22
Q

Where is the cerebellum located?

A
  • in posterior cranial fossa

- separated from cerebrum above by tentorium cerebelli

23
Q

What is the function of the cerebellum?

A
  • coordinates and predicts movements

- enables fluid movement

24
Q

What are the functions of the vestibulocerebellum?

A
  • regulation of gait, posture and equilibrium
  • coordination of head movements w/ eye movements
  • damage (tumour) causes syndrome similar to vestibular disease–> gait ataxia and tendency to fall (even when sitting)
25
Q

What are the functions of the spinocerebellum?

A
  • coordination of speech
  • adjustment of muscle tone
  • coordination of limb movements
  • damage (degeneration and atrophy w/chronic alcoholism) affects legs, causing abnormal gait and stance (wide)
26
Q

What are the functions of the cerebrocerebellum?

A
  • coordination of skilled movements
  • cognitive function, attention, processing of language
  • emotional control
  • damage affects mainly arms/skilled coordinated movements (tremor) and speech
27
Q

What are the main signs of cerebellar dysfunction apparent only on movement?

A
  • ataxia: general impairments in movement coordination and accuracy, disturbances of posture or gait–> wide based, staggering gait
  • dysmetria: inappropriate force and distance for target-directed movements e.g. knocking over cup rather than grabbing it
  • intention tremor:during target-directed movements (nose-finger tracking)
  • dysdiadochokinesia: inability to perform rapidly alternating movements e.g. rapidly pronating and supinating hands/forearms
  • scanning speech: staccato, due to impaired coordination of speech muscles
28
Q

What are alpha motor neurons?

A
  • ‘ventral/anterior horn cells’
  • the lower motor neurons of the brainstem and spinal cord
  • occupy ventral horn of grey matter of spinal cord
  • innervate the extrafusal muscle fibres
  • when activated, cause contraction of muscle fibres
  • motor neuron pool= all alpha motor neurons innervating a single muscle
29
Q

What is a motor unit?

A

a single motor neuron and all the muscle fibres it innervates- stimulation of 1 motor unit causes contraction of all muscle fibres in that unit
*Innervation ratio relates to function of muscle

30
Q

What are the 3 main types of motor unit?

A
  1. slow (S, type 1)
  2. fast, resistant (FR, type IIA)
  3. fast, fatiguable (FF, type IIB)
31
Q

What are the characteristics of the nerve fibres of slow motor units?

A
  • small diameter cell bodies
  • small dendritic trees
  • thinnest axons
  • slowest conduction velocity
32
Q

What are the characteristics of the nerve fibres of FR and FF motor units?

A
  • large cell bodies
  • large dendritic trees
  • thicker axons
  • faster conduction velocity
33
Q

Which type of motor unit generates the most force?

A

fast fatiguable

34
Q

What is recruitment in terms of regulation of muscle force?

A
  • if the CNS determines that more force is required, it can recruit a bigger number of motor neurons and therefore muscle fibres
  • ‘size principle’–> smaller units recruited first (usually slow twitch)
  • more force required–> more units recruited
  • allows fine control e.g. when writing
35
Q

What is rate coding in terms of regulation of muscle force?

A
  • motor unit can fire at a range of frequencies–> slow units fire at lower frequency
  • faster firing rate–> greater force generated
36
Q

What are neurotrophic factors?

A
  • type of growth factor that prevents neuronal death

- promote growth of neurons after injury

37
Q

What is the result of cross innervation where a muscle that is slow has a faster nerve implanted into it? What does this show?

A
  • starts to take on characteristic of a fast muscle
  • the motor neuron has some effect on the properties of the muscle fibres it innervates–> there can be some plasticity within motor unit types
38
Q

What are the most common situations in which motor units change types?

A
  • from IIB to IIA (fast fatiguable–> fatigue resistant) most common following training
  • type I–>II possible with severe reconditioning or spinal cord injury (e.g. microgravity in space results in shift from slow to fast)
  • loss of both type I and II fibres in elderly, but preferential loss of type II–> so larger proportion of type I fibres in aged muscle, leading to slower contraction times
39
Q

What is the Jendrassik manoeuvre?

A
  • when a reflex becomes larger if you clench your teeth, make a fist, or pull against locked fingers at the same time
  • reduces inhibition that CNS usually exerts over reflexes
40
Q

How does the brain influence reflex pathways under normal circumstances?

A
  • higher centres of CNS exert a resting level of inhibition that dampens down reflexes
  • surgical decerebration reveals this–> exaggerated reflexes
41
Q

What are gamma motor neurons?

A

lower motor neurons that don’t contribute to contraction of a muscle, but alter the sensitivity of the sensory organ in skeletal muscle/ intrafusal muscle fibres

42
Q

What is hyperreflexia?

A
  • overactive reflexes
  • due to loss of descending supra spinal inhibition
  • characteristic of upper motor neuron lesions
43
Q

What is clonus?

A
  • involuntary and rhythmic muscle contractions (hyperreflexia)
  • due loss of descending inhibition
  • characteristic of upper motor neuron lesions e.g. stroke
44
Q

What is Babinski sign?

A
  • when sole of foot stroked w/ blunt instrument e.g. spoon, toes curl downwards normally (esp. big toe)
  • if big toe curls upwards–> ABNORMAL in adults- +ve Babinski sign
  • associated w/ upper motor neuron lesion
    N.B. normal in infants
45
Q

What is hypo-reflexia?

A
  • below normal or absent reflexes

- associated w/ lower motor neuron lesions

BRS2 Term 1 (19 decks)

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