Motor Learning and Neurological Syndromes Flashcards

1
Q

Which cortical area is involved with voluntary movement?

A

The Primary Motor Cortex

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2
Q

Voluntary movement follows a monosynaptic pathway from

A

the cortex through an upper motor neuron, which synapses in anterior horn of the spinal cord

the lower motor neuron then synapses at the muscle

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3
Q

Primary Motor Cortex: Which Broddmann area?

A

4

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4
Q

Parasaggital Meningioma:

A

slow brain tumours, very little symptoms or notice symptoms because the tumour grows slowly

causes upper motor neuron symptoms due to pressure on the bones

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5
Q

Upper Motor Neuron Disorders; Signs:

A
  • weakness
  • spasticity
  • brisk reflexes
  • babinski’s sign:
    - normal flexion
    - extension and flaring

upper motor neurons come from the cortex, through spinal cord

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6
Q

Upper or lower motor neuron disease?

A

insert slide

upper motor neuron symptoms:
some flexor muscle movement
stronger extensors
increased tone
brisk reflexes

maintain posture due to spasticity

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7
Q

Lower Motor Neuron Disease: Signs:

A
  • weakness
  • wasting of muscles
  • fasciculations
  • reduction in tone
  • reduced reflexes

anterior horn cell to muscle cell

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8
Q

Hierarchy of Control (3):

A

Strategy Level:
- goal of movement
- association areas of neocortex, basal
ganglia

Tactics Level:
- sequence of muscle contractions to
accurately achieve goal
- motor cortex, cerebellum

Execution Level:
- activation of motor and interneuron
pools to generate movement and
corrections
- brainstem, spinal cord

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9
Q

How Do We Start Planning a Movement?

Higher Cortical Regions

A
  • perceptual mechanisms generate a
    sensory representation of external
    world and individual
  • posterior parietal cortex
  • cognitive processes decide on course of
    action
  • frontal lobes
  • motor plan relayed to action systems to
    implement
  • primary motor cortex
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10
Q

Posterior Parietal Cortex: Brodmann Area:

A
  • area 5
  • area 7
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11
Q

Premotor Area: Brodmann Number:

A

area 6

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12
Q

Movement: Role of the Posterior Parietal Cortex:

A
  • input from the spinothalamic
    tract/dorsal columns via the thalamus
  • input from visual afferents
  • localises body in space
  • integrates sensory and visual
    information
  • passes on information to the premotor
    area
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13
Q

Movement: Posterior Parietal Cortex: Damage:

A
  • damage leads to neglect
  • problem with mental image
  • able to perceive but not attend to
    information
  • eg. drawing clock but all numbers are
    squashed on one side
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14
Q

Movement: Role of the Premotor Area:

A

Lateral Premotor Cortex (PMC):
- input from the posterior parietal
cortex and cerebellum
- output via descending spinal tracts
- important in movements requiring
visual guidance

Medial Supplementary Motor Area:
- input from basal ganglia and the
posterior parietal complex
- output to the primary motor
cortex/spinal cord
- involved in co-ordinating more
complex voluntary movement

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15
Q

Premotor Area:

A

Lateral Premotor Cortex (PMC):
- input from the posterior parietal
cortex and cerebellum
- output via descending spinal tracts
- important in movements requiring
visual guidance

Medial Supplementary Motor Area:
- input from basal ganglia and the
posterior parietal complex
- output to the primary motor
cortex/spinal cord
- involved in co-ordinating more
complex voluntary movement
- involved in the intention to move

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16
Q

Apraxia:

A
  • inability to carry out skilled movements
    in the absence of paralysis
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17
Q

Ideational Apraxia:

A

unable to put together higher sequences to perform action eg show me how to brush your hair

18
Q

Ideomotor Apraxia:

A

unable to use tool
eg. show me show to use these scissors

19
Q

Utilisation Behaviour:

A

lesion in the prefrontal cortex/ supplementory motor area

20
Q

Motor Control of Movement:

A

motor regions feed in to basal ganglia and cerebellum
cerebellum into brainstem then spinal cord
then to sensory receptors

21
Q

Basagl Ganglia/Nuclei:

A

comprises of the striatum:
- caudate nucleu, putamen, nucleus
accumbens

comprises of the globus pallidus (external
and internal which extends to midbrain as a reticular part of substantia nigra)

subthalamic nucleus

pigmented compact part of substantia nigra

22
Q

Basal Ganglia: Movement:

A
  • segregated into circuits to control
    movement
  • circuits begin in the motor cortex
  • cross basal ganglia
  • return to cortex
  • don’t initiate movement but involved in
    control
23
Q

Basal Ganglia: Motor Loops:

A
  • direct pathway promotes activity
  • indirect pathway promotes inhibition
24
Q

Both the direct and indirect pathways of basal ganglia motor loops receive excitatory cortical inputs which are ——ergic

A

glutamatergic

25
Q

Both the direct and indirect pathways of basal ganglia motor loops receive modulatory ——ergic input from the

A
  • dopaminergic
  • substantia nigra
26
Q

Pathways within basal ganglia are —-ergic

A

GABAergic
inhibitory

27
Q

Output from the basal ganglia and thalamus is tonically active but affected by

A

the direct and indirect motor loop pathways

28
Q

Basal Ganglia: Motor Loops: Direct Pathway:

A
  • messages from the sensorimotor cortex
    stimulate the putamen and caudate
    nucleus
  • stimulates inhibitory neurons to the
    globus pallidus
  • the inhibitory neurons REDUCE
    inhibition to the thalamus
  • net result is increase in activity from the
    thalamus to the supplementary motor
    area and back to the motor cortex
  • results in promotion of activity
29
Q

Basal Ganglia: Motor Loops: Indirect Pathway:

A
  • pathway activated by the supplementary
    cortex
  • message from putamen/caudate
    nucleus to globus pallidus externa is
    inhibitory
  • message then reduces inhibitory input
    to the subthalamic nucleus
  • this increase stimulation to the globus
    pallidus interna
  • increases the inhibitory signal to the
    thalamus therefore reducing the output
    to the supplementary motor area
  • promotes inactivity
30
Q

What is the main role of the motor loops of the basal ganglia?

A

to reinforce the chosen motor action
to inhibit unwanted action

31
Q

Loss of inhibition from basal ganglia leads to

A

involuntary movements
hyperkinetic disease
eg: huntington’s disease

32
Q

The cerebellum is connected to the brainstem by

A

the inferior and middle peduncles which are mainly afferents

the superior peduncle which is mainly efferent

33
Q

All input into the cerebellum is excitatory or inhibitory?

A

excitatory

34
Q

Cerebellar: Efferents:

A
  • efferents from the cerebellar cortex are
    from purkinje cells
  • inhibitory (GABA)
  • project to the cerebellar nuclei
  • efferents from cerebellar nuclei are
    excitatory
35
Q

Feedback pathway between the motor cortex and the cerebellum:

A
  • afferents from the cerebral motor
    cortex synapse in the pons with
    afferents into the cerebellum
  • these afferents synapse with fibers in
    the dentate nucleus in the cerebellum
    and are excitatory
  • afferents to the cerebellar cortex also
    stimulate purkinje fibers which inhibit
    the dentate nucleus
  • dentate nucleus feeds back to the
    cerebral cortex via the thalamus
  • influences motor output from the
    primary motor cortex
36
Q

Pathway between the Vestibular Nuclei, Cerebellum and Spinal Cord:

A
  • balance information from the vestibular
    apparatus sends afferents to the
    cerebellum
  • efferents from the fastigial nucleus
    synapse with the vestibulospinal tracts
37
Q

Relationship of Reticular Nuclei and Spinal Tractss:

A
  • afferents from pontine and medullary
    reticular formations
  • efferents to spinal cord via reticulospinal
    tracts
  • facilitates the extension of limbs
38
Q

Tectospinal Pathway:

A
  • originates in the superior colliculus in
    the midbrain
  • input from visual cortex
  • helps create a visual map to coordinate
    eye movements and head control

descending pathway

39
Q

The rubrospinal pathway activates

A

flexor muscles in the arms

40
Q

Midline cerebellar lesions

A

affect trunk and axial muscles
wide based gait seen (gait ataxia)

41
Q

Hemisphere cerebellar lesions cause

A

unilateral deficits
function on same side as lesion

nystagmus
intention tremor