Motor control and Parkinson's disease Flashcards

1
Q

Function of association area in motor control

A

• The idea or decision of a movement originates in cortical association areas

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2
Q

Role of basal ganglia and cerebellum in motor control

A

responsible for modulating movements that has been initiated by primary motor cortex
• Basal ganglia unblock the cortex and allow desired movement to start, blocking any unwanted movement

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3
Q

Role of premotor areas in motor control

A

plans the sequence of muscle contractions that compose a complex movement

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4
Q

Role of pyramidal pathway

A

primary motor cortex is the main contributor to generate neural impulses that pass down to spinal cord/brain stem and gives the command for execution of voluntary movement

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5
Q

Role of voluntary muscles to cerebellum in motor control

A

receives both proprioceptive (sense of position weight of muscles) and kinesthetic (sense of movement) information from periphery
§ To evaluate the strength and type of muscle movements occuring
○ Checks how well the motor comands coming from the cortex are being carried out
§ And what minor adjustments needed to perfect the movement

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6
Q

What are the two sets of motor neurone and their function

A

upper motor neurone transmit impulse to voluntary muscles. • Neurons in layer V of motor cortex, descending fibres cross the medulla (decussation of pyramids),synapse with lower motor neuron is in the ventral horn of spinal cord (corticospinal tract) or in brain stem (corticobulbar tract)

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7
Q

Describe the difference between corticobulbar and corticospinal tract

A

corticobulbar conduct impulses from brain to cranial nerves and Control muscles of face and neck
Involved in facial expression, mastication, swallowing

Corticospinal conduct impulses from brain to spinal cord and are responsible for voluntary movement

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8
Q

Describe corticospinal tract

A
  1. The impulse for movement starts in primary motor cortex receiving input from premotor motor area, somatosensory(skin), proprioceptive (position) and visual stimuli to guide movement
    1. A white matter tract connecting the cortex with the underlying structures - internal capsule
    2. Upper motor neuron is the 1st neuron in pathway
    3. Bundles of upper motor neuron fibres cross the midline (decussate) in the medulla
    4. Descending fibres run through the lateral funiculus of the spinal cord and terminate in the ventral horn
    5. Upper motor neuron synapse directly with lower motor neurons which have cell bodies in ventral horn of spinal cord (cranial nerve nuclei in the corticobulbar tract
    6. Lower motor neurons then exit the spinal cord as spinal nerves and innervate effector muscles
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9
Q

Function of extrapyramidal tract

A

together with basal ganglia and cerebellum to fine tune movement

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10
Q

Function of reticulospinal tract

A

Controls orientation of the body towards or away from stimuli

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11
Q

Function of rubrospinal tract

A

Facilitates flexor movements in the upper limbs

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12
Q

Function of tectospinal tract

A

Neck musculature in response to visual stimuli, orientates the head during eye movement

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13
Q

Function of vestibulospinal tract

A

Help maintain balance, controlling postural adjustments mostly via neck and trunk muscles

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14
Q

What do basal ganglia includes

A

caudate, putamen, globus pallidus , subthalamic nucleus, substantial nivea

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15
Q

function of putamen

A

receives most excitatory input from cortex and thalamus

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16
Q

what is striatum

A

consists of caudate and putamen

17
Q

function of globes pallidus

A

output of basal basal ganglia, sending inhibitory projections to thalamus

18
Q

function of subthalamic nucleus

A

receives afferent from both cortex and other basal ganglia structure, output is excitatory to globes pallid us

19
Q

function of substantia nivea

A

contains dopaminergic neutrons that project to striatum

20
Q

What are the pathways in basal ganglia

A

direct pathways that includes corticostriatial pathway and nigrostiatal and indirect pathways

21
Q

describe corticostriatal pathway and nigrostriatal pathway

A
  1. Coticostriatial pathway
    • Excitatory projections run from cortex to striatum and synapse with striatal inhibitory neurons
    1. Inhibitory neurons from striatum project directly to the globus pallidus internal segment
    2. Thalamus is under tonic inhibition by inhibitory neurons from globus pallidus
      • When Gpi neurons are inhibited -> disinhibition of the thalamus
      Ø Increased output from thalamus
    3. Thalamus send excitatory signals back to the cortex
      • Facilitating intentional movement
    4. Subthalamic nucleus provides tonic stimulation to the substantia nigra
    5. Nigrostriatial pathway
      • Substantia nigra enhances the excitatory input from cortex
      § By releasing dopamine in the striatum, and activation of neurons expressing dopaminergic D1 receptors
22
Q

function of indirect pathway

A
  • Suppresses conflicting movements and actions not related to targeted behaviour
    • Inhibits output from the thalamus
      • Less excitation of the motor cortex and less motor output
23
Q

Describe indirect pathway

A
  1. Excitatory projections from cortex to the striatum synapse with inhibitory neurons
    1. Striatal inhibitory neurons project to the globus pallidus external segment (Gpe)
    2. Inhibitory projection from the Gpe goes to the subthalamic nucleus when these are inhibited
      Ø Result in disinhibition (activation) of subthalamic nucleus
    3. Subthalamic nucleus sends an excitatory projection to the globus pallidus internal segment (Gpi)
    4. Activation of Gpi increases tonic inhibition of the thalamus
      • Different thalamic neurons from those involved in the direct pathway
    5. Resulting in suppression of activation of the cortex
    6. Substantia nigra has inhibitory effect on subthalamic nucleus, in turn sends excitator projections to substantia nigra
      • Controls input to the basal ganglia
    7. Projections from substantia nigra to the striatum release dopamine, which has inhibitory effect on excitatory cholinergic interneurons in the striatum
      • Expresses D2 receptors
24
Q

Function of cerebellum

A
  • Coordinator and predictor of movement and mediates muscles control for skilled manipulation
    • Receives information from periphery concerning position of body parts and muscle tone
    • Compares and integrates information with plans for movement received from cortex
25
Q

What are some lower motor neuron disorder

A
  • Paresis (weakness)
  • Paralysis (loss of movement)
  • Loss of reflexes (efferent limb in reflex arcs is lost)
  • Loss of muscle tone (controlled by tonic activation of the LMNs by muscles spindles )
  • Muscle atrophy (wasting)
26
Q

What are upper motor neurone disorder

A
  • Damage in pyramidal -> Pyramidal motor disorder
    • Corticospinal tract (control muscles of the head and face)
    • Corticobulbar tract
  • Damage in extrapyramidal tracts (lesions of basal ganglia)
27
Q

What are negative extrapyramidal disorders

A
Postural disturbances (when parts of body are held in a fixed position 
	• Also seen in parkinson's disease 

Bradykinesia (slowness or loss of voluntary movement
• Feature of Parkinsons’s disease
• Reduced facial expression, reduced blinking

28
Q

what are positive extrapyramidal disorders

A

Tremor
• Typically at rest

Chorea (irregular, repetitive, jerky movement)
• In Huntington’s disease

Rigidity (increased muscle tone)

Ballismus (violent flinging movements

Athetosis (irregular, repetitive, writhing movements)

Dystonia (slow, sustained, abnormal movements)

Involuntary movements

29
Q

Name cerebellar disorders

A
  • Lesions (due to stroke, trauma, tumours or neurogenerative disease
    * Ataxia (loss of coordination and muscle tone
    * Intention tremor (occurring during movement, as a result of poor coordination of agonist-antagonist contractions)
    * Staggering gait
30
Q

What are characteristics of Parkinsons disease

A
  • Tremors of hand and jar
    • Hypokinesia
      • Ranging from bradykinesia to akinesia (loss of movements
    • Postural disturbances
31
Q

Cause of Parkinsons disease

A
  • Majority is sporadic (occur at irregular intervals)
    • 5-10% of familial with specific gene defects
    • Involve both genetic and environmental factors
    • Signs appear only after 70-90% of nigra neurons degenerated
32
Q

Mechanisms of pathophysiology of Parkinsons disease

A

Protein aggregation in Lewy bodies
• The protein α-synuclein has increased presence in the brains of Parkinson’s Disease patients
• as α-synuclein is insoluble, it aggregates to form Lewy bodies in neurons blocking neurotransmitter release

Disruption of autophagy

• Autophagy is a mechanism by which inner components of the cell are broken down and recycled
• playing a role in brain health, helping to regulate cellular function.
• Disruption of the autophagy mechanism can lead to Parkinson’s disease.
Changes in cell metabolism • mitochondrial function is disrupted, inhibiting energy production
• resulting in death.

33
Q

Effect of loss of dopaminergic neutrons on direct pathway

A

• Loss of this excitatory input to the striatum decreases the amplification of cortical input to the striatum.
Ø results in less excitatory input from the both the cortex and substantia nigra in the direct pathway.

34
Q

Effect of loss of dopaminergic neuron on indirect pathway

A

GpE inhibited and less inhibitory input to subthalmic nucleus
reduced inhibition of the sub thalamic nuclei cause an increased excitatory output to Gpi

Gpi send more inhibitory input to thalamus increasing tonic inhibition and less cortical output
less inhibitory projection from substantial migration to sub thalamic nucleus

Loss of dopamingeric signalling causes reduced inhibition of these excitatory interneurons

35
Q

Treatment of parkinson’s disease

A

COMT inhibitors preserve levodopa
Levodopa replaces dopamine
Dopamine agonists mimic dopamine
MAO-B inhibitors preserve dopamine
anticholinergic drugs to inhibit cholinergic interneuron in striatum
deep brain stimulation of sub thalamic nucleus