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PT2 Neuro 6-9 > Basal ganglia and pathophys of movement disorders > Flashcards

Basal ganglia and pathophys of movement disorders Flashcards

1
Q

primary neurotransmitter released in lower motor neurons

A

acetylcholine

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2
Q

muscle receptors that sense stretch

A

muscle spindle receptors

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3
Q

sensory/afferent neurons

A

1a

1b

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4
Q

sensory neuron that synapses with inhibitory interneuron

A

1b

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5
Q

sensory neuron that synapses with a motor neuron in spinal cord

A

1a

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6
Q

1b fiber causes release of

A

glycine (inhibitory)

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7
Q

1a fiber causes release of

A

glutamate (excitatory)

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8
Q

intermotor neuron is located between

A

1b fiber and motor neuron

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9
Q

intermotor neuron releases what when activated

A

GABA

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10
Q

motor cortex (M1) map

A
  • map of body movement

- amount of cortex is directly related to precision of movement needed

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11
Q

supplementary motor cortex

A
  • thought to be involved in planning and sequencing of movements
  • projects to MI
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12
Q

premotor cortex

A
  • recieves input from sensory/parietal cortex of brain
  • involved in preparatory actions for movement and posture
  • projects to M1, spinal cord, and reticular formation in brainstem
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13
Q

upper motor neurons originate where

A

cell bodies in cortex and brainstem

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14
Q

upper motor neurons synapse with

A

lower motor neurons

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15
Q

pyramidal system

A

direct pathway to movement from cortical association area to premotor and motor cortex

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16
Q

extrapyramidal system

A

basal ganglia and cerebellum pathway to movement refining

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17
Q

damage to upper or lower motor neurons causes

A

paralysis

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18
Q

role of cerebellum

A
  • integrate proprioceptive information and motor plan into smooth movement
  • projections to motor cortex in planning and programming
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19
Q

proprioception

A

sensing of position of ones body is space and around joints

20
Q

basal ganglia is responsible for

A

action selection, how we choose a motor plan

21
Q

basal ganglia is made up of

A
  • subcortical brain structures

- caudate and putamen

22
Q

main input nucleus of basal ganglia

A

caudate/putamen

23
Q

where are dopamine neurons in basal ganglia

A

substantia nigra

24
Q

where do we do deep brain stimulation for parkinson’s

A

globus pallidus and subthalamic nucleus

25
Q

95% of neurons in caudate and putamen are

A

efferent

26
Q

D2 receptor activation leads to

A
  • inhibition of indirect pathway activity, decreases GABA release from caudate/putamen
  • ultimately thalamus excitation of cortex
27
Q

D1 receptor activation leads to

A

-activation of direct pathway activity, increases GABA release from caudate/putamen

28
Q

the main output nucleus of basal ganglia

A

internal globus pallidus

29
Q

sequence of direct (go) pathway of basal ganglia

A
  1. C/P and cortex excitation, D1 activation GABA release
  2. inhibition of GABA release in internal globus pallidus
  3. thalamus is active and releases glutamate
  4. excitation is sent to cortex which promotes a motor action
30
Q

sequence of indirect (no go) pathway of basal ganglia

A
  1. C/P and cortex excitation, D2 activation and GABA inhibition
  2. external globus pallidus not inhibited, so GABA release
  3. subthalamic nucleus is inhibited, so no glutamate release
  4. internal globus pallidus is not activated, no GABA release
  5. thalamus not inhibited, glutamate release
  6. activation in cortex
31
Q

myasthenia gravis pathophysiology

A
  • chronic autoimmune neuromuscular disease
  • antibodies target nicotinic acetylcholine receptors in neuromuscular junction
  • reduces concentration of acetylcholine receptors
32
Q

myasthenia gravis symptoms

A
  • drooping eyelid
  • blurred/double vision
  • slurred speech
  • difficulty chewing and swallowing
  • weakness in arms and legs
  • chronic muscle fatigue
  • all areas of finer muscle movement*
33
Q

treatment of myasthenia gravis

A
  • thymectomy (remove thymus and dampen antibody production)
  • immune suppression
  • plasma phoresis
  • corticosteroids
34
Q

treatment of myasthenia gravis symptoms

A

acetylcholinesterase inhibitors

35
Q

spasticity

A
  • chronic movement disorder in which certain muscles are continuously contracted
  • stems from motor cortex and affects motor neurons
36
Q

spasticity tied to

A
  • spinal cord injury
  • cerebral palsy
  • MS
  • stroke
  • ALS
37
Q

spasticity treatment

A

-decrease lower motor neuron excitation
OR
-increase inhibitory interneuron activity in spinal cord (baclofen)

38
Q

development of parkinson’s

A

degeneration of dopamine receptors in the substantia nigra

39
Q

motor symptoms of parkinson’s disease

A
  • bradykinesia
  • rigidity
  • tremor
  • postural instability (tendency to fall when pivoting)
40
Q

direct pathway in parkinson’s disease

A
  1. less dopamine so less GABA released from caudate/putament
  2. more GABA released from internal glubus palliuds
  3. very low glutamate released from thalamus
  4. decreased cortical activation
41
Q

indirect pathway in parkinson’s disease

A
  1. less dopamine so more GABA release from caudate/putamen
  2. external globus pallidus inhibited so less GABA release
  3. less inhibited subthalamic nucleus so greater glutamate release
  4. more activated internal globus pallidus so more GABA release
  5. greater inhibition of thalamus so low glutamate release and little cortex activation
42
Q

decreased cortical activation leads to

A

less movement

43
Q

cholinergic interneuron of caudate/putamen

A
  • has opposite effect of dopamine receptors
  • inhibits direct pathway
  • activates indirect pathway
  • makes up 5% of neurons in basal ganglia
44
Q

primary motor cortex

A

responsible for planning, initiating, and directing voluntary movements

45
Q

upper motor neurons release what neurotransmitter

A

glutamate

PT2 Neuro 6-9 (5 decks)

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