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NEUROSCIENCE 2 > LECTURE 13 - motor systems 2 > Flashcards

LECTURE 13 - motor systems 2 Flashcards

1
Q

What are the 3 main roles of the cerebellum?

A
  • sensorimotor coordination (circuitry receives info, processes and sends it out again) damage to cerebellum = inhibits persons ability to move
  • control of muscle tone (keep you standing)
  • motor learning e.g. memory about movement
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2
Q

What are the 3 functional and anatomical components of the cerebellum?

A
  1. Spino-cerebellum
  2. Vestibulo-cerebellum
  3. Cerebro- (ponto-) cerebellum
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3
Q

What is the spino-cerebellum?

A
  • medial region
    Connections and functions
  • sensory input from the spinal cord
  • output to the reticular formation and red nucleus then
    –> motor cortex
    –> output to spinal cord
    –> control over axial musculature and posture
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4
Q

What is the vestibulo-cerebellum?

A
  • caudal region
    Connections and function:
  • input from and output to vestibular nucleus (ventromedial pathway)
  • control over posture/ balance, also eye movement
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5
Q

What is the cerebro-cerebellum?

A
  • lateral hemispheres of the cerebellum
    Connections and function:
  • an intracerebral motor loop

cortex –> pons –> cerebellum –> dentate nucleus (deep cerebellar nucleus) –> ventrolateral thalamus –> cortex (M1)

  • instructs the primary motor cortex (M1) regarding movement direction, timing and force
  • sequencing of motor movements that can be sent to different muscle groups
  • compares intended movements with actual movements, sends compensatory instructions to M1
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6
Q

What is ataxia?

A 
- unsteady, staggering gait 
Functional component:
- spino-cerebellum
- cerebro-cerebellum
- vestibulo-cerebellum
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7
Q

What is dysmetria?

A
  • inaccurate termination of movement
  • intention tremor
    Functional component:
  • spino-cerebellum
  • cerebro-cerebellum
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8
Q

What is hypotonia?

A
  • reduced muscle tone
    Functional component:
  • spino-cerebellum
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9
Q

What is nystagmus?

A
  • slow saccades
  • impaired eye movement
    Functional component:
  • vestibulo-cerebellum
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10
Q

What is dysarthria?

A
  • inarticulate speech due to poor oropharyngeal muscular control
    Functional component:
  • cerebro-cerebellum
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11
Q

What layers make up the cerebellar cortex?

A
  • molecular layer
  • Purkinje cell layer
  • granule cell layer
  • white matter
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12
Q

Where do inputs of the cerebellar cortex come from?

A
  1. Climbing fibres get input from inferior olive (receives sensory info from spinal cord) - climbing fibres have an excitatory influence on Purkinje fibres
  2. Mossy fibres from brainstem nuclei - indirectly excite Purkinje via parallel fibres of Granule cells
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13
Q

Where do outputs of the cerebellar cortex arise from?

A
  • only Purkinje cells - project to deep cerebellar nuclei

- only inhibitory signals

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14
Q

What are deep cerebellar nuclei?

A
  • DCN cells can compare input from mossy and climbing afferent input:
    • before (via collaterals from axons to P cell - excitatory) and
    • after cerebellar processing (via inhibitory P cell output)

==> an error signal

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15
Q

Describe the comparator/ timer/ regulator functions of the cerebellum

A
  • able to compare what has happened to what should have happened
  • intended movement = afference copy
  • actual movement = efference copy (sensory feedback)
  • direct input into DCN by mossy fibres and climbing fibres
  • same info sent through cerebellum via Purkinje fibres to see if there is a difference
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16
Q

What is the basal ganglia?

A
  • group of associated subcortical nuclei

- ‘dark basements of the brain’

17
Q

What is the cortico-basal ganglia-cortical loop?

A
  • entire cortex is involved in movement and sends info to basal ganglia
  • integrates motor and sensory info from the cortex
  • input into basal ganglia is all excitatory
  • relays back to the cortex via the thalamus
  • motor circuit output to premotor/ SMA cortex
  • selection and initiation of voluntary movement
18
Q

What is the motor loop?

A
  • another name for cortico-basal ganglia-cortical loop
  • excitatory input from cortex
  • outflow from basal ganglia is inhibiting thalamus
  • signal from PFC switches off outflow, losing inhibition = disinhibition
  • thalamus is now disinhibited so is now excited to send an excitatory signal to SMA to initiate a movement
19
Q

What are the structures of the basal ganglia?

A
  • Striatum (STR)
    • the caudate nucleus
    • putamen
    • nucleus accumbens
  • subthalamic nucleus (STN)
  • globus pallidus (GP): internal (GPi) and external (GPe)
  • substantia nigra
    • reticulata (SNr)
    • pars compacta (SNc) - contains dopaminergic cell bodies
20
Q

Describe the pathways of the internal organisation of the basal ganglia

A

Direct
- striatum –> SNr/Gpi (output stations) –> thalamus –> cortex –> striatum

Indirect:
- projections via GPe and STN

  • opposing effects on thalamocortical output
  • balance between the direct and indirect pathways
  • dopamine, derived from SNc plays a key modulatory role
21
Q

What effect does dopamine have on the direct pathway?

A
  • direct pathway serves to promote movement
  • dopamine acts on excitatory D1 receptors on striato - GPi/SNr
  • dopamine excites cells in striatum to cause more inhibition, decrease activity of SNr/GPi => decreased BG output
  • -> freeing thalamus = increased excitation => facilitated movement
22
Q

What effect does dopamine have on the indirect pathway?

A
  • indirect pathway serves to suppress movement
  • dopamine acts on inhibitory D2 receptors on striato - GPe neurons
  • inhibits output from striatum
  • more inhibition from GPe, less excitation from STN, decrease output from STN, less inhibitory outflow, decreased inhibitory outflow, increase thalamocortical output which leads to movement

Dopamine decreases activity of indirect pathway to facilitate movement

23
Q

What happens if there is an imbalance between direct and indirect pathways?

A

Motor dysfunction
Hypokinetic disorders e.g. Parkinson’s
Hyperkinetic disorders e.g. Huntington’s, Ballism, Tardrive Dyskinesia

24
Q

What is Parkinson’s disease?

A
  • tremor (usually resting tremor)
  • bradykinesia (slowness of movement)
  • rigidity (resistance to passive movement)
  • affects 0.1% of pop under 50; >50 = 1%
  • progressive disorder: –> dementia, depression, bladder disturbance
  • average survival ~ 15 years

Primary pathology
progressive degenerative loss (>80%) of nigro-strial dopaminergic pathway => problem initiating movement
- Lewy bodies are the pathological hallmark of PD

25
Q

Describe the neurobiology of PD i.e. how do we get PD?

A
  • dopamine loss in BG
  • losing influence on both pathways
  • ultimate result is more basal ganglia output than normal
  • excessive inhibition of thalami-cortical pathway
  • accompanied/ driven by increased activity in STN
26
Q

How can we treat PD?

A
  • drugs to boost dopamine in brain
  • L-DOPA (precursor for dopamine)
  • dopamine agonists
  • drugs that reduce dopamine breakdown (MAO-B inhibitors)
  • deep brain stimulation
27
Q

What are the problems with L-DOPA?

A
  • L-DOPA will elevate NAdr synthesis in sympathetic NS
  • so now non-brain penetrating carbidopa or benserazide co-administered to inhibit peripheral DOPA decarboxyl
  • effectiveness diminishes over 2-5 years primarily due to progressive nature of disease (lack of neurones to make dopamine anyway)
28
Q

What are some alternatives to L-DOPA?

A
  • bromocriptine/ pergolide (fairly non-selective)
  • pramipexole / ropinirole (more D2 receptor selective
  • apomorphine - reserved for advanced stage PD
  • selegiline - MAO-B inhibitor
  • amantindine - dopamine releaser
  • muscarinic ACh receptor antagonists e.g. benzhexol (offsets local circuit consequences of DA deficiency on cholinergic stratal interneuron

Problems include

  • nausea/ emetic effects (especially apomorphine)
  • psychotomimetic effects
29
Q

How can surgery be used to treat PD?

A
  • try to lesion or ablate STN

- overstimulation inactivates STN off

30
Q

What is Huntington’s disease?

A
  • excessive choreiform movement
  • uncontrollable, relatively rapid motor patterns

Primary pathology = loss of serial output neurons in indirect pathway

  • -> suppression of STN
  • -> dominance of direct pathway
  • -> decreased BG output
  • -> overactive thalamocortical pathway
  • —> involuntary movement
31
Q

How can Huntingtons disease be treated?

A

Drug treatments are symptomatic relief only

  • tetrabenazine (VMAT inhibitor, decrease DA storage and release)
  • chlopromazine (DA antagonist)
  • Baclofen (GABA-B agonist, decreases spinal reflexes
32
Q

What is hemiballismus?

A

Cause: damage to STN (usually to stroke, unilateral)
Effect: violent flying movements of limbs (contralateral)

33
Q

What is tardive dyskinesia?

A

Cause: increased DA receptor sensitivity, due to long term exposure to antipsychotic drugs (dopamine receptors antagonists)
Effect: uncontrolled movement, especially of facial and trunk muscles (extrapyramidal effects)

NEUROSCIENCE 2 (32 decks)

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