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A PA20023 > Motor pathways and disorders > Flashcards

Motor pathways and disorders Flashcards

1
Q

What are structures and functions in high level of motor control

A
  1. Structures: sensory and association neocortex, basal ganglia
    b. Functions: Planning and strategy
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2
Q

What are structures and functions in middle level of motor control

A
  1. Structures: motor cortex, cerebellum

2. Functions: tactics and preparation and direction

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3
Q

What are structures and functions in low level of motor control

A
  1. Structures: brain stem, spinal cord

2. Executions

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4
Q

What role does the cortico-spinal pathway have

A
  1. From cerebral cortex to spinal cord
  2. Huge long neurons
  3. Provides info to spinal cord to tell what to do
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5
Q

What role does the cortex-brainstem have

A
  1. Cortex- brainstem- VS, RS RuS
  2. In brainstem groups of neurons which are involved in different types of motor activity
  3. Groups of neurons coordinate activity and go to spinal cord
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6
Q

What role does the basal ganglia have

A
  1. Huge group of different neurons

2. With thalamus and cortex- involved in initiation and selection of motor programmes

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7
Q

What role does the cerebellum have

A
  1. Mostly involved in co-ordination and correction of motor activity
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8
Q

What role does the execution system have

A
  1. At spinal level
  2. Coordinate muscle contraction and movement
  3. Sensory receptors in muscles and joints etc involved in feedback to spinal cord to error correct
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9
Q

Describe cortico-spinal tract lateral pathway

A
  1. From motor cortex through mid-brain and medulla into spinal cord
  2. Single neuron
  3. Main pathway- lateral as runs in lateral part of brainstem
  4. Crosses over to opposite side of brain
  5. Voluntary control of movement
  6. Direct cortical control
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10
Q

Describe The rubro-spinal tract pathway

A
  1. From red nucleus through medulla to spinal cord
  2. Some involvement in control of movement- minor function in adults
  3. More important in development
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11
Q

Describe The ventro-medial motor pathways

A
  1. Originate in brainstem and mid brain
  2. Receive output from cortex but not direct
  3. Modify motor output associated with primary information
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12
Q

What does the superior colliculus do

A
  1. Superior colliculus allows coordination of visual information and movement
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13
Q

What does the Vestibular nuclei do

A
  1. Auditory information

2. In control of balance

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14
Q

What is the role of the basal ganglia

A
  1. Involved in passing information from cortex and processing it and sending it back to cortex so it can take into account planning to direct motor output
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15
Q

What are the structures in the basal ganglia

A
  1. Striatum
  2. Globus pallidus
  3. Subthalamic nucleus
  4. Substantia nigra
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16
Q

Describe the striatum

A
  1. Consist of putamen and caudate nucleus

2. If you cut through tissue it has striations

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17
Q

Describe the Globus pallidus

A
  1. Circular pale globular structure
  2. Two segments- internal and external
  3. Different functions between internal and external
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18
Q

Describe the subthalamic nucleus

A
  1. Thalamus processes massive amounts of sensory information and sends to cortex, also receives information from basal ganglia
  2. Thalamus is not part of basal ganglia
  3. It is major recipient of basal ganglia output
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19
Q

Describe substantia nigra

A
  1. Black or dark brown structure

2. Two compartments- Zona reticulata and zona compacta

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20
Q

Describe function of basal ganglia

A
  1. Prefrontal cortex- decision making, planning and execution
  2. Motor cortex- origin of output
  3. Sensory cortex- provides information from which a decision is made
  4. Basal ganglia processes decision making
  5. What motor commands to do and what to ignore
  6. Allows filter of information and pass it on to motor cortex to drive motor output
  7. Output from cortex to basal ganglia is mostly from prefrontal
21
Q

Describe the direct pathway through the basal ganglia

A
  1. Cortex excites CP- Sending excitatory information to caudate/putamen
  2. Caudate/putamen in direct part provides an output
  3. CP inhibits GPi which decreases inhibitory output to thalamus
  4. inhibition of thalamus is reduced
  5. excitatory input to cortex increased
22
Q

Describe the indirect pathway through the basal ganglia

A
  1. Inhibits the other motor commands that cortex wants to send out- refines information
  2. Cortex excites CP
  3. CP inhibits GPe
  4. GPe inhibition of STN is reduced
  5. STN excitation of Gpi increases
  6. GPi inhibition of thalamus is increased
  7. excitatory input to cortex decreased
23
Q

Describe modulation by SNc

A
  1. Nigro-striatal dopamine pathway
  2. Additional level of control – based on reward and motivation for movement
  3. Activates direct pathway via D1
  4. Inhibits indirect via D2
  5. balances the pathways
24
Q

Describe Cortico-cerebellar connections

A
  1. Cerebellar processing is massively complicated!!
  2. moment to moment adjustments
  3. Long term changes - motor learning
25
Q

Where does the cerebellum fit in?

A
  1. Involved in
  2. positional control
  3. directional control
  4. error correction
  5. learning
  6. mainly responds to sensory input instead of decision-making input
26
Q

What are some Motor disorders involving the basal ganglia

A
  1. Parkinson’s disease
  2. Huntington’s disease
  3. Associated disorders
  4. Obsessive-compulsive disorder
  5. Tourette’s syndrome - rapid stereotyped movements or sounds
27
Q

What happens in Parkinson’s disease

A
  1. Hypokinetic - impaired movement, tremor

2. Decreased activity

28
Q

What happens in Huntington’s disease

A
  1. Hyperkinetic - chorea
29
Q

What happens in OCD

A
  1. Lesions in caudate/putamen - repetitive motor responses

2. Treated with SSRIs

30
Q

What happens in Tourette’s syndrome

A
  1. Increased activity in nigro-striatal pathway

2. Treated with dopamine D2 receptor-antagonists

31
Q

What are basics of Parkinson’s Disease

A
  1. 1817 - James Parkinson – shaking palsy
  2. Progressive - dementia - cognitive decline
  3. 0.1% of population, disease of the elderly
  4. Rare at <40 yrs
  5. > 50 yrs - 1%
  6. Increased risk with head trauma
  7. Genetic susceptibility?
  8. Environmental and drug induced
  9. Survival time ~10yrs
  10. Drugs do not alter progression
32
Q

What are Parkinson’s disease symptoms

A
  1. akinesia - the absence or reduction of movement
  2. bradykinesia - slowness of movement
  3. rigidity - resistance to passive movement
  4. tremor - pill rolling
  5. poor balance
  6. speech problems
  7. progressively
  8. depression, anxiety, sleep disturbance, cognitive dysfunction
33
Q

Describe Parkinson’s Disease - pathology

A
  1. Primary - loss of DA cells from SNc
  2. Degeneration of nigro-striatal pathway
  3. Genetic mutations
  4. Parkinsonism - drug induced
34
Q

How can genetic mutations cause Parkinson’s disease

A
  1. Mutant synaptic proteins (alpha-synuclein) – aggregation form big clumps of tissue within the cells
  2. Mutant Parkin (ligase) - prevents proteolysis- leads to big blobs of proteins in cells – Lewy bodies
  3. Protein aggregation - inclusion (Lewy) bodies
  4. Oxidative stress - mitochondrial dysfunction
  5. Cell death
35
Q

How can parkinson’s disease be drug induced

A
  1. Neuroleptics- in schizophrenia patients can get Parkinson symptoms from drugs
  2. MPTP
36
Q

What are the Knock-on consequences of SNc degeneration

A
  1. Loss of DA neurones - imbalance in direct and indirect pathways
  2. Lost influence over striatum
  3. Lose dopamine inhibition so very strong inhibition of STN
  4. increases activation of Gpi via indirect
  5. Decreases inhibition via direct
  6. Increases inhibition of thalamus
  7. Switches off thalamo-cortical pathways
  8. Loss of cortico-spinal output
  9. Decreased movement, rigidity etc
37
Q

How can you treat Parkinson’s

A
  1. Dopamine synthesis and inactivation
  2. Increase DA synthesis
  3. DA receptor agonists- Activating Dopamine receptors
  4. retard degradation
  5. DA release - amantadine
  6. Combination therapy with L-DOPA
  7. Deep brain stimulation with electrodes
  8. Surgery
  9. Thalamotomy
  10. Pallidotomy
  11. nigral transplants
  12. stem cells?
38
Q

Dopamine synthesis and inactivation

A
  1. Inactivation via uptake, MAO and COMT
  2. Uptake transporter specific for DA
  3. L-DOPA elevates synthesis as rate limiting
  4. Can use uptake blockers or stop breakdown
39
Q

How can you increase dopamine synthesis

A
  1. Oral L-DOPA - first line
  2. Converted to DA by DOPA-decarboxylase
  3. Combined with peripheral decarboxylase inhibitors (carbidopa, benserazide).
  4. 80% improvement - 20% full recovery
  5. However…
  6. Time limited - progressive degeneration
  7. dyskinesias
  8. On-Off syndrome (swinging)- effect disappears
  9. nausea
  10. hypotension
  11. anorexia
  12. psychosis
40
Q

Give examples of dopamine receptor agonists

A
  1. bromocriptine, pramipexole, apomorphine
41
Q

What is retard degradation

A
  1. COMT inhibitors - entacapone

2. MAO inhibitors - selegiline

42
Q

What does deep brain stimulation with electrodes affect

A
  1. STN

2. Disruption of GPi

43
Q

What is Huntington’s disease

A
  1. Progressive degenerative
  2. Cognitive decline before motor
  3. Low incidence 0.01%
  4. Appears between 30 and 50yrs (2 > 70)
  5. Inherited disorder - 50% chance of defective gene
44
Q

What are Huntington’s disease symptoms

A
  1. Chorea - involuntary jerking
  2. Grimacing
  3. Balance and gait problems
  4. Cognitive decline, memory loss, depression
  5. Swallowing and speech
  6. Death 10-20 years following diagnosis
45
Q

What is the pathology of Huntington’s disease

A
  1. Primary - cell death in caudate/putamen
  2. Impaired striatal-nigral and striato-pallidal transmission
  3. Nigro-striatal preserved
  4. progressive - degeneration of GP following on from striatal degeneration
  5. Huntingtin protein - normal function unclear
  6. Mutant huntingtin - genetic defect
46
Q

How does mutant huntingtin protein lead to the disease

A
  1. Expanded repeats of codon for glutamine
  2. Overexpression of huntingtin
  3. Dense protein aggregates migrate to nucleus
  4. Apoptosis - cell death
47
Q

What are Knock-on consequences of striatal degeneration

A
  1. Loss of caudate neurones
  2. Lose output from caudate
  3. decreased inhibition of GPe
  4. therefore increased inhibition of STN- so shuts down and provides less input to GPi
  5. Decreased excitation of GPi/SNc
  6. Decreased inhibition of thalamus
  7. Increased thalamo-cortical activity
  8. Increase in cortico-spinal output
  9. Hyperkinesia, facial tics etc
48
Q

How do we treat Huntington’s disease?

A
  1. No cure
  2. Baclofen (antispasticity)- lower output from spinal cord to muscles
  3. D2 antagonists (e.g. chlorpromazine)
  4. Treat symptoms e.g. depression
  5. Neuroprotection
  6. Caspase inhibitors - apoptosis??
  7. Transplantation?- replace caudate tissue- not effective so far
49
Q

What is Ataxia

A
  1. Cerebellar dysfunction
  2. Fine motor control, gait and co-ordination
  3. Multiple types and causes - genetic, trauma, stroke, alcohol and drugs
  4. Degeneration of
  5. cerebellar cortex
  6. spino-cerebellar pathways
  7. ponto-cerebellar pathways
  8. deep cerebellar nuclei
  9. cerebellar-cortico pathways
  10. No cure - treat the symptoms
  11. Some progressive - gradual incapacitation - some not

A PA20023 (19 decks)

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