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PA20023 > Motor pathways and disorders > Flashcards

Motor pathways and disorders Flashcards

1
Q

What is the high level of motor control?

A

It involves the sensory and association neocortex basal ganglia and is involved in the planning and strategy of movement.

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2
Q

What is the middle level of motor control?

A

Tactics, preparation and direction - motor cortex cerebellum.

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3
Q

What is the low level of motor control?

A

It involves the brain stem and spinal cord and is involved in the execution of the movements.

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4
Q

Where does the control of voluntary movement occur?

A

Cortical pathways that go to the spinal cord that direct the actions of motor neurones in the direction and location you want to exert.

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5
Q

What are brain stem outputs involved in?

A

They are involved in specific control associated with sensory inputs - three principal pathways.

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6
Q

What is the basal ganglia involved in?

A

They initiate and select motor programmes to tell the brain what to do.

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7
Q

What does the thalamus do?

A

Provides information to the cerebral cortex to direct the motor output.

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8
Q

What is the cerebellum involved in?

A

Fine motor control.

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9
Q

What are reflexes and motor neurones involved in?

A

The actual movement of muscles.

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10
Q

Where do pyramidal neurones axons (in the motor cortex) project to?

A

All the way through the mid brain, medulla etc. down to the spinal cord.

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11
Q

What control of movement are pyramidal neurones involved in?

A

Voluntary control of movement - direct control from the cortex.

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12
Q

What is the Rubro-spinal pathway?

A

Arises from the red nucleus in the midbrain. This provides a descending input. It directs motor neurons, but doesn’t seem to have much function in humans.

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13
Q

What is the role of the red nucleus?

A

Some element of control limited to upper body muscles. (particularly in infants)

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14
Q

What does the colliculus do?

A

It associates muscle movement with vision

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15
Q

What do vestibular do?

A

Direct movement according to sound.

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16
Q

What are reticular nuclei involved in?

A

Posture control - the ability to stand up straight.

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17
Q

What is the visible structure of the striatum?

A

It has white stripes (striated) throughout it like. Grey and white.

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18
Q

What is not part of the basal ganglia, but the output from the basal ganglia goes via this structure?

A

The thalamus.

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19
Q

What is the substantia nigra?

A

Origin of dopamine pathways in the brain - dark coloured staining in the brain (nigra). It is divided into the zona compacta and zona reticulatar.

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20
Q

What does the basal ganglia do?

A

It narrows down information about cortical decision making, it then sends it to the thalamus back to the cortex as to what the output should be.

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21
Q

What is the prefrontal cortex involved in?

A

Deciding what to do - making a judgement.

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22
Q

What are the direct pathways through the basal ganglia?

A

The cortex excites the caudate/putamen which then excites the GPi. The inhibition of the thalamus is reduced which increases excitatory input to the cortex.

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23
Q

What are the indirect pathways through the basal ganglia?

A

The cortex excites the caudate/putamen which inhibits GPe. This causes inhibition of the STN to be reduced, resulting in increased excitation of the GPi. Inhibition of the thalamus is increased and excitatory input to the cortex is decreased.

24
Q

How can the pars compacta (SNc) modulate direct and indirect pathways through the basal ganglia?

A

The nigro-striatal dopamine pathway activates the direct pathway via D1. This inhibits indirect pathways via D2 and therefore balances the pathways.

25
Q

What is the cortico-cerebellar connections involved in?

A

Moment to moment adjustments and long term changes (motor learning).

26
Q

What are some motor disorders involving the basal ganglia?

A

Parkinson’s disease, Huntingdon’s disease, OCD, Tourette’s.

27
Q

What is Parkinson’s disease?

A

A hypokinetic disorder (decreased movement). There is impaired movement and tremors - an inability to produce muscle movement.

28
Q

What is Huntingdon’s disease?

A

A hyperkinetic disorder - increased, jerky involuntary movements.

29
Q

What is OCD?

A

Obsessive compulsive disorder. It is thought that there are lesions in the caudate/putamen that results in repetitive motor responses.

30
Q

What is Tourette’s syndrome?

A

Rapid sterotyped movements or sound.

31
Q

What causes Tourette’s syndrome and how can it be treated?

A

There is an increased activity in nigro-striatal pathways and it can be treated with dopamine D2 receptor antagonists.

32
Q

What are the statistics about Parkinson’s disease?

A

It is a progressive disorder that mostly affects the elderly. It is rare at below the age of 40. There is an increased risk with head trauma and potentially a genetic susceptibility.

33
Q

What is the survival time after diagnosis of Parkinson’s?

A

Around 10 years due to degradation of the brain.

34
Q

What are the symptoms of Parkinson’s disease?

A

Reduction of movement (akinesia), bradykinesia (slowness of movement), rigidity, tremor (pill rolling), poor balance, speech problems and progressively can cause depression, anxiety, sleep disturbance and cognitive dysfunction.

35
Q

What is the pathological cause of Parkinson’s disease?

A

There is a loss of dopamine cells from the pars compacta (SNc). There is degeneration of the nigro-striatal pathway.

36
Q

What is Parkinsonism?

A

A drug induced condition resulting in symptoms similar to that of Parkinson’s disease. Neuroleptics cause the D2 receptor to be blocked. MPTP also has similar effects.

37
Q

What is the case with dopamine neurones of Parkinson’s sufferers?

A

Their dopamine neurones have degenerated, died and disappeared.

38
Q

What are some of the genetic mutations involved with Parkinson’s disease?

A

Mutant synaptic proteins, mutant parkin, protein aggregation, oxidative stress and cell death.

39
Q

What are some of the knock-on consequences of SNc degradation?

A

No inhibiton of CP from the SNc so there is more inhibition of the GPe and less inhibition of the STN. This results in increased inhibition of the thalamus. Also less direct inhibition of the GPi, so reduced inhibition of the thalamus.

40
Q

What is the overall effect of SNc degradation?

A

There is decreased movement and more rigidity.

41
Q

How can Parkinson’s be treated?

A

Increasing DA synthesis by oral L-DOPA which is then converted to DA by DOPA-decarboxylase.

42
Q

What must oral L-DOPA be used in conjunction with?

A

Peripheral decarboxylase inhibitors - carbidopa, benserazide.

43
Q

What are the problems with the treatments for Parkininson’s?

A

There is progressive degeneration so there are time limits, dyskinesias (other motor symptoms due to increase in dopamine in other areas), nausea, hypotension, anorexia and psychosis.

44
Q

What are some dopamine receptor agonists?

A

Bromocriptine, pramipexole, apomortphine.

45
Q

What can be used to slow degradation of DA?

A

COMT inhibitors such as entacapone or MAO inhibitors such as selegiline.

46
Q

What can be used to cause dopamine release?

A

Amantadine.

47
Q

What are treatments for Parkinson’s used in combination with?

A

L-DOPA.

48
Q

What are some of the surgical ways that have been attempted to treat Parkinson’s?

A

Thalamotomy (destruction of the thalamus), pallidotomy (globus pallidus destroyed), nigral transplants and stem cell use.

49
Q

What is Huntington’s disease?

A

It is a progressive degenerative disorder with cognitive decline before motor. It is an inherited disorder that has low incidence and is common between 30 and 50 years of age.

50
Q

What are the symptoms of Huntington’s disease?

A

Chorea (involuntary jerking), grimacing, balance and gait problems, cognitive decline, memory loss, depression, swallowing and speech issues and death 10-20 yeas after diagnosis.

51
Q

What is the cause of Huntington’s disease?

A

Cell death in the caudate/putamen. This causes impaired striatal-nigral and striato-palladial transmission.

52
Q

What is one of the other causes of Huntington’s disease?

A

There is a mutant Huntington protein due to a genetic defect that causes expanded repeats of the codon for glutamine which can lead to apoptosis due to migration of the dense protein to the nucleus.

53
Q

What are the knock-on consequences of striatal degeneration?

A

Cortico-spinal activity is increased overall and the thalamic output is exaggerated which drives the frontal cortex and the rest of the cortex to become more active. This increases the cortico-spinal output.

54
Q

What can be used to treat Huntington’s?

A

Bacloden for antipasticity, D2 antagonists such as chlorpromazine, neuroprotection, caspase inhibitors to stop apoptosis and potential transplantation.

55
Q

What is ataxia?

A

A group of disorders that affect coordination, balance and speech.

56
Q

What are some of the causes of cerebellar dysfunction?

A

Genetic, trauma, stroke, alcohol and drugs.

57
Q

What can be degraded in cerebellar dysfunction?

A

Cerebellar cortex, spino-cerebellar pathways, ponto-cerebellar pathways, deep cerebellar nucli and cerebellar-cortico-pathways.

PA20023 (17 decks)

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