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cns > Session 5 - Motor disorders > Flashcards

Session 5 - Motor disorders Flashcards

1
Q

what is the basal ganglia?

A
  • the area of the brain known to be involved in motor function
  • it stimulates motor activity in the cerebral cortex
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2
Q

how does the basal ganglia communicate with the motor cortex?

A

via the thalamus

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3
Q

what does increased thalamic activity cause?

A

increased cortical activity

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4
Q

What is the striatum?

A
  • made upon the caudate nucleus - a c shaped nucleus that liens the lateral ventricle **and the putamen
  • the 2 structures are functionally related
  • role in facilitating voluntary movement
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5
Q

what are the different parts of the caudate nucleus?

A

it has a head, body and tail

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6
Q

what is the substantial nigra?

A
  • made up of the pars compact and the para reticular
  • SNc = a source of dopamine in the midbrain
  • Mickey Mouse eyebrows
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6
Q

in what condition does the substantial nigra degenerate?

A

Parkinson’s disease

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7
Q

what are the 2 parts of the globus pallidus?

A

internal and external segment

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8
Q

what is the lentiform nucleus?

A
  • made up of the globus pallidus (medial) and the putamen (lateral)
  • these 2 are anatomically related but not functionally related
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9
Q

what is the subthalamic nucleus?

A

a small area that sits beneath the thalamus

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10
Q

label the following parts of the basal ganglia in this coronal section of the brain

A
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11
Q

what neurones are the pars compacta and substantia nigra made up of?

A
  • dopaminergic neurones - they allow for inhibitory and excitatory control of movement
  • the presence of dopamine allows for an overall excitement giving motor cortex stimulation
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12
Q

what is the role of the basal ganglia?

A

role in reinforcing appropriate movements and removing inappropriate movements

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13
Q

what are the direct and indirect pathways of the basal ganglia?

A
  • direct pathway - reinforces appropriate movements → excitatory to the motor cortex
  • indirect pathway - edits out inappropriate movements → inhibitory to the motor cortex
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14
Q

what is the effect of dopamine on the 2 pathways?

A
  • dopamine facilitates movements by exciting the motor cortex
  • it excites the direct pathway by stimulating excitatory D1 receptors on striatal neurones taking part in the direct pathway
  • it inhibits the indirect pathway by activating inhibitory D2 receptors on striatal neurones taking part in the indirect pathway
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15
Q

what would happen if any part of the basal ganglia was damaged unilaterally in one hemisphere?

A
  • the basal ganglia loop and dopaminergic pathways (substantia nigra) all communicate with the motor cortex on the same side
  • but, the corticospinal pathway supplies the contralateral side and this pathway is kind of like the final pathway between all of them, so that means that damage to any of the basal ganglia structures, would lead to contralateral signs and symptoms
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16
Q

why does basal ganglia damage tend to be bilateral/symmetrical?

A

because damage here is commonly caused by neurodegenerative conditions meaning both sides will be damaged, eg. Parkinson’s and Huntington’s

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17
Q

in which fossa is the cerebellum located?

A

posterior cranial fossa

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18
Q

what does the cerebellum sit above?

A

the 4th ventricle

19
Q

what allows the cerebellum to communicate with the brainstem?

A

3 peduncles

20
Q

what do each of the cerebellar peduncles connect to?

A
  • superior cerebellar peduncle connects to the midbrain
  • middle cerebral peduncle connects to the pons
  • inferior cerebral peduncle connects to the medulla
21
Q

describe the anatomy of the cerebellum

A
  • it has a midline vermis
  • 2 laterally placed hemispheres
22
Q

what do the structures of the cerebellum have a role in?

A
  • vermis deals with the trunk
  • hemispheres deal with the ipsilateral side of the body
23
Q

what is the role of the cerebellum?

A
  • it assesses the position of the limbs via proprioceptors to determine an appropriate sequence for the motor plan
  • sequencing and coordination of movements
  • it uses sensory information to decide the most appropriate sequence of movements to perform an action
24
Q

how do the basal ganglia and cerebellum work together?

A

the basal ganglia decides the most appropriate movements and the cerebellum then sequences these movements

25
Q

how does the cerebellum communicate with the cerebral hemispheres?

A

via the thalamus

26
Q

what happens in the corticopontine pathway?

A
  • neurone from cortex goes down to pons and synapses to a neurone of the pontine nuclei
  • the neurones the pontine nuclei then decussate to the contralateral cerebral hemisphere
27
Q

thought which pathway does the cerebellum communicate with the motor cortex?

A
  • cerebello-thalamo-cortical pathway
  • neurones in the cerebellum hemispheres communicate with the contralateral thalamus
  • then the neurones of the contralateral thalamus communicate back to the motor cortex
28
Q

why does ipsilateral cerebellum damage lead to ipsilateral signs and symptoms in the body?

A
  • the spinocerebellar tract collects info from muscle spindles and the primary sensory neurones carry the information up to the ipsilateral side of the cord to the ipsilateral cerebellum
  • (2) therefore damage to the ipsilateral cerebellum means that the cerebellar hemisphere is unable to process information from the ipsilateral side of the body via the spinocerebellar tracts
  • also, because the cerebellar hemisphere communicates with the contralateral motor cortex (3) and that contralateral motor cortex communicates in turn with the contralateral side of the body (4) there’s no net effect (5)
  • therefore, ipsilateral cerebellar damage leads to ipsilateral signs and symptoms in the body
29
Q

what is dysdiadochokinesia?

A

difficult with rapidly alternating movements

30
Q

what is ataxia?

A
  • incoordination of voluntary movement
  • unsteady gait as a results of difficulty sequencing lower limb muscle contractions as well as loss of unconscious proprioception from lower limbs
31
Q

what is nystagmus?

A

flickering eye movements due to malcoordination of extraoccular muscles

31
Q

what is intention tremor?

A
  • a tremor that worsens as a target is approached
  • past pointing
32
Q

what is slurred speech (dysarthria)?

A
  • caused by maslcoordination of laryngeal and tongue musculature
  • drunk speech
33
Q

what is hypotonia?

A
  • decreased tone
  • pendular reflexes?
34
Q

What is the cause of Parkinson’s disease?

A
  • Degeneration of dopaminergic neurones in the SNc
  • Therefore lose the dopamine driven facilitation of movement in both direct and indirect pathways
  • The loss of dopamine gives less stimulation of putamen. Therefore, GPi is inhibited less so its activity increases. This results in more inhibition of the thalamus which leads to reduced cortex stimulation.
  • Lose activity in the motor cortex
  • causes decreased movement
35
Q

What are the signs and symptoms of Parkinson’s?

A
  • tremor - could be related to dysfunction of the indirect pathway which would normally suppress unwanted movements
  • Rigidity (lead pipe) - loss of balance between direct and indirect pathways/loss of coordination between sntiagnists and agonists
  • Bradykinesia - slow movements due to loss of cortical excitation
  • Hypophonia - quiet speech = bradykinesia of the larynx and tongue
  • Decreased facial movement/mask like fancies - bradykinesia of the face
  • Microphagia - small handwriting = bradykinesia of the hands
  • Dementia - possible progression of currently unknown causative agent eg. protein aggregates
  • Depression - basal ganglia also have a role in cognition and mood - psychiatric features can also be a Sid effect of treatment which increases dopamine
36
Q

what is Huntington’s?

A
  • an autosomal dominant, progressive neurodegenerative disorder due to cell loses within the striatum.
  • therefore the indirect pathway is switched off and there’s constant stimulation fo the motor cortex
  • causes increased movement
37
Q

what’s the onset of huntingtons?

A

early onset - 30-50 years old

38
Q

what are the early stages of Huntington’s associated with?

A
  • loss of inhibitory projections from the striatum to the GPe
  • this leads to hyperkinetic features → increased movements as the ‘brakes’ have been taken off the thalamus
39
Q

what are the features of Huntington’s?

A
  • chorea - dance like movements due to increased motor cortex activation
  • dystonia - uncomfortable contraction of agonists and antagonists simultaneously leading to odd postures caused by over activity in agonist/antagonist muscle circuits and loss coordination between these
  • loss of coordination
  • cognitive decline and behavioural disturbances - related to role of basal ganglia in higher mental function
40
Q

what is the cause of hemiballismus?

A
  • damage to the subthalamic nucleus which normally inhibits the thalamus via GPi
  • can be caused by sub-cortical stroke (lacunar infarct)
  • causes increased movement
41
Q

what does hemiballismus cause?

A

unilateral explosive (ballistic) movements

42
Q

which pathway does hemiballismus affect?

A

the indirect pathway

43
Q

what is motor neurone disease?

A

generative disease affecting both upper and lower motor neurones - therefore will have symptoms of both UMN and LMN damage

44
Q

what are the causes of MND?

A
  • most are sporadic
  • familial causes eg. mutations in the superoxide dismutase gene

cns (7 decks)

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