6 Disorders of the motor system and Parkinson's disease Flashcards

1
Q

what structured form the lentiform nucleus?

A
globus pallidus (interna and externa) 
putamen
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2
Q

what is a DAT SCAN?

A

DaTscan is a tool used to confirm the diagnosis of Parkinson’s disease. It is a specific type of single-photon emission computed tomography (SPECT) imaging technique that helps visualize dopamine transporter levels in the brain. high levels will show as red/blue. low levels as green.

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3
Q

what are the basal ganglia?

A

The basal ganglia are situated at the base of the forebrain and top of the midbrain. The basal ganglia are associated with a variety of functions, including control of voluntary motor movements, procedural learning, habit learning, eye movements, cognition, and emotion.

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4
Q

what are the key components of the basal ganglia?

A

caudate nucleus
putamen
globus pallidus
subthalamic nucleus

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5
Q

what 2 components form the striatum?

A

the caudate and the putamen

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6
Q

what is the substantia nigra?

A

The substantia nigra is a part of the midbrain. Sits deep to the cerebral peduncles. Contains dopaminergic neurones that send their axons up to the striatum in the nitro-striata pathway.

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7
Q

how is the putamen connected to the caudate nucleus?

A

via grey matter bridges

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8
Q

what does the striatum receive input from?

A

the cortex

substantia nigra

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9
Q

what is the function of the basal ganglia?

A

Probable role in reinforcing appropriate movements and

removing inappropriate movements.

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10
Q

how does dopamine facilitate movement?

A

By exciting the motor cortex
(excites direct pathway by stimulating excitatory D1 receptors on striatal neurones taking part in the direct pathway, inhibits indirect pathway by activating inhibitory D2 receptors on striatal neurones taking part in the indirect pathway)

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11
Q

if the substantia nigra is affected unilaterally, how will this manifest?

A

Basal ganglia regulate ipsilateral motor cortex, hence if SNc is affected unilaterally (rare) there will be contralateral signs due to decussation of the corticospinal tract

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12
Q

what is the underlying pathology in parkinsons disease?

A

Caused by degeneration of dopaminergic neurones in SNc
Therefore have lost the dopamine-driven facilitation of
movement via both pathways

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13
Q

what are the signs and symptoms of parkinsons disease?

A

• Tremor (unclear mechanism, but may be related to
dysfunction of indirect pathway which would normally
suppress unwanted movements)
• Rigidity (unknown mechanism, may be related to lack of co-ordination between agonists and antagonists)
• Bradykinesia (best understood mechanism. Slow
movements due to loss of cortical excitation)
• Hypophonia (quiet speech = bradykinesia of larynx and
tongue)
• Decreased facial movement / mask-like faces (bradykinesia of face)
• Micrographia (small handwriting = bradykinesia in hands)
• Dementia (possible progression of currently unknown causative agent (e.g. protein aggregates))
• Depression (basal ganglia also have a role in cognition
and mood)

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14
Q

what is huntingtons chorea?

A

Autosomal dominant, progressive disorder
Early onset around 30-50 years old
Early stages associated with loss of inhibitory projections from striatum to GPe
This leads to hyperkinetic features (increased movement)

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15
Q

what are the features of huntingtons disease?

A

• Chorea (dance-like movements due to increased motor cortex activation)
• Dystonia (uncomfortable contractions of agonists and
antagonists simultaneously leading to odd postures
caused by over activity in agonist/antagonist muscle
circuits and loss of co-ordination between these)
• Loss of co-ordination (similar to above presumably)
• Cognitive decline and behavioural disturbances (related to role of basal ganglia in higher metal functions)

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16
Q

what is hemiballismus?

A

a basal ganglia syndrome resulting from damage to the subthalamic nucleus in the basal ganglia. Hemiballismus is a rare hyperkinetic movement disorder, that is characterized by violent involuntary limb movements, on one side of the body, and can cause significant disability.

17
Q

what can cause hemiballismus?

A

Can be caused by sub-cortical stroke (lacunar infarct) causing damage to the subthalamic nucleus

18
Q

what is the structure of the cerebellum?

A

midline vermis and two laterally placed hemispheres

19
Q

how do the cerebellar hemispheres communicate with the rest of the CNS?

A

through the cerebellar peduncles

20
Q

what is the function of the different cerebellar peduncles?

A
  • Superior cerebellar peduncle connects to midbrain
  • Middle cerebellar peduncle connects to pons
  • Inferior cerebellar peduncle connects to medulla
21
Q

why can cerebellar lesions cause hydrocephalus?

A

as the cerebellum sits above the fourth ventricle and a lesion here can occlude the cerebral aqueduct causing hydrocephalus

22
Q

what is the function of the cerebellum?

A

role in the sequencing and co-ordination of movements.
Uses sensory information to decide upon the most appropriate sequence of movements to perform an action. Works with basal ganglia which decide most appropriate movements. Cerebellum then sequences these movements.

23
Q

what inputs does the cerebellum receive?

A

cerebellum has profuse sensory inputs from

proprioceptive neurones and the sensory cortices

24
Q

what are the outputs of the cerebellum?

A

outputs are to the

contralateral motor cortex

25
Q

does damage to the cerebellum manifest ipsilaterally or contralaterally?

A

ipsilaterally as the corticospinal tract between the PMC and the cerebellar hemisphere decussates. the sensory input into the cerebellum is ipsilateral.

26
Q

what are the signs of cerebellar disease?

A

DANISH

  • Dysdiadochokinesia
  • Ataxia
  • Nystagmus
  • Intention tremor
  • Slurred speech (dysarthria)
  • Hypotonia
27
Q

how is the thalamus associated with the basal ganglia?

A

when the basal ganglia are communicating back with the PMC, impulses have to move through the thalamus.

28
Q

the cerebellum receives sensory input from 2 sources, what are they?

A

contralateral primary sensory cortex
ipsilateral impulse from the spino-cerebellar tract in the spinal cord. carry information from proprioreceptors in the muscles

29
Q

what is the corticospinal pathway?

A

a motor pathway running from the primary motor cortex, through the internal capsule and decussates at the medulla before travelling down the spinal cord to the level of the target muscle. Then synapses at the LMN.
chain of 2 neurones that mediate movement and behaviours.

30
Q

what is the corticostriatal pathway?

A

a pathway that starts at the primary motor cortex. projects down to the ipsilateral striatum (putamen and caudate nucleus). allows motor plan to be analysed by the basal ganglia before the results being sent back to the PMC

31
Q

what is the pallidothalamocortical pathway?

A

a pathway from the globus pallidus via the thalamus to the pmc. llows motor plan to be analysed by the basal ganglia before the results being sent back to the PM. works alongside the corticostriatal pathway to create a loop

32
Q

what is the nigrostriatal pathway

A

pathway between the substantia nigra and the striatum. substantia nigra sits in the midbrain, axon projects up to the striatum to provide a source of dopamine to the basal ganglia

33
Q

what is the corticopontocerebellar pathway.

A

allows the pmc to communicate the motor plan to the cerebellum. 1st neurones is from the pmc to the pons to synapse on a neurone of the pontine nuclei. These then decussate to the contralateral cerebellar hemisphere

34
Q

what is the cerebello-thalamo-cortico pathway?

A

neurones in the cerebellum communicate with the contralateral thalamus to send an impulse of the correct sequence of the motor plan. 2nd neurone from thalamus to the pmc.

35
Q

what is the spinocerebellar pathway?

A

collects information from muscle spindle fibres. sensory pathway travels up in the dorsal spinocerebellar tract to the ipsilateral cerebellar hemisphere

36
Q

the internal capsule is a continuation of which structure?

A

the corona radiata

37
Q

what can be found at the genu of the internal capsule?

A

the axons of the facial UMN