Motor Pathways: Basal Ganglia and Cerebellum Flashcards

1
Q

What are basal ganglia and cerebellum part of ?

A

Extrapyramidal system- this involves tracts like the rubrospinal tract. Basal ganglia and cerebellum are involved in regulating these tracts so are considered part of extrapyramidal system

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2
Q

Broadly speaking, what is the role of this system?

A

Main function is to regulate the motor signals of the pyramidal system (corticospinal tract) from the motor cortex.

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3
Q

Where is the basal ganglion located?

A

White matter in the middle of the brain

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4
Q

What are the different parts of the basal ganglia?

A

Striatum (lentiform (GP+putamen) + caudate)

Substantia Nigra (made of 2 parts: the pars compacta (SNpc) and the pars reticulata (SNpr))

Subthalamic Nucleus

ventral pallidum

nucleus accumbens

nucleus basalis of Meynert

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5
Q

What is the function of the basal ganglia?

A

Smoothness, associated movements and order of movements.
1.It elaborates movements that are associated together(e.g. swinging arms when walking)

  1. Contribute to the smoothness of complex action
  2. Involved in moderating and coordinating movements and performing movements in order

Think of the original motor signal as a coarse signal, the basal ganglia refines the signal (eg suppresses unwanted movements)

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6
Q

Describe the structure of the direct pathway in the basal ganglia.

A

Fibres initially come from the motor cortex to the striatum (caudate and putamen)
Direct Pathway: putamen –> globus pallidus internal segment + substantia nigra pars reticulata

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7
Q

Basal ganglia circuitary

A

slide 31, look at Laz’s notes for more details but no need to know the extra things in laz’s

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8
Q

Which pathway is affected in parkinson’s disease

A

Nigro-striatal pathway. Loss of dopaminergic neurons happens in parkinson’s

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9
Q

Where do the projections go after leaving the basal ganglion structures in the basal ganglia circuitary?

A

They go to the thalamus
From the thalamus they go to the cortex (supplementary motor area and primary motor area = two regions involved in movement preparation and planning)

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10
Q

What causes Parkinson’s disease?

A

Parkinson’s disease is the neuronal degeneration of dopaminergic neurones in the substantia nigra pars compacta
It is caused by the progressive depletion of dopaminergic neurones
NOTE: symptoms only appear when 80% of the dopamine cells in the substantia nigra have died

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11
Q

What are the consequences of this with regards to the circuitry of the basal ganglia? (this is an extra Q that you dont need to know, but it helps for deeper understanding. Read Laz’s for more details on the circuitary then come back to this)

A

The loss of nigro-striatal dopaminergic axons in the caudate and putamen mean that the connection between the striatum (caudate and putamen) and the substantia nigra pars compacta is lost.
This means that the direct pathway is reduced and so the excitation of the motor cortex is reduced.
The lack of excitatory input interferes with the ability of the motor cortex to generate commands for voluntary movement, resulting in poverty of movement.

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12
Q

State the main signs of Parkinson’s disease.

A

Bradykinesia – slow movements eg doing up bottons

Akinesia – hard to initiate movement

Hypomimic face – expressionless face, due to lack of movements that normally animate the face

Tremor at rest

Rigidity – increase in muscle tone (imagine your whole arm stiffens when you remain tensing your biceps)

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13
Q

Describe the Parkinsonian gait.

A

Walking slowly, small steps, shuffling feet, reduced arm swing

Camptocormia- a type of kyphosis

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14
Q

What is Huntington’s disease caused by?

A

Abnormality on chromosome 4 (autosomal dominant), a CAG repeat in the gene coding for Huntingtin protein.

This causes degeneration of GABAergic neurones in the striatum (firstly the caudate and then the putamen)

GABAergic neurons are normally inhibitory. Degeneration of these means theres less inhibition of some things and this leads to the symptoms

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15
Q

Consequences of the loss of inhibition in Huntington’s?

A

Patients will continuously have abnormal movements because less signals from the cortex are inhibited

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16
Q

What are the main signs of Huntington’s disease and how does the disease progress?

A

-Choreic movements – rapid, jerky, involuntary movements of the body
(The hands and face are affected first)

Chorea gradually increases over time until the patients are totally incapacitated by it

  • Speech impairment
  • Difficulty swallowing
  • Unsteady gait
  • At Later stages, cognitive decline and dementia
17
Q

3 functional divisions of cerebellum?

A

vestibulocerebellum
cerebrocerebellum
spinocerebellum

NB theres an anatomical division as well into vermis, anterior and posterior lobes etc.

18
Q

State the 3 layers of the cerebellar cortex.

A

Granule cell layer (deep)
Purkinje cells
Molecular layer (superficial)

19
Q

What is the role of the vestibulocerebellum?

A

Vestibulocerbellum is the flocculonodular lobe
Function= balacne

this includes gait, posture and equilibrium. It is also involved in coordination of head movements with eye movements

20
Q

Which anatomical parts of the cerebellum are part of the spinocerebellum?

A

Vermis and intermediate hemisphere

21
Q

What are the roles of the spinocerebellum?

A
  • Coordination of speech
  • Adjustment of muscle tone
  • Coordination of limb movement
22
Q

Which part of the cerebellum is part of the cerebrocerebellum?

A

Lateral hemisphere

23
Q

From where does the cerebrocerebellum receive inputs and what are its main functions?

A
It receives projections from the cortex  
Main functions are: 
 Coordination of skilled movements  
 Cognitive function  
 Attention 
 Processing of language  
 Emotional control
24
Q

In summary, what are the four main functions of the cerebellum?

A

Maintenance of balance and posture (vestibulo)
Coordination of voluntary movements (spino)
Motor learning
Cognitive functions (cerebro)

25
Q

State three syndromes caused by dysfunction of different parts of the cerebellum.

A
  1. Vestibulocerebellar syndrome/Flocculonodular lobe syndrome
  2. Spinocerebellar syndrome
  3. Cerberocerebellar syndrome
26
Q

What are the symptoms of vestibulocerebellar syndrome?

A

Damage (tumor) causes syndrome similar to vestibular disease (disease of balance) leading to gait ataxia and tendency to fall

27
Q

What behavioural habit is spinocerebellar syndrome associated with?

A

Chronic alcoholism

28
Q

Describe the symptoms of spinocerebellar syndrome.

A

Mainly affects the legs It causes abnormal gait and a wide-based stance

29
Q

Describe the symptoms of cerebrocerebellar syndrome.

A

Damage mainly affects the arms and the skilled/co-ordinated movements that the arms carry out (tremor)

Speech becomes very hesitant and slow (staccato)

30
Q

What are the main signs of cerebellar disorders?

A

Ataxia– general impairments in movement coordination and accuracy

Dysmetria (cannot measure)– inappropriate force and distance for target-directed movements

Intention tremor– increased tremor when an action reaches its target endpoint eg if i ask u to touch ur nose, u get more tremor as you approach your nose compared to the start

Dysdiadochokinesia– ‘bad suceeding (diadochos) movement’ inability to perform rapid alternating movements

Scanning speech– staccato, due to impaired coordination of speech muscles

31
Q

What nucleus projects to the purkinje cells via climbing fibres

A

inferior olivary nucleus (involved in motor coordination and learning)

32
Q

what fibres are involved in the input and output of signals into the granular layer of cerebellum (deepest layer)

A

input - mossy

output- parallel

33
Q

What nucleus do purkinje cells project to first for its output pathway

A

Deep cerebellar nuclei. The neurons from this nuclei can then influence motor cortex and descending motor pathways (see 2 min neuroscience vid slide 43)