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Basal ganglia & cerebellum Flashcards

1
Q

Where are the basal ganglia located?

A

On either side of the thalamus

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2
Q

How many main nuclei are the basal ganglia composed of?

A

4

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3
Q

What are the four main basal ganglia nuclei? What are these composed of?

A
  • The striatum - composed of the caudate nucleus and the putamen
  • The external and internal segments of the globus pallidus
  • The subthalamic nucleus
  • The substantia nigra composed of the pars compacta and the pars reticulata
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4
Q

What does the direct pathway do?

A

Facilitates motor output

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5
Q

What does the indirect pathway do?

A

Inhibits motor output

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6
Q

Draw the direct and indirect pathways

A

See essay plan

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7
Q

Where does most input to the basal ganglia originate from?

A

The frontal or parietal lobes

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8
Q

What is input to the basal ganglia recieved by?

A

Medium spiny neurones

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9
Q

What are the two major outputs of the basal ganglia?

A

Ascending - to the thalamus for form thalamocortical relay
Descending - to upper brainstem structures (such as the superior colliculus and reticular formation)
Output is exclusively to areas involving higher processing of movement - there is no output to the spinal cord

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10
Q

Describe the direct pathway

A

In this pathway, excitatory glutamatergic connections from the cortex excite the GABAergic medium spiny neurons of the striatum
Striatal output inhibits Gpi and SNr, and so reduces GPi inhibition on the thalamus
Hence stimulation of the direct pathway results in disinhibition of the thalamus, allowing the thalamus to release excitatory glutamate to stimulate enhanced activity of the motor cortex
This is disinhibition

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11
Q

Describe the indirect pathway

A

Glutamatergic cortical neurons excite striatal GABAergic neurones which decrease activity of the GABA GPe neurones
This results in disinhibition of neurons in the STN, increasing their activity
These are excitatory
His ultimately leads to increased activity of GABAergic GPi which increases inhibiton of thalamic neurones
This results in decreased motor activity

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12
Q

What is the hyperdirect pathway

A

Inhibitory connection from the cortex to the STN

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13
Q

Where does dopamine input go from and to?

A

SNc to the striatum

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14
Q

What does dopamine do to the direct and indirect pathways?

A

Activates direct

Inhibits indirect

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15
Q

How is it able to have these different effects on the direct and indirect pathways?

A

Binds to different receptors on the GABAergic neurones of the striatum
- Dopamine can bind to D1 receptors, which are Gαs-coupled and so stimulate the neurons in the direct pathway
In contrast, neurons within the striatum involved in the indirect pathway express D2 receptors, which are Gαi-coupled, and so the binding of dopamine inhibits their firing
In both instances, DA therefore facilitates movement.

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16
Q

How are D1 receptors able to activate neurones? What is the underlying mechanism?

A

Stimulate the adenylyl cyclase pathway, where ultimately, PKA is stimulated which is involed in many downstream pathways. For instance, different ion channels may be modulated, such as voltage-gate Na+ channels, Ca2+-activated K+ channels and inwardly rectifying K+ channels. Upregulation of these ultimately leads to larger MSN depolarisation in the direct pathway.

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17
Q

What sort of disorder is PD? Hypokinetic or hyperkinetic?

A

Hypokinetic

think about there being a loss of DA neurones

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18
Q

Characteristic features of PD

A 
A Sexy Boy Rang To Speak 
Akinesia 
Stooped posture 
Bradykinesia 
Rigidity
low frequency Tremour 
Shuffling gait 
Many patients also suffer deficits of cognition as the disease progresses
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19
Q

What causes PD?

A

Deficiency of dopamine in the BG resulting from degenerton of dopaminergic neurones in the SNc

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20
Q

Which nucleus has a similarity to GPi?

A

Pars reticulata

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21
Q

What is thought to be the main role of the BG?

A

Planning and control of complex motor behaviour by selectively activating some movements and suppressing others

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22
Q

Which thalamic nuclei modify signals from the basal ganglia?

A

Ventral anterior and ventral anterior

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23
Q

Describe the principle neruotransmitters involved in this system

A

Excitatory (glutamate) inputs from cerebral cortex to striatum, and from STN to GPi
Inhibitory (GABA) from striatum, GPi and GPe
Dopaminergic from SNc to striatum

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24
Q

How may loss of dopamine explain the symptoms of PD?

A
  • Tremors arise from inability to select movement

- BG plays role in scaling of movement - PD patients have bradykinesia, shuffling gait and cramped handwriting

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25
Q

Describe briefly causes of PD?

A

Single gene mutations - e.g. in alpha synuclein gene cause accumulation of alpha synuclein in DA neurones and formation of Lewy bodies
Environmental contributions - MPTP has toxic effects that can induce PD symptoms

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26
Q

Describe MPTP

A

MPTP is a prodrug for neurotoxin MPP+
Inhibitions complex I of the ETC → cell death
(also decreased ATP → downstream increase in ATP production)

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27
Q

Describe the major may of treating PD

A

L-DOPA → dopamine precursor that crosses BBB
Administered alongside a DOPA decarboxylase inhibitor e.g. carbidopa - which cannot cross the BBB → this prevents peripheral dopamine formation, increasing the amount that reaches the CNS

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28
Q

Problems with L-DOPA

A 
- Dyskinesias 
Effectiveness reduces as the disease progresses 
- as more neurones die, the uptake mechanism of DA by healthy neurones is lost and so large changes in extracellular DA occur → periods of hyperkinesia and hypokinesia 
- Do not prevent disease progression 
- postural hypotension
- dysrhythmias
- depression 
- psychosis
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29
Q

Aside from L-DOPA, what may used used as a treatment of PD?

A

Dopamine agonists

Inhibitors of dopamine uptake such as MAOβ or COMT inhibitors → increase EC DA

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30
Q

Is HD hyper- or hypokinetic?

A

Hyperkinetic

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31
Q

What neurones degenerate in the BG in HD? What does this lead to?

A

Striatal GABA medium spiny neurones of the indirect pathway

Reduces the action of the indirect pathway - bias toward direct

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32
Q

Characteristics of HD

A

ABCDEF
Ballism (undesired violent flinging of the limbs)
Chorea (fragmented, spontaneous and uncontrollable body movements)
Dystonia (slow twisting movements and abnormal posture
Also show personality changes and dementia

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33
Q

Describe hemiballismus

A

Rare movement disorder
decrease activity of STN
ballistic movement of the limbs
Occurs due to stoke, trauma etc

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34
Q

Draw basal ganglia anatomy

A

See online

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35
Q

Cerebellum - ipsi- or contralateral to rest of body?

A

Ipsilateral

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36
Q

Describe the function of the cerebellum

A

sensory-motor integration,

coordination of motor function, comparing ‘intention’ with ‘performance’

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37
Q

What does the cerebellum act in concert with?

A

The motor cortex and the basal ganglia

38
Q

Where does the cerebellum sit?

A

Posterior cranial fossa of the skull

39
Q

What separates the cerebellum and the cerebrum?

A

Tentorium cerebelli

40
Q

What joins the two hemispheres of the cerebellum?

A

The vermis

41
Q

What are the three lobes that the cerebellum can be divided into?

A

Anterior lobe
Posterior (or middle) lobe
Flocculonodular lobe

42
Q

What two fissures divide the cerebellum

A

The primary fissure - separates the anterior and posterior lobe
The posterolateral fissure - separates the flocculonodular lobe and the posterior lobe

43
Q

What are ridges of the cerebellum called?

A

Folia

44
Q

How many lobules of the cerebellum are the?

A

10

45
Q

Describe the cerebellum in terms of grey and white matter

A

Outer layer of grey matter (cortex) and an inner core of white matter surrounding deep cerebellar nuclei

46
Q

What lies ventral and dorsal to the superior vermis?

A

The anterior and posterior cerebellar notches

47
Q

What splits the left and right cerebellar hemispheres?

A

Falx cerebelli

48
Q

What are the large rounded swellings anteriorly on either side of the inferior vermis?

A

Tonsils

49
Q

What is an extension of the inferior vermis (between the tonsils)?

A

Nodule which extends downwards into the uvula

50
Q

Which cerebellar fissure has no functional significance?

A

The horizontal fissure

51
Q

What does the superior vermis extend into?

A

Onto the superior medullary velum, as a single lamella of cortical tissue, the lingula

52
Q

List the cerebellar peduncles

A

Three peduncles

  • the superior cerebellar peduncle
  • the middle cerebellar peduncle
  • the inferior cerebellar peduncle
53
Q

What do the cerebellar peduncles do?

A

They connect the cerebellum to the brain stem

54
Q

What travels through the peduncles?

A

Afferent and efferent cerebellar tracts going to and from the ipsilateral cerebellar cortex

55
Q

What does the superior cerebellar peduncle connect the cerebellum to?

A

Midbrain

56
Q

What does the middle cerebellar peduncle connect the cerebellum to?

A

The pons

57
Q

What does the inferior cerebellar peduncle connect the cerebellum to?

A

Medulla and spinal cord

58
Q

What tracts run through the inferior cerebellar peduncles?

A
  • Afferent tracts carry ipsilateral proprioceptive information from the spinal cord
  • Efferent tract composed primarily of Purkinje cell axon
59
Q

What are the functional divisions of the cerebellum? What do these do?

A

Vestibulocerebellum (balance/posture)
Spinocerebellum (motor execution)
Cerebro-cerebellum (motor planning)

60
Q

Where is the spinocerebellum?

A

Vermis and intermediate zones

61
Q

Where is the cerebrocellum?

A

Lateral hemispheres

62
Q

Where is the vestibulocerebellum

A

Flocculonodular lobe

63
Q

Pneumonic to remember deep cerebellar nuclei

A 
Dont Eat Greasy Food 
- Dentate 
Interposed nucleus made up of:
- Emboliform nucleus
- Globose nucleus 
- Fastigial
64
Q

Where can the dentate nucleus be found?

A

Lateral hemisphere

65
Q

Where can the interposed nuclei be found?

A

Paravermal and vermal area

66
Q

Where can the fastigial nucleus be found?

A

Primarily associated with the flocculnodular lobe (also associated with the vermis)

67
Q

What are the 3 layers of the cerebellum from top to bottom?

A

1 - molecular layer
2 - Purkinje layer
3 - granular layer
The DCN can be found below these

68
Q

What cell types can be found in the molecular layer?

A

Stellate cells
Basket cells
Parallel fibres of the granule cells

69
Q

What cell types can be found in the Purkinje layer?

A

Purkinje neurons

70
Q

Draw the internal circuitry of the cerebellum

A

See OneNote for drawing

71
Q

Describe the 5 cell types that make up the cerebellar circuitry

A

Purkinje – the output neurons. GABAergic, thus the output of the cerebellar cortex is inhibitory. This inhibitory P-cell outflow modulates the activity of the deep cerebellar nuclei.

Granule cells (GCs) – glutamatergic, thus excitatory

3 classes of inhibitory interneurons (GABAergic)…

  • Basket – receive excitatory GC input like P-cells; axons project to neighbouring P-cells forming a basket; excitation reduces activity in adjacent ‘off-beam’ P-cells
    = centre-surround antagonism

Stellate – like basket cells, -act directly on P-cells

Golgi – receive input from and project back to GCs = feedback inhibition to curtail duration of excitement of granule cells by mossy fibres

Furthermore, P-cells receive excitatory inputs from outside the cerebellum:

  • One directly from the climbing fibres
  • The other indirectly from the mossy fibres, via the parallel fibres of the granule cells (GCs)
72
Q

Describe firing of parallel fibres

A

High frequency of 50-100Hz, generating a single action potential in the P cell that appears as a ‘simple spike’ (20-50Hz)

73
Q

How many parallel fibre inputs from granule cells to Purkinje cells are needed to summate to cause simple spikes?

A

~200

74
Q

Where do mossy fibres originate?

A
  • Cerebral cortex
  • Reticular formation
  • Vestibular nuclei
  • Spinal cord
    (VARIOUS SENSORY PATHWAYS)
75
Q

Were do climbing fibres originate?

A
  • Inferior olive
76
Q

How many climbing fibres does one Purkinje cell recieve input from?

A

1!

But makes about 300 synapses

77
Q

Describe the effect that climbing fibres have of Purkinje cells?

A

Each AP in the climbing fibre (1-10Hz) elicits a prolonged depolarisation in the associated P cell, due to the prolonged activation of voltage-gated Ca2+ channels, resulting in a complex spike

78
Q

What are the two types of electrical activity a P cell may elicit?

A

Simple and complex spike

79
Q

Causes of cerebellar lesions

A

Stroke
tumour
trauma
congenital malformations

80
Q

What are the 3 hallmarks of patients with cerebellar damage?

A

1 - postural ataxia → characterised by incoordination of axial muscles and subsequent postural instability and wide-based, staggering gait
2 - action tremors → with oscillations of 3-4Hz that worsen with directed movement due to disruption of the mechanism for detecting and correcting movement errors
3 - hypotonia → as under normal circumstances the deep cerebellar nuclei send ‘reinforcing’ signals to the motor cortex and brainstem motor nuclei, serving to increase tone, thus is the deep nuclei are lost, there is an initial slight decrease in tone (however, after a few months, the motor cortex compensates by increasing its intrinsic activity, and the hypotonia disappears

81
Q

What are other signs of cerebellar lesions?

A

Improper measuring of distance in movements e.g. tendency to over- or under-reach
Difficulty articulating words due to lack of error correction in the movement of neck muscles required to produce speech
Difficulty performing rapid alternative movements e.g. finger-to-nose tests
NYSTAGMUS

82
Q

Which motor system is the cerebellum a part of?

A

Extrapyramidal (does not go through the pyramids of the medulla and descend) - instead sends fibres to branches of descending fibres to modify descending input

83
Q

Discuss efferent tracts from superior cerebellar peduncle

A
  • efferent to the contralateral thalamus (cerebellothalamic tract/dentothalamic)
  • also cerebellorubral (dentorubrothalamic) → to the contralateral red nucleus
  • also rubrospinal (if red nucleus gets activated)
84
Q

Discuss afferent tracts from the superior cerebellar peduncle

A

Most prominent is the ventral spinocerebellar tract

Also tectocerebellar fibres

85
Q

What are the two SCPs connected by?

A

Anterior medullary velum

86
Q

What does the medial cerebellar peduncle do?

A

Cortico-ponto-cerebellar afferents (which can leave via the SCP)

87
Q

What does the ICP receive input from?

A
  • Dorsal spinocerebellar tract (proprioceptive information from the lower trunk and limb)
  • Cuneocerebellar tract (proprioceptive information from the upper limb and neck - from the ipsilateral asscessory cuneate nucleus)
  • Vestibulocerebellar tract (from inner ear)
  • olivocerebellar tract (from proprioceptors - enters as a climbing fibre)
  • reticulocerebellar (all sensory)
88
Q

What does output from the fastigial nucleus output control?

A

MEDIAL DESCENDING SYSTEMS → to proximal muslces

89
Q

What does output from the interposed nuclei control?

A

LATERAL descending systems → more distal mouscles of fine movement control

90
Q

Lesions of vestibulocerebellum

A

Nystagmus, head tilt, circling gate

91
Q

Lesions of spinocerebellum

A

Impaired gait indicative of abnormal spinal control of walking

92
Q

Lesions of cerebrocerebellum

A

Inaccuracy of reaching and clumsiness of hand movements, or impaired voluntary control of body partd

Neuro (23 decks)

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