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HYMS Y1 > Block 5 W4 > Flashcards

Block 5 W4 Flashcards

1
Q

Describe the role of cerebellum and basal ganglia in movement.

A

Cerebellum - coordination of ongoing movement.
Basal ganglia - selection/inhibition of voluntary movements.

Improve accuracy of movements by providing feedback loops with motor and sensory areas in cortex. Modify signals of UMNs.

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2
Q

What are the effects of damage to cerebellum and basal ganglia?

A

Cerebellum - jerky movements, uncoordinated and inaccurate.

Basal ganglia - uncontrolled movement at rest.

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3
Q

Describe the cerebellum.

A

Located in hindbrain.
Folia - folds and ridges.
50% of total neurones in CNS.

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4
Q

Outline the functions of cerebellum.

A

Coordination of planned, voluntary multi-joint movements, balance and muscle tone.
Comparator function - detects difference in ‘motor error’ between intended movement and actual movement. Correction of ongoing movement.
Motor memory - stores learnt movement e.g. riding a bike, driving.

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5
Q

What are the divisions of the cerebellum?

A

Cerebrocerebellum
Spinocerebellum
Vestibulocerebellum

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6
Q

Describe the cerebrocerebellum.

A

Large, inputs from cerebral cortex. Regulates highly skilled movements e.g. speech.

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7
Q

Describe the spinocerebellum.

A

Direct input from SC.
Lateral section - distal muscle movement.
Medial section (vermis) - proximal muscle movement.

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8
Q

Describe the vestibulocerebellum.

A

Includes nodules and flocculus. Inputs from vestibular nuclei in brainstem. Regulates movements underlying posture and balance.

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9
Q

What are the cerebellar peduncles?

A

Attaches cerebellum to brainstem.
Superior cerebellar peduncle -> efferent pathway from cerebellum.
Middle cerebellar peduncle -> afferent pathway to cerebellum via pons.
Inferior cerebellar peduncle -> afferent and efferent pathways.

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10
Q

What are the 3 inputs to the cerebellum?

A
  1. Motor - from cerebral cortex via relay neurones in pons cross over to opposite cerebellar hemisphere (middle cerebellar peduncle).
  2. Sensory inputs (muscle proprioception, vestibular, visual, auditory) on same side convey position and motion info (inferior cerebellar peduncle).
  3. Inferior olive - timing, learning, memory.
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11
Q

What are the deep cerebellar nuclei?

A

Major output structures.
Relay cortical cerebellar info to motor cortex and brainstem to make corrections in movement.
These exit via superior cerebellar peduncles.

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12
Q

What is the nuclei in vestibulocerebellum?

A

Fastigial nucleus or vestibular nuclei

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13
Q

What is the nuclei in spinocerebellum?

A

Interposed (+ fastigial) nuclei.

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14
Q

What is the nuclei in cerebrocerebellum?

A

Dendate nucleus

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15
Q

What are the input microcircuitry of the cerebellum?

A

Climbing fibre

Mossy fibre

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16
Q

What are the output microcircuitry of the cerebellum?

A

Purkinje cells

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17
Q

What are the interneurons of the cerebellum?

A

Granule, stellate, Golgi, basket cells.

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18
Q

Describe the granule cells.

A

Receive input from mossy fibres.

Outputs branch like a ‘T’, each branch - parallel fibres.

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19
Q

Describe purkinje cells.

A

Purkinje axons synapse onto neurones in deep cerebellar nuclei.
Use GABA (inhibitory)
Receives input from ~100,000 parallel fibres.

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20
Q

Describe climbing fibres.

A

Inputs received from inferior olive and twists around purkinje cell dendrites.
Receives input from 1 inferior olive neurone.
Carry error signals which allows for correction by altering effectiveness of the parallel inputs to purkinje cells.

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21
Q

Describe cerebellar damage.

A

Damage disrupts coordination of ongoing movements -> jerky, imprecise (cerebellar ataxia).
Movement errors always on same side as damage to cerebellum.

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22
Q

Describe damage to vestibulocerebellum.

A

Disturbances of balance and eye movements.

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23
Q

Describe damage to spinocerebellum.

A

Impaired gait

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24
Q

Describe damage to cerebocerebellum.

A

Impairments in highly skilled sequences of learned movement.

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25
Q

What is dyssynergia?

A

Loss of synergistic multi-joint movement. Patient touching nose with finger will first move shoulder joint, then elbow, then wrist - no simultaneous movement.

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26
Q

What is dysmetria?

A

Inability to judge distance - wrong location e.g. finger shoots past nose.

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27
Q

What is dysdiadochokinesia?

A

Inability to perform rapid alternating movements.

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28
Q

What is intention tremor and ataxic dysarthria?

A

Tremor when trying to move and slurred speech.

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29
Q

Describe cerebellar damage owing to alcohol.

A

Degeneration of anterior cerebellum:

  • damage specifically affects movement of lower limbs (anterior spinocerebellum)
  • wide and staggering gait but little impairment of arm or hand movements.
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30
Q

What is the basal ganglia.

A

Collection of functionally distinct nuclei.
Caudate nucleus + putamen = striatum (input)
Globus pallidus + substantia nigra = pars reticulata (output)

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31
Q

Outline the functions of basal ganglia.

A

Control of movement - motor cortex produces commands -> BG exerts inhibitory influence to control the initiation and termination of motor commands.
Selection and maintenance of voluntary movements.
Suppresses inappropriate movements.
Modulates movements through complex feedback circuitry.
Non-motor functions -> cognition, working memory, attention.

32
Q

What are the inputs to the basal ganglia?

A
  1. Corticostriatal pathway - inputs from cerebral cortex to striatum - glutamate.
    Frontal lobe - motor cortex and parietal lobe - sensory association areas.
  2. Nigrostriatal pathway - inputs from substantial nigra pars compacts to striatum - dopamine.
  3. Medium spiny neurones.
33
Q

What are the outputs of the basal ganglia?

A

Superior colliculus - eye movement.

Frontal cortex via thalamus - limb and trunk movements.

34
Q

Describe the direct pathway of the basal ganglia.

A
  1. Command from cerebral cortex excites striatum (releases glutamate).
  2. This inhibits globus pallidus internal segment (striatum releases GABA).
  3. GPi releases tonic/ongoing inhibition of thalamus (releases GABA).
  4. Allows thalamus to excite motor cortex, initiating movement.
  5. Substantia nigra facilitates direct pathway via D1 receptors in striatum.
35
Q

Describe the indirect pathway of the basal ganglia.

A
  1. Command from cerebral cortex excites striatum (releases glutamate).
  2. Inhibits the globus pallidus external segment causing:
    - less inhibition of GPi -> increasing tonic inhibition on thalamus
    - less inhibition of subthalamic nucleus -> increases excitation -> increases tonic inhibition on thalamus.
  3. Reduces excitation of motor cortex, inhibiting movement.
  4. Substantia nigra inhibits indirect pathway via D2 receptors.
36
Q

What movement disorder occur due to basal ganglia damage?

A

Parkinson’s
Hemiballismus
Huntington’s

37
Q

Describe hemiballismus.

A

Rapid, flinging and violent movements of limbs on one side of body.
Damage to subthalamic nucleus.
Treatment - deplete dopamine levels.

38
Q

Describe Huntington’s disease.

A

Hyperkinesia genetic disorder.
Excessive uncontrollable, jerky movements (chorea)
1. Death of stratal inputs to GPe.
2. Reduces inhibition of subthalamic nucleus.
3. Reduces excitation of GPi.
4. Leads to less tonic inhibition of thalamus.
5. Causes greater excitation of motor cortex - more movements.
Treatment - tetrabezamine depletes dopamine.

39
Q

Describe Parkinson’s disease.

A 
Hypokinesia disorder.
Peak onset 60yrs.
Causes -> idiopathic, genetic.
Symptoms -> TRAP
Tremor, Rigidity, Akinesia, Postural problems.
40
Q

Describe the neuropathology of Parkinson’s.

A

Degeneration of neurones in substantia nigra -> decrease in dopamine levels -> decreased activity of direct pathway and increased indirect pathway.

41
Q

Describe the effect of Parkinson’s on the pathways.

A
  1. Death of substantia nigra cells reduces dopaminergic effects on D1 and D2 receptors.
  2. leads to reduced excitation of direct pathway.
  3. leads to reduced inhibition of indirect pathway.
  4. Both cause increased inhibition of thalamus and decreased excitation of motor cortex -> reduced movements.
42
Q

What are the treatments of Parkinson’s?

A
  • L-DOPA -> precursor of dopamine, boosts level. Side effects - drug resistance, involuntary movements (dyskinesia), psychosis.
  • Dopamine agonists -> stimulates D receptors in striatum.
  • Foetal cell transplants -> foetal mesencephalic cells in putamen.
  • Deep brain stimulation/surgery -> implanted electrode to inactivate GP/STN/thalamus using high freq stimulation. Remove GP (pallidotomy) or thalamus (thalamotomy).
43
Q

Define the gyri and sulci of the brain.

A

Gyri - mounds

Sulci - grooves

44
Q

What are major sulci of the brain?

A

Central sulcus divides frontal from parietal lobes.
Lateral sulcus divides frontal from temporal lobes.
Longitudinal fissure separates 2 hemispheres.

45
Q

How many peduncles are there?

A

6 (2 superior, middle and inferior).

46
Q

Where is the primary motor cortex?

A

Precentral gyrus

47
Q

Where is primary somatosensory cortex?

A

Postcentral gyrus

48
Q

Describe the motor and sensory homunculi.

A

Areas of cortex represent areas of the body:
- lateral surface -> upper limb, head and neck
- superior surface -> trunk
- medial surface -> lower limbs.
Hand and face - more represented.

49
Q

What are the two major arterial supplies of the brain?

A

Internal carotid

Vertebral

50
Q

Draw the circle of Willis.

A

PIC

51
Q

What does the anterior cerebral artery supply?

A

Medial side of brain - lower limbs - frontal lobe.

52
Q

What does the middle cerebral artery supply?

A

Lateral side of brain - trunk, upper limbs - internal capsule, temporal lobe.

53
Q

What does posterior cerebral artery supply?

A

Midbrain, thalamus, corpus callous - occipital lobe.

54
Q

What will disruption to MCA cause?

A
  • Contralateral upper limb weakness or hemiplegia.
  • Contralateral hemianaesthesia.
  • Homonymous hemianopia, global aphasia, hemineglect.
55
Q

What will disruption to ACA cause?

A
  • Contralateral lower limb weakness or hemiplegia.
  • Frontal lobe behavioural abnormalities.
  • Contralateral hemineglect.
56
Q

What will disruption to PCA cause?

A

Contralateral hemianopia

57
Q

Why will cerebellar lesions produce a ipsilateral defect?

A

Spinocerebellar tract - un-decussated path.
Each half of body represented on ipsilateral hemisphere of the cerebellum -> ipsilateral signs.
Trunk on vermis, lower limb on anterior lobe.

58
Q

Why will motor cortical lesion produce a contralateral defect?

A

Execution of action comes from motor cortex via corticospinal tract (UMN) -> decussates at pyramids -> LMN carries the signal to effector organ.

59
Q

How does extrapyramidal system coordinate control of movement?

A

Vestibulospinal tract - controls balance and posture.
Medial reticulospinal tract - controls voluntary movements and increases muscle tone.
Lateral reticulospinal tract - opposite action.

60
Q

Describe how sensory cortical lesions produces a sensory deficit?

A
  • Primary somatosensory cortex -> contralateral reduced touch, pressure and proprioception.
  • Supramarginal -> tactile and proprioception agnosia, contralateral hemineglect and apraxia.
  • Angular gyrus -> Alexia, dyslexia, agraphia.
61
Q

What is the role of commissural fibres?

A

Links homologous regions (precentral gyri) in right and left side.

62
Q

What is the role of association fibres?

A

Links regions on the same side.

63
Q

Describe the asymmetrical hemispheric functions of handedness.

A

Each hemisphere controls simple movements of the contralateral limb.
Skilled complex motor tasks are programmed by dominant hemisphere.
Lesions of dominant hemisphere -> apraxia.

64
Q

Describe the asymmetrical hemispheric functions of language.

A

Language comprehension - left side dominance.
Lesions of dominant hemisphere -> language dysfunction.
Non-dominant hemisphere specialised for non-verbal functions.

65
Q

What do lesions in Broca’s area produce?

A

Expressive/motor aphasia - slow laboured speech, agraphia.

66
Q

What do lesions in Wernicke’s area produce?

A

Receptive/sensory aphasia - word salad, neologisms, no understanding.

67
Q

What is global aphasia?

A

No understanding and no speech.

Lesion affects both Broca’s and Wernicke’s.

68
Q

What do lesions on one side in the primary auditory cortex do?

A

No effect on hearing as other side compensates.

69
Q

What is the role of the prefrontal cortex?

A

Abstract thinking, decision making/planning, prioritising/sequencing, goal directed behaviour, inhibitions.
Anterior - MCA
Interior - ACA

70
Q

What do lesions in the prefrontal cortex cause?

A

Disinhibition
Subtle changes in personality and social function.
Reduced - concentration, judgement, initiative, problem solving ability.

71
Q

Where does the primary visual cortex sit?

A

Sits perpendicular to parieto-occipital sulcus and either side of calcimine sulcus.
Visual association areas sits around this area.
Supplied by PCA.

72
Q

Differentiate the roles of primary visual cortex and visual association areas.

A

Primary visual cortex - allows sight.

Visual association areas - allows identification and naming of the sight.

73
Q

What do lesions in the primary visual cortex cause?

A

Lose sight

74
Q

What do lesions in the visual association areas cause?

A

Visual agnosia - inability to process the sight and make sense of it.

75
Q

What do lesions in the primary visual cortex and visual association areas cause?

A

Contralateral homonymous hemianopia.

HYMS Y1 (25 decks)

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