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LCRS Neuro > Cortical motor function, basal ganglia and cerebellum > Flashcards

Cortical motor function, basal ganglia and cerebellum Flashcards

1
Q

what is functional segregation?

A

different areas control different aspects of movement

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2
Q

what is hierarchical segregation?

A

some areas coordinate more complex tasks than others
high order: programme and decide on movements, coordinate muscle activity

low order:execution of movement

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3
Q

what is the descending order of the hierarchical segregation?

A

association cortex (highest)
motor cortex
brainstem and cerebellum
basal ganglia and spinal cord (lowest)

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4
Q

what are the 3 main areas of the motor cortex?

describe their locations relative to each other

A

1) primary motor cortex (M1) aka Broadmann’s Area 4
2) premotor cortex aka Broadmann’s Area 6
3) supplementary motor area also Broadmann’s Area 6

  • the primary motor cortex is closest to the midline (precentral gyrus)
  • the premotor cortex lies anterior to the PMC (lateral and inferior)
  • the supplementary motor area also lies anterior to PMC but above the premotor cortex (medial and superior)
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5
Q

where is the primary motor cortex located?

A

frontal lobe on the precentral gyrus

anterior to the central sulcus

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6
Q

what is the function of the primary motor cortex?

A

issues descending commands to lower motor neurons in order to execute basic movements

  • control of fine, discrete and precise voluntary movement
  • provides the descending signals to execute movement
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7
Q

what are the biggest cells of the cerebral cortex?

A

Betz cells (in layer 5)

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8
Q

what are the targets of the corticospinal tracts?

A

motor function:
arms
legs
axial structures (trunk and abdomen)

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9
Q

what are the two main pathways of the corticospinal tract from the PMC?

what do they go?

A

1) lateral corticospinal pathway–> distal muscles of the limbs (MAIN- most fibres)
2) anterior corticospinal tract–> proximal limbs and trunk muscles

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10
Q

what is the pathway of the lateral corticospinal tract?

A
  • right hemisphere cortex
  • internal capsule ipsilateral to the
  • midbrain (cerebral peduncle)
  • medulla oblongata and pyramidal decussation at the base
  • anterior horn of spinal cord (motor)
  • synapse with lower motor neurone
  • innervation to distal muscle

NB lower motor neurone is from spinal cord to muscle

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11
Q

what is the difference in pathways of the LCP and ACP?

A

decussation:
-occurs at the medulla in the pyramids in LCP
heads to distal muscles
- occurs at the level of the spine in the ACP
heads to axial (trunk) and proximal muscles

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12
Q

which type of neurone is the longest?

A

primary neurone, from the brain

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13
Q

what is the pathway for muscles of the face, muscles and neck ?

how does this compare to the pathway for muscles of the body?

A

upper motor synapses in the brainstem and go straight from here to the muscles

the neurones to the body muscles come from spinal cord which receives from the brainstem

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14
Q

what NT is used from upper motor neurone (UMN) to lower motor neurone (LMN)?

A

glutamate

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15
Q

what NT is used from the LMN to the muscle fibres?

A

ACh

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16
Q

what is the significance of Penfield’s motor homunculus ?

A

somatotopic organisation of the PMC

face and hands have a larger area of the brain to control them therefore they have finer movements

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17
Q

where is the premotor cortex located?

A

frontal lobe
anterior to the PMC
lateral brain

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18
Q

what is the function of the premotor cortex?

A
  • planning movement
  • regulating EXTERNALLY cued movements with understanding of intra- and extrapersonal space
    e. g. seeing an apple and reaching out for it requires moving a body part relative to another body part (intra-personal space) and movement of the body in the environment (extra-personal space)

NB different to supplementary motor area that does internally generated movement

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19
Q

where is the supplementary motor cortex located?

A

frontal lobe
anterior to PMC
medial brain

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20
Q

what is the function of the supplementary motor cortex?

A
  • planning complex movements
  • programming sequencing of the movements
  • regulated INTERNALLY driven movements such as speech
  • becomes active before a movement is executed (thought of action)

NB different to premotor cortex that does externally guided movements

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21
Q

what is the significance of the association cortex even though it is not anatomically in the motor region?
what two parts make up the association cortex?

A

provides perceptual experience input and is not directly involved in motor output. Made of two regions

  • posterior parietal cortex
  • prefrontal cortex
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22
Q

what is the function of the posterior parietal cortex of the association cortex?

A

ensures movements are targeted accurately to objects in external space

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23
Q

what is the function of the prefrontal cortex of the association cortex?

A

selection of appropriate movements for a particular course of action

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24
Q

Give examples of UMNs

what can cause an UMN lesion?

A

examples: Corticospinal, corticobulbar

lesion cause: stroke

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25
Q

what are the 2 types of consequences of an UMN lesion?
Loss and Gain consequences

what is the 3rd consequence with neither loss or gain?

A

1) Loss of function: therefore negative symptoms
- Paresis: graded weakness of movements
- Paralysis (plegia): complete loss of muscle activity

2) Increased, abnormal, motor function due to loss of inhibitory descending inputs: therefore positive symptoms
- Spasticity: increased muscle tone
- Hyper-reflexia: exaggerated reflexes
- Clonus: abnormal oscillatory muscle contraction
- Babinski’s

3) Apraxia: disorder of skilled movement (loss of information to do skilled movements)

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26
Q

what features of functional loss (negative symptoms) are seen in UMN lesions?

A

paresis- graded weakness of movement

paralysis (plegia)- complete loss of motor activity

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27
Q

what features of abnormal motor function (positive symptoms) are seen in UMN lesion?

A
  • spasticity-increased muscle tone
  • hyperreflexia- exaggerated reflexes
  • clonus- abnormal oscillatory muscle contraction
  • Babinski’s sign- extensor plantar response
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28
Q

what is apraxia (3rd consequence of UMN lesion)

what causes apraxia?

A
  • disorder of skilled movement (loss of information to do skilled movements). Patient is not paretic i.e. no complete loss hence why its not a -ve effect
  • cause: lesion of the inferior parietal lobe or frontal lobe affecting the premotor cortex and supplementary motor area

most commonly caused by stroke and dementia

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29
Q

what are signs of LMN lesion?

A

displays opposite signs of UMN lesion

  • weakness
  • hypotonia
  • hyporeflexia
  • muscle atrophy
  • fasciculations
  • fibrillations
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30
Q

Give an example of a Motor Neurone Disease?

what is MND?

A

Example: amyotrophic lateral sclerosis (ALS)

MND: group of progressive neurodegenerative disorders ,on a spectrum, affecting both UMNs and LMNs therefore show both sets of signs

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31
Q

What are the signs of Upper MND?

A

Increased muscle tone (spasticity of limbs and tongue).
Brisk limbs and jaw reflexes.
Babinski’s sign.
Loss of dexterity.
Dysarthria – difficult or inarticulate speech.
Dysphagia.

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32
Q

what are the signs of Lower MND?

A 
 Weakness.
 Muscle wasting.
 Tongue fasciculations and wasting.
 Nasal speech.
 Dysphagia.
33
Q

what is required by all the motor cortex areas to function?

A

side loops are required to interconnect all 3 major areas

this is done by basal ganglia and the cerebellum

34
Q

what make up the “side loops” that modulate motor output?

A

basal ganglia and cerebellum

They influence the processing of motor control and modulate the output of the descending pathways without directly causing motor output

35
Q

what make up the basal ganglia (EXTRAPYRAMIDAL)?

A
  • Caudate
  • Putamen.
  • Globus pallidus externa (GPe)
  • Globus pallidus interna (GPi)
  • Substantia nigra pars compacta (SNc)
  • pars reticulata (SNr).
  • Subthalamic nucleus (STN).
  • Ventral pallidum
  • claustrum
  • nucleus accumbens
  • nucleus basalis of Meynert
36
Q

function of the basal ganglia?

A

1) elaborates associated movements e.g. swinging arms when walking
2) moderates and coordinates movement (whilst suppressing unwanted movements)
3) performs movements in order

maintains function the ipsilateral cortex

37
Q

basal ganglia circuit pathway

A

1) PMC wants to make a movement so sends an impulse to basal ganglia
2) impulse then sent to thalamus
3) then motor cortex then to muscles

38
Q

what are the two main pathways in the circuits into basal ganglia

A

1) direct pathway (no projection into Subthalamic nuclei)
- overall excitatory effect on motor cortex

2) indirect pathways (projection into Subthalamic nuclei)
- overall inhibitory effect on motor cortex

these pathways need to be balanced for normal function

39
Q

main neurotransmitters involved in the basal ganglia circuitry

A

dopamine (+)
glutamate (+)
ACh (+)
GABA (+)

40
Q

what types of syndromes are caused by disorder of the basal ganglia?

A

1) hypokinetic disorders- with decreased movement e.g. Parkinson’s Disease
2) hyperkinetic disorders-with increased movement e.g. Huntington’s Disease

41
Q

what happens in Parkinson’s Disease?

A

neuronal degeneration of substantia nigra pars compacta

> 80% loss of dopaminergic cells

42
Q

pathophysiology of Parkinson’s Disease

A

dengeneration of dopaminergic neurones leads to loss of nigra-striatal neurones
there is a disruption in balance of excitation and inhibition
therefore reduced excitation in motor cortex

43
Q

main signs of Parkinson’s Disease

A

Bradykinesia – slow movements.
Hypomimic face – expressionless.
Akinesia – difficulty in initiation of movements.
Rigidity – muscle tone increase.
Tremor at rest – 4-7Hz, and starts in one hand.
Gait and posture – walking slow, small shuffling steps, reduced arm swing and with body and head bent forward and downward.

44
Q

pathophysiology of Huntington’s Disease (hyperkinetic disease)

cause?

A

decreased inhibition, increased excitation:

  • disrupted fine balance
  • motor cortex gets excessive excitatory input and so sends continuous involuntary commands to the muscles.

abnormality in Chr 4
autosomal dominant
degeneration of GABA neurones in striatum (caudate initially then the putamen)

45
Q

what type of disorder is Huntington’s Disease and its consequences-

  • on balance
  • on motor cortex
  • on muscles?
A

hyperkinetic disorder:

  • disruption of fine balance
  • motor cortex gets excess excitatory input
  • therefore sends continuous involuntary commands to muscles
46
Q

main signs of Huntington’s Disease

A
  • Choreic movements (Chorea) – rapid jerky involuntary movements of the body (hands followed by feet affected, then legs and then rest of body).
  • speech affected , dysphagia, unsteady gait.
  • Cognitive decline and dementia.
47
Q

what are the 3 lobes of the cerebellum?

view from inferior up on axial cut

A

1) anterior (motor execution function using medial and lateral descending paths)
2) posterior (motor planning function connecting to motor and premotor cortices)
3) flocculonodular (balance and eye movements connecting to vestibular nuclei)

48
Q

what are the 3 sagittally divided areas of the cerebellum?

A

1) vermis (middle)
2) intermediate hemisphere
3) lateral hemisphere

49
Q

on which side are the connection of cerebellum to:

  • the body ?
  • the cerebral hemispheres?
A

connections with the body are on the same side

connections with the cerebral hemispheres are on the opposite side

50
Q

what are the main NTs used in the cerebellum

A

glutamate (+)

GABA (-)

51
Q

what are the 3 functional divisions of the cerebellum?

A

1) vestibulocerebellum (flocculonodular lobe) –> vestibular nuclei
2) spinocerebellum (vermis+ intermediate cerebellum)–> corticospinal tracts
3) cerebrocerebeluum (lateral cerebellum)–> motor cortices

52
Q

what is the role of the vestibulocerebellum?

A

in flocculonodular lobe:
-regulation of gait, posture and equilibrium

-coordinates head movement with eye movements

53
Q

what is the role of the spinocerebellum?

A

medial cerebellum (vermis+intermediate cerebellum)

  • coordinates speech
  • adjusts muscle tone
  • coordinate limb movements
54
Q

where do the afferents from the body reach the spinocerebellum?
ie. where do they end up in the cerebellum?

A

1) to vermis (medial tract)
spinal afferents from the axial body, dorsal columns, trigeminal, auditory and visual inputs project to the vermis

2) intermediate cerebellum (lateral tract)
afferents from the limbs project to the intermediate hemisphere

these then are sent to the brainstem and cortex to modify the corticospinal tract signals

NB that spinocerebellum makes use of medial corticospinal tracts and lateral

55
Q

what is the role of the cerebrocerebellum?

A

lateral cerebellum:

  • coordinates skilled movements
  • cognitive function
  • attention
  • processes language
  • emotional control
56
Q

main functions of the cerebellum

A

1) maintenance of balance and posture
2) coordination of voluntary movements- coordinates muscle groups to produce smooth body movements
3) motor learning- major role in adapting and fine-tuning motor programmes
4) cognitive functions e.g. language

57
Q

what is vestibulocerebellar/flocculonodular dysfunction?

  • cause of damage
  • effects
A

V/F lobe syndrome:

  • damage due to tumour
  • causes syndrome leading to gait ataxia and tendency to fall

nb vestibulocerebellar function:

  • Regulation of gait, posture and equilibrium
  • Coordination of head movements with eye movements
58
Q

what is spinocerebellar dysfunction?

  • cause of damage
  • effects
A

S syndrome:

  • Damage -degeneration and atrophy associated with chronic alcoholism
  • affects mainly legs, causes abnormal gait and stance (wide-based)

nb spinocerebxllum normally:

  • Coordination of speech
  • Adjustment of muscle tone
  • Coordination of limb movements (hence gait)
59
Q

what is cerebrocerebellar/lateral cerebellar dysfunction?

- cause of damage

A

C/L cerebellar syndrome

  • acquired damage
  • damage affecting mainly the arms or skilled coordinated movements and speech

nb cerebrocerebellar function:

  • Coordination of skilled movements
  • Cognitive function
  • attention
  • processing of language
  • Emotional control
60
Q

when are the deficits of cerebellar syndromes seen?

A

the deficits are only apparent upon movement

61
Q

what are the main signs of cerebellar dysfunction?

A

 Ataxia – general impairment in movement coordination.
 Dysmetria – inappropriate force and distance for target-directed movements.
 Intention tremor – tremor only upon movement.
 Dysdiadochokinesia – inability to perform rapidly alternating movements.
 Scanning speech – staggered speech.

62
Q

example of inherited cerebellar disorder

A

Friedreich’s Ataxia

63
Q

example of acquired cerebellar disorder

Cerebellar means cerebellum

A

MS

64
Q

in which lesions are abdominal reflexes and extensor plantar reflexes ever absent?

A

only in the lesion of the lateral corticospinal tract

  • remember LCT provided for DISTAL muscles
  • abdominal reflexes are axial

all other tracts retain these reflexes

65
Q

what is a fasciculation?

what is a fibrillation?

A

fasciculation: damaged motor units produce spontaneous action potentials, resulting in involuntary abnormal contraction of all the motor fibres in a single motor unit (a visible twitch)
i. e. loads of fibres

fibrillation: spontaneous twitching of individual muscle fibres; recorded during needle electromyography examination
i. e. individual fibres

66
Q

what clinical presentation is unique to upper motor neurone disorders? why?

A

fasciculations (motor unit fibres contract spontaneously)

motor neurone has died so adjacent motor unit axons try to re-innervate the de-innervated motor fibres so there is unstable innervation

67
Q

what kind of lesion does a loss of reflex indicate?

A

lower motor neurone lesion

68
Q

what segments supply the biceps and supinator reflexes ?

A

C5/C6

69
Q

what segments supply the triceps reflex?

A

C6/C7

70
Q

what segment supplies the finger jerk

A

C8

71
Q

why is there no muscle weakness in Parkinson’s disease?

A

does not involve the pyramidal tracts so does not affect power
but rather affects fine control and movement –> pin-roll tremor

Parkinson is extrapyramdidal

72
Q

what are the 3 layers of the cerebellar cortex?

A
  • molecular
  • purkinje/piriform
  • granular
73
Q

what is the corticobulbar pathway outline?

A
  • primary motor cortex
  • internal capsule has corticobulbar tract
  • decussation at medulla (brainstem) where it synapses the contralateral CN5,7,11,12 nuclei
  • some receive contralateral and ipsilateral innervation e.g. CN5, part of CN7 to upper face, and 11 (receive input from both hemispheres)
  • part of CN7 and CN12 receive from the contralateral side
  • CN12:contralateral hypoglossal nerve reaches the intrinsic muscles of the tongue, genioglossus and geniohyoid
74
Q

what is involved in the extrapyramidal system?

what is involved in the pyramidal system?

A

extrapyramidal: basal ganglia and cerebellum
pyramidal: lateral corticospinal tract

75
Q

example of LMN

A

examples: brainstem and spinal cord

76
Q

what are the main collective structures within the basal ganglia?

A

1) corpus striatum (Big Daddy)
- Striatum (input) +Pallidum (output)
- Striatum= caudate nucleus+putamen
- Pallidum= Globus pallidus internus+ Globus pallidus externus

other groupings:
lentiform nucleus= putamen+ globus pallidus

77
Q

motor system hierarchy

A
  • PMC inputs to basal ganglia and cerebellum
  • both basal ganglia and cerebellum feed into the thalamus, but the cerebellum also feeds into the brainstem
  • the thalamus relays to the brain
  • the PMC can directly input to the brainstem and spinal cord
  • the brainstem directly inputs to the muscles of the face, neck and head
  • the brainstem inputs to the muscles of the body via the spinal cord
78
Q

extrapyramidal tracts

A
  • pontine reticulospinal
  • medullary reticulospinal
  • lateral vestibulospinal
  • rubrospinal (from red nucleus)

LCRS Neuro (19 decks)

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