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LCRS 2 > Motor Pathways: Cortical Motor Function > Flashcards

Motor Pathways: Cortical Motor Function Flashcards

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1
Q

Describe the hierarchical organisation of motor control.

A

Association Cortex
Motor Cortex
Brainstem
Spinal Cord

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2
Q

What are postural adjustments and unconscious processing?

A

Postural Adjustments – the motor system has to compensate for changes in the body’s centre of mass during movements
Unconscious Processing – many of the postural adjustments occur without our awareness

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3
Q

What are the three parts of the motor cortex?

A

Primary Motor Cortex
Premotor Cortex
Supplementary Motor Area

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4
Q

What makes up the association cortex?

A

Frontal Cortex
Parietal Cortex
NOTE: this is not exactly part of the motor pathway but it influences the planning and execution of movements

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5
Q

What are the two parts of the pyramidal (descending) system?

A

Corticospinal Tract – starts in the cortex and exits and innervates the muscles in the arms and legs
Corticobulbar Tract – starts in the cortex then exits and innervates the muscles in the face

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6
Q

Describe the side loops of this descending pathway and their role.

A

The descending pathway also has two side loops that go to the cerebellum and basal ganglia
The cerebellum and basal ganglia check the motor information before ittravels to the muscles and has its effect

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7
Q

What are the most important cells in the primary motor cortex?

A

Betz Cells (pyramidal cells)

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8
Q

Where are these cells located within the grey matter and which tracts originate from here?

A

They are found in the 5th layer of grey matter

The corticospinal tracts originate from here

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9
Q

Describe what happens to the upper motor neurones that come from the primary motor cortex.

A

They travel through the brainstem to the pyramidal decussation in themedulla where 90% of the axons cross the midline.
These axons continue down the spinal cord and synapse with a lower motor neurone and exit into a peripheral nerve to the reach the skeletal muscle.
The pathway of the corticobulbar tract is somewhat similar – upper motor neurones go down into the brainstem and synapse with a lower motor neurone and they exit to the muscles of the face

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10
Q

What are the two examples of descending pathway?

A

Lateral and Medial (anterior)

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11
Q

What is the function of each of the lateral and anterior corticospinal pathways?

A 
Lateral  
 Control of proximal and distal musculature
 Voluntary movements or arms and legs
Medial/anterior 
 Control of axial muscles 
 Balance and posture
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12
Q

Describe the structure and function of the lateral corticospinal tract.

A

The lateral corticospinal tract originates in the primary motor cortex from the Betz cells.
Their axons pass down through the brainstem and decussate at the pyramidal decussation in the medulla.
It then passes down the spinal cord and synapses with a lower motor neurone.
It goes onto control mainly the distal musculature.
NOTE: 90% of axons from the primary motor cortex decussate at the medulla (these are the lateral corticospinal tract axons). The 10% that don’t decussate form the anterior corticospinal tract.

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13
Q

Where does the rubrospinal tract originate?

A

Red nucleus of the midbrain

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14
Q

What is the function of the rubrospinal tract?

A

It is an alternative pathway that allows voluntary motor commands to be sent down the spinal cord meaning that the body can compensate for a lesion in the primary motor cortex.
It also has a role in movement velocity.

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15
Q

Describe the structure and function of the vestibulospinal tract.

A

The lateral vestibulospinal tract originates at the lateral vestibular nucleus.
The medial vestibulospinal tract originates at the medial vestibular nucleus.
They mediate postural adjustments and head and eye movements

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16
Q

Describe the structure and function of the reticulospinal tract.

A 
It originates in the reticular formation in the brainstem then goes down the spinal cord to innervate muscle.  
It is involved in complex actions: 
 Orienting 
 Stretching 
 Maintaining a complex posture
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17
Q

Describe the structure and function of the tectospinal tract.

A

It originates in the superior colliculus (brainstem)

Its function is not known but is most likely involved in reflexive turning of the head to orient to visual stimuli.

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18
Q

Describe the structure and function of the anterior corticospinal tract.

A

The anterior corticospinal tract is made up of the upper motor neurone axons coming from the primary motor cortex that do not decussate at the pyramidal decussation.
These fibres cross the midline at the level of the spinal cord It controls proximal musculature.

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19
Q

How can the cortical representation of a muscle in the motor cortex change?

A

The more we use a muscle, the bigger the representation of that muscle in the cortex.

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20
Q

What is the function of the premotor cortex?

A

Plans movements and assembles movements into coordinated actions
NOTE: premotor cortex is anterior to the primary motor cortex

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21
Q

What is the function of the supplementary motor area?

A

Planning complex internally driven voluntary movements e.g. speech
It also becomes active when you are thinking about movement before movement (e.g. rehearsing a dance)

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22
Q

What are the two parts of the association cortex that are involved in motor control? State their functions.

A

Posterior Parietal Cortex – ensures movements are targeted accurately to objects in external space
Prefrontal Cortex – involved in the selection of appropriate movements for a particular course of action

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23
Q

Describe the features of upper motor neurone lesions.

A

Initially you get loss of function of the motor neurones leading to:
 Paresis = graded weakness of movement
 Paralysis = complete loss of muscle activity
After a few weeks, the loss of descending inhibitory pathways leads to increased abnormal motor activity such as:
 Spasticity (increased muscle tone)
 Hyperreflexia (exaggerated reflexes)
 Clonus (abnormal oscillatory muscle contraction)
 Babinski’s Sign
 NO muscle atrophy

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24
Q

What is Babinski’s Sign?

A

You stroke the plantar surface of the foot and in a normal subject you will see flexion of the toes (they curl downwards)
In the case of upper motor neurone lesions, the patient will show an EXTENSOR PLANTAR RESPONSE where their toes fan out and their big toe lifts up.

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25
Why is muscle atrophy not seen in upper motor neurone lesions?
The lower motor neurones are still in tact and they have a role inproviding nutrients to the muscle. There will still be partial atrophy due to muscle disuse.
26
Define apraxia.
A disorder of skilled movement not caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea). It is caused by the loss of information on how to perform skilled tasks rather than loss of motor command to the muscles.
27
Lesions in which part of the brain tend to cause apraxia?
``` Inferior parietal lobe Frontal lobe (premotor cortex and supplementary motor area) ```
28
What are the two most common causes of apraxia?
Stroke and Dementia
29
Describe the features of lower motor neurone lesions.
It is generally the opposite of upper motor neurone lesions.  Hypotonia  Hyporeflexia  Weakness  Muscle Atrophy– the metabolic trophic support to the muscles is lost  FASCICULATIONS– damages motor units produce spontaneous action potentials, resulting in a visible twitch  Fibrillations – twitch of individual muscle fibres (aren’t visible to the naked eye but are picked up on EMG)
30
What is motor neurone disease?
A progressive neurodegenerative disorder of the motor system – it is a spectrum of disorders. MND can affect upper motor neurones, lower motor neurones or both
31
What is the term given for upper AND lower motor neurone disease?
Amyotrophic Lateral Sclerosis (ALS)
32
Describe how the symptoms of ALS change as the disease progresses.
Some patients may present with only upper motor lesion symptoms or only lower motor lesion symptoms but as the disorder progresses, both upper and lower motor neurone signs will be coexistent.
33
List some signs of ALS.
 Increased muscle tone (spasticity in the limbs and tongue)  Brisk limb and jaw reflexes (hyperreflexia)  BABINSKI’s SIGN  Loss of dexterity  Dyarthria – difficulty speaking  Dysphagia – difficulty swallowing
34
Which lower motor neurone controls the tongue?
Hypoglossal Nerve (CN XII)
35
What might you see in the tongue of an MND patient?
Fasciculations and spasticity
36
Function of primary motor cortex
Controls fine, discrete and precise voluntary movement | Provides descending signals to execute movement
37
Role of anterior corticospinal tract
Goes to skeletal muscle of trunk and proximal limbs
38
Role and route of corticobulbar tract
Role is connection of motor cortex to medullary pyramids
39
Where does basal ganglia adjustment go through
Always the thalamus
40
Where does cerebellum adjustment information go through
The thalamus or can go directly on to brainstem and then muscles or spinal chord
41
Location of primary motor cortex
Lies anterior to central sulcus so in posterior part of frontal lobe
42
Role of primary motor cortex
Control all voluntary movement by providing signals for execution
43
Somatotopic organisation to motor cortex ( penfield motor homunculus)
Lower limbs most medial (in sulcus)-> upper limbs-> face then lips
44
Lateral corticospinal motor tract pathway
Begins in motor cortex and one long cell Betts cell passes through basal ganglia to medulla where it decussates to descend in lateral corticospinal tract. When reaches appropriate spinal level enters ventral horn and synapses with lower alpha motor neurone
45
What do descending motor pathways go past in basal ganglia
Internal capsule
46
What do descending motor pathways go through in midbrain
Cerebral peduncle
47
What do descending motor pathways go through in pons
Transverse fibres
48
Anterior corticospinal tract pathway
Pass from motor cortex all the way down the anterior corticospinal tract ipsilaterally to appropriate spinal level where they decussate
49
Muscles supplied by motor lateral corticospinal tract
85% of muscles | Those of distal limbs
50
Musc,es supplied by anterior corticospinal tract
15% | Skeletal muscles of trunk
51
Corticolbulbar pathway
Passes from appropriate region in motor cortex through internal capsule to a nucleus(depending on cranial nerve) in medulla where leaves and goes to muscle
52
Premotor cortex location
Frontal lobe anterior to primary motor cortex
53
Function of premotor cortex
Plans movement | Regulating externally cued movements
54
Function of SMA
Planning a complex movement and the sequence of movements So very active if thinking of carrying out a movement Also regulates speech
55
Role of posterior parietal cortex
Ensures movement is targeted to an object in external space
56
Role of prefrontal cortex
Selects a selection of appropriate movements for a particular action based on personal experience
57
Lower motor motor neurones
Those leaving spine or brainstem
58
Upper motor neurones
Corticospinal or corticobulbar neurones
59
What does pyramidal refer to
Lateral corticospinal tract
60
What does extrapyramidal refer to
Basal ganglia and cerebellum
61
Problems with upper motor neurone lesions
Paresis | Paralysis
62
Paresis
Graded weakness of movements
63
Paralysis definition and alternative word
Complete loss of muscle activity | Plegia
64
2 types of symptoms associated with upper motor lesions
Loss of function (negative signs)- due to loss of excitatory pathways Increased abnormal function (positive signs)- due to loss of inhibitory pathways
65
Positive signs from upper motor lesions
Spasticity Hyper-reflexia Clonus Babinskis sign
66
Spasticity
Increased muscle tone
67
Hyper-reflexia
Exaggerated reflexes
68
Clonus
Abnormal oscillatory muscle contraction
69
Apraxia
Disorder of skilled movement. The patient isn’t necessarily paretic but has lost information on performing a skilled task
70
What are causes of apraxia
Lesion of inferior parietal lobe or frontal lobe Stroke dementia
71
Most common cause of apraxia
Dementia | Stroke
72
What areas are affected by frontal lobe lesion in terms of apraxia
Premotor cortex or SMA
73
Lower motor neurone lesion symptoms
``` Weakness Fasiculations Hypotonia Hyporeflexia Atrophy Fibrillations ```
74
Fasiculations
Damaged motor units produce spontaneous action potentials which result in twitch
75
Muscle fibrillations
Spontaneous twitching of individual muscle fibres
76
Motor neurone disease
Progressive neurodegenerative disease of motor system which has a spectrum of disorders
77
Most common MND
Amyotrophic lateral sclerosis | ALS
78
Progression of MND
Begins distally and moves more centrally | Loss of respiratory muscle effort causes eventual death
79
Upper motor neurone signs of MND
``` Increased muscle tone Brisk limb and jaw reflexes Babinskis sign Loss of dexterity Dysarthria Dysphagia ```
80
Lower motor neurone signs
``` Weakness Muscle wasting Tongue fasiculations and wasting Nasal speech Dysphagia ```
81
What is the basal ganglia
Extrapyrimadimal part of motor system that influences movement
82
Parts of basal ganglia
``` Caudate nucleus Lentiform nucleus Subthalamic nucleus Substantia nigra Series of anatomical parts of brain loosely associated with basal ganglia: Central pallidum Claustrum Nucleus accumbens Nucleus basalis of meynert ```
83
Components of lentiform nucleus
Putamen | External globus pallidus
84
Structure of caudate
Anteriorly forms lateral walls of lateral ventricle | Moving posteriorly becomes thinner
85
What are components of striatum
Caudate nucleus | External globus pallidus and putamen of lentiform nucleus
86
Basal ganglia functions
Elaborated associated movements Coordinating and moderating movements Performing movements in order
87
What would be an example of elaborating associated movements
Swinging arms when walking | Changing facial expression to match emotions
88
What does it mean by moderating movements
Suppressing any unwanted movements
89
Circuitry associated with Parkinson’s
Between striatum and substantia nigra
90
Description of Parkinson’s
Shaking palsy- involuntary motion with lessened muscular power Slight bend forward Difficulty initiating an action Uncontrolled urge to pass from walk to slight run After 8-9 years you get injured intellect and senses
91
Neuropathology of Parkinson’s
Neurodegeneration of dopaminergic neurones originating in substantia nigra that project to striatum
92
Cytopathology of Parkinson’s
In the healthy neurones of substantia nigra a common side product of their metabolism is neuromelanin which makes the substantia nigra appear black. In Parkinson’s patients this is not evident
93
What percentage loss of substantia nigra neurones results in Parkinson’s symptoms
60%
94
Main motor signs of Parkinson’s
``` Bradykinesia Hypomimic face Akinesia Tremor Rigidity ```
95
Bradykinesia
Slowness of movements like doing up a button
96
Hypomimic face
Expressionless as absence of movements that normally initiate the faces emotions
97
Akinesia
Difficulty initiating movements
98
Rigidity
Increased muscle tone so resistance to movements around joints
99
Features of Huntington’s
``` Genetic neurodegenerative disease Chromosome 4 Autosomal dominant CAG repeat-<35= symptoms Degeneration of GABAergic neurones in caudate, putamen and striatum ```
100
Motor and mental signs of Huntington’s
``` Choreic movements Speech impairment Dysphagia Unsteady gait Cognitive decline-> dementia ```
101
Choreic movements
Rapid jerky involuntary movements all over body
102
Progression of choreic movements
Start proximally in head and hands then move distally
103
Location of cerebellum
In posterior cranial fossa | Connected to pons via transverse fibres
104
How many layers to cerebellum
3
105
3 layers to cerebellum
Molecular layer Piriform layer Granular layer
106
What’s in each layer
Molecular- very few neurones(insignificant) Piriform- purkinjie cells Granular- small neurones associated with processing
107
Via what does inferior olive project to purkinjie cells
Climbing fibres
108
Where do climbing fibres synapse
Dendritic trees of purkinjie cells
109
What is input to granule cells
Mossy fibres
110
What is output onwards from granule cells
Parallel fibres
111
Where does output from purkinjie cells go
Deep nuclei in white matter
112
Divisions of cerebellum
Vestibulocrebellum Spinocerebellum Cerebrocerebellum
113
Role of vestibulocerebellum
Regulation of posture and balance | Coordination of head and eye movements
114
Role of spinocerebellum
Coordination of speech Adjust muscle tone Coordination of limb movements
115
Role of cerebrocerebellum
Skilled movement coordination Cognitive function and attention Emotional control
116
Signs of vestibulocerebellum syndrome
Gait ataxia | Tendency to fall
117
Common cause of vestibulocerebrellar syndrome
Tumour
118
Spinocerebrellar syndrome signs
Issues with legs and stance
119
Common cause of spinocebrellar syndrome
Alcoholism and atrophy
120
Cerebrocerebeellar syndrome signs
Speech issues and skilled arm movements
121
Gait
Manner of walking
122
Main signs of cerebrellar dysfunction
``` All to do with movements Ataxia Dysmetria Intention tremor Dysdiadochokinesia Scanning speech ```
123
Ataxia
General issues with movement coordination
124
Dysmetria
Issues with using an inappropriate force and distance
125
Intention tremor
Thought of carrying out an action results in tremor
126
Dysdiadochokinesia
Inability to perform rapidly alternating movements
127
Exact hierarchy to motor system
Motor cortex at core recieving inputs and giving out outputs. Motor cortex receives information from other cortical areas and the thalamus. Outputs go directly to spinal chord (body movements) and the brainstem ( head and neck). The role of the cerebellum and basal ganglia is to adjust and refine these outputs which are fed through the thalamus to the motor cortex
128
What is association cortex
Areas not strictly motor areas but they do play a role in motor signals
129
Hierarchal organisation to motor system
Higher order areas carry out the more complex tasks such as coordination and decisions Lower order areas execute the action
130
How is the motor system organised
Into a number of different areas that control different aspects of movement

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