8. Motor systems Flashcards

1
Q

What tasks are high order and lower level areas involved in?

A
  • High order - more complex e.g. programme and decided on movements, coordinate muscle activity
  • Lower level - execution of movement
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2
Q

The primary cortex supplies innervation to the muscles of the body via which neurones?

A

α neurones in the ventral horn

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3
Q

Which nuclei are responsible for the muscles of the face, head and neck?

A

Brainstem motor nuclei

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4
Q

The cerebellum and basal ganglia are part of which system involved in involuntary movements (and fine tuning output)?

A

Extrapyramidal system

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5
Q

What is the location and function of the primary motor cortex?

A

• Location - precentral gyrus, anterior to the central sulcus
• Function:
- control fine, discrete, precises voluntary movement
- low in the hierarchy

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6
Q

What is the neocortex?

A
  • A 6 layer part of the primary motor cortex (layer 5)
  • High-order function - sensory perception, cognition, generation of motor commands
  • Large pyramidal cells - support a long axon
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7
Q

What is the pathway of motor neurones through subcortical structures known as?

A
  • Internal capsule

* Bisects the basal ganglia

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8
Q

What does the internal capsule become further down?

A

Cerebral peduncle

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9
Q

Why can’t you see the corticospinal tract externally at the level of the pons?

A

Transverse fibres in the pons

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10
Q

Where do 90-95% of the motor fibres decussate?

A
  • The pyramids as the tract re-emerges - base of the medulla

* Pyramidal decussation

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11
Q

In which part of the spinal cord do most of the motor fibres descend?

A

Lateral corticospinal tract (dorsal area of the spinal cord)

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12
Q

In which part of the spinal cord do 5-10% of the motor fibres descend and what do they supply?

A
  • Those that don’t decussate in the brainstem
  • Anterior corticospinal tract
  • Decussate in the spinal cord at the appropriate level
  • Supply the axial musculature
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13
Q

What is the corticobulbar pathway?

A

Pathway from the primary motor cortex to the motor nuclei - within the brainstem

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14
Q

Where is the hypoglossal nucleus?

A

Near the midline of the medulla

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15
Q

What is the location and function of the premotor cortex?

A

• Location - anterior to the motor cortex (M1)
• Function:
- planning of movements
- regulates externally cued movements

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16
Q

How do you describe moving a body part relative to another body part, and movement of the body in the environment?

A

Intra-personal and extra-personal space

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17
Q

What is the location and function of the supplementary motor area?

A

• Location - frontal love anterior to M1, medially
• Function:
- planning complex movements
- programming sequencing of movements
- regulates internally driven movements (plan speech and carry out) (Wernicke’s and Broca’s area)

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18
Q

What is the posterior parietal cortex important for?

A

Ensures movements are targeted accurately to objects in external space

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19
Q

What is the prefrontal cortex for?

A

Involved in selection of appropriate movements for a particular course of action

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20
Q

What are the signs of a loss of function of upper motor neurones?

A
  • Neurones located in the primary motor cortex
  • Paresis - graded weakness of movements
  • Paralysis
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21
Q

How can a loss of inhibitory descending inputs affect upper motor neurones?

A

• Increased abnormal motor function

  • spasticity: increased muscle tone
  • hyperflexia: exaggerated reflexes
  • clonus: abnormal oscillatory muscle contraction
  • Babinski’s sign
22
Q

What is apraxia?

A
  • Disorder of skilled movement
  • Usually related to parietal lobe problems
  • Any disease of the inferior parietal lobe and the frontal lobe can cause apraxia - stroke and dementia are the most common
23
Q

What are the effects of lower motor neurone disease?

A
  • Weakness
  • Hypotonia
  • Hypoflexia
  • Muscle atrophy
  • Fasciculations - visible twitch
  • Fibrillations - spontaneous twitching - recorded during needle electromyography examination
24
Q

What is motor neurone disease?

A
  • Progressive neurodegenerative disorder of the motor system
  • Multiple genetic causes
  • Spectrum of disorders with similar clinical presentations
  • Affects upper and lower motor neurones
  • aka Amyotrophic Lateral Sclerosis (ALS)
25
Q

What are the upper motor neurone signs of ALS?

A
  • Increased muscle tone
  • Brisk limbs and jaw reflexes
  • Babinski’s sign
  • Loss of dexterity
  • Dysarthria
  • Dysphagia
26
Q

What are the lower motor neurone signs of ALS?

A
  • Weakness
  • Muscle wasting
  • Tongue fasciculations and wasting
  • Nasal speech
  • Dysphagia
27
Q

Problems in the basal ganglia underlie which two important motor disorders?

A
  • Parkinson’s

* Huntington’s

28
Q

What structures does the basal ganglia comprise?

A

• Caudate nucleus
• Lentiform nucleus (putamen + external globus pallidus)
(Striatum = caudate + lentiform nucleus)
• Subthalamic nucleus - where surgeons put stimulations in Parkinson’s patients to turn off tremor
• Substantia nigra
• Ventral pallidum
• Claustrum
• Nucleus accumbens - involved in limbic reward
• Nucleus basalis of Meynert - all cholinergic innervation to the cortex (memory)

29
Q

What is the lateral wall of the anterior horn of the lateral ventricle?

A

Caudate nucleus

30
Q

Where is the putamen and nucleus accumbens located with reference to the Caudate nucleus?

A
  • Putamen is more lateral and slightly inferior

* Nucleus accumbens is inferior

31
Q

What are the functions of the basal ganglia?

A
  • Elaborating associated movements e.g. swinging arms when moving, changing facial expressions to match emotion
  • Moderating and coordinating movement
  • Performing movements in order
32
Q

Why is the circuitry of the basal ganglia significant in different disorders?

A
  • Interruption at different components give different clinical presentations
  • Parkinson’s - breakdown in nigrostriatal connectivity (dopaminergic cells project to the striatum)
  • Huntington’s - local circuitry within the striatum
33
Q

What are ballistic movements?

A

Uncontrolled arm movements - generally down to problems in the subthalamic area

34
Q

How do patients with Parkinson’s disease present?

A
  • Slightly stooped in posture
  • Slightly broad based gait - shuffling movement
  • Bradykinesia - slowness of small movements
  • Hypomimic face - expressionless
  • Akinesia - difficulty in initiation of movements
  • Rigidity - muscle tone increase
  • Tremor at rest
  • No external pathological change in brain
  • Lewy Body pathology at microscopic level
35
Q

What does a midbrain look like in a Parkinson’s patient?

A
  • No substantia nigra (black line)

* Dopaminergic neurones that normally project up to the striatum have died

36
Q

Why do younger people have a pale substantia nigra?

A
  • Black substance is neuromelanin
  • Breakdown product of normal dopamine metabolism in dopaminergic neurones
  • Builds up during lifetime, therefore there is less when younger
37
Q

What causes Hungtington’s disease?

A
  • Genetic disease - gene on chromosome 4 (Huntingtin protein), autosomal dominant
  • Triple repeat - CAG repeat (>35 repeats almost certain to get disease)
  • Degeneration of GABAergic inhibitory neurones in striatum, caudate, then putamen
38
Q

What are the motor signs of Huntington’s disease

A
  • Choreic movements - rapid jerky involuntary movements, hands and face affected first, then legs and rest of body
  • Speech impairement
  • Difficulty swallowing
  • Unsteady gait
  • Cognitive decline and dementia at later stages
39
Q

What keeps the cerebellum in place?

A
  • Sits in the posterior cranial fossa

* Covered by the tentorium cerebelli (fold of the dura)

40
Q

How many pathways are there to the cerebellum and what are they?

A
  • 3
  • Inferior cerebellar peduncle - from spinal cord to spino-cerebellar tracts
  • Middle cerebellar peduncle - transverse fibres connecting the 2 halves of the cerebellym
  • Superior cerebellar peduncle - main output pathway to the basal ganglia and thalamus
41
Q

Describe the laminar structure of the cerebellum?

A
  • Outer-molecular layer - lots of glial cells
  • Piriform layer - lots of Purkinje cells
  • Granular layer - granule cells (neuronal as well)
42
Q

Where does the inferior olive (nucleus in the rostral medulla) project to in the cerebellum?

A

• Purkinje cells
• via climbing fibres
- terminate in the molecular layer where the dendritic tree of the purkinje is found

43
Q

Where do all inputs apart from the climbing fibres go in the cerebellum?

A

• Granule cells via mossy fibres
• Onwards via parallel fibres
- innervate purkinje cells
• All output from the purkinje cells is via deep nuclei

44
Q

What are the 3 sections of the cerebellum?

A
  • Vestibulocerebellum
  • Spinocerebellum
  • Cerebrocerebellum
45
Q

Describe the function of the vestibulocerebellum

A
  • Regulation of gait, posture and equilibrium
  • Coordination of head movements with eye movements
  • Connections with the superior colliculus

(small transverse section)

46
Q

What is vestibulocerebellar syndrome?

A
  • Damage (tumour) causes syndrome similar to disease

* Gait ataxia and tendency to fall (even when sitting and eyes open)

47
Q

Describe the function of the spinocerebellum

A
  • Coordination of speech
  • Adjustment of muscle tone
  • Coordination of limb movements
  • Fine control of the main corticospinal output
  • Modulates and refines output to the musculature

(medial vertical section)

48
Q

What is spinocerebellar syndrome?

A
  • Damage (degeneration and atrophy associated with chronic alcoholism) mainly affects legs
  • Abnormal gait and stance (wide-based)
49
Q

Describe the function of the cerebrocerebellum

A
  • Coordination of skilled movements (motor learning)
  • Cognitive function, attention, processing of language
  • Emotional control

(lateral section)

50
Q

What is cerebrocerebellar/lateral cerebellar syndrome?

A
  • Damage mainly affects arms/skilled coordinated movements (tremor) and speech
  • Results in skilled movement loss
51
Q

What are the main motor signs of cerebellar problems?

A

Deficits only apparent upon movement
• Ataxia - impairements in movement coordination and accuracy
• Dysmetria - inappropriate force and distance for target-directed movements
• Intention tremor - increasingly oscillatory trajectory of a limb in a target-directed movement
• Dysdiadochokinesia - inability to perform rapidly alternating movements
• Scanning speech - staccato, due to impaired coordination of speech muscles