Motor Systems Flashcards

1
Q

Hierarchical organisation

A

High order areas of hierarchy: involved in more complex tasks
-Programme and decide on movements, coordinate muscle activity

Lower level areas of hierarchy perform lower level tasks (execution of movement)
-Carrying out the movements – not the planning or coordination

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2
Q

Motor system hierarchy

A

Primary motor cortex
Projects down into the spinal cord
It supplies innervation of muscles in the body via alpha neurones in the ventral horn
Brainstem motor nuclei are responsible for muscles in the face, head and neck

The cerebellum and thalamus are extrapyramidal areas of the brain and fine tune output of the motor cortex

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3
Q

Primary motor cortex location and function

A

Location: precentral gyrus, anterior to the central sulcus

Function: control fine, discrete, precise voluntary movement

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4
Q

Homunculus

A

It is inverted
Lower limb near median/longitudinal fissure
Upper limb and torso are lower and face is the lowest

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5
Q

Significance of homunculus in stroke

A

Lack of blood supply through branches of the middle cerebral artery causes problems in the upper limbs

The middle cerebral artery also supplies subcortical structures (including the basal ganglia)
Therefore middle cerebral artery blockage may result in complete hemiparesis or hemiplegia

Strokes affecting the anterior cerebral artery are likely to have more lower limb consequences

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6
Q

Descending motor pathways

A

Motor neurones pass from the primary cortex through the subcortical structure- through the pathway called the internal capsule

This then becomes the cerebral peduncle- still ipsilateral

Neurones then pass through the pons- but can’t see the corticospinal tract due to transverse fibres

The tract re-emerges at the medulla as the pyramids. At the base of the medulla, 90-95% of fibres cross over (pyramidal decussation).

The fibres descend in the spinal cord in the lateral corticospinal tract (in the dorsal area of the spinal cord).

At the appropriate level, fibres synapse with alpha motor neurones in the ventral horn of the spinal cord. Axons of these neurones go out through the ventral root -> spinal nerve.

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7
Q

Anterior corticospinal tract- what forms it, where they cross and what they supply

A

Formed by the 5-10% of fibres that don’t cross over at the medulla

These cross over at the appropriate level in the spinal cord

These supply the axial musculature (muscle of trunk and head)

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8
Q

Corticobulbar pathways

A

The primary motor cortex to the motor nuclei within the brainstem

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9
Q

Premotor cortex - location and fucntion

A

Anterior to motor cortex

Involved in planning of movements
Regulates externally cued movements

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10
Q

Supplementary motor area- location and function

A

Frontal lobe anterior to M1 (motor cortex)

Planning complex movement and programming sequencing of movements

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11
Q

Association cortex

A

Areas that impact other areas that are involved in motor activity

Posterior parietal cortex- ensures movements are targeted accurately to objects in external space

Prefontal cortex- involved in section of appropriate movement for a particular course of action

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12
Q

Loss of function of upper motor neurone

A

Paresis- graded weakness of movements

Paralysis- complete loss of muscle activity

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13
Q

Increased abnormal motor function of upper motor neurones due to loss of inhibitory descending inputs

A

Spasticity: increased muscle tone

Hyperflexia: exaggerated reflexes

Clonus: abnormal oscillatory muscle contraction

Babinski’s sign- stroke foot and toes fan out

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14
Q

Apraxia

A

Disorder of skilled movement

Usually related to parietal lobe problems

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15
Q

Lower motor neurone disease features

A
  • Weakness
  • Hypotonia (reduced muscle tone)
  • Hypoflexia (reduced reflexes)
  • Muscle atrophy (due to lack of innervation to the musculature)
  • Fasciculations: damaged motor units produce spontaneous action potentials, resulting in a visible twitch
  • Fibrillations: spontaneous twitching of individual muscle fibres
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16
Q

Motor neurone disease

A

Progressive neurodegenerative disorder of the motor system

A disease of both upper and lower motor neurones

17
Q

Upper neurone signs of motor neurone disease

A
  • Increased muscle tone (spasticity of limbs and tongue)
  • Brisk limbs and jaw reflexes
  • Babinski’s sign
  • Loss of dexterity
  • Dysarthria
  • Dysphagia
18
Q

Lower neurone signs of motor neurone disease

A
  • Weakness
  • Muscle wasting
  • Tongue fasciculations and wasting
  • Nasal speech
  • Dysphagia
19
Q

Upper vs lower neurone

A

Upper descends in the spinal cord

Then synapse with lower motor neurones which leave and join the muscle

20
Q

Basal ganglia contents

A
Caudate nucleus
Lentiform nucleus (pitman+ external globes pallidus)
Subthalamic nucleus
Substantia nigra
Nucleus accumbens
21
Q

Function of basal ganglia

A
  • Elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)
  • Moderating and coordinating movement (suppressing unwanted movements)
  • Performing movements in order
22
Q

Basal ganglia circuitry and their relation with diseases

A

For Parkinson’s there is a breakdown in the nigrostriatal connectivity. Dopaminergic cells project to the striatum and are very important in initiation and planning of movement.

Huntington’s disease is affecting neurones within the striatum, and affects local circuitry within the striatum.

Can also get ballistic movements- uncontrolled movement of the arm- due to problems in sub thalamic area

23
Q

Neuropathology of Parkinson’s

A

Black substance is nueormelanin- breakdown product of normal dopamine metabolism in dopaminergic neurones

This is pale in people with Parkinson’s as the dopaminergic neurones die and are cleared

24
Q

Nigro-strial pathway

A

Dopaminergic neurones project from the substantia nigra in the midbrain to the striatum (specifically to the caudate nucleus and the putamen)

In Parkinson’s you lose this input to the basal ganglia

25
Q

Motor signs of Parkinson’s

A

Bradykinesia- slowness of small movements

Hypomimic face- expressionless

Akeneisa- difficulty in initiation of movements

Rigidity- muscle toen increases

Tremor at rest

26
Q

Huntington’s disease genetics and neuropathology

A

Gene on chromosome 4 (codes for Huntingtin protein), autosomal dominant

Triple repeat: CAG repeat(>35 almost certain later in life)

Degeneration of GABAergic inhibitory neurons in the striatum, caudate and then putamen

27
Q

Motor signs of Huntington’s

A

Choreic movements
o Rapid jerky involuntary movements of the body
o Hands and face affected first; then legs and rest of body

  • Speech impairment
  • Difficulty swallowing
  • Unsteady gait ( walking manner)
  • Later stages, cognitive decline and dement
28
Q

Cerebellum vs neocortex laminar structure

A

3 layers in cerebellum vs 6 in neocortex

29
Q

Laminar structure in cerebellum

A

There is an outer-molecular layer (not many neurones, lots of glial cells)

The second layer (piriform layer) has lots of Purkinje cells

Beneath this (granular layer) there are granule cells (neuronal as well)

Inferior olive (nucleus in the rostral medulla) projects to Purkinje cells via climbing fibres
These terminate in the molecular layer where the dendritic tree of the purkinje cell is found

All other inputs go to the granule cells via mossy fibres, and then onwards via parallel fibres
Parallel fibres innervate the purkinje cells
All output from the Purkinje cells is via deep nuclei

30
Q

Divisions of cerebellum

A

Vestibulocerebellum
Spinocerebellum
Cerebrocerebellum

31
Q

Vestibulocerebellum function

A
  • Regulation of gait, posture and equilibrium
  • Coordination of head movements with eye movements
  • Connections with the superior colliculus
32
Q

Vestibulocerebellar Syndrome

A

Damage (tumor) causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open).

33
Q

Spinocerebellum function

A
  • Coordination of speech
  • Adjustment of muscle tone
  • Coordination of limb movements
  • Fine control of the main corticospinal output
  • It modulates and refines output to the musculature
34
Q

Spinocerebellar syndrome

A

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

35
Q

Cerebrocerebellum function

A
  • Coordination of skilled movements – motor learning
  • Cognitive function, attention, processing of language
  • Emotional control
36
Q

Cerebrocerebellar or Lateral Cerebellar Syndrome

A

Damage affects mainly arms/skilled coordinated movements (tremor) and speech. Results in skilled movement loss.

37
Q

Main motor signs of cerebellar problems

A
  • Ataxia: General impairments in movement coordination and accuracy. Disturbances of posture or gait: wide-based, staggering (“drunken”) gait
  • Dysmetria: Inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)
  • Intention tremor: Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)
  • Dysdiadochokinesia: Inability to perform rapidly alternating movements, (rapidly pronating and supinating hands and forearms)
  • Scanning speech: Staccato, due to impaired coordination of speech muscles