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Y2 LCRS 2 - Neuroscience and mental health > Motor Systems > Flashcards

Motor Systems Flashcards

1
Q

COME BACK Explain the concept of the motor system hierarchy.

A

Motor control has a ‘hierarchy’

  • Higher order areas perform more complex tasks
  • Lower order areas perform lower level tasks (i.e. less complex)
  • Certain structures such as the thalamus and cerebellum can modify commands from the cerebral cortex

Levels - lowest to highest:

  • Spinal cord
    • This is mainly involved in reflex movements
  • Brainstem
    • This is the centre of integration of different inputs coming from the vestibular system, the vision system and the auditory system
  • Motor Cortex
    • This is where the movements are programmed and where the voluntary movements are initiated
  • Association Cortex
    • This is not, strictly speaking, part of the motor pathway, but it influences the planning and execution of movements
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2
Q

Where is the motor cortex located and what is it divided into?

A

Location: anterior to the central sulcus

It is divided into three main areas:

  • Primary motor cortex
  • Premotor area
  • Supplementary motor area
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3
Q

What is the location and function of the primary motor cortex (M1)?

A

Location:

  • Precentral gyrus
  • Anterior to the central sulcus

Function:

  • Control of fine, discrete, precise voluntary movement
    • Discrete movements are those that have an observable start and finish (single activity)
    • e.g. lifting a weight
  • Provides descending signals to execute movement
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4
Q

How is the primary motor cortex organised?

A

It has a somatotopic organisation

  • A specific part of the body corresponds to a specific part of the primary motor cortex
  • This organisation is represented by the motor homunculus
    • The size of each body part representation on the motor homunculus is proportional to its complexity of motor function (movement)
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5
Q

What are the two main descending motor pathways?

A
  • Corticospinal tract
    • Supplies the musculature of the body
  • Corticobulbar tract
    • Supplies the musculature of the head and neck
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6
Q

Describe the corticospinal tract.

A

Out of the two descending pathways, the corticospinal tract is the main one

  • It is the route by which motor signals are transmitted from the cortex to the spinal cord
  • It has 2 divisions
    • Lateral corticospinal tract
    • Anterior corticospinal tract
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7
Q

Describe the corticbulbar tract.

A
  • UMN: Primary motor cortex → brainstem
    • Fibres converge and pass through internal capsule to brainstem
    • Internal capsule = large collection of white matter fibres - both motor and sensory
      • ​Includes fibres from corticospinal tract too
  • UMN synapses with LMN in brainstem
    • These LMN are the the cranial nerve motor nuclei
  • LMN: Brainstem → muscles of face and neck via CNs
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8
Q

What is the location and function of the premotor cortex?

A

Location:

  • Frontal lobe
  • Anterior to M1 - laterally

Function:

  • Planning of movements
  • Regulates externally cued movements
    • Externally cued means in response to an external stimuli
  • EXAMPLE: Seeing an apple (external stimuli) and reaching out for it requires:
    • Moving a body part relative to another body part (intra-personal space)
      • You would be moving the arm away from trunk trunk
    • Movement of the body in the environment (extra-personal space)
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9
Q

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

A

Location:

  • Frontal lobe
  • Anterior to M1 - medially

Function:

  • Planning complex movements
  • Programming sequencing of movements
  • Regulates internally driven movements (e.g. speech)
    • Intenally driven means it is essentially a self-initiated process
  • SMA becomes active when thinking about a movement before executing that movement
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10
Q

What is the association cortex?

A

Brain areas which are not strictly motor areas as their activity does not correlate with motor output or action

  • Essentially their level of activity does not correlate with level of motor action
  • As well as having an influence on motor activity, these areas also have other functions

Made up of:

  • Posterior parietal cortex
    • ​Ensures movements are targeted accurately to objects in external space
  • Prefrontal cortex
    • Involved in selection of appropriate movements for a particular course of action
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11
Q

Name different locations of lesions and what they correlate to.

A

If something’s wrong with:

  • Lower motor neurones
    • Problem with the neurons leaving the brainstem or ventral horn of the spinal cord or to the muscle
  • Upper motor neurones
    • Problem with the neurones from the cortex to the brainstem
    • Includes UMNs of the corticospinal and corticobulbar tract
  • Pyramidal
    • Problem with the corticospinal tract
  • Extrapyramidal
    • Problem with the basal ganglia or cerebellum
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12
Q

What are the signs of an UMN lesion?

A

Loss of function (negative signs):

  • Paresis: graded weakness of movements
  • Paralysis (plegia): complete loss of muscle activity

Increased abnormal motor function (positive signs):

  • Spasticity: increased muscle tone
    • Spasticity = increased, involuntary, velocity-dependent muscle tone that causes resistance to movement
    • Clinically: The faster you move the limb, the more resistance you feel
  • Hyperreflexia: exaggerated reflexes
  • Clonus: abnormal oscillatory muscle contraction
  • Babinski’s sign

The positive signs are due to loss of inhibitory descending inputs - these signs are linked to hyperexcitability of muscle

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13
Q

What is apraxia?

A

Apraxia is a disorder of skilled movement

  • Patients are not paretic (i.e. do not have muscle weakeness)
  • But they have lost information about how to perform skilled movements

Lesion of:

  • Inferior parietal lobe
  • Frontal lobe - which would effect the:
    • Premotor cortex
    • Supplementary motor area
    • Makes sense as these two areas are involved in planning of movements

Any disease of these areas can cause apraxia, although stroke and dementia are the most common causes

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14
Q

What are the signs of a LMN lesion?

Come back and explain fasciculations and fibrillations - how they occur

To do with denervation hypersensitivity

A
  • Weakness
  • Hypotonia = reduced muscle tone
  • Hyporeflexia = reduced reflexes
  • Muscle atrophy
    • D**ue to lack of use as patients are unable to use the muscles
  • Fasciculations
    • Damaged motor units produce spontaneous action potentials, resulting in a visible twitch
    • Basically when you have a LMN lesion you get denervation of muscle (loss of nerve supply)
    • In order to compensate, you get increased receptor concentration on muscles (NMJ) - dene
      • This is known as denervation hypersensitivity
    • Therefore, it is much easier than normal to stimulate an AP so you get spontaneous APs being produced on damaged motor units
  • Fibrillations
    • Spontaneous twitching of individual muscle fibres
    • You have denervation hypersensitivity of all the muscle fibres in general due to some denervation of muscle
    • Therefore, the denervated muscle fibres can spontaneously produce APs
      • They are hypersensitive to ACh so even a small amount of ACh in the area can stimulate an AP
    • Recorded during needle electromyography examination

NOTE: Motor unit = all the muscle fibres innervated by a single motor neurone (i.e. single motor axon/nerve fibre)

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15
Q

What is motor neurone disease (MND)?

A
  • Progressive neurodegenerative disorder of the motor system
  • Spectrum of disorders
  • Amyotrophic Lateral Sclerosis (ALS)
    • ​Most common MND
    • Affects both upper and lower motor neurones
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16
Q

What are the UMN signs in MND?

A
  • Increased muscle tone (spasticity of limbs and tongue)
  • Brisk limbs and jaw reflexes
  • Babinski’s sign
  • Loss of dexterity
  • Dysarthria = motor speech disorder
    • You know what to say but there is a problem with your muscles that help produce speech, therefore you cannot formulate/pronounce the words properly
    • With UMN lesion you get spastic dysarthria
  • Dysphagia = difficulty swallowing
    • Increased tone of the muscles used in swallowing would make this action mroe difficult
17
Q

What are the LMN signs in MND?

A
  • Weakness
  • Muscle wasting
  • Tongue fasciculations and wasting
  • Nasal speech
    • Due to flaccid dysarthria
  • Dysphagia = difficulty swallowing
    • Swallowing is a series of muscular contractions
    • If you have weakness of the muscles required to swallow, then this action would be difficult
18
Q

What is the basal ganglia?

STRUCTURE

CIRCUITRY

FUNCTIONAL GROUPING

A
  • The basal ganglia is an accessory motor system within the brain
  • Forms a side loop in the motor systems hierarchy (descending pathway)
    • Therefore it is an extrapyramidal
  • Information from the cerebral cortex gets passed onto the basal ganglia and from there loops back to the cortex via the thalamus
  • This allows the basal ganglia to influence and modulate the activity of motor cortex

NOTE: The same thing happens for the cerebellum - another side loop

19
Q

What structures are included in the basal ganglia?

A

Basal ganglia = group of subcortical nuclei

  • Caudate nucleus
  • Lentiform nucleus
    • Made up of putamen + external globus pallidus
  • Subthalamic nucleus
  • Substantia nigra
  • Ventral pallidum
  • Claustrum
  • Nucleus accumbens
  • Nucleus basalis of Meynert
20
Q

Describe the position of the structures in the basal ganglia.

A

Caudate:

  • Most anterior
  • Tapers as you go back in the coronal plane (head → tail)
  • Makes up the lateral wall of the lateral ventricle anteriorly

Putamen:

  • Lateral and slightly inferior to caudate in coronal plane
  • Links between putamen and caudate

Globus Pallidus:

  • Medial to putamen
  • Two components → internal and external
    • Have different circuitry within the basal ganglia
    • i.e. They are two separate nuclei

Striatum = caudate + putamen + external globus pallidus

21
Q

Be able to label cross sections of the basal ganglia.

A
22
Q

What are the functions of the basal ganglia?

A
  • Elaborating associated movements e.g:
    • Swinging arms when walking
    • Changing facial expression to match emotions
  • Moderating and coordinating movement
    • Involves suppressing unwanted movements
  • Performing movements in order
23
Q

Describe basal ganglia circuitry.

A
  • Input from cerbral cortex → striatum
  • Links between subthalamic nucleus, internal globus pallidus and one part of the substantia nigra
  • Supplementary motor area and thalamus - involved in basal gangla circuitry
  • But thalamus is not part of the basal ganglia

NOTES:

  • Substantia nigra has two parts
    • They have different sets of neurones (GABAergic vs dopaminergic)
  • Ballism = repetitive, but constantly varying, large amplitude involuntary movements of the proximal parts of the limbs
    • Due to decrease in activity of the subthalamic nucleus
24
Q

What is the neuropathology of Parkinson’s disease?

A

Classically the primary pathology involves the neurodegeneration of the dopaminergic neurons that originate in the substantia nigra and project to the striatum

SUMMARY:

  • Neurodegeneration of dopaminergic neurones:
    • Substantia nigra → striatum (nigrostriatal pathway)
25
Q

What will you see in the brain of Parkinson’s patients?

A
  • Normally the substantia nigra is black because the dopaminergic neurones contain neuromelanin
    • Neuromelanin is a normal metabolic by-product in these neurones
  • In PD patients, you lose these dopaminergic neurones
    • They undergo degeneration and therefore you lose the substantia nigra
    • So in the brain you won’t see will see less and less of the black

NOTE: Takes about 60% loss of the dopaminergic neurones before you start to see symptoms.

26
Q

What is the consequence of neurodegeneration of the nigrostriatal pathway?

A

Basal ganglia motor loops are important in modulating the activity of the motor cortex (i.e. voluntary movement)

  • Loss of the nigrostriatal pathway means that the motor cortex is no longer being modulated propely by the basal ganglia which leads to problems
27
Q

What are the main motor signs of Parkinson’s disease?

A
  • Bradykinesia
    • Slowness of (small) movements
    • e.g. Doing up buttons, handling a knife
  • Hypomimic face
    • Expressionless, mask-like
      • Absence of movements that normally animate the face
  • Akinesia
    • Difficulty in the initiation of movements because cannot initiate movements internally
      • Essentially cannot voluntarily move their muscles
  • Rigidity
    • Muscle tone increase, causing resistance to externally imposed joint movements
      • Externally imposed as in when you move their limbs/joints
      • They can’t initiate movements themselves anyway
      • Different from spasticity in that it is not velocity-dependent
  • Tremor at rest
    • 4-7 Hz
    • Starts in one hand (“pill-rolling tremor”) - with time spreads to other parts of the body
      • Pill rolling - looks like you are trying a roll a pill between your thumb and index finger
28
Q

What is Huntington’s disease?

A

Genetic neurodegenerative disorder

  • Autosomal dominant
  • You have a mutation on a gene on chromosome 4
    • This results in several CAG trinucleotide repeats on the gene
    • HTT gene codes for huntingtin protein
    • Mutated gene leads to mutant protein formation which leads to neuronal degeneration
  • Degeneration of GABAergic neurons in the striatum: caudate then putamen
    • Similar to PD, this means that the motor cortex is no longer being modulated propely by the basal ganglia which leads to problems
29
Q

What are the motor signs of Huntington’s disease?

A
  • Choreic movements (Chorea)
    • Rapid jerky involuntary movements of the body
    • Hands and face affected first
    • Then legs and rest of body
  • Speech impairment
  • Difficulty swallowing
  • Unsteady gait
    • i.e. Unsteady when walking
  • Later stages, cognitive decline and dementia
30
Q

Where is the cerebellum located?

A
  • In the posterior cranial fossa
  • Has a fold of dura over it - tentorium cerebelli
  • Lies on the posterior aspect of the pons
31
Q

Describe the structure of the cerebellum.

A

3 layer structure - outer to inner:

  • Molecular Layer
    • Not that many neurones there
  • Piriform Layer
    • Purkinje cells (type of neurone)
  • Granular Layer
    • Granule cells (another type of neurone)
32
Q

Describe the circuitry of the cerebellum.

A
  • Inferior olive projects to Purkinje cells via climbing fibres
    • Inferior olive is a nucleus (collection of cell bodies) in the medulla oblongata
      • ​Also known as inferior olivary nucleus
    • Climbing fibres = axonal projections from inferior olive
  • All other input to granule cells via mossy fibres and then onwards via parallel fibres
    • Mossy fibres from:
      • Cerebral cortex
      • Brainstem
      • Spinal cord
    • Parallel fibres arise from the axons of the granule cells which synapse with Purkinje cells
  • All output from Purkinje cells via deep nuclei
    • The Purkinje cells synpase with deep nuclei in the cerebellum
    • Fibres arising from these deep nuclei then project out of the cerebellum (efferent)

SUMMARY:

  • Climbing fibres from the inferior olive synpase with Purkinje cells
  • Mossy fibres synpase with granule cells
  • Parallel fibres from the granule cells synapse with Purkinje cells
  • Purkinje cells synpase with deep nuclei
  • Cerebellar output originiates from deep nuclei
33
Q

What are the 3 functional divisions of the cerebellum?

A
  • Vestibulocerebellum
  • Spinocerebellum
  • Cerebrocerebellum

NOTE:

  • These divisions are shown in the picture below in order (left to right)
  • The divisions only shown on one side but are present on both sides - cerebellum is symmetrical
34
Q

What is the function of the vestibulocerebellum? What happens if there is damage to this area?

A

Function:

  • Connected with the vestibular
  • Regulation of gait, posture and equilibrium (i.e. balance)
  • Coordination of head movements with eye movements

Vestibulocerebellar syndrome:

  • Damage (tumour) causes syndrome similar to vestibular disease
  • It leads to gait ataxia and tendency to fall
    • Even when patient sitting and have their eyes open
35
Q

What is the function of the spinocerebellum? What happens if there is damage to this area?

A

Function:

  • Coordination of speech
  • Adjustment of muscle tone
  • Coordination of limb movements

Spinocerebellar syndrome:

  • Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs
  • Causes abnormal gait and stance (wide-based)
36
Q

What is the function of the cerebrocerebellum? What happens if there is damage to this area?

A

Function:

  • Coordination of skilled movements
    • Skilled movements are the ones that are developed through training and practice - so they are learned movements
  • Cognitive function, attention, processing of language
  • Emotional control

Cerebrocerebellar (or lateral cerebellar) syndrome:

  • Damage affects mainly:
    • Arms or skilled coordinated movements
      • Leads to tremor
    • Speech
37
Q

What are the main signs of cerebellar dysfunction?

A

REMEMBER: Deficits apparent only upon movement

  • 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
      • e.g. Knocking over a cup rather than grabbing it
  • Intention tremor
    • Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)
    • The amplitude of an intention tremor increases as an extremity (limb) approaches the endpoint of deliberate and visually guided movement
  • Dysdiadochokinesia
    • Inability to perform rapidly alternating movements,
      • e.g. Rapidly pronating (palm down) and supinating (palm up) hands and forearms
  • Scanning speech
    • Staccato, due to impaired coordination of speech muscles
    • Scanning speech is when the normal “melody” or speech pattern is disrupted - you get abnormally long pauses between words or individual syllables of words

Y2 LCRS 2 - Neuroscience and mental health (23 decks)

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