HNS18 Motor System I Flashcards

1
Q

***Key structures of motor system

A
  1. Cortical motor areas
    - Primary motor cortex
    - PMA
    - SMA
    (- Primary sensory cortex)
  2. Pyramidal system
    - Pyramidal tracts
    —> Corticospinal tract
    —> Corticobulbar tract
    - Internal capsule
  3. Basal ganglia + Thalamus
    - Caudate nucleus
    - Putamen (Putamen + Caudate nucleus = Striatum)
    - Globus pallidus (medial to putamen)
    - Subthalamic nucleus
    - Substantia nigra
  4. Brainstem
    - Reticular formation
  5. Cerebellum
    - Spinal cerebellum
    - Cerebral cerebellum
    - Vestibular cerebellum
  6. Spinal cord (Interneuron, Motor neuron, Spinal nerves) —> interact with muscle
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2
Q

Functional overview of motor system

A

Highest level (initial desire to move)
—> Sensorimotor cortex (rough draft of movement design)
—> Basal ganglia, Thalamus (refined movement design)
—> Cerebellum (relay station and further control)
—> Brainstem, Spinal cord (final execution of motor plan)
—> Muscle fibres (activate muscular contraction)

Feedback from Thalamus, Brainstem present

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3
Q

Upper vs Lower motor neurons

A

Upper motor neuron (UMN):

  • Descending tracts from cerebrum (e.g. Primary motor cortex)
  • With/without interneurons in brainstem / spinal cord
  • Ends in brainstem / spinal cord
  • Commands and modulate LMN

Lower motor neuron (LMN):

  • From cranial nerve nuclei in brainstem —> travel within cranial nerves OR
  • From anterior horn cells in spinal cord —> travel within spinal nerves
  • Activates muscle
  • Efferent component of reflex arc
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4
Q

Sensorimotor system

A

Sensory information: Critical to motor functions

Highest level:
- Generates a mental image of the body and its relationship with environment

Middle level:
- Tactical decisions based on memory of sensory information from past experience (muscle memory)

Lowest level:
- Sensory feedback to maintain posture, muscle length, tension before/after each voluntary movement

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5
Q

Connections between regions

A
  • Between higher and lower levels of control / within same level
  • Direct / Indirect influence
  • Parallel non-binary processing (NOT only yes/no)
  • Enable feedback loops, reflexes, memory, purposes, planning etc.
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6
Q

3 stages of brain evolution

A

Reptilian brain (survival response)
—> Paleomammalian brain (emotional processing, limbic system)
—> Neomammalian brain (rational thoughts, complex motor movement)

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7
Q

Human Motor Cortical Areas

A
  • Extend to large areas ***beyond primary motor cortex
  • Capable of purposeful, planned, controlled and complex motor functions
  • Highly evolved **Corticospinal tract to enable **fine complex movement
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8
Q

***Somatotopic organisation of cerebral cortex (Brodmann area)

A
  1. Primary motor cortex (M1, Area 4, in front of central sulcus —> Precentral gyrus)
    - ***Main generator of projecting signals to spinal cord
    - Executes commands via Brainstem, Spinal cord (esp. for distal musculature)
  2. Premotor area (PMA within Area 6)
    - **Sensory guidance
    - **
    Identify targets in space, choose the type of action, programming of movements
    - Act via Area 4, Brainstem, Spinal cord
  3. Supplementary motor area (SMA within Area 6)
    - **Planning, sequence of movement
    - **
    Identify targets in space, choose the type of action, programming of movements
    - Act via Area 4, Brainstem, Spinal cord
  4. Primary sensory cortex (S1 (area 3,2,1), behind central sulcus —> Postcentral gyrus)
    - Sensory input
    - Functionally important for motor activities
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9
Q

Cerebral blood flow

A
  • Correspond to metabolic demands and activities
  • Vary with degree and pattern of involvement, depending on nature of motor movement
    —> seen in functional imaging
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10
Q

Motor homunculus

A

Medial motor cortex:

  • Trunk muscles
  • Lower limb muscles

Lateral motor cortex:

  • Upper limb muscles
  • Hands (occupy large area of motor cortex —> complex, fine, detailed movement)
  • Face
  • Tongue (for speech)

However, the map is an over-simplification
—> many overlaps
—> more likely a map of repertoires of movements than muscle groups

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11
Q

Supplementary motor area (SMA) syndrome

A
  • SMA injured
  • M1 and UMN intact —> No actual paralysis
  • Problem with ***initiating movement
  • Reduced ***spontaneous and voluntary movement
  • Good recovery (vs M1 injury)
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12
Q

Origin of Pyramidal tract

A
  • Cerebral cortex has 6 layers
  • Pyramidal tract mainly from ***layer V of M1 tract
  • Betz cells (from layer V) send out the main UMNs
  • Consists of:
  1. Corticobulbar tract (bulbar: brainstem)
    —> to cranial nerve nuclei (brainstem)
  2. Corticospinal tract
    —> to spinal motor neurons
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13
Q

Pyramidal tract

A
  • Arise from M1 cortex

Travels through:

  1. Internal capsule of cerebrum
  2. Cerebral peduncle of midbrain
  3. ***Ventral pons
  4. Decussate at pyramids of medulla oblongata (forming a bulge at **anterior of brainstem —> pyramids)
    - majority: crossed fibres (
    Lateral corticospinal tract) —> serve limb muscles
    - some: uncrossed fibres (
    **Anterior corticospinal tract) —> serve paraxial muscles (e.g. posture)
  5. Interact with brainstem nuclei
  6. Descend within spinal cord as ***Corticospinal tract
  7. Activates and modulates LMNs
  • Only 10-20% fibres are Corticospinal tract
  • Rest: Cortico-pontine fibres —> connect with Brainstem and Cerebellum
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14
Q

Internal capsule

A

Lateral to Thalamus

3 parts:

  1. Anterior limb
  2. Genu
  3. Posterior limb

Corticospinal area (***Genu of internal capsule):
1. Fibres for medial M1 cortex (lower limb / trunk muscles)
—> posterior of Genu
2. Fibres for lateral M1 cortex (upper limb / face muscles)
—> anterior of Genu

Pathway:
Fibres from M1 cortex (Corona radiata) —> Internal capsule —> finally arrive at midbrain

Other areas of internal capsule:
- fibres for going up to cerebral cortex from other areas of brain

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15
Q

Clinical relevance of pyramidal tract

A
  • Diseases of pyramidal tract (anywhere from cortex to spinal cord) can cause:

UMN lesions:

  1. Loss of cranial nerve motor functions (Corticobulbar tract)
    —> facial / tongue weakness etc. (receive bilateral supply except Lower face + Genioglossus)
  2. Loss of spinal nerve motor function (Corticospinal tract)
    —> contralateral limb weakness / paralysis
  • Pattern of dysfunction is distinct from LMN lesion (affect cranial / spinal nerves themselves)
    —> Enable clinical localisation of the disease
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16
Q

Corticobulbar tract

A
  • Pyramidal UMN fibres that end in brainstem to control motor functions of cranial nerves (CN5, 7, 9, 10, 11, 12) except ocular nerves (CN3, 4, 6)
  • ALL non-ocular LMN supplied by **bilateral UMN except:
    1. CN7 for lower face
    2. CN12 for genioglossus muscle (protrusion)
    —> receive ONLY **
    contralateral UMN supply
  • Extra-ocular movements controlled by a separate system
17
Q

Corticobulbar tract lesion

A
UMN lesion (e.g. cerebral stroke):
- lesion on one side may NOT result in any symptoms due to bilateral supply (except CN7, 12)
LMN lesion (e.g. injury to nerve itself):
- lower motor neuron symptoms on lesion side
18
Q

Facial nerve lesion

A
UMN lesions:
1. Upper facial nerve nuclei:
- receive ***Bilateral UMN input
- function preserved in all UMN lesion
—> e.g. left cerebral stroke —> right upper face unaffected
  1. Lower facial nerve nuclei:
    - receive ***Contralateral UMN input
    - function lost in contralateral UMN lesion
    —> e.g. left cerebral stroke —> right lower face palsy

LMN lesion:
- both upper and lower face affected at the same time
—> e.g. right facial nerve injury —> right upper + lower face palsy

19
Q

Hypoglossal nerve lesion

A

UMN lesion:
- weakness in contralateral genioglossus muscle —> tongue deviates to weakness side (away from lesion side)
—> e.g. **right UMN lesion —> weakness in left genioglossus muscle —> unopposed protrusion by genioglossus muscle —> tongue deviates to **left side

LMN lesion:
- weakness in **ipsilateral genioglossus muscle —> tongue deviates **towards lesion side
—> e.g. **left LMN lesion —> weakness in left genioglossus muscle —> unopposed protrusion by genioglossus muscle —> tongue deviates to **left side

Distinguish between right UMN and left LMN lesion:
—> even though both protrude tongue to left side
—> muscle atrophy ONLY occurs in LMN lesion (UMN lesion ***NO muscle atrophy)

20
Q

Causes of UMN lesions

A
  1. Cerebral infarction
  2. Tumour in corona radiata
  3. Infarction of posterior limb of internal capsule (contralateral lower limb affected)
  4. Pontine infarction
21
Q

Vascular conditions of internal capsule

A

Common site of stroke
- ∵ supplied by ***Lenticulo-striate arteries
—> End artery
—> can be degenerated / occluded / ruptured —> IC infarction / haemorrhage

End result:
- UMN paralysis of contralateral limbs, lower face, genioglossus

22
Q

Key structures of basal ganglion

A

Collection of deep brain nuclei in cerebrum (Thalamus NOT part of basal ganglion even though lies deep to it)

Consists of:

  1. Caudate nucleus
  2. Putamen (Putamen + Caudate nucleus = Striatum / Corpus striatum)
  3. Globus pallidus (medial to Putamen)
  4. Subthalamic nucleus
  5. Substantia nigra

—> Together form a network ***modifying descending internal capsule pyramidal signals

23
Q

Shape of basal ganglion

A

Human brain change shape as it enlarges within confined space of skull
—> caudate nucleus, cerebral ventricles and other structures within cerebrum adopt a “C” shape

24
Q

Key relations of basal ganglion with other structures

A

Caudate nucleus:

  • head + body (sits in frontal lobe)
  • tail (sits in temporal lobe)
  • medial to anterior limb of internal capsule

Putamen + Globus pallidus (exteral + internal) —> Lentiform nucleus

  • separated from head of Caudate nucleus and Thalamus by internal capsule
  • lateral to internal capsule

Subthalamic nucleus: below Thalamus

Substantia nigra: in upper midbrain

25
Q

Corpus striatum (“striated body”)

A

Caudate nucleus + Lentiform nucleus

Striated pattern formation:
- fibres from cortex descend through internal capsule
—> transversing and breaking up connections running between Caudate nucleus and Lentiform nucleus
—> causing striated pattern

26
Q

Function of basal ganglia

A
  • Does NOT directly activate muscles
  • Acts by helping cerebral cortex and brainstem motor regions to **generate and **modulate movements
  • Diseases of basal ganglion —> abnormalities in ***initiation, pattern, speed, rhythm etc. of movement
  • but ***NOT muscle weakness / paralysis
  • Also many functions ***beyond motor function
27
Q

Functional connections of basal ganglion to other regions

A

***Cerebral cortex
—> Caudate + Putamen (Striatum) —> (interact with Substantia nigra)
—> Globus pallidus (Pallidum) —> (interact with Subthalamic nucleus)
—> Thalamus (VA/VL)
—> back to Cerebral cortex

  • Anatomically: Corpus striatum = Caudate nucleus + Lentiform nucleus
  • Functionally: Striatum = Caudate nucleus + Putamen (不包括Globus pallidus)
Striatum: ***Receives signals from Cortex + Thalamus
Globus pallidus (Pallidum): ***Chief output to Cortex + Thalamus
28
Q

***Basal ganglion pathways

A

Associate cortex generates desire to move
—> activates Striatum (which stores programmes)
—> Striatum (initiates movement) —> interact with Substantia nigra
—> Pallidum
—> via Subthalamic + Thalamic nuclei (VA/VL)
—> projects to Premotor cortex (programmes complex movement)
—> carry out though Primary motor cortex
—> UMN —> LMN

29
Q

Abnormalities of Basal ganglion pathways

A

Negative signs:

  • wants to perform but cannot
  • e.g. Bradykinesia, hesitancy, abnormal posture
  • Parkinson’s disease

Positive signs:

  • cannot prevent movement
  • e.g. Rigidity, Dyskinesia, chorea, athetosis, ballismus
  • Huntington’s disease

Parkinson’s disease:
- Loss of dopamine activities in Substantia nigra
—> imbalance between activation and inhibition at various points
- also involve other neurotransmitter in BG (glutamate and GABA)
- symptoms: parkinsonian gait, slowed movement, rigidity, asymmetric resting tremor etc.
- muscles are intact but tone / initiation of movement is abnormal
- treatment: Deep brain stimulation —> generates electrical pulses to correct / override diseased brain circuits

30
Q

Cerebellum

A

Behind Brainstem

3 parts:

  • Right hemisphere
  • Left hemisphere
  • Vermis
3 anatomical lobes:
- Anterior
—> Primary fissure
- Posterior
—> Posterior fissure
- Flocculonodular
31
Q

Functions of Cerebellum

A

does NOT directly activate muscle

  1. **Updates motor commands (by **comparing descending control signals with sensory feedback of movement —> Fine tuning)
  2. Control ***posture (by using vestibular inputs (inner ear))
  3. ***Planning and initiation of movements (via projections to primary motor cortex)
  4. Precision in speed, direction, range of movement
32
Q

Functional division of cerebellum

A
  1. Vestibular cerebellum
    - Flocculonodular lobe
    - Archicerebellum (most primitive)
    - inputs from **vestibular apparatus
    - outputs to **
    axial muscles for ***truncal balance
  2. Spinal cerebellum
    - Anterior lobe
    - Paleocerebellum
    - input from **mechanoreceptors via **spinocerebellar pathway
    - output to **limb via brainstem nuclei —> control muscle **tone and ***coordination for walking and gait stability
  3. Cerebral cerebellum
    - Posterior lobe
    - Neocerebellum (most advanced)
    - input from **cortex via **middle cerebral peduncle
    - output to **thalamus and cortex —> coordination of voluntary movement by motor **planning, learning and memory
33
Q

Connections of cerebellum to brainstem

A
  1. Superior cerebellar peduncle (上面出cortex)
    - Output to Thalamus and Cortex —> fine tune and control movement
    - Output from:
    —> Fastigial nucleus
    —> Globose nucleus, Emboliform nucleus
    —> Dentate nucleus
  2. Middle cerebellar peduncle (中間cortex/pons入)
    - Input from Pons (e.g. Corticopontine fibres / descending tract)
  3. Inferior cerebellar peduncle (下面medulla/spinal cord入)
    - Input from Medulla (esp. Inferior olive) / Spinal cord (e.g. Spinocerebellar tract (proprioceptive information))
34
Q

Cerebellar conditions

A

Distinct from cerebrum conditions:

  • may not be associated with muscle weakness / paralysis
  • ***ipsilateral (unknown reason)
  1. Cerebellar haemorrhage
    - ipsilateral intentional tremor / ***dysmetria
  2. Medulloblastoma
    - tumour of cerebellar vermis
    - truncal ataxia

Clinical signs:

  1. Finger to nose test (***Past-pointing sign)
  2. ***Dysdiadochokinesia test (手板向上向下)
  3. ***Heel to shin test
35
Q

Brainstem: Reticular formation

A

Receive and integrate input from higher motor centres (cortex) and various sensory organs (e.g. eyes / ears / ascending general sensory tracts)
—> 1. Communicate with cortex to modify control (radiations to cortex)
—> 2. Send signals down to spinal cord via descending motor projections
—> forming final motor command

Consists of various brain nuclei such as:

  1. Red nuclei (in Midbrain) —> Rubrospinal tract
    - input from **cerebral cortex + cerebellum
    - output through rubrospinal tract
    - **
    upper limb ***flexor predominant
  2. Lateral Vestibular nuclei (in Medulla oblongata) —> Lateral Vestibulospinal tract
    - equilibrium and balance
    - input from **vestibular apparatus
    - output to **
    limb and **trunk muscles
    - **
    extensor predominant
  3. Reticular nuclei (in Medulla oblongata + Pons) —> Reticulospinal tract
    - Pontine: extensor
    - Medullary: flexor

Run together with pyramidal tracts —> referred to as “extrapyramidal” tracts —> strong influence on spinal cord

36
Q

***Brainstem and motor control

A
  1. ***Process information from
    - Higher level special senses (smell, visual, auditory)
    - Spinal cord (peripheral mechanoreceptors)
  2. ***Modulate activities of:
    - Corticobulbar tract to cranial nerve nuclei
    - Corticospinal tract to spinal nerve nuclei
  3. Send descending fibres in addition to the pyramidal tracts (i.e. extrapyramidal tracts)
    - further ***modulate motor activities within spinal cord
    - sometimes even though pyramidal tracts are diseased
    —> can still have some degree of control on LMN
  4. Critical for **postural adjustments + control of **axial + ***proximal musculature
37
Q

Summary of motor system I

A

Cerebral cortex, Basal ganglion, Thalamus, Cerebellum, Brainstem
—> Refined motor plan

Pyramidal + Extrapyramidal tracts (further modulate motor activities within spinal cord)
—> Execute motor plan