HNS18 Motor System I Flashcards
(37 cards)
***Key structures of motor system
- Cortical motor areas
- Primary motor cortex
- PMA
- SMA
(- Primary sensory cortex) - Pyramidal system
- Pyramidal tracts
—> Corticospinal tract
—> Corticobulbar tract
- Internal capsule - Basal ganglia + Thalamus
- Caudate nucleus
- Putamen (Putamen + Caudate nucleus = Striatum)
- Globus pallidus (medial to putamen)
- Subthalamic nucleus
- Substantia nigra - Brainstem
- Reticular formation - Cerebellum
- Spinal cerebellum
- Cerebral cerebellum
- Vestibular cerebellum - Spinal cord (Interneuron, Motor neuron, Spinal nerves) —> interact with muscle
Functional overview of motor system
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
Upper vs Lower motor neurons
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
Sensorimotor system
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
Connections between regions
- 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.
3 stages of brain evolution
Reptilian brain (survival response)
—> Paleomammalian brain (emotional processing, limbic system)
—> Neomammalian brain (rational thoughts, complex motor movement)
Human Motor Cortical Areas
- 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
***Somatotopic organisation of cerebral cortex (Brodmann area)
- 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) - 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 - 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 - Primary sensory cortex (S1 (area 3,2,1), behind central sulcus —> Postcentral gyrus)
- Sensory input
- Functionally important for motor activities
Cerebral blood flow
- Correspond to metabolic demands and activities
- Vary with degree and pattern of involvement, depending on nature of motor movement
—> seen in functional imaging
Motor homunculus
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
Supplementary motor area (SMA) syndrome
- SMA injured
- M1 and UMN intact —> No actual paralysis
- Problem with ***initiating movement
- Reduced ***spontaneous and voluntary movement
- Good recovery (vs M1 injury)
Origin of Pyramidal tract
- 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:
- Corticobulbar tract (bulbar: brainstem)
—> to cranial nerve nuclei (brainstem) - Corticospinal tract
—> to spinal motor neurons
Pyramidal tract
- Arise from M1 cortex
Travels through:
- Internal capsule of cerebrum
- Cerebral peduncle of midbrain
- ***Ventral pons
-
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) - Interact with brainstem nuclei
- Descend within spinal cord as ***Corticospinal tract
- Activates and modulates LMNs
- Only 10-20% fibres are Corticospinal tract
- Rest: Cortico-pontine fibres —> connect with Brainstem and Cerebellum
Internal capsule
Lateral to Thalamus
3 parts:
- Anterior limb
- Genu
- 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
Clinical relevance of pyramidal tract
- Diseases of pyramidal tract (anywhere from cortex to spinal cord) can cause:
UMN lesions:
- Loss of cranial nerve motor functions (Corticobulbar tract)
—> facial / tongue weakness etc. (receive bilateral supply except Lower face + Genioglossus) - 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
Corticobulbar tract
- 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
Corticobulbar tract lesion
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
Facial nerve lesion
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
- 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
Hypoglossal nerve lesion
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)
Causes of UMN lesions
- Cerebral infarction
- Tumour in corona radiata
- Infarction of posterior limb of internal capsule (contralateral lower limb affected)
- Pontine infarction
Vascular conditions of internal capsule
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
Key structures of basal ganglion
Collection of deep brain nuclei in cerebrum (Thalamus NOT part of basal ganglion even though lies deep to it)
Consists of:
- Caudate nucleus
- Putamen (Putamen + Caudate nucleus = Striatum / Corpus striatum)
- Globus pallidus (medial to Putamen)
- Subthalamic nucleus
- Substantia nigra
—> Together form a network ***modifying descending internal capsule pyramidal signals
Shape of basal ganglion
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
Key relations of basal ganglion with other structures
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
