Somatic Motor System Flashcards

1
Q

What are lower motor neurons?

A

alpha motor neurons
The only neuron that innervate skeletal muscle - final common pathway of nervous system for interacting with external environemtn

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2
Q

What do LMNs use as their neurotransmitter?

A

ACh & skeletal muscle have nicotinic Ach receptors

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3
Q

Describe a Nicotinic Ach Receptor

A

o nAChR are ligand-gated ion channels; when 2 ACh molecules bind to the nAChR, the gate opens, and cations (Na+, K+ and Ca++) can flow through.
• So from resting membrane potential you get binding of ACh to nAChR which trigger the opening of Na+ channels (sodium & calcium in, K+ out) -> membrane depolarizes, AP occurs, channels close & you get repolarization
o Voltage change from AP causes Ca++ channels to open & Ca++ released from SR -> muscle contraction
• The net effect is to depolarize the skeletal muscle membrane (excitatory post-synaptic potential EPSP) enough to reach the threshold potential, so that an AP is generated & then propagated along the full length of the skeletal muscle membrane via voltage gated sodium & potassium channels.

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4
Q

What is the enzyme which breaks down Ach at the synaptic clefts?

A
  • Acetylcholinesterase (AChE) breaks down ACh in the synaptic cleft basal lamina, and the breakdown products can be recycled by the presynaptic terminal
  • A single AP in a LMN causes all of its muscle fibers to fire an AP, hence muscle twitch occurs
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5
Q

What is a motor neuron pool?

A

• A motor neuron pool is all of the LMNs innervating one muscle
o Typically thousands of LMNs supply a single muscle

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6
Q

What is a motor unit

A

• A motor unit is one LMN and all the muscle cells (myofibers) that it innervates
o A motor unit in an extraocular muscle has about 10 cells, while a motor unit in the quadriceps femoris or gluteus maximus has about 1000 muscle cells.
o After an initial development period of multiple innervation, an individual muscle cell is only innervated by a single LMN throughout life

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7
Q

How do you increase the strength of contraction of a muscle

A

To increase the strength of contraction of a muscle, a single LMN can fire action potentials more frequently, leading to the summation of forces generated by individual twitches, up to a maximal response for muscle fibers, called (fused) tetanus. Additionally, more & more LMNs & their muscle fibers (motor units) can be recruited to fire APs, and because of the properties of LMNs, this tends to occur in the order S, FFR, FF motor units as more & more force is required. S fibers can contract for long periods of time (hours), FFR for many minutes, and FF for only about 1 minute.

*S- slow, red: aerobic
F- Fast fatiguable, white- anaerobic
FFR- fast fatigue resistant: intermediate properties or red and white fibres

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8
Q

What happens to a muscle when a LMN dies

A

• If an LMN dies, all its muscle fibers are denervated
o Because only 1 LMN supplies each muscle fiber
• But surviving LMNs nearby can sprout axon collaterals & take over innervation of the surrounding muscle fibers
o May induce a switch (if necessary) in the muscle fiber type
• Leads to ‘type grouping’ (myofibres switch fiber type to new LMN’s type) and larger motor units
o Groups/clusters of different fiber types
• If a muscle loses its motor neuron pool (all LMNs innervating it), this causes complete paralysis of the muscle & severe muscle atrophy over time

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9
Q

Where are LMNs in the spinal cord?

A

Anterior horn

innervate muscles on the IPSILATERAL side

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10
Q

Where are LMNs in the brainstem

A

• LMNs in cranial nerve motor nuclei in the brainstem associated with CN III- XII, except VIII
• Almost all LMNs innervate ipsilateral muscles
o EXCEPTIONs (contralateral)
• Trochlear nucleus – superior oblique (cross before they leave midbrain – so R trochlear nucleus supplies L superior oblique)
• Part of oculomotor nucleus – superior rectus

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11
Q

Names the heirarchical control of LMNs

A

• Direct sensory input
• Interneurons
o integrate a lot of other input – sensory input & input from CPG, UMN systems & indirect influences from other types of cerebral cortex
• Indirect sensory input
• Central pattern generators (CPG)
• Upper motor neurons (UMN)
• Cerebral cortex, cerebellum, basal ganglia
• Input to LMNs may be excitatory or inhibitory
o From interneurons – depending on the neurotransmitter released

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12
Q

Explain the muscle stretch reflex

A
  • The muscle stretch reflex is the simplest reflex, involving only 2 neurons & one synapse (monosynaptic) between the sensory & motor neuron in the CNS (of course, stretching a muscle activates many sensory neurons, which synapse on many motor neurons; to say it is a two neuron reflex & monosynaptic is to discuss only the essence of the organization of the reflex)
  • Muscle spindles detect a stretch of the muscle, which activates Ia afferent fibers (the cell bodies are in the DRG) which synapse (excitatory) directly on LMNs in the ventral horn of the spinal cord. The LMNs innervate the same muscle that was stretched (the homonymous muscle – note, that’s another synapse, so the reflex isn’t really monosynaptic) & cause it to contract, to return it towards its length prior to the stretch. You should revise the main muscle stretch reflexes that are tested clinically, and the related spinal segments, eg S1-2, L3-4, C5-6, C7-8
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13
Q

Explain the flexor reflex (withdrawl reflex)- painful stimuli

A

• It is initiated by cutaneous receptors & involves multiple muscle groups in the affected limb to move the limb away from the noxious stimulus, as well as the contralateral limb & postural muscles to maintain balance
o Particularly when the stimulus is applied to a lower limb, this typically results in a ‘crossed extensor’ response – eg the opposite lower limb is extended to take the weight of the body

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14
Q

what are central pattern generators

A

CPG more complicated than reflex. Reflex just respond to senses.
• CPGs are located in the brainstem & spinal cord
• CPGs are networks of neurons that control LMNs to drive a stereotyped action involving several muscles or groups of muscles (eg breathing, coughing, walking)
o Walking – you are not thinking about which muscle groups are contracting or relaxing.
• Activity of CPG can be modified by descending input & sensory input to adapt to changing conditions
o i.e. not walking on a smooth surface – need to adjust the sequence of contractions, and may involve some reflexes as well

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15
Q

Name some upper neuron systems which influence spinal LMNS

A
  • Corticospinal tract (cerebral cortex)
  • Rubrospinal tract (red nucleus in midbrain)
  • Tectospinal tracts (tectum)
  • Reticulospinal tracts (pontine & medullary reticular formation)
  • Vestibulospinal tracts (medial & lateral vestibular nuclei)
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16
Q

Describe the RUBROSPINAL TRACT

A
  • Cell bodies in red nucleus in rostral midbrain
  • Fibers cross in midbrain
  • Lateral column in spinal cord
  • Act especially on LMNs controlling FLEXORS OF THE UPPER LIMB (ie grasping objects)
17
Q

Describe the TECTOSPINAL TRACT

A
  • Cell bodies in superior colliculus (part of tectum of midbrain)
  • Fibers cross in midbrain
  • Descend close to the midline in the MLF (also has axons related to eye movement)
  • Axons terminate usually in cervical spinal cord
  • Controls reflexive head movements in response to visual & auditory stimuli
18
Q

Describe the VESTIBULO SPINAL TRACT

A

• Cell bodies in vestibular nuclei (medulla, pons)
• Medial VST (mainly ipsilateral) – mainly terminates in cervical spinal cord
o Neck muscles
• Lateral VST (ipsilateral) – connections throughout the spinal cord (cervical to sacral levels)
o Antigravity muscles (axial muscles & extensors) – posture adjustment
• Responding to vestibular/balance information & maintaining upright posture

19
Q

Describe the RETICULOSPINAL TRACT

A
  • Cell bodies in reticular formation (pontine & medullary reticulospinal tracts)
  • Mostly ipsilateral
  • Reticular nuclei receive much input from motor areas of the cerebral cortex & also receive a lot of sensory input
  • Important pathway in voluntary control of movement
20
Q

Describe the location of the UMN tracts in the spinal cord:

IN the lateral column:

A

lateral corticospinal, rubrospinal tracts

o Mainly control LMNs of distal muscles

21
Q

Describe the location of the UMN tracts in the spinal cord:

In the Anterior column

A

(everything else) tectospinal, reticulospinal, vestibulospinal, anterior corticospinal tracts –
o Mainly control LMNs of proximal and axial muscles (muscles of the back & core etc)

22
Q

Describe the CORTICOSPINAL TRACT, what is it FOR

A

FINE MOTOR CONTROL

• Cell bodies in primary motor cortex and nearby structures
• Fibers travel through:
o Internal capsule, posterior limb
o Midbrain – crus cerebri
o Basal pons
o Medulla – pyramid
o Most fibers (>85%) cross in the decussation of pyramids → lateral column of spinal cord
o Some fibers (<15%) do not cross at caudal medulla → descend in anterior column of spinal cord, and most cross via anterior white commissure near interneurons/LMNs they supply
o Hence all innervation still ends up contralateral
• Direct synapses on LMNs for hand musculature; otherwise interneurons (important for integrating information)

23
Q

Describe the CORTICOBULBAR TRACT

A

MOTOR CONTROL OF MUSCLE OF FACE, HEAD AND NECK:

• To V, VII, IX, X, XI, XII LMNs
• Cell bodies in primary motor cortex & nearby
• Fibers travel through:
o Internal capsule (genu or posterior limbs)
• Fibers travel with CST via
o Crus cerebri
o Basal pons
o Medulla
o Upper cervical spinal cord
• Bilateral innervation of brainstem LMNs
o Exception: contralateral only to LMNs of VII (facial motor nucleus), supplying lower 1/3 to 2/3 of face
o More contralateral than ipsilateral to LMNs of V, XI, XII
• Clinical implication of this is that after a stroke you may see some loss of function on contralateral side, but this should resolve within a few days (for muscles of mastication, SCM, trapezius & tongue mm)

24
Q

What are some of the LMN damage signs

A

LMNs maintain metabolism.
• Severe atrophy of muscles
• Weakness or paralysis (depending on amount lost)
• Hyporeflexia or areflexia (reduction in strength of reflex or complete loss of reflex is all the LMNs for the muscle are gone)
• Hypotonia (reduction in tone – so passive movement of the limb will not elicit any resistance that it usually would

25
Q

What are some of the UMN damage signs

A
•	Some or no atrophy of muscles
•	Weakness or paralysis
•	Spasticity
o	Hyperreflexia, Babinski sign
•	Babinski reflex: when you firmly stroke the sole of the foot the big toe points up towards face & the other toes fan out → this is normal in infancy.  However after 2 year, this may indicate a brain or nervous system disorder 
o	Hypertonia
•	(LMNs & reflexes still in tact