Lower Motor Neurones

Lower motor neurons mode of action

Reflexes occur at level of spinal cords regardless of upper input

Definition of LMN (= common final pathway)

• Somatic motor pathway

• Neuron cell bodies located in ventral column/horn of gray matter of spinal cord

• [axons come out of the ventral ROOT]

• LMN also within motor nuclei of CNs containing efferent component

  • e.g. facial nerve innervating muscles in head (orbicularis oculi)

• Brainstem → connection to other nuclei

• Ventrally located neurons that stimulate skeletal muscle

LMN connection/synapses

interneurones/relay → up and down SC

ascending tracts (ipsilateral or contralateral) → sensory

descending tracts (ipsilateral or contralateral)→ motor

commiss-ural tracts (contralateral)- connect left and right brain hemispheres

LMN Influences

UMN

• First order neurons, initiating and modulating muscle contraction

• Pyramidal tracts

  • both inhibitory and facilitatory

• Sensors from muscle/tendons → sensory receptors, creating inputs (muscle spindles, golgi tendon organs)

sensors → spinocerebellar tract → cerebellum ← → cerebrum (primary motor cortex) → pyramidal (corticospinal or cortionuclear) tracts (UMN) → short relay → LMN

• contralateral primary motor cortex → ipsilateral cerebellum → controls fine motor control of ipsilateral muscle

LMN functions

Regulate and control skeletal muscles

• Regulated through voluntary centres in brain (primary motor cortex)

Lower motor neuron types

• Alpha motor neurons

  • Fibers innervate ordinary muscle fibres (extrafusal)

• Gamma motor neurons

  • Fibers innervate intrafusal muscle fibres (muscle spindles/sensors)

Intrafusal fibre

• Specialised muscle fiber sandwiched between normal muscle fibres

• Central region without myofibrils

• Muscle spindles wrapped around central region of intrafusal fiber

• When muscle spindle contracts → central region pulled

  • activates sensory input, engaging spinal cord

• Rate of muscle spindle stretch increases (due to muscle contraction) → either inhibits or stimulates alpha motor neuron depending on whether muscle stretches or contracts

Coactivation and stimulation of skeletal muscles

• Upper motor neuron stimulates both alpha (extrafusal) and gamma (intrafusal) motor neurons → COACTIVATION

• Activation of alpha motor neurons → extrafusal fibres stimulated

• Activation of gamma motor neurons → spindle contracts (stretches) → synchronises stretch between spindle and regular muscle for sensory purposes

Brain (somatomotor cortex) → UMN → LMN

Spinal cord → alpha and gamma motor neurones

Sensory feedback → smooth skeletal muscle control and movement

• Muscle spindles

• Golgi tendon organs

• Skin receptors (pain, touch, temp)

Muscle spindle structure part 1

• Thin intrafusal fibres

• Run parallel to thick extrafusal fibres to insert on either side of tendon

• No contractile apparatus in middle of fibre BUT concentration of nuclei

Intrafusal fibre types [2]

1) nuclear bag → primary annulo-spiral neurones

• wraps around central region

• sensitive to dynamic change → relative length change

2) nuclear chain → flower spray neurones

• sensitive to sustained stretch (static change) → persistent long length

Muscle spindle structure - summary diagram

Before activation of alpha motor neurone (during passively stretch)

Muscle belly and muscle spindle under the same tension

• spindle passively stretches with muscle

• spindle detects changes in tension differences btw muscle and spindle

• there is no change in tension→ spindle & therefore gamma neurone is not activated

Contraction → reduction in size of muscle belly

(concentric contraction)

Muscle contraction (due to alpha neurone stimulation) causes bulge in centre of belly as the extrafusal muscle shortens

• intrafusal fibres in the centre go slack (bend) concomittantly/simultaneously with muscle contraction

• this triggers nuclear bag and chain

• signal sent to spinal cord

• gamma motorneurones discharge

• muscle spindle shortens as polar, striated ends of spindle contracts

• new length of muscle set (slackness removed)

Golgi tendon organ functions

• Monitor tendon tension caused by contraction of muscle

• Overstretching → sensory signals reach spinal cord relay neuron

• Relay neuron sends inhibitory signal to alpha neurons → prevents further muscle stretch

Aim - eliminate muscle tension by inhibiting contraction or shifting position

• Found exclusively in tendons

• Act on postural muscles

key difference btw golgi tendon organ and muscle spindle

MS - both sensory and motor neurones

GTO - sensory component only

Golgi tendon organ before sensory neuron activation

When no active tension/non-excessive tendon stretching GTO sends inhibitory signals

• no contraction of muscle

• communicates to spinal cord - no overstretching taking place

GTO when overstretching of muscle

• GTO activates sensory neuron

• Sensory neuron signals to spinal cord relay neuron

• Discharge to alpha motor neuron for muscle contraction → prevents excessive overstretch of tendon and muscle

Patella reflex (mono-synaptic reflex control)

• NO RELAY NEURONE (one synapse)

  • sensory x motor → excitatory

1. striking patellar ligament → stretches tendon and quadriceps femoris

2. stretch activates muscle spindles

3. sensory neurone activated

4. sensory neurone DIRECTLY activates alpha motorneurone

5. alpha motorneurone stimulates extrafusal fibres

6. quadriceps (femoris) contracts

   UMN - can intervene → interrupts common pathway → quadriceps remain relaxed

Di-synaptic reflex control

• 2 synapses

  • sensory x relay → stimulatory

  • relay x motor → inhibitory

1. Overstretching on muscle stretches tendon

2. Golgi tendon organ senses tension

3. Sensory neuron activation

4. Sensory neurone stimulates relay neurone

5. Relay neurone inhibits ALPHA motor neurone

6. Tension on tendon reduced due to lack of extrafusal contraction

Multi-synaptic reflex control - reciprocal innervation

• Agonist muscle contracts via monosynaptic reflex (stimulatory synapse)

  • sensor = muscle spindle → slackness

• Antagonist muscle relaxes via disynaptic reflex (inhibitory relay x motor synapse)

  • sensor = golgi tendon organ → over-stretch

Patellar reflex example

• quads contract via monosynaptic (stifle extensors)

• hamstrings relax (inhibited) via disynpatic (stifle flexors)

Another example

• biceps and triceps

• any two opposing muscles

Posture control is multi-synaptic

Long spinal reflex

Different segments of spinal cord involved in execution of reflex (or postural control)

Example: reflex in response to pain or pinching is called the withdrawal reflex (also known as the flexor reflex).

• Sensory recognition of pain (spinoreticular or spinothalamic tracts) → go into somatosensory cortex by travelling up spinal cord

• Reflex aspect remains in spinal cord

Crossed extensor reflex → postural control

• Lift one foot up → other foot goes down to compensate by weightbearing

• Rising (ipsilateral) foot: (e.g. due to withdrawal reflex/pain)

  • Flexor contracts

  • Extensor relaxes

• Lowering (contralateral) foot:

  • Extensor contracts

  • Flexor relaxes

• Only IPSILATERAL sensory neuron activated

• Relay neurons on both ipsilateral and contralateral sides (decussate) allow bilateral innervation

• contralateral decussating interneurone = commissural neurone

LMN lesion potential clinical signs [5]

• Muscle atrophy (if nerve cut through or injured)

• Fasciculations (muscle twitching) if muscle overstimulated

• Decreased reflexes

• Decreased muscle tone

• Flaccid paralysis (if no stimulation received)

LMN potential disorders

• Polio-myelitis → selective alpha motor neuron destruction

• Amyo-trophic lateral sclerosis → degeneration of LMNs at ALL levels of spinal cord → muscle atrophy, paralysis, death (diaphragm/larynx → breathing and swallowing)

• Poly-myositis (cause not well known)

  • muscle disease that causes progressive, symmetric muscle weakness, mainly affecting the proximal muscles (like the hips, thighs, shoulders, and neck).

• Myasthenia gravis → autoimmune targeting of ACh receptors (type 2 hypersensitivity → antibody blocking)