Download MOTOR SYSTEM – Muscle, LMC, Spinal cord mechanisms of control

MOTOR SYSTEM – Muscle, LMC, Spinal cord mechanisms of control
- Motion around a certain joint creates a mechanical effect such that each successive joint is
disturbed and must be stabilized
- To localize lesion in motor system is presence of absence of weakness
-Upper motor neurons (UMNs) lower motor neurons (LMNs), NMJ, Muscle fibers
present weakness if damaged (motor cortex  muscles)
- Motor cortex gets input form basal ganglia (via thalamus), cerebellum (via thalamus),
and other cortical areas; Damage to one of these does not result in weakness, but produces
disorders of the quality of movement
2. – A muscle is innervated by several hundred LMNs (cell bodies in anterior horn of spinal
cord)
- A motoneuron, with its axon and all the muscle fibers that it innervates is called a motor unit
- Each muscle fiber innervated by single LMN and has a single NMJ
- AP along LMN reaches nerve terminal at NMJ  calcium ions enter nerve terminal due to
depolarization and Ach is released from the nerve terminal
- Ach binds its receptor on surface of muscle fiber  depolarization  AP along full length of
myofiber (both directions)
- As AP spreads along surface of myofiber, it travels into T-tubules (transverse tubules)  long
invaginations of plasma membrane into the myofiber
- T-tubules aligned along junction between A-band and I-band; T-tubules are closely apposed to
sarcoplasmic reticulum (SR). Two cistern of SR associated with single T-tubules  triad.
- At each triad, voltage-gated calcium channels in T-tubule membrane are coupled to a different
class of calcium channel in SR channel
- AP in the T-tubule causes release of Ca2+ from SR  rise in [Ca2+] causes activation of
sarcomeres and contraction of myofiber
- One AP in LMN caused one AP in each of the muscle fibers it innervates
1. EMG – electrodes detect sum of electrical activity of active muscle fibers; APs of each
muscle fiber belonging to a single motor unit add up to produce a compound AP (EMG records
a sum of compound APs)
Myopathic disease
- Muscle fiber dysfunction  no APs in muscle fibers  fewer surviving muscles in each motor
unit that can generate an AP  amplitude of EMG record is reduced
Neurogenic disease
- Damage to LMN has abnormal findings
- fibrillations  spontaneous contractions of individual muscle fibers (small spikes on EMG
record); small potential, low frequency; fibrillations arise from increased expressions of Na and
Ca channels in denervated muscles  nearby intact fibers activated previously and residual
ionic currents cause depolarization in adjacent denervated fibers (with increased channels)
-fasciculations  spontaneous activation of motor units (spontaneous activation of LMN
involving Ach); visible as twitching; can be abolished by Ach blocker and induced by AchAse
blocker;
- EMG can detect Giant units  abnormally large compound APs (show when voluntary
movements are attempted); occurs due to sprouting: motoneurons die and lose innervation of
muscle fibers  nearby intact motoneurons make new collateral branches and send those
branches to innervate vacant slots on denervated muscle  surviving motor units include
more muscle fibers  recorded compound AP increases in seize
Hyperactive reflexes  UMN lesion (motor cortex of CST)
Normal or reduced reflexes  LMN or muscle lesion (including NMJ); to distinguish between
LMN and muscle look at EMG (fibrillations, fasciculation, etc.  LMN, reduced amplitude 
muscle if constant weakness or NMJ if fluctuating weakness)
3. Automatic functions of spinal cord – automatic regulation of muscle force
Types of motor units
Motor Unit Type
Motoneurons
Muscle Fiber
Histological Type of
Properties
Properties
muscle fiber
Slow twitch (S)
Small, slow
Low force, slow
Type I (smallest)
conducting axons
contraction, fatigueresistant, oxidative
metabolism
Fast-twitch, fatigue
Medium size,
Moderate-high forces, Type IIa (medium
resistant (FR)
moderate-fast
fast contraction,
size)
conducting
fatigue-resistant
Fast-twitch, fatigable Large, fast-conduction High force, fast
Type IIb (largest)
contraction, fatigable
(FF)
- Properties of motoneurons match properties of muscle fibers they innervate
- Muscles contain a mixture of the 3 types of motor units
4. How muscle force is increased – 1) increase number of motor units activated, 2) increase
discharge rates of already firing motor units
Rule #1 – Fixed order of recruitment according to size principle; smallest motoneurons activated
first, and successively larger motoneurons activated as more force needed; S  FR  FF
- Smaller motoneuron has fewer parallel ion channels and has a higher total cell input
resistance
- Larger motoneuron has more parallel ion channels and has a lower total cell input resistance
- according to V=IR (I is constant as the CST UMN); R is high in small motoneurons and low in
large motoneurons
- V of the small LMN is higher, and V of the large LMN is lower; small motoneurons will
reach threshold first, and the large motoneurons will reach threshold later
Rule #2 – fixed sequence for firing rate of motoneurons; when first activated, a motoneuron may
fire at 10 Hz; when it receives more excitation is will increase its firing up to 25 Hz
- Increasing the discharge rate of an already active unit increases its force output until it
reaches maximum force (tetany)
- Both rules lead to increases in force that are smooth
5. - A network of interneurons responsible for generating an automatic rhythmical movement is
called central pattern generator (CPG); CPGs are in the spinal cord and brainstem for
respiration, chewing, swallowing, and locomotion
- once a CPG is activated it can product the complex muscle instruction by its own subroutine;
does not need descending cortical input or sensory feedback
- A CPG reduces the amount of planning that the nervous system at other levels need; A CPG
established the timing signals and basic motor pattern at a lower level; cortical areas and
sensory feedback modulate these elementary instructions
Locomotor central pattern generator – network of interneurons residing in spinal cord; most
unconscious and automatic part of the motor system (like walking)
- capability for rhythmical stepping after cord transection and deafferentation; CPG is
dependent on descending influences; the locomotor CPG provides timing instructions for
alternating activity in flexor and extensor muscles at each joint of the leg: hip, knee, ankle
- locomotor CPG requires sensory sources and cortical, higher motor center sources:
cutaneous sense, position sense, and force feedback from limbs
6. Reflexes during walking – the network of spinal cord circuitry for reflexes must interact with
the circuitry for the locomotor CPG
- If the dorsum of the foot is pinched during the swing phase of locomotion  withdrawal
response in which flexor muscles of the stimulated leg are activated  foot is drawn up and
away for stimulus
- If the dorsum of the foot is pinched during the stance phase of locomotion (leg is accepting
body’s weight)  extensor muscles are activated to produce an extension response in the
standing leg to move away from the stimulus
7. Brainstem – CPGs for breathing, chewing, and swallowing; receive sensory and cortical
input to adapt the basic instructions for the functional and environmental context
Respiration – nuclei in pons/medulla; two medullary centers  a dorsal and ventral
respiratory group in reticular formation, pons, and medulla  timing instructions to
inspiratory and expiratory muscles;
- output of two respiratory centers activates trigeminal, facial, glossopharyngeal, vagus, and
hypoglossal nerve (and spinal input to diaphragm via phrenic nerve and intercostals,
abdominal muscles)
- neurons in respiratory groups include pacemaker neurons  spontaneous rhythmical
oscillations  APs to quiet to APs; CPG provides alternating EPSPs and IPSPs to respiratory
motoneurons
- breathing requires sensory and cortical input to respiratory CPG
- chemoreceptors, pulmonary stretch receptors and muscle spindles, provide sensory feedback
about blood gases and muscle work to regulate breathing muscle pattern
- cortical input necessary for adjusting breathing pattern to hold breath, whistle, talk.
Chewing – repetitive jaw opening and closing; initial prep phase  food from anterior to
posterior of mouth; reduction phase  food is torn and crushed to form bolus
- the CPG for chewing isolated to gigantocellular reticular nucleus in reticular formation in
medial pons/medulla to motoneurons (trigeminal and facial)
-sensory and cortical inputs sculpt the rhythmical jaw movements into everyday patterns of
chewing; muscle spindle information (trigeminal mesencephalic nucleus) for jaw closure
muscles modifies timing of switch from jaw opening to jaw closing; feedback from pressure
sensors in teeth modify force and timing of chewing (jaw closure); cortical input involved in
modulating chewing pattern
Swallowing – three phase: oral, pharyngeal, and esophageal;
Pharyngeal phage:
1. Hyoid bone elevated and moved anteriorly
2. Larynx is adducted
3. Soft palate elevated
4. Pharynx is constricted
5. Esophageal sphincter is relaxed
- Muscles receive alternating excitatory and inhibitory input t p produce sequenced EMG
pattern producing these steps
- CPG in nucleus of Solitary tract and dorsal motor nucleus (X)  LMN (nucleus ambiguus)
- CN X (Superior laryngeal nerve)  on-switch for pharyngeal CPG (activated by cortical or
sensory input)
- sensory/cortical info; chemoreceptors at dorsum of tongue, epiglottis, pharynx walls carries
with V3, IX, and X  modify duration of EMG and force of muscle contractions of
swallowing pattern; cortical areas  voluntary swallowing