Module 14 - Lecture 10.5 - Clinical LMN vs UMN Lesions Flashcards
How does the stimulus of a “larger” stretch change the stretch reflex?
The main thing is with a larger stretch, the muscle spindle itself will detect a larger change and that leads to a larger change in the receptor potential and more 1a afferents would discharge at a higher rate. (If there is more AP discharge, then more calcium enters the presynaptic terminal for a longer period of time, which causes an increase a higher number of neurotransmitter release → this recruits more motor neurons and they reach their threshold faster which causes a larger contraction) The more activity in the 1a afferents, the more homonymous motor neurons will reach threshold and discharge faster. This would produce a larger contraction.
How does the UMN modulate reflexes, like the stretch reflex?
Reflexes can be modulated by voluntary changes in the UMN activity. This is due to the fact that UMN activity can modify the postsynaptic potential explained by summation of the lower motor neuron.
Understand what would happen if the gamma motor unit itself were activated or if it were co-activated with the stretch reflex
The motor neuron forms synaptic junctions with either extrafusal muscle fibers (skeletal muscle) or intrafusal muscle fibers (muscle spindles). Stimulation of these motor neurons induces contraction or shortening of the muscle fibers. Alpha motor neurons induce the contraction of extrafusal muscle fibers upon stimulation, whereas gamma motor neurons induce the contraction of intrafusal muscle fibers upon stimulation. Alpha motor neurons control muscle contraction involved in voluntary movement, whereas gamma motor neurons control muscle contraction in response to external forces acting on the muscle. In response to these external forces, the gamma motor neurons induce the involuntary, reflexive movement called the stretch reflex. Intrafusal motor neurons adjust the length of intrafusal muscle fibers to maintain an appropriate level of tension on the muscle spindle receptor. The control of intrafusal muscle fibers occurs independently of the length of skeletal muscle fibers. This independent function allows the spindle to maintain a high degree of sensitivity over a wide range of muscle lengths, and in effect acts as a means of encoding muscle length. In other words, If the gamma motor neurons were excited it may want to say that the muscle is actually not in the right position, that could then increase the 1a afferent activity and that could excite the LMN of the alpha LMN to cause excitation and contraction of the extrafusal muscles. This would put us in a whole new position, but it would be gamma driving/leading the alpha. → this is the reason why it is called a feedback time.
What structures would be lesioned to lead to LMN syndrome? What would be the observed symptoms?
The structures:
Lesion to the actual neurons in the cranial nerve motor nuclei (recall that these are considered as LMN) or in the cells of our LMN that reside in ventral horn
Could be damage to the neuron but it could also be damage to the axon, all the motor efferent fibers such as ventral root, spinal nerve, plexus, peripheral nerve.
The symptoms:
Weakness/flaccid paralysis of innervated region Hyporeflexia - Hypoactive reflexes (decrease in the deep tendon reflexes)
Muscle atrophy/wasting
Hypertonia - Decreased muscle tone
Fibrillations and possible fasciculations (visible to the naked eye)
What structures would be lesioned for sensory afferent dysfunctions? The symptoms and how it might impact the stretch reflex.
The structures:
Neurons in the dorsal root ganglia
Could be damage to the axon, to be specific to the dorsal root, the spinal (afferent) nerve, the plexus and the peripheral nerve
The symptoms:
Loss of somatic sensation of innervated regions
Neuropathic pain (not related to receptor dysfunction)
Hyporeflexia - Hypoactive reflexes (decreased deep tendon reflexes )
Hypotonia - Decrease muscle tone
Strength normal - could be less coordinated
What structures would be lesioned to lead to UMN syndrome? What would be the observed symptoms? Tip pathological reflexes= reflexes presented after birth (Babinski, grasping, rooting) that are inhibited as voluntary UMN control is utilized in humans.
The structures:
Neurons in the cortex and brainstem
Inclusive of white matter such as corona radiata, internal capsule, individual tracts
The symptoms:
Weakness/flaccid paralysis of specific movements
Hypereflexia - Hyperactive reflexes (Increase in the deep tendon reflexes)
No muscle atrophy (wasting) → however could have disuse atrophy if muscle is not used
Hypertonia - increased muscle tone
Positive Babinski reflex - extensor plantar response
Critical thought (maybe fun for your discussion board). Would a spinal cord injury be a UMN or LMN lesion and why?
Patients with complete spinal cord injury can present with either an upper motor neuron lesion or a lower motor neuron (LMN) lesion. LMN lesions are characterized by disruption of the final common pathway, effectively leading to denervation of peripheral skeletal muscle. Clinically, this is manifested as weakness or paralysis, loss of muscle tone (flaccidity), loss of reflexes, and muscle atrophy. When the lumbar and sacral spinal cord are involved, one can see (1) flaccid, atrophic, paralyzed lower limbs; (2) absent lower limb deep tendon reflexes; (3) absent sacral reflexes (ie , bulbocavernosus reflex, anal wink); (4) a flaccid , areflexic gastrointestinal tract below the splenic flexure; (5) a flaccid, areflexic bladder; and (6) loss of reflex penile erections.
All of the descending spinal pathways that can influence or modify activities of the LMN constitute the UMN. UMN lesions are characterized by disruption of the descending pathways, leading to loss of voluntary motor control and inhibitory input to more caudal reflex arcs. The final common motor pathway remains intact, and peripheral skeletal muscle continues to be innervated by LMNs and their associated axons. Clinically, when the UMN lesion occurs above the lumbar spinal cord, one can see paralysis, hypertonia, and spasticity (hyperreflexia) involving the lower limbs. The Babinski sign is also frequently present. If the injury is complete, sacral reflexes to the lower gastrointestinal tract, bladder, and genitals remain intact, although they are not subject to volitional control.
Critical thought (maybe fun for the general discussion board) If an individual was voluntarily flexing their knee, and the knee was then suddenly stretched into a “more flexion”. How would the quadriceps stretch reflex differ (stronger or weaker) than if the individual were to receive the same stretch when 1) in a static position, 2) while voluntarily extending their knee. Explain why?
Stretch reflex while flexing the knee compared to in a static position…
If the individual was voluntarily flexing their knee, the muscle is lengthening and therefore the muscle spindle is stretched more than compared to a static position. That being said, the nerve activity of the muscle spindles increases since their main function is to maintain the muscle at a constant length. This will cause an increase in the alpha motor neuron activity, causing the muscle fibers to contract, maybe more than what they would have in a static position.
Stretch reflex while flexing the knee compared to while voluntarily extending their knee
If the individual was voluntarily extending their knee, the muscle is shortening and therefore the muscle spindle is slack compared to a static position. That being said, the nerve activity of the muscle spindles decreases. This will cause an decrease in the alpha motor neuron activity, causing the muscle fibers to contract, maybe less than what they would have in a static position. To sum up, the muscle spindles would become slack and the reflex would cease to function.
