Discussion of skeletal muscle reflex physiology with a clinical scenario.
A patient, Andrew, is paralyzed from the waist down due to a car accident.
Initial examination shows hyperreflexia in the patellar reflex.
A year later, the same patient shows absent reflexes. Discussion of causes.
Reflexes are rapid, predictable, and involuntary motor responses to stimuli.
Mediated by neural pathways called reflex arcs.
Designed to protect us, with local stimuli integration at a simplistic integration center, the reaction will be predictable since it's simple.
Five components of a reflex arc:
Receptor
Sensory neuron
Integration center (brainstem or spinal cord)
Motor neuron
Effector (muscle or gland)
Skeletal muscle reflexes can be simple with a monosynaptic reflex arc.
Monosynaptic reflex arcs involve only two neurons: a sensory neuron synapsing directly with a motor neuron in the spinal cord.
The patellar reflex involves tapping the patellar tendon.
Receptors: Proprioceptors in muscle fibers sense the stretching of the tendon.
Sensory neurons: Primarily from lumbar nerves L2, L3, and L4 (mainly L4).
Integration center: Spinal cord at the lumbar level (intact in this case).
Motor neurons: Somatic motor neurons from L2, L3, and L4 (working fine).
Effector: Quadriceps muscles (healthy and intact initially).
All five components of the reflex arc are functional, resulting in a reflex.
For each muscle, there is an opposing muscle.
These muscles resist movement and are innervated by the corticospinal tract, which maintains muscle tone.
Normally, reflexes are examined by distracting the patient to reduce muscle tone in the opposing muscles.
In the initial case, the patient's paralysis indicated an injured corticospinal tract, thus eliminating the need for distraction as the muscle tone was already reduced.
This injury in the corticospinal tract is also the reason his reflex was exaggerated.
A year after the accident, the patient's leg muscles have atrophied (gotten significantly smaller).
Repeat patellar reflex examination shows absent reflexes.
Initially, all five components of the reflex arc were intact.
After a year of paralysis, there is no innervation to the skeletal muscles.
The lack of use leads to disuse atrophy of the muscles.
When the patient is examined a year later, the atrophied skeletal muscles (the effector) are no longer capable of producing the reflex movement.
Therefore, the reflex is absent because the fifth component (skeletal muscle) is no longer functional.
Detailed discussion of skeletal muscle reflex physiology with a clinical scenario to enhance understanding.
A patient, Andrew, is paralyzed from the waist down due to a severe car accident, leading to neurological deficits.
Initial examination reveals hyperreflexia in the patellar reflex, indicating upper motor neuron damage.
A year later, the same patient shows absent reflexes in the lower extremities. Discussion of potential causes including changes in muscle tone, nerve function, and muscle health over time.
Reflexes are rapid, predictable, and involuntary motor responses to stimuli, crucial for quick responses to environmental changes.
Mediated by neural pathways called reflex arcs, which ensure efficient and consistent responses.
Designed to protect us, with local stimuli integration at a simplistic integration center, making the reaction predictable due to its simplicity. This predictability is vital for survival.
Five essential components of a reflex arc:
Receptor: Specialized sensory receptors that detect the initial stimulus.
Sensory neuron: Transmits afferent impulses from the receptor to the spinal cord or brainstem.
Integration center (brainstem or spinal cord): Processes the sensory information and generates an appropriate motor response.
Motor neuron: Conducts efferent impulses from the integration center to the effector.
Effector (muscle or gland): Responds to the motor commands, producing the reflex action.
Skeletal muscle reflexes can be simple, involving a monosynaptic reflex arc for rapid responses.
Monosynaptic reflex arcs involve only two neurons: a sensory neuron synapsing directly with a motor neuron in the spinal cord, allowing for minimal delay in the reflex response.
The patellar reflex involves tapping the patellar tendon to assess the integrity of the spinal reflex arc.
Receptors: Proprioceptors (muscle spindles) in muscle fibers sense the stretching of the tendon, initiating the reflex.
Sensory neurons: Primarily from lumbar nerves L2, L3, and L4 (mainly L4), transmitting sensory information to the spinal cord.
Integration center: Spinal cord at the lumbar level (intact in this case), where sensory input is processed and motor commands are generated.
Motor neurons: Somatic motor neurons from L2, L3, and L4 (working fine), conducting motor commands to the quadriceps muscles.
Effector: Quadriceps muscles (healthy and intact initially), which contract to extend the knee in response to the stimulus.
All five components of the reflex arc are functional, resulting in a normal reflex response. This indicates that the basic neural circuitry is intact at the time of the initial examination.
For each muscle, there is an opposing muscle (antagonist) that helps control movement and maintain balance.
These opposing muscles resist movement and are innervated by the corticospinal tract, which plays a crucial role in maintaining muscle tone and regulating voluntary movements.
Normally, reflexes are examined by distracting the patient to reduce muscle tone in the opposing muscles, allowing for a clearer assessment of the reflex response. Distraction techniques help minimize voluntary interference.
In the initial case, the patient's paralysis indicated an injured corticospinal tract, thus eliminating the need for distraction as the muscle tone was already reduced due to the upper motor neuron lesion.
This injury in the corticospinal tract is also the reason his reflex was exaggerated. The loss of inhibitory control from the brain leads to an overactive reflex response, known as hyperreflexia.
A year after the accident, the patient's leg muscles have atrophied (gotten significantly smaller) due to chronic disuse and lack of neural stimulation.
Repeat patellar reflex examination shows absent reflexes, indicating a significant change in the functionality of the reflex arc.
Initially, all five components of the reflex arc were intact, allowing for a normal reflex response.
After a year of paralysis, there is no innervation to the skeletal muscles, leading to muscle degeneration and loss of function.
The lack of use leads to disuse atrophy of the muscles, reducing their size and strength. This atrophy affects the muscles' ability to respond to stimuli.
When the patient is examined a year later, the atrophied skeletal muscles (the effector) are no longer capable of producing the reflex movement. The muscle's reduced mass and strength impair its ability to contract effectively.
Therefore, the reflex is absent because the fifth component (skeletal muscle) is no longer functional. The muscle's inability to respond to the motor neuron signal results in the absence of the patellar reflex.