Upper & Lower Motor Neurons & their Lesions part 1

Name: Upper & Lower Motor Neurons & their Lesions part 1
Uploaded: 2024-01-25T14:22:19.000Z
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Understanding Upper and Lower Motor Neuron Lesions

Overview of Motor Neurons

The discussion focuses on the clinical presentations and complications associated with upper motor neuron lesions (UMNL) and lower motor neuron lesions (LMNL).

Lower motor neurons are defined as those that exit the central nervous system, connecting to neuromuscular junctions, serving as the final common pathway for motor control.

Biceps Muscle Innervation

The biceps muscle is used as an example to illustrate innervation; it is supplied by cervical segments C5 and C6 of the spinal cord.

A diagram is referenced to show a cross-section of the spinal cord at the cervical region, highlighting connections to both left and right biceps muscles.

Muscle Fiber Types

Biceps consist of extrafusal fibers (contractile units) and intrafusal fibers (sensory units), which play roles in muscle contraction and stretch detection.

Extrafusal fibers connect to tendons via Golgi tendon organs, while intrafusal fibers act as stretch receptors within muscle spindles.

Neuromuscular Junction Functionality

Alpha motor neurons innervate extrafusal fibers at neuromuscular junctions, releasing acetylcholine (ACh), which binds to nicotinic receptors.

The binding of ACh leads to depolarization through sodium influx via nicotinic receptors coupled with potassium channels.

Muscle Contraction Mechanism

Action potentials generated in alpha motor neurons stimulate calcium release in muscle cells, facilitating actin-myosin interaction necessary for muscle contraction.

Muscle spindle sensory endings continuously report stretch information back to the spinal cord, influencing reflex actions and proprioception.

Role of Gamma Motor Neurons

Gamma motor neurons provide stimulation specifically to muscle spindles, enhancing their sensitivity during muscle contractions.

Stimulation of gamma motor neurons can lead to contraction within the spindle itself, affecting overall muscle tone and reflex responses.

Muscle Spindle Function and Deep Tendon Reflexes

Understanding Muscle Spindles

Muscle spindles have a miniature contractile function that leads to slight contraction, which is insufficient for whole muscle contraction. However, this contraction produces stretch at the ends of the spindle.

The stretching of muscle spindles generates more action potentials directed towards the spinal cord, stimulating Alpha motor neurons and resulting in the contraction of extrafusal fibers, leading to overall muscle contraction.

Role of Gamma and Alpha Motor Neurons

Different descending pathways connect with gamma motor neurons and Alpha motor neurons. Stimulation of gamma motor neurons activates muscle spindles, increasing stretch on their ends.

This increased stretch results in heightened stimulation of Alpha motor neurons, enhancing muscle tone through greater degrees of contraction.

Deep Tendon Reflex Mechanism

The deep tendon reflex involves striking a tendon (e.g., biceps jerk), which initiates a reflex arc. Key components include stimulus/receptor, sensory pathway to the central nervous system (CNS), central integration system, motor pathway output, and effector unit.

When a tendon is struck with a hammer, it stimulates the associated muscle (e.g., biceps), causing it to contract and produce a reflexive jerk.

Pathways Involved in Reflexes

Understanding how deep tendon reflexes work requires knowledge about sensory pathways and receptors involved when hitting tendons. For example:

Ankle jerk: S1

Knee jerk: L2-L4

Biceps: C5-C6

Misconceptions About Deep Tendon Reflexes

It’s important to note that "deep tendon reflex" is misleading; it should be termed "muscle stretch reflex." The actual receptor stimulated during these actions is not the Golgi tendon organ but rather muscle stretch receptors.

Striking the tendon causes brisk transient stretching of the entire muscle rather than directly stimulating Golgi tendon organs.

Mechanism Behind Stretch Responses

When hitting a tendon lightly with a hammer, it stretches both the tendon and consequently pulls on the entire muscle. This creates an immediate stretch response in intrafusal fibers within muscle spindles.

The transient brisk stretch increases information sent to the CNS via Ia fibers due to activation from stretched intrafusal fibers.

Resulting Action Potentials and Contractions

The brief stretch leads to increased traffic of action potentials toward the spinal cord, resulting in temporary overstimulation of Alpha motor neurons.

This overstimulation translates into slightly increased activity at neuromuscular junctions for short durations, culminating in transient contractions—hence why we observe positive responses like biceps jerks during testing.

By understanding these mechanisms thoroughly, one can appreciate how deep tendon reflexes operate fundamentally through complex interactions between various neural pathways and muscular responses.

Understanding Muscle Reflexes and Their Mechanisms

Overview of Muscle Stretch Reflex

The discussion begins with the distinction between tendon reflex and muscle stretch reflex, emphasizing that striking a tendon induces a transient stretch across the entire muscle.

When the muscle is stretched, muscle spindles become activated, leading to overfiring of alpha motor neurons associated with that muscle, resulting in brief contractions.

Testing Reflex Pathways

During reflex testing, several components are evaluated: functionality of muscle spindles, integrity of sensory pathways to the spinal cord, central integration processes, motor output effectiveness, and neuromuscular junction capabilities.

A normal reflex indicates that all these components—muscle spindles, sensory pathways, spinal cord segments, and motor outputs—are functioning properly.

Understanding Golgi Tendon Organs (GTO)

The speaker addresses when Golgi tendon organs (GTO) are stimulated; understanding their activation helps clarify why they may not respond under certain conditions.

An example is provided where holding a weight causes biceps contraction; as weight increases on the tendon, it leads to further stretching of muscles and increased action potentials sent to the spinal cord.

Progressive Weight Increase and Muscle Response

As more weight is added progressively during an exercise scenario, there’s an increase in tension on both tendons and muscles which stimulates further action potentials from alpha motor neurons for greater contraction.

Eventually, if too much weight is applied beyond muscular capability or safety limits (threatening locomotor integrity), GTO will activate to inhibit alpha motor neuron activity regardless of voluntary effort.

Role of GTO in Preventing Injury

The critical moment occurs when excessive tension activates GTO; this prevents potential injury by inhibiting muscle contraction through interneurons releasing inhibitory neurotransmitters.

It’s clarified that while mild to moderate stretches stimulate muscle spindles for contraction enhancement during deep tendon reflexes, GTO only activates under excessive tension threatening structural integrity.

Understanding GGI Tendon Reflex and Muscle Stretch Reflex

Differentiating Between Reflex Types

The distinction between muscle stretch reflex and GGI tendon reflex is crucial. The muscle stretch reflex occurs when a mild to moderate stretch stimulates the muscle spindle, leading to contraction.

In the muscle stretch reflex, the stimulus is a stretch, resulting in muscle contraction through alpha motor neuron activation.

Common tests for these reflexes include ankle jerk, knee jerk, biceps, and triceps reflexes.

Mechanisms of Reflex Action

Excessive stretching activates inhibitory receptors (GGI tendon organs), which are less easily stimulated than muscle spindles. This leads to relaxation of the muscle via inhibition of alpha motor neurons.

When stimulated, GGI tendon organs send signals through 1B fibers that activate interneurons releasing inhibitory neurotransmitters.

Relationship with Upper and Lower Motor Neurons

Understanding these reflexes is essential for grasping concepts like rigidity, spasticity, hypertonia, and hyperreflexia related to upper and lower motor neuron lesions.

The structure includes extrafusal fibers for force generation and intrafusal fibers within the spindle for sensing stretch.

Pathways Influencing Motor Neuron Activity

Alpha motor neurons are classified as lower motor neurons influenced by both muscle spindles (increasing activity) and GGI tendon organs (decreasing activity).

Muscle spindles act as monosynaptic pathways while GGI tendon reflexes involve polysynaptic pathways.

Upper Motor Neuron Influence on Lower Motor Neurons

Upper motor neurons originate from cortical areas influencing alpha motor neurons primarily through interneurons rather than direct connections.

Various descending pathways (e.g., corticospinal pathway, rubrospinal pathway) modulate lower motor neuron behavior.

Defining Lower vs. Upper Motor Neuron Lesions

A practical demonstration involves comparing changes in biceps muscles following lower versus upper motor neuron injuries to illustrate their distinct manifestations.

Understanding Lower Motor Neuron Lesions

Definition and Characteristics of Lower Motor Neuron Lesions

Lower motor neuron lesions manifest from the alpha motor neuron to various points, including the anterior root, trunk of the spinal nerve, or neuromuscular junction.

Any injury affecting lower motor neurons, such as polio or nerve cuts, results in a lower motor neuron lesion characterized by loss of function at these sites.

The term "lower motor neuron lesion" encompasses any interruption along the final common pathway that affects muscle control.

Clinical Implications of Nerve Injury

An example is an injury to the nerve supplying the biceps (C5 and C6), which interrupts spinal cord signals to muscles.

After three months post-injury, key assessments include muscle mass, power, tone, and reflexes (e.g., tendon stretch reflex).

Effects of Denervation on Muscle Mass

If a nerve is cut and not allowed to regenerate, denervation occurs leading to significant muscle atrophy due to loss of trophic signals from acetylcholine release.

Acetylcholine normally maintains muscle mass through small physiological releases; without it, muscles cannot sustain their size.

Consequences of Loss of Nerve Supply

Denervation leads to autophagic processes within muscle cells resulting in rapid loss of mass—up to 70%–80% can be lost within two to three months.

Distinction Between Upper and Lower Motor Neuron Lesions

In cases where upper motor neurons are damaged but lower motor neurons remain intact (e.g., spinal cord injury), this results in an upper motor neuron type lesion with preserved trophic action but reduced muscle power.

Muscle Atrophy and Neural Control: Understanding Upper and Lower Motor Neuron Lesions

Mechanisms of Muscle Mass Loss

Muscle mass loss occurs due to two primary factors: the trophic action of nerves and muscle usage. When lower motor neurons are damaged, there is a complete termination of trophic action.

In cases where both denervation atrophy and disuse atrophy occur, significant muscle mass loss can be observed—up to 80% in severe cases due to lack of nerve supply and muscle use.

In contrast, when discussing upper motor neuron lesions, only about 20-30% muscle mass loss is noted because some trophic action remains intact despite reduced power.

Comparison Between Upper and Lower Motor Neuron Lesions

The left side (lower motor neuron lesion) shows more significant mass loss compared to the right side (upper motor neuron lesion), which retains more muscle mass but still experiences some reduction.

Power dynamics differ between the two types of lesions; while upper motor neuron lesions result in partial power retention, lower motor neuron lesions lead to total power loss.

Functional Implications of Upper vs. Lower Motor Neuron Lesions

Despite losing control over lower motor neurons in upper motor neuron lesions, these neurons remain functional, allowing for some preservation of muscular power compared to normal muscles.

The degree of power retention in upper motor neuron conditions is better than that seen in lower motor neuron conditions where drastic changes occur.

Tone Maintenance and Its Dependence on Neural Activity

Muscle tone maintenance relies heavily on gamma motor neurons. If these are lost alongside alpha motor neurons, it leads to hypotonia or flaccidity as muscle spindles become relaxed.

A lack of stimulation from relaxed muscle spindles results in diminished signals sent to spinal cord pathways necessary for maintaining tone.

Consequences of Upper Motor Neuron Damage

Following damage to upper motor neurons, lower motor neurons may exhibit altered firing patterns leading to potential overactivity or underactivity depending on the context. This affects overall muscular function significantly.

Understanding Motor Neuron Function and Reflexes

Mechanisms of Gamma Motor Neurons

When lower motor neurons begin to overfire, gamma motor neurons also start to overfire, leading to excessive contraction of muscle spindles. This results in increased sensory input.

Overfiring of gamma motor neurons causes the ends of the spindle to overstretch, which translates into excessive action potential traffic to the spinal cord.

Effects on Alpha Motor Neurons

Continuous overfiring of alpha motor neurons occurs due to loss of inhibition and overstimulation from stretch reflexes, resulting in increased muscle tone (hypertonia or rigidity).

In contrast, lower motor neuron lesions lead to flaccidity and loss of power, while upper motor neuron lesions result in rigidity with some retained power.

Tendon Reflex Responses

The tendon reflex can be disrupted if sensory pathways are disconnected; even if the muscle is stretched, it may fail to elicit a proper motor response.

In cases of lower motor neuron lesions, deep tendon reflexes may be diminished or absent (hyporeflexia).

Comparison Between Upper and Lower Motor Neuron Lesions

In upper motor neuron lesions, despite overstimulation causing excessive firing in alpha motor neurons, the output remains intact leading to exaggerated tendon reflex responses (hyperreflexia).

Hyperreflexia can manifest as clonus; prolonged stretching leads muscles to contract repeatedly.

Muscle Atrophy and Tone Maintenance

Lower motor neuron damage results in significant muscle atrophy due to disuse and denervation. Upper motor neuron damage leads only to disuse atrophy since lower motor neurons remain functional.

Muscle tone is primarily maintained by gamma motor neuron activity; when both types of neurons are compromised, stimulation fails leading to loss of muscle tone.

Understanding Muscle Tone and Reflexes in Upper and Lower Motor Neuron Lesions

Muscle Tone Changes in Motor Neuron Lesions

Loss of muscle tone leads to flaccidity and hypotonia in lower motor neuron lesions, as the control is lost.

In upper motor neuron lesions, there is an overactivity of lower motor neurons, resulting in hypertonia due to the overfiring of both alpha and gamma motor neurons.

Deep Tendon Reflexes vs. Muscle Stretch Reflexes

Deep tendon reflexes are more accurately termed muscle stretch reflexes; they occur when a muscle is stretched, stimulating muscle spindles.

In lower motor neuron lesions, brisk stimulation may not effectively drive the alpha motor neuron due to dysfunction, leading to diminished reflex responses (hyperreflexia or areflexia).

Comparison of Reflex Responses

In upper motor neuron lesions, overfiring gamma motor neurons cause muscle spindles to be contracted; thus, hitting the tendon results in exaggerated reflex responses due to overstretched spindles.

The comparison shows that lower motor neuron mass decreases while upper motor neuron mass increases; power decreases significantly in lower motor neurons but slightly increases in upper ones.

Babinski's Reflex: Normal vs. Pathological Responses

Babinski's sign indicates how normal physiological responses change with different types of neuronal damage; it involves withdrawal reflexes when stimulating the foot's outer part.

In infants, local spinal reflexes function without fully developed cortico-spinal pathways; this allows for primitive withdrawal responses upon irritation. However, as infants grow and learn to walk, these pathways mature and reverse the response from withdrawal to maintaining contact with surfaces (plantar flexion).

Implications of Corticospinal Pathway Damage

If corticospinal pathways are damaged at specific levels (e.g., C4), it results in loss of control over muscles below that level leading to hyperreflexia and hypertonia indicative of upper motor neuron lesions affecting overall function.

Understanding Upper Motor Neuron Lesions

Impact on Corticospinal Pathway

The discussion centers around the effects of upper motor neuron lesions, specifically how they impact the corticospinal pathway responsible for voluntary movement.

When the upper motor neuron is affected, it abolishes the ability to reverse withdrawal reflexes from the foot, indicating a significant disruption in normal reflex pathways.

The foot's operation becomes reliant solely on spinal reflexes or higher-level spinal reflexes due to this disruption.

A key point raised is whether stimulating the outer part of the foot will result in downgoing responses; however, this response is compromised due to the lesion.

The downgoing response was previously expected but is now absent because of the altered functioning of neural pathways following an upper motor neuron lesion.