Muscle Spindle And Lower Motor Neurone
Lower Motor Neurone
The lower motor neurone (LMN) is defined as the neurone whose cell body lies in either the anterior or ventral horn of the spinal cord or cranial nerve nuclei of the brainstem and which directly innervates the muscle via its axon. The number of muscle fibres innervated by a single axon is termed the motor unit. The smaller the number of fibres per motor neurone (MN) axon, the finer the control (e.g. the extraocular muscles).
The MNs of the anterior horn are divided into two types:
• α-MNs (70 μm in diameter) which innervate the muscle itself (the force generating extrafusal fibres);
• γ-MNs (30 μm in diameter) which innervate the intrafusal fibres of the muscle spindle.
The muscle spindle is an encapsulated sense organ found within the muscle, which is responsible for detecting the extent of muscle contraction by monitoring the length of muscle fibres. It is the muscle spindle and its connections to the spinal cord that mediates the tendon reflexes:
• Sudden Stretching Of A Muscle By A Sharp Tap Of A Tendon Hammer Transiently Activates The Ia Afferent Nerve Endings Which, Via An Excitatory Monosynaptic Input To The MN, Causes That Muscle (The Homonymous Muscle) To Contract Briefly (E.G. The Knee Jerk).
• In Addition, The Ia Afferent Input From The Muscle Spindle, While Activating Other Synergistic Muscles With A Similar Action To The Homonymous Muscle, Also Inhibits Muscles With Opposing Actions (Antagonist Muscles) Through A Ia Inhibitory Interneurone (IN) In The Spinal Cord.
However, it must be stressed that tendon jerks reflect not only the integrity of this circuit but the overall excitability of the MN, which is increased in cases of an upper MN (UMN) lesion (see Chapter 37).
The muscle spindle lies in parallel to the extrafusal muscle fibres and consists of the following:
• nuclear bag and chain fibres which have different morphological properties: the bag 1 or dynamic fibres are very sensitive to the rate of change in muscle length, while the bag 2 or static bag fibres are like the nuclear chain fibres in being more sensitive to the absolute length of the muscle;
• γ-MN – which synapses at the polar ends of the intrafusal muscle fibres and which can be one of two types: dynamic or static, with the latter innervating all but the bag 1 fibres. Both types of γ-MN are usually coactivated with the α-MN so that the intrafusal fibres contract at the same time as do the extrafusal fibres, thus ensuring that the spindle maintains its sensitivity during muscle contraction. Occasionally, the γ-MN can be activated independently of the α-MN, typically when the animal is learning some new complex movement, which increases the sensitivity of the spindle to changes in length;
• two types of afferent fibres and nerve endings a Ia afferent fibre associated with an annulospiral nerve ending winding around the centre of all types of intrafusal fibres (primary ending); and a slower conducting type II fibre which is associated with flower spray endings on the more polar regions of the intrafusal fibres (with the exception of the bag 1 fibres; the secondary ending). The stretching of the intrafusal fibre activates both types of fibre. However, the Ia fibre is most sensitive to the rate of change in fibre length, while the type II fibres respond more to the overall length of the fibre rather than the rate of change in fibre length.
The spindle relays via the dorsal root to a number of sites in the central nervous system (CNS) including:
• Mns Innervating The Homonymous And Synergistic Muscles (The Basis Of The Stretch Reflex);
• Ins Inhibiting The Antagonist Muscles;
• The Cerebellum Via The Dorsal Spinocerebellar Tract;
• The Somatosensory Cortex;
• The Primary Motor Cortex Via The Dorsal Column Medial Lemniscal Pathways.
Thus, the muscle spindle is responsible for mediating simple stretch or tendon reflexes as well as muscle tone, and it is also involved in the coordination of movement, the perception of joint position (proprioception) and the modulation of long latency or transcortical reflexes (see Chapter 39).
Effects of damage to this structure
Damage to the spindle afferent fibres (e.g. in large-fibre neuropathies) produces hypotonia (as the stretch reflex is important in controlling the normal tone of muscles), incoordination, reduced joint position sense and, occasionally, tremor with an inability to learn new motor skills in the face of novel environmental situations.
In addition, large fibre neuropathies disrupt other somatosensory afferent inputs (see Chapters 31 and 54).
Golgi tendon organ
The Golgi tendon organ is found at the junction between muscle and tendon and thus lies in series with the extrafusal muscle fibres. It monitors the degree of muscle contraction in terms of the mus- cular force generated and relays this to the spinal cord via a Ib afferent fibre. This sensory organ, in addition to providing useful information to the CNS on the degree of tension within muscles, serves to prevent excessive muscular contractions (see Chapter 37). Thus, when activated it inhibits the agonist muscle.
Motor neurone recruitment and damage
The principle of recruitment corresponds to the order in which different types of muscle fibres are activated. The smallest α-MNs, which are those most easily excited by any input, innervate type 1 (not to be confused with the bag 1 intrafusal fibres found in the spindle) or slow-contracting fibres (which are responsible for increasing and maintaining the tension in a muscle).
The next population of MNs to be activated are those that innervate the type 2A or fast contracting/resistant to fatigue fibres, which are responsible for virtually all forms of locomotion. Finally, the largest MNs are only activated by maximal inputs, which innervate type 2B or fast contracting/easily fatigued fibres that are responsible for running or jumping.
The order of recruitment of MNs to a given input follows a simple relationship known as the size principle, which allows muscles to contract in a logical sequence.
Lower Motor Neurone Lesions
The α-MN itself can be damaged in a number of different conditions but in all cases the clinical features are the same:
• Wasting of the denervated muscles;
• Weakness of the same muscles;
• Reduced or absent reflexes (an lmn lesion).
In some cases one can also see fasciculations (muscle twitchings), as the loss of the motor neuronal input to the muscle leads to a more random redistribution of the acetylcholine receptors away from sites of the old neuromuscular junction.
The features of an LMN lesion are very different from a UMN lesion (see Chapter 37). Causes of a LMN lesion including infection (poliomyelitis); neurodegenerative disorders (motor neurone disease) as well as entrapment as the nerves exit the spine (radiculopathies) and in the limb itself (e.g. carpel tunnel syndrome).