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).
Muscle spindle
Structure
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.
Connections
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).
