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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2817_Библиотеки_им_академика_М_И_Перельмана.pdf
Association motor cortex (SMA, PFC, PM)
Motor cortex
Inhibitory connection
Functions:
programmes for desire to move – planning,
initiation, direction
Cerebrocerebellum
Cerebellum
Function:
coordinating movement
Anterior
lobe
Flocculonodular
lobe
Basal ganglia
Function:
gating initiation
of movement
9
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
Primary motor cortex
Function:
command to move
−
Thalamus
Brainstem upper motor neurons
Functions:
postural reflexes and basic movements
−
Pyramidal tract system
(corticobulbar)
(corticospinal)
Vestibular apparatus
Function: balance
Skeletal muscles
Intrafusal muscle fibres (proprioceptors)
Functions:
detect muscle stretch
Fig. 9.1 Schematic representation of circuits involved in motor function. PFC, Prefrontal cortex; PM, premotor cortex; SMA, supplementary motor
area.
The third and fourth systems are arranged in parallel
with the hierarchical organization of LMNs and UMNs.
These are the cerebellum and basal ganglia, which are
large collections of nuclei that modify movement on a
minute- to- minute basis. They do not project directly to
LMNs but are important for successful motor performance. Their output regulates the activity of UMNs. The
basal ganglia and cerebellum receive information from
the motor cortex and both structures send information
back to it via the thalamus. The output of the cerebellum
to the motor cortex is excitatory, while the basal ganglia
are inhibitory (in that they reduce thalamic activation of
the motor cortex, see Chapter 10). The balance between
Extrafusal muscle fibres
Function:
produce movement
formed by the autonomic nervous system (ANS). The
LMNs of this system reside outside the spinal cord, in
the paravertebral and prevertebral sympathetic chain
ganglia, in the parasympathetic postganglionic ganglia
near the target organ, or in the gut wall itself in the case
of the enteric system. Their function is controlled by the
hypothalamus, brainstem reticular formation and spinal
cord autonomic centres. The importance of autonomic
control of organs, such as the heart, bladder and sexual
organs, and the pharmacological means of modulating
its function makes visceral motor control systems an
important topic in clinical medicine (see Chapter 1).
these two systems allows for smooth, coordinated movement. The cerebellum acts as a motor performance error
detector, whereas the basal ganglia function to suppress
iour is produced, it is necessary to begin by considering
the interaction between LMNs and skeletal muscles.
Extra-pyramidal
tract pathways
Brainstem and spinal cord
Interneurons
Functions:
reflex integration
and modulation
Lower motor neurons
Function:
muscle contraction
Involuntary motor control of smooth muscle is per-
In order to understand how voluntary motor behav-
unwanted movements as well as to prepare the motor
cortex for the initiation of movements (see Chapter 10).
All levels of the motor hierarchy, except the basal gan-
Skeletal muscle contraction
glia, receive information from somatic proprioceptors
that continually inform the motor system about the position and movement of the body and limbs. Disturbances
to any of these structures lead to paresis (weakness),
paralysis or spasticity of movement, as demonstrated in
the case history described in Box 9.1.
Voluntary movements occur by the active contraction of
skeletal muscles. Striated muscles make up approximately
40% of the mass of an adult human and attach to the
skeleton by tendons. They act in pairs, with the contrac-
tion of one muscle being associated with the relaxation
THE NERVOUS SYSTEM
179
9
Box
Case history
9.1
David is a 63- year- old retired actor who sought help
because of progressive weakness of his arms and legs,
along with slurred speech. He complained of frequent muscle cramps in his legs. Neurological examination showed
bilateral loss of strength in his arms, shoulders and feet.
There was some wasting of the muscles of the hands and
of the feet and fasciculations were observed in the tongue.
Stretch reflexes were hyperactive in his arms and legs,
and the Babinski sign was present bilaterally. There was
increased resistance to passive flexion of the elbow and
knee, which was strong at the beginning of the movement
but collapsed towards the end of the movement. Clonus
was present in response to Achilles’ tendon reflex stimulation. All sensations and mental status were normal. David
was prescribed the drug riluzole. He became progressively
weaker during the next 3 years, with increasing atrophy
and fasciculations in the limb and trunk muscles and difficulty in breathing. He became confined to a wheelchair
and died 4 years after the initial examination.
This case gives rise to the following questions:
1. What are the causes of the various symptoms?
2. What nervous system regions are affected?
3. Why was David given riluzole?
Box
Diseases of the neuromuscular
9.2
junction
Normally, large amounts of acetylcholine (ACh) are
released from motor neurons with each action potential,
which is more than enough to ensure excitation of the
motor unit. However, there are certain conditions in which
this does not occur and muscle weakness ensues. In myasthenia gravis auto-antibodies are produced that destroy
nicotinic ACh receptors so the muscle cannot respond
to the ACh released. The cardinal sign is variable muscle
weakness with the head, eyes and proximal muscles being
more commonly involved than distal limb muscles. Muscle
tone, reflexes, bulk and sensations are normal. Treatment
consists of using acetylcholinesterase inhibitors, such as
neostigmine and pyridostigmine, and immune suppression.
In Lambert–Eaton syndrome, auto-antibodies are directed
against the presynaptic voltage- dependent Ca2+ channels,
which allow the influx of Ca2+, triggering exocytosis of
vesicles containing ACh. This reduces the amount of ACh
released. Patients present with proximal weakness, and
sensory and autonomic disturbances.
The binding of two molecules of ACh to each nAChR
opens this ligand- gated ion channel to allow the flow of
Na+ and K+ ions. The subsequent depolarization of the
endplate is sufficiently large to exceed the threshold for
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
of the opposing (antagonistic) muscle. Each muscle consists of muscle fibres and each muscle fibre receives input
from a single LMN.
When the LMN axon reaches the muscle, it branches,
and each branch forms a specialised synapse called the
firing an action potential in the muscle plasma membrane and this triggers Ca
stores, in sufficient amounts to cause muscle contraction.
In some diseases auto-antibodies bind to the nAChR to
prevent activation (Box 9.2).
neuromuscular junction (NMJ). Upon stimulation, the
LMN axon releases acetylcholine (ACh) into the synaptic
Blocking activity at the neuromuscular junction
cleft. The region of the muscle that lies under the synapse
is the motor endplate and contains a high density of nicotinic acetylcholine receptors (nAChRs).
The NMJ is an unusual synapse compared with other
synapses in the vertebrate central nervous system (CNS).
It releases only a single type of neurotransmitter onto a
single type of postsynaptic receptor (in invertebrates and
in the ANS more than one neurotransmitter is released),
and each action potential releases a large number (200–
300) of vesicles into the synaptic cleft.
The release of so many vesicles leads to a rapid rise
(within 200 μs) in the concentration of ACh to approximately 1 mM. The postsynaptic membrane of the endplate is highly folded and contains abundant nAChRs
and an enzyme—acetylcholinesterase (AChE)—which
is responsible for the breakdown of ACh released into
the cleft. It is present as both soluble and membraneassociated forms and, by hydrolysing ACh into choline
and acetate, reduces the concentration of ACh back to
baseline levels within 1 ms. The choline is then transported back into the motor axon, where it is recycled to
produce ACh.
Activation of the NMJ can be affected by ACh antagonists, which act either presynaptically or postsynaptically. Certain toxins, such as the botulinum toxin, from
the bacterium Clostridium botulinum, can prevent presynaptic ACh release. It prevents the exocytosis of ACh vesicles, by destroying the proteins that allow fusion of the
vesicle to the presynaptic membrane, thus paralysing the
muscle. Severe botulism can be fatal and recovery takes
several weeks. Today, local Botox injections are used by
cosmetic surgeons to paralyse facial muscles, thus reducing wrinkles, and by clinicians to treat enduring muscle
spasms and spasticity.
The poison curare, used by indigenous South
American hunters, is a mixture of plant alkaloids that
act by inhibiting the postsynaptic nAChRs of the NMJ.
A similar mechanism of action occurs in cobra snakebites. Here, one of the peptides in the venom—α
bungarotoxin—binds tightly to the nAChRs, taking days
to be removed from the receptor. Both produce muscle
weakness and respiratory arrest. Prey caught in this way
can be safely eaten as neither poison is absorbed in the
2+
release from intracellular
-
180 SYSTEMS OF THE BODY
9
gut. One of the alkaloids in curare—tubocurarine—was
first used to produce blockade of skeletal muscle during surgery but has now been replaced by other similar
drugs (e.g. gallamine, pancuronium, vercuronium, atracurium, rocuronium, cisatracurium and mivacurium),
which vary in their duration of action (15–60 min). All
are competitive antagonists of ACh that bind to nAChRs
to prevent the depolarization of the motor end plate and
are therefore called non-depolarizing blocking agents.
They also act on presynaptic receptors, interfering with
2+
influx, which causes inhibition of the release of
Ca
ACh. These agents do not cross the blood–brain barrier. Their action can be rapidly reversed by the administration of AChE inhibitors, such as neostigmine. This
prevents breakdown of ACh released into the cleft, effectively increasing the local concentration of ACh, which
can then compete with the blocking agent. Neostigmine
is considered the drug of choice for routine practice in
the reversal of neuromuscular blocking agents in the
paediatric population.
Another class of drugs used to induce neuromuscular blockade are agonists of nAChR. These drugs, which
have some structural similarity to ACh, act by producing
a sustained depolarization of the endplate and are therefore called depolarizing blocking agents. This makes
the muscle unresponsive to stimulation, as the voltagesensitive Na+ channels that produce the muscle action
potential are all inactivated. The only clinically relevant
member of this group is suxamethonium (Box 9.3). Its
blocking action occurs in two phases. In phase 1 there
is an initial brief depolarization of the skeletal muscle
fibres, causing small contractions (fasciculations), and
repolarization is inhibited. In phase 2, desensitization
blockade occurs. After the drug has been present for a
period of time, the motor endplate loses its sensitivity
and depolarization cannot occur. Desensitization continues for several minutes, even after drug is no longer
present. Therefore this dual block effect delays recovery.
The motor unit
Box
Suxamethonium and genetic
9.3
variability
Suxamethonium chloride is the gold standard neuromuscular blocking agent (NMBA) used in clinical anaesthesia.
It is used as a muscle relaxant to facilitate endotracheal
intubation, mechanical ventilation and a wide range of
surgical and obstetric procedures, due to its rapid onset
of effect (3060 s) when injected intravenously, and short
duration of action (2–6 min), despite adverse effects such
as anaphylaxis, hyperkalaemia and malignant hyperthermia. It is rapidly hydrolysed by non-specific cholinesterase
enzymes, called pseudocholinesterases, present in plasma
and normally its effect wears off within 5–10 min as the
drug is metabolized. However, in approximately 1 in 3000
individuals the effects are longer lasting and may continue for many hours. This is due to an autosomal- recessive
genetic variation that causes the production of a form of
plasma cholinesterase that cannot metabolize suxamethonium. In this case the patient requires ventilatory support.
Suxamethonium should be used with caution in patients
with atypical plasma cholinesterase or with muscle diseases.
In 2008 sugammadex was approved in the UK for use
in clinical practice as an alternative drug to neostigmine
because it could rapidly reverse neuromuscular blockade of
the longer- lasting, non-depolarising paralysing agents roncuronium and vercuronium. This means that roncuronium
can be given at sufficiently high doses to work quickly and
reliably (for situations such as laryngeal surgery where
the laryngeal muscles are relatively resistant to neuromuscular blockade) without the adverse effects of suxamethonium. However, sugammadex is costly compared with
other NMBAs and this limits its routine use. If sugammadex
becomes cheaper and more widely available, it is possible
that rocuronium will become the only non-depolarising
NMBA used and sugammadex will become the reversal
agent of choice.
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
The smallest functional component of the motor system is the motor unit. This consists of the LMN and the
muscle fibres that it innervates. Although each muscle
fibre is supplied by only one motor neuron, each motor
neuron innervates between three and a few thousand
muscle fibres (precision vs power functions). This is the
innervation ratio, which determines the precision with
which a muscle is controlled. Muscles with a low innervation ratio, such as the extraocular muscles (ratio of
three fibres per motor neuron), which control eye movements, are very finely regulated, whereas muscles with a
high ratio, such as the gastrocnemius (ratio of 1000–2000
fibres per motor neuron), are less precisely regulated.
Additionally, this organization reduces the chance that
damage to one or a few motor neurons will significantly
affect the muscle action. If a single LMN dies, some of
the muscle fibres that were innervated by the motor axon
become innervated by an adjacent motor neuron, which
sprouts new connections and takes over control of the
denervated muscle fibres. Thus the average size of the
motor units in the muscle increases but with functional
consequences: instead of smaller motor units with finer
control there are now fewer, but larger, units and muscle
precision decreases.
The types of motor unit can be distinguished by the
properties of the muscle fibre and the firing characteristics of its LMN. The most numerous are slow muscle
units, which innervate muscle fibres rich in haemoglobin. They are found in muscles that are important for
activities requiring sustained contractions, such as postural control (anti-gravity muscles). Prolonged activation
of these units produces little reduction in muscle force
even after an hour or more. Fast muscles have less haemoglobin, appear paler and fatigue more quickly. These
181THE NERVOUS SYSTEM
9
AB C
50 ms 500 ms 1 s
contain fast fatigue units, whose activity is important
for muscle contractions that require large forces, such as
during activities like jumping and sprinting. Repetitive
activation of these units causes a rapid decline in the
force of contraction after approximately 30 s. In addition, some motor units are fast- fatigue- resistant and can
sustain activity for approximately 5 min before declining. These different motor units allow the nervous
system to produce movements appropriate to the circumstances and also help to explain the different types
of structural composition of muscles. For example, the
muscle of a 100- m sprinter contains more fast- fatigue
muscle fibres—essential for producing power—than
those of a marathon runner, whose muscles are conditioned for endurance and therefore have more slow
muscle fibres.
Slow muscle fibres are innervated by small α
neurons, while fast fibres are innervated by large α-
motor neurons. This relationship is important, as soma
size determines the order in which motor units are
recruited during a voluntary movement: the smallest ones first, then fast- fatigue- resistant and finally
fast- fatigue. This is known as the size principle. Motor
neurons are deactivated in reverse order as the voluntary movement is terminated. Recruiting an increased
number of motor units generates the increased force of
contraction. During a submaximal contraction of each
muscle, each motor unit fires a small burst of action
potentials and then rests. Greater force is generated by
having more motor units active and reducing the pause
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
time. For finely controlled movements, such as hand
movements, small motor units are used; for more powerful ones, such as quadriceps activation, larger motor
units are recruited.
A single impulse in the motor neuron causes a single
contraction in the muscle, a twitch (Fig. 9.2). This lasts
much longer than the refractory period of the action
potential so if a second impulse arrives before the muscle relaxes; the second twitch is superimposed on the
first. This generates more force in the muscle. Trains of
action potentials will cause twitches to summate. At low
frequencies (12 Hz), this will produce a force that oscillates about a plateau value (unfused tetanus) but as the
frequency increases (30 Hz) the force becomes smooth
and reaches a plateau that is the maximum force attainable by that motor unit. This is called a fused tetanus and
there are no longer peaks and troughs corresponding to
individual twitches evoked by the motor neuron action
Fig. 9.2 Summation of muscle contraction. (A) Single twitch.
(B) Unfused tetanus (12 Hz). (C) Fused tetanus (30 Hz).
- motor
potential. Asynchronous firing of different motor neurons produces a steady- state input to muscles, causing
the contraction of a relatively constant number of motor
units, and averages out the changes in muscle tension
due to contractions and relaxations of different motor
units. This allows movements to be executed smoothly.
The firing frequency of motor neurons also regulates the
muscle tension produced by motor units.
Motor pools
The motor neurons that innervate the same muscle are
called a motor pool and the various motor neuron pools
are topographically organised: LMNs innervating flexors
are separate from extensors and LMNs innervating distal muscles are spatially separate from those innervating
proximal muscles (see Fig. 4.4B). The force of contraction
of a whole muscle depends on the frequency of firing of
the individual motor neurons and also the proportion of
the motor pool that is active. Initially, increases in force
are brought about by increases in firing rate but larger
increases in force are provided by increasing the number of active motor units. This is called recruitment. All
the neurons within a motor pool are excited by common inputs in the spinal cord. Which neurons fire first
will depend on both their size and the specific arrangement of synaptic inputs. Smaller neurons are more easily
excited than larger ones and neurons with more inputs
are excited more easily than more sparsely innervated
ones.
There are two types of LMN found in the same pool:
- and γ- motor neurons. α- Motor neurons are larger and
α
innervate the striated (extrafusal) muscles that generate
the forces needed for movement and postural balance. γ
Motor neurons are smaller and only innervate the muscle
spindle sensory receptors embedded within capsules in
the muscle, called intrafusal fibres. Their function is to
regulate the tension of the muscle spindle by setting the
muscle fibres to a set length (see later).
-
Reflexes
A reflex is the simplest motor response to sensory input.
The reflex directly couples the sensory signal to a motor
output to produce simple, stereotyped responses to
particular sensory inputs. Reflexes occur in both the
autonomic and somatic nervous systems. The neural
pathways involved are called reflex arcs and, in their
simplest form, consist of a sensory neuron and a motor
neuron; this is called a monosynaptic reflex. Sensory
receptors have their cell bodies in the dorsal root ganglion of the peripheral nervous system (PNS) and synapse on the cell bodies of LMNs in the spinal cord or
brainstem. The axons of the LMNs travel in the spinal
nerve of the same spinal segment, and axon collaterals
may travel up and down the spinal cord to affect motor
neurons in adjacent segments.
182 SYSTEMS OF THE BODY
9
Dorsal root
ligament
Group II af
Flower spray
Capsule
bag fibre
bag fibre
Monosynaptic reflexes
In humans there is only one type of monosynaptic reflex,
called the stretch (or the myotatic or deep tendon) reflex
(Fig. 9.3). It occurs when the tendon of a muscle is hit
using a reflex hammer (see Chapter 3) with adequate
force to cause stretching of the muscle. This elicits a brief
contraction of that muscle via activation of the intrafusal
and extrafusal muscle fibres. The reflex acts to prevent
rapid muscle stretch when the force on it increases rapidly and returns the muscle back to its original length.
This reflex is most prominent in extensor (anti-gravity
and postural) muscles and is most easily seen in the
knee- jerk reflex. When the patellar ligament is tapped
just below the knee there is a rapid contraction of the
quadriceps muscles, which swings the lower leg forward. The contraction is stimulated by input from the
muscle spindles, which are embedded in the muscle
and act directly on the large α
- motor neurons supplying
the muscle. As there are no other synapses between the
sensory neuron and the motor neuron the reflex is very
rapid and is all or none, that is, once initiated it cannot
be stopped. Tendon reflexes are used to assess the functional integrity of the spinal cord at specific levels (Table
9.1). All stretch reflexes are ipsilateral, so any reflex
ganglion
testing must be performed on both sides to determine if
there is a difference.
Muscle spindles
The extrafusal muscle fibres form most of the muscle
bulk and produce the contraction. In parallel with these
are specialised sensory receptors called muscle spindles
(Fig. 9.4). These detect the force acting on the muscle and
provide sensory input to the spinal cord about the length
and rate of change of length (velocity) of the muscle.
Muscle spindles consist of a small capsule containing
a small number (∼8–10) of modified muscle fibres called
intrafusal fibres, which have a central region that is noncontractile and around which the ends of sensory nerves
are wrapped. Intrafusal fibres are arranged in parallel
with the extrafusal muscle fibres. There are two types
of intrafusal fibre: nuclear bag fibres and nuclear chain
fibres.
Nuclear bag fibres are modified multinucleated muscle
fibres, swollen in the middle to form a non-contractile baglike structure. They are innervated by myelinated afferent
nerves. There are two types of nuclear bag fibre: dynamic
ending
Extrafusal
fibre
Intrafusal
fibres
Annulospinal
ending
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
Ia afferent
Spinal
cord
Fig. 9.3 The stretch reflex arc. Stimulation of the patellar ligament
stretches the quadriceps muscle, exciting the muscle spindle, which
fires action potentials to stimulate the α- motor neuron in the
lumbar spinal cord. The motor axon releases acetylcholine at the
neuromuscular junction causing the homonymous muscle to contract.
Table 9.1 Main deep tendon reflexes
Muscle (joint) assessed Spinal level assessed
Supinator (wrist) C5–C6
Biceps (elbow) C5–C6
Triceps (elbow) C7
Quadriceps (knee) L3–L4
Gastrocnemius (ankle) S1
α-Motor neuron
Quadriceps muscle
Neuromuscular
junction
Muscle
spindle
Patella
Patellar
ferents
Iα muscle
spindle
γ-Motor neuron
α-Motor neuron
Fig. 9.4 Anatomy of a muscle spindle (simplified). A muscle spindle
contains two types of intrafusal fibre: nuclear bag fibres and nuclear
chain fibres. Bag fibres are innervated by Ia spindle afferents while
chain fibres are innervated by group II muscle afferents. Intrafusal
fibres have their own motor innervation from γ- motor neurons. αMotor neurons synapse on extrafusal fibres.
axon
axon
Nuclear chain fibres (two)
Dynamic nuclear
Static nuclear
183THE NERVOUS SYSTEM
9
primary Ia afferents, which are large in diameter (∼16 μm),
and static secondary (II) afferents, which are smaller in
diameter (8 μm). These differ in their responses to muscle
stretch: static fibres are stiffer than dynamic ones and so
signal muscle length rather than velocity. Ia fibres are rapidly adapting, whereas group II fibres are non-adapting
and so fire even though the muscle has stopped moving.
The peripheral endings of Ia afferents are called annulospiral endings, while those of the group II muscle spindle
afferents are called flower spray endings.
Nuclear chain fibres are slender and have nuclei
arranged along their length in a chain- like fashion. They
are innervated by both Ia and II afferents. They are stiff,
like static fibres, and respond to length.
Each muscle spindle contains at least one dynamic
and one static fibre and a variable number (3–5) of chain
fibres. The distal portion consists of striate muscle with
contractile properties. It is the group II static afferents
that allow the brain to know the position of the muscle when it is still, such as when you are holding your
arms outstretched with your eyes shut (unconscious
proprioception).
When the tendon is tapped, the rapid, phasic component of the monosynaptic reflex is triggered by
the stretching of the dynamic Ia afferents in the central non-contractile part of the muscle spindle so that
they fire action potentials that are relayed to the spinal
cord. Subsequently, as the non-contractile pole ends of
the intrafusal fibres are also stretched, they elongate
slowly, which reduces the firing of the Ia neurons. The
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
remaining tension produces static responses in both
the Ia and II afferents. The longer- lasting tonic component is maintained by the static responses of the
muscle spindles. This is very important in maintaining
posture.
Gamma (γ) motor neurons
The muscle spindle is the only sensory receptor to have
its own motor supply. γ
striated portions of the intrafusal fibres, and are therefore called fusimotor neurons. Stimulation of γ
neurons does not cause movement of the joint to which
the extrafusal muscles are attached. It only places tension
on the central portion of the intrafusal fibres. Therefore,
although they are not part of the stretch reflex per se,
they set the sensitivity of the muscle to stretch by regulating the tension of the intrafusal fibres; that is, they
keep the muscle spindle taut. γ
little peripheral afferent input; most of their input is from
supraspinal descending pathways, such as the reticulospinal and vestibulospinal pathways.
Appreciating the relationship between extrafusal and
intrafusal fibres is important in understanding motor
function. As the extrafusal fibres of the muscle contract,
stretch on the muscle spindles is reduced and sensory
information from the muscle spindles stops unless the
muscle spindles themselves also shortened. During
intentional activity, at the same time as the α
- Motor neurons innervate the
- motor
- Motor neurons receive
- motor
neurons fire to produce shortening of the extrafusal
fibres, the γ- motor neurons are stimulated to shorten the
intrafusal fibres. This α- γ co- activation ensures that the
muscle spindle is shortened at the same rate as the muscle and the sensitivity of the muscle spindles is maintained despite shortening of the muscle. γ
conduct action potentials more slowly than α- motor neurons. This means that the intrafusal fibres will contract
fractionally later than the extrafusal fibres, allowing time
for the sensory systems to respond.
Reciprocal and synergistic innervation
Skeletal muscles act in antagonist pairs. Contraction
of one muscle is prevented by the tone of the opposing
muscle, unless that muscle is simultaneously relaxed.
During the knee- jerk reflex, as well as stimulation of α-
motor neurons supplying the quadriceps muscles, there
is reciprocal inhibition of the hamstring muscles at the
back of the thigh. This occurs via an inhibitory interneuron in the spinal cord, which is stimulated by the sensory
input from the muscle spindles of the quadriceps. This is
a disynaptic reflex.
The quadriceps muscle group comprises four leg
extensor muscles that function synergistically to extend
the lower leg about the knee joint. The majority of the
muscle spindle input is to the motor neurons in the
same motor pool (the homonymous muscle). However,
approximately 40% of the synapses occur with motor
neurons going to all the other leg extensors. Thus activation of the muscle spindles in one extensor muscle will
produce synergistic contractions in all four muscles.
Supraspinal control of stretch reflexes
Stretch reflexes are subject to descending modulation via
direct or indirect connections between UMNs and α
γ- motor neurons. Most of the axons from descending
pathways do not form synapses directly with α- motor
neurons but terminate on these interneurons. Alterations
in the activity of these pathways may affect the size or
threshold for activation of the reflex. For example, the
amplitude of the reflex can be reinforced by various
measures, including clenching of the teeth, pulling interlocked fingers (Jendrassic manoeuvre; see Box 9.4) and
general distraction of attention. These measures only
work when the reinforcement is at a higher level than the
reflex being tested, and the reinforcement is thought to
be due to the removal of tonic inhibition from the LMNs.
Golgi tendon organs
As well as muscle spindles, muscles have a second
type of sensory organ called the Golgi tendon organ
(GTO) that is found in the tendons. These are placed in
series with the muscle fibres and measure muscle tension. An increase in muscle tension activates a negative
(autogenic) feedback reflex of the homonymous muscle
called the inverse myotactic reflex (Fig. 9.5), which prevents further increases in tension. This reflex protects the
- Motor neurons
- and
184 SYSTEMS OF THE BODY
9
antagonist muscle
Golgi tendon organ
α-Motor neuron
Striated
Box
Excitatory
interneuron
Jendrassic manoeuvre
9.4
In patients with reflexes that are difficult to elicit or appear
absent, the use of reinforcement techniques may be helpful in observing a response. This is the Jendrassic manoeuvre. It is most often used when testing lower limb reflexes;
the patient is asked to interlock their fingers and try to
pull their hands apart while keeping the fingers interlocked. Clenching the teeth can be added to this task if
necessary. The tendon is struck during this process. A positive response (if none was present before) or an enhanced
response (f the response was weak previously) is to be
expected in the absence of any pathology. This indicates
that the reflex is under some level of supraspinal inhibition.
The main idea behind the reflex is that when the brain is
asked to focus on a specific, focal voluntary movement such
as pulling the hands apart, it ‘forgets’ about other body
regions and so the descending drive is reduced. The reinforcement task must be at a neurological level above the
reflex to be tested. Remember that most descending motor
axons do not directly activate α- motor neurons but synapse
with inhibitory interneurons that regulate the size of the
reflex. When this inhibition is temporarily reduced, the
reflex gets bigger, and this is reminiscent of what is seen in
patients with stroke or other upper motor neuron lesions.
Ib afferent
Muscle
Inhibitory
interneuron
tendon from being injured by too much tension. It also
plays a role in mechanisms related to muscle fatigue and
joint hyperextension/flexion.
GTOs consist of collagen fibres that contain the endings of Ib afferent neurons at the tendon- muscle interface. GTOs are relatively insensitive to passive stretch
but are sensitive to active contraction when most of the
force acts directly on the tendon. When muscle tension
increases the collagen fibres are stretched, causing Ib
afferents to fire. The frequency of firing is proportional to
the level of tension. These afferents synapse onto interneurons, which, in turn, synapse onto the α
- motor neurons of both the homonymous (inhibitory action) and
antagonistic (facilitatory action) muscles. Thus the function of this reflex is to ‘switch off movement’ and allow
the muscle to relax.
The sensory inputs involved in the myotactic and
inverse myotactic reflexes affect the same motor neurons but with opposite effects (Fig. 9.6). Sometimes, in
pathological situations, these two systems get trapped in
a loop where they alternatively trigger each other. This
causes the muscle to alternately contract and relax several times a second. This is termed clonus. It can be seen
in ankle stretch reflexes where the foot oscillates about
the ankle.
Control of muscle tone (stiffness)
All muscles are under some degree of stretch and this is
responsible for resting tension in the muscle called muscle
tone. The stretch reflex, which maintains muscle length in
response to increased load, and the inverse myotactic reflex,
which maintains a constant tension, work in opposition.
When the load on a muscle is increased, either the mus-
= inhibitory interneuron
+
= excitation
−
= inhibition
Golgi tendon organ
Ib
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
α-Motor neuron
(homonymous)
–
+
Fig. 9.5 Inverse myotactic reflex arc. The Golgi tendon organ
fires in response to an increase in tension and activates spinal cord
interneurons that inhibit the α- motor neurons innervating the
homonymous and synergistic muscles, thereby relieving excess muscle
tension and relaxing the muscle. At the same time connections
with other sets of interneurons allow excitation of α- motor neurons
innervating the antagonistic muscles, causing their contraction (not
shown). +, Excitation; - , inhibition.
α-Motor neuron to
Ia/II
Muscle spindle
+
I
+
−
Fig. 9.6 Cooperation of myotactic reflexes. Activity of Ia and group II
fibres produces α- and γ- motor neuron co- activation, which produces
muscle contraction while maintaining its sensitivity during contraction.
Stimulation of the Golgi tendon organ (Ib) fibre inhibits α- motor
neurons (and γ- motor neurons), producing relaxation. Differences in
the conduction velocity (Ib fibres are slower than Ia/II fibres) and the
presence of inhibitory interneurons allow contraction and relaxation
to occur.
γ-Motor neuron
muscle
185THE NERVOUS SYSTEM
9
12
postural support
E
cle must lengthen or the tension must increase. Working
together, these reflexes control the tone of the muscle. If the
load on a muscle increases but the length is maintained,
the contraction is isometric. This is normally the case for
postural muscles. Alternatively, if the load is moved by
shortening the muscle, this isotonic contraction maintains
a constant tension. Damage to LMNs or descending pathways will change the level of tone within muscles.
may be important in maintaining balance as the centre of
gravity changes. For example, treading on a sharp object produces a withdrawal of the foot with extension of the other leg
in order to support the extra weight (see Fig. 9.7).
Flexion reflexes differ from myotactic reflexes in that
they involve several interneurons between afferent axons
and motor neurons. This gives the brain opportunities to
override, modulate or control these reflexes via activity in
descending pathways. This is impossible for the monosyn-
Polysynaptic reflexes—Flexor and crossed extensor
reflexes
These two linked reflexes are stimulated by noxious
stimuli, both actual (such as a sharp object) and perceived (such as threatening behaviour). These polysynaptic reflexes trigger a complex set of actions (Fig. 9.7).
The flexion reflex is an important protective reflex.
Stimulation produces a withdrawal of the entire threatened
limb from the harmful stimulus on the ipsilateral side, with a
compensatory extension of the opposite side. These reflexes
aptic and synaptic reflexes from proprioceptors. Damage
to descending pathways can alter flexion reflexes.
Spinal motor function
A considerable amount of local processing of sensory
information occurs in the spinal cord and this influences motor output. Motor reflexes are simple patterns
generated in the spinal cord but the spinal cord is also
involved in producing the complex patterns involved
in locomotion. During locomotion, networks of neurons
produce cycles of activity in order to contract groups of
muscles in a carefully timed sequence. These networks,
which are called central pattern generators, are initiated
by descending input and are modified by reflexes. They
are more prominent in quadrupeds than in bipeds, as is
evidenced by the observation that when the spinal cord
is transected in animals such as cats and rats, there is
+
−
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
greater recovery of locomotion than in humans.
Descending pathways
= Excitatory
interneuron
= Inhibitory
interneuron
= α-Motor neuron
= Extensor muscle
= Flexor muscle
F
Nociceptor
−
+
EF FE
As outlined in Chapter 4, several descending motor pathways that originate in the brain and brainstem modulate
LMN function (Table 9.2). The name of the individual
tract indicates where it originates and terminates. Unlike
LMNs, they use glutamate as their neurotransmitter.
There are three main functionally distinct pathways.
The pyramidal pathway arises in the motor cortex and
is essential for planning, initiating and directing voluntary movements and complex spatiotemporal sequences
of movements. It provides for fine, precise movement
and voluntary control of distal muscle groups. The other
functionally distinct pathways are termed extrapyramidal, because they arise from the brainstem. They are
Flexion
to painful
stimulus
(response;
withdrawal)
Extension for
responsible for orientating the body, head and eyes in
response to somatic, auditory, visual or vestibular stimuli
and for regulating muscle tone. The medial brainstem
pathways arise from cells in the reticular formation,
vestibular nuclei and tectum. These motor pathways
Fig. 9.7 The flexor (1) and crossed extensor (2) reflex arcs. These are
polysynaptic reflexes. The flexor withdrawal reflex has a protective
function. A noxious stimulus activates nociceptors that stimulate spinal
cord interneurons in several spinal segments to excite the ipsilateral
flexor α- motor neurons, which withdraw the limb from the stimulus.
At the same time, the antagonistic extensor muscles are inhibited.
The crossed extensor reflex is a contralateral response to an ipsilateral
stimulus to maintain balance. Here, nociceptors activate interneurons
that excite the α- motor neurons of the extensor muscles of the
contralateral leg, while inhibiting the flexors of that leg.
provide for reflex movements related to posture and balance, usually involving many muscle groups—particularly anti-gravity muscles—to prevent the body or head
from being destabilised. A lateral brainstem pathway
originates in the red nucleus and provides for voluntary
movements of the arms but not the individual digits.
Each of these main motor pathways terminates in the spinal cord in a different pattern, which reflects the modality of
movement controlled by that motor pathway (Fig. 9.8).
186 SYSTEMS OF THE BODY
Table 9.2 Summary of the main functions of the descending tracts
Motor system Tract Origin
Pyramidal Lateral corticospinal
Anterior
corticospinal
Corticobulbar Motor cortex Bilateral
Extra- pyramidal:
lateral
Extra- pyramidal:
medial
ANS, Autonomic nervous system; LMNs, lower motor neurons.
Rubrospinal Red nucleus of
Medial
reticulospinal
Lateral
reticulospinal
Lateral
vestibulospinal
Medial
vestibulospinal
Tectospinal Superior colliculus Crossed
Motor cortex Crossed
midbrain
Pons Ipsilateral
Medulla Bilateral
Lateral vestibular
nucleus
Medial and inferior
vestibular nuclei
Distribution
and cord
levels
Bilateral
All levels
Crossed
Crossed
Cervical cord
All levels
All levels
Ipsilateral
All levels
Bilateral
Cervical cord
Cervical cord
Decussation
(where
appropriate)
Spinomedullary
junction
Spinal cord
Pons and medulla
Midbrain and pons
Midbrain
Ventral tegmentum
— Axial and proximal
— Proximal limb flexors Axial and proximal
— Axial and proximal
— Axial ipsilateral Axial contralateral Stabilises head position while
Midbrain
Dorsal tegmentum
Main action on lower motor neurons
(LMNs) Function
Excitatory to Inhibitory to
Hand and finger
flexors
Trunk flexors
Mixed cranial nerve
motor nuclei (V,
VII, IX, X, XII)
Oculomotor nuclei
(III, IV, VI)
Limb flexors Limb extensors Control of gross limb movements
limb extensors
limb extensors
Neck extensors Neck flexors Coordinating head and eye reflex
Hand and finger
extensors
Trunk extensors
Mixed cranial nerve
motor nuclei (V,
VII, IX, X, XII)
Proximal limb flexors Facilitates extensor reflexes,
limb extensors
Axial and proximal
limb flexors
Control of fine voluntary
movement
Control of brainstem motor
nuclei
inhibits flexor reflexes, and
increases muscle tone in axial
and proximal limb muscles
Facilitates flexor reflexes,
inhibits extensor reflexes and
decreases muscle tone in axial
and proximal limb muscles.
Autonomic activation of ANS
preganglionic LMNs
Stimulates extensor and inhibits
flexor muscles to aid postural
control of the body (balance)
body is moving (balance)
responses to auditory, visual
and somatic cues
187THE NERVOUS SYSTEM
9
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
9
Tr unk
Anterior CST
n
biased tracts
spinal cord
MOTOR SYSTEMS I: DESCENDING PATHWAYS AND CEREBELLUM
Arm
Hand
Head
Internal
capsule
Leg
Cortex
Superior colliculus
Red nucleus
Midbrain
Key
Corticospinal tract
Rubrospinal tract
Tectospinal tract
Reticulospinal tract
Ver tibulospinal tract
Pons
MVST
Medulla
LVST
Cervical
Lateral CST
Flexors
Extensors
Lateral RST
Lateral RST
Medial RST
Fig. 9.8 Location of the descending pathways along the neuraxis. The
locations of the main descending pathways in the spinal cord in relation
to the topographic organization of muscles are shown schematically.
Pathways that act mainly on extensor motor neurons are located in the
ventral funiculus, while those acting on flexor motor neurons run in the
lateral funiculus. The schematic positions of these pathways at higher
levels of the neuraxis are shown. ICP, Inferior cerebellar peduncle; ION,
inferior olivary nucleus; LVST, lateral vestibulospinal tract; MVST, medial
vestibulospinal tract; RST, reticulospinal tract.
Medial RST
Corticospinal tract
(to body)
Corticobulbar tract
(to head)
RST
PT
Distal
Limb
Tr unk
ICP
ION
Location of flexor
biased tracts
Proximal
To pographic organizatio
of α-motor neuron pools
Location of extensor
The pyramidal system comprises the corticospinal and
corticobulbar tracts. Approximately 60% of the neurons
are in the primary, supplementary and premotor areas
of the frontal lobe. The rest are in the somatosensory cortex (30%) and the posterior parietal cortex (10%). Their
axons pass through the internal capsule (genu and posterior limb) and descend in the basal part of the brainstem
but they differ in their termination sites. Corticobulbar
fibres terminate on LMNs in the brainstem and control
facial movements. Corticospinal axons bypass the brainstem LMNs and terminate in the spinal cord to control
limb movements. Corticospinal tract (CST) axons are
often called pyramidal tract axons (after the area in the
medulla where the axons cross the midline—the spinomedullary junction—Fig. 9.9). The CST is concerned with
generating voluntary movements of the hands (see Table
9.2) that require precision, speed and agility. It has very
little effect on the lower limbs.
At the spinomedullary junction 85% of the corticospinal axons decussate to form the lateral CST. The remaining 15% are uncrossed fibres that form the anterior CST,
and these fibres decussate in the spinal cord at the same
segmental level where they synapse. Both tracts are excitatory and most of these axons synapse with spinal cord
interneurons; some lateral CST axons synapse directly
with α
- motor neurons, especially those involved in
movement of the fingers whereas the anterior CST axons
synapse bilaterally on interneurons to control voluntary
movements of the axial muscles. The terminal distribution of the corticospinal motor pathway partly overlaps
with those of the other lateral and medial extrapyramidal
pathways.
The rubrospinal tract is a small contralateral pathway that ends on interneurons in the spinal cord; these
convey motor commands to cervical motor neurons for
the control of limb muscles (see Table 9.2). As an evolu-
tionary old pathway, its function differs across species.
In quadrupeds, like rodents, it is involved in intra- and
inter- limb coordination during locomotion. In primates
its function is associated with skilled forelimb movements. In humans rubrospinal axons are intermingled
with those of the lateral CST and the function of the
rubrospinal tract has largely been taken over by the latter. The majority of red nucleus axons do not project to
the spinal cord but relay information to the motor cortex
from the cerebellum via the thalamus and inferior olivary
nucleus (ION) and are involved in complex cognitivemotor functions, such as motor learning, error encoding,
timing and control of ongoing movement (see later).
The medial brainstem motor pathways are represented by the anterior CST, reticulospinal, vestibulospinal and tectospinal tracts. They are associated with
balance and postural control via the temporal and spatial coordination of movements. Their axons travel in
the brainstem tegmentum (and are therefore spatially
separate to the pyramidal system) and the spinal cord
ventrolateral funiculus (see Fig. 9.8) and end mainly on
interneurons in the medial third of the spinal cord grey
matter. These interneurons carry the motor commands
188 SYSTEMS OF THE BODY