|
A REGIONAL AND SYSTEMIC OVERVIEW OF FUNCTIONAL
NEUROANATOMY
INDIANA UNIVERSITY
SCHOOL OF MEDICINE
TERRE HAUTE CENTER FOR MEDICAL EDUCATION
MEDICAL NEUROBIOLOGYDR. WILLIAM J. ANDERSON
I. ORGANIZATION OF THE NERVOUS SYSTEM
A. THE THREE-NEURON NERVOUS SYSTEM
The human nervous system is extremely complex; it receives
and interprets all outside stimuli. it integrates information
from the outside world with that from inside the body, and it
initiates appropriate responses to the environment, including
all movements and all behavioral acts. The human central nervous
system (CNS) contains close to a trillion (1012)
neurons, and connections between these neurons approach ten
thousand trillion (1016). The connections are not
random, but are highly organized and precise. These connections
can be considered as specific systems performing specific
functions and processing specific information. The Organization
of neural tissue into systems becomes clearer if we examine the
nervous system of a primitive animal, the sponge. This will
permit a brief look at steps in the evolution of the human
nervous system.
The nervous system appears in sponges as a derivative of
the ectoderm in contact with the external environment. This
modified ectoderm responds to noxious stimuli and causes the
organism to withdraw from them. This primitive nervous system is
a one neuron nervous system in which a single type of
nerve cell receives external stimuli and initiates a withdrawal
response by initiating a contractile action in effector tissue
(Fig. 1-1). Direct contact of nervous tissue with the external
environment has persisted throughout evolution and is still
present in the human (e.g., cutaneous receptors). However, to
permit a diversity of response, the same neuron in humans that
responds to external stimuli does not directly contact effector
tissue. As the nervous system developed phylogenetically,
specialization of neural tissue into sensory neurons in contact
with the environment, and motor neurons in contact with effector
tissue, occurred. This specialization produced a two-neuron
nervous system, such as that found in some coelenterates
(Fig. 1-2). The sensory neuron in this system no longer
interacts directly with the effector tissue. Rather, the sensory
neuron conveys the stimulus to a second neuron, the motor
neuron, which then communicates with the effector tissue,
initiating a motor action in response to the sensory input. The
motor neuron is no longer in contact with the external
environment but is totally within the organism.
The direct communication between sensory input neurons and
motor output neurons has persisted throughout evolution and can
be seen in humans in the form of muscle stretch reflexes
(sometimes called deep tendon reflexes). This reflex is
initiated by applying a sensory stimulus to a muscle tendon (a
tap or stretch of the tendon with the reflex hammer). The
stretching of the muscle activates the receptor of a sensory
neuron. The sensory neuron communicates directly with a motor
neuron in the spinal cord. The motor neuron communicates
directly with the muscle being stretched and causes the muscle
to contract. The same organization of neurons that originally
evolved to allow quick response to noxious stimuli has persisted
in the human as a system that permits the unconscious regulation
and maintenance of a particular state of muscle activity.
Such a reflex mechanism, through just two types of neurons,
sensory and motor, allows little flexibility in the behavior of
the organism. Direct contact between sensory and motor neurons
permits only a contraction or non-contraction of the effector
tissue, an all-or-none response. It does not allow for a
partial, or graded, response, nor does it allow the response to
be integrated with other stimuli being received by the organism.
Advanced behavior and adaptive responses require more complex
processing between the sensory input and the motor output. This
intermediate system of information processing is made possible
by the addition of a third kind of neuron to the two-neuron
nervous system, the intermediate neuron. This final
neuronal addition to nervous system evolution is present in more
advanced animals, including humans. It is designated the
three neuron nervous system and represents the most advanced
and flexible or nervous system patterns (Fig. 1-3). The
intermediate neuron (sometimes called interneuron)
provides more processing of incoming information and allows more
flexibility in the response.
This three-neuron nervous system has reached its highest
level of development in the human brain. Specialization and
complex communication networks have expanded the role of
intermediate neurons to the point to which the entire human
brain, with the exception of a few million motor neurons
supplying muscles of the head and neck, consists entirely of
intermediate neurons. Our ability to think, write, speak, and
perform any complex action is based upon the functioning of
them. These intermediate neurons are not in direct contact with
either the external environment or the effector tissue but are
clustered together into a complex central network--the CNS.
As complex as the human nervous system is, it can be broken
down into basic components for study. The human nervous system
can be thought of as having two basic parts: (1) a peripheral
nervous system (PNS) that is in contact with the external
and internal environment; and (2) a central nervous system
(CNS) that is responsible for processing information and
providing an appropriate response to the environment. The PNS
has a somatic component consisting of sensory input (sensory
receptors and neurons) and motor output (axons and the
neuromuscular junction of motor neurons) that was classically
described as controlling the contraction of skeletal muscles.
The PNS also has an autonomic component that controls smooth
muscles, cardiac muscle, and secretory (or exocrine) glands,
allowing for the continuous regulation of both basal homeostatic
and stress-related functions of the body. More recent evidence
shows many other targets of the autonomic nervous system such as
hepatocytes, brown fat cells, and cells of the immune system
within lymphoid organs. This autonomic nervous system (ANS)
is further subdivided into two components, the sympathetic
nervous system (SNS) and the parasympathetic nervous
system (PsNS). The sympathetic component is a widespread
system that responds to stress or a demand for activity by
causing a general arousal and readiness of the body to cope with
the perceived situation, often called a "fight or flight"
response. The parasympathetic component is responsible for the
control of homeostatic functions necessary for the well being,
basic maintenance, and repair of the body. An example of PsNS
function is normal digestion. A third subdivision of the
autonomic nervous system, the enteric nervous system, consists
of approximately 100 million neurons within the gut, many of
which are autonomous, not in contact with parasympathetic or
sympathetic neurons.
The CNS is composed of a brain and a spinal cord. The
spinal cord receives axons of sensory neurons bringing
information into the CNS from the body. It also contains the
cell bodies of the motor neurons whose axons leave the spinal
cord to innervate skeletal muscles of the body. The bulk of the
spinal cord is made up of interneurons that mediate incoming
sensory information and outgoing motor and autonomic
information, and fiber tracts that represent ascending and
descending communication channels interconnected with higher
structures in the brain. The brain can be divided into a
brain stem and a forebrain. The brain stem has three
basic anatomical subdivisions continuing upward (rostrally) from
the spinal cord. These are the medulla, the pons,
and the midbrain. The cerebellum is a large
convoluted structure derived from the pons but associated with
all three of the other subdivisions that has a major role in
smoothing and coordinating motor activity. The medulla, pons,
and cerebellum are parts of the rhombencephalon, while
the midbrain is synonymous with the mesencephalon. The
brain stem receives sensory input from general and special
sensory systems of the head and neck and contains motor and
central autonomic neurons supplying the head and neck, and
portions of the viscera. In this manner, the organization of the
brain stem is similar to that of the spinal cord. In addition,
the brain stem contains mechanisms and structures for more
sophisticated sensory, motor, and autonomic processing that are
capable of integrating and coordinating more complex activities
(e.g., respiratory rhythm, control of body tone, eye movement
responses to head position). The forebrain (prosencephalon)
can be divided into a diencephalon, including mainly
the thalamus and the hypothalamus, and a telencephalon,
including the olfactory system, the limbic system,
the basal ganglia (corpus striatum), and the neocortex.
The functional role of these higher centers of the brain
will be discussed later in this chapter.
In addition to the organization of neuronal structures of
the brain, the study of the nervous system must also include its
coverings, the meninges, and two fluid systems, the blood
supply and the cerebrospinal fluid. The meninges comprise three
layers of membranes covering the brain.
The innermost layer, the pia, adheres very closely
to the surface of the brain and follows all of the convolutions.
The second layer, the arachnoid, encloses both the
subarachnoid space, which contains the CSF, and the arteries and
veins supplying the cortex; it stretches across the sulci
without following the folds. The third or outer layer, the dura,
is a tough protective membrane; itself composed of two layers
(Fig. 1-4). Major venous sinuses that drain blood from the brain
lie between its two layers. The outermost layer is tightly
adherent to the bones of the skull.
The blood supply to the brain comes from two sources: (1) two
vertebral arteries that unite to form the basilar artery on the
ventral midline surface of the pons, supply most of the brain
stem: and (2) the internal carotid arteries supply most of the
forebrain. The two arterial systems are connected at the base of
the brain by communicating branches, the anterior and posterior
communicating arteries, forming the circle of Willis
(Fig. 1-5). The venous blood drains into the major venous
sinuses through superficial and deep veins. The sinuses then
drain into the internal jugular veins. The cerebrospinal
fluid (CSF), found in both the subarachnoid space and the
ventricles within the brain, is an ultrafiltrate of blood. CSF
is produced by the choroid plexus from arterial blood and by
leakage of the extracellular fluid into the ventricular cavities
of the brain. The CSF circulates through the ventricular system
(from lateral ventricles of the forebrain, into the third
ventricle of the diencephalon, into the aqueduct of the
midbrain, and into the fourth ventricle of the rhombencephalon),
escapes into the subarachnoid space through foramina (the
foramen of Magendie in the midline and the lateral
foramina of Luschka) at the caudal end of the fourth
ventricle in the medulla, circulates around the external surface
of the brain and spinal cord in the subarachnoid space and its
enlargements, called cisterns, and is absorbed into the
venous blood through specialized one-way valve structures of the
arachnoid, the arachnoid villi. The CSF provides a
hydraulic cushion to protect the brain from contact with the
hard bone of the skull and may provide a communication channel
for CSF-borne substances to influence neurons.
The foregoing discussion provides a very general plan of the
nervous system. Understanding the nervous system requires
knowledge of how the neuron functions and how groups of neurons
function together as systems. The characteristics and properties
of the neuron will be discussed next. The nervous system itself
can be organized and studied in two different but complementary
ways, regionally and systemically. Both of these organizations
will be used to provide a framework for study. The PNS,
including both somatic and autonomic components, will be
discussed first, followed by a regional overview of the central
nervous system. Finally, the nervous system will be studied
longitudinally, according to functional systems.
II. NEURONS AND SUPPORTING CELLS
1. The Neurons
a. Morphological Characteristics of Neurons
The neuron is the fundamental unit of the nervous
system. Its function is to communicate coded information over a
distance. That distance may be very short, as with a local
interneuron, or very long, as with a motor neuron whose cell
body is in the spinal cord and whose axon terminates on a muscle
of the foot. The neuron achieves this conduction of information
by carrying an electrical potential down its axon. The shape of
the neuron is particularly conductive to the transport of
information. Typically, the cell body (soma) has two
kinds of processes, called neurites, extending from it.
Dendrites are extensions of cytoplasm from the cell body
that generally are considered to receive information from other
neurons and pass that information toward the cell body (Fig.
1-6). The branching patterns of dendrites may be very
distinctive, reflecting the type and amount of information that
a specific process received; these dendritic arborizations can
range from sparse and small (only a few microns), or elaborately
branched and huge, extending over millimeters of distance. The
second type of neurite is the axon. It usually originates at the
cell body (or primary dendrite) and is a long process of
constant diameter through which the neuron communicates with
other neurons or effector structures. Each neuron has at most
one axon leaving the cell body or a dendrite, but that axon may
branch to form many processes called axon collateral’s,
each of which may communicate with different parts of the
nervous system. In its course of travel, the axon may give rise
to many small bulges called axon terminals (also called
boutons or varicosities). The terminal is in close
proximity either to another neuron or to the effector tissue in
the case of the outflow of the PNS. This gap between one neuron
and another, or between neuron and effector tissue, is called a
synapse. The flow of electrical information in a neuron
is generally from the dendrites to the cell body, and then down
the axon to the terminals, carrying the message toward the next
neuron in that chain of communication, or toward the effector
tissue. Figure 1-6 shows a schematic representation of the basic
neuron and a few examples of neurons with specific shapes.
The form and structure of each neuron reflects the role of
that neuron. Very specific connections exist between neurons,
establishing communication channels that may extend over long
distances and may be composed of a chain of many neurons. The
anatomy of these communication channels, called neuronal
connections or projections, determines the
hierarchical relationships and influences that one neuron
population exerts over other neurons. A knowledge of these
connection patterns is essential for the adequate evaluation of
neurological disorders and their therapy. For example, a spinal
cord injury removes motor neurons from the control of higher
centers in the brain by severing or damaging descending
pathways. Removal of this control, which normally holds these
neurons in check and regulates their response to incoming
sensory stimuli, results in hyperexcitability and
over-responsiveness (called release phenomena, or
disinhibition) of spinal cord lower motor neurons (LMNs) to
certain types of stimuli, manifested in the patient as
spasticity. A knowledge of which connections were destroyed and
which connections remain intact provides a rational basis for
the therapy of such a patient.
b. Electrical Properties of Neurons
Understanding how neurons transfer information and how that
information can be altered by outside influences can help to
explain the mechanisms by which groups of neurons act together
as integrated systems. The neuron has two properties that allow
it to transfer information, conductivity and
neurotransmission. The neuronal cell membrane is an
excitable membrane; it is capable of conducting an electrical
impulse over a distance. Because of the ionic balance that
exists between the cytoplasm of a neuron and the extracellular
fluid, based upon the differentially permeable neuronal
membrane, an electrical potential, called the resting
potential, exists across the cell membrane. The resting
potential is produced by the properties of the neuronal membrane
itself, particularly the differential permeability of the
membrane to sodium (Na+) and potassium (K+)
ions, and the metabolic pumps that help to main the unequal
distribution of these ions. The resting potential is normally a
voltage of approximately -70 to -80mV. Excitation or inhibition
of the membrane causes the potential to change. If an excitatory
stimulus is strong enough to allow the membrane potential to
reach a higher specific voltage, called the threshold,
the neuron fires an action potential. The action potential
represents a specialized way of conducting an electrical
impulse over a long distance, the entire length of the axon,
without dying out. That is to say, the action potential is
non-decremental (does not decrease in amplitude) over the length
of the axon, even a meter or more. The action potential occurs
because of a rapid increase in sodium conductance through the
sodium channels that is brought about by a stimulus that
depolarizes the membrane to threshold, thereby opening the
sodium channel and permitting the sodium ion to move across the
membrane. The resultant depolarization, in turn, increased the
potassium conductance, thus permitting potassium to move out of
the axon, restoring the axoplasm. to a polarized state. The
sodium and potassium ions then are moved out of, or into the
axon, respectively, by energy dependent ion pumps. The action
potential is propagated down the axon by re-initiation at each
adjacent increment of axon, or at each bare site of a myelinated
axon (node of Ranvier); a process called saltatory
conductance because the action potential appears to skip
from node to node. The reinitiating of the action potential is
brought about by current flow along and within the axon that
brings the next node or next patch of axon membrane to
threshold. The action potential is in contrast graded
potentials, small changes of the membrane voltage away from
the resting potential in either direction, that will decay or
die out after a short distance if it does not reach threshold,
and will diminish with time. In general, dendrites and cell
bodies carry graded potentials, while action potentials are
carried by axons. The graded potential allows a great deal of
flexibility in processing in the nervous system because it can
be summed. In contrast to the action potential that, if it
fires, is always a constant amplitude and velocity for a given
axon. The graded potential may be increased by several inputs
arriving at the neuron at the same time (spatial summation)
or by individual inputs that act on the membrane
repetitively, before the resultant graded potential has had an
opportunity to die out (temporal summation). This means
that increasing the input to a given neuron can bring it to
threshold and cause it to fire an action potential, or that an
input can bring a neuron to a more excitable state; closer to
threshold for firing an action potential, even though that input
itself does not cause an action potential directly (called
subliminal excitation). It also means that if one
form of input is lost due to injury or disease, resulting in a
failure of a given population of neurons to function, those
neurons may then be caused to fire by increasing the input from
another source. This principle is the basis for therapy of some
disorders.
Neurotransmission
When an action potential reaches an axon terminal or
a varicosity, it causes the membrane potential of that terminal
to increase (i.e., to go from -70 mV toward 0). This change
reduced the negativity of the potential across the membrane and
is called depolarization. Depolarization of the nerve
terminal results in the release of a chemical messenger called a
neurotransmitter. The release of neurotransmitter depends
on the presence of calcium ion (Ca++), which enters
the cell during depolarization and permits the release of the
neurotransmitter from the cytoplasm or from the prepackaged
subcellular compartment, the synaptic vesicle, by a process
called excitation-secretion coupling. The vesicles in most
terminals’ range from 20-100 nm in diameter, contain the
neurotransmitter, can combine with the nerve terminal membrane
in the presence of Ca++, and release the transmitter
into the synaptic cleft. The vesicle membrane is recycled later
(Fig. 1-7) by a process of pinocytosis (pinching off a
membrane). The membrane of the axonal terminal pinches off
fuzzy-coated vesicles inside the terminal, which then merge to
form a cisternal apparatus. This apparatus then pinches off
recycled synaptic vesicles, ready for use again in the process
of neurotransmission. The interaction of a
neurotransmitter with its receptor (a surface protein) causes a
change in the membrane of the target cell, initiated through a
second messenger such as a cyclic nucleotide. The change can
cause (1) a decrease in the potential difference or voltage
across the cell membrane (making it more positive), called a
depolarization, or (2) an increase in the potential
difference across the cell membrane (making it more negative),
called hyperpolarization. Both these post-synaptic
potentials (PSPs) are graded potentials and can be summed. A
depolarization raises the potential toward the threshold, making
it easier for the cell to fire an action potential. If a single
depolarization is strong enough or if enough depolarization’s
occur, threshold may be reached and the neuron will fire an
action potential. A hyperpolarization, on the other hand, lowers
the potential away from the threshold, making it more difficult
to fire an action potential. If a neurotransmitter (ligand)
-receptor interaction cause the depolarization of the cell
membrane, it is excitatory, and the neurotransmitter stimulating
it is called an excitatory neurotransmitter, and the
synapse is considered an excitatory synapse. If a
ligand-receptor interaction causes a hyperpolarization of the
target cell membrane, it is inhibitory, and the neurotransmitter
stimulating it is called an inhibitory neurotransmitter.
This synapse is an inhibitory synapse. Recent evidence has shown
that a single terminal may contain more than one
neurotransmitter (for example, a catecholamine and a peptide),
so this simplistic scheme of excitatory and inhibitory neurons
may require extensive modification.
A nomenclature problem has developed as neurotransmitter
research has demonstrated that a neurotransmitter can be
excitatory at one kind of synapse and inhibitory at another.
This seeming paradox is easily explained if it is realized that
the single factor which determines whether the transmitter is
excitatory or inhibitory is the receptor on the target cell, not
the transmitter itself. The target cell membrane may possess
receptors for many neurotransmitters
The evolution of chemical transmitters interacting with
specific receptors provides the nervous system with additional
flexibility in the processing of information. The neuron can sum
information received from different sources, received at
different rates, and received from both excitatory and
inhibitory sources, and can integrate it to provide a single
response based on the processing of a large amount of diverse
information. It should be noted that other chemicals besides
neurotransmitters might interact with receptors. Various drugs
exploit an interaction with receptors in order to restore
function when there is a lack of transmitter released, when the
releasing neuron has been damaged, or when it is necessary to
block the release or activity of a transmitter present in too
high a quantity. These receptor interactions, whether excitatory
or inhibitory, can be used to treat numerous disease states,
such as Parkinson's disease, depression, and spasticity.
d. Patterns of Neuronal Connections and Interactions
Additional flexibility in information processing is brought
about by diverse patterns of connections between
neurons. The axon of one neuron may synapse with the dendrites
of another neuron. This type of synapse is called an
axo-dendritic synapse. Other types of synapses can occur,
such as axons synapsing on cell bodies, called axo-somatic
synapses; axons synapsing on axons, called axo-axonic
synapses, dendrites synapsing on dendrites, called
dendro-dendritic synapses, and so forth. Figure 1-8
illustrates the synaptic patterns just described. Because
dendrites and cell bodies usually carry only graded potentials
that may die out, it seems logical that synapses on these
structures, especially if they are far from the axon, are less
likely to lead to an action potential than a synapse near the
origin of the axon. Synapses closest to the point at which the
axon leaves the cell body, called the axon hillock (Fig.
1-6), or on the initial segment of the axon, appear most likely
to cause the firing of an action potential because the action
potential originates at this point. A similar situation exists
with inhibitory synapses. However, recent evidence suggests that
a synapse on a distal dendrite may exert a greater influence on
the excitability of the hillock region than geometry alone would
predict due to variability in the membrane resistance.
Of particular interest is the axo-axonic inhibitory synapse
on the axon terminal. It is a highly effective way of preventing
the axon's action potential from releasing neurotransmitter at
the axon terminal. If the terminal does not release its
neurotransmitter(s), no message is communicated farther along
the neuronal chain, even though an action potential did fire
initially, and propagate down the axon. This phenomenon, called
presynaptic inhibition, depends upon an axo-axonic
synapse, brought about when a neurotransmitter from the afferent
axon terminal acts upon receptors on the second (post-synaptic)
terminal, depolarizing it and preventing neurotransmitter
release even when the action potential invades that terminal.
Using a combination of excitatory and inhibitory synapses,
sophisticated neuronal chains of control can be established. For
example, Figure 1-9 illustrates a chain of three neurons. Each
of the three neurons are excitatory, as indicated by the open
cell body (closed cell bodies indicate inhibitory neurons). If A
receive a stimulus, it can excite B, which can excite C, which
will excite the target tissue, T. In Figure 1-10, an inhibitory
neuron has been introduced at B. A stimulus exciting A causes A
to excite B. B, however, inhibits C and prevents it from firing.
The target tissue therefore is not excited. Figure 1 - 11 adds a
further complication. Both A and B are inhibitory. A will
inhibit B and prevent it from inhibiting C. If C can receive an
excitatory input from another source, or if it can fire
spontaneously, the target tissue will be excited. This process
of removing an inhibition is called disinhibition (or a
release phenomenon). Disinhibition can occur when a previously
inhibitory neuron is damaged, or when another inhibitory neuron
inhibits the firing of the original inhibitory neuron. This
happens in many motor disorders, such as spasticity, athetosis,
and other involuntary movement disorders.
One more example of the possibilities of neuronal control
mechanisms illustrates the process of feedback inhibition.
Figure 1- 12 shows neuron A exciting neuron B, which in turn
excites the target tissue. However, an axon collateral from
neuron B excites an inhibitory interneuron, C, which inhibits
the firing of neuron A, causing the system to be shut off. It is
clear from the foregoing discussion that neuronal control
mechanisms can become very complicated and can involve chains of
dozens, or perhaps even hundreds of neurons. There are other
examples of neuronal control that will be discussed with the
systems in which they are active.
2. Neural Response to Injury and Manipulation
The foregoing discussion can aid in the understanding of
the manipulations that can be performed on a damaged or
defective nervous system. Generally, neurons are not capable of
replication in the adult brain, and only certain kinds of small
neurons are still able to replicate during neonatal development.
A dead neuron cannot be replaced or regenerated by cell
division, in contrast to other organs such as liver or skin that
can heal with new, functional cells. When a neuron is destroyed,
its specific functions are permanently lost. When a neuron is
damaged, it may cease to function altogether for a period of
time, it may undergo a period of suboptimal or diminished
function, it may totally recover its function and perform
normally, or it may function in a hyperexcitable and excessive
manner (producing seizure activity). If an axon is damaged in
the PNS, regeneration of the distal portion of the axon may
occur, accompanied by readjustments of metabolism by the cell
body, a process called central chromatolysis. If an axon
is damaged in the CNS, it is unlikely that appropriate
regeneration of that axon or complete restoration of that
function will occur. In the CNS, neuronal damage or cell loss
can result in an anatomical and functional reorganization of
remaining, intact neurons, but not the destroyed neurons. When a
specific input to a particular neuron, such as a motor neuron,
is lost, as occurs in spinal cord injury, remaining neurons in
the spinal cord or the dorsal root ganglion cells that are not
damaged can sprout additional axonal terminals to reinnervate
the partially denervated neuron. Neurons may be facilitated
therapeutically to assume wider functional roles, such as when
vestibular neurons are manipulated to influence motor tone in a
cortically damaged patient. Perhaps neurons also may be
manipulated therapeutically to assume new functional roles.
The limitations of therapy in neurological dysfunction must
be understood clearly. The available therapeutic approaches,
some occurring naturally and some aided by a neurologist or
therapist, include the following: (1) reinnervation and
restoration of function in the PNS due to regeneration,
generally achieved by nature, or aided by microsurgical
reanastomoses of severed nerve fascicles; (2) recovery of
function of neurons that have been temporarily but reversibly
damaged, such as may occur in a stroke; (3) manipulation or
stimulation of an intact system to overcome an imbalance
produced by damage to another system (for example, use of
vestibular manipulation to alter postural tone in a cortically
damaged patient, or administration of an anti-cholinergic drug
to counterbalance the loss of a dopaminergic system in
Parkinson's disease); (4) manipulation (stimulation or
inhibition) of a reorganized or reorganizing system following
neurological damage (for example, training or eliciting reflex
responses for bladder emptying or for sexual function following
a spinal cord injury); (5) drug manipulation of intact neurons
through alterations in neuronal metabolism, neuronal
communication, or neuronal excitability, often through use of
agents directed towards specific receptors; (6) surgical
intervention to remove a mass, to restore a balance of
functions, to alleviate pain temporarily, or to alter the
hormonal milieu of the nervous system; and; (7) transplantation
of neurons or other neurotransmitter-producing cells (e.g.
adrenal medulla) into a damaged adult brain.
Autotransplantation of adrenal medullary chromaffin cells
into the striatum of patients with Parkinson's disease already
has been attempted in humans at several medical centers. The
results have been equivocal. It is not yet known whether these
systems, if they do provide any benefit to the patient, act
through the release of a neurotransmitter, through release of a
trophic agent, or only appear to have a beneficial role because
of lesion-induced effects from the considerable trauma of
surgical transplantation, or from a placebo effect and the added
attention such a patient receives. On the other hand, the
transplantation of fetal dopamine neurons into the striatum of
drug-induced Parkinsonian African green monkeys has shown a
remarkable degree of recovery from severe movement impairment.
Thus, the use of transplanted cells into brain circuitry has
considerable promise, but the underlying mechanisms, even in
experimentally successful models, is only poorly understood. The
future role of such therapy in the treatment of human
neurological deficits still requires careful evaluation because
of scientific, ethical, and social hurdles that must be
overcome.
An additional approach to therapy involves altering
neuronal functioning by environmental and other intangible
influences not often viewed as part of current therapy for
neurological disorders. Significant improvement of a patient's
condition due to emotional and motivational factors is a real
phenomenon and may exert a powerful influence on the progress of
a neurological damaged patient. While the neuroscience’s cannot
yet explain how these mechanisms work, or how emotional and
cognitive factors interact in recovery from neurological
disease, the empirical recognition and utilization of these
phenomena is not to be overlooked. In some neurological
conditions, the concern, determination, friendship, or empathy
of the family and the medical staff may be equally as important
as the actual physical or medical benefits of therapy. It is
admittedly difficult to teach a physician or therapist how to
persist in the face of overwhelming odds; how to truly care for
the emotional well-being of a debilitated elderly patient; or
how to empathize with the hurt, the uncooperative, or the
unlovely, but those who possess such capabilities should be
given encouragement.
3. Supporting Cells
Neurons are supported by non-excitable cells, called
glia in the CNS, and Schwann cells in the PNS.
These cells help to insulate, separate, and protect neurons and
may assist the neurons metabolically. These cells respond to
injury by forming scar tissue and by phagocytosis of debris. In
the CNS the glia are of three types: astrocytes,
oligodendroglia, and microglia. In addition,
supporting ependymal cells line the ventricles of the brain and
separate the cerebrospinal fluid (CSF) from the substance of the
brain.
Astrocytes are responsible for forming scar tissue
in response to injury. Within a week of the initial injury,
astrocytes begin laying down fibrous processes that fill in
spaces left by the injury, and add strength to the areas of
necrosis and damage. Unfortunately, the astrocytic scar tissue
also can form an irritating focus that can initiate seizure
activity. Astrocytes also send endfeet (processes with
bulbous endings) to contact the basement membranes of
capillaries in the brain. Although tight junctions between
adjacent cells linking the blood vessels exclude certain
substances from the brain and form the cellular basis for a
blood-brain barrier, the astrocytic endfeet may play a secondary
role in the barrier by sequestering products, guarding the
extracellular space, or inducing enzymes in the endothelial
cells. Astrocytes also separate nerve cell bodies and processes
by physically sending astrocytic processes between them.
Astrocytic endfeet also form a layer of contact with the pia
(pial glial membrane) as a protective covering of the brain.
Recent evidence suggests that astrocytes may provide support to
neurons through regulation of the ionic milieu (sequestration of
potassium), or may produce active substances that can interact
with neurons directly (e.g. production of interleukin. In
addition, astrocytes also appear to posses the capability to act
as antigen-presenting cells, when their major histocompatibility
(MHC) antigens are up regulated in the presence of gamma
interferon from lymphocytes. These cells may play a roll in the
immunological protection of the CNS.
Oligodendroglia are responsible for myelinating the axons
of central neurons. Myelin is formed by the concentric wrapping
around an axon of an oligodendroglial process that was formed
from its cell membrane. The cytoplasm in the oligodendroglial
processes is squeezed out during the wrapping, causing the
membranes to abut each other, and forming a lamellar arrangement
of wrapping around the axon. Myelin, which forms during fetal
development through adolescence, is essential for normal nerve
function. Its main purpose is to permit an increased speed of
electrical conduction of the action potential down the axon.
Proper speed permits accurate neuronal functioning. Any
demyelinating disorder such as multiple sclerosis, or
interference with normal myelination, results in slowed
conduction velocity and incompetent functioning of the affected
axons.
Microglia are small phagocytes found in CNS in response
to an injury. They are the first glial cells to arrive at the
injury and are found in abundance at the site for at least a
week. As debris is removed, astrocytes move in and lay down
fibrous scar tissue. A major task of microglia is removal of
debris in the CNS. Some microglia in the CNS appear to be of
mesodermal origin, from the periphery, and probably are invading
macrophages. Other evidence points to an origin for some
microglial cells from neuroectoderm. Microglia also may
be able to present antigens and functionally immunologically in
the CNS.
Schwann cells are the supporting cells in the PNS.
Their major functions are to separate, insulate, and myelinate
axons. All peripheral axons have at least one layer of Schwann
cell cytoplasm, called a Schwann sheath, surrounding
them. Larger axons (greater than 2 um) will have a complete
myelin sheath formed from many concentric layers of Schwann cell
membrane. Schwann cells also can respond to injury or to a
degenerative process such as demyelination by
phagocytosis of debris. They then can divide and form new cells,
which will remyelinate the axon. A Schwann cell can myelinate
only one segment (one millimeter or so) of one peripheral axon,
in contrast to oligodendroglia, which can myelinate one segment
of many different central axons.
C. PERIPHERAL NERVOUS SYSTEM
1. Components
The extent of the peripheral nervous system (PNS) is
easiest to define by exclusion: it comprises all the neural
elements not in the brain and spinal cord. Because primary
sensory, motor, and autonomic elements all are connected with
the central nervous system (CNS), each has a peripheral as well
as a central component. The peripheral components can be
subdivided into somatic and autonomic portions in the following
manner.
a. Somatic Component
1. Sensory component, including receptors, primary
sensory axons and primary sensory cell bodies (found in the
dorsal root ganglia).
2. Motor component, including the axons of lower motor
neurons (LMNs) and the neuromuscular junction.
b. Autonomic Component
1. Sympathetic component, including preganglionic axons,
ganglion cells, and their postganglionic axons.
2. Parasympathetic component, including preganglionic axons,
ganglion cells, and their postganglionic axons.
2. Gross Anatomy of the PNS
There are two kinds of peripheral nerves, spinal nerves
and cranial nerves. There are 31 pairs of spinal
nerves. These are all mixed nerves containing more than one of
the aforementioned sensory, motor, or autonomic components to
the body. The cranial nerves supply these same functional
components to the head and neck. The only difference, other than
their area of supply, is that the individual cranial nerves are
more specialized. Some of them are almost purely sensory, some
are purely motor, and some are partially autonomic. Spinal
nerves distribute to the body in a fairly regular pattern
(called somatotopic distribution), based on their origin from
the spinal cord. The 31 spinal nerves are distributed as
follows: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1
coccygeal.
The cervical nerves leave the spinal canal through the
vertebral foramina rostral to their respective vertebrae except
for cervical nerve 8, which leaves caudal to vertebra 7 (because
there are only 7 cervical vertebrae). The rest of the spinal
nerves leave the vertebral column caudal to their vertebrae.
These nerves are numbered for their vertebral levels in the
following manner. The first cervical nerve is designated C1, the
second, C2, and so forth. The first thoracic is T1; the third
lumbar is L3. The cervical nerves supply the shoulder and the
upper limb. The thoracic nerves supply the body trunk in the
thoracic and abdominal region. The lumbar and sacral nerves
supply the lower limb and perineal region. Figure 1- 13 shows
the spinal nerves as they exit from the vertebral column.
Cranial nerves are designated by Roman numerals I through XII
as well as by their individual names. Because their areas of
distribution and their functions are not as regular as the
spinal nerves, a brief summary has been provided in the section
of this chapter on Regional Neuroanatomy (Table 1-4). These
cranial nerves have been subdivided into their sensory, motor
and autonomic components. For a more complete and detailed
review of these nerves as well as the precise distribution of
the individual spinal nerves, one of the neuroanatomy textbooks
should be consulted. Such detailed consideration is beyond the
scope of this overview. Even though cranial nerves I (olfactory)
and II (optic) have been included in the summary, they are
really peripherally located tracts of the CNS, and should be
considered part of the brain.
3. Sensory Aspects of the PNS
There are many kinds of sensory receptors, but they
all have one thing in common- they all act as transducers to
convert various types of external stimuli into electrical
impulses. We will not describe the anatomy of these receptors
because we are more concerned here with the kinds of information
they can transform. For a detailed recounting of receptor
anatomy, consult one of the major neuroanatomy textbooks. Bear
in mind that there is still no absolute correlation of
morphological receptor types and the functional transduction
they perform for specific modalities. For the body, these types
of information (modalities) can be arranged as follows:
a. Epicritic Modalities (Somatic Sensation)
- Fine, discriminative touch, vibration, two-point
discrimination, stereognosis (the ability to determine the
size, shape, and texture of an object by tough alone)
- Proprioception, information concerning the action and
position of muscles and joints
- (a) Conscious proprioception-joint position
- (b) Unconscious proprioception-muscle position and
movement
b. Protopathic Modalities (Somatic Sensation)
- Pain (both fast, localized pain and slow, excruciating,
poorly localized pain)
- Temperature
- Light moving touch
c. Special Senses
- Vision
- Olfaction
- Audition
- Vestibular proprioception, the position of the head in
space (linear and angular acceleration)
- Taste
d. Visceral Sensation
- Painful sensation from the viscera
- Non-painful sensation from the viscera
Information
transduced by the receptor is conveyed into the
CNS by a
primary sensory axon. Its most distal
part is the receptor and the initial segment immediately
adjacent to the receptor. The initial segment is the portion of
the axon in which the action potential is initiated, analogous
to the axon hillock, except that it is not next to the cell
body. The receptor functionally can be considered a
dendrite.
The rest of the
neurite can be considered the axon, which continues
into the spinal cord as part of a spinal nerve. The cell body of
the primary sensory neuron for somatic sensation is in the
dorsal root ganglion, near the spinal cord. It does not have a
direct role in carrying or initiating the action potential. The
primary sensory cell body therefore serves mainly a
trophic role to help nourish and
maintain the process. After the axon passes through the dorsal
root ganglion, it enters the spinal cord through the dorsal
root. See Figure 1- 14 for a
summary of the anatomy and connections of a primary sensory
neuron. The central processing of the information conveyed by
the primary sensory neurons will be discussed in more detail
under the sections of spinal cord and sensory systems.
4. Motor Aspects of the PNS
The only component of the motor system found in the
periphery is the axon of the lower motor neuron
(LMN). Cell bodies of
LMNs are
found in the spinal cord anterior horn (anterior horn
cells) and in motor cranial nerve nuclei in the brain
stem. The axon leaves the CNS with
a cranial nerve, or with a spinal nerve after exiting through a
ventral root. LMNs
innervate skeletal muscle. Each motor axon
innervates more than one muscle fiber and establishes a
functional motor unit (the
LMN and all muscle fibers it
supplies). When the axon carries an action potential to the
terminals, all fibers of the motor unit contract together. In
conditions in which
LMNs are damaged or
degenerating, aberrant discharges in
LMNs lead to motor unit
twitches (fasciculations),
which can be visualized directly. The junctional complex, or
synapse, between a
LMN and the muscle is called a
neuromuscular junction
(NMJ),
and the terminal of the
LMN is called a motor end
plate.
An action
potential arriving at the terminal of a
LMN
depolarizes the terminal, causing the release of the
neurotransmitter acetylcholine
(ACh). ACh
diffuses across the synaptic cleft, which in the case of the
neuromuscular junction is thrown
into numerous secondary folds, thus expanding the surface area
of muscle membrane possessing receptors with which the
ACh will
interact. ACh combines with
specific receptors on the muscle membrane, causing it to
depolarize, resulting in muscle
contraction. These ACh receptors
can be activated by nicotine, and are called nicotinic
(N)
cholinergic receptors. In the total absence of
ACh or other compounds that would
bind with the receptor, the muscle will be unresponsive and
flaccid. This is also true if the LMN
itself is destroyed so that no
neurotransmission can take place. The
cholinergic receptors on the muscle
also respond to destruction or cutting of the nerve. Normally,
receptors are concentrated densely at the
NMJ. When the nerve is lost, the nicotinic receptors
proliferate across the surface of the muscle, where they are
sensitive to ACh or
cholinomimetic compounds from any
source. Muscle twitches in this circumstance are not the result
of normal neurotransmission from an
intact nerve, but reflect the
denervation hypersensitivity of the receptors. These
twitches, called fibrillation’s, cannot be observed
visually, but can be detected by electrical recording, called
electromyography.
ACh is removed from the
synaptic cleft and is broken down by the enzyme
acetylcholinesterase
(AChE), found also on the muscle
membrane and in the motor terminals. It is extremely important
for normal nerve function that this enzyme be present and that
it break down (hydrolyze) ACh. If
it is not present and functioning properly, or if this enzyme is
inhibited by an anti-cholinesterase
agent (e.g. nerve gas), the
ACh persisting at the
NMJ will cause continued
stimulation of the nicotinic receptors and continued contraction
of the muscle that is no longer under complete
neural control. With prolonged
persistence of ACh in the cleft,
the muscle membrane is chronically
depolarized, resulting in total muscle paralysis and
death.
Certain drugs have been developed that can be used to augment
the action of ACh. For example, in
the disease myasthenia
gravis,
there are not enough receptors available to interact with the
ACh that is released from the motor
end plate because of antibodies against the nicotinic
ACh receptors. A drug that blocks
the action of AChE, called an
anti-cholinesterase (or
cholinesterase inhibitor) is given
so that the transmitter can persist in the synaptic cleft
longer, increasing the chance that it will combine with
receptors and will augment muscle contraction. It should be
clear that manipulation of the
neurotransmitter (its synthesis, release, combination
with a receptor, or its removal from the synapse and eventual
metabolism) could be extremely important in controlling muscle
activity. It also should be clear that without the presence of a
LMN, the skeletal muscle can’t be
made to function properly, or to respond to commands from the
CNS, no matter how much of a drug
or manipulative therapy is used. Fortunately, peripheral nerves
have the capacity to regenerate and repair themselves to
some extent, if the cell body has not been destroyed. In
addition, other LMNs may be able to
sprout and reinnervate
muscles previously denervated, as
happens in polio when the polio virus destroys some, but not
all, LMNs. However, when the cell bodies have been destroyed, as
in polio with total death of LMNs,
or a spinal cord crush injury at the level of total destruction,
the neurons die and are not replaced. In these cases, no amount
of treatment will help muscle tone or will restore even a small
degree of movement.
5. Autonomic Aspects of the PNS
In general, the autonomic nervous system exists as a
two-neuron chain. The first neuron has its cell body in the
CNS and is called the
preganglionic cell. Its axon, the
preganglionic axon, is
myelinated, leaves the
CNS, and synapses in an autonomic
ganglion. The ganglion contains cell bodies for the second
neuron is called the postganglionic
neuron. The postganglionic
axons are mainly
unmyelinated. The autonomic nervous
system has two divisions, the sympathetic and the
parasympathetic, which will be discussed separately.
a. Sympathetic Nervous System
The general action of the sympathetic nervous system is to
activate or arouse the organism to prepare for "fight or flight"
activity. The response of this system is widespread, preparing
the whole body for activity. It usually is activated by the
perception of stress and is not so much a reaction to a specific
stimulus as a reaction to the nervous system's interpretation of
that stimulus. It is particularly important for a therapist to
realize that a patient may respond to therapeutic manipulation
intended to assist in motor activities as if it were stressful.
The resultant activation of the sympathetics, with the
concomitant tensing of muscles, increase in heart rate and
respiration, and decrease in homeostatic mechanisms such as
digestion may be undesirable, and may interfere with therapy.
natomy of the sympathetic nervous system reflects its widespread
effects. The preganglionic cell
bodies are located in the spinal cord intermediate gray (Fig. 1-
15) of segment T1 through
L2, also called the
thoracolumbar region. These
cell bodies often are described as residing in the lateral
horn, or intermediolateral
cell column. However, recent evidence has demonstrated the
presence of additional preganglionic
sympathetic neurons in the medial regions of intermediate gray
and in the dorsal commissural gray
just above the central canal. The sympathetic
preganglionic
axons leave the spinal cord, and travel with the
LMN axons
through the ventral root to sympathetic chain ganglia
(paravertebral ganglia) that are
attached to the spinal nerve near the vertebral column. The
chain ganglion attaches to the spinal nerve by
rami
communicantes. The white ramus
communicans
(distal) contains myelinated
preganglionic
axons entering the ganglion, while the gray
ramus
communicans (proximal) contains
unmyelinated postganglionic
axons leaving the ganglion. There
is a sympathetic chain ganglion for almost every spinal nerve,
even though only the TI to
L2 segments of spinal cord have
preganglionic: sympathetic cells.
This occurs because while some of the
preganglionic axons synapse
on postganglionic cells located in
the chain ganglion of the same level, many
preganglionic fibers go right through the ganglion and
ascend or descend through connecting processes
(rami) to other ganglia. Therefore,
the chain ganglia are found from the neck (superior cervical
ganglion) all the way down to the pelvis.
The chain ganglia supply specific structures in the head
and neck and in the thoracic, abdominal, and pelvic viscera, and
also supply blood vessels (vasomotor
fibers), arrector
pili muscles
(pilomotor fibers), and sweat glands
(sudomotor fibers) in the
periphery. These postganglionic
fibers leave the chain ganglia through the gray
rami
communicantes and travel with the spinal nerves to their
target structures, often hitchhiking along a blood vessel to
reach their final destination.
Some preganglionic
axons do not synapse in chain
ganglia at all. They pass through the ganglia, forming bundles
called splanchnic nerves,
and eventually synapse in collateral sympathetic ganglia
(prevertebral ganglia) that are
near the target organs. The postganglionic
axons leave these ganglia to
synapse on the target tissue directly. See Figure 1- 15 for a
diagram of sympathetic neurons. These synaptic structures are
not like the usual motor nerve terminals. They occur along the
length of the axon, as illustrated by Figure
1-16. The individual terminals are
called varicosities, and this kind of synapse is called a
terminal en passage because the axon does not end there.
These synapses are different from central synapse; they may have
very wide "synaptic clefts" so that the
neurotransmitter must diffuse over a much wider area. The
presynaptic ending does not always
sit in close proximity to the postsynaptic
site, as does the cholinergic nerve
ending at the NMJ or central
synapses.
Because the collateral ganglia are located near the organ
innervated, the cell bodies often are intermingled with nerve
terminals in this area. This combination of
preganglionic
axons and terminals, collateral ganglion cells, and
postganglionic
axons and terminals, is called a
plexus. A plexus may contain both sympathetic and
parasympathetic components. Therefore, the conglomeration of
neural elements found on the ventral surface of the aorta and
large blood vessels, and in or near many organs innervated, are
located in autonomic plexuses. For details of the anatomy of the
many peripheral plexuses, consult one of the major
neuroanatomy or gross anatomy
textbooks.
The spreading out of the sympathetics
from the relatively restricted
preganglionic cells to the widely distributed ganglia,
and the less specific nature of the synapses, or
neuroeffector junctions,
provide the anatomical basis underlying the basic principal that
the action of the sympathetic nervous system is widespread. In
addition, the adrenal medullary
chromaffin cells, which produces the hormones
epinephrine (80 per cent) and
norepinephrine (20 per cent) for release into the
blood, can be considered a component of the
SNS. The greater
splanchnic nerves, arising from
the thoracic chain ganglia (but not
synapsing in them), contain
preganglionic sympathetic axons
that synapse on chromaffin cells of
the adrenal medulla. Stimulation of these axons results in the
release of epinephrine and norepinephrine into the blood, which
carries these compounds to effector tissues, augmenting the
action of the sympathetic nervous system. These hormones of
adrenal derivation can interact with receptors directly, and
also can be taken up by the sympathetic postganglionic
noradrenergic nerve terminals, stored, and used subsequently for
release as a neurotransmitter. This is an example of a compound
with both hormonal and neurotransmitter roles. It also should be
noted that adrenal glucocorticoids, released by the action of
ACTH (adrenal corticotrophic hormone), a stress hormone from the
anterior pituitary, can enhance production of catecholamines in
the adrenal medullary chromaffin cells, further enhancing
general sympathetic arousal.
The peripheral distribution of sympathetic nerves, once they
leave the ganglia, usually follows blood vessels. For example,
the sympathetic supply to the head comes almost entirely from
the superior cervical ganglion, the rostral-most ganglion
of the sympathetic chain. Many of the postganglionic fibers
travel along the surface of the carotid artery and it branches
to reach their eventual terminations on smooth muscles
(pupillary dilator muscle) and glands (mucosal glands) of the
head. Some sympathetic fibers travel with nerves, but only
rarely is a nerve composed mainly of postganglionic sympathetic
fibers (the splenic nerve is the best example).
In general, the sympathetic nervous system can function as a
single entity to prepare the body to cope with stress,
particularly a dangerous or frightening situation. The pupils
dilate, skin and gut blood vessels constrict, muscle blood
vessels dilate, bronchioles dilate to allow passage of more air,
heart rate increases, and more blood is pumped with each beat.
Table 1 - 1 summarizes the actions of the sympathetic nervous
system on various tissues.
The postganglionic sympathetic fibers achieve their effects
on peripheral tissue by releasing the neurotransmitter
norepinephrine (except for sweat glands, innervated by ACh
fibers). For this reason, they are called noradrenergic
or adrenergic neurons. Many available drugs affect
these neurons. The preganglionic cells use ACh as their
neurotransmitter, as do the LMNs, and are called cholinergic
neurons. The receptors on the ganglion cells are different
from those on skeletal muscle cells, although they both respond
to nicotine and are considered to be nicotinic cholinergic
receptors. They respond to the same transmitter ACh, but they
respond differently to other drugs that are applied to them.
This is important pharmacologically because it allows the
manipulation of one kind of receptor without necessarily causing
the same effect on the other receptors. For example, a drug
might be given that will partially block cholinergic: receptors
on muscle, causing relaxation of that muscle, but that drug will
not block cholinergic: preganglionic fibers from synapsing with
ganglion cells of the autonomic nervous system. More details
will be supplied concerning the pharmacological manipulation of
the autonomic nervous system following the next section on the
parasympathetic nervous system.
Parasympathetic Nervous System
The action of the parasympathetic nervous system is
mostly homeostatic, allowing the maintenance and repair of the
body. This particularly is the case with the process of
digestion, which depends extensively on the parasympathetic
system. Sympathetic arousal virtually shuts digestion down.
Parasympathetic stimulation is necessary for gut contractility,
motility, and peristalsis, and secretion of digestive enzymes
and other gut secretory products.
Anatomically, the parasympathetics are similar to the
sympathetics in having a two-neuron chain, with preganglionic
and postganglionic neuronal elements- but there the resemblance
stops. The parasympathetic preganglionic neurons have their cell
bodies in two areas of the CNS. The first area, the cranial
portion, is in the brain stem. Four cranial nerve nuclei contain
parasympathetic preganglionic cells. These are: (1) the
Edinger-Westphal nucleus, the parasympathetic portion of the
oculomotor nucleus that sends fibers with cranial nerve III; (2)
the superior salivatory nucleus that sends fibers with
cranial nerve VII; (3) the inferior salivatory nucleus
that sends fibers with cranial nerve IX; and (4) the dorsal
motor (or efferent) nucleus of the vagus, whose fibers
contribute to cranial nerve X. Figure 1-17 depicts a schematic
view of the brain stem with the approximate locations of
preganglionic cell bodies of the parasympathetic nervous system.
The second area of preganglionic cell bodies is in the sacral
spinal cord. These cells are located in the intermediate gray
of levels S2 to S4, the same zone of gray matter that
contains some preganglionic sympathetics in the thoracolumbar
regions. Because of the two locations of preganglionic cells,
this parasympathetic portion of the autonomic system is often
referred to as the craniosacral system.
The postganglionic neurons have their cell bodies in ganglia
that are usually very close to, or actually part of, the organ
innervated. In other words, preganglionic fibers of the
parasympathetic nervous system are long, traveling to the organ
innervated, while sympathetic preganglionic fibers are short,
traveling to chain or collateral ganglia. As a result, the
postganglionic parasympathetic fibers are rather short in
comparison to the postganglionic sympathetic fibers that must
travel to the organ innervated from their position closer to the
spinal cord. In the head, there are specific ganglia associated
with specifically innervated structures. Most of the remaining
postganglionic cell bodies are located in plexuses near the
aorta and its branches or in the organs themselves (called
intramural ganglia). For example, the parasympathetic supply
to the gut is located (1) in a plexus of cells between the
longitudinal and circular smooth muscle layers of the gut wall (myenteric
plexus, or Auerbach's plexus); and (2) in a
submucosal plexus (Meissner's plexus). These particular
arrangements allow coordinated constriction of the gut in order
to pass its contents along. Table 1-2 gives the location of
preganglionic's, postganglionic's, tissues innervated, and
function of parasympathetic stimulation in that tissue.
Blood vessels are not supplied with parasympathetic fibers,
but stimulation of the parasympathetic nervous system does
affect the circulatory system by inhibiting the sympathetics.
The result is dilation of gut and skin blood vessels, and
dilation of the blood vessels involved in engorgement of
erectile tissues.
Preganglionic parasympathetic cells are cholinergic (use ACh
as a neurotransmitter) just like the preganglionic sympathetics;
the postganglionic cells are also cholinergic, unlike the
noradrenergic postganglionic sympathetics. But the cholinergic
receptors on effector tissue differ in their chemical and
pharmacological characteristics, and are stimulated by muscarine
(muscarinic receptors), not nicotine.
Sympathetics and parasympathetics can exert their actions in
one of two ways - they can cause primary effects by stimulating
the target tissue or one can act to inhibit the other. This
accounts for the effects of parasympathetics on blood vessels
even though they have no parasympathetic innervation. In this
case, parasympathetics inhibit sympathetic tone or constriction
and thereby cause dilation. In fact, both of these activities
may occur at once. In the gut, sympathetics stop digestive
processes partly by direct action and partly by inhibiting
parasympathetic action. Often the sympathetics and
parasympathetics oppose each other in action, but there are
systems in which they complement each other, such as erection
and ejaculation. In addition, during some behavioral states such
as chronic stress, both systems may be active. The sympathetics
may cause the release of catecholamines and generalized arousal,
while the parasympathetics increase gastric secretion,
contributing to the production of stress ulcers.
c. Autonomic Neurotransmission
It is essential to have a general understanding of the
actions of drugs on the autonomic nervous system, because
many drugs given to patients affect autonomics either directly
or indirectly. Terminology is a problem in discussing autonomic
neurotransmission, so the following distinctions should be made
before the details are given.
1. Adrenergic (or noradrenergic) neurons are cells that use
norepinephrine as a neurotransmitter.
2. Adrenergic receptors (adrenoceptors) are receptors
that recognize and respond to norepinephrine, epinephrine, and
dopamine, such as the sympathetically innervated effector
tissues.
3. Cholinergic neurons are cells that use ACh as a
neurotransmitter.
4. Cholinergic receptors are receptors that recognize and
respond to ACh, such as those on ganglion cells, on
parasympathetically innervated effector tissue, or on skeletal
muscles.
Even though all preganglionic autonomic axons, postganglionic
parasympathetic axons, and LMN axons use ACh as a
neurotransmitter to stimulate postsynaptic receptors, that
receptor react differently to other drugs. It is known that
nicotine will stimulate the cholinergic receptors normally
stimulated by ACh from preganglionic autonomics and from LMNs,
but not those normally stimulated by ACh from postganglionic
parasympathetics. These postganglionic parasympathetic receptors
are instead stimulated by muscarine and are called muscarinic
receptors. Receptors sensitive to nicotine are called nicotinic
receptors. This choice of designation is perhaps unfortunate
because all nicotinic receptors are not equal. While they
all respond to nicotine, they respond differently to still other
drugs. For example, ganglionic blockers block the nicotinic
receptors on ganglion cells normally stimulated by ACh, but not
the receptors at the NMJ, which are also nicotinic.
Adrenergic receptors are also of at least two different
kinds. These are designated alpha and beta-adrenergic
receptors. These types of receptors not only respond to
different drugs, but cause different effects on the postsynaptic
site. In general, alpha-receptors are excitatory except in the
gut, where they are inhibitory; beta-receptors are inhibitory
except in the heart, where they are excitatory. Beta-receptors
can be further subdivided into beta1 receptors
(Cardiac muscle, fat cells) and beta2 receptors
(bronchi, blood vessels, lymphocytes). Alpha-receptors also have
been subdivided into at least two classes, alpha1
(mainly postsynaptic) and alpha.2 (mainly
presynaptic). These subdivisions are not rigid but may vary from
one system to another.
The actions of many drugs take place on the receptors. Drugs
that block receptors are usually named for the kind of receptor
they block (cholinergic blockers, ganglionic blockers,
adrenergic blockers, beta-blockers, alpha-blockers). They are
also called antagonists. Two very common antagonists for
the cholinergic system are (1) the muscarinic blockers,
atropine and scopalarnine; and (2) the nicotinic
blocker, curare. Common antagonists for the adrenergic
receptors are (1) alpha-blockers, phentolamine and
phenoxybenzamine, and (2) the beta-blocker, propranolol.
Drugs that mimic the effects of neurotransmitters are called
mimetics (sympathomimetics, parasympathomimetics, and
cholinomimetics). They also are called agonists.
6. Response of Peripheral Nerves to Injury
Peripheral neurons can be damaged in a number of ways-
trauma, disease, toxic chemicals, and nutritional deficiencies-
resulting in a peripheral neuropathy. If the cell body is
killed, no regeneration of the neuron can occur. After birth,
peripheral neurons do not divide, and new neurons are not
usually formed. However, if the injury occurs to the axon, if
the damage is not too severe, and if the distal and proximal
ends of the neuron are still close together, reinnervation can
occur. The distal portion of the axon dies and is phagocytosed
by Schwann cells (Wallerian degeneration). Sprouts
extend from the proximal end of the damaged axons, grow into the
intact "tube" left by the distal basement membrane, and travel
to the target effector tissue, where reinnervation occurs. When
the whole neuron is killed, it is possible that nearby neurons
can sprout axonal processes and reinnervate the tissue.
Sympathetic postganglionic axons (noradrenergic) are
particularly able to sprout and reinnervate a denervated tissue.
Another kind of injury can occur to peripheral nerves. The
neuron is dependent on the integrity of its myelin sheath for
proper function. Demyelinating diseases can damage axons
secondarily. If the Schwann cells cannot recover and cannot
remyelinate the neuron, the neuron will first lose conduction
velocity and eventually the unmyelinated segment can die. This
problem can alter the function of sensory, motor, and autonomic
nerves. However, since only the preganglionic autonomic axons
are myelinated within the ANS, this problem is mainly restricted
to those components.
D. SPINAL CORD
1. Gross Anatomy
The spinal cord lies in the vertebral canal, is surrounded by
meninges, and is bathed in cerebrospinal fluid (CSF), as is the
rest of the central nervous system (CNS). The spinal cord is
divided into segments based on the spinal nerves
associated with each segment. There are 31 segments grouped into
four major regions. From rostral to caudal these divisions are:
(1) cervical spinal cord, with 8 segments; (2) thoracic spinal
cord, with 12 segments; (3) lumbar spinal cord, with 5 segments;
and (4) sacral spinal cord, with 5 segments, and a single
coccygeal segment usually grouped with the sacral spinal cord.
During development, the vertebral column grows more rapidly
than the spinal cord it encloses. Therefore, in the adult,
vertebral levels do not correspond with spinal segments, even
though they are often designated in the same way. For example,
the designation C7 may refer to a vertebral level, to a spinal
nerve, or to a segment of spinal cord. In this chapter we will
use such a designation for the spinal segment only and will
refer to the others more specifically as C7 vertebral level, or
C7 spinal nerve. For example, an injury to an adult patient at
the T8 vertebral level will injure the spinal cord at
approximately the T10 segment. The spinal nerves are derived
from cord segments of the same number. For instance, the T8
spinal nerve is derived from spinal cord segment T8 and must
travel caudally within the vertebral canal to the T8 vertebral
level (opposite T10 spinal cord segment) before it leaves the
canal. In general, the cervical segments are one segment
different from the cervical vertebral levels. (The C5 vertebral
level is approximately at the C6 spinal cord level.) The
thoracic segments are approximately two segments different (the
T6 vertebral level is approximately at the T8 spinal cord
level). The T11 and T12 vertebral bodies correspond to the five
lumbar spinal cord segments. The adult spinal cord ends at
approximately the lower Ll vertebral level (see Fig. 1- 13). The
tapering end of the spinal cord in this area, composed of sacral
spinal segments, is called the conus medullaris.
Caudal to the conus medullaris, the vertebral canal is filled
with spinal nerves traveling to their appropriate vertebral
levels of exit. This bundle of spinal roots in the vertebral
canal is called the cauda equina (or horse's tail). A
spinal tap done to remove a sample of CSF is done in this distal
lumbar vertebral region because entry of the needle will be
below the caudal end of the spinal cord and is unlikely to
damage the spinal roots. The spinal nerves consist of components
carrying both input and output. The input (sensory component)
enters the spinal cord mainly through the dorsal roots.
The output (motor and autonomic components) exits the spinal
cord through the ventral roots. The dorsal and ventral
roots unite for each segment to form the spinal root for
that segment. In actuality, the dorsal and ventral root for each
segment is made up of six or more rootlets.
The spinal cord consists of two types of tissue, gray
matter and white matter, as does the rest of the CNS.
The gray matter consists of cell bodies arranged into clusters
called nuclei (not to be confused with the nucleus of an
individual cell). The white matter consists of axonal processes,
appearing white because of the presence of myelin surrounding
the larger fibers. Clusters of fibers are arranged into
tracts. These tracts are variously called pathways, columns,
channels, funiculi, fasciculi, lemnisci, and so on, but they are
all axonal processes communicating with other cells at a
distance.
In the spinal cord the gray matter is arranged in a
butterfly, or "H," pattern in the center of the cord and can be
subdivided further into a dorsal horn, a region of
intermediate gray, and a ventral horn. In the spinal
cord, dorsal is used synonymously with posterior and ventral
with anterior. In thoracic and upper lumbar segments, a lateral
horn is present at the lateral edge of the intermediate gray.
The white matter is arranged into dorsal, lateral, and ventral
funiculi, anatomical zones of tracts subdivided by the dorsal
and ventral horns. The gray matter can be subdivided further
into 10 lamina, or layers, called lamina of Rexed (Fig.
1-18). In the dorsal horn, lamina I (marginal layer) is
associated with spinothalamic projections, laminae II and III
(substantia gelatinosa) are associated with slow pain
processing, and laminae IV and V (nucleus proprius) are
associated with the processing of both slow and fast pain. The
dorsal horn is separated from the dorsolateral sulcus by the
entrance zone of the dorsal root fibers, called Lissauer's
zone. In the intermediate gray, laminae VI, VII, and VIII
contain interneurons. In the ventral horn interneurons of
laminae VII and VIII are present along with clusters of LMNs,
which collectively are called lamina IX. Lamina X is the
commissural gray found around the central canal, and in its
dorsal portion contains some preganglionic autonomic cell
bodies.
The spinal cord contains major processing zones for sensory,
motor, and autonomic portions of the CNS. Somatic input and some
visceral input enter the spinal cord through the dorsal roots,
and motor and autonomic output leaves the spinal cord through
the ventral roots. In addition, local neuronal processing in the
dorsal, intermediate and ventral gray matter regulates reflex
activity in the spinal cord. Converging supraspinal influences
from the brain regulate the final outflow from motor and
preganglionic autonomic neurons. The spinal cord also serves as
a diverging channel for ascending sensory information, destined
for both unconscious proprioceptive responses and conscious
interpretation. These secondary sensory channels and components
are understood most easily by subdividing them into their
individual components, which include reflex channels,
cerebellar channels, and lemniscal channels. Refer to
Table 1-3 for a summary of these components.
The tracts listed in Table 1-3, forming the spinal cord white
matter, will be discussed under the heading Systemic
Neuroanatomy. Specific areas of cells in the gray matter will
also be discussed as necessary with their functional
descriptions.
2. Spinal Reflexes
a. Introduction
A spinal reflex is an appropriate motor response to a
sensory stimulus, not requiring supraspinal input or higher
processing. Such a reflex will occur even if supraspinal
connections are removed or destroyed because of injury or
disease. As long as sensory input and lower motor neuron (LMN)
output are intact, a spinal reflex can occur. In fact, a spinal
reflex may be hyperresponsive in a cord-injured patient (for
example, mass reflexes or spastic muscle stretch reflexes). If
LMNs are destroyed, as in polio, these reflexes cannot occur
because no motor response is possible. Destruction of the
sensory input is more difficult because it is often much more
diffuse, but if all sensory input is destroyed, the reflex
cannot occur. This can occasionally be seen in severe peripheral
neuropathies.
The simplest example of a spinal reflex is the
monosynaptic reflex. In this reflex, a sensory neuron
synapses directly on a LMN. This reflex can be considered a
holdover from the primitive two-neuron nervous system. It is
fast and effective but not very flexible. In higher animals,
upper motor neuronal control, especially through cortical
regulation, can over-ride some reflexes or use this circuitry
for performing complex movements. However, the supraspinal
control present in intact animals makes the study of such
reflexes difficult. In order to study spinal reflexes in
isolation from upper motor neuronal or supraspinal control,
experiments are sometimes done on animals with lesions that cut
off supraspinal input (such as spinal or decerebrate
preparations). These experiments show what happens locally,
either in individual segments or in the whole spinal cord, but
do not show how these reflexes are integrated into more complex
motor behavior. The following discussion will include only
spinal responses, but it should be remembered that upper motor
neurons (UMNs) are extremely important for keeping LMNs and
reflex pathways in a state of readiness for voluntary movements,
as well as for initiating those movements.
There are basically two kinds of spinal reflexes,
cutaneous (or exteroceptive) reflexes and muscle
reflexes. The cutaneous reflexes are polysynaptic,
while muscle reflexes may be polysynaptic (Golgi tendon organ
[GTO] reflexes, reciprocal inhibition reflexes, distant
responses to muscle stretch reflexes) or monosynaptic (the
muscle stretch reflex). The cutaneous reflexes are a motor
response to cutaneous stimulation. They also are called
withdrawal reflexes or flexor reflexes. The term
flexor reflex is actually a misnomer because the motor response
does not have to be flexion. The only requirement is that the
motor response must be appropriate to the cutaneous stimulus.
Most withdrawals are flexion movements, but an extensor muscle
may also carry out appropriate movements. The second kind of
spinal reflexes, the muscle reflexes, adjust the tone and
reactivity of muscles.
b. Cutaneous Reflexes
Cutaneous reflexes permit withdrawal from noxious or
nociceptive stimuli. The sensory input originates from receptors
in the skin and deeper tissue. Because these receptors are on
the exterior of the body rather than in the viscera, they
sometimes are referred to as exteroceptors and the resultant
cutaneous reflexes as exteroceptive reflexes. Exteroceptors are
responsive to heat, cold, touch, and pain. There are several
different morphological types of receptors, and it has been
suggested that each type may report a different kind of
stimulus. Unfortunately, the question of which receptor reports
which stimulus (or even whether a single receptor reports a
single modality) has not been answered fully and will not be
discussed further. Consult a major textbook for the many
receptor types described by anatomists, and bear in mind that
few absolute statements regarding modalities conveyed by these
receptors can be made at present.
Painful or noxious stimulation of appropriate receptors
causes the withdrawal (usually by flexion) of the entire limb,
and sometimes of the entire body. Figure 1-19 shows a schematic
of the simplest kind of polysynaptic reflex, with a receptor R,
a primary sensory neuron S, synapsing on an interneuron I 1,
which in turn synapses on LMN A. LMN A innervates a flexor
muscle, F1. Stimulation of the receptor causes an
action potential to fire in the primary sensory neuron. The
primary sensory neuron synapses on the interneuron I1,
exciting this neuron. The interneuron synapses on the LMN,
causing it to fire an action potential in turn. The LMN action
potential depolarizes its terminal at the motor end plate and
releases acetylcholine as its neurotransmitter, which crosses
the neuromuscular junction and causes the muscle to contract,
completing a cutaneous reflex.
The actual mechanism of the reflex is usually more
complex than the simple reflex just described. When a
finger is burned (a noxious cutaneous stimulus), the whole arm
withdraws, not just the finger, or local flexor. Many muscles
contract in a coordinated fashion to cause the withdrawal. This
is done through interneurons that control the degree to which
other LMNs will fire, and therefore the degree to which other
muscles will contract. Generally speaking, the stronger, the
stimulus, the more interneurons will be recruited, and the more
muscles will be involved in the reflex. Figure 1-20 illustrates
this principle schematically. This schematic is similar to
Figure 1-19, but to it has added an additional excitatory
interneuron, I2 (remember that excitatory neurons are
represented by white or undarkened cell bodies and inhibitory
neurons have black or darkened cell bodies). A second LMN, B;
and a second flexor muscle, F2, that represents a
synergistic muscle; one that works with the first muscle. In
this case, excitation of the receptor and the primary sensory
neuron causes interneuron I1 and subsequently LMN A
to fire and muscle F1 to contract; but it also causes
the interneuron I2 to fire, exciting LMN B, resulting
in the contraction of muscle F2. Adding more
interneurons increases the possibility of greater responses and
provides an appropriate response for a given stimulus. The whole
body does not have to withdraw; only the part actually in danger
will withdraw, but the withdrawal has to be both effective and
quick, and sometimes will involve a total body response.
Withdrawal reflexes affect more than just the muscles on the
side of the body that receives the stimulus. Muscles on the
opposite side of the body may respond as well, because of
activation through interneurons. This is particularly true of
withdrawal of the foot and leg, perhaps from stepping on a tack.
The foot that steps on the tack withdraws by flexion of that
leg, but in order to maintain balance, the other leg must extend
to provide a strong pillar to keep the body from falling over.
This kind of reflex is called a flexion-crossed extension
reflex.
The processing that goes on in the spinal cord is diagrammed
schematically in Figure 1-21. On the right side, Figure 1-21 is
the same as Figure 1-20. The left side represents the left side
of the spinal cord. Stimulation to receptor R will ultimately
cause flexion of muscles F1 an F2 just as
in Figure 1-20, but the primary sensory neuron also stimulates
excitatory interneurons 13 and 14 on the
left side of the spinal cord. These interneurons excite LMNs C
and D, which in turn cause the contraction of extensor muscle E1
and its synergistic muscle represented by E2. Any
further processing diagrammed schematically in this manner will
become too complex to follow, so the following simplification
will be made. Figure 1-22 represents the same system as Figure
1-21. It is understood that the primary sensory neuron excites
interneurons that in turn excite LMNs. The LMNs will be
designated FLX for those exciting flexor muscles and EXT for
those exciting extensor muscles. For simplicity, the muscles
have been left out of the diagram.
Not only are flexors on the side of the stimulus and
extensors on the side opposite the stimulus excited. In order
for them to have optimal effect, the extensors on the side of
the stimulus and the flexors on the opposite side from the
stimulus are inhibited so that they will not be working against
the withdrawal reflex. This process is diagrammed in Figure
1-23. The inhibition of antagonist muscle groups is mediated
through inhibitory interneurons (dark circle), and the process
is called reciprocal inhibition. If a stimulus is
presented on the right, as it is in the diagram, the LMNs for
flexor muscles on the right will be excited, while those for
extensors on the right will be inhibited. LMNs for extensors on
the left will be excited, while those for flexors on the left
will be inhibited.
Maintaining balance while withdrawing a whole leg may require
more than simply extending the other leg. Movement of the arms
may be needed as well, to offset the loss of balance. Therefore,
these reflexes can involve all four limbs and the trunk at once.
These reflexes are often referred to as long spinal reflexes,
but the movement of each limb is appropriate to withdrawal
from the noxious stimulus and maintenance of balance during the
movement, and will involve both flexion and extension.
The preceding discussion has considered what happens when one
noxious stimulus is presented alone. It is important to note
that when more than one such stimulus is presented, one stimulus
may have priority over the others, preventing appropriate
responses to the latter. Pain usually has precedence over other
reflexes. For example, if a scratch reflex is being elicited
from a dog, pinching the dog’s foot can stop it. The foot will
then be withdrawn. When the painful stimulus is stopped, the
scratch will resume.
c. Muscle Reflexes
Muscles have two specialized kinds of receptors: muscle
spindles and Golgi tendon organs (GTOs). These receptors are
responsible for reporting information about muscles to the
spinal cord for spinal reflexes and to special nuclei in the
spinal cord and medulla that relay the information to the
cerebellum (see the discussion of cerebellar channels). Muscle
spindles report static information concerning the length or
amount of stretch of individual muscle fibers, and dynamic
(phasic) information concerning the speed with which an active
muscle fiber is being stretched. The GTO reports the amount of
tension on a tendon from the passive stretch or contraction of
the muscle. This information is called proprioceptive
information and is necessary for two kinds of processing:
(1) in the spinal cord, it provides input to LMNs and
interneurons for local reflexes such as the muscle stretch
reflex; and (2) in the cerebellum, via synapses in the spinal
cord or medulla, it reports the state of the muscles so that the
cerebellum can coordinate the superimposition of voluntary
movements directed by the cortex, or adjustments in tone and
posture directed by brain stem UMNs.
d. Muscle Spindles
The muscle spindle is a sophisticated sensory receptor
that reports sensory information from muscles to the CNS and has
its own motor innervation through by which it can be adjusted by
the CNS. This mechanism assists the CNS by providing continuous
sensory feedback from the muscles.
(1) Anatomy of the Muscle Spindle. The muscle spindle is
made up of special types of muscle fibers called intrafusal
fibers, attached in parallel with the skeletal muscle
(extrafusal) fibers. It is attached at both ends to inelastic
collagen tissue associated with a skeletal muscle fiber. The
extrafusal fibers are responsible for generating the contractile
power of the muscle (Fig.1-24A). The muscle spindle is
surrounded by a capsule, which is attached at each end to the
connective tissue of the skeletal muscle fiber about which it is
reporting information. The spindle contains two types of
intrafusal fibers attached to the capsule on the inside,
chain fibers and bag fibers (Fig. 1-24B). These
fibers have an equatorial or middle region that contains
cell nuclei and a polar or end region that can contract
in response to motor input to increase tension on the equatorial
regions. The bag fiber has its nuclei arranged bag-like, in a
central cluster, and the chain fiber has its nuclei arranged
chainlike, in a row. Each muscle spindle usually has four to six
chain fibers and one to two bag fibers. Fibers that are
intermediate between the bag and chain fibers have been
described, but their function is not well understood at present.
(2) Innervation. The muscle spindle has both sensory and
motor innervation (Fig. 1-25). The sensory innervation consists
of group Ia fibers and group II fibers, which are sensitive to
the tension of the equatorial regions of the bag and chain
fibers. Group la endings wrap mainly around the
equatorial zone of the bag fibers. These Ia fibers are also
called primary endings, or annulospiral endings.
Group II endings innervate mainly the chain fibers. They
are also called secondary endings, or flower spray
endings. A stretch or tension on the equatorial
region of the group Ia and II fibers will cause them to fire
action potentials. The sensory input goes into the spinal cord,
as discussed earlier, and synapses on LMNs or their
interneurons, and on relay nuclei sending information to the
cerebellum.
The motor innervation is derived from two types of gamma
motor neurons (fusimotor neurons), gamma1 and
gamma2, to be distinguished from alpha motor
neurons (skeletomotor neurons). Gamma1 endings,
also called plate endings, innervate mainly the polar
ends of the bag fibers, and gamma2 endings,
also called trail endings, end mainly on the chain fiber,
near the polar region. Firing of these fusimotor neuron's
results in contraction of the polar region of the muscle
spindle, stretching or putting tensions on the equatorial
region. Stretching of the equatorial region causes the sensory
la and II fibers to fire. The resultant stimulation of
skeletomotor neurons in the anterior (ventral) horn of the
spinal cord causes the skeletal muscle fibers to contract.
Experimental stimulation of the fusimotor neurons causes spindle
fibers to contract, but adds negligible strength or power to the
contraction of the skeletal muscle without the stimulation of
skeletomotor neurons. A tightening of the muscle spindle causes
the Ia and II fibers to report specific kinds of sensory
information to the CNS.
(3) Function. Changes in skeletal muscle activity cause
changes in the muscle spindle. Passive stretch of the muscle by
tapping on a tendon, or experimental stretch of a muscle by
hanging a weight on it, will cause the muscle spindle to
stretch. As the spindle stretches, tension is put on the
equatorial regions, causing firing of la and II fibers.
Increased activity in the Ia fiber’s results in contraction of
the extrafusal muscle fibers, increasing the tension produced by
the skeletal muscle fibers. This shortening of the extrafusal
muscle fibers causes the spindle to slacken. Spindle slackening
decreases tension on the equatorial region and decreases the
firing of Ia and II fibers. In summary, the spindle reflex
responds to a stretch on the muscle by contracting the
extrafusal fibers, restoring the muscle to its original state
before the stretch. The spindle reflex therefore is a mechanism
for maintaining a muscle at a fixed state of contraction.
Relaxation of a muscle that has been contracted produces a
response of the spindle similar to stretching the muscle; the
sensory fibers increase their firing.
Gamma motor neurons act to modulate the length, and
consequently the tension, in the muscle spindle so that the
information reported to the CNS can be controlled. Contraction
of a muscle causes slackening of the spindle so that little or
no information goes into the CNS. Under these conditions, the
spindle would fail to report sensory information whenever the
muscle contracts. However, a resetting of spindle sensitivity is
achieved by the gamma motor neurons. These neurons, when
stimulated, contract the bag and chain fibers of the muscle
spindle by the gamma1 and gamma2 motor
fibers and cause the resumption of sensory information reporting
to the CNS. Figure 1-26 shows what happens to the firing of
group Ia and group II fibers during various activities. Type II
fiber's report only static information; that is, they report the
tension of the spindle, corresponding to the length of
the extrafusal muscle fiber. Group la fibers also report static
information to the CNS, but are even more important in reporting
dynamic information as well. In this capacity, they report the
speed with which the extrafusal muscle fibers are changing their
length (velocity).
In Figure 1-26A, the skeletal muscle is stretched passively
to a new length, which also stretches the muscle spindle. The
group II fibers respond to the new tension by increasing
their base rate of firing. The group Ia fibers also
respond with a new rate of firing, but during the time the
muscle fiber is changing its length there is a rapid burst of
activity that can be equated with velocity (or change in length
with respect to time) of muscle stretch. When stretching stops
and a new tension is reached, the group la fiber reports that
new static tension with a new firing rate. In Figure 1-26B, the
skeletal muscle is contracted, causing the muscle spindle to
slacken. Group II fiber’s decrease their firing to report the
new length. Group Ia fibers are silent during the period of
collapse, then resumes firing at a reduced rate corresponding to
the new extrafusal fiber length. It should be noted that when
contraction is initiated voluntarily or is adjusted by
supraspinal signals, those controlling signal’s are sent to both
the alpha and gamma motor neuron’s, thereby adjusting both the
extrafusal and intrafusal muscle fibers to maintain the muscle
spindle afferents in responsive range for the new extrafusal
length. In Figure 1-26C, the muscle tendon is tapped in order to
elicit a muscle stretch reflex. Group II fibers do not change
their firing rate because the tap is too fast for them to
respond. Group Ia fibers report a burst of firing during the
stretch part of the tap. It is this |
