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Glossary Figures
Chapter 6
The nervous system is made up of three types of organs: the brain,
the spinal cord, and nerves (Fig.
6.1). The brain and the spinal cord are referred to as the central
nervous system (CNS) because they are along the midline
of the body. The nerves constitute the peripheral nervous system
(PNS), extending from the brain and spinal cord to the farthest
reaches of the body. The functions of the brain, spinal cord, and nerves are
performed by the highly specialized nerve cells (i.e., neurons)
they contain.
Main Functions for Homeostasis
The overall goal of the nervous system is to regulate the
operations of parts of the body to make sure they contribute to homeostasis and
a satisfactory quality of life. The nervous system regulates muscles and glands
directly by sending impulses to those structures. Among the glands controlled
by the nervous system are the sweat glands and salivary glands. This system
regulates other parts of the body indirectly by adjusting the amounts of
hormones produced by some of the endocrine glands.
The nervous system performs six main functions to carry out
its overall goal. Three operations stem from the three
steps in negative feedback systems: monitoring, communicating, and adjusting.
Many of the neurons in the brain and nerves monitor conditions in and around
the body. These neurons do very little if conditions are proper and fairly
stable. However, they are affected by harmful conditions and are sensitive to
any change in conditions. When conditions are unfavorable for the cells or when
there is a change (a stimulus), the neurons respond by starting
messages (nerve impulses) within themselves.
The initiation of impulses by neurons leads to the second
main function: communicating. The neurons carry impulses to other parts of the
nervous system, where they are passed to other neurons, which pass them to
still other neurons, and so on. Thus, many parts of the nervous system are
informed that a change has occurred. They are also informed of the nature of
the change, its extent, and where it is happening. For example, if an insect
bites a person, that person feels that something is happening. He or she also
knows that it is a bite rather than something soft brushing against the skin,
has a sense of the severity of the bite, and knows where to scratch or hit to
remove the insect.
Communicating leads to the third function: stimulating. In
the case of an insect bite, the nervous system activates muscles in the arms to
remove the source of irritation. Note that the nervous system does not actually
perform the adjustment, which is the third step in negative feedback. It only
stimulates other parts of the body to do so.
These three functions can activate responses to promote
beneficial changes as well as eliminate harmful ones. For example, when neurons
in the stomach sense that it is empty and brain neurons detect that the
nutrient level in the blood is low, a person feels hungry. If other neurons
detect the sound of someone cooking in the kitchen while other neurons detect
dinner aromas, the nervous system will activate muscles so that the hungry
person will go to the kitchen and obtain nourishment. When the stomach has
become full and blood nutrient levels begin to rise, other neurons initiate a
negative response, causing the person to stop eating.
Making adjustments often requires the contributions of many
parts of the body, and the nervous system must stimulate them so that they all
work in harmony. At the same time, parts of the body that can interfere with
achieving the desired outcome must be inhibited from acting. The nervous system
provides these stimulations and inhibitions through its fourth main function:
coordinating. For example, to walk to the kitchen, a person must activate some
muscles while inhibiting others in order to step forward with one foot at a
time.
When a person must adjust to a new situation, it may take
quite a while for all the necessary impulses to reach their destinations,
especially when the situation is complicated and the proper response requires
the coordinated stimulation of many structures. Furthermore, sometimes mistakes
are made and the wrong response occurs. This is when remembering, the fifth
main function of the nervous system, becomes helpful.
By remembering, the nervous system stores information about
past experiences that includes the recollection of a situation, the responses
that were made, and the degree of success that was provided by each response.
Then, when faced with the same situation, a person can avoid trial and error by
remembering what to do. This procedure saves time and prevents costly mistakes.
Simple examples include remembering the way home after traveling the route a
few times and remembering the answers to test questions using information that
was studied many times.
The benefits of remembering are used on an unconscious level
as well. For example, when one is practicing an activity
such as walking, playing an instrument, or riding a bicycle, the nervous system
remembers the sequences of muscle contractions that resulted in failure or
success. With enough practice, one need only consciously start the activity.
One can then continue to perform well without thinking about the activity
because, like a recording, the nervous system plays the rest of the program of
successful commands for the muscles.
Memory also recalls situations that led to favorable or
unfavorable outcomes. When the nervous system recognizes the presence of such
situations, it will alert a person to proceed or take evasive action. This is
why an experienced child will reach out for candy but back away from fire.
Remembering tends to provide the same type of successful
response every time a person is in the same circumstance. The more successful
the same response is in the same situation, the faster and more accurately that
response will occur. However, remembering does little when a person is faced
with a new situation. That person must try to find the correct response by
trial and error or by mentally imagining different responses and the results
they might cause. Creating mental images of new courses of action and their
possible outcomes is the sixth main function of the nervous system: thinking.
Thinking depends on memory to provide initial mental images
and information. In thinking, a person intelligently rearranges the remembered
images and information to create new images that have not been experienced
before. Many alternatives can be mentally explored in a few seconds without
actually trying any of them. People are thinking when they make plans, solve
problems by analysis, and create mental images of things that do not occur
naturally. Thinking provides the variety of acting that many people believe
separates humans from other living things.
Thinking allows people to decide the best response to a new
situation quickly, accurately, and without having to risk the consequences of
untested attempts. It can even produce new responses to situations that have
been created by people. For example, this is how people return to the Earth
from a trip to the moon.
All the billions of neurons in the nervous system have three
basic parts. The nerve cell body contains the nucleus of the cell
along with cytoplasm and organelles (e.g., mitochondria and ribosomes) (Fig.
6.2a). The nerve cell body supplies the other two parts of the neuron with
the materials and energy they need. It can also pick up messages from other
neurons.
There are three types of nerve cells based on the number of
extensions from the nerve cell body (Fig.
6.2b). A unipolar neuron has one extension, which branches very close
to the nerve cell body into a dendrite and an axon. A bipolar neuron has two
extensions, a dendrite and an axon. A multipolar
neuron has more than two extensions from the cell body; two or more dendrites
and one axon.
Each dendrite can branch up to several hundred times. Like nerve cell bodies,
dendrites can pick up messages from other nerve cells. They are also the parts
of the sensory cells that monitor conditions. A dendrite being activated by
another neuron or by a stimulus starts nerve impulses that travel along the
dendrite to the nerve cell body, which passes the impulses to the third part of
the neuron: the axon.
Each neuron has only one axon, which extends out from the
nerve cell body. Each axon may have up to several hundred branches (axon
collaterals). The impulses that are passed to the axon travel the
entire length of each of its branches. Each branch then passes the impulses to
another structure. Axons can pass impulses to other neurons, muscle cells, and
gland cells, although all the branches from one neuron's axon can go to only
one of these types of cells.
Reception All neurons perform three main functions. Reception
involves having impulses generated in response to environmental conditions or
messages from other neurons. Dendrites and nerve cell bodies are the parts that
usually perform reception (Fig.
6.3a).
Conduction The second function - conduction
- refers to the movement of impulses along the neuron to the end of the axon (Fig.
6.3a). Conduction in longer dendrites and axons occurs through a special
mechanism called an action potential. This mechanism involves
several activities of the neuron cell membrane that carefully control the
inward and outward movement of ions, especially sodium and potassium ions.
Transmission Once impulses have been conducted to the end
of the axon, they are passed to the next structure by the third neuron
function: transmission (Fig.
6.3a). The place where transmission occurs between neurons is called a synapse.
Transmission to muscle cells occurs at neuromuscular junctions,
and transmission to gland cells takes place at neuroglandular junctions.
The process of transmission is essentially the same in all three cases.
At a synapse, when an action potential reaches the end of an
axon, it causes small packets (synaptic vesicles) at the end of
the axon terminal to burst like blisters (Fig.
6.3b). These packets contain a chemical called a neurotransmitter,
which is then released into the small space (synaptic cleft)
between the neurons. Most neurons can release only one type of neurotransmitter.
The neurotransmitter diffuses to the dendrite or cell body of the next neuron,
where it attaches to receptor molecules on the cell membrane.
Each type of receptor molecule is designed to bind to only one type of
neurotransmitter.
Once enough neurotransmitter has been bound to the receptor
molecules, the receiving neuron responds. Depending on the type of
neurotransmitter and the type of neuron, the receiving neuron will be
stimulated to perform reception and start its own impulses or will be inhibited
from acting. The nervous system uses stimulatory transmissions to start or
speed up an activity; it uses inhibitory transmissions to slow down, stop, or
avoid an activity. A neurotransmitter continues to have its effect on the next
cell until it is eliminated or counteracted. Neurotransmitters can be
counteracted when antagonistic neurotransmitters are sent into the synapse.
Although a few synapses involve one neuron transmitting to
one other neuron, synapses often have many neurons converging to transmit
messages to a single neuron. The amount and length of the response by the
receiving neuron depend on the balance between the amount of stimulatory and
inhibitory neurotransmitters it receives at any moment from the many neurons
connected to it. Thus, by changing the combinations of neurotransmitters at
synapses, the nervous system can provide exquisitely precise adjustments to its
impulses and the resulting body activities. The effect of such an interplay of
stimulatory and inhibitory transmitters is experienced, for example, by a
person whose hands are being burned by a hot beverage but who puts down the cup
slowly and carefully to avoid spilling the beverage.
The branching of axons allows for divergence. Thus, impulses
in one neuron can spread to many muscle cells, gland cells, or neurons. One can
experience the effects of divergence when hearing a frightening sound or
noticing a flirtatious glance. The heart pounds, the breathing increases, the
stomach tightens, and the legs may become weak and shaky.
Another important function of synapses is to keep order in
the nervous system. Since messages can pass only from axons to the next neuron,
synapses ensure that impulses move through the system only in the correct
direction. Finally, synapses play an essential role in remembering.
The CNS contains neuroglia cells, which
provide a variety of services for the neurons (e.g., support and defense).
These cells do not perform reception or conduct or transmit nerve impulses. One
type makes a material called myelin, which forms a coating on CNS
axons. The myelin coating on an axon resembles beads on a string. It causes
impulses to travel faster by making them jump along the neuron (Fig.
6.2a). Since myelin is white, it causes the regions that contain it to
become white in appearance; these areas are referred to as the white
matter of the brain and spinal cord.
The areas of the CNS that do not have myelin possess the
pinkish gray color of plain neurons; these regions constitute the gray
matter. The gray matter is important because it contains the synapses.
All the complicated nervous system functions, including coordination,
remembering, and thinking, require these synapses.
Neurons in the PNS are assisted by Schwann cells.
These cells produce myelin on dendrites and axons; this myelin is structurally
and functionally similar to CNS myelin (Fig.
6.2a).
Recall that there are two main subdivisions of the nervous
system - the central nervous system and the peripheral
nervous system
- and that the two parts of the CNS are the brain and the
spinal cord (Fig.
6.1). The neurons in different regions of these two organs are specialized
to contribute to one or more of the main functions of the nervous system. For
example, certain areas of gray matter in the brain monitor conditions such as
temperature and the level of CO2, others start impulses that
stimulate muscles to contract, and still other areas are for remembering.
Myelinated axons in the white matter allow regions of gray matter to
communicate with each other.
Sensory Portion The sensory portion of
the peripheral nervous system contains sensory neurons, which
monitor body conditions outside the brain and spinal cord. They also monitor
conditions on the surface of the body and in its surroundings. Each type of
sensory neuron is designed to monitor only one type of condition. For example,
one kind responds to changes in temperature, while another is activated by
pressure. Those in the nose and on the tongue respond to chemicals.
Most sensory neurons are long thin cells that extend through
nerves from the regions they monitor to the brain or spinal cord. For example,
sensory neurons from the fingertips extend through nerves in the arm all the
way up to the middle of the back, where they enter the spinal cord. Once a
sensory neuron performs reception in response to a condition, it carries
impulses to communicate information about that condition to the brain or spinal
cord (Fig.
6.5).
Sensory neurons that do not have myelin release two
substances (i.e., calcitonin gene-related peptides, substance P) at sites of
wound injury. The combined effects are providing adequate inflammation while
promoting healing.
Motor Portion The motor portion of
the PNS consists of motor neurons that control the activities of
muscles and glands. Somatic motor neurons control muscles that
are attached to bones. Usually there is voluntary control of these muscles,
although sometimes the nervous system causes them to contract involuntarily.
Somatic motor neurons extend from the brain and spinal cord,
through nerves, to the muscles they control (Fig.
6.20a). For example, the motor neurons that enter and stimulate the muscles
in the lower leg begin in the spinal cord just below the middle of the back.
Other motor neurons make up the autonomic
portion of the PNS. Autonomic motor neurons control many of the
functions of the integumentary, circulatory, respiratory, digestive, urinary,
and reproductive systems by regulating many glands and also muscles that are
usually not under voluntary control. The sweat glands and salivary glands, for
example, are under autonomic control. Muscles under autonomic control include
the heart and the smooth muscle in the walls of blood vessels, the bronchi, the
stomach, and the urinary bladder.
Autonomic motor neurons are of two types: sympathetic
and parasympathetic (Fig.
6.20b, Fig.
6.20c). Though a few structures (e.g., sweat glands, skin vessels) are
controlled by only one type of autonomic motor neuron, most receive both
sympathetic and parasympathetic motor neurons. In places where both types are
present, one type of autonomic motor neuron stimulates the structure and the
other type inhibits it. By balancing the amount of stimulation and inhibition,
the autonomic nervous system can precisely control the speed and strength of
activity of a structure. For example, sympathetic motor neurons increase the
rate and strength of the heartbeat while parasympathetic motor neurons decrease
them. By automatically adjusting the ratio between sympathetic and
parasympathetic impulses, the autonomic nervous system varies the rate and
strength of the heartbeat as the amount of blood flow needed by the body
fluctuates.
The individual components of the nervous system work
together to regulate the operations of parts of the body in order to maintain
homeostasis. The simplest level of regulation involves a reflex,
which is an involuntary response to a stimulus. Reflexes that use somatic
neurons include blinking when something moves close to the eyes, coughing when
something gets caught in the throat, and withdrawing from something that is
painful. All activities controlled by autonomic neurons are reflex responses.
Many reflexes are built into the nervous system as it
develops before birth. Others are acquired reflexes which develop
when a person repeats the response every time a certain stimulus occurs. These
reflexes involve the use of unconscious remembering.
A reflex occurs in basically the same way every time a
particular stimulus occurs because the nervous system pathway that causes it is
firmly established. Sensory neurons detect the stimulus and communicate through
synapses with specific neurons in the CNS, and the CNS neurons quickly
communicate with specific motor neurons. In a few reflex pathways, such as the
one for the knee jerk, sensory neurons synapse directly with motor neurons. In
either case the motor neurons complete the pathway by sending impulses to a muscle
or gland, causing it to make the response.
Note that reflex pathways involve monitoring, communicating,
and stimulating (or inhibiting). In many reflexes the adjustment caused by the
response prevents or reverses the situation created by the stimulus. For
example, the cough reflex removes material that enters the airways. These
reflexes therefore are negative feedback systems that help maintain
homeostasis. The responses produced by other reflexes contribute to homeostasis
by improving conditions for the body. For example, the sight and smell of
appetizing food cause a reflex that increases the secretion of saliva, which
will be useful when the person begins to eat because it makes swallowing
easier.
Some reflexes simultaneously use sensory impulses from
several types of sense organs, such as the eyes, ears, skin receptors, and
proprioceptors. Proprioceptors detect motion and tension in muscles and at
joints. Some reflexes require a considerable amount of coordination by both
brain and spinal cord interneurons and synapses. Some are influenced by
voluntary motor impulses or by higher brain activities such as emotions and
thinking, which send modifying impulses into the reflex synapses.
Reflex Pathways The specific parts and activities in a
reflex pathway must be understood to appreciate the effects of aging on
reflexes. The withdrawal reflex that occurs when a sharp object jabs the bottom
of the foot provides a good example (Fig.
6.4).
When sensory neurons in the skin of the left foot detect the
intense pressure caused by stepping on a sharp object, their dendrites carry
out (1) reception. This causes the dendrites to (2) conduct impulses up through
the nerve in the leg. These impulses reach and enter the gray matter in the
back of the spinal cord via the sensory neuron axons, which (3) transmit them
through synapses to other neurons in the spinal cord gray matter. Since these
next neurons extend from one neuron to another, they are called interneurons.
The interneurons (4) transmit the impulses to somatic motor neurons in the
front part of the gray matter of the spinal cord. The impulses are then (5)
conducted down the motor axons in the nerves in the left leg to certain muscles
in the thigh and calf. Neurotransmitters from the motor axons (6) stimulate
these muscles to contract, causing the response of lifting the foot and thus
relieving the intense pressure and protecting the foot from harm.
Proper reflex responses may require coordination in addition
to monitoring, communicating, stimulating, and unconscious remembering. For
example, to prevent loss of balance when lifting the foot, cooperation by a
second reflex must occur. Branches of the sensory axons transmit impulses to
other interneurons that cross over to the right side of the spinal cord. These
crossing interneurons (7) transmit the impulses to other somatic motor neurons
in the right side of the gray matter. Impulses in these motor neurons are (8)
conducted down the nerves in the right leg. The impulses cause certain muscles
in the right leg to contract, resulting in a straightening of the right leg at
the same time that the left leg is bending and lifting the foot off the object.
In this way, the right leg supports the weight of the body so that the person
does not fall down.
Another aspect of coordination is shown by the withdrawal
reflex. As the interneurons stimulate motor neurons to the muscles that will
make the appropriate actions occur, the interneurons send (9) inhibitory
impulses to motor neurons controlling leg muscles that would interfere with the
proper movements. This prevents antagonism among the muscles.
The reflex pathway for the withdrawal reflex is a fairly
simple one. Other reflex pathways may involve interneurons that extend up or
down the spinal cord or through several areas of the brain. Countless synapses
may become involved before the impulses are finally transmitted to the motor
neurons. Autonomic reflexes are further complicated by the synapses in the PNS.
This increased complexity permits more coordination and modulation in
responses. However, more complicated reflex pathways operate in essentially the
same manner as simple reflex pathways.
Though a reflex is completely involuntary and requires no
conscious awareness, a person may feel the stimulus. For example, a person
feels a sharp object jabbing the foot because the sensory neurons may synapse
with other interneurons extending up to the brain. These other neurons help
form the conscious sensory pathways in the nervous system.
Information from perceived sensations is used to initiate
and adjust voluntary actions so that people can respond properly to conditions
in their bodies and the world around them. These sensations provide information
necessary for learning. Finally, conscious sensation provides much of the
enjoyment that makes life worthwhile.
All conscious sensory pathways begin in the same way as do
reflex pathways. That is, sensory neurons that have carried out reception
conduct impulses into the CNS (Fig.
6.5). Sensory neurons that monitor regions below the head extend into the
spinal cord, while those which monitor the head region pass into the brain.
Once in the CNS, sensory impulses are passed to interneurons extending into the
gray matter of the brain.
Impulses in each type of sensory neuron and from each part of
the body are directed by synapses to the part of the brain designed to monitor
that type of stimulus from that region. For example, impulses from the eyes are
sent to vision centers, while impulses from the auditory parts of the ears are
sent to hearing centers. The impulses are interpreted as perceived sensations
when they reach the appropriate areas of the cerebral cortex, a
layer of gray matter on the surface of the cerebral hemispheres.
The postcentral gyrus is a raised area of the cortex on each cerebral
hemisphere that is concerned mostly with conscious sensations from the
integumentary, muscle, and skeletal systems (Fig.
6.5). Other regions of the cortex are used for the special senses, such as
vision, hearing, and smell.
In many situations a person voluntarily chooses to move or
not move in response to stimuli. One can also choose the type and degree of
motion to make. For example, if someone calls, a person can choose to answer or
not answer. If that person answers, the response may include a variety of
motions or sounds. If the response is vocal, the sounds produced may be loud or
soft, enunciated quickly or slowly, and projected with different intonations.
In addition to deciding whether to move in response to
conscious stimuli, one can decide whether to take action on the basis of
internal thought processes. Again, the type and degree of motion are usually up
to the individual. Thus, one need not be called in order to decide to move or
say something. A person may spontaneously decide to start a conversation or
simply to sing.
Voluntary movements allow a person to take what he or she
judges to be an appropriate action to optimize conditions in a given situation.
Unlike reflex responses, voluntary movements allow freedom to select among many
options rather than forcing a person to respond in a particular way.
Whether voluntary motion is initiated by stimuli or by
thought processes in the brain, the nervous system pathway causing the motion
is the same. It is called the somatic motor pathway because it
controls voluntary muscles. The somatic motor pathway begins in a band of the
cerebral cortex running down the side of each cerebral hemisphere. Each band is
called a precentral gyrus (Fig.
6.6).
Each region of a precentral gyrus is designed to control the
voluntary muscles in one area of the body. To move, a person (1) starts
impulses from the area of the precentral gyrus that controls the muscles for
the part of the body to be moved. Impulses from the precentral gyrus begin to
(2) travel down the brain through white matter. As the impulses descend, they
pass through areas of gray matter, where they are modified as they move through
the gray matter synapses. In this way, the motion is performed at exactly the
speed, strength, and distance chosen. Several important areas of gray matter
that modify the motor impulses are called the (3) basal ganglia,
located inside the cerebral hemispheres. In general, the basal ganglia dampen
motor impulses so that motions are not exaggerated.
Descending motor neurons are also channeled through the gray
matter of the (4) cerebellum, which lies behind and below the
cerebral hemispheres. Its gray matter forms a wrinkled coating called the (5) cerebellar
cortex. The synapses in the cerebellar cortex modify the impulses so
that the resulting motion starts and stops smoothly, at the proper time, and
within the desired distance. The cerebellar cortex also adds impulses to ensure
that all muscles that can assist in the motion are stimulated appropriately.
The additional impulses activate muscles that move in the same direction and
muscles that hold other parts of the body still or prevent loss of balance. At
the same time the cerebellar cortex blocks impulses that would cause muscle
contractions antagonistic to the desired action.
The cerebellar cortex continues to work throughout the time
during which the desired action is occurring. It monitors the motion that is
occurring and, if the motion is not exactly what was intended, provides
impulses to muscles that can correct the error. With practice, the cerebellar
cortex improves its ability to adjust the action, leading to increasing skill
at performing that action. Similar control activities occur in the part of the
cerebral cortex in front of the precentral gyrus.
Other synapses in the descending somatic motor pathways
modify impulses to a lesser degree. Finally, the impulses reach (6) synapses to
the dendrites and cell bodies of the somatic motor neurons. These synapses are
the last places where the impulses can be modified. Once within the somatic
motor neurons, the impulses leave the CNS and travel along the (7) motor axons
in the nerves.
Upon arriving at the ends of the motor axons, the impulses
cause the (8) release of the neurotransmitter acetylcholine. Like
neurotransmitters in synapses, acetylcholine binds to the receptor molecules on
the cell membranes of muscle cells. Once enough acetylcholine is bound, the
muscle cells initiate the steps that lead to contraction, producing the desired
action, Enzymes from the muscle cells then destroy the acetylcholine, and the
cells relax until the next nerve impulses arrive.
The brain improves the efficiency of this process by sending
some impulses to somatic motor neurons just before the person attempts a
motion. Some of these anticipatory impulses are sent to motor neurons
controlling the muscles that will contract, making them more sensitive to the
main impulses telling the muscle to contract. The result is that when the
motion should occur, the correct muscle moves faster and stronger while muscles
that oppose its motion are inactivated.
The nervous system is also involved in activities that
produce conscious remembering, thinking, interpretations, emotions, and
personality traits. All these higher‑level functions take place in the
brain.
The neuron pathways that produce these activities are poorly
understood. There seem to be complicated interactions among several areas of
the brain for each activity. Also, each activity seems to influence and
interact with the others. However, many of the areas of the brain that are
involved with these higher‑level functions have been identified, and some
of the details of their operations have been discovered.
Age Changes in Sensory Functioning
Age changes that affect the sensory neurons are important
because by providing monitoring and communication, these neurons initiate
reflexes and start or influence many voluntary actions, memories, thoughts, and
emotions. Therefore, alterations in sensory functioning can affect homeostasis
and the quality of life.
Aging causes a gradual decline in sensory functioning as a
result of a reduction in the numbers of several types of sensory neurons, a
decline in the functioning of the remaining sensory neurons, and changes within
the CNS. The following section concentrates on changes in PNS sensory neurons
other than those involved in vision, hearing, and other inner ear functions.
In the skin there is little change in either the number of
sensory neurons for touch that are associated with hairs or the number of pain
receptors. However, touch receptors called Meissner's corpuscles,
which are not associated with hairs, and pressure receptors called pacinian corpuscles decrease in
number and become structurally distorted. In addition, the capsule in each pacinian corpuscle becomes thicker. Further reductions in
sensations from the skin seem to result from a weakening of the action
potentials that conduct impulses to the CNS. Alterations in action potentials
may be due to age changes in neuron cell membranes or thickening of the myelin
that surrounds many sensory neurons.
The age changes in Meissner's corpuscles and pacinian corpuscles lead to a decreased ability to notice
that something is touching or pressing on the skin; identify the place where
touch or pressure is occurring; distinguish between being touched by one object
and being touched by more than one at the same time; and identify objects by
touching them. In addition, some skin sensory neurons require more time to
respond to stimuli; this may contribute to the declining ability to feel
vibrations, particularly those with higher frequencies. An age‑related
increase in impulse speed in some sensory neurons may partially compensate for
these changes.
In addition to the effects of age changes on sensory
neurons, the monitoring of conditions in and on the skin may be altered by changes
in the thickness of the skin and the subcutaneous layer; the quality and
distribution of hair; the ability of the CNS gray matter to respond to and
interpret impulses from sensory neurons; and psychological status. Because of
these factors, the effects of aging on the perception of temperature and pain
are ambiguous.
Decreases in the ability to detect, locate, and identify
objects touching or pressing on the skin result in decreases in the ability to
respond to those objects. As a consequence, harmful objects may be encountered
more frequently, more severely, and for longer periods. There is also a decline
in the ability to perform precise actions that depend on good sensory input,
such as moving the lips when forming words and manipulating small objects with
the fingers. Reductions in skills may lead to problems in certain professions
and loss of satisfaction with hobbies. Furthermore, reduced sensation means
reduced pleasure from favorable physical contact, and this can have
psychological and social consequences. Since sensory neurons associated with
pain release substances that promote wound healing, age-related decreases in
these neurons or in processing impulses from them may contribute to the
age-related slowing of healing.
Aging causes decreases in the number of sensory neurons for
smell. These neurons are called olfactory neurons and are high in
the nasal cavities. Aging also causes deterioration of the pathways that carry
olfactory impulses through the brain. All these changes cause a decline in the
ability to detect and to identify aromas. The degree of change is difficult to
measure, however, because of the influence of changes in other brain functions
(e.g., memory, emotional state) and of previous experiences. Furthermore, the
degree of change seems to be highly variable among individuals.
Since much of what is commonly referred to as flavor is
actually aroma, age changes in the sense of smell reduce the pleasure derived
from eating and can contribute to malnutrition. Reduced olfaction also means a
reduced ability to detect harmful aromas such as toxic fumes and dangerous
gases. Finally, a declining ability to notice offensive odors can lead to
socially embarrassing situations.
The sense of taste accounts for only four of the sensations
that many people call flavors; all other flavors are due to the sense of smell.
The four taste flavors are salt, sweet, sour, and bitter. Aging seems to cause
slight decreases only in the ability to detect salty and bitter substances. The
amount of change is highly variable among individuals, and the ability to
detect salt declines the most.
Even in the oldest individuals, the threshold
levels for these four taste sensations are well below the levels in
ordinary foods. The threshold for a stimulus is the lowest level of that
stimulus which causes a response. If the threshold for tastes approaches the
values found in foods, adding more of the ingredient that produces the flavor
can compensate for this age change. Therefore, unlike the sense of smell, age
changes in the sensory neurons for taste normally do not have a significant
effect on food selection or diet. Of course, this may not be true for persons
with medical problems such as high blood pressure because these individuals may
be on restricted diets that prohibit the use of flavorings such as salt. It may
also be untrue for individuals who smoke because smoking greatly reduces taste
sensations.
A main reason for the small age change in the sense of taste
may be the lifelong ability of these sensory neurons to reproduce rapidly and
thus replace taste receptors lost to aging or injury (e.g., from hot foods).
Other types of sensory neurons that seem to have reduced
functioning because of aging include those which monitor blood pressure in
arteries; materials in the throat; thirst; amount of urine in the urinary
bladder; amount of material in the rectum (the end of the large intestine); and
positions, tensions, and lengths of the joint structures, muscles, and tendons.
Additional decrements in these sensory functions may derive from changes in the
ability of the organs being monitored to stretch and from alterations in the
ability of the CNS to respond to sensory impulses.
Corresponding outcomes from these decreases in sensory
functioning include high blood pressure; dehydration; swallowing and choking
problems; urinary incontinence; constipation or bowel incontinence; and reduced
control and coordination of voluntary movements.
Age Changes in Somatic Motor Functioning
Important age changes in somatic motor neurons involve their
numbers, action potentials, and transmission sites. The first two changes are
similar to those we have noted in sensory neurons.
Number There is a decrease in the number of motor
neurons, and this reduces the number of cells that can be stimulated in a
muscle. Therefore, the maximum strength of contraction that muscles can produce
declines. In the lumbar region of the spinal cord, which controls muscles in
the lower half of the body, as many as 50 percent of the somatic motor neurons
are lost by age 60. Muscle cells that lose their motor neurons degenerate
completely because they are no longer stimulated.
The resulting decrease in muscle strength can be minimized
by increasing the strength of contraction provided by muscle cells that retain
their motor neurons. This effect can be achieved on a short‑term basis by
increasing the amount of stimulation by the surviving motor neurons. However,
using this strategy puts extra strain on the stimulated muscle cells. It also
can produce the feeling that one must work harder to perform a strenuous
activity which formerly was not difficult. Over the long term much of the
strength of each muscle can be retained through programs of physical training
and ordinary activities that require very strong muscle contractions.
Action Potentials The second age change in motor neurons is a
slight decrease in the speed of action potentials in their axons. The amount of
slowing is different in different neurons. The changes in speeds caused by
aging increase the original differences in speed found among young neurons. As
a result, when an aging muscle is supposed to contract, the burst of impulses
sent to it by the motor neurons arrives over an increasingly long period.
Therefore, the contractions of muscle cells are spread out over a longer
period.
Slower action potentials in motor neurons may result from
age changes in motor neuron cell membranes, myelin, or blood vessels within the
nerves. Aging causes some myelin in peripheral nerves to separate from its
axons. Damaged myelin is removed by macrophages, and its replacement occurs
more slowly with age. Age changes in blood vessels were described in Chap. 4.
These changes reduce blood flow in the nerves and therefore decrease the supply
of nutrients and the elimination of wastes.
Alterations in muscle contraction resulting from slower
action potentials and the spreading of muscle cell contractions include slower
contraction, lower peak strength of contraction, and slower relaxation.
Age-related decreases in anticipatory impulses increase these changes. All
these alterations reduce the maximum amount of strength a muscle can produce
when it performs very quick movements.
Neuromuscular Transmission The third age change is a substantial
decrease in the speed of transmission from motor neurons to muscle cells. This
decline may be from the formation of irregularities at the ends of aging motor
axons. Slower transmission results in further delay in starting a motion.
All three age changes mean that activities that require
strong and/or fast actions cannot be performed as well. This can have a
significant impact on individuals whose careers or recreational activities
depend on such actions. For other people, modifying or changing strategies to
achieve their goals can help compensate for the slow decline in strength and
speed.
Age Changes in Autonomic Motor Functioning
Aging of the autonomic motor neurons has not been as well
studied as aging of other parts of the nervous system because of difficulties
in distinguishing such changes from other age‑related changes. Therefore,
little can be said with confidence about the effects of aging on autonomic
motor neurons. However, some aspects of the aging of these neurons are coming
to light. In general, aging seems to have little effect on their ability to
regulate body functions under normal conditions. This is due in part to overall
slow loss of sympathetic motor neurons in the spinal cord (i.e., 5 percent to 8
percent per decade). Additionally, sympathetic motor neurons compensate for
some age changes by modifying their dendrites and axons throughout life.
However, when conditions become unfavorable, the autonomic neurons controlling
certain structures have difficulty causing adequate adjustments to preserve
homeostasis.
An apparently inadequate autonomic response occurs when
older people stand up or remain standing for long periods. Normally,
sympathetic neurons prevent a substantial drop in blood pressure by stimulating
the heart and causing constriction of many blood vessels. The ability of the
sympathetic neurons to cause these adjustments decreases in many people. The
resulting low blood pressure when one is in an upright position orthostatic hypotension can cause dizziness, light‑headedness, and fainting.
This is a major cause of falls and physical injury (e.g., fractures).
Orthostatic hypotension does not occur in all older individuals, and some cases
result from abnormalities in the circulatory system.
Aging of autonomic neurons can lead to elevated blood
pressure as well as low blood pressure. Normally, parasympathetic impulses slow
and weaken the heartbeat to keep blood pressure down while a person is at rest,
when a person ends vigorous physical activity, and during each inspiration.
Aging causes this parasympathetic function to decline and therefore diminishes
the ability of these neurons to prevent blood pressure from exceeding the
proper levels.
Age changes in autonomic neurons may also contribute to a
decrease in the ability to adjust to extremes in temperature. Normally,
sympathetic impulses cause blood vessels in the skin to constrict when a person
is getting cold; this helps stabilize body temperature by reducing the rate of
heat loss. With increasing age, there is a decrease in such constriction. Thus,
older individuals are at greater risk of developing hypothermia. This age
change may be due largely to age changes in blood vessels.
Another age change that may be due in part to aging of
autonomic neurons involves erection of the penis. Normally, erection occurs
when parasympathetic neurons cause dilation of blood vessels in the penis
during sexual arousal, increasing blood flow into the penis and causing it to
enlarge and become stiffer. With advancing age, these processes occur more
slowly and to a lesser degree. These age‑related changes may be due to
reduced parasympathetic functioning or to age changes or disease in penile
vessels. Parasympathetic control of other blood vessels is not changed by
aging.
Another age change believed to result from aging of
autonomic nerves is a decrease in the responsiveness of the pupil. Normally,
sympathetic nerves stimulate muscles in the iris that cause dilation of the
pupil and parasympathetic nerves stimulate muscles in the iris that cause
constriction of the pupil. Balancing these autonomic influences results in
letting enough light enter the eye for vision while preventing the entry of
excess light, which can hinder vision and damage the eye. With advancing age,
there is a decrease in the amount of pupillary dilation and slower constriction
of the pupil, which reduces adaptation by the eye. Both changes may be caused
by changes in the autonomic neurons or in the iris.
Finally, there is a decrease in the number of neurons
controlling the movements of the esophagus during swallowing. Normally, when
solids or liquids enter the esophagus from the throat, these materials are
pushed down to the stomach by a wave of muscular contraction in the esophagus.
The contraction is initiated by the swallowing reflex and is coordinated by a
group of motor neurons (Auerbach's plexus) in the esophagus. With
aging, the number of neurons in Auerbach's plexus decreases. Swallowing becomes
more difficult because the wave of contraction starts later, is weaker, and is
less well coordinated. Sometimes the esophagus fails to empty completely,
resulting in considerable discomfort.
Sympathetic functioning is also affected by changes at
neuromuscular and neuroglandular junctions. Sympathetic neurons become
especially active when conditions become unfavorable and homeostasis is
threatened or when such a threat is suspected or anticipated. The effects of
sympathetic activity include increases in heart functioning, blood pressure,
and perspiration as well as dilation of the airways. At the same time,
sympathetic neurons inhibit certain activities, including digestions, urine
production, and the functioning of the reproductive organs. Overall, these
effects are adaptive and beneficial because they channel more of the body's
energies into actions that help the individual overcome or escape danger. The
combination of effects caused by the sympathetic neurons is often referred to
as the fight‑or‑flight response, which is part of the
body's reaction to stress.
Most sympathetic motor neurons use norepinephrine
as a neurotransmitter at neuromuscular and neuroglandular junctions. At the
direction of sympathetic neurons, norepinephrine is also produced and secreted
into the blood by a gland called the adrenal medulla (Chap. 14).
Norepinephrine from the adrenal medulla increases the intensity and duration of
the effects of sympathetic norepinephrine.
Aging affects blood levels of norepinephrine in three ways:
1. The concentration of norepinephrine in the blood of
resting individuals rises.
2. When a stressful situation is encountered, the level of
norepinephrine increases faster.
3. Once the stress has passed, the level of circulating
norepinephrine returns to its resting concentration more slowly.
There seem to be two reasons for the higher levels of
norepinephrine in older individuals. One may be the stiffening of arteries
(Chap. 4). The other seems to be a compensatory response for an age‑related
decline in the effectiveness of norepinephrine in some organs. This decline may
be due to age changes in receptor molecules (e.g., lungs) or in reactions
within cells (e.g., heart).
In conclusion, although the effects of age changes in
autonomic neurons are not unimportant, such changes are few compared with the
number of autonomic functions that seem to be unaffected by aging. Autonomic
neurons can provide proper regulatory impulses to most of the structures they
control regardless of age or the degree of stress placed on the body.
Since aging causes many detrimental changes in sensory and
motor neurons as well as in myelin, it produces deleterious effects on the
reflexes that use those structures. Some of these effects were mentioned in the
sections on sensory, somatic, and autonomic neurons. The decrease in number and
the decline in sensitivity of certain sensory neurons mean that more
stimulation is required to start many reflexes. It takes more time for the
response to begin because reception takes longer and action potentials are
weaker and slower. Changes in action potentials, together with decreases in the
number of motor neurons and the effectiveness of certain neurotransmitters,
cause the response to be weaker and of longer duration.
Age changes in the structures that surround the sensory neurons,
such as the skin and blood vessels, further alter reflexes by preventing
sensory neurons from properly detecting stimuli. Reflex responses are also
reduced by age changes in the glands and muscles producing the responses and in
the skeletal system.
Reflexes also seem to be detrimentally affected by age
changes in the CNS. It has been observed that the more complicated the pathway
in the CNS, the more dramatic the effect of aging on reflexes. In addition to
reflexes occurring more slowly and weakly, there is a decline in the amount of
coordination provided by the CNS in complicated reflex responses. Reflex
contraction of large muscles is a good example.
The simplest muscle reflexes in the body are those which
help maintain posture. These stretch reflexes or deep
tendon reflexes use few synapses and no interneurons. A stretch reflex
is initiated when a muscle is stretched, as occurs when a person's posture
begins to change because of slumping, an external force causes a joint to bend,
or an object hits a tendon. When the impulses in the reflex pathway reach the
muscle that has been stretched, it contracts to restore the body to its
original posture. The knee‑jerk reflex is an example of a stretch reflex.
Such simple reflexes become weaker but only slightly slower with age. The
degree of weakening indifferent individuals is highly variable. The degree
ranges from virtually no change in the strength of the response to essentially
total loss of the response. However, many cases of very weak or absent stretch
reflex responses result not from aging but from abnormal or disease conditions
such as traumatic injury, atherosclerosis, arthritis, and diabetes mellitus.
In contrast to stretch reflexes, reflexes that maintain
balance while one is standing in place require the proper timing of a sequence
of many muscle contractions. Keeping one's balance while there is movement of
either the body or the surface on which a person is standing requires an even
more complicated series of muscle contractions. Though the same sensory and
motor neurons involved in stretch reflexes may be used, many interneurons and
synapses in various parts of the brain and spinal cord are involved in these
pathways. Sensory inputs from the eyes, ears, and skin may assist in these
reflexes.
Complex reflexes such as those which maintain balance show a
substantially greater slowing with age than do simple muscle reflexes. Aging
also causes disturbances in the coordination required for such reflexes. For
example, there is a change in the sequence in which the muscle contractions
occur during these reflexes and an increase in the number of antagonistic
muscle contractions. In comparison to simple reflexes, some of the additional
slowing and much of the decline in coordination seen in complex reflexes seem
to be due to age changes in the synapses and interneurons in the CNS.
Interestingly, some age changes in the CNS seem to involve
adjustments in reflex pathways that compensate for diminished sensory
functioning, muscle strength, skeletal system functioning, and confidence in
one's ability to maintain balance. This can be observed in the age change in
gait. Part of walking involves voluntary activity, but many of the muscles used
for walking are controlled by acquired reflexes. Older individuals walk with
smaller steps, at a slower pace, and with the feet more widely spread. Such a
gait minimizes the risk of losing one's balance. Gradually modifying voluntary
actions and reflexes to walk in this manner seems to reduce the demands on the
muscles, joints, and reflexes needed to maintain balance.
In summary, reflexes undergo several age changes. They
require more stimulation to be activated, and it takes longer for a response to
begin. The response is weaker, takes longer to occur, and shows less
coordination. These changes are caused by alterations in both the PNS and the
CNS. With more complicated reflexes, aging of the CNS makes a larger
contribution to alterations in reflexes than do age changes in the PNS. As
aging diminishes the functioning of reflexes, it reduces their ability to
provide automatic, fast, and accurate responses to changes in internal and
external conditions and therefore to maintain homeostasis.
Age Changes in Conscious Sensation and Voluntary
Movements
As with reflexes, aging affects conscious sensation and
voluntary movements because of age changes in sensory neurons, motor neurons,
myelin, and CNS neurons and synapses. Since conscious sensation and voluntary
movement use even more CNS synapses and interneurons than are used in reflexes,
age changes in the CNS have a greater impact on these activities.
The results of PNS and CNS age changes on conscious
sensation include a declining ability to detect, recognize, and determine
levels of stimuli. These decrements make selecting and performing appropriate
voluntary actions more difficult, inhibit learning, and diminish enjoyment from
experiences.
The ability to maintain homeostasis and the quality of life
is decreased further because aging of nerve pathways used for voluntary
movements causes such movements to become slower, weaker, less accurate, and
less well coordinated. Since these changes occur gradually, individuals are
able to make adjustments in their activities and minimize the undesirable
effects.
Correlations between the alterations in reflexes, conscious
sensation, and voluntary movements and age changes in the structure and
functioning of the CNS are not well understood. The reasons for this ambiguity
include (1) the necessity of studying brains obtained from autopsies, which
have undergone variable degrees of postmortem changes, (2) the difficulty in
determining how much, if any, disease was present in the brain or in other
organs, and (3) the paucity of psychological or behavioral information about
the people whose brains are studied. However, as these correlations become
clear, it may become possible to influence the decreases in nervous system
functioning caused by aging.
In the white matter, there is an age-related decrease in the
motor neurons, especially of motor neurons that control somatic motor
functions. These neurons carry anticipatory impulses and main impulses from the
brain to lower somatic motor neurons in spinal cord gray matter. Within the
gray matter, the average loss of motor neurons is approximately 25 percent
during adulthood and into very old age. The rate is highly variable, and may be
two to three times higher in some individuals. There seems to be a preferential
loss of somatic motor neurons. This corresponds with the loss of motor units in
muscles (see Chapter 8).
Dimensions Many studies report that there is a decrease in the size and weight of the brain as age increases. The fluid‑filled cavities inside the brain enlarge, the raised ridges (gyri) on the surface shrink, and the grooves (sulci) between the gyri become wider (Fig. 6.7). (Suggestion 131.02.Fig. 6.7)
How much of the age‑related shrinkage of the brain is
due to aging and how much is due to diseases such as atherosclerosis has not
been determined. One reason for the overall shrinkage may be a decrease in the
number of neurons in several areas of the brain. The cause of this neuron death
is not known, and there is no indication that what is considered to be a normal
amount of overall shrinkage has any effect on brain functioning.
Numbers of Neurons Some parts of the brain show a substantial
decline in the number of neurons, and this may affect specific functions. In
the cerebrum, these parts include areas that control voluntary movements, areas
for vision and hearing, and possibly areas involved in other conscious
sensations. Other parts of the cerebral cortex seem to lose few if any neurons.
The cerebellar cortex, which coordinates muscle movements and controls many
complicated muscle reflexes, and the basal ganglia, which are also involved in
modifying muscle actions, lose many neurons (Fig.
6.5,
Fig.
6.6).
The regions of the brain other than the cerebral hemispheres
and the cerebellum are referred to as the brain stem. The only
regions of the brainstem that seem to lose neurons because of aging are the nucleus
of Meynert, which produces acetylcholine for
short‑term memory, and the locus coeruleus, which produces
norepinephrine and helps regulate sleep (Fig.
6.8).
It has been suggested that neuron losses in these areas
contribute to age‑related detrimental changes in the functions to which
they contribute: voluntary movements, conscious sensation, muscle reflexes,
memory, and sleep. However, there is no conclusive evidence that localized loss
of brain neurons caused by aging has any effect on the functions performed by
the areas that incur neuron loss.
One reason why neuron loss may have no effect is that the
remaining brain neurons can branch and produce many new synapses. The new
neuron pathways created by the new synapses may compensate for the decrease in
neurons. Second, there may initially be many more neurons in the brain than are
needed, and these additional neurons may constitute a reserve capacity. Third,
the loss of neurons may actually improve the brain by eliminating neurons that
are not used or have made errors. The brain may be able to recognize and
eliminate unused or undesirable neuron pathways and thus improve its
efficiency. This process may constitute part of the development of wisdom.
Neuron Structure and Functioning Many neurons
remaining in the aging brain undergo several age changes. For example, the cell
membranes of brain neurons become less fluid and stiffer. These changes may
contribute to age‑related alterations in brain functioning by altering
reception, conduction, and transmission. Second, internal membranes (e.g.,
endoplasmic reticulum) become irregular in structure, and many neurons have an
accumulation of lipofuscin. The effects of abnormal amounts of lipofuscin are
not known.
A third change in brain neurons is the formation of neurofibrillar tangles.
Normally, neurons contain long thin structures called neurofibrils.
These structures are present in the cell bodies and extend down the axons.
Neurofibrils seem to be important in the movement of neurotransmitters from
their sites of production to the ends of the axon. The formation of tangled
neurofibrils may mean that not enough neurotransmitter is reaching the end of
the axon; this could result in a decrease in or an elimination of transmission
by neurons with neurofibrillar tangles. The result
would be a decrease in the functioning of synapses.
Synapses Because most research on changes in brain
synapses has been directed toward alterations caused by disease, the effects of
aging are not well understood. For example, there may be dozens or even
hundreds of different neurotransmitters in the brain, and much confusion and
contradictory information exist about age changes in these. All that can be
said at this point is that aging seems to cause decreases in some
neurotransmitters in some areas of the brain. There are few or no cases where
the amount of a neurotransmitter increases with aging.
Information about age changes in the number of synapses in
various brain areas is also incomplete. It is known that the number of synapses
in an area may increase or decrease depending on how much use is made of that
area. Neurons that are heavily used increase their number of synapses by
growing new axon branches or new dendrites and dendrite branches (dendritic
spines). The ability of neurons to do this decreases with age. There is
also evidence that at least in some areas, neurons that get little use reduce
their number of dendrites or dendritic spines and thus decrease the number of
synapses in those areas of the brain.
The interpretation of information about changes in the
number of synapses is complicated because the effectiveness of synapses depends
not only on their numbers but also on changes in their neurotransmitters and in
the exact neuron pathways that are gained or lost. For example, many
inefficient synapses may be replaced by a few efficient ones, resulting in an
improvement rather than a decline in functional capacity.
Adding to the confusion is the fact that synapses undergo
age changes in structure as well as number. For example, though there is a
decrease in the number of synapses in the precentral gyrus, the remaining
synapses become broader. This may mean that these synapses work better and
therefore compensate for those which are lost.
Perhaps the best-known age change in synaptic structure is
the buildup of the protein called amyloid. A mass of amyloid in a
synapse is called a plaque. As with other age changes, different
amounts of plaques develop in different areas of the brain. It is believed that
plaques decrease the functioning of synapses. Normally, however, a person does
not form enough plaques to alter brain functioning to a detectable degree.
Aging of Other Brain Functions
The process of consciously remembering information is
referred to as memory. Memory is a very complicated process that is
not well understood. Though certain areas of the brain, such as the hippocampus,
(Fig. 6.8
video) are especially important, many areas in the cerebral cortex and
other brain regions act cooperatively to provide memory.
Memory can be divided into two broad types: short‑term
memory and long‑term memory. Information that is
stored in short‑term memory is retained for brief periods (seconds or
minutes). The brain may be temporarily storing this information by continuously
repeating the impulses containing the information, and the information is
forgotten as soon as the impulses fade away. The information is also easily
forgotten if a person is distracted by different information that sends other
impulses through the neurons.
It is possible to increase the time information is stored in
short‑term memory by keeping the impulses going. This can be done by
repeating the stimulus over and over, just as a person can keep a wheel
spinning by giving it a push now and then. This technique is used when people
remember a telephone number for a short period by repeating it until the number
is dialed.
Long‑term memory can store information for many years.
For example, remembering an incident from childhood requires the use of long‑term
memory. Apparently, information is stored in long‑term memory when
impulses produce physical changes in the neurons processing the information. The
more times impulses about an incident pass through the neurons, the greater the
chances that they will cause the physical changes. This is why a person studies
material over and over to remember it for a test.
Two types of changes are believed to occur in neurons that
store information in long‑term memory. In one case, new molecules are produced in the neurons. Alternatively
or additionally, the synapses in the nerve pathway are altered. In either case
the impulses for the information travel much more easily. Then a small stimulus
can trigger the neurons to produce the same impulses, resulting in the person
consciously remembering the information.
Memory can also be classified according to the types of
information stored. Incidental memory involves remembering
information or skills that were self-taught. Procedural memory
involves recalling how to perform a process or series of steps. Both types may
include explicit memory and implicit memory. Explicit memory (declarative
memory) involves remembering specific facts that a person tried to
learn so they could be remembered. Implicit memory involves
remembering specific facts that a person did not try intentionally to learn so
they could be remembered. For example, a person may be unaware of learning procedures,
processes, motor skills, or vocabulary by experience. Episodic memory
involves recalling the times and places events happened. The events are
mentally separated and oriented correctly regarding their proper time,
sequence, and locations of occurrence. Working memory involves
holding information at or close to the level of consciousness so it can be used
in cognitive processing, such as solving a problem or planning a complex
activity.
Age Changes in Memory Aging causes a decline in short‑term memory
in most people. The rate of decline varies highly between individuals. This may
be due in part to differences in the rate of age changes within the nervous
system, but it is caused by other factors to a greater degree. These factors
include differences in general health, diet, presence of specific diseases,
past patterns of mental activity, motivation, and diverse psychological,
social, and economic parameters. So many features affect memory that it is
impossible to predict which changes have occurred or will occur in a particular
individual.
On the average, the decline in short‑term memory is
gradual and slow until approximately age 60 and then becomes ever more rapid,
especially after age 70. However, the total amount of loss in memory
functioning in a normal individual is relatively slight regardless of age. In
many cases changes in memory can be noticed only in carefully controlled
experimental situations, and because people develop compensatory strategies,
such age changes usually do not affect ordinary activities significantly.
The greatest decline in short‑term memory occurs for
information that is presented quickly and verbally. Information about
completely unfamiliar things also becomes much harder to remember. Older people
have more difficulty recalling information than simply recognizing it. For
example, questions that require an older person to supply the answer are harder
than those which require the person to select the correct answer from among
several incorrect ones. To help elderly people remember, information should be
presented slowly, in an organized manner, using relevant and concrete examples
and visual aids. People are better able to recall information when cues such as
notes and mnemonic devices are used and when they are allotted additional time
to study and respond. It is also helpful to make adjustments to compensate for
deficits in vision and hearing.
The reasons for the decline in short‑term memory are not understood but may include age changes in the number
of neurons, the number or structure of synapses, and the amounts of different
neurotransmitters present in memory pathways.
Long‑term memory seems to be largely unaffected or to
improve as people get older.
Age changes in incidental memory and procedural memory depend
upon whether they use explicit memory or implicit memory. Explicit memory
decreases with aging, especially when the facts had to be learned quickly or
they must be remembered quickly. Aging has much less effect on explicit memory
when more time is used to learn or to remember facts. Implicit memory shows
little decline when elders unknowingly experience or are given prompts related
to the passed information, such as being placed in a familiar setting. Implicit
memory shows the greatest age-related decline when a person tries intentionally
to remember. Because of different age-related changes in these two types of
memory, elders largely retain their ability to perform even complex procedures
they have practiced, but they may have difficulty explaining how to carry them
out. Episodic memory also decreases with age. Failure of episodic memory
results in erroneously remembering widely separate events as having occurred
together or being unable to connect related events.
Working memory decreases with aging. Therefore, while the
ability to remember specific information does not decline much, the ability to
use multiple pieces of information in complex cognitive activity declines
significantly. This may result from age-related reductions in effectively
selecting, retrieving, and processing information consciously.
Elders can increase their memory functions through
educational and training programs about memory. Memory training programs may
emphasize specific memory techniques. Examples of such techniques include using
written notes; mentally repeating information often; organizing material into
large meaningful blocks rather than many unrelated details; making up sentences
or words where letters (e.g., first letter in each word, letters of the words)
stand for the items being remembered; mentally picturing information, images,
or processes; putting information into a story, rhyme, or song; sketching
pictures or diagrams; finding experiences in life that are relevant or related
to the information. Factors that help learning information include studying
when energy levels are high, but not after eating a large meal; avoiding large
quantities of aspartame artificial sweetener (e.g., diet beverages); avoiding
distractions when learning; getting restful REM sleep.
Other memory training programs take less direct approaches.
Sometimes using cognitive restructuring to promote positive expectations in
memory performance produces greater and more lasting beneficial effects on
memory. This may result from using practical techniques in only similar
situations, while cognitive restructuring techniques are often used in diverse
situations.
Knowledge of the associations between memory and aging are
important for improving outcomes from training programs for elders. For
example, modifying job training programs to accommodate age changes in memory
becomes more important as the numbers and ages of older workers increase.
Like conscious memory, thinking occurs entirely within the brain,
but it is an even more complicated and less well understood process. Thinking
includes problem solving, planning, and other activities that may be called
intelligence. Intelligence may be divided into two categories. Crystallized
intelligence involves using cognitive skills with familiar learned
activities. Fluid intelligence involves using cognitive skills in
new situations. Examples of fluid intelligence include learning novel problem
solving, motor activities, or reasoning. It involves more flexibility in
dealing with situations. No attempt will be made here to explain how the brain
performs thinking.
As with age changes in short‑term memory, there is on
the average a slow and gradual decline in thinking to approximately age 60; the
rate of decline increases more each year after that, especially after age 70.
Note, however, that the loss of thinking ability is relatively slight
regardless of age and that changes can be noticed only through careful testing.
The small amount of change, coupled with the use of compensatory strategies,
usually means that there is not a significant effect on ordinary normal
activities. There is much variability
among individuals in regard to age‑related changes in thinking because of
variations in aging of the nervous system and differences in other factors that
affect thinking. As a result, no one can anticipate how aging will affect an
individual's ability to think. Some individuals show no changes in thinking,
and up to 10 percent of older people show an increase in thinking ability. This
increase seems to be due to continued use of thinking, ongoing education, or
good economic status. Among those whose thinking declines with aging, thinking
becomes slower and changing one's train of thought becomes more difficult.
Aging has little effect on crystallized intelligence, and
many people show age-related increases. Fluid intelligence usually shows
age-related decreases. Men show earlier decline in crystallized intelligence;
women show earlier decline in fluid intelligence. Deterioration in the ability
to solve problems and make decisions quickly and accurately is most evident
when these processes require the consideration of many factors.
Language functions rely heavily upon memory and
intelligence. There is little or no age-related change in knowing the meanings
of words, though vocabulary may increase throughout life. Age-related changes
in conversation include using more short and simple sentences; sentence fragments;
pronouns and less specific terms; vague adjectives; vague references to time
and place. Working vocabulary, ability to find the right word, and adherence to
one topic decline. These changes increase as background distractions increase
(e.g., noise, motion). Comprehension of conversations decreases as the content
of a conversation becomes more complex; more disjointed; more novel; faster;
and with increased distractions. These age-related changes usually do not
prevent elders from carrying on meaningful conversations. The changes seem to
result from age-related changes in memory and in cognition, including changes
in methods of processing verbal information.
Supporting memory and intelligence
Factors that reduce age-related decreases in memory and intelligence
and often improve these functions include good health; exercise; passed and
continuing education; activities requiring complex mental functions;
self-determination and self-direction; and a sense of self-efficacy. Estrogen
therapy in postmenopausal women improves some aspects of memory and cognition
including short term verbal memory, abstract reasoning, logical thinking, and
overall cognitive functioning. Using proper prevention, intervention, and
cognitive training programs for elders help to sustain and improve memory and
intelligence as age increases.
Personality includes many facets, including levels of
anxiety, depression, self‑consciousness, vulnerability, impulsiveness,
hostility, warmth, assertiveness, gregariousness, and emotions.
Age Changes in Personality Personality
undergoes changes up to about 30 years of age, after which most of its aspects
are extremely stable. However, major upsetting events in a person's life, such
as a major illness, may significantly alter one's personality.
Personality greatly influences the choices made throughout
life, particularly in matters related to education, exercise, diet, and health
care. All these parameters influence the length and quality of life. Also,
personality is a major determinant of an individual's ability to adapt to
changing circumstances. Since personality becomes stable, the nature of its
contribution to the ability to adjust remains about the same throughout life.
Therefore, knowledge of personality can be useful in predicting an individual's
future ability to adapt to the new life situations that develop with aging.
The effects of aging on sleep are of great interest. One
reason for this is the perception that older individuals are sleepier during
the day. Second, there is evidence that compared with wakeful (daytime) values,
body functions are different during sleep and at night. To fully understand
aging, the body must be studied in the sleeping as well as the wakeful state.
Age Changes in Sleep As people get older, several changes in
sleep usually occur. Complaints about sleep difficulties rise from 15 percent
among young adults to almost 40 percent among elders. With aging, more time is
needed to fall asleep, there are more awakenings during the night, and wakeful
periods are longer. Reasons for the increased number of awakenings include a
higher incidence of indigestion, pain (e.g., arthritis), rhythmic leg
movements, sleep apnea, and circulatory problems (e.g., irregular heartbeat).
Some individuals have more awakenings because a decline in the capacity of the
urinary bladder requires them to void urine more often. The rise in the level
of norepinephrine may also contribute since norepinephrine increases alertness.
The increase in awakenings is greater in men than in women. Even though sleep
becomes more fragmented, the total amount of time spent asleep in each 24‑hour
period remains about the same because more time is spent in bed as age
increases.
Changes occur in the type of sleep as well as in its
continuity. While there is increasing variability among people as they get
older, there is an average increase in the time spent in stage 1 sleep, the
least restful of the five types. The existence and significance of age changes
in amounts of stage 2 and stage 3 sleep are uncertain.
While asleep, people switch between stage 4 sleep and rapid
eye movement (REM) sleep every 80 to 100 minutes. These
are the most restful stages of sleep. There is an age‑related decline in
the amounts of time spent in stage 4 sleep and REM sleep, although the decrease
in REM sleep becomes substantial only in very old age.
It is difficult to determine how much or which of the
changes in sleep are due to aging of the brain and which are due to other age‑related
factors, such as having diseases, taking more medication, being past menopause,
having different daily routines because of retirement, having more freedom for
daytime napping, and experiencing altered social situations such as death of a
spouse or a move to a different home or institution.
Sleep can be improved by keeping to a schedule; adhering to
bedtime routine; creating an environment conducive to sleep (e.g., quiet,
dark); exercise; treating medical problems and sleep apnea; entraining
circadian rhythms with bright light therapy; biofeedback training; and mental
relaxation techniques. Things to avoid include daytime naps; stimulants (e.g.,
caffeine) late in the day; strenuous activity shortly before bed; using the bed
and bedroom for work, worrying, or solving problems; medications that adversely
affect sleep (e.g., diuretics at bedtime); and chronic use of sedatives, hypnotics,
and other sleep inducers;
The effects of age‑related changes in sleep include a
reduction in the quality of sleep and alterations in the time when it occurs
during each 24‑hour period. These effects probably explain why more
people feel sleepy during the day as they get older. However, this is not a
normal part of aging. When daytime sleepiness interferes with regular
activities, it should be considered abnormal and warrants further diagnosis.
The presence of age‑related increases in abnormal sleepiness has
contributed to the stereotype of the older person who nods or falls asleep at
inappropriate times.
Many activities in the body show regular cyclic fluctuations
or biorhythms. One of these is a daily biorhythm that repeats
itself approximately every 24 hours. It is aptly called the circadian
rhythm, meaning "approximately daily rhythm. Perhaps the most obvious manifestation is the cycle of
sleeping and being awake. Another well-known biorhythm is the menstrual cycle
in women, which recurs approximately every 28 days. Faster cycles include the
cardiac cycle and the breathing cycle. People also exhibit annual rhythms that
accompany seasons of the year.
In the body, the circadian rhythm is controlled primarily by
the brain. When light entering the eyes causes impulses to be sent to the
brain, many of the impulses reach a brain area called the suprachiasmatic
nucleus (SCN). The SCN is in the hypothalamus,
located between the basal ganglia (Fig.
6.8, Fig.
14.1). Impulses from the SCN travel an indirect route to the pineal
gland of the brain. The pineal gland is in the crevice between the
cerebral hemisphere and the cerebellum (Fig.
6.8, Fig. 14.1).
The pineal gland secretes the hormone melatonin. When less light
enters the eyes, more impulses travel from the SCN to the pineal, causing more
melatonin secretion. More light entering the eyes causes the opposite effect.
Both the intensity and wavelengths of light influence its effects on melatonin
secretion.
Since usually more light enters the eyes during the day and
light decreases during the evening, remaining very low during the night,
melatonin secretion increases during the evening and remains low during the
day. Melatonin influences many body functions including the SCN, and it
produces some manifestations of the circadian rhythm. However, even with no
light entering the eyes, the SCN causes melatonin to be secreted in a circadian
rhythm. The SCN in the main regulator of the body's circadian rhythm. The
circadian rhythm is influenced by other factors including environmental cues,
physical activity, and eating.
Body circadian rhythms include sleep:wakefulness; stages of sleep; lowering of body
temperature, blood pressure, and urine production at night; and oscillations in
blood levels of many substances including hormones (e.g., melatonin,
glucocorticoids, growth hormone, testosterone, estrogen, progesterone).
Oscillations of these hormones cause manifestations of the circadian rhythm (see Chap. 14). The
importance of maintaining normal circadian rhythms is evident when they are
disrupted. Examples include "jet lag,” working night shifts, or having sleep:wakefulness cycles disrupted
by environmental irregularities (e.g., nighttime noise).
Aging causes changes in circadian rhythms. Many changes
begin during the third decade and increase after that through old age. In
general, manifestations of the circadian rhythm have lower peak intensities.
Examples include difficulty falling asleep; poorer sleep quality; more urine
production at night; and lower peak hormone levels.
The circadian rhythm tends to shorten, and most
manifestations begin up to one hour earlier in the 24-hour day. However, phase
shifts are unequal, and some manifestations of the circadian rhythm occur later
rather than earlier. The result is an age-related loss of synchrony among
manifestations of the circadian rhythm. Perhaps the most obvious troublesome
consequence is the age-related deterioration of the sleep:wakefulness cycle accompanied by deterioration
of sleep quality.
Age changes in circadian rhythms may be due to a combination
of age changes in the brain and the eyes. Weak or disrupted circadian rhythms
can be brought toward normal by regulating exposure to bright light, by
voluntarily regulating routines (e.g., physical activity), and by carefully
timed melatonin supplementation.
In general, there are only small age changes in seasonal
rhythms. Exceptions include levels of clinically important substances in the
blood (e.g., creatinine, urea, urate, blood proteins).
Understanding and accounting for age-related changes in
circadian rhythms and seasonal rhythms are important because circadian rhythms
influence patient evaluations and effects of medications. The changes should
also be considered in research studies so that measurements are taken at proper
times of the 24-hour day.
In spite of age changes, the normal nervous system can help
maintain homeostasis and sustain a satisfactory quality of life for many
decades. However, as with other body systems, the comfort derived from these
conclusions may diminish when one considers the frequency and effects of
nervous system diseases that increase with age.
Diseases of the Nervous System
Strokes are the fourth leading cause of death among people
over age 65, accounting for approximately 9 percent of all these deaths.
Beginning at a rate of less than 6 percent at age 65, the percentage of deaths
from strokes rises steadily as age increases, surpassing 12 percent for those
over age 85.
Heart disease accounts for 4.5 times as many deaths, and
cancer, which is the second leading cause of death among the elderly, accounts
for more than twice as many deaths among people above age 65. While the death
rate from cancer has remained stable for many years, the death rates from
strokes and heart disease have declined steadily since about 1960. These
declines are probably due in large part to better prevention of atherosclerosis
and better diagnosis and treatment of strokes and heart disease. (Suggestions:
Chap 06 - 137-2-6)
Many people who have a stroke survive. Therefore, not only
the percentage of deaths but also the overall incidence of strokes increases
with age, especially after age 65. About 4.5 percent of those between 65 and 75
years of age have a stroke, and the rate among those over age 75 is about 7.3
percent. Strokes occur more frequently in men than in women and much more
frequently in Blacks than in Whites. Those who survive are often left with
serious lifelong disabilities.
|
Causes
of death for all ages |
|||
|
Rank |
Cause
of death |
Number
(thousands) |
Percent
of total |
|
|
All causes |
2,814 |
100.0 |
|
1 |
Diseases of heart |
647 |
23.0 |
|
2 |
Malignant neoplasms |
599 |
21.3 |
|
3 |
Chronic lower respiratory
diseases |
170 |
6.0 |
|
4 |
Cerebrovascular diseases |
160 |
5.7 |
|
5 |
Alzheimer disease |
146 |
5.2 |
|
6 |
Diabetes mellitus |
121 |
4.3 |
|
7 |
Accidents (unintentional
injuries) |
84 |
3.0 |
|
8 |
Influenza and pneumonia |
56 |
2.0 |
|
9 |
Nephritis, nephrotic syndrome and
nephrosis |
51 |
1.8 |
|
10 |
Parkinson disease |
47 |
1.7 |
|
|
All others (approx.) |
780 |
26.0 |
|
Causes
of death for all ages 65 year and older |
|||
|
Rank |
Cause
of death |
Number
(thousands) |
Percent
of total |
|
|
All causes |
2,067 |
100.0 |
|
1 |
Diseases of heart |
519 |
25.1 |
|
2 |
Malignant neoplasms |
427 |
20.7 |
|
3 |
Chronic lower respiratory
diseases |
136 |
6.6 |
|
4 |
Cerebrovascular diseases |
125 |
6.1 |
|
5 |
Alzheimer disease |
120 |
5.8 |
|
6 |
Diabetes mellitus |
59 |
2.9 |
|
7 |
Accidents (unintentional
injuries) |
55 |
2.7 |
|
8 |
Influenza and pneumonia |
46 |
2.3 |
|
9 |
Nephritis, nephrotic syndrome and
nephrosis |
41 |
2.0 |
|
10 |
Parkinson disease |
31 |
1.5 |
|
|
All other causes |
503 |
24.4 |
Causes and Types To understand how and why strokes occur,
some additional information about the brain must be understood. Most of these
facts are also true of the heart.
Brain neurons are always very active and therefore need a
constant supply of energy. This energy is obtained by breaking down glucose in
processes that consume oxygen and thereby prevent the formation of lactic acid
and other harmful waste products. Flowing blood delivers the glucose and oxygen
to the brain. If the supply of glucose or oxygen drops, the brain neurons will be
injured or killed. A low oxygen supply for a few seconds will cause the neurons
to malfunction, and a very low oxygen supply for several minutes can result in
neuron death. The brain can adjust the amount of blood flow it receives by
signaling the heart to adjust cardiac output, directing blood vessels
throughout the body to adjust blood pressure, and constricting or dilating its
own blood vessels.
Blood being pumped to the brain by the left ventricle passes
first through part of the aorta and then through the arteries (carotid and
vertebral arteries) that lead up the neck and into the skull (Fig.
6.9). Blood can be felt pulsing through the carotid arteries on either side
of the neck. Branches from these ascending arteries carry blood over the
brain's surface and deep into the brain.
Strokes occur when blood flow to and through the brain is
disrupted. Because of the sudden and devastating effects on the brain, the
victim may appear to have been struck with a heavy blow, hence the name
"stroke." Since strokes affect the brain and are almost always caused
by abnormalities in the blood vessels or heart, they are also called cerebrovascular
accidents (CVAs).
The most common circulatory system problem resulting in
strokes is atherosclerosis. As in all arteries, atherosclerosis in brain
arteries reduces blood flow by causing them to become narrow, rough, and stiff.
Recall that roughness leads to thrombus and embolus formation, blocking blood
flow, and that stiffness prevents an artery from dilating when necessary (Fig.
4.7, Fig.
6.10). Blood flow to the brain can also be reduced by emboli formed on a
myocardial infarction that causes roughness of the inner lining of the heart.
Additional causes of blocked brain arteries include emboli or pieces of plaque
that break free from the wall of an artery leading to the brain. Coronary
artery disease may decrease blood flow by reducing heart functioning. Since all
these strokes prevent adequate blood flow in the brain, they are called ischemic
strokes. Ischemia means inadequate blood flow, and about
80 percent of all strokes are ischemic strokes.
Thrombus formation, narrowing, and stiffening in brain
arteries develop gradually, and there is some time for enzymes in the blood to
dissolve some of the thrombus and for blood vessels to compensate for the
reduced flow by dilating. Sometimes this restores blood flow sufficiently so
that even though neurons are injured, they survive. Additional neuron injury
occurs when blood flow is restored because the increase in O2
combined with injured cells causes an increase in free radical production and
damage. Injured neurons can repair themselves and regain their normal
functions.
Ischemic strokes from emboli tend to produce greater injury
and more neuron death because they cause blood flow to be stopped suddenly and
completely. Even if the blocked artery dilates, the embolus is likely to slide
farther along until it gets stuck at the next narrowing. Furthermore, since a
rough spot in the heart or in an artery may continue to produce emboli, many
brain regions may be affected and many strokes can occur in succession.
After a stroke, the neurons that were killed are not
replaced since neurons cannot reproduce. However, the remaining neurons may
form new dendrites and synapses to compensate for the dead neurons. The
surviving neurons may be trained to take on some of the jobs previously
performed by the killed neurons.
Atherosclerosis of brain arteries also causes strokes in
another way. Arteries weakened by atherosclerosis can rupture and bleed,
causing hemorrhagic strokes. These constitute the remaining 20
percent of all strokes. Since they are often associated with high blood
pressure, hemorrhagic strokes are also referred to as hypertensive
hemorrhagic stokes.
When an artery in the brain ruptures, the region it supplies
no longer receives adequate blood flow because some of the blood is leaking.
Neurons near the site of the rupture are injured as blood sprays on them and
pushes them apart and aside. The hemoglobin that leaks out of the red blood
cells further injures these neurons. Part of the injury is from free radicals
produced in the presence of iron in hemoglobin.
Hemorrhagic strokes cause additional brain damage because as
more blood leaks from the artery, it increases the pressure inside the skull.
This condition begins to damage neurons in all parts of the brain. The pressure
also tends to compress vessels, reducing blood flow to many parts of the brain.
If the blood pushes the brain far out of position, more neurons will be torn
and crushed and more blood vessels will be squeezed shut. Pressure within the
skull increases further when inflammation in the injured areas causes the brain
to swell, and all areas of the brain can be injured. If the brain regions
controlling the heart, respiration, or blood pressure are affected, the
victim's life is severely threatened.
Since hemorrhagic strokes can injure many parts of the
brain, they are more serious than ischemic strokes and are much more likely to
cause death. About 80 percent of all hemorrhagic strokes in people with high
blood pressure are fatal.
Signs and Symptoms Malfunctioning of the brain starts as soon
as a stroke begins. Depending on which regions are injured and the severity of
the damage, the malfunctions are apparent as any of a wide variety of signs and
symptoms. Some more common ones are tingling, numbness, and muscle weakness or
paralysis in one or more parts of the body. These alterations often occur on
only one side of the body. Other frequently encountered changes include loss of
balance or muscle coordination, altered vision, difficulty speaking, mental
confusion, and diminished or lost consciousness.
Sometimes the signs and symptoms disappear in a few seconds
or hours. Strokes of this type are called transient ischemic attacks
(TIAs) because they result from a brief decline in blood flow and
the injured neurons recover quickly. TIAs frequently occur over and over in
exactly the same way because a thrombus forms in the same place in a brain
artery. Though TIAs may appear to be unimportant, they are often followed by
more serious strokes.
The signs and symptoms of other strokes last for days or
weeks and subside very gradually, if at all. Strokes of this type are referred
to as reversible ischemic neurological deficits (RINDs)
because the brain is able to regain some of its functions.
The third type of stroke is called a completed stroke
because the signs and symptoms develop quickly and show no improvement.
Treatments
The best way
to reduce the effects of strokes is prevention. Since most strokes result from
atherosclerosis, this entails reducing the risk factors for atherosclerosis.
This process should begin as soon as possible and continue throughout one's
life (Chap. 4).
Other ways of reducing the risk of a stroke in individuals
of advanced age include reducing high blood pressure, treating blood disorders,
and avoiding exhaustion. When a person seems to be having a stroke, medical
attention should be obtained immediately to minimize possible complications.
Treatments for strokes involve reducing the risk of having
another stroke and may include medications or surgery. During and after medical
treatment, steps should be taken to provide psychological and social support
for the stroke patient and the members of his or her family. Physical therapy
and rehabilitation often help the patient improve or compensate for functions
detrimentally affected by the stroke.
Many stroke patients are disabled for the rest of their
lives. The disabilities not only adversely affect their ability to care for
their physical needs but also may impinge heavily on their self‑image,
mental health, interactions with others, and ability to support themselves
economically. The cost of treatment and care may add substantially to the
economic difficulties.
Dementia
is a broad category of diseases, all of which involve a serious decline in
memory accompanied by a major decline in at least one other mental function.
Three other criteria must be met before a person can be said to have dementia.
First, the person must be affected to such an extent that he or she has
significant difficulty carrying out normal activities and interacting with
other people. Second, these difficulties must be present on a continuing and
long‑term basis rather than sporadically. Third, they must be caused by
an identifiable physical abnormality or at least must not be caused by an
identifiable mental illness such as depression. Functions that are often
reduced in patients with dementia include abstract thinking; speaking, reading,
and writing; making judgments; solving problems; identifying common objects;
and performing simple voluntary tasks.
The number and rate of cases of dementia are increasing
because the number of older people and the proportion of the population made up
of older people are growing. In addition, since better diagnostic tests are
being developed and the social stigma attached to the diagnosis of dementia is
declining, more cases are being identified and reported. However, incidence
rates and death rates are only estimates because of
difficulty with diagnosis, and other diseases can mask the presence of
dementia. Also, dementias contribute to other causes of death, leaving cases of
dementia unreported as the cause of death.
The incidence of dementia increases with the age of a
population. The incidence rate rises exponentially, meaning the greater the
age, the faster the rate of incidence rises. Very few cases occur in people
below age 60, and less than 2 percent of all people between the ages of 60 and
65 have dementia. The percentages approximately double for every five years
above age 65, so that more than 30 percent of those over age 85 suffer from
dementia to some degree. Overall, between 16 and 24 percent of the population
over age 65 suffer from mild dementia and up to 8 percent of those over age 65
have severe dementia. Among those over age 65, the number of people with
dementia is greater than the number who have strokes. For adults, the death
rate from dementias approximately doubles with each decade of life until age
90, when the death rate begins to plateau.
There are more than 60 different types of dementia. Some
forms are reversible, including dementia caused by medications; drugs; alcohol;
anemia; malnutrition; CNS infection; malfunction of the thyroid gland or
adrenal glands; and malfunction of organs such as the liver and kidneys. Some
forms of dementia are irreversible, including the forms associated with
Alzheimer's disease and Parkinson's disease and those caused by strokes, heart
failure, repeated head injury, AIDS, and Huntington’s disease.
Some individuals have more than one type of dementia. Others
have dementia along with nervous system disorders such as delirium and depression.
As a result, a definitive diagnosis of dementia is quite difficult to obtain.
At present, cases can be diagnosed with about 90 percent accuracies.
The many causes of dementia occur as follows: 10 percent to
20 percent from atherosclerosis or, occasionally, another circulatory system
disease: at least 55 percent from Alzheimer's disease; 8 percent from
Parkinson's disease; 4 percent from head trauma; 12 percent from a mixture of
these causes; and 6 percent from other causes. Approximately 70 percent of
cases after age 60 are caused by Alzheimer's disease.
Dementia caused by circulatory disease is often called multi‑infarct
dementia because it results from having many areas of the brain die
from inadequate blood flow. Free radicals also cause damage. The amount of
infarction usually increases over an extended period because the victim has one
stroke after another or because arteries remain nearly completely blocked.
Therefore, multi‑infarct dementia becomes progressively worse. Sometimes
one large stroke will leave the patient with dementia. Since almost all cases
of multi‑infarct dementia result from atherosclerosis, taking steps to
prevent atherosclerosis reduces the risk of multi‑infarct dementia.
Alzheimer's
disease (AD) is named for
Alois Alzheimer, who first described the disease in 1907. The rate of
occurrence of Alzheimer's disease doubles every five years after age 60 up to
age 90. The earliest cases occur at about age 40. However, less than 1 percent
of those under age 65 have AD, compared with up to 20 percent of those over age
80. Overall, 10 percent to 15 percent of people over age 64 have Alzheimer's
disease, and it affects approximately 50 percent of those over age 84.
Alzheimer's disease occurs more frequently in women compared with men.
There are now four million people with AD. The number is
expected to reach nine million by AD. 2040. Alzheimer's disease is now the fourth
leading cause of death in the U.S., causing 100,000 deaths per year. AD is becoming more important, as death rates
from cardiovascular disease and strokes continue to decline, the elder
population continues to increase, and the proportion of very elderly people
increases. Older statistical tables do not list AD as a major cause of death
among older people because widespread and accurate diagnosis of AD has occurred
only in recent years. By AD. 2020, costs from AD are expected to exceed costs
from heart disease and cancer. Costs come from physicians, health care
providers, social workers and in-home care givers; diagnostic procedures and
medications; hospitalizations and nursing homes; special apparatus, diets, and
living accommodations; and loss of income and productivity. These costs bear on
families, insurance companies, and society as a whole. Non-economic costs
include social costs (e.g., disrupted family life, isolation, increased
conflicts) and personal costs (e.g., stress, fatigue, psychological detriments
such as depression and anger, reduced quality of life). These costs increase
synergistically as the disease progresses and as other disorders develop.
Types Alzheimer's
disease can be subdivided into two types. One type is early onset AD
or familial AD (FAD). Onset occurs before age 65,
usually during the sixth decade of life. The second is late onset AD
or senile dementia of the Alzheimer's type (SDAT),
with onset usually after age 60. SDAT, also called sporadic Alzheimer's
disease, is the most common form of AD.
Causes Though the
causes of most AD cases are not known, as many as 50 percent are probably
caused by genetic abnormalities since AD tends to run in families. Other
factors must be involved because when one identical twin develops AD, the other
may not develop the disease (see Genetics of AD, below). A main difficulty in
finding causes of AD is that no animals are known to develop AD or conditions
very similar to AD. Therefore, research is limited.
Some scientists propose that AD is not a disease but is part
of normal aging. They point out that all aging brains develop the same physical
changes found in brains from AD victims, though to a lesser degree. Perhaps
like other age changes, AD develops in everyone, though at different rates.
They suggest that if people lived long enough, everyone might eventually
develop AD.
Though the causes of some forms of AD remain unknown, risk
factors have been identified. The greatest risk factor is increasing age. Other
risk factors include having relatives with AD; suffering head trauma (e.g.,
boxing); being exposed to aluminum; having high blood cholesterol; having low
education; and for women, being postmenopausal. Factors that seem to reduce the
risk for AD include education; taking anti-inflammatory medications (e.g.,
steroids, ibuprofen) or folic acid supplements; smoking; and for postmenopausal
women, taking estrogen supplements.
Effects The effects of Alzheimer's disease develop in a steady and
fairly predictable sequence. At first there is a decrease in short‑term
memory. Because the change is gradual and resembles the normal decrease, it is
not uncommon for normal individuals to fear that they have Alzheimer's disease
when the ability to remember begins to decline. Conversely, individuals with
Alzheimer's disease may attribute their memory impairment to aging.
With AD, however, memory function declines to such an extent
that affected individuals have considerable difficulty performing ordinary
daily activities such as preparing food, dressing, and shopping. Patients with
AD become disoriented with respect to location and have trouble learning new
information. Early in the disease some patients begin to have trouble with
language skills such as speaking. Perhaps because of fear of some of these
changes or because of the disease itself, personality changes such as
irritability, hostility, and agitation may appear. Often affected individuals
tend to withdraw from social contact.
As AD progresses, loss of short‑term memory becomes severe
enough to dramatically decrease the ability to learn information or new skills,
solve problems, and perform the ordinary tasks of daily living or working.
Abstract thinking and making judgments become increasingly impaired. Language
functions such as speaking, reading, and writing decline. Affected individuals
become easily disoriented not only in terms of where they are but also with
regard to time and date. Confusion occurs easily and frequently. Many patients
wander away from home and become lost. Long‑term memory, including
recognizing familiar people, may also diminish.
Major personality changes that commonly accompany these more
advanced effects of Alzheimer's disease may include high levels of agitation,
paranoia, hostility, and aggressiveness. These patients may have verbal and
physical outbursts of anger or other emotions. They may strike out violently.
These changes make cooperation and acceptable interactions with others
difficult. For many people, social withdrawal becomes more intense.
By this stage affected individuals require a great deal of
care. They need to be bathed, dressed, and fed.
Their behavior must be monitored so that they do not engage in
destructive actions or wander off. Eventually the care must extend for 24 hours
a day. The changes in personality and behavioral traits caused by AD make
providing such care emotionally draining on family members. Families that
cannot provide adequate care are faced with the financial burden of paying
others to provide it. All these problems intensify as the disease progresses.
In the most advanced stages of Alzheimer's disease patients
lose essentially all memory and intelligence capabilities. Performing any task
and talking with others become impossible. Apparently, there is a complete loss
of awareness of one's surroundings. Bladder and bowel incontinence develop. The
nervous system seems to forget how to stimulate muscles so that walking,
eating, and other voluntary motions dwindle and finally cease. Curiously, long‑lasting
muscle spasms may occur. The victim becomes bedridden and paralyzed. The final
result of Alzheimer's disease is death, which is caused by complications from
immobilization. The complications may include infections of the skin and
respiratory systems, thrombus and embolus formation, malnutrition, and
respiratory failure.
Though this sequence of events occurs in most patients with
Alzheimer's disease, individual cases vary considerably. For example, changes
in personality may be the first noticeable indication that something is wrong.
In other cases, problems with speaking may occur early in the disease or not
until most of the other effects have developed.
There is also much variation in the time that passes from
the diagnosis of AD until death occurs; this period may range from 2 to 20
years. The average length of time from diagnosis to death is eight years. More
rapidly progressing and serious cases are correlated with an earlier age of
onset. Alzheimer's disease almost always progresses at a steady rate. There is
never a period of improvement.
Diagnosis Diagnosing Alzheimer's disease by observing
changes in behavior is difficult until the disease has progressed into more
advanced stages because at first these changes seem to be normal fluctuations.
Only specific tests can detect early abnormalities in mental status. Repeating
tests every few years to detect changes associated with AD may help detect AD
at earlier stages.
Making a definitive diagnosis of Alzheimer's disease remains
difficult even after the recognition of abnormal behaviors because similar
behavioral changes can be caused by many other factors (e.g., medications,
depression, altered social situations) and by other diseases of the nervous
system or other systems. Furthermore, the simultaneous presence of other types
of dementia can mask the presence of AD. Researchers continue developing other
diagnostic procedures including tests at the chemical, genetic, and cellular
through system levels. Being able to detect and diagnose AD earlier could lead
to developing effective treatments.
Eventually, after all other possible causes of the
behavioral signs and symptoms have been ruled out, a clinical diagnosis of Alzheimer's
disease can be made with an accuracy of over 90 percent. Only an autopsy
examination of the brain can determine conclusively that a person had
Alzheimer's disease.
A brain from an Alzheimer's patient can be identified because
it has two characteristics: an excessive number of senile plaques and neurofibrillar tangles (Fig.
6.12). A third important finding is a low level of the neurotransmitter
acetylcholine. These features are especially prevalent in brain areas involved
in memory. The functioning of synapses in these areas may be hampered because
the neurons produce inadequate neurotransmitter, the tangles may prevent enough
neurotransmitters from reaching the ends of the axons; and the plaques may
block transmission at synapses.
Senile plaques
(SPs) are round microscopic masses having
various mixtures and densities of materials. They are at or near synapses. SPs
usually contain a protein called beta-amyloid (β-A),
dead neurons and neuroglia cells, pieces of synapses, and fibrous material
called neurofibrillar tangles
(NTs) (Fig.
6.12). Neurofibrillar tangles are composed of one
or two protein fibers twisted into a helix. Much of the protein is tau
protein (τ-protein). NTs also contain other
materials including enzymes, inflammatory molecules, β-A, a lipoprotein
called apolipoprotein E (APOE), and
carbohydrate/protein complexes. NTs also form in neuron cell bodies, axons, and
dendrites.
SPs and NTs appear first in the hippocampus region, which is
near the center and bottom of the cerebral hemispheres. The hippocampus has a
major role in memory functions. Later, SPs and NTs appear in wider areas near
the bottom of the hemispheres. Later still they appear in upper regions of the
cerebral cortex. Eventually, all regions of the cerebral cortex develop SPs and
NTs. Neuron connections to the nucleus of Meynert
also develop many SPs and NTs, and SPs form in the cerebellum. The final
distribution of SPs and NTs in brain areas corresponds to the sequence in which
they appear. Areas showing SPs and NTs first developing the highest densities
of them.
As SPs and NTS form, neurons are damaged and die, and
synapses are destroyed. Scientists do not know if SPs and NTs form and then
cause damage to neurons or if neurons damage occurs first, causing SPs and NTs
to develop. Neurons that interconnect other neurons (i.e., association neurons)
are affected much more than sensory neurons and motor neurons.
As AD progresses, brain vessels also change. Small vessels
accumulate much β-A in their middle layer. Vessels become twisted,
shrunken and broken, which reduces blood flow in the brain. The cerebral
hemispheres shrink dramatically (Fig.
6.11). Some scientists believe that reduction in blood flow causes the SPs,
NTs, and other neuronal and synaptic changes in the AD brain.
Beta-amyloid Many cells in the body produce amyloid protein.
There are more than 10 types of amyloid protein. The type called β-amyloid
(β-A) is found in AD. Its function is unknown. Beta-amyloid may be
produced by neurons and by blood vessels. It is produced when an enzyme breaks
a protein called amyloid precursor protein (APP),
which extends across cell membranes. Breaking normal APP produces a small
amount of soluble short β-A. In AD, APP is abnormal. When it is broken by
enzymes, much abnormal long β-A is produced and released from the cell
membrane.
The abnormal "sticky" β-A binds easily to APOE
and to τ-protein, forming many SPs quickly. The abnormal β-A
increases free radicals, inflammation, cell membrane damage, and neuron
apoptosis. Excess glycation of proteins also occurs. All these processes seem
to promote each other synergistically. Finally, APP itself binds to
τ-protein and to APOE, suggesting that it can contribute to the formation
of NTs and SPs.
The causes, method of formation, sources of β-A and
NTs, and sequence in which these materials are deposited are unknown.
Tau protein Brain cells produce other proteins called tau proteins
(τ-proteins). Their functions are unknown, though they seem
to promote microtubule formation. The brain contains at least six types of
τ-protein, and their proportions vary from childhood through adulthood.
Abnormal modifications of τ-proteins (e.g., glycation, adding phosphate
groups) cause τ-proteins to help form NTs.
APOE Many cells produce apolipoprotein E (e.g., brain, liver,
adrenals). Most brain APOE comes from neuroglia cells and macrophages. Though
neurons do not produce APOE, it enters them. APOE helps move cholesterol and
other lipoproteins from cell to cell and through cell membranes. APOE also
seems to help in neuron development and repair.
Brain APOE has different forms including APOE-ε3 and APOE-ε4.
APOE-ε4 seems to promote the formation of SPs and NTs. The mechanisms are
not clear, but they may involve disruption of neuron membranes; formation of
free radicals; excess accumulation of β-A; and the formation of abnormal
microtubules in neurons. Interactions between the β-A and the abnormal
microtubules seem to result in SPs and NTs.
Presenilins The last groups of brain proteins to mention are the presenilins. Two important forms of
presenilin in the brain are presenilin-1 (PS-1) and
presenilin-2 (PS-2), which are membrane proteins.
Their functions are unknown.
In summary, AD may be caused by or promoted by abnormal
protein formation; chronic inflammation; inadequate blood flow; free radical
damage from brain proteins, metal ions, damaged endothelium, or
neurotransmitters; decreased *FR defenses; mitochondrial malfunctioning;
reduced insulin sensitivity; immune responses; or abnormal apoptosis of
neurons. Regardless of the causes or mechanisms, the results are the same; too
many SPs, too many NTs, too much neuron death, and too much loss of synapses.
Genetics of AD There are several genes that promote different types of AD.
Though these genes are in different chromosomal locations, have effects at
different ages, and may act by different mechanisms, they all produce the same
outcomes in the brain and the same manifestations of AD. Some genes that
promote or modify AD have not been identified. One or more of these genes may
contribute to a form of AD that begins after age 70. These latter genes may be
on chromosomes 12 or 3.
Three genes for one type of familial Alzheimer's disease
(FAD) are on chromosomes 21. The mutated forms of the genes cause
the production of abnormal "sticky" ß-amyloid, resulting in 7 percent
of AD cases and 25 percent of FAD cases. Age of onset is between ages 45 and
65, with most cases developing before age 60. The mutations are present in
approximately 19 families. An individual with only one copy of one of the
mutated genes has a 100 percent chance of developing AD because each mutated
gene is a dominant gene.
Certain forms of a gene on chromosome 19
promote SDAT. The gene has three forms (i.e., three alleles), each of which
contains the genetic information for producing APOE-ε. One
form codes for APOE-ε4, one form
for APOE-ε3, and one for APOE-ε2. Since a
person has two copies of chromosome 19, each person has two of these genes. The
pair of genes may be in any combination (i.e., ε4:ε4,
ε4:ε3, ε4:ε2, ε3:ε3, ε3:ε2, ε2:ε2).
In the general population, the genes are found in the proportion ε4:ε3:ε2::14:78:8.
The genes are codominant, meaning that each produces its
form of APOE-ε regardless of which other forms of the gene are present.
Having two ε4 genes provides the highest risk from APOE genes and makes
the AD occur at earlier ages. The risk for developing AD is eight times higher
in people with two ε4 genes than in people with two ε2 genes.
However, people with two ε4 genes do not always get AD.
The different combinations of APOE-ε genes provide
decreasing risk of getting AD and increasing average age of onset in the order ε4:ε4 (age 68), ε4:ε3 (age 71), ε3:ε3
(age 74). Still, age of onset shows great variability with any of these
combinations. Very few people with even one ε2 gene develop AD.
The APOE-ε gene influences other problems. Having an ε4
gene increases the age-related decline in cognitive functions even if AD does
not develop. The ε4 gene also promotes amyloid formation in blood vessels,
so people with the ε4 gene are at higher risk for developing
atherosclerosis. Having an ε2 gene reduces the risk of atherosclerosis.
Chromosome 14
has the gene for PS-1, and chromosome 1 has the gene for PS-2.
Nearly 50 percent of
FAD cases are associated either with mutations in the APP gene on
chromosome 21 or a presenilin gene. Nearly 70 percent of cases of FAD are
associated with mutations in the PS genes. Mutations in either presenilin gene
increase the risk of developing AD, apparently because abnormal PS-1 and
abnormal PS-2 increase the production of "sticky" β-A.
The PS-1 mutation is known to occur in nearly 50 families.
The PS-2 mutation is known to occur in descendants from certain German families
(i.e., Volga Germans). For people with the PS-1 mutation, average age of onset
is in the fifth decade, but cases develop as early as age 30. The PS-1 mutation
also promotes late onset SDAT. For people with the PS-2 mutation, the average
age of onset is higher than with the PS-1 mutation, but onset may occur before
age 30.
Treatments There are no effective treatments to slow,
stop, or reverse the effects of Alzheimer's disease. Therapies being
investigated include antioxidant supplements; anti-inflammatory drugs;
medications that increase brain acetylcholine (e.g., tacrine); medications that
slow atherosclerosis or reduce blood clotting; and for women, estrogen
supplements. Until effective treatments are found, all that can be done is
reduce the signs and symptoms and maintain as much functioning as possible. In
the early stages of the disease memory aids such as notes and verbal reminders
help. Various medications can alleviate the behavioral and psychological
problems. Maintaining social contacts and providing emotional support for the
patient and his or her families are important components in a complete
treatment program.
As the disease progresses, outside help from support groups
and social agencies is usually required. Day care centers can relieve the
burden of full‑time care by family members. Attention must be paid to
preventing complications such as malnutrition and infections. Finally, full‑time
institutionalization may be necessary.
Though the incidence of Parkinson's disease is
less than half that of strokes or Alzheimer's disease, it remains a leading
disease of the nervous system among older Americans. Its rate of occurrence is
extremely low before age 50, but the rate increases gradually after that until
about age 75; after that age it diminishes steadily. About 2 percent of those
over age 50 will develop Parkinson's disease. This disease occurs with equal
frequency in men and in women and among people of different races.
Causes The cause of true, or primary,
Parkinson's disease is unknown, and it does not tend to run in
families. Scientists suspect the involvement of free radicals and reduced blood
flow. Many cases of what appear to be Parkinson's disease actually result from
abnormalities such as CNS infections, atherosclerosis, brain tumors or other
brain diseases, head injury, toxins, and medications. These cases are called secondary
parkinsonism.
Effects The development of Parkinson’s disease is shown primarily by
changes in the control of muscle contractions. These changes usually occur in the
same sequence. At first, ongoing movements of the fingers and hands occur. The
movements of the fingers give the appearance that the victim is rolling pills
between the fingers. (Suggestion:
Chap 06 - 146-1-3)
Tremors of the hand, arm, and leg muscles often develop
next. The movements are rhythmic, with alternating contractions between muscles
that bend the joints and muscles that straighten them. Four to eight
contractions occur each second. The tremors are greatest when the person is
awake but resting. They diminish during voluntary movements and stop when the
patient falls asleep.
Further progress of the disease causes muscle stiffness and
difficulty moving rapidly and smoothly. As control of muscle contraction
diminishes further, the patient may find it impossible to complete a motion
once it has been started. For example, a person who is walking may suddenly
stop in the middle of taking a step. Ordinary motions occur ever more slowly.
Performing ordinary tasks and job‑related activities becomes difficult or
impossible.
As normal contractions of muscles continue to diminish,
facial expressions disappear. The voice becomes soft and loses inflection.
Weaker, slower, and fewer contractions of leg, trunk, and arm muscles cause
walking to occur more slowly and with shuffling of the feet, a stooped posture,
and little swinging of the arms. Muscle contractions for swallowing and
breathing also weaken and slow.
Declining muscle control and muscle activity causes
drooling. Constipation is not uncommon because patients are less active and
have weaker contraction of the abdominal muscles that normally help with bowel
movements.
Gradually, coordination of muscles declines to such an
extent that the person has trouble with balance. Not only do these patients
tend to fall more frequently, they make little or no effort to slow or stop
themselves as they are falling.
Parkinson's disease often produces effects other than those
involving control of muscles. During the night, patients tend to wake up and
have difficulty going back to sleep. They become restless and begin to wander
about. Because of declining muscle coordination and balance, they are at great
risk of physical injury from falls. The interrupted sleep also causes these
patients to be sleepy during the day.
Psychological changes may begin at any stage in the disease.
Many patients experience depression, loss of interest in activities, and other
mood changes. These psychological alterations seem to be caused partly by the
disease itself and partly by the awareness of its effects. Reductions in very
short-term memory are common. Parkinson's disease causes dementia in over 15
percent of patients.
While the sequence of changes caused by Parkinson's disease
is fairly regular and progresses steadily, the rate of change varies greatly
from one person to another. A few cases reach extreme conditions in as few as
five years, although most cases progress more slowly, so that severe disability
is delayed for many years.
Nervous System Changes The mechanism by
which Parkinson's disease affects muscle control is fairly clear. Recall that
impulses controlling voluntary movements are modified as they descend through
the somatic motor pathway. Some areas of modification are in the basal ganglia
inside the cerebral hemispheres (Fig.
6.7). The normal impulse modifications occurring in the basal ganglia
actually result from the interplay among several neurotransmitters in the basal
ganglia. Acetylcholine tends to increase the impulses and thus increases muscle
contractions. Dopamine (DOPA) and another
neurotransmitter (gamma‑aminobutyric acid) tend to dampen the impulses
and the movements they cause.
In Parkinson's disease a major decline in the amount of DOPA
in the basal ganglia creates an imbalance among the antagonistic transmitters.
This imbalance causes impulses and the muscle contractions they produce to
become excessive and uncontrolled. Hence, muscle contractions occur.
Neurotransmitter imbalances also cause the other effects of this disease.
Diagnosis Parkinson's disease is accompanied by a
decrease in certain CNS chemicals that are used by the brain to manufacture
dopamine. Dopamine is a neurotransmitter that is present in inadequate amounts
in patients with Parkinson's disease. Because this and the other effects of the
disease are somewhat different from those of other diseases and the effects
develop in a fairly regular sequence, Parkinson's disease can be diagnosed
accurately.
Treatments There is no cure for Parkinson's disease and
no way to slow its progress. However, its effects can be greatly diminished by
administering levodopa because this chemical
boosts brain production of DOPA. Dosages must be carefully monitored and
adjusted during the disease to minimize adverse side effects such as increased
uncontrolled movements. Since increasing the level of DOPA seems to be so
important, attempts have been made to implant into the brains of Parkinson's
disease patients’ tissues that produce DOPA. Pieces of adrenal medulla and
pieces of brain regions from aborted human fetuses have been used. Transplants
of adrenal medulla have not yet produced satisfactory results. However,
experiments using fetal brain tissue have resulted in dramatic and long‑term
improvements in muscle control in individuals having severe cases of Parkinson's
disease. As the controversial and experimental techniques employing fetal brain
tissue improve and become more standardized, they may gain widespread
acceptance and use.
Other medications can relieve certain signs and symptoms
sometimes. However, the specific types and amounts of substances used to treat
Parkinson's disease vary from case to case because individuals have such varied
responses to these medications and because their responses change as the
disease progresses.
Besides medications, treatment of Parkinson's disease should
include physical therapy to help sustain the movements used in ordinary tasks
and in the patient's occupation. Speech therapy and psychological support are
also important components of a treatment plan.
Dementia with Lewy bodies is a newly classified type of age-related dementia. It has
been identified in nearly 20 percent of the brains from people who died after
developing any dementia. Lewy bodies are round masses of clumped microfilaments
in neurons. They occur in all areas of the brain. (Fig.
6.14) This type of dementia also shows amyloid deposits.
© C©
Copyright 2020: Augustine G. DiGiovanna, Ph.D.,
Salisbury University, Maryland
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