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BRAIN PARTS AND STUFF

Amygdala
The amygdala is a small structure lying in the medial temporal lobe which is important for the emotional
content of new memories.

Basal Forebrain
The basal forebrain is a term for a group of structures that lie near the bottom of the front of the brain,
including the nucleus basalis, diagonal band, medial septum and substantia innominata. These
structures are important in the production of a brain chemical called acetylcholine, which is then
distributed widely throughout the brain. Acetylcholine affects the ability of brain cells to transmit
information to one another, and also encourages plasticity, or learning. Thus, damage to the basal
forebrain can reduce the amount of acetylcholine in the brain and impair learning. This may be one
reason why basal forebrain damage can result in memory impairments such as amnesia and
confabulation. One common cause of basal forebrain damage is aneurysm of the anterior communicating
artery.

Cerebellum
The cerebellum is the portion of the brain which lies behind and under the cerebral cortex. It is involved
in fine control and coordination of skeletal muscles. It plays an important role in movements which
require careful timing and interaction of many muscles: maintaining posture, walking, eating, playing
musical instruments, tracking movements with the eyes, etc.. Individuals with cerebellar damage may still
be able to walk, gesture and eat, but the movements may appear difficult and clumsy.

Cerebral Cortex/Cortex

Technically, a cortex is an outer layer of an organ; thus, there is a cerebral cortex (in the brain) as well
as an adrenal cortex (the outer layer of the adrenal gland), a renal cortex (the outer layer of the kidney),
and so on. However, in cmmon parlance, cortex is usually taken as a shorthand for cerebral cortex.
Likewise, the adjective cortical usually refers to the cerebral cortex. The cerebral cortex forms the outer
layer of the brain, including its recognizable gray, wrinkled surface. The gray substance is actually the
cell bodies of nerve cells, or neurons; underneath lies the so-called white matter, formed of the output
processes (axons) of these neurons. The wrinkled surface reflects the fact that, in humans and other
primates, the brain has grown at a faster rate than the skull, and so the surface of the brain is folded to fit
inside the skull. If the human cortex were smoothed out, it would appear as a sheet about the size of a
tabloid newspaper, about 3 millimeters thick.

The cerebral cortex has left and right halves which, to a first approximation are mirror images of each
other. In most cases, structures which appear on the left side (or hemisphere) have an analogous
structure on the right side (or hemisphere). There are a few exceptions: notably, areas of the left
hemisphere are specialized for language processing in most right-handed people. In general, sensory
information from the left side of the body is processed in the right hemisphere, and vice versa; motor
commands to the left side of the body also originate from the right hemisphere, and vice versa. The
cortex is often divided into large regions, called lobes, based on anatomical structure and also on
function. These include the frontal lobes, the parietal lobes, the occipital lobes and the temporal lobes.

Frontal Lobes
The frontal lobes lie at the front of the brain. They contain brain structures that are important for
executive functions, such as planning, judgment and self-control. The frontal lobes are also involved in
motor control, including the ability to form speech.
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Parietal Lobes
The parietal lobes lie at the top of the brain, on each side of the midline. They contain brain structures
that are involved in processing sensory information, such as where on the surface of the body a touch
stimulus occurred.

Occipital Lobes
The occipital lobes lie at the rear of the brain, above the cerebellum. They contain brain areas which are
important for visual processing.

Temporal Lobes
The temporal lobes of the brain are located on each side of the brain. They are so-named because they
lie under the temples. They contain brain areas which are important for auditory processing, including the
ability to understand spoken words. They also contain structures such as the hippocampus which are
important for new memory formation.

Dementia
Dementia is a broad term that refers to a progressive cognitive decline, especially marked by memory
deficit. The symptoms may include memory deficits, impaired abstract thinking, poor judgment,
disorientation, depression, agitation and nervousness, and sleep disorders. In the late stages of the
disease, patients become dependent on caregivers for the activities of daily living, including eating,
dressing and bathing. Dementia itself is not directly fatal, but patients may die of complications
associated with immobility or reduced resistance to infectious diseases such as pneumonia.
Alzheimers disease is the most prevalent type of dementia. Dementia may also be caused indirectly by
brain tumors, head injury, viral inflammation, substance abuse, syphilis, long-term epilepsy, etc.
Dementia is also a component of the late stages of Parkinsons disease, Huntingtons disease and AIDS,
and may also appear in individuals who are chronic abusers of alcohol. In some cases (e.g. Alzheimers
disease), symptoms progress gradually over a course of years; in others (e.g. vascular dementia),
symptoms appear over a relatively short period of time and may appear to worsen in increments.
Normally, when a patient is diagnosed with dementia, doctors first attempt to establish whether the
dementia is associated with some pre-existing disease or condition such as Parkinsons disease or
substance abuse, or with some trauma such as head injury or stroke. Other conditions such as
depression and sleep disorder can also cause memory deficits and other cognitive problems superficially
related to dementia. A diagnosis of probable Alzheimers disease is only made after other causes of
dementia are ruled out, while a definite diagnosis of Alzheimers disease can only be made at autopsy.

Hippocampus
The hippocampus is a brain structure which lies under the medial temporal lobe, one on each side of the
brain. It is sometimes grouped with other nearby structures including the dentate gyrus and called the
hippocampal formation. The hippocampus is critical for the formation of new autobiographical and fact
memories. It may function as a memory gateway through which new memories must pass before
entering permanent storage in the brain. Hippocampal damage can result in anterograde amnesia: loss
of ability to form new memories, although older memories may be safe. Thus, someone who sustains an
injury to the hippocampus may have good memory of his childhood and the years before the injury, but
relatively little memory for anything that happened since. Some memories, such as the memory for new
skills or habits, can sometimes be formed even without the hippocampus. A current research area is to
determine exactly what kinds of learning and memory can survive hippocampal damage, and how these
kinds of learning can be used to guide rehabilitation.
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The hippocampus is especially sensitive to global reductions in oxygen level in the body. Thus, periods of
oxygen deprivation (hypoxia) which are not fatal may nonetheless result in particular damage to the
hippocampus. This could occur during a heart attack, respiratory failure, sleep apnea, carbon monoxide
poisoning, near-drowning, etc. The hippocampus is also a common focus site in epilepsy, and can be
damaged through chronic seizures. It is also sometimes damaged in diseases such as herpes
encephalitis, and is one of the first brain areas to show damage in Alzheimers disease.

Huntingtons Disease
Huntingtons Disease is a motor disease, in which patients develop involuntary dance-like movements.
It is an inherited disease, which means that if a parent passes the appropriate gene to a child, that child
will eventually develop the disease. Huntingtons disease results from degeneration of a brain area
known as the basal ganglia, which is important in generating voluntary movements. Early in the course of
the disease, patients may also show emotional problems, typically fits of depression or irritability. Later in
the disease, subcortical dementia occurs. (In some cases, though, memory loss is among the earliest of
symptoms.) There is no cure and no good treatment; tranquilizers may be used to control the involuntary
movements and alleviate depression, but they cannot reverse the disease nor stop mental deterioration.

Parkinsons Disease
Parkinsons Disease is a progressive neurological disease involving deterioration of neurons in a region
of the brain called the substantia nigra. The causes are unknown. It is named after James Parkinson
(1755-1824), an English neurologist who studied the disease. Symptoms include a tremor in muscles
that are at rest, rigidity in movement, and problems maintaining posture. The onset of these symptoms is
usually gradual, and patients may go for a long time without appreciable worsening. Symptoms are
usually intermittent in the early stages of the disease, but may become continual late in the course of the
disease. In late stages, the face becomes expressionless, eye blinking is infrequent, speech is slow, and
the patient may find it difficult to stand upright without falling. Drugs such as levodopa (trade name
Sinemet) can often combat these symptoms for a long time, but the substantia nigra continues to
degrade and drugs eventually become ineffective.
Approximately 25%-30% of Parkinsons patients develop dementia. It is not known whether this is a side
effect of the disease, or whether these patients are coincidentally more susceptible to develop
Alzheimers disease.

Korsakoffs Disease
Korsakoffs disease is a brain disorder which is named after Sergei Korsakoff (1854-1900), a Russian
neurologist who first described the disease. It arises from a dietary deficiency of thiamin (Vitamin B-1),
which the body uses to convert carbohydrates into energy. Over time, thiamin deficiency can cause
damage to several brain areas critical for memory: including the thalamus, mammillary bodies and basal
forebrain. In rare cases, this damage culminates in Korsakoffs disease.
A common cause of Korsakoffs disease is alcoholism. Alcohol interferes with the bodys ability to
metabolize thiamin; additionally, alcoholic individuals tend to have poor diets, further reducing intake of
thiamin. Individuals with Korsakoffs disease tend to show general intelligence which is just as good as
chronic alcoholics without the disease - which is to say, slightly impaired but not abnormal. Attention may
also survive quite well. However, Korsakoffs disease can include both anterograde amnesia (loss of
ability to form new memories) and retrograde amnesia (disruption of pre-existing memories). One
interesting aspect of Korsakoffs disease is that patients become unable to use time relationships: thus,
asked about his autobiography, a Korsakoffs patient may report serving in the army before entering high
school. Both recollections may be correct, but their ordering is wrong, and the patient may be unable to
perceive the error.
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Although Korsakoffs patients may show severe memory deficits, they tend also to show other
impairments associated with chronic alcoholism, including disorientation for time and place, apathy, and
emotional blandness broken by sudden, momentary irritability, anger or pleasure. Thus, if a Korsakoffs
patient performs poorly on a particular neuropsychological test, it is difficult to assess whether this poor
performance reflects a true deficit or merely a lack of attention during the test-taking. For this reason,
many researchers studying anterograde amnesia prefer not to lump Korsakoffs patients together with
other patients who sustained more localized memory impairments as a result of stroke or other injury.
Some improvement can be seen in Korsakoffs patients given thiamin replacement early in the course of
the disease, but most patients who develop serious symptoms (e.g. amnesia) do not regain enough
capacity to allow independent living. While the non-memory symptoms of the disease often improve
following thiamin treatment, the amnesia typically does not.

MEMORY
Memory refers to the storage, retention and recall of information including past experiences, knowledge
and thoughts. Memory for specific information can vary greatly according to the individual and the
individuals state of mind. It can also vary according to the content of the information itself; thus
information which is novel or exciting tends to be better remembered than information which is
uninteresting or ordinary. Failure of memory can normally result from failure to adequately store the
memory in the first place, failure to retain the information (forgetting), and failure to retrieve the
information later.
The precise biological mechanisms of memory are not fully understood, but most scientists believe that
memory results from changes in connections or connection strengths between neurons in the brain. One
possible mechanism is long-term potentiation (LTP). Roughly stated, LTP refers to a process whereby if
two neurons are usually active together, the connection between them will be strengthened; over time,
this means that activity in one neuron will tend to produce activity in the other neuron.

Categories of Memory Systems

Psychologists and memory researchers often divide memory into categories defined by the duration for
which the memory is expected to last.
Sensory memory refers to the fact that, after experiencing a stimulus, information about that stimulus is
briefly held in memory in the exact form it was received, until it can be further processed. Typically,
sensory memories may last only a few seconds before decayingor being overwritten by new, incoming
information. But, while they last, sensory memories contains detailed information: almost like an internal
copy of the stimulus, in perfect detail. For example, psychologists have assumed that there is a
memory area (called a buffer) where incoming visual information is stored as a picture or icon. This is
sometimes called iconic memory. While visual information remains in iconic memory, an individual can
answer detailed questions, such as what is the third row of numbers in a numerical display.
Psychologists have assumed that there is also an echoic memory for auditory information (stored as an
echo) and other buffers for information related to the other senses: taste, smell and touch.
Short-term memory refers to memories which last for a few minutes. Unlike sensory memory, which is
stored in the exact form it was experienced, short-term memory has received some processing; thus, A
is stored not as a visual stimulus, but as an abstract concept of the letter A.
Short-term memory is of limited capacity, usually 5-9 items (7-plus-or-minus-two). Beyond this capacity,
new information can bump out other items from short-term memory. This is one form of forgetting.
Objects in short-term memory can be of indefinite complexity: thus short-term memory can hold several
numbers, or several words, or several complex concepts simultaneously. Thus, while an individual may
only be able to remember seven random digits, it may be possible to remember more digits if they are
chunked into meaningful objects: thus, 1776-2001-1941 represents twelve separate digitswell
beyond most peoples capacitybut only three easily-remembered chunks. Items can be maintained
indefinitely in short-term memory by rehearsal: e.g. by repeating the information over and over again.
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An example would be a seven-digit phone number, which is maintained in short-term memory by
repetition until the number is dialed, and then fades from short-term memory once the conversation
starts. Repetition may also increase the probability that items in short-term memory will enter permanent
storage in long-term memory. Intermediate-term or working memory is sometimes considered a
synonym for short-term memory.
However, memory researchers often consider this a specialized term referring for information about the
current task. Thus, even though a specific phone number may occupy short-term memory, working
memory contains the information that lets you remember that you are in the process of phoning the gas
company to complain about a recent billing error. Long-term memory is memory that lasts for years or
longer. It contains everything we know about the world, including semantic and factual information as
well as autobiographical experience. In general, long-term memory is organized so that it is easy to
reach a stored item by a number of routes. For example, the concept umbrella may be retrieved by
seeing an umbrella, experiencing a rainstorm, hearing the words to the song Let a smile be your
umbrella, and so on.
Retrieval of an item also facilitates other related items: so that retrieving information about a cat can lead
to retrieval of information about dogs, lions, specific instances of cats (Grandmothers tabby), the
Cheshire Cat from Alice in Wonderland, and so on.
NOTE: Clinicians (e.g. neurologists) often use a slightly different classification, in which short-term
memory is memory for events which occurred recently (e.g. a few days or weeks ago) and long-term
memory is memory for events which occurred in the distant past (e.g. childhood).

Kinds of Long-term Memory

There are several different ways to classify long-term memories according to their content. Declarative
memory is a term for information which is available to conscious recollection and verbal retrieval (i.e., it
can be declared). Two subclasses of declarative memory are episodic memory, which is
autobiographical information, and semantic memory, which is factual information about the world
(vocabulary items, knowledge of what a hammer is used for, memory of multiplication tables, etc.).

Brain Structures involved in Long-Term Memory

Most types of memory appear to be stored in the cortex. Different areas of cortex specialize in different
kinds of information, so that visual information about the Statue of Liberty may be stored in one location
(e.g., the inferior temporal cortex), while information about its associations to liberty and immigration
might be stored in another (e.g., the frontal cortex). High linkage between these two areas means that
seeing a picture of the Statue of Liberty can retrieve memory about its associations. At the same time,
damage to specific areas of cortex can produce specific memory deficits. For example, damage to a
specific region within the temporal lobe can produce a memory deficit in which the patient loses
knowledge about living things (e.g. dogs, lions, birds) but maintains knowledge about other categories
(e.g. inanimate objects such as furniture and utensils).
Formation of new declarative memories depends on the hippocampus and related structures in the
medial temporal lobe. When these structures are damaged, a condition of anterograde amnesia can
result, in which older declarative memories are largely spared, but few if any new declarative memories
are acquired. At this point, the process whereby the hippocampus and other medial temporal lobe
structures contribute to long-term memory formation is still incompletely understood. Some researchers
believe that the hippocampus acts as a temporary store for new information, which is then gradually
transferred to permanent storage in the cortex. Other researchers believe that the hippocampus never
actually stores information itself, but is needed by the cortex in the process of devel ping new memories.
Another important structure is the amygdala, which lies near the hippocampus in the medial temporal
lobes. The amygdala is critically involved in emotional memory; an individual with damage to the
amygdala may remember the details of a traumatic (or joyful) event but not the emotional content of that
event.
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Pathology of Memory
Memory can be impaired by various injuries and diseases. Damage to the medial temporal lobe and
hippocampus can devastate the ability to acquire new declarative memory; damage to the storage areas
in cortex can disrupt retrieval of old memories and interfere with acquisition of new memoriessimply
because there is nowhere to put them.
Another critical factor is attention. Items are more likely to be remembered if they are attended to in the
first place; this is why novel or exciting items are more likely to be remembered than dull or ordinary
ones. Damage to the frontal lobes, which disrupts attention, may affect memory.
Various psychiatric disorders such as paranoia and schizophrenia may affect memory adversely, either
by disrupting attention or by disrupting the biological bases of memory, or both. Alzheimers disease
causes memory impairments from the early stages, probably because of cell death in the basal forebrain,
an area that produces the chemical acetylcholine which facilitates plasticity (learning). Recent memories
tend to be poorly remembered, while there may be good memory for long-ago events.
Other conditions such as viral infections, depression and use of drugs (including medication) can affect
memory by disrupting brain chemicals as well. Although a mild memory impairment is a common feature
of old age, there is currently much debate over whether memory loss is inevitable with aging, or whether
it is a by-product of conditions (such as Alzheimers disease and cardiovascular disease) which are more
common in old age than in youth. (See also: Age-associated Memory Impairment.)

AMNESIA
Posttraumatic Amnesia
Posttraumatic amnesia is a memory disruption following injury, such as a blow to the head. Often, the
injury leads to a period of coma (unconsciousness) which can last a few seconds or minutes or, in severe
cases, can last weeks. When consciousness is recovered, the patient typically experiences a period of
confusion. When the confusion clears, testing may reveal that the patient has a permanent retrograde
amnesia for the events leading up to the injury and a permanent anterograde amnesia for events which
followed the injury (e.g. during the period of confusion). The window of amnesia may be limited to a few
minutes before and after the injury, or may be more extensive. Outside this window, memory for prior and
subsequent events is normal.
Psychogenic Amnesia
Fugue State, Dissociative Amnesia

Psychogenic amnesia (also called functional amnesia) is a form of amnesia which occurs in otherwise
healthy peoplei.e., it is not the result of a brain injury. It involves loss of important personal information.
Another term for this condition is functional amnesia.
In one form of psychogenic amnesia, called fugue state, individuals may forget not only their pasts but
their very identities. Despite the many Hollywood movies depicting this phenomenon, fugue state is
extremely rare in real life. Fugue state normally resolves with time, particularly with the help of therapy.
A more common form of psychogenic amnesia is dissociative amnesia. In this state, an individual may
experience memory loss which is restricted to a particular period of time, such as the duration of a violent
crime. This memory loss is too extensive to be explained by ordinary forgetting, and instead may reflect
the fact that the information is too stressful or traumatic to be remembered. Dissociative amnesia is a
psychological phenomenon, rather than a physiological one, and may often be resolved with the help of
therapy.
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Retrograde Amnesia
Retrograde amnesia is a form of amnesia resulting from brain injury in which the individual loses
memories for the time period just prior to the injury. This time period may stretch from a few minutes to
several years, and typically it is worst for event which occurred just before the injury.
Very rarely, there have been reported cases in which an individual sustains pure retrograde amnesia as a
result of a physical brain injury. More often, retrograde amnesia occurs in an individual who also has
anterograde amnesia. In this case, the individual will have near total loss of memory for events occurring
after the injury, and some loss of memory for events which occurred before the injury.

Anterograde Amnesia
Anterograde amnesia is a selective memory deficit, resulting from brain injury, in which the individual is
severely impaired in learning new information. Memories for events that occurred before the injury may
be largely spared, but events that occurred since the injury may be lost. In practice, this means that an
individual with amnesia may have good memory for childhood and for the years before the injury, but
may remember little or nothing from the years since. Short-term memory is generally spared, which
means that the individual may be able to carry on a conversation; but as soon as he is distracted, the
memory of the conversation fades.

It is now becoming apparent that while anterograde amnesia devastates memory for facts or events, it
may spare memory for skills or habits. Thus, an individual with amnesia can be taught a new skill, such
as how to play a game or how to write backwards. The next day, the amnesic individual will claim to have
no memory of the prior session, but when asked to try executing the skill, can often perform quite well -
indicating that some memories have been formed. It is an important area of current research to
document exactly which kinds of memory can be formed in amnesia, and how this may be used to help
rehabilitate amnesic individuals.
Anterograde amnesia can occur following damage to at least three distinct brain areas. The first, and
most well-studied, is the hippocampus and associated areas in the medial temporal lobes of the brain.
The hippocampus seems to act as a gateway through which new fact information must pass before
being permanently stored in memory. If it is damaged, no new information can enter memory - although
older information which has already passed through the gateway may be safe.
Damage to the hippocampus (and medial temporal lobes) can occur following stroke or aneurysm to one
of the arteries which supplies blood to these areas, as well as following epilepsy, encephalitis, hypoxia,
carbon monoxide poisoning, near-drowning or near-suffocation, and the earliest stages of Alzheimers
disease. Some damage to the hippocampus also occurs in the course of normal aging.
Anterograde amnesia can also occur following damage to the basal forebrain, a group of structures
which produce acetylcholine, a chemical which helps cells in the brain store new information during
learning. The basal forebrain can be damaged by aneurysm of the anterior communicating artery, which
supplies blood to the basal forebrain.
Finally, anterograde amnesia can sometimes occur following damage to the diencephalon - a set of
structures deep in the brain including the medial thalamic nuclei. Currently, there is no good
understanding of why damage to these brain areas should sometimes result in a selective memory deficit
such as amnesia. Korsakoffs disease is a syndrome which can damage the diencephalon and cause
anterograde amnesia.

Dementia
Dementia is a cognitive disorder that includes both deterioration of intellectual ability and
alterations in the persons emotional and personality functions. Alzheimers disease, vascular
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dementia, general medical conditions (brain tumors, brain trauma, metabolic disorders, kidney,
liver, heart, or lung disoders) or multiple etiologies all cause dementia.
A neurologist and a psychiatrist should closely follow persons with this disorder. Medication is
often needed to reduce agitation and assist in controlling acting out behavior and wondering.
Confusion is common in dementia as is psychotic behaviors. While dementia patients can
become floridly psychotic, illusions, paranoia, and agitation are most common.
Often a very small dosage of Neuroleptic is useful to control agitation and psychosis.
Often, a consultation will be arranged with a neuropsychologist who will continue to follow the
patient. It is the job of the neuropsychologist to monitor the mental status of the patient. Often,
baseline tests are conducted to monitor change in mental status over time. It is also imperative
to monitor and control the patients environment so as not to ad to their confusion. The patients
room should have a large calendar in a primary location. A sign identifying the patients current
location (e.g., such and such hospital, this is Donnas room in the harbor manner nursing home,
etc.) helpful. Items the patient is familiar with should be available. Keeping a stable and
consistent environment will help to minimize confusion and agitation.
Dementia is usual a chronic and progressive disorder. Alzheimers is usually evenly progressive
over time, while vascular dementias are often stepwise. In Alzheimers, the patients family may
not notice changes for a long time. However, when asked to think back, they can usually identify
significant changes in memory or personality that they chose to ignore, or chalk up to old age.
Alzheimers has an insidious course, beginning with memory loss, confusion and personality
changes and eventually leading to death. After the first signs of Alzheimers are identified, a
patient will generally live no more than 5 to 10 years.
Alzheimers type dementia is considered untreatable. No form of psychosocial or medical
therapy has been shown successful in slowing the progression of the disease. Other untreatable
dementias include Huntingtons Chorea and Parkinsons Disease among others. Huntingtons and
Parkinsons are especially tragic in that patients suffer significant distress and depression as the
disease progresses. Alzheimers patients often only suffer in the early stages, as they generally
loose higher cortical functions and self-awareness as the disease progresses.
Vascular dementia on the other hand is considered treatable. Vascular Dementia has rapid
onset often due to a significant cerebral event (e.g., multiple thromboemolic episodes or
cerebral infarctions). The course of vascular dementia is usually stepwise, more focal in area of
impairment, and may be less insidious in course.

QUESTION OF THE DAY:

Hypomanic episodes are characterized by:
(a) marked impairment of social/occupational functioning
(b) none of these are correct
(c) persistent elevated, expansive mood lasting at least four days
(d) physiological effects of drug abuse, medication, or treatment

ELLIS (RATIONAL-EMOTIVE THERAPY) ABCDE MODEL

Rational-emotive therapy, RET, is a cognitive-behavioral therapy. This theory believes that
individuals have the potential for rational thinking. Self-talk is the source of emotional
disturbance.
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A Activating event
B Belief
C Consequent affect
D Disputing of the irrational belief
E Effect

Rational emotive therapy was developed by Albert Ellis in the 1950s. It envisions emotional
consequences as being created by an individuals belief system rather than by significant causal
events with individual intrapersonal and interpersonal life being the source of growth and
happiness. Each of us is born with abilities to create or destroy, to relate or withdraw, to choose
or not choose, or to like or dislike. These abilities are all affected by our individual culture and
environment, family, and social group. The counselors aim is to use rational-emotive methods
to help the client to desire rather than to demand. The counselors aim is to also positively
change those parts of the client that he or she wants to change, and accept what cannot be
changed.

QUESTION OF THE DAY:

Moral judgments based on rules made by recognized authorities as a stage of moral
development is indicative of one of the following, according to Kohlberg:
(a) postconventional morality
(b) conventional morality
(c) preconventional morality
(d) realistic morality