IV. Developmental and cognitive
disorders
A. Developmental disorder

Identifying the disorder at an early age
is important

Deficit at one stage influences another stage
Early detection leads to prevention of other
disorders
such
as
language
and
communication
Interaction between biological factors and
learning factors



Accurate
understanding
symptom is important
of
the
- for example, echolalia is an aspect of
normal development
- consequently, echolalia which we
can observe in the behaviors of
autistic children is not a sign of a
disorder, but a delayed learning
1. Attention Deficit / hyperactivity
Disorder; ADHD)
< Clinical description >




Have trouble with concentration
don’t pay attention when others speak
start many tasks but seldom finishes one
Inattention, motor hyperactivity, impulsivity
Difficulty sustaining their attention on a
task or activity (Popper et al., 2003)
Unable to sit still for more than an few
minutes





Act without thinking beforehand
Respond to a question, before a teacher
finished his sentence.
Impairment both in social relationship and
academic achievement
The most common reason a child is
referred to a clinic
DSM-IV-TR differentiates 3 types of
symptoms
i) inattention
don’t listen to others
lose books or tools, forget school
assignments
ii) hyperactivity
fidgeting, having trouble sitting
for any length of time, always
being on the go
iii) impulsivity
blurting out answers before
questions have been completed.
and having trouble waiting turns

Either the first or the second and third
domains of symptoms must be present for
someone to be diagnosed with ADHD

Academic performance tends to suffer
ADHD children are likely to be unpopular and
rejected by their peers


Frequent negative feedback from parents and
teachers often result in low self esteem
among these children (Johnston et al, 1985)
1. Statistics




Prevalence rate 6% (Popper et al., 2003)
Boys outnumbering girls roughly 4 to 1
Identified as around 3-4 years old
they are described as active,
mischievous, slow to toilet training,
and oppositional (Conners et al., 2001)
The symptoms become increasingly
obvious during the school years

The problem usually continues through
adolescence. 68% of children have ongoing
difficulties through adulthood

Impulsivity goes down as the patient gets old
But inattention lasts



ADHD continues in adulthood
10% have severe symptoms of ADHD in adult
=> these patients violate traffic law and get
involved frequently in traffic accidents
2. Cause

Genetic factors

ADHD is more often found in families
whose members show ADHD

Until recently it has been regarded as a
brain damage. It was called “minimal
brain dysfunction” (Ross & Pellham,
1981)

Three areas of the brain of ADHD children
are smaller.
Frontal cortex, basal ganglia and the
cerebellar vermis (Popper et al., 2003)


Feingold(1975) diet
The theory that food additives such as
artificial colors, flavorings, and preservatives
are responsible for the symptoms of ADHD
has had a substantial impact.

Feingold
presented
this
view
with
recommendations for eliminating these
substances as a treatment for ADHD.
Hundreds of thousands of parents put their
children on the Feingold diet, despite
evidence that it has little or no effect on the
symptoms of ADHD

Maternal smoking
Mothers who smoke during pregnancy may
be up to three times more likely to have a
child with ADHD than mothers who do not
smoke (Linnet et al., 2003)

Negative responses by parents, teachers,
and peers to the affected child’s impulsivity
ad hyperactivity may contribute to his or her
feelings of low self-esteem (Barkley, 1989)

Which in turn can have a negative impact
on their ability to make friends.
3. Cause

Biological treatment
=> decrease of impulsivity, hyperactivity

Psychosocial treatment
=> improvement of school work, control of
inattentive behavior, enhancing social skill
recently combining both methods

stimulant medication can be effective such as
Ritalin, Dexedrine, Cylert => effective to
70% of the patients
=> reduction of hyperactivity, impulsivity,
enhanced attention

Anti depressant such as imipramine or a
drug used to treat high blood pressure
(clonidine) is known to have some effect
(Popper et al., 2003)

But
these drugs don’t
enhance
academic performance .
And their effect do not usually last over
the long term when the drugs are
discontinued.






Some children don’t respond to the
medication
Side effects such as insomnia,
drowsiness, or irritability
Combined with psychosocial treatment
Increasing the amount of time the child
remains seated by reinforcement and
punishment
Increasing the number of math papers
completed
Appropriate play with peers
2. Learning Disorders
< Clinical description >





Performance that is substantially below what
would be expected given the person’s age,
IQ, and education
Learning deficit in reading, writing, math
Low self esteem
Reading disorder
Cannot remember most of the content of what one
read


Can remember better when one reads aloud or
listens to recorded voice
Writing disorder => difficulty in writing
a story or a poem
1. statistics


5-10% (Young & Beitchman, 2001)
Difficulties with reading 5-15% of the
general population (Popper et al., 2003)





Math disorder 6%
American children 4 million
More boys than girls
34% drop out of school (Wagner, 1990)
Low employment rate (60 – 70%)
2. Cause


Genetic factors
Family members of learning disability
children tend to show higher rate than
general population (Popper, 2003)





Identical
twin
study
shows
100%
concordance rate (Vandenberg, Singer, &
Pauls, 1986)
Genes on chromosomes 2, 3, 6, 15 and 18
are linked to reading disorder (Kaminen et
al., 2003)
Problems in brain structure and function
among children with learning disability
They fails in distinguishing between the
sound “da” and “ga”
Individual difference in disorder depending
on parent’s expectation, socioeconomic
status, educational attitude, school support
system
3. Treatment





Medication is ineffective except when it is
comorbid with ADHD
Educational intervention is important
Teaching students visual and auditory
perception skills
Improving
cognitive
skills
through
instruction in listening, comprehension and
memory
Behavioral skills to compensate for
specific problems the students may have
with reading, math, or written expression


Computer game that helps children
distinguish sounds
Developing behavioral strategies such as
re-reading material and ask questions
about what they read
3. Communication and related disorders
3.1 stuttering
- disturbances in speech fluency
repeating syllables or words
prolonging certain sounds
- Making obvious pauses
substitutes words to replace ones that
are difficult to articulate
1. Statistics




Boys outnumbers girls more than twice
In many cases begins younger than 3 age
98% of the children begins before 10 years
old (Mahr & Leith, 1992)
80% of the children who stuttered before
they enter school will no longer stutter after
they have been in school a year or so
(Yairi & Ambrose, 1992)
2. Cause



Rather than anxiety cause stuttering,
stuttering makes people anxious (Miller &
Watson, 1992)
Multiple brain pathways appear to be
involved
Genetic influence
3. Treatment
- parent education
- regulated breathing method


instructed to stop speaking when stuttering
episodes occurs and then to take a deep
breath before proceeding
haloperidol => serious side effect
verapamil may decrease the severity of
stuttering in some individuals
3.2 Expressive language disorders


Limited speech in all situations
Expressive language is significantly below
their usually average receptive language
1. Statistics




2.2% of 3 years old infants
Boys are almost 5 times as likely as girls to
be affected
Unfounded psychological explanation
-> parents may not speak to them enough
A biological theory is that middle ear
infection is a contributory cause
2. Treatment

Without special intervention, many of them
can self-correct the problem
3.3 Selective mutism

Persistent failure to speak in specific
situations such as school, despite the
ability to do so
1. Statistics



Less than 1% of children
More prevalent among girls than boys
Most often between the ages of 5 and 7
2. Causes


Not much is known
Anxiety is one possible cause
3. Treatment

Contingency management :
giving children praise and reinforces for
speaking while ignoring their attempts to
communicate in other ways
3.4 Tic disorders

Involuntary motor movements
such as head twitching,
or vocalizations happen in
idiosyncratic or stereotyped ways

In Tourette's disorder, involuntary
repetition of obscenities
1. Statistics

Of all children 12-24% show some
tics during their growing years
(Ollendick & Ollendick, 1990)

2-8 out of every 10,000 have Tourette’s disorder
(Leckman et al., 1997)
2. Cause


Genetic influence
Anxiety
3. Treatment
self monitoring, relaxation training, and habit
reversal
haloperidol and more recently pimozide and
clonidine
4. Autistic Disorder
< Clinical description >





Significant impairment in social interaction
and communication
Restricted patterns of behavior, interest and
activities
Don’t play with other children
Also restricted contact with adults
Only as an instrument to acquire needed
objects




Not the amount of contacts, but the quality of
contact is the problem
Don’t smile at the sight of mother
Prefer to be mother’s side in stress situation
(Dissanayake & Crossley, 1996)
Lack of joint attention
( when sitting with a parent in front of a favorite toy,
young children will typically look back and forth the
parent and the toy, smiling, in an attempt to engage
the parent with the toy. However, this skill in joint
attention is noticeably absent in children with autism)
Show a picture of an autistic adult






Nearly always have severe problems with
communicating
About 50% never acquire useful speech
Those who have some speech show unusual
communication
Some repeat the speech of others
=> echolalia
Often repeats not only words,
intonations
Maintenance of sameness
but

Things must be always in the same place
become extremely upset if a small change is
introduced

Spend countless hours in stereotyped and
ritualistic behaviors such as :
- spinning around in circles
- waving their hands in front of their eyes
with their heads cocked to one side
or biting their hands
< Jim’s self report >

27 year old graduate school students in
psychology

Diagnosed as autism in childhood
=> hospitalized at the age of 9 years old
because of autism

Acquired considerable social skills through
his own efforts

Still have many difficulties
- Information processing
- Cannot do several things
simultaneously
- Have to turn off the radio to read
a traffic sign


Involuntary movements come out when
stressed
Have to try hard to learn social skills that are
necessary in social interaction
1. Statistics





Prevalence 2 out of 10,000 (Gillberg, 1984)
More girls IQ level below 34
More boys IQ level above 34
Found in most cultures
Onset before 36 months (APA, 1994)



IQ of autistic patients vary
In ¾ of the cases comorbid with mental
retardation
Better prognosis for patients with high IQ and
language ability
2. Cause




Cannot find a single cause
Psycho-social influence
Classic theory -> difference in parental
education
Perfectionistic, cold, aloof
rejected in recent research (Koegel et al.,
1983)

Classic theory -> lack of self-awareness was
attributed as a cause
(Do you want something to drink ?
-> he wants something to drink,
instead of I want … )

Also rejected in recent research
self-concept may be lacking because of
cognitive disabilities or delays,
not because of autism itself

It is now regarded as a matter of delayed
development


Stimulus over-selectivity
Too much attention is given to details of
things in learning

Only the name of things on the right
edge of the table are remembered =>
this is also a problem of delayed
development

They are also observable in the
development of the normal children

Echolalia, self injurious behavior can be
also observed in the normal children in
their early phase of development

The deficit of social interaction is the
key factor of autism

Poor parenting is not responsible for
autism
Biological dimensions

Rubella virus, hypsarhythmia
(간질의 특이 EEG), tuberous sclerosis (뇌, 폐,
신장의 종양), cytomegalo-virus, difficulties
during pregnancy and labor etc.

Although a few mother who was exposed to
rubella virus have children with autism, most
of others don’t have the problem

We still don’t know why certain conditions
sometimes result in autism
Genetic influences






It is now clear that autism has a genetic
component (Cook, 2001)
Families that have one autism child
have a 3-5%
Risk of having another child with this
disorder
Michael Rutter’s research (1971)
11 identical twins 36% concordance
10 not identical twins 0% concordance


If other developmental disorder included:
identical twins 82% concordance
Not identical twins 10% concordance
Neurobiological influences



¾ of autism patients have mental retardation
30-75% have neurobiological anomalies
MRI -> part of autism patient show reduced
size of cerebellum(소뇌)
3.Treatment
Still today there is no effective therapy
that would eliminate the social problems of
autistic patients
 Enhancing their communication and daily
living skills and reducing problem
behaviors such as tantrums and self-injury

Psychodynamic approach
-> inappropriate parenting
-> not proven yet


Behavior shaping, social skill training







Foods and praise are offered as a
reinforcer
Imitation of other people’s speech->
shaping + physical prompting
Long term research of Ferster & Lovaas
Mainly
focuses
on
enhancing
communication and social interaction
There is no successful treatment yet which
would
improve
social
interaction
remarkably
UCLA prof. Lovaas
40 hours weekly training -> improvement in
intellectual and academic performance
-> possibilities of early intervention
expenses and effectiveness of investment






Integrating treatment with regular class in
school -> inclusion
special psychological programs, and
psychotherapy
Supported living arrangement and work
settings -> integrated into community
community home, foster home
No effect of medication
Restricted effect on specific symptoms
5. Mental Retardation
< clinical description >





Far below the average intelligence
Low social adjustment
Difficult to carry out independent daily life
Individual differences in personality and
capabilities
Also differences in communication,
socialization and learning abilities
Mental retardation is included on Axis II
of DSM-IV-TR. Separating disorders by
axes serve two purposes:
First, indicating that disorders on Axis II
tend to be more chronic and less
amenable to treatment.
Second, reminding clinicians to
consider whether these disorders, if
present, are affecting an Axis I disorder.
< Three conditions required by DSM-IV to be
diagnosed as mental retardation >
1) IQ below 70
2)
Deficit
in
adaptive
functioning
(communication, self care, home life, use of
community resources, goal setting, academic
performances, occupational activities, leisure,
health, safety behaviors etc)
3) onset below 18 age (brain abnormality,
dementia are excluded)
< 4 levels of mental retardation >
1) Mild -> IQ 50-70
home living, academic performance possible
2) Moderate -> IQ 35-49
home living, academic performance possible
3) severe -> IQ 20-34
language use and daily life severely
impaired
4) Profound -> IQ below 19
language use and daily life severely
impaired
1. Statistics
90% of MR fall under the label of mild
mental retardation (IQ of 50 to 70)
 Mild mental retardation
-> 3-4 out of 1,000 general population
 Including severe MR
-> 6-8 out of 1,000 general population





do not recover, become chronic
Through education and support => daily life
possible
Male outnumbers female (1.6 : 1)
No sexual differences in severe MR
2. Cause
Environmental -> deprivation, abuse, neglect
 prenatal -> disease, drugs while in the womb
 perinatal->difficulties during labor
and delivery
 postnatal -> infections, head injury
 Heavy use of alcohol among pregnant women
-> fetal alcohol syndrome => learning disability



Lack of oxygen during birth
Malnutrition and head injuries
developmental period
during
the
In 75% of cases, specific causes are not found
(Zigler & Hodapp, 1986)
< Biological dimensions >






Usually multiple genes are involved
Certain dominant, recessive, or X linked genes
In most cases , MR are not likely to marry and
give their genes to their children -> natural
selection, even though some mild MR people do
marry
Phenylketonuria(PKU)
Patients who cannot digest phenylalanine
if they intake phenylalanine -> their children
become MR
Every one out of 14,000 newborn baby is
diagnosed
Now it is possible to detect and prevent by diet
< Chromosomal influences >


In 1956, the number of chromosomes in
human cells was first correctly identified as
46
Gene anomalities that lead to MR are more
than hundred different way
< Down Syndrome >

First identified in 1866
physician Langdon Down
by
an
British

It was called first mongoloidism, because of
resemblance of these patients to mongolian and
then replaced later by the term “Down Syndrome”

The disorder is caused by the presence of an
extra 21st chromosome
Folds in their upwardly slanting eyes
Flat nose, small mouth, protruded tongue




Heart malformation
After 40 age, develop dementia Alzheimer’s
type
Correlates with the age of mother’s age
 Woman’s ova (egg) are all produced in
youth
-> exposed to harmful substances
-> disorder of division of chromosome



Hormonal change with aging
-> disorder in chromosome division
Possible to detect Down syndrome by
amniocentesis by testing a sample of the
fluid that surrounds the fetus in the
amniotic sac
< Fragile X syndrome >



Abnormality on the x-chromosome
A mutation that makes the tip of the
chromosome look as if it were hanging from
a thread, giving it the appearance of
fragility
Mostly males are affected, because they
don’t have a second x-chromosome to
balance out the mutation

Women who carry fragile x syndrome
commonly display mild to severe learning
disabilities

Men with fragile x syndrome display moderate
to severe levels of MR and have higher rates
of hyper activity, short attention spans, gaze
avoidance
Large ears and testicles


1 of every 2,000 males is born with fragile x
syndrome (Dykens et al., 1988)
< Psychological and social dimensions >

Up to 75% of the MR is caused by cultural and
familial retardation

These individuals tend to score mild mental
retardation and have relatively good adaptive skills
Specific mechanisms that lead to this type of MR is
not yet known




Psychological and biological influence combined
Or just delayed development
MR group influenced by psycho-social influence
such as abuse, neglect, social deprivation
-> higher IQ compared to those influenced
by biological factors
2. Treatment
Biological treatment



Currently not available
Rat experiment
-> Healthy brain cell transplantation
Gene examination -> gene treatment
psychological treatment



The same principle used to LD, autism
Basic skills to live in community





Task analysis tailored to individual
need
Shaping through praise and access to
objects and activities the person desires
(reinforcers)
Learning communication skills
Severe MR -> learning sign language
Augmentative communication strategies
-> teaching the person to make a
request by pointing to a picture

Communication with the help of computer
one can press a button to produce a
complete sentence (would you please come
here ? I need your help.)
-> reduction of self destructive, aggressive
behavior

More effective treatment programs need to
be developed
-> more investments are needed

Occupation and community need to be
integrated
B. cognitive disorder
There are three categories in cognitive disorder,
namely, delirium, dementia, and amnestic
disorder
-
-
They used to be called in the past as
"organic mental disorder“
In DSM-IV-TR the name “organic” was
dropped, because all other psychological
disorders are also more or less organically
influenced

Memory, attention, perception,
thinking are impaired
and

Consequencies of the disorder
influence person’s behavior,
personality

Intense anxiety and depression are
common, especially among people with
dementia
1. Delirium
< Clinical description >






Confused, disoriented,
Out of touch with the surroundings
Impairment of attention, memory, language
Confusion of consciousness
Lasts hours or several days
Disappears relatively quickly
1. Statistics



10-30% of emergency cases of old people
Most common illness among the elderly
Most prevalent among older adults, people
undergoing medical procedures, cancer patients,
and people with AIDS
2. Cause



Intoxication by drugs and poisons, withdrawal
from alcohol
Infections, head injury, and brain trauma
Age, lack of sleep, physical exercise, stress




Improper use of medication
among elderly =>
fall -> hip fracture (annually 32,000)
Traffic accidents (annually 16,000명)
High fever or drug -> delirium of children
Also in the process of dementia (Wolanin & Philips,
1981)
3. Treatment


Delirium caused by withdrawal of alcohol
-> benzodiazepine
Delirium by infection, brain injury, brain tumor
-> medical treatment


Acute delirium
-> haloperidol
Agitation, anxiety, hallucination
-> psychotherapy

Patient’s participation in the process of
decision making
-> enhanced feeling of self control

Supervision of drug use
-> prevention
2. Dementia
1. clinical description and statistics





Impairment of judging, memory, language
Medication, drug abuse, rupture of blood
vessel by stroke
Syphilis and HIV, parkinson’s disease,
Huntington’s disease, Alzheimer’s disease
Progress slowly
Memory of several years ago remain






Cannot remember events happened
hours ago
Agnosia -> cannot recognize an object
Facial agnosia -> cannot recognize
faces of family members or friends
Accompanies delusion
Anxiety, agitation, depression, aggression,
feel helpless
Difficult to establish cause-and-effect
relationship








Interplay between disease, anxiety, social
isolation
Age 75-79 : 2.3%
Age 80-84 : 4.6%
Age above 85 : 8.5% (Paykel et al., 1994)
No difference between sex, education,
socio-economic states
More women in Alzheimer’s dementia
Medical and economical burden
Severe social and familial burden
< 6 kinds of dementia >
1) Alzheimer's type
2) vascular dementia
3) dementia due to general medical
conditions
4) substance-induced persisting dementia
5) dementia due to multiple etiologies
6) dementia not otherwise specified
2.1 Dementia of the Alzheimer's type







In 1906, German psychiatrist
Alois Alzheimer
Progressive complex cognitive disorder
Memory disorder -> difficulty to process new
informations
Forget objects, appointments
Diminished social activities
Aphasia, apraxia, agnosia
Difficulty in planning,
organizing, integrating informations

Examination of mental status
- orientation, registration, attention and
calculation

Recall, name of objects
Research with catholic nuns in a
longitudinal study
Problem of restricted sampling
Diary -> idea density is related to dementia
Both at the early and last stage
-> progress slowly
In the middle phase
-> progress quickly










Can live in average 8 years after the onset
In most cases, begins at 60-70 age
Those who begins in 40-50age -> pre-senile
dementia
50% of all dementia -> Alzheimer’s type
In U.S : 4 millions
More among low education level
High education -> compensation by intellectual
strategies => prevention of or delaying the
development of dementia (Stern et al., 1994)

High prevalence among women
=> unexplainable only by longer
life expectancy
the role of estrogen

Estrogen treatment after menopause
=> late onset or reduced incidence of
Alzheimer’s disease (Lambert, coyle, &
Lendon, 2004)

Differences in different racial group
Japan, Nigeria, Cherokee American Indian

2.2 Vascular Dementia







high percentage next to Alzheimer’s disease
As a result of stroke
Similar symptoms to those of Alzheimer’s
disease
Impairment of memory, cognition
Abnormalities in walking and weakness in the
limbs
Prevalence of men 4.7%
Prevalence of women 3.8%
2.3 Dementia due to other general medical
conditions



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HIV virus, brain injury
Parkinson’s disease, Huntington’s disease
Pick’s disease, Creutzfeld-Jakob’s disease
Hydrocephalus (excessive water in the
cranium because of brain shrinkage)
Hypothyroidism ( an under-active thyroid
gland)
Brain tumor and vitamin B12 deficiency
< Infection of HIV virus >
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Cognitive slowness,
Impaired attention,
Forgetfulness, clumsy,
Tremors, weakness,
Become apathetic,
Socially withdrawn
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29-87% of AIDS patients
-> impairment of cognitive function
30%
-> diagnosed as having dementia
(Heaton et al., 1994)
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AIDS, parkinson’s disease, Huntington’s disease
-> sub-cortical dementia (The inner areas of the brain
below outer layer called cortex )
-> impairment of the motor skills
-> severely depressive, anxious
Alzheimer’s dementia, Pick’s dementia
-> cortical dementia
-> aphasia (language disorder)
< head trauma >
 Brain damage through traffic accident or other
accidents
-> disorder of cognitive functioning, memory
< Parkinson’s disease >
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I out of every 1,000 people
Stooped
posture,
slow
body
movements (called bradykinesia)
Tremors, and jerkiness in walking
Speaks in a soft monotone
Damage to dopamine pathways
Prevalence twice as high as in general
population
< Huntington’s disease >
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Involuntary movements of limbs
20-80% of Huntington’s disease develops
dementia
Strong heredity
Abnormality in chromosome 4
2.4 substance-induced persisting dementia
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Drug abuse, alcohol abuse, inhalation of glue or
gasoline, sedative, hypnotic and anxiolytic drugs
Similar symptoms to those in Alzheimer’s dementia
Impairment in memory, language
movements, recognition, organizing and planning
2. Cause

Alzheimer’s disease
neurofibrillary tangles
dead cells of neurons (amyloid plagues or nuritic
plaques)
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Too small to be observed in a living organ, which
is why a definitive diagnosis of Alzheimer’s
disease requires an autopsy
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Atrophy of brain cells
Multiple genes are related
Chromosome 21, 19, 14, 1
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Abnormality of chromosome 21 in Down syndrome
-> high prevalence of dementia Alzheimer’s type
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Abnormality of chromosome 14
-> early onset (30-60 age)
Abnormality of chromosome 19
-> late onset ( after age 60 )
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Individual’s life style
diet, exercise, stess
-> vascular dementia
Education, cultural factors
-> influences on the process of dementia
-> low expectancy of social activity to the elderly
3. Treatment
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There is no absolute cure, because neurons are
currently irreparable
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Preventive certain conditions such as
- substance abuse, reduction of stress
- trying to stop the brain damage from
spreading and becoming worse
- attempting to help these individuals and their care
givers cope with the advancing deterioration.
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Education of coping strategies
- more than 50% of the family members
are severely depressed and stressed
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High doses of vitamin E delayed
progression of dementia compared with
a placebo
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Tacrine hydrochloride (cognex)
Donepezil (Ariecept)
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Aspirine, nonsteroidal
anti-inflammatory drugs
Estrogen treatment
=> temporary effect
Psycho-social treatment
- Cognitive strategies
- memory wallets
- name, short career, memory cards
- improve dialogues
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Safety line
-> red line is drawn on the floor
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Verbal and nonverbal aggressive
behavior
-> caregivers need to be protected
-> self assertive behaviors
-> prevention of patients abuse
3. Amnestic disorder
1. Clinical description and statistics
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Inability to change from a short term memory to a
long term memory
Apple, bird, roof
Counting backwards from 100 extracting 3 each time
Remembering 5 words for 5 minutes
- checking the memory intermittently
- no impairment in high cognitive functioning
- relatively simple memory disturbance
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Normal language, able to count simple
numbers
Difficulty in recalling recent events
unstable orientation
Cannot remember what he or she ate as a
breakfast
Forget names, the anniversary of one’s
marriage, home address
Change in personality
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Wernicke-Korsakoff syndrome
Impairment of thalamus
=> station of information transmission
influence of brain injury, drug abuse,
alcohol abuse
Alcoholics
-> deficiency of vitamin B1
-> vitamin therapy
-> no long term effectiveness