Psychological Testing

on Attention-Deficit Hyperactivity
Disorder (ADHD)and Learning Disability
(LD)

A Case Study

Submitted to Mrs. Helen C. Jagmis

In partial fulfillment of the requirements in

Research II

Sarah Mae B. Sincero

IV-1 Acts

February 2008
 PERSONAL PROFILE

Name: Christian A. Santos

Nickname: Chris

Address: San Jose, Rizal

Birthday: February 29, 1994

Age: 12 years old

Father: Rafael Santos

Occupation: businessman

Mother: Cristy Santos

Occupation: accountant

Disorder: Attention- Deficit Hyperactivity Disorder (ADHD)

Description of the Chosen Respondent

The child with ADHD who is hyperactive/impulsive is

described by the following observations. I have classified

my observations into three sections: hyperactivity,

impulsivity, and inattention to further elaborate his

social behavior, psychological status and mental

disabilities. These three are the following:

I. Hyperactivity

• Runs or climbs excessively when inappropriate

• Has difficulty playing or engaging in leisure

activities quietly
• Often talks excessively

• Fidgets with hands or feet or squirms in seat

• Leaves seat in classroom or in other situations in

which remaining seated is expected

II. Impulsivity

• Interrupts or intrudes on others (for example, butts

into conversations or games).

• Blurts out answers before questions have been completed

• Has difficulty waiting for a turn

III. Inattention

• Does not seem to listen when spoken to directly

• Does not follow directions and fails to complete

schoolwork, tests, chores, or on-the-job duties

• Is often forgetful in daily activities

• Fails to pay close attention to details or makes

careless mistakes and is easily distracted

• Has difficulty maintaining attention in tasks or play

activities, has difficulty organizing tasks or activities

Review of Related Literature and Studies

 According Reyes (1998), Attention-Deficit

Hyperactivity Disorder (ADHD), or Hyperkinetic Disorder, is

a neurobehavioural developmental disorder affecting about

3-5% of the world's population under the age of 19. It

typically presents itself during childhood, and is

characterized by a persistent pattern of inattention and/or

hyperactivity, as well as forgetfulness, poor impulse

control or impulsivity, and distractibility. ADHD is

currently considered to be a persistent and chronic

condition for which no medical cure is available. ADHD is

most commonly diagnosed in children and, over the past

decade, has been increasingly diagnosed in adults. About

60% of children diagnosed with ADHD retain the condition as

adults. It appears to be highly heritable, although 1/5 of

all cases are estimated to be caused from trauma or toxic

exposure. Methods of treatment usually involve some

combination of medications, behaviour modifications, life

style changes, and counseling.

Sarmiento (1996) writes that ADHD is a developmental

disorder, in that, in the diagnosed population, certain

traits such as impulse control significantly lag in

development when compared to the general population. Using

magnetic resonance imaging, this developmental lag has been

estimated to range between 3 years, to 5 years in the

prefrontal cortex of those with ADHD patients in comparison

to their peers; consequently these delayed attributes are

considered an impairment. ADHD has also been classified as

a behavior disorder and a neurological disorder or

combinations of these classifications such as

neurobehavioural or neurodevelopmental disorders.

Garcia (1999) says that the most common symptoms of

ADHD are distractibility, difficulty with concentration and

focus, short term memory slippage, procrastination,

problems organizing ideas and belongings, tardiness,

impulsivity, and weak planning and execution. Not all

people with ADHD have all the symptoms. Most ordinary

people exhibit some of these behaviors but not to the point

where they seriously interfere with the person's work,

relationships, or studies or cause anxiety or depression.

Children do not often have to deal with deadlines,

organization issues, and long term planning so these types

of symptoms often become evident only during adolescence or

adulthood when life demands become greater. Hyperactivity

is common among children with ADHD but tends to disappear

during adulthood. However over half of children with ADHD

continue to have symptoms of inattention throughout their

lives.
 According to a majority of medical research in the

United States, as well as other countries, ADHD is today

generally regarded as a chronic disorder for which there

are some effective treatments, but no true cure. Evidence

suggests that hyperactivity has a strong heritable

component, and in all probability ADHD is a heterogeneous

disorder, meaning that several causes could create very

similar symptomology. Candidate genes include dopamine

transporter (DAT), dopamine receptor D4 (DRD4), dopamine

beta-hydroxylase (DBH), monoamine oxidase A (MAOA),

catecholamine-methyl transferase (COMT), serotonin

transporter promoter (SLC6A4), 5-hydroxytryptamine 2A

receptor (5-HT2A), and 5-hydroxytryptamine 1B receptor (5-

HT1B). Researchers believe that a large majority of ADHD

arises from a combination of various genes, many of which

affect dopamine transporters. Suspect genes include the 10-

repeat allele of the DAT1 gene, the 7-repeat allele of the

DRD4 gene, and the dopamine beta hydroxylase gene (DBH

TaqI).

Genome wide surveys have shown linkage between ADHD

and loci on chromosomes 7, 11, 12, 15, 16, and 17. If

anything, the broad selection of targets indicates the

likelihood that ADHD does not follow the traditional model

of a "genetic disease" and is better viewed as a complex

interaction among genetic and environmental factors. As the

authors of a review of the question have noted, "Although

several genome-wide searches have identified chromosomal

regions that are predicted to contain genes that contribute

to ADHD susceptibility, to date no single gene with a major

contribution to ADHD has been identified." Chromosomes

disaffecting health or life expectancy are not expressed by

everyone with the same DNA, and have only been found in

combination with one or more other chromosomes. One reason

for this may be that nature selects against genetic

abnormalities that do not have any advantage.

Studies show that there is a familial transmission of

the disorder which does not occur through adoptive

relationships. Twin studies indicate that the disorder is

highly heritable and that genetics contribute about three

quarters of the total ADHD population. While the majority

of ADHD is believed to be genetic in nature,roughly 1/5 of

all ADHD cases are thought to be acquired after conception

due to brain injury caused by either toxins or physical

trauma prenatally or postnatally.

Additionally, SPECT scans found people with ADHD to

have reduced blood circulation, and a significantly higher

concentration of dopamine transporters in the striatum

which is in charge of planning ahead.A study by the U.S.

Department of Energy’s Brookhaven National Laboratory in

collaboration with Mount Sinai School of Medicine in New

York suggest that it is not the dopamine transporter levels

that indicate ADHD, but the brain's ability to produce

dopamine itself. The study was done by injecting 20 ADHD

subjects and 25 control subjects with a radiotracer that

attaches itself to dopamine transporters. The study found

that it was not the transporter levels that indicated ADHD,

but the dopamine itself. ADHD subjects showed lower levels

of dopamine across the board. They speculated that since

ADHD subjects had lower levels of dopamine to begin with,

the number of transporters in the brain was not the telling

factor. In support of this notion, plasma homovanillic

acid, an index of dopamine levels, was found to be

inversely related not only to childhood ADHD symptoms in

adult psychiatric patients, but to "childhood learning

problems" in healthy subjects as well.

Although there is evidence for dopamine abnormalities

in ADHD, it is not clear whether abnormalities of the

dopamine system are the molecular abnormality of ADHD or a

secondary consequence of a problem elsewhere. Researchers

have described a form of ADHD in which the abnormality

appears to be sensory overstimulation resulting from a

disorder of ion channels in the peripheral nervous system.

An early PET scan study found that global cerebral

glucose metabolism was 8.1% lower in medication-naive

adults who had been diagnosed as ADHD while children. The

image on the left illustrates glucose metabolism in the

brain of a 'normal' adult while doing an assigned auditory

attention task; the image on the right illustrates the

areas of activity in the brain of an adult who had been

diagnosed with ADHD as a child when given that same task;

these are not pictures of individual brains, which would

contain substantial overlap, these are images constructed

to illustrate group-level differences. Additionally, the

regions with the greatest deficit of activity in the ADHD

patients (relative to the controls) included the premotor

cortex and the superior prefrontal cortex. A second study

in adolescents failed to find statistically significant

differences in global glucose metabolism between ADHD

patients and controls, but did find statistically

significant deficits in 6 specific regions of the brains of

the ADHD patients (relative to the controls). Most notably,

lower metabolic activity in one specific region of the left

anterior frontal lobe was significantly inversely

correlated with symptom severity. These findings strongly

imply that lowered activity in specific regions of the

brain, rather than a broad global deficit, is involved in

ADHD symptoms. However, these readings are of subjects

doing an assigned task. They could be found in ADHD

diagnosed patients because they simply were not attending

to the task. Hence the parts of the brain used by others

doing the task would not show equal activity in the ADHD

patients.

The estimated contribution of non genetic factors to

the contribution of all cases of ADHD is 20 percent. The

environmental factors implicated are common exposures and

include alcohol, in utero tobacco smoke and lead exposure.

Lead concentration below the Center for Disease Control's

action level account for slightly more cases of ADHD than

tobacco smoke (290 000 versus 270 000, in the USA, ages 4

to 15). Complications during pregnancy and birth—including

premature birth—might also play a role. It has been

observed that women who smoke while pregnant are more

likely to have children with ADHD. This could be related to

the fact that nicotine is known to cause hypoxia (lack of

oxygen) in utero, but it could also be that ADHD women have

more probabilities to smoke both in general and during

pregnancy, being more likely to have children with ADHD due

to genetic factors.
 Head injuries can cause a person to present ADHD-like

symptoms, possibly because of damage done to the patient's

frontal lobes. Because these types of symptoms can be

attributable to brain damage, the earliest designation for

ADHD was "Minimal Brain Damage".

Michelson (1993) says that there is no compelling

evidence that social factors alone can create ADHD. Many

researchers believe that attachments and relationships with

caregivers and other features of a child's environment have

profound effects on attentional and self-regulatory

capacities. It is noteworthy that a study of foster

children found that an inordinate number of them had

symptoms closely resembling ADHD. An editorial in a special

edition of Clinical Psychology in 2004 stated that "our

impression from spending time with young people, their

families and indeed colleagues from other disciplines is

that a medical diagnosis and medication is not enough. In

our clinical experience, without exception, we are finding

that the same conduct typically labeled ADHD is shown by

children in the context of violence and abuse, impaired

parental attachments and other experiences of emotional

trauma." Furthermore, Complex Post Traumatic Stress

Disorder can result in attention problems that can look

like ADHD, as can Sensory Integration Disorders.

 Despite the lack of evidence that nutrition causes

ADHD, studies have found that malnutrition is correlated

with attention deficits.

According to an advanced high-precision imaging study

by researchers at the United States National Institutes of

Health's National Institute of Mental Health, an actual

delay in physical development in some brain structures,

with a median value of three years, was observed in the

brains of 223 ADHD patients beginning in elementary school,

during the period when cortical thickening during childhood

begins to change to thinning following puberty. The delay

was most prominent in the frontal cortex and temporal

cortex, which are believed responsible for the ability to

control and focus thinking, attention and planning,

suppress inappropriate actions and thoughts, remember

things from moment to moment, and work for reward, all

functions whose disturbance is associated with a diagnosis

of ADHD; the region with the greatest average delay, the

middle of the prefrontal cortex, lagged a full five years

in development in the ADHD patients. In contrast, the motor

cortex in the ADHD patients was seen to mature faster than

normal, suggesting that both slower development of

behavioral control and advanced motor development might

both be required for the restlessness and fidgetiness that

characterize an ADHD diagnosis. Aside from the delay, both

groups showed a similar back-to-front development of brain

maturation with different areas peaking in thickness at

different times. This contrasts with the pattern of

development seen in other disorders such as autism, where

the peak of cortical thickening occurs much earlier than

normal.

The same laboratory had previously found involvement

of the "7-repeat" variant of the dopamine D4 receptor gene,

which accounts for about 30 percent of the genetic risk for

ADHD, in unusual thinness of the cortex of the right side

of the brain; however, in contrast to other variants of the

gene found in ADHD patients, the region normalized in

thickness during the teen years in these children,

coinciding with clinical improvement.

Cruz (1994) affirms that many studies point to

synthetic preservatives and artificial coloring agents

aggravating ADD & ADHD symptoms in those affected. Older

studies were inconclusive quite possibly due to inadequate

clinical methods of measuring offending behavior. Parental

reports were more accurate indicators of the presence of

additives than clinical tests. Several major studies show

academic performance increased and disciplinary problems

decreased in large non-ADD student populations when

artificial ingredients, including artificial colors were

eliminated from school food programs.

According to Geronimo (1993), any of the symptoms of

ADHD occur from time to time in everyone. In those with

ADHD the frequency of these symptoms occur frequently and

impair regular life functioning typically at school or at

work. Not only will they perform poorly in task oriented

settings but they will also have difficulty with social

functioning with their peers. No objective physical test

exists to diagnose ADHD in a patient. As with many other

psychiatric and medical disorders, the formal diagnosis is

made by a qualified professional in the field based on a

set number of criteria. A review of 102 studies estimated

ADHD's worldwide prevalence in people under the age of 19

to be 5.29%. There was wide variability in prevalence

estimates, mostly due to the methodological characteristics

of studies (for example, diagnostic criteria used) and, to

a lesser extent, geographic location (North America having

a significantly higher rate of ADHD than Africa and the

Middle East). 10% of males, and (only) 4% of females have

been diagnosed in the U.S. This apparent sex difference may

reflect either a difference in susceptibility or that

females with ADHD are less likely to be diagnosed than

males.
 Aquino (2000) defined Psychological tests that are

written, visual, or verbal evaluations administered to

assess the cognitive and emotional functioning of children

and adults. Psychological tests are formalized measures of

mental functioning. Most are objective and quantifiable;

however, certain projective tests may involve some level of

subjective interpretation. Also known as inventories,

measurements, questionnaires, and scales, psychological

tests are administered in a variety of settings, including

preschools, primary and secondary schools, colleges and

universities, hospitals, outpatient healthcare settings,

social agencies, prisons, and employment or human resource

offices. They come in a variety of formats, including

written, verbal, and computer administered.

According to Mendoza (2002), for children, academic

achievement, ability, and intelligence tests may be used as

a tool in school placement, in determining the presence of

a learning disability or a developmental delay, in

identifying giftedness, or in tracking intellectual

development. Intelligence testing may be used with adults

to determine vocational ability (e.g., in career

counseling) or to assess adult intellectual ability in the

classroom.
 Personality tests are administered for a wide variety

of reasons, from diagnosing psychopathology (e.g.,

personality disorder, depressive disorder) to screening job

candidates. They may be used in an educational or

vocational setting to determine personality strengths and

weaknesses, or in the legal system to evaluate parolees.

Patients who have experienced a traumatic brain

injury, brain damage, or organic neurological problems (for

example, dementia) are administered neuropsychological

tests to assess their level of functioning and identify

areas of mental impairment. They may also be used to

evaluate the progress of a patient who has undergone

treatment or rehabilitation for a neurological injury or

illness. In addition, certain neuropsychological measures

may be used to screen children for developmental delays

and/or learning disabilities.

Santos (1991) defines learning disability as a

neurological disorder. In simple terms, a learning

disability results from a difference in the way a person's

brain is "wired." Children with learning disabilities are

as smart or smarter than their peers. But they may have

difficulty reading, writing, spelling, reasoning, recalling

and/or organizing information if left to figure things out

by themselves or if taught in conventional ways.

 A learning disability can't be cured or fixed; it is a

lifelong issue. With the right support and intervention,

however, children with learning disabilities can succeed in

school and go on to successful, often distinguished careers

later in life.

Adelino (2001) advises that parents can help children

with learning disabilities achieve such success by

encouraging their strengths, knowing their weaknesses,

understanding the educational system, working with

professionals and learning about strategies for dealing

with specific difficulties.

The good news about learning disabilities is that

scientists are learning more every day. Their research

provides hope and direction.

If parents, teachers, and other professionals discover

a child's learning disability early and provide the right

kind of help, it can give the child a chance to develop

skills needed to lead a successful and productive life. A

recent National Institutes of Health study showed that 67

percent of young students who were at risk for reading

difficulties became average or above average readers after

receiving help in the early grades.

Parents are often the first to notice that "something

doesn't seem right." If you are aware of the common signs

of learning disabilities, you will be able to recognize

potential problems early.

Statement of problem

The general problem of the research is:

Does a child with Attention- Deficit Hyperactivity

Disorder possess learning disability?

The specific problems are the following:

a. Is there a significant difference between

Attention- Deficit Hyperactivity Disorder of a child and

the child’s learning disability?

b. Can learning disability be assessed through the use

of the psychological test made by the researcher herself?

Hypotheses

No, a child with Attention- Deficit Hyperactivity

Disorder does not possess learning disability.

There is a significant difference between the

Attention- Deficit Hyperactivity Disorder of a child and

the child’s learning disability ( H0: uA = uB)

 Yes, learning disability can be assessed through the

use of the psychological test made by the researcher

herself.

Instrumentation

Self-Made Test

Name:____________________________

Age:____

Direction: Answer each of the five questions. Base your

answer in the given figures.

1. What is the color of the rectangle?

2. What is the shape with the blue color?

3. What is the color of the circle?

4. What is the shape of the triangle?

5. What is the color of the oval?

Four Standardized Tests

MEMORY TEST
Question:

1. What is the color of his pants?

2. What object is he holding?

3. What kind of slippers is he wearing?

4. What is the color of his nose?

5. What is the color of the slippers?

MATHEMATICAL ABILITY

1. What is 45+23?

2. If I have 78 eggs and my mom give me 98 how many do

I have all in all?

3. What is 65-45?

4. What are 8 multiplied to 2?

5. What do you get if in a basket with 43 flowers you

pick 13?

GENERAL INFORMATION

1. What is the capital of Germany?

 2. How many states are there in US?

3. What is the former name of Iraq?

4. What is the capital of Japan?

5. How many stars are there in the flag of USA?

Methodology

This chapter presents the materials used, the

procedure to be followed in order to assess the respondent

precisely and the statistical treatment of data.

A. Materials

1. sheet of paper containing the psychological test

2. timer

3. tally sheet

B. Procedure

1. Present the psychological test to the respondent.

2. Read the directions clearly before him.

3. Allow the respondent to answer the assessment for 10

minutes.

4. Collect the test sheet and tally the results.

Statistical Treatment of Data

Table 1: Results of the Psychological Test

Items (n) Score (x)

1 5
2 5

3 1
4 5
5 2

N=5 Σ x = 18

Legend:

5-the child’s answer is the correct one

4-the child’s answer is closely related to the correct one

3-the child’s answer is fairly related to the correct one

2-the child’s answer is somewhat related to the correct one

1-the child’s answer is incorrect

1. H0: uA = uB

There is a significant difference between Attention-

Deficit Hyperactivity Disorder of a child and the child’s

learning disability.
2. Ha: uA = uB

There is no significant difference between Attention-

Deficit Hyperactivity Disorder of a child and the child’s

learning disability.

3. Compute for the Mean, Mode and Range

Mean:
x= Σx Mode: 5

n Range:
= 18 R= HR - LR
5 = 5-1
= 3.6 =4
5. Graph

Figure 3. Graph of Computed mean and the Treatment Group

Mean
6. Computed Value > Critical Value

3.6 > 4

Accept H0, Reject Ha

7. Conclusion

There is a significant difference between Attention-

Deficit Hyperactivity Disorder of a child and the child’s

learning disability.

Results and Discussion

 This chapter contains the major finding of the study

and answers all the questions raised according to she

chronological sequence of problems presented in the

statement of the problem. It also contains a discussion on

the analysis of the relationship between the variables

included in the study.

The result of the computation for mean, which is 3.6,

is close to the accepted value 4.0. This indicates that the

answers of the child all in all are closely related to the

correct ones, and therefore the special child has a good

test result. This signifies that the respondent, the child

with the ADHD, has no learning disability, rather he has a

good capability of thinking. Based on his answers to the

queries given, he has no deficits in cognitive functioning.

A child with Attention- Deficit Hyperactivity Disorder

does not necessarily possess learning disability. Not all

children affected by ADHD have learning disabilities. Some

may even excel among those children who have no disorder at

all.

There is a significant difference between the

Attention- Deficit Hyperactivity Disorder of a child and

the child’s learning disability. Although ADHD may cause

learning disabilities due to the behavior of the child, it

does not necessarily mean that a child with ADHD is born

having learning disabilities.

Learning disability can be assessed through the use

of the psychological test made by the researcher herself.

The psychological testing is said to be successful based on

its results. Therefore, the psychological test made by the

researcher herself can be effective in assessing a child

with ADHD.

Summary, Conclusion, Recommendation

This chapter presents the overview of the study,

summary of the significant findings, the conclusions drawn,

and the recommendations made.

A child with Attention- Deficit Hyperactivity Disorder

does not necessarily possess learning disability. Moreover,

it is proved by this research that ADHD is not the same as

learning disability. The researcher therefore concludes

that the psychological testing done using the assessment

she made can be utilized the same way as the standardized

psychological tests are used.

 The researcher then recommends that parents should

take advantage of all the support and education that's

available, and a parent should be able to help her child

with ADHD navigate his or her way to success. She recommends

parent education and support groups to help family members

accept the diagnosis and to teach them how to help their

child organize his or her environment, develop problem-

solving skills, and cope with frustrations. Parent training

can also teach parents to respond appropriately to their

child's most trying behaviors and to use calm disciplining

techniques. Individual or family counseling may also be

helpful.

A parent is a stronger advocate for his child when she

fosters good partnerships with everyone involved in her

child's treatment - that includes teachers, doctors,

therapists, and even other family members.

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