AN ANALYTICAL STUDY OF FACTORS

INFLUENCING ANXIETY AND DEPRESSION OF

PERSONS WITH MENTAL RETARDATION

A THESIS

Submitted by

SOUMEE CHAKRABORTY

Reg Number: 80187610100803

in partial fulfillment for the award of the degree

of

DOCTOR OF PHILOSOPHY

FACULTY OF PSYCHOLOGY

CMJ UNVIERSITY

SHILLONG

2012

UNDER THE SUPERVISION OF

DR. SUBHOD KUMAR

BONAFIDE CERTIFICATE

Certified that this thesis titled AN ANALYTICAL STUDY OF FACTORS

INFLUENCING ANXIETY AND DEPRESSION OF PERSONS WITH

MENTAL RETARDATION is the bonafide work of SOUMEE

CHAKRABORTY who carried out the research under my supervision.

Certified further that to the best of my knowledge the work reported

herein does not form part of any other thesis or dissertation on the basis of

which a degree or award was conferred on an earlier occasion of this or

any other candidate.

SIGNATURE

RESEARCH SCHOLAR

SIGNATURE

SUPERVISOR

DECLARATION

I hereby declare that the dissertation titled " AN ANALYTICAL STUDY OF FACTORS

INFLUENCING ANXIETY AND DEPRESSION OF PERSONS WITH MENTAL

RETARDATION " is the research work carried out under the guidance of Dr. SUBHOD

KUMAR , submitted in the partial fulfillment of the requirements for the award of degree of

Doctor of Philosophy in Management and the dissertation has not formed the basis for the

award of any degree of any academic course.

Place: _____Sign_______________

SOUMEE CHAKRABORTY

Date: _____Sign_______________

Dr. SUBHOD KUMAR

Ph.D PSYCHOLOGY

ACKNOWLEDGEMENTS

I extend my sincere gratitude to Dr. SUBHOD KUMAR , for giving me the

opportunity to do this study and undergo the process of learning. I thank him for all

the trust and faith he posed in me and I only hope that I have been able to live up to

his expectations. Her guidance and support was helpful.

I would like to express my sincere gratitude to Dr. Nimita Khanna, Director Isara

Institute, My faculty guide who encouraged me and guided me to prepare this report

and helped me in carrying out my task.

_____Sign_______________

SOUMEE CHAKRABORTY

Contents

1. INTRODUCTION ........................................................................................................................... 8

1.1 ANXIETY, DEPRESSION AND HEALTH .......................................................................... 9

1.2 ASSESSMENT OF ANXIETY AND DEPRESSION ........................................................... 12

1.3 COMORBIDITY ........................................................................................................... 17

1.4 RISK FACTORS ........................................................................................................... 21

1.5 B-vitamins and its effects on depression .................................................................. 25

1.6 Psychosocial factors .................................................................................................. 29

1.7 Socioeconomic status ............................................................................................... 30

1.8 A meta-analysis ......................................................................................................... 30

1.9 Indicators of SES and anxiety and depression .......................................................... 31

1.10 Impact of childhood anxiety disorders on childhood and adult ............................... 35

1.11 Aims for the current study ........................................................................................ 37

2. LITERATURE REVIEW .............................................................................................................. 42

2.1 MENTAL RETARDATION ........................................................................................ 42

Diagnosing Mental Retardation ............................................................................................ 43

Families ............................................................................................................................ 44

Children ............................................................................................................................ 45

Adults ................................................................................................................................ 45

2.2 DEPRESSION ............................................................................................................ 47

2.3 SURVEY OF LITERATURE ....................................................................................... 50

3. Hypothesis ............................................................................................................................... 54

4. ADULTS WITH MENTAL RETARDATION AND MENTAL DISORDERS ................................ 56

4.1 Presentations of mental disorders in people with mental retardation?............. 56

4.2 Mental disorders in adults with mental retardation? .......................................... 58

4.3 Factors Involved in assessment of mental disorders in adults with mental

retardation? ......................................................................................................................... 61

4.4 Psychological treatments which are mostly used? ............................................... 63

5. RESULTS & FINDINGS ............................................................................................................. 68

6. RECOMMENDATIONS FOR FURTHER RESEARCH ............................................................... 79

7. REFERENCES ........................................................................................................................... 82

1. INTRODUCTION

This dissertation addresses two of the most common mental ailments, namely

anxiety and depression in Mental Retardation. For an understanding of these

vaguely defined and multi- factorial symptoms and disorders, a wide spectrum of

research approaches is required. Various concepts of psychopathology and

assessment methods illuminate different aspects of anxiety and depression, and the

reciprocal relation between these constructs. Examination of the co-occurrence of

anxiety and depression, as well as their co-morbidity with somatic illnesses

elucidates the broad role of anxiety and depression within the field of health care.

Likewise, studying associations with neurobiological and psychosocial factors will

give a more comprehensive understanding of the mechanisms involved in the

development of anxiety and depression.

Hence, the studies of this dissertation address how anxiety and depression can be

assessed by a simple questionnaire, how the relation between anxiety and depression

can be viewed by two different approaches to psychopathology, how anxiety and

depression are co-occurring with some somatic illnesses and symptoms, and finally

how anxiety and depression are related to some neurobiological and psychosocial

factors. Health surveys have a long tradition in the studies of major health problems

such as tuberculosis and cardiovascular illnesses. Recently, mental disorders have

received status as a major health problem in society, and, therefore, measurements

of anxiety and depression have become a major goal of the national health surveys

(1).

1.1 ANXIETY, DEPRESSION AND HEALTH

Prevalence

Anxiety disorders and depression are among the most frequently occurring mental

disorders in the general population. However, prevalence estimates vary markedly

in different studies. In the Epidemiologic Catchment Area Study (ECA) (2) the 12-

month prevalence of a major depressive episode was 5.8%, compared to 10.3% in

the National Comorbidity Study (NCS) (3), and 7.3% in a recent study from Oslo,

Norway (4). The 12-month prevalence of any anxiety disorder in ECA was 12.7%,

and in NCS 17.2%. In the Oslo study the overall prevalence of anxiety disorders was

not reported, but the prevalence of the separate anxiety disorders were lower than in

NCS. Although this may reflect real differences geographically or historically, the

main explanation is probably differences in assessment instruments and their

relation to different classification systems. ECA used the Diagnostic Interview

Schedule (DIS) (5) which gave diagnoses according to the Diagnostic and Statistical

Manual of Mental Disorders, third edition (DSM-III) (6). In contrast, the Composite

International Diagnostic Interview (CIDI) (7) was used in NCS and the Oslo study,

giving diagnoses according to DSM-III-R (8) and the International Classification of

Diseases, version 10 (ICD-10) (9). The sampling procedures also differed; while

ECA was a multi-site study, NCS included a nationally representative sample, and

the Oslo study included a locally representative sample.

The findings of a relatively high prevalence of mental disorders, e.g. 29% of any

one-year DSM-III-R mental disorder in NCS, have questioned the clinical

significance of the diagnoses achieved in such studies (10). This issue has recently

been considered in a re-analysis of ECA and NCS (11), where clinical significant

symptoms had to be related to self-reported use of health services, medication, or

impairment. By this approach the prevalence of the anxiety disorders and major

depression generally decreased, and the revision concluded with a one-year

prevalence of any anxiety disorder of 11.8% and major depressive episode of 4.5%.

The one-year prevalence of the anxiety disorders differed considerably, the most

prevalent was simple phobias (4.3%), followed by posttraumatic stress disorder

(3.6%), social phobia (3.2%), generalised anxiety disorder (2.8%), agoraphobia

(2.1%), obsessive-compulsive disorder (2.1%), and panic disorder (1.4%).

Dysthymic disorder (low-grade, chronic depression) and bipolar disorder (I/II)

(recurrent depressive and manic/hypomanic episodes) had a one-year prevalence of

0.7% and 1.7%, respectively. Since the one-year prevalence of having any of these

mental disorders was 14.9%, the public health impact of depression and anxiety

disorders should be evident.

Impact on public health, costs and need for research

Depression was ranked as the fourth most important specific cause of global

disability-adjusted life years (DALY, sum of life years lost due to premature

mortality, and years lived with disability adjusted for severity) by the Global

Burden of Disease Study (GBD) (12) and was predicted to advance to the second

most important cause by year 2020 (13). The role of anxiety disorders was not

addressed in the GBD, but analyses from the NCS estimated the annual costs of

anxiety disorders (panic disorder, posttraumatic stress disorder, agoraphobia,

social phobia, simple phobia and generalised anxiety disorder) to be 54 % of the

total costs due to treatment for somatic illness, and 31 % of the costs due to

treatment for mental illness (14). The total cost of affective disorders (major

depression, dysthymia and bipolar disorder) was very similar to the total cost of

anxiety disorders.

Measures to prevent these widespread, deteriorating, and costly disorders should be

of great interest to society. However, much is still unknown about the etiology and

prevention of anxiety disorders and depression. Population-based epidemiological

studies collecting comprehensive information on both mental and somatic health as

well as characteristics of personal environment, lifestyle, use of health services, and

biological measures, are warranted to identify modifiable risk factors. Such studies

have not been abundant, but in Norway some have been performed during the last

two decades. Data from three of these health surveys are the basis of the studies

included in this dissertation.

1.2 ASSESSMENT OF ANXIETY AND DEPRESSION

Mental disorders are assessed by registration of subjective symptoms, behavioural

patterns, and impairment during a specified period, either through interviews or

questionnaires. However, there is a controversy about which features should

characterise the constructs of anxiety and depression, and whether these

conditions should be considered as categorical diagnoses or continuous

phenomena. Both approaches, therefore, are used in this dissertation . However,

before the assessment methods are presented, different approaches to the

understanding of anxiety and depression will be reviewed.

What is anxiety and depression?

Anxiety is usually described as the emotion of fear involving feelings of tension,

worry, apprehension, and dread for something considered dangerous in the future

(15). Depression is associated with the emotion of sadness, in addition to feelings of

sorrow, hopelessness, gloom, lack of energy, and anhedonia (16). These symptoms

are sometimes considered as normal psychological responses, equivalent to physical

pain, on a continuous scale from being absent to a maximum intensity. This

approach is often described as dimensional (17). In contrast, the categorical

approach views anxiety and depression as discrete psychopathological entities, or

disorders. Such disorders are classified as being present or not according to a

threshold for specific diagnostic criteria (17).

The categorical approach

From a public health and clinical point of view it is necessary to identify individuals

suffering from anxiety disorders and depression in order to make decisions about

planning of health services and treatment. Researchers also address anxiety and

depression by the categorical approach in order to get a reliable description of their

samples. The classification is based upon distinctive symptoms, such as panic or

depressed mood, and their impact, most often on functional impairment, as well as

their duration. The validity of categorical diagnoses can be settled by converging data

from clinical, family, populationbased, and laboratory studies (the Washington

University criteria) (18, 19).

A syndrome is defined by the presence of a set of co-occurring symptoms, and may

be considered as a valid diagnosis if it has a predictable clinical course, treatment

response, and pattern of familial aggregation (20). Accordingly, the current

classification systems, DSM-IV (21) and ICD-10 (9), are meant to be atheoretical,

solely describing the characteristic of the diagnoses, mainly without consideration of

etiology or hierarchical organisation of the disorders. Moreover, in the expanding

revision of DSM-III-R (8), which aimed to include all kinds of psychopathology,

there was no assumption that each mental disorder is a discrete entity with sharp

boundaries (discontinuity) between it and other mental disorders (p. xxii).

In both ICD-10 and DSM-IV anxiety is classified as different anxiety disorders,

while depression is mainly classified as unipolar or bipolar disorder with a variety

of subtypes.

The dimensional approach

A limitation of the categorical approach is the need to define sharp, clear-cut

thresholds between normality and pathology. Sub-threshold conditions of

depression as well as of anxiety disorders have been found to have significant

clinical impact in terms of functional impairment, mortality, treatment, and

prognosis (22-27). However, simply lowering the diagnostic threshold does not

solve the problem of categorization (28). Thus, it has been suggested that anxiety

and depression are dimensional phenomena with no thresholds between pathology

and normality (29). Hence, the use of symptom scores opposed to categorical

diagnoses has been proposed for research addressing anxiety and depression (17).

Models for underlying dimensions

By use of latent trait analyses of GHQ scores from primary care patients,

Goldberg and colleagues (30) identified the highly correlated dimensions of

anxiety and depression underlying the common mental illnesses presented in these

patients. Later, Goldberg proposed a dimensional model for common mental

disorders, including anxiety, depression and somatisation (31). Other similar

models of non- psychotic psychopathology have been developed, such as

Kruegers model (32) that identified an externalising and an internalising

dimension, the latter encompassing the anxious-misery and fear sub-dimensions.

After having reviewed nearly 400 studies addressing symptoms of anxiety and

depression among patients and non-patients, Clark and Watson (33) suggested a

tripartite model. First, the model contains a common factor for anxiety and

depression consisting of general distress or Negative Affect including both anxious

and depressed mood, insomnia, and poor concentration. Second, a specific factor for

anxiety, consisting of tension and anxious arousal manifested as shortness of breath,

dizziness or light-headedness, and dry mouth was described. Third, the depression

factor was described as anhedonia and absence of Positive Affect, i.e. loss of interest

and feeling that nothing is interesting or enjoyable. However, subsequent testing of

this model failed in confirming such a simple concept. Hence, Mineka, Watson and

Clark (34) proposed an integrative hierarchical model of anxiety and depression,

not very different from the original tripartite model, but where each individual

anxiety disorder and depression had their own unique component that differentiated

them from all the others. Later, Watson has suggested more specific factors for the

various anxiety disorders (35).

Assessment of anxiety and depression in epidemiological studies

In epidemiological studies focusing mainly on mental health, standardised

interviews performed by trained lay people have been the gold standard. As

described in the ECA, DIS was used, while CIDI was used in the NCS and the Oslo

study. Such interviews are suitable for collecting comprehensive information as to a

variety of mental symptoms, and yield categorical diagnoses according to the ICD-

10 and DSM-IV classification systems. However, in large-scale health surveys the

diagnostic information is mostly obtained from short questionnaires, resulting in a

limited number of data on each topic.

Rating scales

Rating scales are widely used for clinical as well as scientific purposes. They yield

scores that may be used as continuous measures (dimensional approach), or they

may be used as diagnostic tests to identify cases by defined cut-off values

(categorical approach). Several questionnaires that assess anxiety and depression are

applicable in many settings due to their low cost. In epidemiologic studies the

following instruments are mostly used: Center for Epidemiological Studies of

Depression Scale (CES-D) (36); Becks Depression Inventory (BDI) (37);

Spielberger State-Trait Anxiety Inventory (STAI) (38); Hopkins Symptom Check

List (HSCL) (39); General Health Questionnaire (GHQ) (40); and Hospital Anxiety

and Depression Scale (HADS) (41). Some assess both anxiety and depression

(HADS, HSCL, GHQ) while others assess only anxiety (STAI) or depression (CES-

D; BDI).

1.3 COMORBIDITY

The co-occurrence, or comorbidity, of two or more diseases is relatively common

both in psychiatry and in somatic medicine, in particular in older age groups (47).

Various combinations of diseases may occur simply by chance. However, the term

comorbidity is usually applied when the risk (e.g. odds ratio) for a co-occurring

disease is more than by chance (48). Some critics claim that comorbidity is simply

an artefact of splitting nosological entities into separate classes. Hence, two

disorders that have some common diagnostic criteria, are more prone to co-occur,

which is called diagnostic comorbidity (49). Furthermore, when the co-occurring

condition is a consequence of the other, e.g. when panic disorder is followed by

agoraphobia, it has been referred as pathogenic comorbidity (49). As long as the

diagnostic hierarchy

with one main diagnosis introduced by Jaspers in 1913, was accepted, comorbidity

was non-existing. The idea to make hierarchy-free diagnoses was suggested in

1984 (50), and was accepted in DSM-III-R in 1987, after which comorbidity

ensued as an important issue. However, due to lack of consensus as to definition,

the reported extent of comorbidity varies across studies (51).

Comorbidity between anxiety and depression

Varying degrees of comorbidity between anxiety disorders and depression have

been reported in different studies. In NCS (52) the comorbidity between the 12

month prevalence of major depressive disorder (MDD) and any anxiety disorder

was 51 %. In the international WHO Study on Psychological Disorders in Primary

Health Care (53) the rates were somewhat lower. Among cases of depression 39%

had an anxiety disorder, and among cases of anxiety disorder 44% had a

depression. In a clinical sample panic disorder and generalised anxiety disorder

were found to be more common in bipolar disorder than in MDD (54), while this

pattern was not seen in a population-based study (55).

Anxiety disorders and depression has several consequences including increased

symptom severity (56), impaired treatment response to antidepressive medication

(57), impaired recovery rate from depression, increased time to recovery,

decreased time to relapse (58, 59) as well as increased risk for suicide (60).

Studies addressing comorbidity have almost exclusively applied a categorical

approach (61). Since the dimensional approach is seen as complementary to the

categorical (62), it is paradoxical that the dimensional approach to anxiety and

depression has hardly been applied when studying the causes or consequences of

such comorbidity. In co-occurring anxiety and depression the contribution from

each may vary from a minimum to a maximum of symptom load, resulting in an

anxiety- depression ratio varying from zero to infinite.

Although it is well known that anxiety and depression are highly correlated (34), a

correlation coefficient alone cannot describe whether the relationship between the

two is the same in the lower and upper parts of the symptom scales. The lower

parts (i.e. few symptoms) are of special interest because sub-threshold conditions

have been reported to be of clinical significance (22), and because most individuals

have scores in that range.

The high correlation between anxiety and depression does not necessarily mean that

they are similarly associated with other mental or somatic conditions, or with

various risk factors. However, in studies addressing depression, comorbid anxiety

disorders or co-occurring anxiety symptoms are frequently not accounted for, and

vice versa for studies addressing anxiety disorders. Hence, it is not known whether

the findings are mainly caused by the anxiety or the depression component.

Anxiety and depression, and somatic disease

The prevalence of anxiety disorders and depression among individuals reporting

somatic illness in the general population (63) or among patients in general practice

(64, 65), is higher than the prevalence among somatically healthy individuals. The

hospital stay of patients with such comorbidity has been reported to be significantly

longer than for somatic patients without co-occurring anxiety or depression (66). In

an international study the economic consequences of depression were influenced to

a greater extent by the presence of somatic comorbidity than by depressive symptom

severity alone (67).

The majority of studies have examined cardiovascular disease, such as

myocardial infarction (68-73), stroke (74), and arterial stiffness (75), and found

increased prevalence of depression. Increased prevalence of depression has been

reported as well in diabetes (76, 77), Parkinsons disease (78), rheumatoid

arthritis (79), and back pain (80). Increased prevalence of anxiety has been

reported among patients with peptic ulcer (81). Among patients with functional

gastrointestinal complaints (82), cancer (83-85), HIV-infection (86-88), and

multiple sclerosis (89) the prevalence of both anxiety and depression is

increased.

The mechanisms linking anxiety and/or depression with somatic disease are not

known in part due to the presumed complexity of such mechanisms, as well as the

heterogeneity of both mental disorders and somatic diseases included in the various

studies (90-92). In addition, there is a paucity of longitudinal studies and most of

these have addressed depression only (47).

Three theoretical explanations for these associations have received some support.

First, anxiety/depression may cause or aggravate somatic disease, second, somatic

disease may cause or aggravate anxiety/depression, or, third, there may be some

common pathophysiological mechanisms for both anxiety/depression and somatic

disease (92). Some studies suggest a reciprocal relationship between depression

and somatic health problems (93, 94) merging the two first theoretical alternatives.

Common pathophysiological mechanisms may involve the effect of hormonal

dysfunction, nutritional deficiencies, toxic agents, or neurodegenerative or

inflammatory processes.

It is also possible that the observed comorbidity may be due to one or more

uncontrolled confounding factors in the studies (95). These may include age or

gender, as well as socioeconomic status, psychosocial factors or health behaviours

(smoking, alcohol consumption, unhealthy dietary habits and lack of physical

exercise). Finally, many studies have examined either anxiety or depression, and if

they have included both, they usually have not accounted for the close association

between the two. If the subjects studied have a depression with co-occurring

anxiety (or vice versa) it may be hard to tease apart whether the association with a

somatic disease is mainly due to the depression or the anxiety (20). We are aware

of only one study (N=711) (96) addressing the occurrence of somatic illness in

comorbid anxiety and depression. Hence, the patients with panic disorder and

comorbid major depressive disorder were reported to have higher rates of somatic

illness (peptic ulcer, angina pectoris, and thyroid disease) than patients with

anxiety disorder without depression. However, the specific rates were not reported,

nor tests of statistical difference between them.

1.4 RISK FACTORS

A risk factor may be defined as An aspect of personal behaviour or life-style, an

environmental exposure, or an inborn or inherited characteristic, that, on the basis

of epidemiological evidence, is known to be associated with health-related

condition(s) considered important to prevent (97). However, the term is frequently

inconsistently and imprecisely used (98), and should be differentiated into e.g. risk

markers, determinants and modifiable risk factors (97).

In the social sciences intermediate factors in a causal pathway from e.g.

socioeconomic status (SES) to e.g. anxiety and/or depression, are often denoted

mediators (99). However, to identify a mediator, a longitudinal study design with

at least two follow-up points is necessary to establish the causal direction between

various factors (100). In a cross-sectional study, or when there is only one follow-

up, it might be difficult to decide whether a factor is a mediator or a confounder.

Contrary to a mediator, a confounder should not be caused by the exposure (101),

which is difficult to prove without three consecutive measurements as well.

Specific risk factors may be difficult to identify when the validity of the outcome is

questionable, e.g. due to extensive comorbidity (see section 4.3.1.) or overlapping

criteria with other outcomes. In the search for risk factors in mental disorders,

strong associations are therefore not to be expected. Alternatively, other phenotypes

of neurophysiological, biochemical, endocrinological, neuroanatomical, cognitive,

or neuropsychological (including configured self-report data) nature, called end

phenotypes, have been suggested (102).

Different theoretical approaches to mental disorders have emphasized their unique

etiological models. Hence, research addressing biological, psychological, as well as

social risk factors has been conducted. These different perspectives are, however,

artificially separated, and an explicit integrated bio psychosocial model

acknowledging the multi factorial diathesis of disease in general, and mental

disorders in particular, was proposed by Engel (103) and has been implemented to a

certain extent. Our knowledge of neurobiological and psychosocial risk factors is

incomplete, as well as how they interplay in precipitating mental disorders (104). In

the following sections some of these factors will be reviewed as to current status

and unanswered questions.

Biological factors

Genetics

A meta-analysis including twin studies of anxiety disorders has revealed a

heritability between 30-40% (105), while another meta-analysis of major

depressive disorder found 37% heritability (106). However, the limited reliability

of life-time diagnosis in, for example, major depression (107) is likely to cause too

low estimates of the heritability due to overestimation of the individual specific

environmental factors (108). The genetic factor in bipolar disorder is assumed to be

even stronger than in major depression (109).

There is some evidence for common etiologic factors for anxiety and depression.

Female twin studies have shown that the genetic factors of MDD and generalized

anxiety disorder seemed identical (110), while the association between the genetic

factors of MDD and other anxiety disorders was modest (111). Obsessive

compulsive disorder seemed to be genetically unrelated to depression or other

anxiety disorders (112), but related to Tourettes syndrome (113).

Some studies have shown associations between a single nucleotide polymorphism

in the promotor region of the serotonin transporter gene and neurotisism (114),

anxiety (115) and depression (116), but others have not (117). Moreover, a study

using functional magnetic resonance imaging demonstrated an association

between this polymorphism and an increased response in amygdala, (the

neurophysiological substrate for normal and abnormal fear behavior) to fearful

stimuli (118).

Neuro Science

Most studies examining neurobiological factors in mental disorders compare

clinical samples to healthy controls. To measure such factors expensive and

sometimes unpleasant or painful procedures are necessary, limiting the sample size

and the chance of participation at follow-up assessments. Accordingly, in the

paucity of longitudinal population-based studies, it may be difficult to decide

whether the factors identified in cross-sectional association studies are

determinants or only markers of the disorder. Hence, frequently short-cuts are

made directly from clinical cross-sectional observations to randomised clinical

trials (RCT).

In mental disorders neurotransmission is compromised in various ways, which has

lead to the development of drugs influencing receptors and transport mechanisms for

neurotransmitters. Benzodiazepines binding to the gamma amino butyric acid

benzodiazepine receptor complex have a tranquillising effect on anxiety (119), while

different drugs inhibiting the serotonin reuptake in the synapses have a relatively

good effect on depression and anxiety as well (120).

The hypothalamic-pituitary-adrenal (HPA) axis is affected in both anxiety and

depression. Anxiety is characterised by hypocortisolemia, supersuppression after

dexamethasone, and increased number of glucocorticoid receptors. In contrast,

depression is characterised by hypercortisolemia, non-suppression after

dexamethasone and decreased glucocorticoid receptors (121). Abnormal regulation

of sex-hormones (122), thyroid hormones (123, 124), and melatonin (125, 126) is

observed in patients with anxiety disorder and depression. Elevated levels of

cytokines, as seen in some infections and immunotherapy of cancer and hepatitis,

may induce depression and possibly anxiety as well (127).

1.5 B-vitamins and its effects on depression

Deficiency of nutritional factors, such as fatty acids (128), tryptophan (129), folic

acid, and cobalamin have all been associated with depression. The evidence for

folic acid and cobalamin will be reviewed more closely in this section.

Folate is a B-vitamin of major importance for methylation processes (one- carbon

metabolism) in the brain. By transferring a methyl group from 5-methyl-

tetrahydrofolate (5mTHF), the cobalamin dependent methionine synthetase

converts homocysteine into methionine (figure 3). Folate deficiency may be

caused by an inadequate dietary intake, increased metabolic demands due to

cancer, or certain drugs (130), or due to a single nucleotide polymorphism of

methylenetetrahydrofolate reductase gene (MTHFR 677C T) reducing the

availability of 5mTHF (131). Cobalamin deficiency may also be caused by an

inadequate intake (e.g. among strict vegetarians) as well as gastrointestinal disease

(in particular atrophic gastritis among elderly) (130). Low levels of both folate

(132) and cobalamine (133) are associated with elevated levels of serum homo

cysteine .

Four decades ago Victor Herbert (134) treated successfully his self-induced folate

deficiency symptoms of insomnia, irritability, and impaired memory by folate

supplementation. However, our understanding of the role of folate, and one-carbon

metabolism in general, in mental disorders is still insufficient. Most studies on

folate and depression are cross-sectional and compare folate status in depressed

patients with the status in patients with other mental disorders or in healthy

subjects. These studies suggest that low folate status is associated with depression,

especially with more severe forms, prolonged episodes and weak treatment

response (135). The limitations of these studies are related to lack of longitudinal

design, small sample size, highly selected patients and lack of adequate control

groups. Notably, two population-based studies (136, 137) controlling for possible

confounders demonstrated no association between folate status and depression.

Indications that folate deficiency increases the risk for depression, have been

obtained mainly from biochemical and in vitro studies, but also from a recent study

of dietary habits (138). Folate metabolism is linked to biopterin-dependent

neurotransmitter synthesis (139) (figure 4) and methylation of biogenic amines and

phospholipids in the central nervous system (CNS) (140).

Only two studies (141) have shown an association between serum total

homocysteine and depression, while other studies have not (137, 142, 143).

Homocysteine, or its metabolites, may have a direct excitotoxic effect on the

N- methyl-D-aspartate glutamate receptors in the CNS, or may inhibit the S-

adenosylmethionine (SAM)-dependent methylation via S-adeno

sylhomocysteine (140).

Investigations on a possible role of cobalamin status in neuropsychiatric disorders

have been motivated by the central nervous system damage caused by overt or

subtle cobalamin deficiency (145, 146). Data regarding the association between

serum cobalamin levels and depression are ambiguous (137, 143, 147-149).

Elevated levels of the cobalamin marker, methylmalonic acid, have been found

among depressed physically disabled older women in a population-based study

(137). Moreover, higher baseline serum cobalamin has been associated with a

better outcome in treated depressed outpatients (150). Cobalamin is a co-factor in

the methylation of homocysteine to methionine, which in turn affects the levels of

both homocysteine and SAM.

MTHFR 677CT affects MTHFR activity and thus folate distribution and

homocysteine remethylation (131). Inconsistent results on the association between

depression and the MTHFR 677C T polymorphism have been obtained (151, 152).

In case such a relation can be confirmed, it will support the hypothesis that altered

folate status may precede the onset of depression.

Despite our incomplete understanding of the relation between methylation and

mood, several clinical trials examining the effect of folate in antidepressant

treatment have been conducted. The results are promising, though the samples are

small, and in only four of the studies were patients randomised to folate or placebo

(153-156). The largest (n=127) and best designed study (154) showed a significant

beneficial effect only in women. The lack of significance in men could be due to the

small sample size or an insufficient dosage of folate. Still, we do not know which

patients should be supplemented with folate, the duration of treatment, the dosage

(135) or the safety of high dosage folate supplementation (157).

There is of the extensive comorbidity between depression and anxiety (52, 53), we

have found no more than three studies (148, 158, 159) addressing the possibility of

impaired one carbon metabolism in anxiety disorders. Only one of theses suggests

such an association, namely between low cobalamin and anxiety (148).

1.6 Psychosocial factors

Environmental influences are strong and pervasive on mental health (160). Since

World War II various kinds of stress have been addressed as determinants of

anxiety and depression (161). Childhood adversities, such as loss of a parent,

parental psychopathology, parental aggression, physical or sexual abuse, or life-

threatening accidents, are associated with later anxiety and depression (162, 163).

Likewise, adverse life events in adulthood, such as unemployment, homelessness,

violence, breakdown of a relationship, loneliness, and lack of social support, have

been observed to have similar effects on anxiety and depression (161, 164).

Psychosocial factors have been associated with a worsened prognosis in bipolar

disorder, however the relationship between such factors and bipolar disorder is

more ambiguous (109).

In the Islington study from London, some common environmental risk factors for

developing both anxiety and depression in women were found (165). These were

parental indifference and physical and sexual abuse in childhood. In adults, loss (of

a person, a position or resources) and lack of social support predicted depression,

while danger or threats (of a future loss, or a serious threat to life), predicted

anxiety. The combination of loss and threat predicted comorbid anxiety and

depression. A common feature of many of these adversities is their association with

social inequalities (166), in that individuals belonging to the lower social classes

have higher risk for being exposed to such unfortunate influences.

1.7 Socioeconomic status

Socioeconomic status (SES), which most often is characterised by length of

completed education, households annual income, and/or occupation, has consistently

been associated with poor somatic and mental health (166, 167). However, due to

differences in study design, use of indicators for SES, and assessment of mental

status, the relationship between SES and anxiety and depression is still ambiguous.

Moreover, despite the role of psychosocial factors in both SES and mental health, the

mechanisms causing this relationship are unknown.

1.8 A meta-analysis

In a recent meta-analysis Lorant et al found compelling evidence for socioeconomic

inequalities in depression (168). Low-SES individuals had a significantly higher risk

of being depressed (OR=1.81) compared to high-SES individuals in the 51 cross-

sectional studies, where a dose-response relation was observed both for education and

income. In the few longitudinal studies (n=7) similar socioeconomic inequalities in

depression were observed: a slight association in the incidence studies (OR=1.24) and

a moderate to strong association in the persistence studies (i.e. persistence of

depression from baseline to follow-up) (OR=2.06). However, after excluding the

studies not addressing education, the most frequently used SES indicator, the results

of the studies on incidence (169, 170) and persistence (170-172) were inconsistent.

The discrepancy may be due to differences in sample size and follow-up period

between the studies. Moreover, only one of the studies that examined SES included

education as the main predictor of depression (169).

1.9 Indicators of SES and anxiety and depression

The indicators of SES usually vary from study to study, and despite being only

moderately intercorrelated, such indicators are seldom addressed specifically.

Likewise, the assessment of anxiety and depression varies between studies, however,

according to Dohrenwend the use of different measures for mental health is welcomed

in this field, because until diagnosis is less dependent on interviews, it is important

to use a variety of methods (166).

Although anxiety disorders are closely related to depression (52, 53), we are not

aware of longitudinal studies of their relation to education.

The association between SES and depression is not fully understood. In contrast to

e.g. schizophrenia, there is most evidence that depression is a consequence, rather

than a cause, of low SES, at least in women (168, 173). However, some studies (174,

175) support the selection theory; (176) that is, depression may be an obstacle to

upward social mobility, and may promote downward social mobility.

Mechanisms Mediators

Assuming SES is a determinant, little is known about how SES influences the

development of new cases or the maintenance of chronic cases of depression. The

effect on depression of measures of SES other than education has been explained by

work characteristics (SES measure: occupational grade) (177), health behaviours

(SES measure: economic situation) (178), and psychosocial factors (SES measure:

income) (170). In longitudinal studies the effect of education has mainly been

explained by depressive symptoms at baseline (171, 172) and prior to baseline (172).

Anxiety as a Unidimensional or a multidimensional concept

First, anxiety can be defined as either Unidimensional (trait) or multidimensional in

nature. Anxiety as a trait refers to a broad, underlying single factor that may form a

vulnerability to each of the anxiety disorders. There are several theoretical frameworks

in which this single factor has been elaborated. These concepts include negative

affectivity, neuroticism, harm avoidance, or behavioural inhibition (see Zinbarg &

Barlow, 1996). There are some empirical indications that provide support for a

Tommon underlying factor. First, anxiety disorders tend to co-occur: Anderson (1994)

concluded that around 50% of children and adolescents in a clinical sample had a

concurrent anxiety disorder, which may imply the existence of an underlying

construct. Second, - different anxiety disorders tend to respond positively to the same

drug and cognitive-behavioural treatment components (e.g. Kendall, 1994), and

treatment outcome was independent of specific primary anxiety disorder (Cobham et

al.,1998; Barrett et al., 1996; Berman et al., 2000), suggesting that the disorders may

have common underlying features. Third, comorbid anxiety disorders tend to fade with

successful treatment of the primary anxiety disorder.

Unidimensional concept of anxiety, the multidimensional concept emphasizes that

clusters of anxiety symptoms reflect meaningful syndromes. The

Diagnostic and Statistical Manual of Mental Disorders (4th edition, DSM-IV,

American Psychiatric Association, 1994) is an extended example of this description of

different nosologies. Also in clinical practice, the clinician typically requires

information about the clustering of specific patterns of anxiety problems. Such

information may provide indications as to the type of situations that the child finds

difficult and may guide the content of treatment.

Many authors have found evidence for a hierarchical model. Zinbarg and collaegues

(1996) described both a higher order factor of trait anxiety and, in addition, lower

order factors providing the basis for differentiation among patient groups. Brown,

Chorpita, and Barlow (1998) also found separate factors of anxiety, namely

generalised anxiety disorder, panic disorder, obsessive-compulsive disorder, and social

phobia. In the so-called tripartite model (Clark & Watson, 1991), a general negative

affectivity component is defined as being the higher order factor for both anxiety and

depression, with anxiety and depression consisting of distinct symptomatology at a

lower level. This model has been replicated in children and adolescents (see Laurent

& Ettelson, 2001).

Anxiety as a dimensional or a categorical concept The second issue in the definition of

anxiety disorders is the discussion between a dimensional and a categorical concept. In

the field of psychology, anxiety is mostly perceived as a dimensional feature, as

existing on a continuum. Children differ in their level of anxiety, and those with high

levels of anxiety tend to experience greater problems in adaptive functioning. In the

categorical concept, which is based on the medical model, a child has an anxiety

disorder when meeting certain criteria for that disorder. If a child meets too few

criteria, there is no disorder. Three disadvantages of this model are that (1) it does not

allow for evaluation of the severity of the disorder, (2) the artificial severity cut-off is

quite arbitrary in dividing the two groups with and without the disorder, and (3)

individuals in the same category may not share the same symptoms (e.g. in separation

anxiety disorder, 3 of 8 symptoms are required in DSM-IV; APA, 1994). Researchers

have claimed the necessity of viewing anxiety as a dimensional (versus a categorical)

and a multidimensional (versus a unidimensional) concept in both theory and

assessment (Endler et al., 2001).

Questionnaires of anxiety in children

The development of self-report questionnaires of anxiety in children, the two issues of

unidimensional versus multidimensional, and of dimensional versus categorical, have

been prominent. Traditionally, child-completed anxiety questionnaires have aimed to

measure broad anxiety constructs and symptoms rather than specific symptoms of

anxiety that reflect diagnostic subtypes of anxiety. Over the past decade, several

measures have been developed to assess clusters of anxiety symptoms in young

people. These include the Multidimensional Anxiety Scale for Children (MASC;

March et al., 1997), the Screen for Child Anxiety Related Emotional Disorders

(SCARED; Birmaher et al., 1997), and the Spence Childrens Anxiety Scale (Spence,

1997). The last two measures are related to the DSM-IV structure of anxiety disorders.

The current study psychometrically evaluated the SCAS.

1.10 Impact of childhood anxiety disorders on childhood and

adult

Anxiety disorders in children are associated with low levels of adaptive functioning.

Compared to non anxious children, children with anxiety disorders show impairment

in peer relations, self-esteem, school performance and social behavior (Strauss, Frame,

& Forehand, 1987). They have more negative social expectations, report lower social

self competence, and their parents and teachers rate them as more socially maladjusted

(Chansky & Kendall, 1997). Also, many anxiety disordered adolescents report

psychosocial impairment (Essau, Conradt, & Petermann, 2000). Children with anxiety

disorders were 2.9 times more likely than children without any disorder to fail to

complete secondary school (Vander-Stoep, Weiss, McKnight, Beresford, & Cohen,

2002) and may thus be at risk for less adult economic success, and greater instability

at home and at work. In social phobia, children showed a high level of general

emotional over-responsiveness and loneliness, had significantly poorer social skills

(Beidel, Turner, & Morris, 1999), and reported lower levels of social functioning and

lower self esteem (Ginsburg, La Greca, & Silverman, 1998).

Generalized anxiety symptoms in children were associated with a higher risk of

alcohol consumption in adolescence (Kaplow, Curran, Angold, & Costello, 2001).

Formerly, anxiety symptoms were assumed to be passing phases in childhood and

adolescence, but researchers found the level of anxiety symptoms to be relatively

stable during childhood in both clinical (Beidel, Fink, & Turner, 1996) and normal

children (Verhulst & van der Ende, 1992; Ialongo, Edelsohn, Werthamer-Larsson,

Crockett, & Kellam, 2000; Heymens Visser, van der Ende, Koot, & Verhulst, 1999).

Research has demonstrated that children with an anxiety disorder were still likely to

fulfil the diagnostic criteria up to 8 years after the onset of the disorder (Kovacs &

Devlin, 1998). The content of anxiety symptoms, however, may differ over time.

Costello et al. (2003) reported that children with an anxiety disorder at one point were

likely to continue suffering from the anxiety disorder, or develop depression or

substance abuse.

Anxiety disorders in childhood may have impact on later development: 50% of

anxiety disordered adults reported anxiety disorders in childhood (Pollack, Otto,

Sabatino, & Majcher, 1996). Prospectively, clinically referred children with anxiety

disorders seem to be at risk for development of new mental disorders later in life

(Last, Perrin, Hersen, & Kazdin, 1996). Epidemiological research has shown that in

80% of the young adult cases, social phobia in adolescence preceded depression,

substance misuse, or other anxiety disorders (Wittchen, Stein, & Kessler, 1999). With

regard to adjustment, results of one study were more positive: young adults with a

history of only anxiety disorder did not show more impairment than normal controls.

The only difference found was that they were less likely to be living independent from

their family. The group that was at risk for high levels of impairment later in life

included anxious children with comorbid depression (Last, Hansen, & Franco, 1997).

This group was less likely to be working or in school, and reported more

mental problems.

1.11 Aims for the current study

Participants

In this study we have taken a sample size of , 76 children with anxiety disorders and

depression. They were 50% boys and aged 7-17 years (mean age 11.0, SD=2.4). Most

children lived in two parent households (n=68, 90%). All children had a primary

diagnosis of an anxiety disorder, namely separation anxiety disorder (n=23, 30%),

social phobia (n=29, 38%), generalized anxiety disorder (n=17, 22%), and panic with

or without agoraphobia (n=7, 10%). A majority of children (n= 57, 75%) had one, two

or three comorbid disorders.

The research involves the SCAS has, to date, focused primarily upon community

samples, and questions remain as to the validity of its factor structure, reliability and

convergent/ divergent validity with clinical populations. The present study had several

aims. First, it used confirmatory factor analysis to determine the degree to which the

pattern of anxiety symptoms amongst a clinical sample of children is in keeping with a

model based largely on the DSM-IV classification of anxiety disorders. It was

predicted that anxiety symptoms in clinically anxious children would cluster in a

manner that is consistent with the DSM-IV classification of anxiety disorders and

consistent with the findings for children in community populations. It was also

examined whether, consistent with findings in community samples, the inter-

correlations between factors would be satisfactorily explained by a single higher order

factor. In order to test this hypothesis, four models were examined and compared with

a null model which posits complete independence of all observed measurements and

all relations are constrained to be zero (Byrne, 1989). The models selected for

evaluation were based on theoretical grounds. The first comparison model (Model 1)

was a single factor model in which all symptoms are viewed as reflecting a single,

homogenous dimension of anxiety, with minimal variance left to be explained by

separate anxiety disorder factors. From a theoretical perspective, Model 1 examined

whether the high level of comorbidity of anxiety disorders in children reflects the lack

of distinct anxiety categories, with symptoms simply reflecting a single dimension of

anxiety.

Model 2 involved a six factor model reflecting the hypothesized position in which it is

proposed that anxiety symptoms will cluster within the factors proposed by DSM-IV,

namely panic disorder (with agoraphobia), social phobia, separation anxiety disorder,

generalized anxiety disorder, and obsessive compulsive disorder. The SCAS also

includes symptoms relating to a sixth dimension of physical injury. This latter

dimension was included in the original SCAS in response to the suggestion that fears

in children cluster into distinct social and physical domains suggesting the possibility

of a fear of physical injury dimension (Campbell & Rapee, 1994). In Model 2, the

factors were considered to be independent, thereby reflecting distinct, unrelated

clusters of symptoms.

Model 3 was defined according to the same structure as Model 2, but allowed the 6

factors to be inter-correlated. In view of comorbidity between anxiety disorders in

children, it was predicted that this model would provide a better fit than Models 1 and

2. However, in keeping with DSM-IV classification system, the model assumed that

although anxiety symptoms would cluster onto the 6 hypothesized factors, there would

be sufficient unique variance to justify acceptance of separate categories of anxiety

disorders.

Model 4 was a higher-order model, which examined the degree to which the data

could be explained by 6 clusters of anxiety symptoms, the covariation of which could

be accounted for by a single, higher-order factor of anxiety. Such a model is in

keeping with DSM-IV, which outlines an overall category of anxiety disorder within

which lie subtypes of anxiety disorders.

Aim of the study was to examine the construct validity of the scale in terms of the

association of SCAS scores and diagnostic classification based on structured clinical

interviews. In exploring its construct validity, Spence (1998) examined a clinical

sample, comprising 20 children with social phobia and 20 with comorbid social phobia

and separation anxiety disorder, compared with 20 non-anxious matched controls. As

predicted, clinically anxious children showed significantly higher SCAS scores than

the non-anxious controls, with comorbid anxious children showing significantly

higher total scores than those with pure social phobia. Importantly, the socially

anxious children reported higher scores on the social phobia subscale, but not other

subscales (except physical fears), in comparison to non-anxious children. Children

with both social phobia and separation anxiety reported higher levels of anxiety on all

subscales in comparison to non-anxious children and higher scores than the social

phobic group on the separation anxiety subscale.

Our study also examined whether significant differences in SCAS scores would be

evident in comparing clinically anxious children versus a general community sample,

and whether significant differences in subscale scores would be evident between

clinically anxious children presenting with different clinically diagnoses. The study

was to examine the internal consistency and convergent, divergent, and discriminant

validity of the SCAS in a large clinical sample of children with different anxiety

disorders. Given that data were obtained from both Dutch and Australian samples, a

subsidiary goal was to compare findings across the two populations.

2. LITERATURE REVIEW

Almost every primary research study begins with a review of the literature. The

purpose of the literature review section of a research article is to provide the reader

with an overall framework for where this piece of work fits in the big picture of

what is known about a topic from previous research. Thus, the literature review

serves to explain the topic of the research and to build a rationale for the problem

that is studied and the need for additional research

2.1 MENTAL RETARDATION

The essential features of mental retardation are a significantly sub-average general

intellectual function, accompanied by significant deficits in social functioning in areas

such as social skills, communication and in addition difficulties in attaining personal

independence and social responsibility. The onset of mental retardation must be before

the age of 18. Traditionally, intellectual functioning has been measured by IQ tests and

a significantly sub-average intellectual functioning was defined as an IQ of 70 or

below. However IQ tests are now treated with some flexibility that might permit the

exclusion from the diagnosis of mental retardation of some people with IQ's lower

than 70. This is the case if it is felt that there are no significant deficits in adaptive

function (the person's effectiveness in areas such as social skills, communication, daily

living skills, etc) Mental retardation can be further broken down into borderline, mild,

moderate, severe and profound according to IQ. The IQ level gives an approximate

guide to the individual's general level of functioning.

Diagnosing Mental Retardation

Chromosomal abnormalities and metabolic disorders often are diagnosed by doctors

during prenatal testing or at birth. In other cases, however, a parent, caregiver, or

teacher may be the first to notice that a baby or young child is not demonstrating new

skills at the same pace as his or her peers. For example, the child may not crawl, walk,

or talk by the expected age.

Using thorough physical and psychological examinations, doctors try to rule out other

possible causes of the child's delays, such as hearing or vision problems,

neuromuscular disorders, emotional or behavioral problems, learning or speech

disorders, abuse, or a troubled home life. Pediatricians use blood tests, brain scans,

genetic testing, and other medical tests to look for underlying physical disorders.

Psychologists use developmental tests to help determine whether babies and children

actually are behind peers, and they use standardized intelligence tests to compare the

abilities of school-aged children to those of average children in the same age group.

Psychologists also may observe the child at play, in school, and interacting with

family members before making a diagnosis of mental retardation. Because

developmental delays are not always linked to mental retardation, and because they

may improve with physical treatment or changes in the child's environment,

psychologists often schedule repeated evaluations over time to measure delays and

assess improvements in intelligence and adaptive behaviors.

Living with Mental Retardation

Families

Parents who learn that an infant or child has mental retardation often are shocked, and

they may be overwhelmed by feelings of sadness, helplessness, or anger until they

adjust to the news. Family counselors and support groups often are needed to help

parents learn how to meet the special needs of mentally retarded children and balance

those needs with other family responsibilities, particularly to siblings who also must

adjust to the situation. To help children with mental retardation, many families work

with a team of specialists that includes psychologists, speech and language

pathologists, physical and occupational therapists, social workers, and special

education teachers.

History

In 1975, the U.S. Congress passed Public Law 94-142, the Education for All

Handicapped Children Act, which was renamed the Individuals with Disabilities

Education Act (IDEA) in 1990. IDEA guaranteed all children with disabilities a "free

appropriate public education." It said that children with disabilities should be educated

alongside their nondisabled peers "to the maximum extent appropriate," a practice

known as "mainstreaming." Since then, teachers, principals, parents, civil rights

advocates, and even courts of law have debated whether or not students with mental

retardation should be educated in the same classrooms as their nondisabled peers.

Some argue that this practice places too great a burden on teachers.

In general, current policy favors including students with mental retardation in regular

classrooms to whatever extent is possible. Under IDEA, every disabled child has the

right to an annual, written individualized education plan (IEP) starting at age 3.

Teachers, therapists, and parents work together to develop the best plan for educating

the child, which may mean full inclusion in regular classes, partial inclusion

supplemented by special education classes, or separate classes full-time. IDEA also

ensures that children with special needs get free access to any education-related

services they need, including transportation, counseling, and special therapy.

Children

Children with mental retardation face many emotional challenges. They may know

that they are "different" from their peers in ways that they may not understand. They

may think that their families consider them a burden or an annoyance or a reason for

shame, and they may be aware that they are "special needs" students in school.

However, children with mental retardation can benefit from treatment and support in

learning academic skills and the adaptive behaviors needed for everyday living. They

also may get a boost in self-esteem by realizing that they, like other children, are

unique and valuable individuals.

Adults

Adults with severe or profound mental retardation requiring constant supervision often enter

nursing homes or other residential facilities that offer intensive 24-hour care. However, the

majority of adults with mild to moderate mental retardation can achieve varying degrees of

independence. Because they may want or need some support and guidance, many continue to

live with family members or in group homes, apartment clusters, or hostels designed

especially for people with special needs. Some are able to hold jobs and participate in

community events such as the Special Olympics, which can help them develop greater self-

esteem. Others are able to get married and start their own families.

Borderline / Mild Mental Retardation

They represent about 80% of people with mental retardation and their appearance is

usually unremarkable and any sensory or motor deficits are slight. In adult life most of

these people are never diagnosed. Most of these people can live independently in

ordinary surroundings, although they may need help with housing and employment or

when under some unusual stress.

Moderate Mental Retardation

People in this group account for about 12% of the learning disabled population. Most

of them can talk or at least learn to communicate and they take3 care of themselves

with some supervision. As adults they can usually undertake simple or routine work

and find their way about.

Severe Mental Retardation

This group accounts for about 7% of the learning disabled population. In preschool

years their development is usually greatly slowed. Eventually they may acquire some

skills to look after themselves although under close supervision. They may also be

able to communicate in a simple way. Association adults they can undertake simple

tasks and engage in limited social activities.

Profound Mental Retardation

People in this group account for less than 1% of the learning disabled group. Few of

them learn to care for themselves although some eventually acquire some simple

speech and social behavior.

2.2 DEPRESSION

Depression is a normal response to loss or misfortune. Depression is abnormal when

it is out of proportion of the misfortune or unduly prolonged. Depressive mood is

closely coupled with other changes, notably a lowering of self-esteem, self-criticism

and pessimistic thinking. Depression occurs in many psychiatric disorders. It is the

defining feature of the depressive disorders and it occurs commonly in schizophrenia,

anxiety and obsession disorders and in eating disorders. (M. Gelder, R. Mayon & P.

Cowen, 1983)

Depression may be defined in terms of the following attributes:

A. A specific alteration in mode: sadness, loneliness, apathy.

B. A negative self concept associated with self reproaches and self- blame.

C. Regressive and self punitive wishes: desires to escape, hide or die.

D. Vegetative changes: anorexia, insomnia, loss of libido.

E. Changes in activity level: retardation or agitation.

The cognitive manifestations of depression include a member of diverse phenomena.

One group is composed of the patients distorted attitudes toward himself, his

experience and his future. This group includes low self evaluations, distortions of

body image and negative expectations. Another symptom, self blame, expresses the

patients notion of casualty; He is prone to hold himself responsible for any difficulties

or problems that he encounters. A third kind of symptom involves the area of decision

making. The patient typically vacillates and is indecisive. (Aaron. T. Beck, 1967)

COGNITIVE & MOTIVATIONAL MANIFESTATIONS OF DEPRESSION:

FREQUENCY AMONG DEPRESSED AND NON-DEPRESSED PATIENTS

D e p t h o f D e p r e s s i o n

None Mild Moderate Severe

Manifestation % % % %

n=224 n=228 n=377 n=86

1) Low Self-

Evaluation 38 60 78 81

2) Negative

Expectation 22 33 72 87

3) Self-blame &

Self-Criticism 43 67 80 80

4) Indecisiveness 23 48 67 76

5) Distorted Self-

image 12 33 50 66

6) Loss of

Motivation 33 63 83 86

7) Suicidal

wishes 12 31 53 74

n = Number of Patients

A striking feature of the characteristic motivation of the depressed patients in their

regression nature. The term regressive is applicable in that patient seem drawn to

activities that are the least demanding for him either in terms of the degree of the

responsibility or initiative required or the amount of energy to be expended. He turns

away from activities that are specifically associated with the adult role and seeks

activities that are more characteristics of the childs role. When confronted with a

choice, he prefers passivity to the activity and dependence to independently

(autonomy); he avoid responsibility and escapes from his problems rather than trying

to solve them; he seeks immediate but transient, gratification instead of delayed, but

prolonged satisfactions. (Aaron. T. Beck, 1967)

The behavioural characteristics of persons with mental retardation shows greater

tendency towards the above symptoms than the normal.

One of the major components to the response to stressful events is an emotional

response, with somatic accompaniments which are of two kinds. Anxiety responses

with autonomic arousal leading to apprehension, irritability, tachycardia, increased

muscle tension and dry mouth. Depressive response with poor appetite and reduced

physical activities. Anxiety responses are generally associated with events that pose a

threat, whilst depressive responses are usually associated with events that involve

separation or loss. These features of these responses are similar to, but intense than,

the symptoms of anxiety and depressive disorder. (M. Gelder, R. Mayon, P.

Cowen, 1983)

2.3 SURVEY OF LITERATURE

Holden and Gitelson (2003) conducted a study on Prevalence on Psychiatric

Symptoms in Adults with MR and Challenging behaviour Here a sample of

165 persons with mental retardation was surveyed for the presence of psychiatric

symptoms, level of mental retardation and self injurious and other types of

challenging behaviour. The results indicate increased prevalence of psychiatric

symptoms, especially anxiety and psychosis in mentally retarded persons. No

association between anxiety and self injurious behaviour was found.

Carvill, Sue and Marston, G (2002) made a study on People with intellectual

disability, sensory impairment and behaviour disorders It is found that

Sensory Impairments (SIs) are more prevalent in people with intellectual

disability (ID). Both conditions lead to higher rates of emotional and behavioral

problems than in general population.

Glenn, Elizabeth, Bihm, Elson M and Lammer, William J (2003) conducted a

study on Depression, Anxiety and relevant cognitions in persons with MR

They assessed depression, anxiety and relevant cognitions in persons with MR by

administering modified versions of Reynolds Child Depression Scale, the Beck

Anxiety Inventory, the Automatic Thoughts Questionnaire and the Cognitions

Checklist to 46 persons with borderline to moderate MR, consistent with research

with other groups. Self reports of depression and anxiety were highly correlated in

these individuals and cognitions were strong predictors of negative affect.

Subscales measuring cognitions related to depression and anxiety were also

highly related, limiting Cognitive-Specificity hypothesis.

Arthur, Anderen R (2003) conducted a study on The Emotional lives of people

with learning disability The emotional lives and difficulties of people with

leaning disabilities are much neglected. There is evidence to suggest the presence

of a significantly higher level of emotional developmental problems and

disturbance in people with learning disability. This problem requires

multidisciplinary attention if progress in improving quality of life is to be

maintained.

Merikangas, Kathleen Ries, Zhang, Heping, Avenevoli, Shelli, Acharyya,

Suddhasatta et al. conducted a study on Comorbid Anxiety and Depression

Comorbid Anxiety and Depression tended to be far more persistent than either

syndrome alone. Individuals with anxiety states alone tended to develop either

depression alone or comorbid anxiety and depression as they progressed through

adulthood. In contrast, depression alone and depression comorbid with anxiety

tended to be more stable than anxiety alone over time. The patterns of stability

were similar for subthreshold and threshold level disorders.

Mellinger, David and Lynn, Steven Jay (2003) conducted a study on How to

face you fear and anxiety and live your life It offers a menu of techniques to

help confront and calm fear, to understand inner workings of personal anxiety and

to rebuild individual reactions from the ground up.

Moon, Henry, Hollenbeck, John R, Humphrey, Stephen E and Maue (2003)

conducted a study on The Tripartite model of Neuroticism and The Suppression

of Depression and Anxiety within an Escalation of commitment dilemma The

results demonstrate a positive relationship between anxiety and level of

commitment. On the other hand, results also demonstrate a relationship between

depression, anxiety and commitment, the broad factor of neuroticism does not

demonstrate any relationship with the level of commitment and the significant

effects of anxiety and depression on commitment is contingent upon partialling

the effect of the other facet of neuroticism.

Lenze, Eric J. M.D.; Rogers, Joan C. Ph.D.; Martire, Lynn M. Ph.D American

Journal of Geriatric Psychiatry: Spring 2001 - Volume 9 - Issue 2 - p 113-135

Special Article Depression and anxiety disorders are associated with excess

disability. The authors searched the recent geriatric literature for studies

associating late-life depression or anxiety with physical disability. Studies showed

depression in old age to be an independent risk factor for disability; similarly,

disability was found to be a risk factor for depression. Anxiety in late life was also

found to be a risk factor for disability, although not necessarily independently of

depression. Increased disability due to depression is only partly explained by

differences in socioeconomic measures, medical conditions, and cognition.

Physical disability improves with treatment for depression; comparable studies

have not been done for anxiety. The authors discuss how these findings inform

current concepts of physical disability and discuss the implications for future

intervention studies of late-life depression and anxiety disorders.

3. Hypothesis

Hypothesis 1:

Stability of instruments - A comparison of self- and informant-report measures of

Depressed Mood, Social Support and Life Events.

Hypothesis 1 A: Self- and informant-report measures of depressed mood will be

positively correlated as an indicator of agreement among raters.

Hypothesis 1 B: Self- and informant-report measures of social support will be

positively correlated as an indicator of agreement among raters.

Hypothesis 1 C: Self- and informant-report measures of life events, both frequency

and impact ratings, will be positively correlated as an indicator of agreement among

raters, using intra-class correlation coefficients. 32 Specific Aim 10: Depressed Mood

related to Social Skills and Social Support

Hypothesis 2:

Hypothesis 2 A: Self- and informant-report measures of depressed mood will be

negatively correlated with informant-reports of social skills. High levels of depressed

mood will be associated with low levels of social skills.

Hypothesis 2 B: Self- and informant-report measures of depressed mood will be

negatively correlated with self- and informant-reports of social support. High levels of

depressed mood will be associated with low levels of social support.

Hypothesis 3: Relationship between Life Stress and Life Events

Self-report frequency measures of life stress will be moderately positively correlated

with self- and informant-reports of the frequency of life events. Self-report impact

measures of life stress will be moderately negatively correlated with self- and

informant-reports of impact ratings of life events.

Hypothesis 4: Relationship between measures of Depressed Mood Informant-report

measures of depressed mood will not differ between those participants who complete

and those who do not complete the self report measures.

4. ADULTS WITH MENTAL RETARDATION AND MENTAL

DISORDERS

What is the prevalence of mental disorders in adults with mental retardation?

Adults with mental retardation are at increased risk of developing mental

disorders due to the complex interaction of biological, psychological, social and

family factors. Prevalence studies have consistently shown that 20-40% of people

with mental retardation also have some form of mental disorder.

Professionals and staff unaccustomed to working with adults with mental

retardation may inappropriately attribute signs of a mental disorder to a person's

mental retardation per se - a phenomenon known as 'diagnostic overshadowing'.

4.1 Presentations of mental disorders in people with

mental retardation?

The presentation of a mental disorder in an individual with mental retardation will

depend on his or her usual levels of cognitive, communicative, physical and social

functioning, and usual behavioral repertoire, together with past and present inter-

personal, cultural and environmental influences. Generally, the signs and

symptoms of mental disorders presented by adults with mild mental retardation

and reasonable verbal communication skills are similar but less complex than

those presented by adults with normal intellect.

However, due to their less well-developed cognitive and communication skills, as

well as increased risks of physical impairments, adults with moderate and severe

mental retardation are more likely to exhibit disturbed and regressed behaviours,

physical signs, and complaints as presentations of mental disorders. The

possibility of underlying mental illness in people presenting with newly arisen

behaviour disturbance must be considered.

An individual may present with overlapping signs and symptoms of two or more

related mental disorders at a given time, as the clinical examples below illustrate:

Example A:

A man with mild mental retardation and epilepsy presented with long-standing

excessive attention to his personal hygiene due to an obsessional personality

disorder, together with recent panic attacks and hyperventilation due to an anxiety

disorder.

Example B:

A middle-aged woman with Down syndrome and moderate learning disabilities

presented with a recent onset of low mood, disturbed sleep and appetite due to a

depressive disorder, set against a background of gradually declining social and

self-care skills due to Alzheimer dementia.

Example C:

A teenager with severe mental retardation, no speech, social indifference, fear of

water and finger flicking since childhood due to autism, presented with self-

injurious and sexually inappropriate challenging behaviours following changes in

his daytime activity programme.

4.2 Mental disorders in adults with mental retardation?

Adults with mental retardation suffer from the same types of mental disorder as

people with normal intellectual functioning. In adults with severe mental

retardation, autism and behavioural disorders are common, but psychoses are

often difficult to diagnose when individuals are unable to verbalise complex

experiences such as odd ideas and hearing voices. The diagnosis of organic

psychoses and personality disorders is difficult in most adults with mental

retardation, as it is hard to obtain an accurate base line and long-term account of

functioning, behaviours and symptoms.

The main types of mental disorders in adults with mental retardation are:

Psychoses

These disorders may be misdiagnosed in adults with mental retardation

exhibiting stress-related confusion, odd behavior, muddled speech and

suspiciousness. Classic symptoms are usually present but may be difficult to

identify and be masked / overshadowed by atypical features, which can lead to

diagnostic problems in schizophrenia and paranoid psychosis. Hysterical

symptoms, pseudo-seizures, and visual hallucinations are common. Affective

(manic-depressive) psychoses often run in families and can present as cyclical

manic, depressive or mixed disorders. Disturbed activity levels, biological and

social functioning often accompany irritability in mania, and bodily complaints in

depression. Regression, confusion, vomiting, self-injurious and aggressive

behaviours may represent "depressive equivalents". Rapid cycles of bipolar

disorder are particularly associated with mental retardation.

Neuroses

These disorders are generally under-diagnosed, especially in adults with moderate

or severe mental retardation. Reactive depression commonly follows a life event

such as the loss of a significant carer, friend or pet, or placement changes, but is

often not recognised. Anxiety states may develop in response to stress and

environmental changes including resettlement. Anxiety may present with panic

attacks, agitation, low mood, pseudo-seizures, and hypochondriacal, self-injurious

and acting-out behaviours.

Phobias tend to be over-diagnosed - a refusal to try something new may represent

more general avoidance of possible failure. However, specific phobias of dogs,

scissors, dirt, water or heights.

Example, do occur, particularly in people with autism. The repetitive thoughts

and ritualistic behaviours that are resisted and cause anxiety to those with

obsessive-compulsive disorder may be misdiagnosed as autistic features.

Personality Disorders

Adults with mental retardation exhibit the full range of personality assets,

difficulties and disorders. There is no universal agreement among specialists as to

the existence of personality disorders in adults with mental retardation because of

their different developmental process of personality due to their impaired

intellectual and social functioning. However chronic maladaptive patterns of

behaviour which are not adequately explained by other developmental or mental

disorders, may be best explained as due to a personality disorder. Whilst

personality disorders are more easily diagnosed in adults with mild and moderate

mental retardation, similar presentations in adults with severe mental retardation

are more likely to be seen as challenging behaviours.

Organic Disorders

Delirium is probably under-diagnosed. Acute confusion caused by constipation,

medication, infections, or epilepsy may not be noticed. It usually resolves with

treatment of the underlying causes.

Dementia is increasingly diagnosed as more adults with mental retardation

survive into old age. Roughly 8% of adults with Down syndrome aged 35-50

years and 65% of those aged over 60 years will develop Alzheimer's dementia.

Dementia may present with loss of skills, social withdrawal, behaviour problems,

epilepsy, depression or incontinence. The inevitable functional and physical

decline may be rapid. Reduced functioning in ageing adults with Down syndrome

may also be due to their increased risk of developing a hearing loss, cataracts,

depression and thyroid underactivity.

4.3 Factors Involved in assessment of mental disorders in

adults with mental retardation?

Multidisciplinary assessment is always indicated in mental retardation. Specialist

psychiatric assessment is necessary, given the complex combination of mental

health, physical health and social care needs presented by people with mental

retardation and mental disorders. Psychiatric assessment focuses on whether or

not the adult with mental retardation has a mental disorder; i.e. should the

individual be considered as having 'dual diagnosis' i.e. mental retardation and

mental illness or disorder? Ideally, the multidisciplinary approach is adopted

involving the client, carers and other agencies to maximise the gathering of

developmental, background, functional, behavioural and observational data.

Assessment should cover the client's usual and recent communication skills,

functioning, personality, relationships, environments, service inputs, behaviours,

medication and physical health (for example: epilepsy) to determine any changes.

Verbal communication, hearing