INTRODUCTION TO BDI

INTRODUCTION TO DEPRESSION
Sadness, discouragement, pessimism, and hopelessness about matters improving are fami
liar feelings to most people. Feelings of depression are unpleasant when we are experienc
ing them, but they usually do not last long, dissipating on their own after a period of days
or weeks or after they have reached a certain intensity level. Indeed, mild and brief depre
ssion may actually be "nor- mal'' and adaptive in the long run. By slowing us down,mild
depression sometimes saves us from wasting a lot of energy in the futile pursuit of unattai
nable goals (Keller & Nesse, 2005; Nesse, 2000). Usually, normal depressions would be
expected to occur in people undergoing painful but common life events such as significan
t personal, interpersonal, or economic losses.
Symptoms of Depressive Episode (F32)
In the usual occurrences of mild, moderate, and severe depressive episodes (F32.0, F32.1,
F32.2, and F32.3), individuals typically experience feelings of sadness, lack of interest in
things they used to enjoy, and decreased energy, resulting in heightened fatigue and reduc
ed physical activity. Feeling extremely tired even after minimal exertion is a frequent sy
mptom. Other frequent symptoms are:
(a) reduced concentration and attention;
(b) reduced self-esteem and self-confidence;
(c) ideas of guilt and unworthiness (even in a mild type of episode);
(d) bleak and pessimistic views of the future;
(e) ideas or acts of self-harm or suicide;
(f) disturbed sleep;
(g) diminished appetite.
The consistent low mood doesn't change much from day to day and is often not influence
d by situations, but it might exhibit a predictable daily pattern.The way manic episodes ar
e displayed clinically can vary significantly among individuals, especially during adolesc
ence where atypical presentations are common. Sometimes, symptoms like anxiety, distre
ss, and restlessness might be more noticeable than the depression itself. Mood changes co
uld be obscured by other behaviors like irritability, excessive alcohol consumption, attent
ion-seeking actions, or worsening of existing phobias, obsessions, or health concerns. To
diagnose depressive episodes of any severity, a minimum duration of around 2 weeks is t
ypically required, but shorter periods could be considered in cases of severe and sudden s
ymptoms. Certain symptoms, like loss of interest in enjoyable activities, reduced emotion
al response to pleasurable situations, early morning awakening, more intense morning de
pression, observable psychomotor slowing or restlessness, significant appetite reduction,
substantial weight loss, and pronounced decrease in libido, might develop and carry speci
al clinical significance. Usually, this group of somatic symptoms is only considered prese
nt if about four of them are clearly observed.
Mild depressive episode (F32.0) : Commonly seen as the key signs of depression, feelin
gs of sadness, disinterest, and exhaustion are typically considered the most typical indicat
ions, with at least two of these being required for a clear diagnosis (for F32.-). None of th
e symptoms should be too severe. The entire episode should last for a minimum of about
two weeks. Someone experiencing a mild depressive episode is usually bothered by these
symptoms and may find it somewhat challenging to carry on with regular tasks and social
engagements, but they are unlikely to completely stop functioning.
Moderate depressive episode (F32.1) : For a diagnosis of mild depressive episode (F32.
0), it is required that at least two out of the three most common symptoms are present, alo
ng with a minimum of three (preferably four) other symptoms. While several symptoms a
re likely to be significantly experienced, it's not necessary if there is a wide range of sym
ptoms overall. The episode must last for approximately two weeks, and someone with a
moderately severe depressive episode will typically struggle to maintain social, work, or
household tasks.
Severe depressive episode without psychotic symptoms (F32.2) : In cases of severe de
pressive episodes, the standard symptoms, along with at least four additional symptoms (s
ome being severe), are typically required. However, if significant symptoms like agitation
or retardation are present, the patient might struggle to describe many symptoms. In such
situations, a classification of a severe episode might still be appropriate. Normally lasting
for around 2 weeks, a diagnosis can be made in less time if the symptoms are extremely s
evere and rapidly appear. During a severe depressive episode, the individual will likely fi
nd it extremely challenging to engage in social, work, or household activities, except to a
very limited extent.
Severe depressive episode with psychotic symptoms : A severe episode of depression t
hat fulfills the criteria described in F32.2, accompanied by the presence of delusions, hall
ucinations, or depressive stupor. The delusions often involve ideas related to guilt, povert
y, or imminent disasters, for which the patient might assume responsibility. Auditory or o
lfactory hallucinations usually consist of accusatory voices or disturbing odors. Profound
psychomotor slowing can escalate to a state of stupor. If necessary, the delusions or hallu
cinations may be specified as consistent with the individual's mood or not consistent with
it (refer to F30.2).
Includes: single episodes of major depression with psychotic symptoms, psychotic depres
sion, psychogenic depressive psychosis, reactive depressive psychosis.
Depressive Episode : DSM-5 Criteria
Depressive disorders consist of the following Disorders:
● Disruptive mood dysregulation disorder
● Major depressive disorder (including major depressive episode)
● Persistent depressive disorder (dysthymia)
● Premenstrual dysphoric disorder
● Substance/medication-induced depressive disorder
● Depressive disorder due to another medical condition
● Other specified depressive disorder
● Unspecified depressive disorder
Etiology
Biological causal factors:
It has long been known that a variety of diseases and drugs can affect mood, leading som
etimes to depression and sometimes to elation or even mania. Indeed, this idea goes back
to Hippocrates (c. 400 B.C.), who hypothesized that depression was caused by an excess
of "black bile" in the system. As we will discuss, in the past half century investigators att
empting to establish a biological basis for uni-polar disorders have considered a wide ran
ge of factors.
Genetic Influences: Family studies have shown that the prevalence of mood disorders is
approximately two to three times higher among blood relatives of per- sons with clinicall
y diagnosed uni-polar depression than it is in the population at large (e.g., Levinson, 2006,
2009; Wallace et al., 2002). Twin studies, which can provide much more conclusive evid
ence of genetic influences on a disorder, also suggest a moderate genetic contribution to
MDD. Monozygotic co-twins of a twin with MDD are about twice as likely to develop th
e disorder as are dizygotic co-twins, with about 31 to 42 percent of the vari- ance in liabil
ity due to genetic influences (Sullivan, Neale, & Kendler, 2000). The estimate is substanti
ally higher (70 to 80 percent) for more severe, early-onset, or recurrent depressions (see a
lso Levinson, 2009; McGuffin et al., 2007). Notably, however, even more variance in the
liability to most forms of MDD is due to nonshared environmental influences (i.e., experi
ences that family members do not share) than to genetic factors.
Neurochemical Factors : Ever since the 1960s, the view that depression may arise from
disruptions in the delicate balance of neurotransmitter substances that regulate and mediat
e the activity of the brain's nerve cells has received a great deal of attention. A large body
of evidence suggested that various biological therapies (discussed later in this chapter) th
at are often used to treat severe mood disorders-such as electroconvulsive therapy and ant
idepressant medications-affect the concentrations or activity of neurotransmitters at the sy
n- apse. Such early findings encouraged the development of neurochemical theories of th
e etiology of major depression.
Abnormalities of Hormonal Regulatory and Immune System : Research interest has f
ocused on possible hormonal causes or correlates of some forms of mood disorder (South
wick et al., 2005; Thase, 2009a). The majority of attention has been focused on the hypot
halamic-pituitary-adrenal (HPA) axis, and in particular on the hormone cortisol, which is
excreted by the outermost portion of the adrenal glands and is regulated through a comple
x feedback loop. The human stress response is associated with elevated activity of the HP
A axis, which is partly controlled by norepi- nephrine and serotonin. The perception of str
ess or threat can lead to norepinephrine activity in the hypo- thalamus, causing the release
of corticotropin-releasing hormone (CRH) from the hypothalamus, which in turn triggers
the release of adrenocorticotropic hormone (ACTH) from the pituitary. The ACTH then t
ypically travels through the blood to the adrenal cortex of the adrenal glands, where cortis
ol is released. Elevated cortisol activity is highly adaptive in the short term because it pro
motes survival in response to life-threatening or overwhelming life circumstances. Howe
ver, sustained elevations are harmful to the organism, including promoting hypertension,
heart disease, and obesity (which are all elevated in depression) (Stetler & Miller, 2011;
Thase, 2009a). Blood plasma levels of cortisol are known to be elevated in some 20 to 40
percent of outpa- tients with depression and in about 60 to 80 percent of hospitalized pati
ents with severe depression (Thase et al., 2002). Sustained elevations in cortisol-a "hall-
mark of mammalian stress responses"-can result from increased CRH activation (for exa
mple, during sustained stress or threat), increased secretion of ACTH, or the failure of fee
dback mechanisms.
Neuropsychological and Neuroanatomical Influences : Exciting neurophysiological re
search in recent years has followed up on earlier neurological findings that damage (for e
xample, from a stroke) to leads to depression (Davidson et al., 2009; Robinson & the left,
but not the right, anterior prefrontal cortex often Downhill, 1995). This led to the idea tha
t depression in people without brain damage may nonetheless be linked to lowered levels
of brain activity in this same region. A number of studies have supported this idea. Studie
s measuring the electroencephalographic (EEG) activity of both cerebral hemispheres in
people who are depressed reveals an asymmetry or imbalance in the EEG activity of the t
wo sides of the prefrontal regions of the brain. People with depression show lower activit
y in the left hemisphere in these regions and higher activity in the right hemisphere (Davi
dson et al., 2009; Stewart et al., 2010, 2011). Similar findings have been reported using p
ositron emission tomogra- phy (PET) neuroimaging techniques (Davidson et al., 2009; Ph
illips et al., 2003). Notably, patients in remis- sion show the same pattern (Henriques & D
avidson, 1990; Stewart et al., 2010, 2011), as do children at risk for depression (Bruder et
al., 2007). These latter find- ings hold promise as a way of identifying persons at risk bot
h for an initial episode and for recurrent episodes. Indeed, a recent study found that left fr
ontal asymmetry in never-depressed individuals predicted onset of major and minor depre
ssive episodes over a 3-year period (Nusslock et al., 2011). The relatively lower activity o
n the left side of the prefrontal cortex in lev- depression is thought to be related to sympto
ms of reduced positive affect and approach behaviors to personal rewarding stimuli, and i
ncreased right-side activity is hen thought to underlie increased anxiety symptoms and in
creased negative affect associated with increased vigilance for threatening information (P
izzagalli et al., 2002).
Sleep and other Biological Rhythms : Al-though findings of sleep disturbances in patie
nts with depression have existed as long as depression has been studied, only recently hav
e some of these findings been linked to more general disturbances in biological rhythms.
Sleep Sleep is characterized by five stages that occur in a relatively invariant sequence thr
oughout the night (Stages 1-4 of non-REM sleep and REM sleep make up a sleep cycle).
REM sleep (rapid eye movement sleep) is characterized by rapid eye movements and dre
aming as well as other bodily changes; the first REM period does not usually begin until
near the end of the first sleep cycle, about 75 to 80 minutes into sleep. This normal sleep-
wake cycle is thought to be regulated by the suprachiasmatic nucleus of the hypothalamu
s (Steiger, 2007; Thase, 2009a). People who are depressed often show one or more of a v
ariety of sleep problems, ranging from difficulty falling asleep, to periodic awakening dur
ing the night (poor sleep maintenance), to early morning awakening. Such changes occur
in about 80 percent of hospitalized patients with depression and in about 50 percent of ou
tpatients with depression, and are particularly pronounced in patients with melancholic fe
atures.
Biological Explanations for Sex Differences : Before we leave the topic of possible biol
ogical causal factors for depression, we should note that it has been suggested that hormo
nal factors such as normal fluctuations in ovarian hormones account for sex differences in
depression (Deecher et al., 2008). However, studies examining this hypothesis have yield
ed inconsistent results and overall are not very supportive (Nolen-Hoeksema & Hilt, 200
9). It seems that for the majority of women, hormonal changes occurring at various points
(e.g., at the onset of puberty, before menstruation, in the postpartum period, and at menop
ause) do not play a significant role in causing depression. However, it remains possible th
at there is a causal association that has not yet been discovered because of real methodolo
gical difficulties in conducting conclusive research on this topic (Naninck et al., 2011; Sa
nborn & Hayward, 2003). Moreover, for a small minority of women who are already at hi
gh risk (for example, by being at high genetic risk), hormonal fluctuations may trigger de
pressive episodes, possibly by caus- ing changes in the normal processes that regulate neu
rotransmitter systems (Deecher et al., 2008; Nannck et al., 2011). Some studies have sugg
ested that women have a greater genetic vulnerability to depression than men, but many o
ther studies have not supported this idea (e.g., Nolen-Hoeksema & Hilt, 2009; Wallace et
al., 2002).
Psychological Causal Factors :
The evidence for important psychological causal factors in most unipolar mood disorders
is at least as strong as the evidence for biological factors. However, it is likely that the eff
ects of some psychological factors such as stressful life events are mediated by a cascade
of under- lying biological changes that they initiate. One way in which stressors may act i
s through their effects on bio- chemical and hormonal balances and on biological rhythms
(Hammen, 2005; Monroe, 2008).
Stressful Life Events as Causal Factors : Environmental stressors are known to be invo
lved in the onset of a variety of disorders, ranging from some of the anxiety disorders to s
chizophrenia, but nowhere has their role been more carefully studied than in the case of u
nipolar major depression. Many studies have shown that severely stressful life events ofte
n serve as precipitating factors for unipolar depression (e.g., Hammen, 2005; Monroe et a
l., 2009). This is especially true for young female adults for whom stressful life events are
more likely to show a stronger stress-depression rela- tionship than is the case for men (H
arkness et al., 2010). Most of the episodic stressful life events involved in precipitating de
pression concern loss of a loved one, serious threats to important close relationships or to
one's occupation, or severe economic or serious health problems (Monroe et al., 2009). T
he stress of being the caregiver to a spouse with a debilitating disease such as Alzheimer's
is also known to be associated with the onset of both major depression and generalized an
xiety disorder in the caregiver.
Different Types of Vulnerabilities for Unipolar Depression : In addition to genetic var
i- ables, there are a host of other psychological and social variables that may make some
people more vulnerable, and other people less vulnerable, to developing depres- sion after
experiencing one or more stressful life events.
Personality and cognitive diathesis; Researchers have concluded that neuroticism is the
primary personality variable that serves as a vulnerability factor for depres- sion (and anx
iety disorders; Klein et al., 2009; Zinbarg et al., 2011). Recall that neuroticism, or negativ
e affectivity, refers to a stable and heritable personality trait that involves a temperamenta
l sensitivity to negative stimuli. Thus, people who have high levels of this trait are prone t
o experiencing a broad range of negative moods, includ- ing not only sadness but also an
xiety, guilt, and hostility. Moreover, several studies have also shown that neuroticism pre
dicts the occurrence of more stressful life events, which frequently lead to depression (Ke
ndler, Gardner, & Prescott, 2003; Uliaszek et al., 2012). In addition to serv- ing as a vuln
erability factor, neuroticism is associated with a worse prognosis for complete recovery fr
om depression. Finally, some researchers attribute sex differences in depression to sex dif
ferences in neuroticism.
Early adversity as a diathesis; A range of adversities in the early environment (such as f
amily turmoil, parental psychopathology, physical or sexual abuse, and other forms of int
rusive, harsh, and coercive par- enting) can create both a short-term and a long-term vuln
erability to depression. Such factors operate, at least in part, by increasing an individual's
sensitivity to stressful life events in adulthood, with similar findings having been observe
d in animals (Slavich et al., 2011). The long-term effects of such early envi- ronmental ad
versities may be mediated by both bio- logical variables (such as alterations in the regulat
ion of the hypothalamic-pituitary stress response sys- tem) and psychological variables (s
uch as lower self- esteem, insecure attachment relationships, difficulty relating to peers, a
nd pessimistic attributions; Good- man & Brand, 2009; Harkness & Lumley, 2008). Ho
w- ever, it is also important to realize that certain individuals who have undergone early a
dversity remain resilient, and if the exposure to early adversity is moderate rather than se
vere, a form of stress inoculation may occur that makes the individual less susceptible to t
he effects of later stress (Parker et al., 2004). These stress-inoculation effects seem to be
mediated by strengthening socioemotional and neuroendocrine resistance to subsequent st
ressors.
Theoretical Aspects
There are five major psychological theories of depression that have received much attenti
on over the years, they are ;
Psychodynamic Theories: In his classic t "Mourning and Melancholia" (1917), Freud no
ted the important similarity between the symptoms of clinical depression and the sympto
ms seen in people mourning the loss of a loved one. Freud and his col- league Karl Abrah
am (1927) both hypothesized that when a loved one dies the mourner regresses to the oral
stage of development (when the infant cannot distinguish self from others) and introjects
or incorporates the lost person, feeling all the same feelings toward the self as toward the
lost person. These feel- ings were thought to include anger and hostility because Freud be
lieved that we unconsciously hold negative feelings toward those we love, in part because
of their power over us. This is what led to the psychodynamic idea that depression is ange
r turned inward. Freud hypothesized that depression could also occur in response to imagi
ned or symbolic losses. For example, a student who fails in school or who fails at a roma
ntic relationship may experience this symbolically as a loss of his or her parents' love. Lat
er psychodynamic theorists proposed a number of variants on Freud and Abraham's early
psychodynamic theories (Levy & Wasserman, 2009). Perhaps the most important contrib
ution of the psychodynamic approaches to depression has been their noting the importanc
e of loss (both real and symbolic or imagined) to the onset of depression and noting the st
riking similarities between the symptoms of mourning and the symptoms of depression
(Bowlby, 1980).
Behavioral Theories: In the 1970s and 1980s, several theorists in the behavioral traditio
n developed behavioral theories of depression, proposing that people become depressed e
ither when their responses no longer produce positive reinforcement or when their rate of
negative experiences increases (Ferster, 1974; Lewinsohn & Gotlib, 1995). Such theories
are consistent with research showing that people with depression do indeed receive fewer
positive verbal and social reinforcements from their families and friends than do people
who are not depressed and also experience more negative events. Moreover, they have lo
wer activity levels, and their moods seem to vary with both their positive and their negati
ve experiences rates (Lewinsohn & Gotlib, 1995; Martell, 2009). Nevertheless, although
such findings are consistent with behavioral theories, they do not show that depression is
caused by these factors. Instead, it may be that some of the primary symptoms of depressi
on, such as pessimism and low levels of energy, cause the person with depression to expe
rience lower rates of rein- forcement, which in turn may help maintain the depres- sion. I
nterestingly, exciting new research has demonstrated that a novel form of behavioral treat
ment inspired by these behavioral theories-behavioral activation treatment-seems to be an
effective treatment for depression (Dimidjian et al., 2011; Martell, 2009).
Beck's Cognitive Theory: Since 1967 one of the most influential theories of depression
has been that of Aaron Beck (b. 1921), a psychiatrist who became chanted with psychody
namic theories of depression early in his career and developed his own cognitive the- ory
of depression (Beck, 1967, 2005). Whereas the most prominent symptoms of depression
have generally been considered to be the affective or mood symptoms, Beck hypothesize
d that the cognitive symptoms of depres- sion often precede and cause the affective or mo
od symptoms rather than vice versa (see Figure 7.3). For example, if you think that you ar
e a failure or that you are ugly, it would not be surprising for those thoughts to lead to a d
epressed mood. Beck's theory, a diathesis-stress theory in which negative cognitions are c
entral, has become somewhat more elaborate over the years while still retaining its primar
y ten- ets (Beck, 1967, 2005; Clark & Beck, 2010). First, there are the underlying dysfunc
tional beliefs, known as depressogenic schemas, which are rigid, extreme and counterpro
ductive.
The Helplessness and Hopelessness Theories of Depression: Whereas Beck's theory str
ewed out of his clinical observations and research on the pervasive patterns of negative th
inking seen in patients with depression, the learned helplessness theory of depression orig
inated out of observations in an animal research laboratory. Martin Seligman (1974, 197
5) first proposed that the laboratory phenomenon known as learned helplessness might pr
ovide a useful animal model of depression. In the late 1960s, Seligman and his colleagues
(Maier et al., 1969; Overmier & Seligman, 1967) noted that laboratory dogs who were fir
st exposed to uncontrollable shocks later acted in a passive and helpless manner when the
y were in a situation where they could control the shocks. In contrast, animals first expos
ed to equal amounts of controllable shocks had no trouble learning to control the shocks.
Seligman and his colleagues (Maier et al., 1969; Overmier & Seligman, 1967) developed
the learned helplessness hypothesis to explain these effects. It states that when animals or
humans find that they have no control over aversive events (such as shock), they may lear
n that they are helpless, which makes them unmotivated to try to respond in the future. In
stead they exhibit passivity and even depressive symptoms. They are also slow to learn th
at any response they do make is effective, which may parallel the negative cognitive set i
n human depression. Seligman's observations that the animals looked depressed captured
his attention and ultimately led to his proposing a learned helplessness model of depressi
on (Seligman, 1974, 1975). Subsequent research demonstrated that helpless animals also
show other depressive symptoms such as lower levels of aggression, loss of appetite and
weight, and changes in monoamine neurotransmitter levels. After demonstrat- ing that lea
rned helplessness also occurs in humans (Hiroto & Seligman, 1975), he went on to propo
se that learned helplessness may underlie some types of human depression. That is, peopl
e undergoing stressful life events over which they have little or no control may develop a
syndrome like the helplessness syndrome seen in animals.
Hopelessness theory of depression; Theory of Depression A further revi- sion of this th
eory, known as the hopelessness theory, was later presented (Abramson et al., 1989; see
Alloy et al., 2008). Abramson and colleagues (1989) propose that hav- ing a pessimistic a
ttributional style in conjunction with one or more negative life events was not sufficient t
o pro- duce depression unless one first experienced a state of hopelessness. A hopelessnes
s expectancy was defined by the perception that one had no control over what was going t
o happen and by the absolute certainty that an important bad outcome was going to occur
or that a highly desired good outcome was not going to occur. They also proposed that th
e internal/external dimension of attributions was not important to depression. Specifi- call
y, they proposed that depression-prone individuals not only tend to make global and stabl
e attributions for negative events but also tend to make negative inferences about other lik
ely negative consequences of the event (e.g., that this means more bad things will also ha
ppen) and negative inferences about the implications of the event for the self-concept (e.
g., that one is unworthy or deficient; Abramson et al., 2002).

Beck Depression Inventory

The Beck Depression Inventory (BDI) is a 21-item, self-report rating inventory that meas
ures characteristic attitudes and symptoms of depression (Beck, et al., 1961). The BDI ha
s been developed in different forms, including several computerized forms, a card form
(May, Urquhart, Tarran, 1969, cited in Groth-Marnat, 1990), the 13-item short form and t
he more recent BDI-II by Beck, Steer & Brown, 1996. (See Steer, Rissmiller & Beck, 20
00 for information on the clinical utility of the BDI-II.) The BDI takes approximately 10
minutes to complete, although clients require a fifth-sixth grade reading level to adequate
ly understand the questions (Groth-Marnat, 1990) Internal consistency for the BDI ranges
from 73 to 92 with a mean of 86 (Beck, Steer, & Garbin, 1988). Similar reliabilities have
been found for the 13-item short form (Groth-Marnat 1990) The BDI demonstrates high i
nternal consistency, with alpha coefficients of 86 and 81 for psychiatric and non-psychiat
ric populations respectively (Beck et al. 1988) BDI one of the most widely used psychom
etric tests for measuring the severity of depression Its development marked a shift amoun
t mental health professionals who had until In its current version, the BDI-II is designed f
or individuals aged 13 and over, and is composed of items relating to symptoms of depres
sion such as hopelessness and irritability. cognitions such as guilt or feelings of being pun
ished, as well as physical symptoms such as fatigue, weight loss, and lack of interest in se
x

There are three versions of the BDI-the original BDI, first published in 1961 and later rev
ised in 1978 as the BDI-1A, and the BDI-II, published in 1996. The BDI is widely used a
s an assessment tool by health care professionals and researchers in a variety of settings.

The BDI was used as a model for the development of the Children's Depression Inventor
y (CDI). first published in 1979 by clinical psychologist Maria Kovacs.

BDI-II

The BDI-II was a 1996 revision of the BDI, developed in response to the American Psych
iatric Association's publication of the Diagnostic and Statistical Manual of Mental Disord
ers, Fourth Edition, which changed many of the diagnostic criteria for Major Depressive
Disorder

Items involving changes in body image, hypochondriasis, and difficulty working were re
placed Also, sleep loss and appetite loss items were revised to assess both increases and d
ecreases in sleep and appetite. All but three of the items were reworded, only the items de
aling with feelings of being punished, thoughts about suicide, and interest in sex remaine
d the same Finally, participants were asked to rate how they have been feeling for the pas
t two weeks, as opposed to the past week as in the original BDI.
Like the BDI, the BDI-II also contains about 21 questions, each answer being scored on a
scale value of 0 to 3 Higher total scores indicate more severe depressive symptoms. The s
tandardized cutoffs used differ from the original

0-13 minimal depression

14-19 mild depression

20-28 moderate depression

29-63. severe depression !!!!

One measure of an instrument's usefulness is to see how closely it agrees with another si
milar instrument that has been validated against information from a clinical interview by
a trained clinician. In this respect, the BDI-II is positively correlated with the Hamilton D
epression Rating Scale with a Pearson r of 0.71, showing good agreement The test was al
so shown to have a high one-week test-retest reliability (Pearson r=0.93), suggesting that
it was not overly sensitive to daily variations in mood. The test also has high internal con
sistency (u=91)
Types of items included in BDI: The beck depression inventory (BDI), the 21 item, self-
rated scale that evaluates key symptoms of depression including mood, pessimism, sense
of failure, self-dissatisfaction, guilt, punishment, self-dislike, self-accusation, suicidal ide
as, crying, irritability, social withdrawal, indecisiveness, body image change, work diffic
ulty, insomnia, fatigability, loss of appetite, weight loss, somatic. preoccupation and loss
of libido (Beck and Steer, 1993, Beck, Steer and Garbing, 1988).
Psychometric Properties
Rationale for selecting BDI
Rationale for selecting BDI II is that it has undergone two major revisions in 1978 as the
BDI-IA and in 1996 as the Beck Depression Inventory-II (BDI-II). The updated BDI-II ta
ps psychological and somatic manifestations of 2-week major depressive episodes, as ope
rationalized in the DSM-IV. This version was modified to reword and replace some items.
Population for which BDI is designed; The Beck Depression Inventory (BDI) is a widel
y used 21-item self-report inventory used to assess variety levels in adults and adolescent
s. It has been used in multiple studies, including in treatment outcome studies for individu
als who have experienced traumas Although the age range for the measure is from 17 to 8
0, the measure has been used in peer-reviewed studies with younger adolescents Notes un
der "Construct Validity" for studies and ages of adolescents). In a comparative analysis of
the research output on clinical measures of anxiety (Psycinfo citation analysis for 1991-1
998), the "BAI ranks aped 12 and older (see third, behind the State-Trait Anxiety Invento
ry and the Fear Survey Schedule, in terms of use in research (Piotrowski, 1999)
Scoring and norms: The original HDI, first published in 1961 consisted of twenty-one q
uestions about how the subject has been feeling in the last week Fach question has a set o
f at least four possible answer choices,
For example

I do not feel sad

I feel sad

I am sad all the time and I can't snap out of it

I am so sad or unhappy that I can't stand it

When the test is scored a value of 0 to 3 is assigned for each answer and then the total sco
re is compared to a key to determine the depression's seventy The standard cut-offs are as
follows

0-9 indicates minimal depression

10-18 indicates mild depression

19-29: indicates moderate depression

30-63 indicates severe depression

Higher total scores indicate more severe depressive symptoms

When the test is scored, a value of 0 to 3 is assigned for each answer and then the total sc
ore is compared to a key to determine the depression's severity. The standard cut-offs are
as follows:

For example

I do not feel sad

1 feel sad

I am sad all the time and I can't snap out of it.

When the test is scored, a value of 0 to 3 is assigned for each answer and then the total sc
ore is compared to a key to determine the depression's severity. The standard cut-offs are
as follows

0-9 indicates minimal depression

10-18 indicates mild depression

19-29 indicates moderate depression

30-63: indicates severe depression

Higher total scores indicate more severe depressive symptoms

Higher total scores indicate more severe depressive symptoms.

Limitations :
● The BDI-II shares the common issue with other self-administered assessments, w
here individuals can manipulate their scores by exaggerating, downplaying, or fals
ifying their responses.
● Factors like completing the assessment in the presence of others or within a clinic
al setting might lead to different outcomes.
● People with co-existing medical conditions tend to overstate physical problems lik
e fatigue and sleep disturbances, artificially inflating BDI scores even when actual
depressive symptoms are absent.

Reference
Hooley, J. M., Butcher, J. N., Nock, M., & Mineka, S. (2017). Abnormal psychology. Bo
ston: Pearson 17th ed.
World Health Organization(WHO). (1993). The ICD-10 classification of mental and beha
vioural disorders. World Health Organization.
A short textbook of psychiatry (7th ed.) (nd) jaypee brothers medical publications LibGui
des DSM-5. Depressive Disorders (nd) Retrieved September 29, 2022, from https://wireg
rass libguides.com/c.php'g-1044445&p=7583274
American Psychiatric Association. (2022). Title of chapter. In Diagnostic and statistical
manual of mental disorders (5th ed., text rev.). DOI of chapter

EXPERIMENT NO: ASSESSOR: NA

DATE: ASSESSEE: JJ

Aim
To assess the seventy of the client's depressive symptoms by administering Beck's Depres
sion Inventory-II.

Materials Required

Beck's Depression Inventory-11

Norms for interpretation

Writing Materials

Plan

Administer the Beck's Depression Inventory II. on the patient to assess the severity of the
client's depressive symptoms

Procedure

Seat the client comfortably After establishing appropriate rapport, the Beck's Depression
Inventory II is placed in front of the subject. The subject is instructed to read each statem
ent carefully and select a response that best suits his condition since the past 2 weeks. Aft
er the client completes the test, has responses are scored and interpreted according to the
norms

Instructions

"On this inventory there are groups of statements Please read each group of statemen care
fully, and then select one statement which best describes the way you love en feeling in t
he past 2 weeks and circle the number against the appropriate statement. Be sure to read a
ll the statements in each group before making your choice: Do not leave any question una
nswered, and answer as honestly as possible

Analysis Of Results
The score for each item is given based on the number corresponding to each statement e g
if the client marks the 0th item he obtains a score of 0 and if he marks the 3rd item he obt
ains a score of 2 The total obtained from all these items for each of the symptoms constit
utes the total score which is interpreted based on the norms.

Results
The table shows the raw score and interpretation of the patient JJ;

Name Raw Score Interpretation

JJ 49 Severe Depression

Behavioral Observation
JJ is a 45 year old woman from Vadakara. She belongs to a nuclear family . Her general
appearance was hygienic, but less cooperative. JJ established eye contact but not
maintained. Rapport was established with effort. Psychomotor activity was retarded.
voice and speech is less audible, coherent and monotonous voice. Reaction time was
delayed and non-goal directed.

Discussion
The aim of the experiment was to assess the client's depressive symptoms by administerin
g Beck's Depression Inventory-II. Depression is a common mental disorder, which is
characterized by persistent sadness and a lack of interest or pleasure in previously
rewarding or enjoyable activities. It can also disturb sleep and appetite; tiredness and
poor concentration are common.
The objective of the test is used to assess the intensity of depression by using Beck
Depression Inventory. BDI can be used for screening purposes and also for clarifying the
diagnosis.

The patient JJ has obtained a total score of 49, indicating that the subject has severe level
of depression. The patient JJ has a feeling of loss of interest, change in sleeping pattern,
irritability, difficulty in concentration, tiredness, poor social interaction, suspiciousness,
suicidal thought, increased thoughts, and crying.

Conclusion
The total score of the patient JJ indicates Severe Level of Depression.