lecture 3 - mental health conditions 1 Flashcards
Defining (a)typicality
Defining normal behaviour – determining atypical behaviour(s)?
Normal psychological processes -> unhelpful outcome
No single definition works for all cases, but together they provide a framework for understanding
Definitions change with social norms, cultural differences, strata of society, new advances
Need to define what is ‘normal’ for particular society…. (quite tricky?!)
normal behaviour is
➢ Statistically frequent (common)
➢ Positive bias to society/personally
➢ Socially normal
➢ Does not lead to personal distress
or harmful dysfunction
➢ Expected and appropriate
abnormal behaviour is
➢ Statistically infrequent (rare)
➢ Negative bias to society/personally
➢ Socially deviant
➢ Leads to personal distress and
harmful dysfunction
➢ Unexpected and inappropriate
social anxiety/ phobia 1
‘an exaggerated fear of one or more situations . . . In
which the person is exposed to possible scrutiny by
others and fears that he/she may do something or act
in a way that will be humiliating or embarrassing’
Like most phobias…
generally learned behaviour:
directly or
vicarious - have anxious parents
60% sufferers generally remember the first time
90% teased/mocked at school
96% criticised for having anxiety symptoms
(blushing etc) – reflects on self-image
➢ Fear of judgement (criticised, ridiculed, humiliated)
➢ Blushing, sweating, heart rate changes, nausea, wooziness
➢ Avoidance of similar situations
➢ Anxiety – anticipation – fear may cross to other social situations
➢ Recurrent thoughts…
Social anxiety can affect everyday
activities such as shopping, job
interviews, talking on the phone, eating
in public …
Other phobias similar
e.g. haemophobia - could be directly learned so happened to them or passed on from parents talking about it and acting on it
social anxiety / phobia 2
By definition – a fear of other people
Conflict between internal representation of self and –ve external indicators
Evolutionary predisposition – fear of dominant/aggressive stimuli
shown by facial expressions
NB quicker processing/increased vigilance of negative facial expressions than positive
e.g. Mogg et al., 2004,
increased attentional bias to angry faces
=> interpret ambiguous social events
in negative way
looked at where people were looking on screen
stimuli - faces, happy, sad - looked at eye gaze how quality is shifted
people with social anxiety are sensitive to the facial expressions of other people
social phobia / other specific phobias eg haemophobia
Aetiology
Preparedness hypothesis (Seligman) – we have an evolutionary bias to fearful stimuli
Phobias are maintained by cognitions – more alert to stimuli, more attentive
Temperament/personality will affect development/onset (e.g. high neuroticism)
(behaviourally inhibited toddlers potentially more at risk)
Previous life experience – behavioural/learning
Learning effects : escapable vs inescapable situations (conditioning)
post-conditioning experience
Could be genetic tendency – reasonable concordance in MZ twins for animal-related phobias
Treatment
Exposure therapy – best treatment (systematic desensitisation)
controlled exposure to stimuli (flooding)
participant modelling - virtual reality?
Cognitive behaviour therapy (CBT)
OCD
2-3% of UK population – female>male
“what if ” disorder – worried something terrible will happen
Occurrence of unwanted and intrusive thoughts or images - accompanied by compulsive behaviours
Compulsive behaviours an attempt to neutralise thoughts or prevent further events - Inability to inhibit these
Obsessions
Recurrent and persistent thoughts, impulses, images:
Must be intrusive and anxiogenic
Not simply worries from normal life
Attempt to suppress or ignore
(use some other action/thought)
Compulsions
Repetitive behaviours or mental acts
in response to an obsession or rigid rules
To prevent/reduce stress or prevent a dreaded
event or situation
DSM5
Recognised as unreasonable and/or excessive
Cause marked distress/interfere with normal functioning (>1hr/day
OCD - aetiology/ treatments
Defence mechanisms – occupy the mind to displace painful thoughts
Psychosocial factors
Behavioural – classical conditioning – avoidance learning
- normal neutral stimuli become anxiety inducing
- anxiety reduced by different behaviour (displacement behaviours)
use of CBT to restructure thought processes - rationalise obsessive thoughts and compulsive behaviours - reduce the impact they have on persons mind
Resistance of obsessive thoughts
Presence of intrusive thoughts
Inability to exclude irrelevant stimuli
Biological factors
Genetics – high concordance rate in MZ twins - high prevalence in 1st degree relatives - suggest genetic component
Abnormal brain functions
MRI show differences in brain regions: orbitofrontal cortex
caudate
cingulate cortex
Regions involved in motor inhibition/response control
Neurochemical differences
Use of serotonergic agents in treatment – Selective serotonin reuptake inhibitors
(SSRIs) - Prozac
WCST - Wisconsin card sorting test
➢ inductive reasoning task
➢ 3 rules – shape, number, colour
➢ main DV is perseverative responses - how long does it take someone to correctly know the new rule
Assesses frontal function
schizophrenia and WCST
Haut et al., 1996
Compared SCZ to controls and people
with brain tumours in different parts of
the brain – right frontal (RF) and
elsewhere (NF)
SCZ differed from controls and NF
Same as RF
schizophrenia - ‘split mind’
Heterogeneous disorder
Unitary disorder
+
subtypes
or Many different
disorder
0.7% of UK population – female<male
spectrum
Undifferentiated
Catatonic
Paranoid +ve
Disorganised -ve
See also schizotypy - presentation of +/- symptoms more than normal population but not as much as people with SZ
main types 14 subtypes in DSM5
disordered thought patterns
positive symptoms
Thought disorder
Hallucinations
Delusions
Poor impulse control
(Jump to conclusions)
Negative symptoms
Flattened emotions
Poor speech
Lack of initiative
Social withdrawal
Prognosis
Law of thirds: 1/3 institutionalised for life
1/3 remission and cured
1/3 symptomatic for life, generally
getting worse
symptoms can get worse overtime
difficult diagnosis to make
schizophrenia risk factors
Genetic influence (predisposition, maybe) – may need environmental aspect
Neurochemical – major candidate dopamine: the dopamine hypothesis
Neurological – brain structure and brain regions
Neurodevelopmental – in utero, seasonal births
Family – high expressed emotion
optimum treatment = antipsychotic drugs
mood disorders
Extremes of emotion/affect – hence affective disorders
Dysthymia – more mild form – less severe but chronic
Cyclothymia – more mild form of bipolar disorder
Depression:
lack of interest for most of day, for most days, for at least 2 weeks
significant weight loss or gain
insomnia or hypersomnia
psychomotor agitation/retardation
fatigue/loss of energy
feelings of worthlessness/guilt
ability to think/concentrate
recurrent thoughts of death/suicide (ca. 15%)
Mania – wildness, exuberance,
unrealistic activity
rapid speech/thoughts
flighty behaviour
delusions
Episode ca. 6mths long – longer=chronic depressive disorder – remit=2mths clear
Generally co-morbid with anxiety, high level of recurrence
Most common form
of MHD: 10-20% -
bipolar has periods of depression and periods of exuberance. Bipolar 1 has higher levels of mania than Bipolar II
MD aetiology and management
Cognitive - becks cognitive triad - different outlook on life – negative view of self, self-blame, pessimism
result of distorted view of reality (negative view of the world)
self-inadequacies lead to state of life (negative view of the future)
Neurochemical imbalance – reduction in the neurotransmitters: noradrenaline and serotonin ( aka 5HT)
Genetics – increased risk in families, 40% concordance in MZ twins
bipolar may be more heritable than MD
few candidates at present – 5HTT gene changes
example of a gene*environment interaction
(Caspi et al., 2003)
5HTT – serotonin transporter, removes 5HT
from the synapse
Cognitive behavioural therapy (CBT) – corrects distorted thinking
works by discussing views and logic
understand from different perspective
Anti-depressant drugs
Tricyclics
monoamine oxidase inhibitors (MAOI)
Selective serotonin reuptake inhibitors (SSRIs) – e.g. Prozac
NB: lithium for bipolar disorder
bipolar may be more heritable than depression
those with bipolar can easily be misdiagnosed with depression
bipolar disorder
0.5-1.5% lifetime prevalence, = , mean age of onset 21yrs
Different to unipolar – but similar depressive symptoms
Bipolar – experienced mania ± depression – “manic-depressive”
>1 manic episode – singly or mixed/alternating with depressive episode
Easy to misdiagnose as unipolar – important w.r.t. treatment options
Bipolar I – depression + mania
Bipolar II – depression + hypomania
Cylothymia – less severe
Mania = extreme defence against/reaction to depression
Higher genetic correlations/concordance in MZ twins (70%)
Use of mood stabilisers - bidirectional – lithium
cause for concern
- Prevalence of mental disorders and trauma mean that approximately 25% of
people are affected at some time in their lives - About 75 here!
discussion of the items covered in the lectures, may be a sensitive issue for some
of you….
so please speak to your personal tutor
or the student counselling service if you have any concerns
anxiety disorders
Anxiety is a sense of apprehension or doom that is accompanied by certain physiological reactions, such as accelerated heart rate, sweaty palms and tightness in the stomach. It is the most commonly reported mental illness. The prevalence of anxiety internationally ranges between 1 and 28 per cent, depending on the study and overall prevalence is 7 per cent (Baxter et al, 2013). It is twice as common in Europe/Anglicised countries than in African countries. It is more common in women and in those aged between 15 and 34 (Baxter et al, 2014a). The increase in this, and in other mental illnesses, is probably driven more by population growth, rather than an increase in the disease (Baxter et al, 2014b).
Several types of mental disorders are classified as anxiety disorders, which have fear and anxiety as their most prominent symptoms. Three of the most important anxiety disorders are generalised anxiety disorder, panic disorder and specific phobia. Two anxiety disorders previously described as such in DSM-IV – obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD) – now either occupy their own category (OCD is now found under its own category – Obsessive-Compulsive and Related Disorders) or have been moved to a new category (PTSD is now found under Trauma- and Stressor-Related Disorders).
generalised anxiety disorder - description
The principal characteristic of generalised anxiety disorder (GAD) is excessive worry about all matters relating to the individual’s life: health, money, work, relationships and so on. These worries must be present on most days and will have occurred over a period of at least six months. The anxious individual finds it difficult to control the worry and shows at least three symptoms out of the following: restlessness, being easily fatigued, difficulty concentrating, irritability, muscle tension and sleep disturbance.
Anxious individuals spend considerably longer making decisions. For example, Tallis et al (1991) asked a group of controls and clinically anxious individuals to respond if a target was present on a computer monitor. Although there was no difference between controls and anxious individuals when the target was present, the anxious group took significantly longer to make a decision when the target was absent. This finding demonstrates that anxious individuals seem to attend more to tasks that require them to make absolutely correct decisions
generalised anxiety disorder - aetiology
Several models exist which try to explain GAD; some of these also apply to other mental disorders but this section limits itself to those which account for GAD explicitly. One explanation (Borkovec, 1994) suggests that GAD arises from the individual’s drive to set and anticipate a set of goals that are desirable. In this context, the anxiety arises when a history of a frustrated failure to achieve affects the perception of cues associated with these goals. Anxiety is reflected in the individual’s need to anticipate all possible outcomes, for fear of failing or not achieving.
Eysenck (1992) has argued that although Berkovec’s model (described in full in Berkovec (1994)) might explain pathological worry, it does not explain normal worry. Eysenck’s model attempts to explain both by suggesting that worry or anxiety serves as an ‘alarm function’ which brings information concerning threat-related stimuli into awareness. In a sense, worry acts as a behaviour that will prepare an individual for future behaviour; it prompts the individual to anticipate future situations and their solutions.
Gray’s (1982) model suggests a similar mechanism to Eysenck’s but ties it to neurophysiology and certain brain systems. According to Gray, anxiety is evoked by signals of punishment, lack of reward, novel stimuli and innate fear stimuli. The individual detects such threats by means of a behavioural inhibition system (BIS) which also generates the anxiety. An important function of the BIS is that it helps the organism (Gray’s theory applies to humans and other animals) to evaluate the threat content of a stimulus or event. The neurophysiology of the system is vast and complicated, involving neuroanatomical and neurochemical interaction between a number of brain regions. The BIS is thought to be represented by the septum and hippocampal formation
generalised anxiety disorder - two factor model
The two-factor model of anxiety suggests that individuals exhibit a vulnerability to anxiety owing to high trait anxiety and poor coping skills. There is a strong correlation between neuroticism and almost all major anxiety disorders (Andrews et al, 1989; Andrews, 1991). There also seems to be a loss of control exhibited by anxious individuals and anxiety is often preceded by stressful life events (Last et al, 1984), as Borkovec’s model also suggests. Individuals with panic disorder and GAD have been found to rate their parents as less caring and as overprotective (Silove et al, 1991), indicating perhaps one cause of the perceived lack of control. High trait anxiety individuals have been found to be very similar to clinically anxious patients in terms of their perception that events are out of their control and in terms of parental overprotection (Bennett and Stirling, 1998).
generalised anxiety disorder - information- processing models
A number of studies have suggested that individuals high in trait anxiety and those suffering GAD exhibit attentional biases. That is, they are significantly biased towards responding to threat- or anxiety-related material. Anxious people are more vigilant when reacting to threatening faces than non-threatening faces, for example (Bradley et al, 1999). There is a relationship between anxiety and negative interpretation of ambiguous events in children and adolescents and this relationship becomes stronger as the child gets older and when the ambiguity is related to the type of anxiety the child experiences (Stuijfand et al, 2017).
There are various ways of measuring this attentional bias and three of the most common measures are the dot probe, the emotional Stroop test and the interpretation of ambiguous sentences (Eysenck et al, 1991; Wells and Matthews, 1994).
The dot probe task involves the presentation of two words, one above the other, on a computer monitor. Individuals are asked to read aloud the word at the top; this word is either neutral or is an anxiety or threat-related word. After a short pause, the individual is presented with either another pair of words or a dot where the top or bottom word appeared. The individual has to press a key when such a dot appears. MacLeod and his colleagues (MacLeod et al. 1986; Matthews et al, 1990) have reported that latencies are shorter for anxiety-related words in GAD patients.
Similar biases are reported for the emotional Stroop task. In this, individuals have to read the colour in which a word is written. These words are either neutral or anxiety related. GAD patients and individuals high in trait anxiety exhibit a bias towards the anxiety-related words, although the effects found with the Stroop are not as robust as those seen in the dot probe (Williams et al, 1996)
brain anxiety network
The brain anxiety network involves a series of interconnected regions and structures which detect threat and allows us to produce defensive responses (Kirouac, 2021). Some of these include the shell of the nucleus accumbens, the dorsolateral region of the bed nucleus of the stria terminalis, and the lateral central nucleus of the amygdala. Kirouac also suggests that the paraventricular nucleus of the thalamus may also play a role, acting as a relay node integrating signals from the cortex and hypothalamus and projecting them to the areas mentioned above.
Each model of GAD has some merit; that Eysenck’s and Gray’s models flag anxiety as indicating an alarm system that prepares an individual for future action suggests that anxiety results from excessive monitoring for and detection of threat. The findings from attentional bias studies support this view. Why the anxiety should be produced by this appraisal in some individuals and not in others, however, is still unclear. Borkovec’s model is useful in that it specifies previous non-reward and frustration as a cause of being unable to achieve goals. Gray’s model is useful because it ties this appraisal down to one neuropsychological system.
In a meta-analysis of the role of brain activation in anxiety, Etkin and Wager (2007) suggest that the brain contains a ‘fear circuit’. This involves the amygdala, insula, inferior frontal gyrus, fusiform gyrus and superior temporal gyrus. When people experience fear, increased activation is found in these areas bilaterally. When people take medication, or receive some other treatment, this activation decreases. The type and nature of activation, and the structures and regions involved, depend on the specific anxiety disorder.
treatment
The most common form of treatment for GAD is psychopharmacological, with drug administration sometimes coupled with CBT. The drugs used to combat anxiety disorder are called anti-anxiety drugs or anxiolytics and include barbiturates, benzodiazepines and antidepressants. Barbiturates are sedatives and include drugs such as Phenobarbital. However, because they are highly toxic and foster dependence, they are not widely used. Benzodiazepines are anticonvulsant and sedative drugs and they are the most widely prescribed. Two common benzodiazepines are chlordiazepoxide (Librium) and diazepam (Valium), both of which are low in toxicity.
A meta-analysis of 65 studies comparing CBT and/or pharmacological interventions with a control condition for the treatment of GAD, found that CBT was a significantly better treatment than was no treatment (Mitte, 2005). When studies directly compare CBT with drug intervention, there was no significant difference in efficacy.
The evidence for the efficacy of pharmacology in anxiety is inconsistent with one review concluding that a placebo effect is strong. Benzodiazepines have been found to be effective for GAD, panic disorder and social anxiety disorder but these have side effects such as cognitive impairment, sedation and dependence (Baldwin et al, 2014). Drugs that are normally the first choice in anxiety are serotonin-specific reuptake inhibitors (which were developed as antidepressants). These, too, have side effects such as nausea, insomnia and sexual dysfunction (Baldwin et al, 2014).
A recent innovation in treatment has been the development of online interventions (this has been developed for depression, too). The problem with CBT, as a non-pharmacological intervention, is that it is expensive, its availability is limited, and it requires attendance at a practice, office or clinic. Internet-based CBT has been developed which has had positive outcomes for depression and social anxiety disorder (Robinson et al, 2010). In one version of this online treatment, the Worry Programme has been used which comprises six online lessons that challenge the individual’s beliefs about their worries, challenges their core beliefs and ensures that relapse is prevented. In one study, anxious individuals were placed into different conditions randomly (Robinson et al, 2010). One group received technician-assisted online treatment which involved a weekly email and telephone call which followed a specific script. One group received clinician-assisted treatment which involved weekly email or telephone calls plus involvement in online discussions. Each took 10 minutes a week. A control group received no treatment for 11 weeks. Both treatment groups showed reduced worry scores and GAD scores and had sustained this improvement three months later; the clinician-assisted group’s anxiety was reduced the most.
panic disorder - description
Panic has been described as a fear of fear (Foa et al, 1984). Individuals who experience panic are threatened by the presence or the potential presence of fear-related physical states. People with panic disorder suffer from episodic attacks of acute anxiety, that is, periods of acute and unremitting terror that grip them for lengths of time lasting from a few seconds to a few hours. The lifetime prevalence for panic attacks is around 13 per cent and most people who experience one will experience another (De Jonge et al, 2016). Those who do experience more than one are likely to experience other mental illnesses. Onset is most common at the age of 32 (De Jonge et al, 2016).
Panic attacks include many physical symptoms, such as shortness of breath, sweating, racing heartbeat (trachycardia), physical tension, cognitive disorganisation, dizziness and fear of loss of support (jelly legs). The individual feels as if he or she is about to collapse and is on the point of death. Such catastrophic thoughts and feelings only exacerbate the physical symptoms and so the individual becomes involved in a self-fulfilling prophecy.
Between panic attacks, people with panic disorder tend to suffer from anticipatory anxiety, that is, a fear of having a panic attack (Ottaviani and Beck, 1987). Because attacks can occur without apparent cause, these people anxiously worry about when the next one might strike them. Sometimes, a panic attack that occurs in a particular situation can cause the person to fear that situation. The anxiety we all feel from time to time is significantly different from the intense fear and terror experienced by a person gripped by a panic attack, as the case study below illustrates.
panic disorder - aetiology
There seems to be a hereditary component to panic disorders: the concordance rate for the disorder is higher between identical twins than between fraternal twins (Torgerson, 1983). Almost 30 per cent of the first-degree relatives (parents, children and siblings) of a person with panic disorder also have panic disorder (Crowe et al, 1983). According to Crowe et al, the pattern of panic disorder within a family tree suggests that the disorder is caused by a single, dominant gene.
Panic attacks can be triggered in people with histories of panic disorder by giving them injections of lactic acid (a by-product of muscular activity) or by having them breathe air containing an elevated amount of carbon dioxide (Woods et al, 1988; Cowley and Arana, 1990). People with family histories of panic attack are more likely to react to sodium lactate, even if they have never had a panic attack previously (Balon et al, 1989). Some researchers believe that what is inherited is a tendency to react with alarm to bodily sensations that would not disturb most other people.
panic disorder - clark’s model
The most comprehensive (and cognitive) model of panic disorder is that proposed by David Clark. Clark (1986, 1988) argues that panic attacks are produced by the catastrophic misinterpretation of bodily events. Slight changes in bodily sensation are interpreted as symptomatic of a physical threat which makes the individual anxious. The more anxious the individual becomes, the more intense the bodily sensations become (the self-fulfilling prophecy referred to above). According to Clark’s model, two processes contribute to the maintenance of this misinterpretation. The first is hypervigilance: the individual repeatedly checks for changes in bodily sensations; the second is avoidance strategies: the individual avoids those behaviours they feel will exacerbate the bodily sensations. For example, a person who is afraid that he is about to have a heart attack will avoid exercise (although this prevents the individual from discovering that exercise will not cause a heart attack).
Seligman (1988), however, has argued that the catastrophic misinterpretation theory is questionable on the grounds that the realisation that death will not accompany panic attacks will eventually dawn on these patients. Seligman suggests an alternative suggestion based on evolutionary preparedness, the notion that we are evolutionarily predisposed to respond in a specific way to some stimuli because it is to our advantage to do so (Seligman, 1971). Panic, in this context, is the individual’s response to biologically prepared bodily sensations. However, as Power and Dalgleish (1997) argue, the failure to realise that death does not follow bodily sensations arises because individuals avoid situations and stimuli that would induce such bodily sensations in the first place. Seligman’s formulation may not, therefore, be necessary (for the reason he suggests).
Interestingly, some patients maintain that they do not misinterpret their bodily sensations catastrophically and some are more difficult to convince that these sensations will not lead to death (McNally, 1990). These findings point to a degree of variation in panic disorder patients. The anxiety sensitivity hypothesis (Reiss and McNally, 1985), for example, suggests that some individuals are more anxiety-sensitive than others. The degree of sensitivity depends on pre-existing beliefs about the harmfulness of bodily sensations. These pre-existing beliefs predispose the individual to interpret bodily events negatively and erroneously. This leads to panic.
panic disorder - treatment
Treatment for panic disorder can be both cognitive behavioural or pharmacological. CBT, for example, is effective at reducing panic attacks. Such therapy would involve breathing and relaxation techniques, cognitive restructuring (altering misconceptions about the consequences of bodily sensations) and eliciting bodily sensations in the individual to demonstrate the non-harmful nature of such changes (Craske et al, 1997). Antidepressants and anxiolytics are sometimes used to treat panic attacks with some success. Some individuals react badly to the drugs, however, and while they treat the anxiety generated during panic, they do not address the core problem of catastrophic misinterpretation.
social anxiety disorder
Social anxiety disorder (SAD) is the second most common anxiety disorder (Wittchen et al, 2011) and describes an illness in which people have extreme fear of social situations and interacting with others, especially people who are unfamiliar. Often, they fear that they will be scrutinised by others and, consequently, might be criticised.
The aetiology of SAD is multifarious: various studies have suggested genetic and biological influences, parenting, peer relationships and adverse life events (Spence and Rapee, 2016). The difficulty in deterring which, if any, is more important has been hampered by the lack of longitudinal studies. Studies of SAD ask participants to engage in various tasks such as recognising emotion in faces, experiencing social transgressions or criticism, engaging in self-referential thoughts, exposing them to scrutiny and examining their anticipation of public speaking.
Studies of brain activation in SAD have found a network of regions that are active under various conditions in three individuals. For example, a meta-analysis of brain activation during the recognition of emotion in people’s facial expressions found that SAD patients showed activation in these areas, compared to a neutral task: bilateral amygdala, left medial temporal lobe, the right anterior cingulate, right globus pallidus and right post central gyrus (Hattingh et al, 2013). These, and the right insula, anterior cingulate cortex, left DLPFC and medial PFC and the occipitotemporal area bilaterally, are consistently activated in SAD but not in control groups (Bruhl et al, 2014). No region is more active in controls than in SAD.
Treatment can be offered either in the form of medication or cognitive behavioural therapy. People with SAD who receive these show less activation in the occipital and temporal cortex; antidepressants have been associated with decreased activation in the amygdala in three studies (Bruhl et al, 2014).
The amygdala is particularly interesting in the context of anxiety because the volume of the structure has been associated with increased trait anxiety (Baur et al, 2012) and blood flow is greater here in post pubertal women who are high in trait anxiety (Kaczkurkin et al, 2016)
phobia - description
Phobias – named after the Greek god Phobos, who frightened his enemies – are irrational fears of specific objects or situations.
Most individuals have one or more irrational fears of specific objects or situations, and it is difficult to draw a line between these fears and phobic disorders. If someone is afraid of spiders but manages to lead a normal life by avoiding them, it would seem inappropriate to say that the person has a mental disorder. Similarly, many otherwise normal people are afraid of speaking in public. The term ‘phobic disorder’ should be reserved for people whose fear makes their life difficult.
Agoraphobia (agora means ‘marketplace’ in Ancient Greek) is a fear of open spaces and is the most serious and common of the phobic disorders. It occurs in between 50 and 80 per cent of phobic disorders (Matthews et al, 1981). It is reported three times as often in women as in men. Onset is sudden and individuals are usually in their early twenties (Clarke, 1992). The term was coined by Westphal in 1871 to describe four (male) cases who feared open spaces.
Agoraphobia can be severely disabling. Some people with this disorder have stayed inside their house for years, afraid to venture outside. Supermarkets and queuing are especially anxiety-provoking for agoraphobics. Features of supermarket layout such as stairways and diminished access, for example, are regarded as anxiety-provoking by agoraphobic individuals (Jones et al, 1996).
Specific phobias include fear of spiders, blood, snakes, darkness or heights. These phobias are often caused by a specific traumatic experience and are the easiest of all types of phobia to treat.
The lifetime prevalence rate for simple phobia is estimated to be about 14 per cent for women and about 8 per cent for men (Robins and Regier, 1991), but approximately one-third of the population sometimes exhibit phobic symptoms (Goodwin and Guze, 1984)
phobia - aetiology
Animal phobias are sometimes surprising because in Europe, for example, there are no indigenous lethally poisonous spiders, although spider phobias are common. One explanation for this anomaly is that we fear animals that have potentially lethal consequences; we are, therefore, predisposed to fear them. This is the preparedness hypothesis (Seligman, 1971) described in the section on panic disorder. Evidence for this hypothesis comes in the form of the deliberate conditioning of fear of spiders. These conditioning experiences are the most difficult to extinguish – more difficult than non-threatening stimuli (Ohman et al, 1985; McNally, 1987). Preparedness argues that there are some organisms that we are conditioned to fear because they have been likely to cause harm or present a threat throughout evolution and so this threat should be difficult to extinguish. An analysis of 32 fear-conditioning studies measuring whether autonomic condition of fear to images of snakes and spiders were subject to greater resistance to extinction than were exposure to neutral images (Ahs et al, 2018) found extinction resistance to these animals in only 31 per cent of studies; 69 per cent did not show this predicted pattern.
Also, if we are adaptively predisposed to fear the stimuli producing simple phobias, what adaptive purpose does a fear of snails, moths and slugs serve? As McNally (1995) points out, we can ascribe adaptive significance to a fear of any object if we are creative enough. One theory suggests that phobias develop from a pairing of a phobic object with an aversive stimulus so that phobic stimuli become phobic by association. However, only 40–50 per cent of animal phobias appear to be accounted for in this way. Davey (1992) also reported that only 8 out of 118 spider phobics recall having a traumatic experience with spiders.
Matchett and Davey (1991) suggest an alternative explanation: that some stimuli become the object of phobia because of our inherent fear of contamination or disease. Animals (such as spiders, slugs, cockroaches) become feared because they seem disgusting, and we would reject them as food on the basis of this disgust (although some individuals would be immune to such disgust responses; snails are considered a delicacy in certain parts of Europe). In fact, sensitivity to disgust may be an important determinant of the level of fear (Webb and Davey, 1993). To investigate whether some animal phobias were disgust- or fear-related, Davey et al (1998) conducted a cross-cultural study of phobia in seven countries. An analysis of the data suggested that phobic stimuli could be divided into one of three categories: fear-irrelevant (for example, chicken, hamster, cow), fear-relevant (for example, lion, bear, alligator) and disgust-relevant (for example, cockroach, spider, maggot, worm). Disgust was consistent across cultures (although there were some cross-cultural differences with Indian respondents reporting lower levels of fear to the disgust stimuli and Japanese respondents showing higher levels of fear). This finding suggests that not all stimuli may be feared for the same reasons (perhaps the term ‘simple phobia’ is too simplistic, as Curtis et al (1998) suggest).
how specific is specific phobia?
Some innovative work in neuroimaging has found that as an object a person fears comes closer to them, activity is increased in an area of the brain called the bed of the nucleus stria terminalis. When a person holds a feared object, such as a snake, however, and moves it closer to their own person, activation is found in the ventromedial prefrontal cortex (VPC) (Nili et al, 2010; Somerville et al, 2010). The studies suggest that our brain has a network of regions and structures that allows us to appraise threat-related objects, determine our reaction to them and to overcome our fear of them. The volume of the amygdala on the left has been found to be greater in people who were afraid of spiders and this structural characteristic also correlated with disgust sensitivity, trait and anxiety and the duration of the illness (Fisher et al, 2013).
Fearful objects look bigger than they are; we over-estimate their size (Vasey et al, 2012). The actual size of a spider correlates with the degree of fear arachnophobics experience. We also think that heights are taller if we make estimates from the top of a building, than the bottom, but this could be that we have more information on which to make a judgement in the top condition (Proffitt et al, 1995). If people are afraid of spiders, they also estimate its distance to them to be shorter than it actually is (Cole et al, 2013). Mobbs et al (2010) have shown, using fMRI, that when a tarantula is placed closer to a person’s foot (seen via a live video feed), a series of brain regions become activated as feelings of threat increase. These include the periaqueductal grey, the amygdala and the stria terminalis. The amygdala and terminalis activation increased as the spider moved closer to the participant. As the spider moved away, activation became more pronounced in the orbitofrontal cortex (OFC).
But are such regions activated to every phobia? Or do some phobias have features not shared by others? Animal phobias, for example, are known to activate the amygdala, insula and anterior cingulate cortex (ACC) (Shin and Liberzon, 2010).
Lueken et al (2011) used fMRI and galvanic skin response (GSR) to compare two groups of phobics: those with ophidiophobia (snake; animal) and those with dental phobia (blood–injection–injury) as participants watched a fear-inducing video of their feared stimulus/situation. The fear of snakes was associated with increased activation in the amygdala, insula, thalamus and in GSR. Individuals with dental phobia showed activation in the PFC and OFC and less GSR. These data suggest that these two phobias differ, with different underlying neural characteristics
phobia - treatment
Phobias are sometimes treated by systematic desensitisation (described in the general section on treatment) or modelling. Bandura (1971), for example, has described a modelling session with people who had a phobic fear of snakes. The therapist himself performed the fearless behaviour at each step and gradually led participants into touching, stroking and then holding the snake’s body with gloved and bare hands while the experimenter held the snake securely by head and tail. If a participant was unable to touch the snake following ample demonstration, they were asked to place their hand on the experimenter’s and to move their own hand down gradually until it touched the snake’s body. After participants no longer felt any apprehension about touching the snake under these secure conditions, anxieties about contact with the snake’s head area and entwining tail were extinguished. The therapist again performed the tasks fearlessly, and then he and the participant performed the responses jointly. As participants became less fearful, the experimenter gradually reduced his participation and control over the snake, until eventually participants were able to hold the snake in their lap without assistance, to let the snake loose in the room and retrieve it, and to let it crawl freely over their body. Progress through the graded approach tasks was paced according to the participants’ apprehensiveness. When they reported being able to perform one activity with little or no fear, they were eased into a more difficult interaction. This treatment eliminated fear of snakes in 92 per cent of those who participated.
Modelling is successful for several reasons. Participants learn to make new responses by imitating those of the therapist and their behaviour in doing so is reinforced. When they observe a confident person approaching and touching a feared object without showing any signs of emotional distress, they probably experience a vicarious extinction of their own emotional responses. In fact, Bandura (1971, p. 684) reports that ‘having successfully overcome a phobia that had plagued them for most of their lives, subjects reported increased confidence that they could cope effectively with other fear-provoking events’, including encounters with other people.
CBT has also been applied to agoraphobia (Ost et al, 1993). In an experiment in which the effect of exposure (graded exposure to the phobic stimuli) was compared with exposure and CBT (combating negative thoughts and dysfunctional attitudes), Burke et al (1997) found no difference in the effectiveness of the two therapies at six months following the therapy: both were equally effective. Similar combinations have also been found to be effective for social phobias (Scholing and Emmelkamp, 1996).
Exposure therapy was also associated with a reduction in amygdala activation in a study of arachnophobic individuals (Bjorkstrand et al, 2020). Such individuals show increased responsiveness in the amygdala when they see spiders, and a decreased response when the phobia is treated via, for example, CBT (Ipser et al, 2013). Bjorkstrand et al observed that neuroimaging studies of brain activation in phobia involved recording before and after therapy. They, instead, decided to examine brain activation during exposure therapy with spider stimuli. Forty-five people with spider phobia were repeatedly exposed to pictures of spiders. The researchers found that as exposure to the pictures increased, amygdala activation receded. What is more, this attenuation was associated with object avoidance, even six months later. That is, the greater the amygdala activation attenuation, the more likely participants were to avoid spiders.
A recently developed treatment has taken the idea of exposure but added a technological element: virtual reality (VR) technology. This has many practical benefits. and has been applied to a number of anxiety disorders, successfully, including social anxiety disorder (Bouchard et al, 2016).
PTSD - description
Post-traumatic stress disorder (PTSD) made its first appearance in DSM-III in 1980 and refers to anxiety that follows a traumatic event. This event poses a threat to the individual’s life or the lives of others. Symptoms of the disorder include the re-experiencing of feelings related to the event (such as intrusive memories, thoughts and images related to the event), avoidant behaviour (such as denial and emotional numbing) and arousal (such as hypervigilance for trauma-related information).
A review of symptoms suggests that they can be grouped into four types: intrusions, avoidance, dysphoria and hyperarousal (Yufik and Simms, 2010). Sadness, guilt and anger are also associated with the disorder (Shore et al, 1989). People with PTSD seem to express emotional facilitation of cognition; trauma-related information is processed faster and more accurately than information unrelated to the trauma. They also show emotional interference – the impairment of processing of some trauma-related information (Brown and Morey, 2012). These latter symptoms are important because PTSD seldom appears alone but with other disorders or additional diagnoses (McFarlane, 1992; Bleich et al, 1997). PTSD is a controversial disorder because its validity has been challenged. Some researchers point to the ease with which PTSD symptoms can be faked (Burges and McMillan, 2001).
The prevalence rate is around 25–30 per cent in the general population, and rape is associated with the greatest prevalence (Green, 1994). A recent review of 35 studies in which PTSD following a terrorist incident was recorded, found that the prevalence of PTSD was between 33–39 per cent in direct victims (the primary targets of the attack), 5–6 per cent in emergency/rescue services and 17–29 per cent in relatives and friends of the person injured or killed by the attacks (Garcia-Vera et al, 2016). Other events which can produce PTSD are road traffic accidents (Stallard et al, 1998; Murray et al, 2002), bank robberies (Kamphuis and Emmelkamp, 1998), war (Fontana and Rosenheck, 1993) and natural or human-made disasters (Freedy et al, 1994).
Onset of the disorder may be delayed by many years (Blank, 1993). As with GAD and panic disorder, there is a greater Stroop interference for words related to the trauma (Thrasher et al, 1994).
In a study of 96 victims of physical or sexual assault, Dunmore et al (1999) found that some factors were common to both onset and maintenance whereas others were specific to onset. Factors associated with both were appraising the event and the consequences of the event (dwelling on the assault and its aftermath) and adopting poor coping strategies (such as avoidance). Factors which were related to onset were feeling detached during the assault and being unable to perceive positive responses from others. The researchers suggest that these cognitive factors may contribute to PTSD in a number of ways. They may prevent recovery by encouraging poor coping strategy or by generating a sense of immediate threat.
PTSD - aetiology
Horowitz’s (1979, 1986) model suggests that information about the trauma in PTSD is processed because of a mechanism called completion tendency. Completion tendency refers to the need for new information to be integrated into existing patterns of thought and memory. Power and Dalgleish (1997) describe how there is first a stunned reaction to the traumatic event and then a feeling of information overload as the individual realises the enormity of the trauma. Such information cannot be accommodated by existing mental schemata, and defence mechanisms, such as denial and numbing, provide a means of coping with this lack of accommodation. Completion tendency, however, insists on keeping the memory of the event alive (Horowitz calls this ‘active memory’) through flashbacks and nightmares. The anxiety results from the vacillation between these two processes: defence mechanisms and completion tendency. Although an honourable attempt at explaining PTSD, Power and Dalgleish (1997) query whether the model explains some features of the disorder. Why do only some individuals develop PTSD, for example? And why is PTSD delayed in some individuals?
It has been suggested that those individuals exposed to trauma who go on to develop PTSD have a pre-existing disposition to respond over-sensitively to trauma. Alternatively, they develop oversensitivity as a consequence of the trauma. The hippocampus, amygdala and anterior cingulate cortex, for example, have been found to be smaller in PTSD (Morey et al, 2012). The amygdala is especially sensitive to emotional stimuli in PTSD. One model suggests that during trauma reinstatement, activation is found in the dorsal anterior cingulate and ventral PFC when people are cognitively processing information, and in the amygdala and insula when they are responding to the emotional content of the stimulus (Brown and Morey, 2012). However, the type of activation may be content-specific. The insula might be hyperactive when it assigns value to a particular threat and this threat contains emotional information but is hypoactive when it responds to trauma-related information.
hypoactive when it responds to trauma-related information.
The structures of brain that have been implicated in PTSD include the amygdala, hippocampus and prefrontal cortex but the findings are very mixed and not conclusive, largely because in neuroimaging studies employed to explore brain activation or inactivation, sample sizes have been small and appropriate control groups have not been common (Heningsberg et al, 2019; Kredlow et al, 2021).
Some studies have shown increased activation in the amygdala and others show no difference between PTSD and controls (Heningsberg et al, 2019) and even among PTSD patients, consistent changes in the amygdala are not observed. In one study, the only PTSD symptom associated with increased amygdala activation was re-experiencing traumatic symptoms (Stevens et al, 2018).
The evidence for volume changes is no more consistent; a meta-analysis found that left amygdala volume was smaller in PTSD adults than in controls (Karl et al, 2006) whereas others found no differences or found a reduction in the right amygdala (Heningsberg et al, 2019). Whether any changes are the result of the PTSD or a cause/risk factor is unclear. One hypothesis argues that these changes in the brain might represent risk factors; that is, people who have these atypical brain features may be more prone to PTSD when they are exposed to serious trauma. Lower hippocampal volume was observed in one study of 1,868 PTSD patients (Logue et al, 2018) but the same issue of cause or response still applies. Another feature might be reduced activation in the ventromedial PFC
PTSD - treatment
Various forms of treatment have been attempted with PTSD with varying success (Shalev et al, 1996; Foa and Meadows, 1997). Debriefing appears to be ineffective (Deahl et al, 1994) but drug treatment meets with mixed success (O’Brien and Nutt, 1998). Treatment based on exposure seems to be effective (Foa and Meadows, 1997).
A more unusual treatment has been based on the electronic game Tetris. In Tetris, seven differently coloured and shaped blocks descend from the top of the screen to the bottom and the aim is to build a wall of shapes horizontally. To do this, the player can move the blocks to the left or the right. If the blocks build up to the top without the wall being completed, the game is lost. Research has found that when people play this visuospatial game during or after the experience of trauma, the number of traumatic intrusions later in an experiment is lower than if participants had not played the game or had completed a word game (e.g. Green and Bavelier, 2003; Deeprose et al, 2012; James et al, 2015). The explanation for this is that the game taxes working memory to such an extent that the rehearsal of trauma-related material cannot take place or cannot be consolidated because resources have been shifted elsewhere.
OCD - description
Individuals with obsessive-compulsive disorder (OCD) suffer from obsessions – thoughts that will not leave them – and compulsions – behaviours that they cannot keep from performing. In one study, impaired control of mental activities, checking, urges involving loss of motor control and feeling contaminated were found to be the major classes of obsession and compulsion among a large sample of American college students (Sternberger and Burns, 1990). The lifetime prevalence rate is estimated to be about 2.5 per cent (Robins and Regier, 1991; Bebbington, 1998).
Unlike people with panic disorder, people with OCD have a defence against anxiety, their compulsive behaviour. Unfortunately, the need to perform this compulsive behaviour often becomes more and more demanding of their time until it interferes with their daily life. Obsessions are seen in many mental disorders, including schizophrenia. However, unlike persons with schizophrenia, people with OCD recognise that their thoughts and behaviours are senseless and wish that they would go away. The types of obsession and compulsion seen in these individuals are summarised in.
There are two principal kinds of obsession: obsessive doubt or uncertainty, and obsessive fear of doing something prohibited. Uncertainties, both trivial and important, preoccupy some people with OCD almost completely. Others are plagued with the fear that they will do something terrible – swear aloud in church, urinate in someone’s living room, kill themselves or a loved one, or jump off a bridge – although they seldom actually do anything antisocial. And even though they are often obsessed with thoughts of killing themselves, fewer than 1 per cent of them actually attempt suicide.
Most compulsions fall into one of four categories: counting, checking, cleaning and avoidance. For example, people might repeatedly check burners on the stove to see that they are off and windows and doors to be sure that they are locked. Some people wash their hands hundreds of times a day, even when they become covered with painful sores.
Other people meticulously clean their homes or endlessly wash, dry and fold their clothes. Some become afraid to leave home because they fear contamination and refuse to touch other members of their families. If they do accidentally become ‘contaminated’, they usually have lengthy purification rituals
OCD - aetiology
Several possible causes have been suggested for OCD. Unlike simple anxiety states, this disorder can be understood in terms of defence mechanisms. Some cognitive investigators have suggested that obsessions serve as devices to occupy the mind and displace painful thoughts.
Cognitive researchers also point out that persons with OCD believe that they should be competent at all times, avoid any kind of criticism at all costs, and worry about being punished by others for behaviour that is less than perfect (Sarason and Sarason, 1993). Thus, one reason people who have OCD may engage in checking behaviour is to reduce the anxiety caused by fear of being perceived by others as incompetent or to avoid others’ criticism that they have done something less than perfectly.
Family studies have found that OCD is associated with a neurological disorder called Gilles de la Tourette’s syndrome, which appears during childhood (Janowic, 1993). Gilles de la Tourette’s syndrome is characterised by muscular and vocal tics, including making facial grimaces, squatting, pacing, twirling, barking, sniffing, coughing, grunting or repeating specific words (especially vulgarities). It is not clear why some people with the faulty gene develop Gilles de la Tourette’s syndrome early in childhood and others develop OCD later in life.
OCD appears to show different patterns of activation than other anxiety disorders. It has been associated with dysfunctional activation in the nucleus accumbens and with abnormal connectivity to the frontal lobe (Figee et al, 2011)
OCD - treatment
There are usually two forms of treatment employed in OCD. The first is behavioural therapy in which the individual may be exposed to the object, situation or event that provokes the ritualistic behaviour (Emmelkamp, 1993). One example may be to deliberately dirty the hands of an individual who ritualistically washes their hands 20 or 30 times a day and not allow them to wash their hands (Rapoport, 1989). This type of therapy has met with some success in serious cases of OCD. However, behavioural treatment appears to be more successful at eliminating compulsive than obsessive behaviour (Emmelkamp, 1993). Drug treatment appears to eliminate both successfully. These drugs are two serotonin-specific reuptake inhibitors (described in more detail in the section on depression below) and act by increasing the amount of the neurotransmitter, serotonin, in the brain.
A more radical form of intervention is Deep Brain Stimulation (DBS) which you read about in Chapter 4 when we discussed Parkinson’s disease. One study has suggested that DBS can reduce the symptoms of OCD by decreasing the excessive connectivity between the frontal lobe and the striatum (Figee et al, 2013)
dissociative disorders
In dissociative disorders, anxiety is reduced by a sudden disruption in consciousness, which in turn produces changes in one’s sense of identity. The term comes from Freud: according to psychoanalytical theory, a person develops a dissociative disorder when a massive repression fails to keep a strong sexual desire from consciousness. As a result, the person resorts to dissociating one part of their mind from the rest.
The most common dissociative disorder is psychogenic amnesia, in which a person ‘forgets’ all their past life, along with the conflicts that were present, and begins a new one. The term ‘psychogenic’ means ‘produced by the mind’. Because amnesia can also be produced by physical means – such as epilepsy, drug or alcohol intoxication, and brain damage – clinicians must be careful to distinguish between amnesias of organic and psychogenic origin.
A psychogenic fugue is a special form of amnesia in which a person deliberately leaves home and starts a new life elsewhere (fugue means ‘flight’). You read about this in the memory at the movies section in Chapter 8.
Dissociative identity disorder is a very rare, but very striking, dissociative disorder that is marked by the presence of two or more separate personalities within the individual, either of which may be dominant at any given time. Only about 100 cases of dissociative identity disorder have been documented, and some investigators believe that many, if not most of them, are simulations, not actual mental disorders.
An interesting example of dissociative identity disorder is the case of Billy Milligan as told in the book The Minds of Billy Milligan (Keyes, 1981). Milligan was accused of rape and kidnapping but was deemed not guilty by reason of insanity. His psychiatric examination showed him to have 24 different personalities. Two were women and one was a young girl. There was a Briton, an Australian and a Yugoslav. One woman, a lesbian, was a poet, while the Yugoslav was an expert on weapons and munitions, and the Briton and Australian were minor criminals. Dissociative identity disorder has received much attention; people find it fascinating to contemplate several different personalities, most of whom are unaware of each other, existing within the same individual. Bliss (1980) suggests that dissociative identity disorder is a form of self-hypnosis, established early in life and motivated by painful experiences. In fact, the overwhelming majority of people diagnosed as having multiple personality disorder report having been physically abused when they were a child (Kluft, 1984)
personality disorders
The DSM-V classifies abnormalities in behaviour that impair social or occupational functioning as personality disorders. There are several types of personality disorder which the DSM has grouped into three clusters. Cluster A, for example, refers to the ‘eccentric cluster’ of schizotypal and paranoid personality disorders; Cluster B (the dramatic cluster) includes the narcissistic and antisocial personality disorders; and Cluster C (the anxious cluster) includes avoidant and dependent personality disorders. Another general cluster accounts for other personality disorders not covered by these clusters. Because there are so many personality disorders, this chapter focuses on just one in depth: antisocial personality disorder. Table 17.6 provides a description of the several other personality disorders. According to a meta-analysis of four studies, pathological personality is associated with extreme scores on The Big Five (Gøtzsche-Astrup and Moskowitz, 2016)
antisocial persoanlity disoder and psychopathy - description
Antisocial personality disorder (ASPD) refers to a failure to conform to standards of decency, repeated lying and stealing, a failure to sustain long-lasting and loving relationships, low tolerance of boredom and a complete lack of guilt. The first edition of the DSM used the term ‘sociopathic personality disturbance’, which was subsequently replaced by the present term, ‘antisocial personality disorder’. Most clinicians still refer to such people as psychopaths or sociopaths, but this is probably incorrect. There is good evidence, for example, that antisocial personality disorder/sociopathy and psychopathy are different disorders; the former is characterised by antisocial behaviour, usually criminal, whereas the latter is characterised by these antisocial activities plus other, more emotive factors such as lack of empathy for others, remorselessness and manipulativeness. Edens et al (2001) investigated whether the structured clinical interview for ASPD from DSM-IV could predict institutional aggression and physical or verbal violence in a group of 298 male and 55 female prison inmates from four prisons. The DSM criteria did not predict misconduct in jail.
The symptoms of psychopathy were based, originally, on Cleckley’s (1976) 16 characteristics of antisocial personality disorder. Psychopathy is considered the prototype personality disorder (Crego and Widiger, 2014). Cleckley’s list of features provides a good picture of what most psychopaths are like.
They are unconcerned for other people’s feelings and suffer no remorse or guilt if their actions hurt others. Although they may be superficially charming, they do not form real friendships; thus, they often become swindlers or confidence artists. Both male and female psychopaths are sexually promiscuous from an early age, but these encounters do not seem to mean much to them. According to Hare and Hart (1993), they are ‘social predators who charm, manipulate, and ruthlessly plan their way through life . . . Completely lacking in conscience and feeling for others, they selfishly take what they want and do as they please, violating social norms and expectations without the slightest sense of guilt or regret’ (p. xi).
Psychopaths habitually tell lies, even when there is no apparent reason for doing so and even when the lie is likely to be discovered. They steal things they do not need or even appear to want. When confronted with evidence of having lied or cheated, psychopaths do not act ashamed or embarrassed and usually shrug the incident off as a joke.
Psychopaths do not easily learn from experience; they tend to continue committing behaviours that get them into trouble. They also do not appear to be driven to perform their antisocial behaviours; instead, they usually give the impression that they are acting on whims. When someone commits a heinous crime such as a brutal murder, normal people expect that the criminal had a reason for doing so. However, criminal psychopaths are typically unable to supply a reason more compelling than ‘I just felt like it’. They do not show much excitement or enthusiasm about what they are doing and do not appear to derive much pleasure from life. Although they are capable of understanding the difference between right and wrong, the consequences of immoral behaviour and the possession of this knowledge is unimportant to them (Cima et al, 2010).
Psychopathy is diagnosed, conventionally via the Hare Psychopathy Checklist-Revised (PCL-R). This is a part interview, part 20-item questionnaire-based measure that generates a two-factor structure. Respondents are scored from 0 to 2 (‘does not apply’ to ‘definitely applies’) and a score of 30 is the cut-off point for diagnosis of psychopathy. One factor measures behavioural aspects of antisocial behaviour (called lifestyle/antisocial – violence, theft, not caring about others); the second (affective/interpersonal) measures the more emotional, affective components of the disorder such as the manipulativeness and the remorselessness. The two-factor model has been extended to four – each of the traits within each factor – and you can see these listed in Table 17.7. This table also includes the traits for the Youth Version (YV) and the Short Version (SV). The original measure was developed using US participants, but it has since been validated across cultures and sexes and has been found to predict violent and sexual re-offending (Boduszek and Debowska, 2016). The most consistent predictor of later crime commission is scores on the antisocial factor.
When Hassall et al (2015) administered the PCL-R to a group of students, business students scored higher on all four factors than did psychology students and a similar result is found in the corporate world (Babiak et al, 2010). This is why one of Hare’s books was called Snakes in Suits. When Boduszek and Debowska (2016) attempted to determine whether the factor structure of the PCL-R could be obtained across 11 studies, they reported inconsistent results.
A meta-analysis of 431 studies with 123,414 participants which explored the relationship between psychopathy, antisocial personality and empathy found that cognitive empathy was impaired in ASP but affective empathy was more impaired in psychopathy (Campos et al, 2022). The analysis showed that psychopathy and ASD had separate empathy profiles and supports the argument that these two are distinct disorders which share some features, but which differ in important ways
types of personality disorders
aranoid
Suspiciousness and extreme mistrust of others; enhanced perception of being under attack by others
Schizoid
Difficulty in social functioning; poor ability and little desire to become attached to others
Schizotypal
Unusual thought patterns and perceptions; poor communication and social skills
Histrionic
Attention-seeking; preoccupation with personal attractiveness; prone to anger when attempts at attracting attention fail
Narcissistic
Self-promoting; lack of empathy for others; attention-seeking; grandiosity
Borderline
Lack of impulse control; drastic mood swings; inappropriate anger; becomes bored easily and for prolonged periods; suicidal
Avoidant
Oversensitivity to rejection; little confidence in initiating or maintaining social relationships
Dependent
Uncomfortable being alone or in terminating relationships; places others’ needs above one’s own in order to preserve the relationship; indecisive
Obsessive-compulsive
Preoccupation with rules and order; tendency towards perfectionism; difficulty relaxing or enjoying life
Passive-aggressive
Negative attitudes; negativity is expressed through passive means; complaining, expressing envy and resentment towards others who are more fortunate
Depressive
Pervasive depressive cognitions and self-criticism; persistent unhappiness; feelings of guilt and inadequacy
personality disorder - aetiology
The causes of psychopathy are unclear and studies of some of the biological candidates – changes in brain structure/activation, changes in brain volume, deficient levels of serotonin, the presence of the MAO-A gene, the SNAP25 t-snare protein gene or the gene that enables oxytocin production, OXT – have produced inconsistent findings (Frazier et al, 2019).
Cleckley (1976, p. 371) suggested that the psychopath’s defect ‘consists of an unawareness and a persistent lack of ability to become aware of what the most important experiences of life mean to others . . . The major emotional accompaniments are absent or so attenuated as to count for little.’ Some investigators have hypothesised that this lack of involvement is caused by an unresponsive autonomic nervous system (ANS). If a person feels no anticipatory fear of punishment, they are perhaps more likely to commit acts that normal people would be afraid to commit. Similarly, if a person feels little or no emotional response to other people and to their joys and sorrows, they are unlikely to establish close relationships with them.
Many experiments have found that psychopaths do show less reactivity in situations involving punishment. For example, Hare (1965) demonstrated that psychopaths show fewer signs of anticipatory fear. All participants in Hare’s study watched the numerals 1 to 12 appear in sequential order in the window of a device used to present visual stimuli. They were told that they would receive a very painful shock when the numeral 8 appeared. Psychopathic subjects showed much less anticipatory responsiveness than did normal control subjects or non-psychopathic criminals.
According to Hare (1996, p. 46), ‘In some respects, it is as if psychopaths lack a central organiser to plan and keep track of what they think and say.’ The part of the brain that is more responsible than any other for monitoring, organising and integrating sensory input and behaviour, is the frontal cortex. People with damage to the frontal cortex have also been shown to exhibit irregularities in ANS functioning such as a lack of heart rate responsiveness and GSR in contexts that require an assessment of risk.
Over many years, Adrian Raine, James Blair and others in the UK and US have published controversial data linking frontal lobe dysfunction with psychopathic behaviour and antisocial personality disorder. In general, psychopaths tend to show less activity or less volume in this area, a region known to mediate some aspects of emotional and social behaviour (see Chapter 13). In what they describe as a study showing the ‘first evidence for a structural brain deficit in antisocial personality disorder’ (APD), Raine et al (2000) compared the brain volume of 21 community volunteers having the DSM-IV TR ratified APD with control groups and found that the prefrontal brain volume of the APD group was 11 per cent less than other groups. They also showed little autonomic response when undertaking the social stressor task – they had their behaviour videotaped as they talked about their faults.
A review of neuroimaging findings from psychopathy has highlighted the importance of four areas of the brain: the OFC, the amygdala, the anterior/posterior cingulate and nearby limbic structures (Anderson and Kiehl, 2012). A meta-analysis of brain volume in psychopathy found that prefrontal cortex reductions were the most commonly reported (Santana, 2016). These areas of reduction included the OFC, the medial PFC, the inferior frontal gyrus and the anterior cingulate cortex. At the level of function, connections between the prefrontal lobe, the amygdala and the parietal lobe were reduced in the psychopaths (Motzkin et al, 2011).
When psychopaths had to make decisions regarding moral violations, activity in the ventromedial PFC and temporal cortex was reduced compared to a control group (Herenski et al, 2010). A review (Pascual et al, 2013) has summarised the brain areas involved in moral decision-making.
tTo date, neuroimaging studies have focused on ‘unsuccessful’ psychopaths, that is, those who have been caught and jailed. It has been suggested that successful psychopaths – those who are not caught and jailed – are behaviourally very similar to their incarcerated counterparts but are physiologically different (Widom, 1978). Ishikawa et al (2001) recruited people from temporary employment agencies and administered the Hare Psychopathy Checklist to determine the degree of psychopathy in the sample. The researchers found that, when compared with the control group, the successful psychopaths showed heightened heart rate activity and performed better than the unsuccessful psychopaths at a test of frontal lobe function. The authors suggest that this reactivity reflects the successful psychopath’s greater awareness of changes in the social environment; they are better than unsuccessful psychopaths at assessing or making risky decisions; unsuccessful psychopaths show little ANS reaction to risk and it may be this lack of feedback from the ANS that leads to their slipping up.
personality disorder treatment
There is no standard, effective treatment for APD or psychopathy and the treatments used have normally been designed for other purposes such as anger management or reducing deviant sexual behaviour (Oltmans and Emery, 1998). Whereas evidence suggests that there is some temporary effect on the behaviour, the effect does not generalise to other settings in the long term. One predictor of success, when it does happen, is a person’s adherence to a treatment programme: the more successful complete the programme (Reid and Gacono, 2000)
schizophrenic spectrum and other psychotic disorders
Schizophrenia, the most common psychosis, is not a unitary illness but a group of varied disorders each with a distinctive set of symptoms (Arnedo et al, 2014).
The common symptoms are distortions of thought, perception and emotion, bizarre behaviour and social withdrawal. Around 8 to 40 cases per 1,000 are reported per year worldwide and the disorder appears to recognise no cultural or international boundaries. It is higher in urban areas and there is a lifetime risk of 0.7 per cent of developing the illness (and this is greater in men). It is highest in people of lowest socio-economic status, has its onset in adolescence or early adulthood, and genetic factors account for 80 per cent of the disorder’s appearance (Tandon et al, 2008a). According to the WHO (2016), 21 million people worldwide suffer from the disorder. Schizophrenia is probably the most serious of the mental disorders. It tends to manifest itself in the patient’s mid-twenties, although there will have been evidence of subtle clinical symptoms and decline of function prior to this – the so-called prodromal stage of the illness (Addington et al, 2007). It is highly heritable – if a close relative has the illness, this increases the likelihood of developing the disorder (Rees et al, 2015).
In his book, Better To Live, an examination of his own depression and how he tries to manage the disorder, Alastair Campbell describes his brother Donald’s schizophrenia and how poorly people understand the illness. ‘Imagine a cacophony of voices in your head,’ he writes, ‘screaming, telling you to do things you normally know you shouldn’t. Then imagine plugs, sockets and light switches, road signs and shop signs, talking to you. Imagine sitting in a public place busy with people going about their business and thinking every single word being thought by everyone is about you. Imagine watching TV and being sure everyone is talking about you. And then imagine snakes coming out of the floor and wild cats charging through the walls and ceilings. Donald had all that and more when he was in crisis.’ (Campbell, 2020, p12–13).
The word ‘schizophrenia’ literally means ‘split mind’, although it is commonly misinterpreted as ‘split personality’. The individual does not suffer from split personality or multiple personality (those are other mental disorders) but from disordered thought and affect. The man who invented the term, Eugen Bleuler (in 1911), intended it to refer to a break with reality caused by such disorganisation of the various functions of the mind that thoughts and feelings no longer worked together normally.
Many studies of people who become schizophrenic in adulthood have found that they were different from others even in childhood. One study obtained home movies of people with adult-onset schizophrenia that showed them and their siblings when they were children (Walker and Lewine, 1990). Although the schizophrenia did not manifest itself until adulthood, viewers of the films (six graduate students and one professional clinical psychologist) did an excellent job of identifying the children who were to become schizophrenic. The viewers commented on the children’s poor eye contact, relative lack of responsiveness and positive affect, and generally poor motor coordination.
The prognosis for schizophrenia is described by the ‘law of thirds’. Approximately one-third of the people who are diagnosed as having it will require institutionalisation for the rest of their lives. About one-third show remission of symptoms and may be said to be cured of the disorder. The final third are occasionally symptom-free (sometimes for many years) only to have the symptoms return, requiring more treatment and perhaps even institutionalisation. It has the worst prognosis of the psychiatric illnesses apart from dementia (Jobe and Harrow, 2010). After about five years, however, the illness stabilises and does not worsen.
Schizophrenia is characterised by two categories of symptoms: positive and negative. Positive symptoms include thought disorders, hallucinations and delusions. A thought disorder – a pattern of disorganised, irrational thinking – is probably the most pronounced symptom of schizophrenia. People with schizophrenia have great difficulty arranging their thoughts logically and sorting out plausible conclusions from absurd ones. In conversation, they jump from one topic to another as new associations come up. Sometimes, they utter meaningless words or choose words for their rhyme rather than for their meaning. Delusions are beliefs that are obviously contrary to fact. Delusions of persecution are false beliefs that others are plotting and conspiring against oneself. Delusions of grandeur are false beliefs in one’s power and importance, such as a conviction that one has god-like powers or has special knowledge that no one else possesses. Delusions of control are related to delusions of persecution; the person believes, for example, that they are being controlled by others through such means as radar or tiny radio receivers implanted in their brain.
The third positive symptom of schizophrenia is hallucinations, which are perceptions of stimuli that are not actually present. The most common schizophrenic hallucinations are auditory, but such hallucinations can also involve any of the other senses. The typical schizophrenic hallucination consists of voices talking to the person. Sometimes, they order the person to act; sometimes, they scold the person for their unworthiness; sometimes, they just utter meaningless phrases. Sometimes, those with schizophrenia may also hear a voice that keeps a running commentary on their behaviour, or they hear two or more voices.
In contrast to the positive symptoms, the negative symptoms of schizophrenia are known by the absence of normal behaviours: flattened emotional response, poverty of speech, lack of initiative and persistence, inability to experience pleasure, and social withdrawal.
types of schizophrenia
The DSM identifies four types of schizophrenia: undifferentiated, catatonic, paranoid and disorganised. Most cases of schizophrenia, however, do not fit exactly into one of these categories. Many individuals are diagnosed with undifferentiated schizophrenia, that is, the patients have delusions, hallucinations and disorganised behaviour but do not meet the criteria for catatonic, paranoid or disorganised schizophrenia. In addition, some patients’ symptoms change after an initial diagnosis, and their classification changes accordingly.
Catatonic schizophrenia (from the Greek katateinein, meaning ‘to stretch or draw tight’) is characterised by various motor disturbances, including catatonic postures – bizarre, stationary poses maintained for many hours – and waxy flexibility, in which the person’s limbs can be moulded into new positions, which are then maintained. Catatonic schizophrenics are often aware of all that goes on about them and will talk about what happened after the episode of catatonia subsides.
The pre-eminent symptoms of paranoid schizophrenia are delusions of persecution, grandeur or control. The word ‘paranoid’ has become so widely used in ordinary language that it has come to mean ‘suspicious’. However, not all paranoid schizophrenics believe that they are being persecuted. Some believe that they hold special powers that can save the world or that they are Christ, or Napoleon or the president of the USA.
Individuals with paranoid schizophrenia are among the most intelligent of psychotic patients, so, not surprisingly, they often build up delusional structures incorporating a wealth of detail. Even the most trivial event is interpreted in terms of a grand scheme, whether it is a delusion of persecution or one of grandeur. The way a person walks, a particular facial expression or movement, or even the shapes of clouds can acquire special significance. An example of a case study of paranoid schizophrenia appears in the Psychology in action section.
Disorganised schizophrenia is a serious progressive and irreversible disorder characterised primarily by disturbances of thought. People with disorganised schizophrenia often display signs of emotion, especially silly laughter, that are inappropriate to the circumstances. Also, their speech tends to be a jumble of words: ‘I came to the hospital to play, gay, way, lay, day, bray, donkey, monkey’ (Snyder, 1974, p. 132). This sort of speech is often referred to as a word salad
schz - aetiology
Research into the causes of all kinds and forms of schizophrenia throughout this century and the last reflects the challenge that psychologists face in attempting to understand how psychological and biological factors interact to influence behaviour. Schizophrenia appears to result from one or more inherited, biological predispositions that are activated by environmental stress
schz - genetic causes
The heritability of schizophrenia, or more precisely the heritability of a tendency towards schizophrenia, has now been firmly established by both twin studies and adoption studies. Identical (monozygotic, MZ) twins are much more likely to be concordant for schizophrenia than are fraternal (dizygotic, DZ) twins, and the children of parents with schizophrenia are more likely themselves to become schizophrenic, even if they were adopted and raised by non-schizophrenic parents (Kety et al, 1968; Farmer et al, 1987). Twin studies of schizophrenia compare the concordance rates of MZ twins with the concordance rates of siblings of different genetic relatedness who were reared either together or apart. The risk of one MZ twin developing the disorder if the other has it is between 50 and 70 per cent; in DZ twins, this is between 9 and 18 per cent. If both of a child’s parents are affected, it has a 40–60 per cent chance of developing the illness (Tanda et al, 2008).
If a person has been diagnosed with schizophrenia, there exists the possibility that other family members have the disorder, too. It is important to note that although the likelihood of developing schizophrenia increases if a person has schizophrenic relatives, this disorder is not a simple trait, like eye colour, that is inherited. Even if both parents are schizophrenic, the probability that their child will develop schizophrenia is 30 per cent or less.
Current findings provide strong evidence that schizophrenia is heritable, and they also support the conclusion that carrying a ‘schizophrenia gene’ does not mean that a person will necessarily become schizophrenic (see Figure 17.6). These figures suggest that the environment may be an important trigger for the activation of the biological predisposition. Other risk factors can be seen in Figure 17.7.
Genome-Wide Association Studies (GWAS) (see Chapter 3) attempt to identify genetic features which cluster in a group of individuals. Forty-two single-nucleotide polymorphisms have been identified which have been associated with a 70 per cent risk of developing schizophrenia; 34 have been confirmed in high-risk schizophrenia, although it has been difficult to replicate these findings (Arnedo et al, 2014). Yet other studies, suggest that over 1000 alleles are involved in schizophrenia (Cross-Disorder Group, 2013). A GWAS study of 36,989 cases of schizophrenia and 113,075 controls identified 128 independent alleles (Schizophrenia Working Group, 2014). Some studies have associated schizophrenia with genetic mutation such as copy number variations – these are higher in schizophrenia than in controls. The first to be identified was 22q11.2. At least 15 of these have been identified in schizophrenia and have been associated with a risk of developing schizophrenia (Robinson et al, 2014b). The most significant association is thought to be on the short arm of chromosome 6. There is also an association between schizophrenia and the gene which encodes the dopamine D2 receptor and genes which code the regulation of dopamine synthesis, pathways which are also responsible for our response to stress (Howes et al, 2016)
schz - neurochemical causes
The dominant neurochemical hypothesis concerning schizophrenia involves dopamine and the evidence for dopamine’s involvement was originally indirect. Cocaine and amphetamine, for example, can cause symptoms of schizophrenia, both in schizophrenics and in non-schizophrenics; antipsychotic drugs, on the other hand, can reduce them. Because both types of drug affect neural communication in which dopamine serves as a transmitter substance, investigators hypothesised that abnormal activity of these neurons was the primary cause of schizophrenia. The dopamine hypothesis, therefore, states that schizophrenia is produced by the overactivity of synapses (increased dopamine synthesis), especially those in the striatum, that use dopamine as a transmitter substance (Howes et al, 2016; Weinstein et al, 2016; Maia and Frank, 2016).
schz - neurological causes
Two meta-analyses have found that there is greater loss of brain volume in schizophrenia than in controls, although whether this loss is due to the illness or the drugs used by individuals is not clear (Veijola et al, 2014). There is also evidence of decreased white matter connectivity in schizophrenia (Kochunov and Hong, 2014). There seem to be specific abnormalities in the fibres connecting the frontal and temporal lobes (Wheeler and Voineskos, 2014). A meta-analysis of 15 such studies found that there was a significant reduction in left frontal white matter and left temporal white matter (Ellison-Wright and Bullmore, 2009). In first-episode patients, there is a loss in white matter in the right frontal lobe and left temporal lobe, but some studies find no such differences (Yao et al, 2013). The severity of negative symptoms has been associated with lower white matter in the bilateral uncinate fasciclus and inferior frontal areas (Szesko et al, 2014). Unaffected family members also show decreased left PFC and medial temporal lobe white matter (Hao et al, 2009). There appears to be a reduction in connectivity between other areas such as the frontal cortex and the limbic system (Wheeler and Voineskos, 2014).
Despite these findings, there is no confirmed and consistent biological marker of schizophrenia at the neural level. The lack of consistency is due to methodological differences between studies investigating neural bases, the heterogeneity of symptoms presented in schizophrenia, the inclusion of a range of sub-types, a variety of proposed causal mechanisms, and differences in moderator variables (studies vary by participants’ age, sex, age of onset) (Wheeler and Voineskos, 2014)
schz - cognitive and environmental causes - family and expressed emotion
A study carried out in Finland has suggested that being raised by a ‘mentally healthy’ family helps to protect against the development of schizophrenia (Tienari et al, 1987). The researchers examined the children of schizophrenic mothers who had been adopted away early in life. Following interviews and psychological tests, the families who adopted the children were classified as well adjusted, moderately maladjusted or severely maladjusted. The children adopted by the well-adjusted families were least likely to show signs of mental disturbance, including schizophrenia. These findings suggest that the environment may be either an important cause or mediator of schizophrenia.
The personality and communicative abilities of either or both parents appear to play an influential role in the development of schizophrenic symptoms in children. Several studies have shown that children raised by parents who are dominating, overprotective, rigid and insensitive to the needs of others later develop schizophrenia (Roff and Knight, 1981). In many cases, a parent may be verbally accepting of the child yet in other ways reject them, which establishes a conflict for the child called a double-bind. For example, a mother may encourage her son to become emotionally dependent on her yet continually reject him when he tries to hug her or sit on her lap.
Another environmental factor which could account for the development of schizophrenia is expressed emotion or EE (Hooley et al, 1996). Brown et al (1966; Brown, 1985) identified a category of behaviours of families of individuals recovering from schizophrenia that seemed to be related to the patients’ rates of recovery. They labelled this variable expressed emotion, which consists of expressions of criticism, hostility and emotional overinvolvement by the family members towards the patient. Patients living in a family environment in which the level of expressed emotion was low were more likely to recover, whereas those in families in which it was high were likely to continue to exhibit schizophrenic symptoms. Perceived criticism also appears to be important: in depressed patients, perceived criticism predicted a relapse in the mental disorder more reliably than did actual criticism (Hooley and Teasdale, 1989); mood disorder patients with high-EE families appear to be more non-verbally negative than patients from low-EE families (Simoneau et al, 1998). Expressed emotion has been found to increase with illness duration and patients are more likely to relapse if they come from high-EE families (Hooley, 2010).
schz - treatment
The commonest form of treatment for schizophrenia is psychopharmacological although there is no cure for the disorder and treatment is a combination of pharmacological intervention – the primary treatment – and behavioural/psychological support. Success is variable with treatments often resulting in adverse effects, relapses, failure to adhere, and persistent negative symptoms (Maroney, 2020). Negative symptoms persist because a dominant drug therapy involves acting on the dopaminergic system which can reduce positive symptoms, but which leave negative symptoms untreated (Krogman et al, 2019). Guidelines from professional societies, such as the American Psychiatric Association, recommend a bespoke approach to treatment where treatment is based on an individual patient’s need and symptoms.
With these drugs, such as chlorpromazine, hallucinations diminish or disappear, delusions become less striking or cease altogether, and the patient’s thought processes become more coherent. These drugs are not merely tranquillisers; for example, they cause a patient with catatonic immobility to begin moving again as well as cause an excited patient to quieten down. In contrast, true tranquillisers such as Librium or Valium only make a schizophrenic patient slow-moving and lethargic.
Antipsychotic drugs block dopamine receptors and prevent them from becoming stimulated. The focus of the drugs appears to be the D2 receptor in the striatum: around 70 per cent of these receptors are occupied by antipsychotic medication which blocks their action (Lidow et al 1998). Cocaine, conversely, activates this receptor. The only effective means of treating the disorder is by D2 antagonists. These antipsychotic drugs help to reduce the effects of schizophrenia apparently by blocking dopamine receptors in the brain. Presumably, overactivity of dopamine synapses is responsible for the positive symptoms of schizophrenia, which is why treatment is effective at combating the positive symptoms but has limited success in combating the negative symptoms (Keshavan et al, 2008). Although dopamine-secreting neurons are located in several parts of the brain, most researchers believe that the ones involved in the symptoms of schizophrenia are located in the cerebral cortex and parts of the limbic system near the front of the brain. There is evidence that the education of the family/patient about the disorder reduces the likelihood of a relapse and that social skills training also improves outcome (Keshavan et al, 2008).
The drug of choice is the second-generation antipsychotics because they are associated with fewer adverse effects than the first-generation drugs such as clozapine. These adverse effects are called ‘extrapyramidal side effects’ and include conditions such as akathisia – restless movement – and symptoms similar to Parkinson’s disease. The second-generation class are not effect-free; they can also result in adverse effects such as weight gain and diabetes (Keepers et al, 2019). Another side effect – tardive dyskinesia in which movements are either very slow or very jerky – can be reduced by changing antipsychotic medication.
A new treatment approved in the US in 2019 and the only transdermal treatment currently available can be applied on the skin via patches or under the tongue. The drug, asenapine, has met with initial success in randomised trials but there is no release date for the product (Maroney, 2020). Other drugs developed or under development include selective serotonin agonists, lumateperone and pimavanserin, a mu-receptor agonist, olanzapine/samidorphan, and a TAAR-1 receptor agonist (Maroney, 2020).
Most drug treatments target, and are successful in reducing, the positive symptoms of schizophrenia although some individuals are resistant to antipsychotic medication. The negative symptoms, such as anhedonia, blunted affect, social withdrawal and poverty of speech (alogia), are difficult to treat and are often core symptoms of the disorder (and are called primary negative symptoms) or may arise from other disorders (e.g. depression) or even from positive symptoms themselves. The main drug strategy involves administration of medication which acts on the dopamine, choline and serotonin systems (Capatina et al, 2021).
Some first-generation antipsychotics, which block D2 dopamine receptors are not effective at reducing primary negative symptoms. Second generation antipsychotics such as clozapine and amisulpride (also known as atypical antipsychotics) which act on D2 and D3 dopamine receptors and other amine receptors seemed to be successful in reducing these symptoms (Capatina et al, 2021). Cariprzine, which is a D3/D2 partial agonist and a 5-HT1A partial agonist seems to be effective in reducing negative symptoms compared with placebo (Earley et al, 2019). 5-HT3 receptor antagonists were also found to be successful according to one meta-analysis (Kishi et al, 2014). Acetylcholineesterase inhibitors might also be effective (Singh et al, 2012).
The positive symptoms of the illness have been addressed using CBT. One aim of CBT is to improve the patient’s social skills by changing his/her cognition. A meta-analysis of social skills training in schizophrenia found that they led to improvements in the acquisition of skills, assertiveness, social interactions and a general reduction in symptoms (Kurtz and Mueser, 2009). More modest improvements are seen in social activities such as behaving appropriately at a supermarket.
depressive disorders
Everyone experiences moods varying from sadness to happiness to elation. We are excited when our team wins a game, saddened to learn that a friend’s father has had a heart attack, thrilled at news of a higher-than- expected grade in an exam, and devastated by the death of a loved one. Some people, though, experience more dramatic mood changes than these. They may be characterised by a deep, foreboding depression or by a combination of depression and euphoria.
DSM-V describes what we consider to be chronic and persistent unhappiness as major depressive disorder (MDD). According to DSM-V, individuals with MDD, have depressed mood, have diminished interest and pleasure, weight/appetite increase or decrease, insomnia or hypersomnia, psychomotor agitation, loss of energy, feelings of worthlessness, inappropriate guilt, lack of concentration, diminished thinking and recurrent thoughts of deaths or suicide. Depressed people also show impairment in some cognitive functions such as executive functions, especially if they are currently experiencing severe depression and if they are taking relevant medication (Snyder, 2013). Depressed people cannot always state why they are depressed.
The ‘walking, waking dead’, according to the World Health Organization (2021), is estimated to account for 5 per cent of the global population (www.who.int). This is a total of 280 million people.
There are some issues with the diagnosis of the disorder, however, which may explain why some people present with some symptoms and not others, why some people are responsive to medication and some not and how degrees of depression vary. For example, Fried et al (2022) have raised the nature of the measures used to diagnose depression and highlight the low validity and reliability of these measures. In an earlier review of depression measures (seven of them), Fried identified 52 symptoms of depression and many of these were not common to all seven (Fried, 2017)
depressive disorders - aetiology - cognitive causes
People with mood disorders do not have the same outlook on life as others. Specifically, they make negative statements about themselves and their abilities: ‘Nobody likes me’, ‘I’m not good at anything’, ‘What’s the point in even trying, I’ll just mess it up anyway’. Because they are so negative about themselves, depressed people are particularly unpleasant to be around. The problem is that the depressed individual is caught in a vicious circle: negative statements strain interpersonal relationships, which result in others withdrawing or failing to initiate social support, which, in turn, reinforces the depressed individual’s negative statements (Klerman and Weissman, 1986).
Beck (1967, 1991) suggested that the changes in effect seen in depression are not primary but instead are secondary to changes in cognition. That is, the primary disturbance is a distortion in the person’s view of reality. For example, a depressed person may see a scratch on the surface of their car and conclude that the car is ruined; or a person whose recipe fails may see the unappetising dish as proof of their unworthiness; or a nasty letter from a creditor is seen as a serious and personal condemnation. According to Beck, depressed people’s thinking is characterised by self-blame (things that go wrong are always their fault), overemphasis on the negative aspects of life (small problems are blown out of proportion) and failure to appreciate positive experiences (pessimism). This kind of pessimistic thinking involves negative thoughts about the self, about the present and about the future, which Beck collectively referred to as the cognitive triad. In short, depressed people blame their present miserable situation on their inadequacies and a lack of hope for improving the situation in the future. Depressive symptoms can be measured via the Beck Depression Inventory.
The negative view of the self and events, however, seems to be time specific. Depressed individuals who are asked to describe themselves ‘right now’ use negative terms but use less negative terms when they describe how they usually feel (Brewin et al, 1992). Depressed patients are also likely to be negative when discussing things globally but not when discussing specific issues (Wycherley, 1995).
Beck’s original model argued that cognition caused the emotional disorder, but his later reformulation of the theory suggested that cognition is part of a set of interacting mechanisms that include biological, psychological and social factors (Kovacs and Beck, 1978). In the reformulation, Beck argued that people might be predisposed to develop depression under certain circumstances. He called this a diathesis–stress theory. Central to the theory is that there is a set of schema – a stored collection of knowledge that affects encoding and understanding of all other processed information – which, when activated, sets off a series of negative thoughts and experiences. If the schema is depressogenic – characterised by depressive features – then an event which might activate these schemata leads to the person processing information very negatively. However, if a person is not exposed to these triggers, they will think or behave no more depressively than a person who does not possess depressogenic schemata. A study of undergraduates found that students with dysfunctional attitudes – those who were identified as having depressogenic schemata – felt more depressed after learning they had been refused a place at a university of their choice than when learning that they had, a pattern not seen in students whose attitudes were not dysfunctional (Abela and D’Alessandro, 2002).
Beck also distinguished between two types of depression: sociotropic depression in which the abnormal belief derived from a dependence on others, and autonomous depression in which the individual was goal-oriented and relied little on others. The evidence for these two types as distinct varieties of depression, however, is mixed (Power and Dalgleish, 1997).
Another causal factor in depression appears to involve the attributional style of the depressed person (Abramson et al, 1978, 1989). According to this idea, it is not merely experiencing negative events that causes people to become depressed: what is more important are the attributions people make about why those events occur. People who are most likely to become depressed are those who attribute negative events and experiences to their own shortcomings and who believe that their life situations are never going to get any better. A person’s attributional style, then, serves as a predisposition or diathesis for depression. In other words, people prone to depression tend to have a hopeless outlook on their life: ‘I am not good at anything I try to do and it will never get any better. I am always going to be a useless person.’ According to this view, depression is most likely when people with pessimistic attributional styles encounter significant or frequent life stressors (Abramson et al, 1989). The pessimistic attributions are then generalised to other, perhaps smaller, stressors, and eventually a deep sense of hopelessness and despair sets in. Thus, the original formulation of the theory was called the helplessness theory whereas the later reformulation became known as the hopelessness theory.
Such people also appear to suffer a double dose of hopelessness.
Not only do they perceive negative outcomes as being their own fault, but they also perceive positive outcomes as being due to circumstance or to luck. In addition, they apply pessimistic attributions to a wide range of events and experiences and apply positive attributions only to a very narrow range of events and experiences, if any.
However, there is mixed evidence for a strong version of the hopelessness attribution theory. Swendsen (1998) reported that attributional style did not predict immediate depressed or anxious mood in a group of 91 individuals who were asked to report negative events, cognitions, anxiety and depression five times a day for one week. However, attributional style did predict ‘individual’ specific causal attributions made to negative events. Similar findings have been reported in other studies (Kapci, 1998). Lynd-Stevenson (1996, 1997) reports that hopelessness does not mediate the relationship between attributional style and depression but that there is a mediating effect when measures of hopelessness are relevant to the individual’s ongoing life (in Lynd-Stevenson’s sample’s case, hopelessness related to unemployment). Attributional style, therefore, seems to apply only in certain, relevant contexts.
depressive disorders - genetic causes
Like schizophrenia, depressive disorders have been the subject of a search to discover an underlying genetic cause. One study of 9,000 people with major depression found no genetic sequences which were associated with depression (MDDWG, 2013). In 2015, the first two genetic markers linked to depression were discovered (CONVERGE Consortium, 2015). A study of 5,303 Chinese women with depression and 5,337 without, found that two sequences were associated with the illness – one next to an enzyme whose function is not completely understood and another next to S1RT1, a gene that codes for mitochondria, cells which produce energy (Flint and Kendler, 2014). This was later confirmed in a study of 3,000 men and women with depression.
depressive disorders - neurochemcial causes
Drug treatments for depression (which are described in detail below) have shed some light on the biochemical causes of schizophrenia. Antidepressants such as imipramine, for example, stimulate synapses that use two transmitter substances, norepinephrine and serotonin. Other drugs such as reserpine, which is used to treat high blood pressure, can cause episodes of depression. Reserpine lowers blood pressure by blocking the release of norepinephrine in muscles in the walls of blood vessels, thus causing the muscles to relax. However, because the drug also blocks the release of norepinephrine and serotonin in the brain, a common side effect is depression. This side effect strengthens the argument that biochemical factors in the brain play an important role in depression.
Such data have suggested a biological amine theory of depression: depression results from a depletion in the monoamines, dopamine, norepinephrine or serotonin. The serotonin hypothesis is a variant of this general theory. The serotonin hypothesis suggests that this neurotransmitter (the lack of it) may be more involved in depression because blocking reuptake of serotonin is more effective than blocking norepinephrine. Given that most antidepressants augment serotonin (perhaps by different mechanisms), perhaps the involvement of other neurotransmitters is peripheral.
In addition to the amines, levels of the neurotransmitter gamma-aminobutyuric acid (GABA) have been found to be lower in the cerebrospinal fluid (CSF) and plasma of individuals with unipolar depression (Brambila et al, 2003). When depressed individuals are given drugs which increase the level of serotonin at serotonergic neurons or are given ECT, the decrease in GABA concentration seen in the occipital cortex is reversed (Sanacora et al, 2002, 2004). The roles of the two classes of GABA (the a and b classes) in depression, however, are unclear.
Another possible chemical cause of depression is vitamin D deficiency. The receptors for vitamin D are present on neurons in the cingulate cortex and hippocampus and several studies have found a correlation between depression and vitamin D deficiency. However, as Anglin et al (2013) note, eight reviews of the evidence have found insufficient evidence for the involvement of vitamin D. In their own review of 14 studies including 31,424 people, they found that significant effects were found in some types of study and not others. They also suggest that the field may be susceptible to publication bias – negative results are not published
depressive disorders - neuropathological causes
in a neuroimaging study, activity in the PFC near the top of the corpus callosum was reduced in individuals with unipolar and bipolar depression (Drevets et al, 1997). This part of the PFC is called the ACC and a specific region within the cingulate – which has been called subgenual region sg24 – is less active in people with mood disorder.
Drevets et al found that the volume of this region was lateralised to the left hemisphere, which is consistent with the data and model of normal emotion (described in Chapter 13). These findings were subsequently replicated in a group of people with severe mood disorder (Hirayasu et al, 1999).
A further study, using a larger sample, found cell density and goal cell reduction in a group of individuals with major and bipolar depression but only in a subset with a family history of the disorder (Torrey et al, 2000). These cells carry neurotransmitter receptors and help to transport neurotransmitters, which may explain why their reduction is associated with depression; the reduction might also explain why this area is seen as smaller in people with depression and bipolar depression.
There is also evidence that connectivity in the brain at rest differs between people with major depressive disorder and control groups (Berman et al, 2011; Zeng et al, 2012). This resting state abnormality has been thought to underlie the rumination that depressed individuals engage in. People with depression attend preferentially to negative information but the brain regions underlying this are not completely known; some suggest that the amygdala becomes active during exposure to negative information and the ventral striatum responds to positive information and is less active in depressed individuals (Groenewold et al, 2013).
Muller et al’s (2017) meta-analysis of PET and fMRI studies of cognition and emotion in unipolar depression found no aberrant brain activation in the depressed samples when compared with the controls. Fifty-seven studies comprising 99 individual experiments and 1,058 patients were included and 34 of the experiments measured cognitive processing and 65 measured emotional processing.
When the experiments were split into those investigating positive and negative emotion, and memory, there was no significant difference between experimental groups and controls, which provides evidence that the lack of a main finding was not attributable to camouflaged effects elsewhere at a more specific level, that is, there may not have been a difference in emotion studied in general but there may have been a difference for positive emotion (but not negative). Medication, co-morbidity and age did not alter this conclusion.
The researchers suggest that the reasons for the null result include small samples, choices of analysis software and statistical analysis, and heterogeneity in methods. ‘Our results,’ they conclude, ‘ may reflect that the current imaging literature on unipolar depression is so heterogeneous that no generalized effects can be found’ (p 7). Too few studies, they argue, are similar enough to make proper comparisons meaningful.
depressive disorders - treatments
The treatments available for depression are well established but their success is variable. The Sequenced Treatment Alternatives to Relieve Depression (STARD) study, for example, found that only a quarter of individuals improved after one treatment (Fried and Nesse, 2015). One reason for this might be that DSM guidance indicates that it is the number of symptoms which determines a diagnosis of illness, not the type of specific symptom. Given the heterogeneity of symptoms in depression – DSM lists nine, as you saw earlier – and the severity of these symptoms, it may not be surprising that not all treatments are effective for all individuals. According to Fried and Nesse (2015), for example, two individuals with MDD may not have a symptom in common (based on the current diagnostic system) and 227 symptom profiles are possible. In their review of 3,703 individuals in the STARD study, the most common symptom profile was found in only 2 per cent. Fourteen per cent showed a symptom profile not shared by any other person, suggesting a high degree of heterogeneity in the symptoms and diagnosis of the illness. There is evidence that a combination of treatments – psychotherapy and medication – can lead to more successful outcomes. A meta-analysis of studies combining these two approaches in depression and anxiety found that the combination led to a clinically meaningful improvement in people’s health, even two years after treatment (Cuijpers et al, 2014).
The two principal treatments for major depressive disorder are cognitive therapy and antidepressant medication
depressive disorders - treatment - CBT
Beck’s cognitive therapy begins by arguing that the negative beliefs held by depressed individuals are seen as conclusions based on faulty logic (Beck, 1967). A depressed person concludes that they are ‘deprived, frustrated, humiliated, rejected or punished’ (Beck et al, 1979, p. 120). Beck views the cognitions of the depressed individual in terms of a cognitive triad: a negative view of the self (‘I am worthless’), of the outside world (‘The world makes impossible demands on me’) and of the future (‘Things are never going to get better’).
Even when confronted with evidence that contradicts their negative beliefs, depressed individuals often find an illogical means of interpreting good news as bad news (Lewinsohn et al, 1980). For example, a student who receives an A grade in an exam might attribute the high grade to an easy, unchallenging exam rather than to their own mastery of the material. The fact that few others in the class received a high grade does little to convince the depressed person that they deserve congratulations for having done well. The depressed student goes on believing, against contrary evidence, that the good grade was not really deserved.
Once the faulty logic is recognised for what it is, therapy entails exploring means for correcting the distortions. The therapist does not accept the client’s conclusions and inferences at their face value. Instead, those conclusions resulting from faulty logic are discussed so that the client may understand them from another perspective, changing their behaviour as a result.
Meta-analyses suggest that CBT can be a very effective means of combating depression and may even be more effective than tricyclic antidepressants (see below) in the long term (Hensley et al, 2004). Recent advances in CBT and CBT-like treatments include the availability of online interventions, as you saw for anxiety. For example, van Ballegooijen et al (2014) note that guided online therapy is more successful than unguided therapy and that people adhere to face-to-face CBT better than guided therapy
depressive disoder treatment - diet
Some evidence that a change in diet is association with a reduction in depressive symptoms in a non-clinical sample (Firth et al, 2019), and with a reduction in clinical samples especially if the diet is a Mediterranean one (Parletta et al, 2019; Francis et al, 2019). While these studies suggest that a change in diet can be beneficial to health, there is no evidence that diet can prevent depression. Various mechanisms have been proposed for why this relationship exists, mostly based on animal studies, including a change in the pathways which lead to inflammation and oxidative stress, the gut microbiome and the hippo-pituitary axis amongst others (Marx et al, 2020).
depressive disorders - treatment - Brain stimulation
rTMS and tDCS have also been used as potential treatment interventions, but the mechanism is unknown and unclear (Cukic, 2020). fMRI studies suggest that aberrant connections between frontal and limbic regions reflect the pathology of depression.
antidepressant drugs
Antidepressant drugs are a class of drugs used to treat the symptoms of major depression. Antimanic drugs are used to treat the symptoms of bipolar disorder and mania. The earliest used antidepressant drugs were derived from the family of chemicals known as tricyclics, which refers to their ‘three-ring’ chemical structure (Lickey and Gordon, 1983).
Although the biology of depression is not well understood, the most widely accepted theory is that depression may result from a deficiency of the catecholamine neurotransmitters norepinephrine and serotonin. Each of these neurotransmitters may be involved in different types of depression, although researchers are not sure how. Antidepressant drugs seem to slow down the reuptake of these neurotransmitters by presynaptic axons. Although tricyclic antidepressants do not work for all people, about 60–80 per cent of those whose depression has brought despair to their lives gradually return to normal after having been placed on tricyclics for two to six weeks (Hughes and Pierattini, 1992). Unfortunately, tricyclics have many side effects, including dizziness, sweating, weight gain, constipation, increased heart rate, poor concentration and dry mouth.
Monoamine oxidase inhibitors
Another class of antidepressants, introduced in the late 1950s, is the monoamine oxidase inhibitors (MAOIs), which take one to three weeks to begin alleviating depression. MAOIs prevent enzymes in the synaptic gap from destroying dopamine, norepinephrine and serotonin that have been released by presynaptic neurons. These drugs can have many side effects, many of them fatal. The tyramine cheese reaction, for example, arises from the eating of foods containing tyramine such as some wines, milk products, coffee and chocolate. Because the monoamine oxidase does not oxidise tyramine, tyramine displaces epinephrine at epinephrine receptors. This produces severe hypertension and blurred vision, impotence, insomnia and nausea. It can also be fatal if leading to a haemorrhage. MAOIs also have been shown to be more effective in treating atypical depressions such as those involving hypersomnia (too much sleep) or mood swings (Hughes and Pierattini, 1992).
Serotonin-specific reuptake inhibitors
A relatively new class of drugs is serotonin-specific reuptake inhibitors (SSRIs), which, as their name suggests, block the reuptake of serotonin in nerve cells. As a result, the common feature of all SSRIs is that they enhance the transmission of serotonin. Perhaps the most common SSRI is fluoxetine (Prozac), first authorised for medical use in 1988. Fluoxetine inhibits the reuptake of serotonin, leaving more of that neurotransmitter in the synaptic cleft to stimulate post-synaptic receptors, and is the drug of first choice when tricyclic drug treatment has failed. SSRIs produce fewer negative side effects than do tricyclics and the MAOIs, although some individuals do experience headache, gastrointestinal discomfort, insomnia, tremor and sexual dysfunction. There is evidence, however, that antidepressants have no clinical advantage over placebo in minor depression (Barbui et al, 2011).
depressive disorders - other pharmacological treatments
Two developments in the psychopharmacology of depression have been second generation (atypical) depressants which block either norepinephrine reuptake or dopamine reuptake, and dual-action antidepressants which block certain serotonin receptors while inhibiting its reuptake. An example of the former, nefazodone, was released in 1995; an example of the latter, mirtazapine, was released in 1997. Neither type of drug has been authorised in all European countries and, because of their youth, little research is available evaluating their long-term efficacy.
The important factor in assessing the effect of antidepressant medication is the maintenance phase of the treatment. In the initial period of drug-taking, there is an acute phase in which the acute symptoms begin to stabilise. This period can last up to three months (Hirschfeld, 2001). The next period extends between the end of the acute period and the end of the depression itself, a period that can take up to 6–12 months. The danger is that if patients had stabilised in the acute phase, then they would have medication withdrawn. According to Hirschfeld (2001), however, around one-third to one-half of people who successfully stabilise in the acute phase, will relapse if medication is not sustained, hence the importance of monitoring behaviour closely during this period.
In a review of 21 antidepressants’ efficacy for treating major depression in adults, Cipriani et al (2018) found that all antidepressants were more effective than placebo. From 522 trials of 116, 477 participants, seven of the drugs were found to be more effective than the others: agomelatine, amitriptyline, escitalopram, mirtazipine, paroxetine, venlafaxine and vortioxetine. The least effective were fluoxetine, fluxovamine, reboxetine and trazodone. The most tolerable drugs (i.e. participants kept taking them and did not drop out) were agomelatine, citalopram, escitalopram, fluoxetine, sertraline, and vortioexetine. The highest drop-out rates were found for amitriptyline, clomipramine, duloxetine, fluvoxamine, reboxetine, trzodone and venlafaxine.
bipolar disorder
Bipolar disorder is characterised by alternating periods of depression and mania. Mania (the Greek word for madness) is characterised by wild, exuberant, unrealistic activity not precipitated by environmental events. During manic episodes, people are usually elated and self-confident; however, contradiction or interference tends to make them very angry. Their speech (and, presumably, their thought processes) becomes very rapid. They tend to flit from topic to topic and are full of grandiose plans, but their thoughts are not as disorganised as those of people with schizophrenia. Manic patients also tend to be restless and hyperactive, often pacing around ceaselessly. They often have delusions and hallucinations, typically of a nature that fits their exuberant mood. Impairments in ‘frontal lobe’ function such as set-shifting, verbal memory and sustained attention have been reported (Clark et al, 2002), and the experience of the disorder has been related to an oversensitive frontal cortex (Harmon-Jones et al, 2002).
Bipolar disorder (BD) is one of the most difficult disorders to diagnose because distinguishing it from major depressive disorder takes time and the depression episode might be wrongly misdiagnosed as depression because the manic period had not manifested itself. Baldessarini et al (2020) reviewed studies showing that diagnosis and treatment can be delayed by as much as 6–8 years for this reason and that 40 per cent of people who later develop BD were initially diagnosed as showing major depressive disorder (Shen et al, 2018). Seventy-five percent of the time spent ill was with depression according to a study by Forte et al (2015). They also note that people with BD are afraid of seeking help for their depression and may not realise that a change in libido, increases in mood and activity are actually reflections of their mania. They may even find these pleasurable.
Suicide in BD is much higher than the international average suicide rate: around 20 in every 100, 000 (Baldessarini et al, 2019a) and risk is higher in BD than in major depression, especially in the days after the patient has been discharged from hospital (Forte et al, 2019). The treatments for BD include drugs, such as antidepressants, anticonvulsants and lithium, ECT and psychological interventions. Lithium appears to be the best protection against suicide attempts although the data are not universally consistent (Baldessarini et al, 2020). Baldessarini et al cite ten, placebo-controlled studies, for example, that have found a five to sixfold reduction in suicide attempts by patients taking lithium and so this is the recommended drug treatment for BD patients at risk of suicide.
While the drug may have beneficial effects on suicide attempts, drug interventions are not highly effective in treating the depressive or manic components of the disorder and there are risks associated with proscribing antidepressant medication (McGirr et al, 2016), which is a common proscription given the dominance of the depressive aspect of the disorder.
bipolar disorder - lithium carbonate
Lithium carbonate is most effective in the treatment of bipolar disorders or simple mania (Young and Newham, 2006). People’s manic symptoms usually decrease as soon as their blood level of lithium reaches a sufficiently high level (Gerbino et al, 1978). In BD, once the manic phase is eliminated, the depressed phase does not return. People with BD have remained free of their symptoms for years as long as they have continued taking lithium carbonate. This drug can have some side effects, such as a fine tremor or excessive urine production; but in general, the benefits far outweigh the adverse symptoms. However, an overdose of lithium is toxic, which means that the person’s blood level of lithium must be monitored regularly. Psychotherapy has also been associated with some benefits, but this treatment is more successful for depression than mania (Scott, 2006).
The major difficulty with treating BD is that people with this disorder often miss their ‘high’. When medication is effective, the mania subsides along with the depression. But most people enjoy at least the initial phase of their manic periods, and some believe that they are more creative at that time. In addition, many of these people say that they resent having to depend on a chemical ‘crutch’. As a consequence, many people suffering from BD stop taking their medication. Not taking their medication endangers the lives of these people because the risk of death by suicide is particularly high during the depressive phase of bipolar disorder.
brain impairments in adults
The causes of neurocognitive disorders are often much
more specific than is the case for many of the disorders we
have discussed elsewhere in this text. In DSM-5, the disor-
ders that used to be known as “Delirium, Dementia, and
Amnestic andOtherCognitive Disorders”are nowgrouped
into a new diagnostic category called “Neurocognitive Disorders.” This term is more straightforward than its pre-
decessor. It is also more conceptually coherent. Disorders
in this category are those that involve a loss of previously
attained cognitive ability and where the presumed cause is
brain damage or disease. Subsections of this diagnostic cat-
egory include delirium, major neurocognitive disorder
(which includes the former diagnosis of dementia), and a
new category of mild neurocognitive disorder. The dis-
tinction between major and mild neurocognitive disorder
is based on severity. As the Thinking Critically about DSM-5
box illustrates, the inclusion of a mild neurocognitive dis-
order in DSM-5 raises some important issues.
Within each broad diagnostic category, the specific
diagnosis is determined by what is thought to be the cause
of the problem. For example, the diagnosis of major neuro-
cognitive disorder associated with Alzheimer’s disease is
used for patients thought to have Alzheimer’s. For patients
whose brain damage is caused by a traumatic brain injury
the diagnosis would be major (or mild) neurocognitive dis-
order associated with traumatic brain injury. In this way
the diagnosis provides information about both the cause of
the neurocognitive disorder as well as its degree of severity.
clinical signs of brain damage
With a few exceptions, cell bodies and neural pathways in
the brain do not appear to have the power of regeneration,
which means that their destruction is permanent. When
brain injury occurs in an older child or adult, there is a loss
in established functioning. Often, the person who has sus-
tained this loss is painfully aware of what he or she is no longer able to do, adding a pronounced psychological
burden to the physical burden of having the lesion. In other
cases, the impairment may extend to the loss of capacity
for realistic self-appraisal (a condition called anosognosia),
leaving these patients relatively unaware of their losses
and hence poorly motivated for rehabilitation.
The degree of mental impairment is usually related to
the degree of damage to the brain. However, this is not
invariably so. Much depends on the nature and location of
the damage as well as the premorbid (predisorder) compe-
tence and personality of the individual. In some cases
involving relatively severe brain damage, mental change is
astonishingly slight. In other cases of seemingly mild and
limited damage, there may be quite marked alterations in
functioning,
diffuse vs focal damage
The disorders discussed in this section are characterized by
neurocognitive problems, although psychopathological
problems (such as psychosis or mood change) may also be
associated with them. Some of these disorders are gener-
ally well understood, with symptoms that have relatively
constant features in people whose brain injuries are compa-
rable in location and extent. For example, attention is often
impaired by mild to moderate diffuse—or widespread—
damage, such as might occur with moderate oxygen depri-
vation or the ingestion of toxic substances like mercury.
Such a person may complain of memory problems due to
an inability to sustain focused retrieval efforts, while his or
her ability to store new information remains intact.
In an illustration of this, LoSasso, Rapport, and Axelrod
(2001, 2002) foundthat nailsalon technicians reported signifi-
cantly more cognitive and neurological impairments than
controls did. The nail salon technicians also performed more
poorly than the controls on tests of attention andinformation
processing. This is likely due to routine exposure to (meth)
acrylates and a variety of organic solvents such as toluene,
acetone, and formaldehyde that are known to be potentially
damaging to the central nervous system. Such findings
highlight the consequences of even low-level exposure to neurotoxic substances that can be found in places where
many people work and where many others routinely visit.
In contrast to diffuse damage, focal brain lesions
involve circumscribed areas of abnormal change in brain
structure. This is the kind of damage that might occur
with a sharply defined traumatic injury or an interruption
of blood supply (a stroke) to a specific part of the brain.
Figure 14.1 explains how a stroke occurs.
The location and extent of the damage determine what
problems the patient will have.As you are aware, the brain
is highly specialized. Although the two hemispheres are
closely interrelated, they are involved in somewhat differ-
ent types of mental processing. At the risk of oversimplify-
ing, it is generally accepted that functions that are
dependent on serial processing of familiar information,
such as language and solving mathematical equations,
take place mostly in the left hemisphere for nearly every-
one. Conversely, the right hemisphere appears to be gener-
ally specialized for grasping overall meanings in novel situations; reasoning on a nonverbal, intuitive level; and
appreciating spatial relations. Even within hemispheres,
the various lobes and regions mediate specialized func-
tions (see Figure 14.2).
Although none of these relationships between brain
location and behavior can be considered universally true, it
is possible to make broad generalizations about the likely
effects of damage to particular parts of the brain. Damage
to the frontal areas, for example, is associated with one of
two contrasting clinical pictures: (1) being unmotivated
and passive and with limited thoughts and ideas or (2) fea-
turing impulsiveness and distractibility. Damage to specific
areas of the right parietal lobe may produce impairment of
visual-motor coordination, and damage to the left parietal
area may impair certain aspects of language function,
including reading and writing, as well as arithmetical abili-
ties. Damage to certain structures within the temporal
lobes disrupts an early stage of memory storage. Extensive
bilateral temporal damage can produce a syndrome in
which remote memory remains relatively intact but noth-
ing new can be stored for later retrieval. Damage to other
structures within the temporal lobes is associated with dis-
turbances of eating, sexuality, and emotion. Occipital dam-
age produces a variety of visual impairments and visual association deficits, the nature of the deficit depending on
the particular site of the lesion. For example, a person may
be unable to recognize familiar faces. Unfortunately, many
types of brain disease are general and therefore diffuse in
their destructive effects, causing multiple and widespread
interruptions of the brain’s circuitry.
