Treasure, J., Claudino, A. M., & Zucker, N. (2010). Eating disorde.docx

Treasure, J., Claudino, A. M., & Zucker, N. (2010). Eating
disorders. The Lancet, 375(9714), 583-93. Retrieved from
http://search.proquest.com/docview/199059169?accountid=8731
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Eating disorders
Treasure, Janet; Claudino, Angélica M; Zucker, Nancy.The
Lancet375.9714 (Feb 13-Feb 19, 2010): 583-93.
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Abstract (summary)
TranslateAbstract
[...] binge eating disorder is often associated with obesity.
Investigators of a study of a large sample of American children
aged 9-14 years reported that 7.1% of boys and 13.4% of girls
displayed disordered eating behaviours.35 The pivotal effect on
health has led to the inclusion of eating disorders among the
priority mental illnesses for children and adolescents identified
by WHO.36 Eating disorders have been reported worldwide both
in developed regions and emerging economies such as Brazil
and China.37,38 The lifetime prevalence of eating disorders in
adults is about 0.6% for anorexia nervosa, 1% for bulimia
nervosa, and 3% for binge eating disorder.19,20 Women are
more affected than are men, and the sex differences in lifetime
prevalence in adults could be less substantial than that quoted in
standard texts: 0.9% for anorexia nervosa, 1.5% for bulimia
nervosa, and 3.5% for binge eating disorder in women; and

0.3%, 0.5%, and 2.0%, respectively, in men.20 Many people
with eating disorders, who were detected in community studies
in the USA, do not seek treatment.20 Pathogenesis A
comprehensive review published in 2004 summarised the risk
factors for eating disorders,39 and a position paper from the
Academy of Eating Disorders outlined the evidence supporting
these diseases as biologically-based forms of severe mental
illnesses.40 In this section we draw attention to some present
areas of emphasis.
Full Text
TranslateFull text
Headnote
This Seminar adds to the previous Lancet Seminar about eating
disorders, published in 2003, with an emphasis on the biological
contributions to illness onset and maintenance. The diagnostic
criteria are in the process of review, and the probable four new
categories are: anorexia nervosa, bulimia nervosa, binge eating
disorder, and eating disorder not otherwise specified. These
categories will also be broader than they were previously, which
will affect the population prevalence; the present lifetime
prevalence of all eating disorders is about 5%. Eating disorders
can be associated with profound and protracted physical and
psychosocial morbidity. The causal factors underpinning eating
disorders have been clarified by understanding about the central
control of appetite. Cultural, social, and interpersonal elements
can trigger onset, and changes in neural networks can sustain
the illness. Overall, apart from studies reporting
pharmacological treatments for binge eating disorder, advances
in treatment for adults have been scarce, other than interest in
new forms of treatment delivery.
Introduction

This Seminar adds to the previous Lancet Seminar about eating
disorders, which was published in 2003.1 We provide a concise
review of eating disorders in young people, focusing on factors
of particular relevance to the clinician such as diagnosis,
epidemiology, pathogenesis, treatment, and prognosis. In this
Seminar we draw attention to biological factors that could
contribute to new interventions. Eating disorders also occur in
prepubertal children, but studies in this age group are scarce
and there is no consensus about either diagnosis or treatment.
Classification and diagnosis
Diagnosis is challenging because diagnostic symptoms and
associated behaviours substantially overlap across the range of
eating disorders. For example, extreme dietary restraint, binge
eating, and overvalued ideas about weight and shape can be
present in all forms of eating disorder. Additionally, the
subjective interpretation and justification behind diagnostic
behaviours is often not clear or is limited by developmental
constraints (as in childhood anorexia nervosa), further
complicating diagnosis.
In the diagnostic and statistical manual of mental disorders
fourth edition (DSM-IV),2 three broad categories are
delineated: anorexia nervosa, bulimia nervosa, and eating
disorder not otherwise specified. The international classification
of diseases tenth revision (ICD-10) has three categories:
anorexia nervosa, bulimia nervosa, and atypical eating
disorder.3 Briefly, anorexia nervosa is characterised by
extremely low bodyweight and a fear of its increase; bulimia
nervosa comprises repeated binge eating, followed by
behaviours to counteract it. The category of eating disorder not
otherwise specified encompasses variants of these disorders, but
with subthreshold symptoms (eg, menstruation still present
despite clinically significant weight loss, purging without

objective binging). The panel shows some key symptoms of
eating disorders in general (more detailed information about the
clinical features of each disorder is available in the previous
Seminar1). The weight criteria used for diagnosis need to be
adjusted for age,4 height, sex, and the developmental weight
trajectory of the individual.
More than 50% of cases in the community fall into the category
termed eating disorder not otherwise specified (or atypical).5
Proposals to reduce the specificity of some of the diagnostic
criteria in anorexia nervosa and bulimia nervosa have been
made, which would reduce the proportion of cases that fall
within the not-otherwisespecified category.6 Subgroups within
obesity with mental or behavioural components, such as binge
eating disorder and night eating syndrome, can be delineated.7
Binge eating disorder is a subcategory of eating disorder not
otherwise specified, and is defined as frequent binge eating
distinguished from bulimia nervosa by the absence of recurrent
inappropriate compensatory behaviours. Hence binge eating
disorder is often associated with obesity. Transition from severe
restriction into binge eating behaviour is common;8 however,
the reverse process (a shift from binge eating into restriction) is
less usual. The criteria for diagnosis of binge eating disorder in
DSM-IV appendix B include associated behavioural and
affective features,2 and these criteria have been extensively
used in research in the past 15 years. Support is growing for
recognition of binge eating disorder as a specific entity9 on the
basis of taxometric analyses,10 family aggregation studies,11
treatment response research,12 and studies of clinical course.13
Furthermore, interest is growing in a transdiagnostic approach
to eating disorders, both within14 and outside the category of
eating disorders, with proposals for links to the obsessive
compulsive and autistic spectrum of disorders15 and anxiety
and mood disorders.16,17 Several articles present the arguments

for diagnostic change in DSM-V.7,18
Psychiatric comorbidity
Comorbidity is the rule rather than the exception for patients
with eating disorders.19,20 Developmental dis orders (eg, those
of the autistic spectrum and attention-deficit hyper activity
disorder) have been reported to affect about a fifth of patients
with anorexia nervosa.21,22 Moreover, a small propor tion of
adults with attention-deficit hyperactivity disorder have
additional symptoms of eating disorders.23 Obsessive
compulsive traits24,25 or disorder,26 and anxiety
disorders27,28 and some borderline traits,25 have been reported
both before and after the onset of eating disorders, and are also
diagnosed in family members.29,30 Bulimia nervosa and binge
eating disorder are associated with affective disorders31,32 and
with alcohol33 or substance34 misuse.
Epidemiology
Eating disorders and related behaviours are common in young
people. Investigators of a study of a large sample of American
children aged 9-14 years reported that 7.1% of boys and 13.4%
of girls displayed disordered eating behaviours.35 The pivotal
effect on health has led to the inclusion of eating disorders
among the priority mental illnesses for children and adolescents
identified by WHO.36 Eating disorders have been reported
worldwide both in developed regions and emerging economies
such as Brazil and China.37,38 The lifetime prevalence of
eating disorders in adults is about 0.6% for anorexia nervosa,
1% for bulimia nervosa, and 3% for binge eating disorder.19,20
Women are more affected than are men, and the sex differences
in lifetime prevalence in adults could be less substantial than
that quoted in standard texts: 0.9% for anorexia nervosa, 1.5%
for bulimia nervosa, and 3.5% for binge eating disorder in
women; and 0.3%, 0.5%, and 2.0%, respectively, in men.20

Many people with eating disorders, who were detected in
community studies in the USA, do not seek treatment.20
Pathogenesis
A comprehensive review published in 2004 summarised the risk
factors for eating disorders,39 and a position paper from the
Academy of Eating Disorders outlined the evidence supporting
these diseases as biologically-based forms of severe mental
illnesses.40 In this section we draw attention to some present
areas of emphasis.
Genetic factors
The most potent risk factor is female gender. How much this
association can be attributed to biological rather than social
factors is uncertain. Sexual divergence is less pronounced in
binge eating disorder23 and in prepubertal anorexia nervosa.41
Twin and family studies suggest that anorexia nervosa, bulimia
nervosa, and binge eating disorder are complex genetic
diseases, and for each disorder the estimated heritability ranges
between 50% and 83%.11,42,43 Linkage studies have identified
loci for anorexia and bulimia nervosa and for associated
behavioural traits such as compulsivity.44-46 About a third of
genetic risk for eating disorders and depression,47 anxiety
disorders,48 and addictive disorders49 is shared. All the above
studies are limited because of low power; however,
international collaborations are working at pooling cases and
using newer forms of analysis such as genome-wide
associations.
Biological factors
Although many of the biological findings in eating disorders
can be best understood as results of starvation and disturbed
eating behaviours, some are causally linked as risk or

maintaining factors. The brain is particularly vulnerable to the
consequences of poor nutrition since it uses around 20% of the
caloric intake and is especially dependent on glucose.
Therefore, poor nutrition has a general effect on brain function
in addition to the specific effect on the appetite system. Most
eating disorders emerge during adolescence-a vulnerable period
of brain reorganisation-and malnutrition during this crucial
period can negatively affect illness trajectories.
Starvation shrinks the brain and is associated with many
behavioural and psychosocial disturbances such as rigidity,
emotional dysregulation, and social difficulties.50 Many
symptoms resolve with weight gain and when brain mass is
restored.51 Concentrations of brain-derived neurotrophic factor,
a regulator of brain plasticity, in blood are reduced in acute
anorexia nervosa,52 and genetic studies suggest a trait-related
disturbance in this system.53
The characterisation of the central control of appetite54,55
could improve our understanding of eating disorders. A
simplified heuristic is to consider three components. First is the
homoeostatic system that is centred mainly in the brain stem
and hypothalamus, which integrates peripheral metabolic
markers with information from the gastrointestinal tract to
affect subjective states of hunger, satiety, and autonomic
nervous activity. Second is the drive system, with distributed
neural circuitry within the mesolimbic cortex and striatum that
has afferent inputs from sense organs and neural structures that
are implicated in learning and memory. This system registers
the reward value associated with food and is involved in the
motivation to seek food and eat. Third is the selfregulation
system, within which a form of so-called topdown control
contextualises appetite within life goals, values, and meaning.
Abnormal changes in all three of these systems have a role in
the risk and maintenance of eating disorders. A hypothesis

suggests that these disorders could result from pervasive
deficits in self-regulatory systems.56 Furthermore, eating
disorder behaviours affect the drive system, as shown by models
of binge eating in laboratory rodents for which scientists have
replicated the conditions implicated in the increase of binge
eating-ie, food restriction, gastric drainage (an analogue of
vomiting), stress, and intermittent access to highly palatable
food- and produced animals with an addiction to food. The
investigators noted that not only did these animals binge eat,
but they also showed withdrawal effects. Moreover, they had a
propensity to relapse after a time, and crosstolerance to alcohol
and cocaine.57,58 Under pinning these behavioural changes are
alterations in the chemical transmitters (dopamine and opioids).
Finally, the response to changes in food intake of the putative
homoeostatic system could contribute-eg, anorexia nervosa is
often linked to premorbid and familial leanness,59 whereas the
reverse is the case for bulimia nervosa and binge eating
disorder.60
Brain monoamine function in eating disorders has been studied
in the acute state (which can be confounded by illness effects)
and after recovery with specific ligands and positron emission
tomography. These findings for anorexia nervosa have been
synthesised into an explanatory model.61 5HT2A receptors are
reduced and 5HT1A receptors are increased in both the acute
and recovered state, and dopamine receptors (DA2) within the
striatum are increased after recovery.62 Less research has been
done into binge eating disorders and bulimia nervosa, but
anomalies in the dopamine system could heighten food
reward.63
Abnormalities in both illness-related (food and body shape) and
non-illness-related information processing are detected in eating
disorders. An attentional bias is evident towards food and body
shape64 associated with increased activation in distributed
neural networks connected with self-regulation and hedonic

motivation.61,65 General problems include difficulties in
decision making,66 abnormal striatal activation by reward,67,68
reduced flexibility69 associated with decreased activation in the
striatum and associated areas,70 a bias towards focusing on
detail at the expense of seeing the general picture (weak central
coherence),71 problems in social cognition,72 and dysfunctional
emotional regulation.73 These functional anomalies can
maintain eating disorder behaviours. For example, an eye for
detail and inflexibility can allow an individual to understand the
laws of thermodynamics in relation to energy intake and
expenditure and succeed in weight loss, whereas impaired social
and emotional regulation could isolate the individual.
Environmental context
The environment shapes the developmental course of the
individual beginning at the time of conception. For example,
mothers of people who later develop an eating disorder might be
more exposed to stress during pregnancy.74 Birth-related
perinatal complications (eg, cephalohaematoma) and premature
delivery increase the risk of development of an eating
disorder.75 Epigenetic mechanisms or damage to the brain from
hypoxia can also mediate these effects.
In some developed countries, the excess value placed on
thinness encourages extreme dieting and weight control
practices. Negative comparisons between an individual's body
shape and that of the ideal contributes to poor self-esteem.76
Criticism, teasing, and bullying focused on food, weight, and
shape issues specifically increase the risk of developing an
eating disorder.77 The tension between the stigmatisation of
fatness, idealisation of thinness, and easy access to highly
palatable foods, perhaps eaten in secret, could lead to weight
control behaviours that can have a destabilising effect on the
biology of appetite control. In addition to food-related and
weight-related harmful experiences, general adversity (neglect

and physical and sexual abuse) also increases the risk of
developing an eating disorder.
Interactions between the environment and individual biology
The postpubertal years are a crucial time of vulnerability.
Developmental changes of puberty (the hormonal fluxes and
synaptic pruning and myelination within the brain), stressful
events, and challenges (eg, changes in social affiliation and
ranking) could trigger eating disorder behaviours. The
consequent nutritional deficits can induce factors that maintain
the illness. These factors have been grouped into four broad
domains: the medical effect on the body and brain, the
interpersonal effect, the exaggeration of avoidant coping, and
obsessive compulsive traits.78
Treatment
Medical complications
Although eating disorders can begin in adulthood, the highest
incidence is between 10 and 19 years of age,79 potentially
disrupting optimum growth and development. Most
pathophysiological complications are reversible with improved
nutritional status or remittance of abnormal eating and purging
behaviours. However, some physical consequences can be life-
threatening, such as electrolyte imbalances (eg, hypokalaemia)
due to excessive vomiting or laxative and diuretic misuse.
Additionally, nutritional deficiencies increase the risk of
cardiac arrhythmias and intercurrent infection. Comprehensive
reviews80,81 and the previous Seminar1 discuss the physical
abnormalities of eating disorders in great depth.
Many practice guidelines discuss how to measure and assess
medical risk.82-84 Children and adolescents have less
nutritional reserve than do adults, so their risk can rapidly

escalate. Body-mass index (BMI) is not a useful index of
nutritional compromise for men, children, tall and muscular
individuals, and those with water retention. Other comorbid
medical disorders also increase vulnerability and might need
regular monitoring, such as diabetes mellitus, which can
increase risk at any level of BMI. Apart from these caveats,
standard forms present a means of giving both personalised and
normative feedback on medical risk. (Examples include the
Maudsley BMI chart and the Risk Assessment in Eating
Disorders). Table 1 shows an abridged set of markers of
nutritional and cardiovascular decompensation that signal the
need for increased or urgent care. These markers should be
considered in the context of the complete clinical picture,
expertise of the treating team, and local availability of eating
disorder units. Signs of increased medical risk suggest the need
for immediate specialist consultation or inpatient treatment, or
both, especially in people with a recent, acute onset.
The deficits in anorexia nervosa gradually evolve and are
general rather than specific. Therefore they should be rectified
slowly, orally, and with food supplemented with multivitamin
and multimineral preparations. In the first phase (3-7 days), a
soft diet of about 5-10 kcal/kg per day with thiamine and
vitamin B co-strong in small portions throughout the day, and
foods with high phosphorus content (eg, milk-based products)
accords with guidelines from the UK National Institute for
Health and Clinical Excellence (NICE) describing refeeding of
severely undernourished patients, and reduces the risk of
refeeding syndrome.85 On special units with skilled nursing,
feeding by tube is rarely necessary. At moderate levels of risk
the aim is to produce a weight gain between 250 g and 450 g per
week in outpatients, and around 1 kg in those treated in
hospital.83
Some weight change strategies-such as vomiting or misuse of
diuretics, laxatives, or caffeinated and carbonated drinks-can

result in underhydration or overhydration and electrolyte
imbalance. Acute renal failure can occur in severe cases. Oral
replacement is usually the first line of management, but the full
clinical diagnosis and level of risk (table 1) decide the
appropriate setting and method of replacement. Persistent
hypokalaemia can be linked to low calcium and magnesium
(which also need rectification), or to sustained purging
behaviours. Proton-pump inhibitors to inhibit gastric acid
secretion reduce metabolic alkalosis and help to conserve
potassium.86 They can also prevent oesophageal and tooth
damage.
Long-term effects on physical health
Some medical consequences of eating disorders can be
irreversible or have later repercussions on health, especially
those affecting the skeleton, the reproductive system, and the
brain. Dental problems, growth retardation, and osteoporosis are
some of the long-term problems. Bone loss in lumbar spine,
radius, and proximal femur can be detected within a year of
illness and progresses to produce fractures, kyphoscoliosis, and
chronic pain. Weight gain alone improves bone density,
especially if it is sufficient to restore menses. Several
treatments have been investigated, including antiresorptive
agents, oestrogens, insulin growth factor, and calcium
supplementation, but none can be recommended on the basis of
present evidence.87
The fertility and maternity rate of women with anorexia nervosa
is reduced; a Swedish study88 suggested that the rate of fertility
was 70% of that in the general population. Infant birthweight is
lower in mothers with anorexia nervosa89 but higher in those
with bulimia nervosa.90 The miscarriage rate for women with
bulimia nervosa is higher than for healthy women-those with
bulimia nervosa were twice as likely to have two or more
miscarriages compared with the general population.89 Perinatal

problems can be increased,91 and feeding difficulties reducing
infant growth have been reported.92 Infertile and pregnant
women should be screened for eating disorders and offered
treatment to optimise the wellbeing of their offspring.82
Pathways of care
High levels of health-care use are common across all forms of
eating disorders.93 The management of bulimia nervosa and
binge eating disorder can be complicated by medical (eg,
diabetes and obesity) and psychiatric (eg, affective disorders
and addictions) comorbidity, but acute medical risk is less of a
problem than it is for anorexia nervosa, and care is typically
delivered on an outpatient basis in adult services.
NICE guidelines recommended that people with anorexia
nervosa should first be offered outpatient treatment82 and that
inpatient care be used for those who do not respond or who
present with high risk and little psychosocial resources.
Whether inpatient admissions should be short to alleviate acute
risk or prolonged to attain full weight restoration (thought to
reduce relapse) is controversial.94 Models of day treatment
provide an intermediate service model.95
Practice recommendations emphasise the importance of
specialised care for the treatment of eating disorders, but such
care is not often accessible. Hence, new forms of service
delivery (eg, e-mailing, text-messaging) with use of treatment
directed via mobile phones, the internet, or telemedicine (eg,
cognitive behavioural therapy [CBT] delivered by a therapist
via the internet) are being assessed.96-99 A systematic
review98 of self-help interventions (computerised or manual)
modelled after empirically validated approaches concluded that
with professional oversight (guided self-help) these
interventions could have benefit in bulimia nervosa and binge
eating disorder, although some uncertainty still

remains.98,100,101
Evidence-based treatments
Anorexia nervosa
The evidence base relating to the treatment of anorexia nervosa
is meagre.82 Two main factors contribute to difficulties in trials
of treatment for this disease: clinician- instigated protocol
withdrawal because of failure to stabilise risk, and patient
withdrawal and difficulties in recruitment because of poor
accept ability of treatments. Thus, treatment guidelines rely on
expert recom mendations. These recommendations emphasise
the importance of a multi disci plinary approach including
medical, nutritional, social, and psycho logical com ponents.82-
84 Psychotherapy can be delivered individually or with the
family. The involve ment of families in treatment depends on
several factors-eg, age of the patient, living arrangements, the
patient's level of risk and dependence, and the ethos of the
treatment team.
For adolescents with anorexia nervosa, family psychotherapy as
practised according to the Maudsley method is recommended
(table 2).102 6 months of treatment can be sufficient unless
there is obsessive compulsive comorbidity or non-intact
families.103 Families with extremes of overprotection or
criticism have better outcomes in separated family therapy
(child and parents seen separately) than in combined family
therapy.104 Parents are distressed and burdened by symptoms
and behaviours of eating disorders.105 These feelings can be
alleviated by group educational interventions.106
A Cochrane collaboration review (updated in 2008) concluded
that the evidence accumulated so far does not lend support to
any one particular psychotherapeutic method for adults with
anorexia nervosa, although support from a non-specialist

clinician might be less efficacious than might that from a
specialist delivering a specific form of psychotherapy.107
No strong evidence lends support to drug treatment either in the
acute or maintenance phases of the illness.108,109 A few
randomised controlled trials have been done since the last
Seminar. The previous expectation that fluoxetine could have a
role in prevention of relapse in anorexia nervosa110 weakened
after the negative findings from a large and thorough study.111
Interest has been renewed in the potential use of atypical
antipsychotic drugs to target dopaminergic dysregulation and
comorbid features of this disease.112 The idea is that by
reducing distorted cognitions and anxiety symptoms, resistance
to weight gain decreases. Initial, small randomised
studies113,114 report decreases in obsessive symptoms and an
increased rate of weight gain. Larger trials are necessary,
however, to substantiate these benefits and elucidate harms with
this drug, such as a potential increase of QTc interval with the
risk of cardiac arrhythmias.
Bulimia nervosa
The evidence base115 for the original CBT model of bulimia
nervosa116 and its use as the first-line treatment is strong.
Although CBT has good acceptability, binge remission rates
(cessation of binge eating or purging) at the end of treatments
are only 30-40%.117,118 An enhanced form of CBT with a
broader focus including interpersonal factors, emotional
tolerance, perfectionism, and self-esteem did not substantially
improve this outcome.119 Furthermore, combining
antidepressants (tricyclics or fluoxetine) with CBT did not
significantly add to the effect of CBT alone.117 Interpersonal
therapy is efficacious as a treatment alternative, although it
showed a slower response of symptom change than did CBT
(similar results to CBT only after 1 year of follow-up).115,117
Other models of treatment are being considered for use in

bulimia nervosa, such as those with a focus on emotional
regulation (eg, dialectical behaviour therapy).120
Two studies have assessed the role of family-based
psychotherapy for adolescent bulimia nervosa.121,122 One
suggested that guided CBT could have advantages compared
with family-based treatment in terms of cost and speed of
response,121 whereas the other suggested that family-based
treatment had advantages compared with individual supportive
therapy.122
A 2004 review of treatment for bulimia nervosa and binging
included seven trials in which participants with the form of
eating disorder not otherwise specified that was similar to
bulimia nervosa formed part of the sample.123 The conclusion
from this and from a recent trial119 is that CBT is as effective
for non-specified eating disorder similar to bulimia nervosa as
it is for bulimia nervosa itself.
Pharmacotherapy has been recommended in the treatment of
bulimia nervosa and binge eating disorder, especially if
psychotherapy is either unavailable or unacceptable.82,83
Evidence from pharmacological trials in bulimia nervosa is
strong, and it is increasing in studies of binge eating disorder,
but this finding mainly indicates efficacy in the acute stage
after short-term treatment. Overall, evidence for long-term
effects after medication is scarce. Additionally,
pharmacological agents have been mainly tested in adults, and
the results might not be generalised to adolescents and children.
Moreover, use of antidepressant drugs in children and young
people is controversial because of increased suicidal risk.124
Three systematic reviews detected strong evidence for the use
of antidepressants to treat bulimia nervosa in the short term
(around 8 weeks).115,117,125 However, the pooled effect from
one meta-analysis (with eight studies, 901 patients) was judged

only moderate for clinical improvement, which was defined as
the number of patients with 50% or more reduction of binge
eating (57% of patients receiving antidepressants vs 33%
receiving placebo), and remission rates with antidepressants
were usually less than 20% (similar to placebo).125 Overall
acceptability of antidepressant treatment is low (around 40%
dropout rates) when drugs are given alone.125 Fluoxetine is the
main drug tested in trials and approved for use in bulimia
nervosa by health regulatory agencies; it is recommended in a
dose (60 mg per day) that is higher than is usually necessary to
treat depression (20-40 mg per day).115 There is less evidence
of efficacy for other serotonin reuptake inhibitors (citalopram,
sertraline, fluvoxamine).117,126 Whether antidepressant
treatment can prevent relapse in bulimia nervosa is not yet
known, since the few trials that were done were limited by their
high attrition rates.115,117,127 Topiramate can be effective in
reduction of bulimic and purging symptoms, but the safety
profile of this drug still needs to be established in this
disease.117,128,129
Binge eating disorder
Psychological interventions that have shown efficacy in
treatment of bulimia nervosa have also been tested in binge
eating disorder with positive results, particularly modified CBT,
interpersonal therapy, and dialectical behaviour therapy.130
Large effect sizes in a metaanalysis have been reported for CBT
compared with a control for reduction of binge frequency and
for binge abstinence.100 An additional challenge in the
treatment of binge eating disorder is weight management, since
individuals are often classified as being overweight or obese. So
far, psychological interventions for this disorder have not
consistently shown clinically relevant weight losses.100
However, behavioural weight loss treatments have shown a
moderate reduction in weight and improvement in binge
abstinence.100 Binge abstinence is an important treatment goal

because it has been associated with increased weight loss in
both psychological and pharmacological trials.131,132 A few
studies with long-term follow-up suggest that abstinence from
bingeing could persist for 12 months132,133 and 24 months.134
Systematic reviews130 and meta-analyses100,135 of treatments
for binge eating disorder suggest that drug treatments show, at
least, a moderate effectiveness in reduction of binge frequencies
and promotion of binge remission in the short term, with a
remission rate of 48.7% reported with pharmacotherapy
(including antidepressants, anticonvulsants, and obesity drugs)
compared with 28.5% with placebo.135 Several guidelines
recommend short-term treatment with antidepressants (mainly
serotonin reuptake inhibitors) as an alternative first approach to
CBT. Although antidepressants are usually effective in reducing
binges,100,135 some studies have reported negative
findings,130,136 and their effect on depressive symptoms and
on weight is uncertain.135,137
Modest weight loss and binge remission have been reported
with drugs approved for use in obesity,135 such as
sibutramine138,139 and orlistat,140 and with drugs associated
with weight loss, such as topiramate,141 zonisamide, 142 and
atomoxetine.143 Sibutramine and topira mate have both been
tested in multicentre trials and showed binge remission rates
greater than with serotonin reuptake inhibitors compared with
placebo.138,139,144 Supple mentation of CBT or behavioural
weight loss treatments with the obesity drug orlistat145 or
topiramate144 might increase weight loss.146 Although these
drugs can be considered as part of the available regimen to treat
binge eating disorder, the short-term duration of trials (12-24
weeks), high dropout rate, and placebo-response rates restrict
the conclusions about their use.100,130 Additionally, the risk-
benefit balance is uncertain since intolerable adverse effects
have been reported with some drugs (eg, zonisamide,
topiramate).117,130,142

Prognosis
Recovery from anorexia nervosa becomes much less likely the
longer that the illness has persisted. This finding contrasts with
that of bulimia nervosa, for which the chance of recovery
becomes higher the longer the illness duration.147 A systematic
review148 has compiled data for all outcomes for eating
disorders and reported an increased mortality rate for anorexia
nervosa (the reported range is wide, varying with case mix and
length of follow-up) and persistent psychiatric problems in
many cases.
In anorexia nervosa, a young age at onset and short duration of
illness was associated with a good outcome, and somatic and
psychiatric comorbidity with a poor outcome.149 This disease
disrupts education150 and vocational functioning, which
contributes to difficulties in independent living in 20% of cases
up to 10-20 years after the onset of the illness.88 Less is known
about the effect of other eating disorders in this domain of life.
Little research has been done into the long-term outcome of
bulimia nervosa and binge eating disorder. Of a cohort of
patients with both these diseases admitted for hospital treatment
in Germany, a third had an eating disorder diagnosis 12 years
later; 36% of patients with binge eating disorder and 3.6% with
bulimia nervosa had a BMI greater than 30 kg/m^sup 2^.151
Conclusions
This Seminar has attempted to synthesise new developments in
eating disorders that have arisen since the previous Lancet
Seminar, and to integrate these developments into the
knowledge that is relevant for clinicians. The diagnostic criteria
for anorexia nervosa and bulimia nervosa are under
consideration and could be broadened in DSM-V, reducing the

size of the population in the category for eating disorders not
otherwise specified. Binge eating disorders will probably be
accepted as an additional form of eating disorder.
Eating disorders arise from an interaction between environ
mental events and the biological and developmental features of
the individual. Abnormal eating behaviours produce both
medical and psychosocial results. The psychosocial
consequences derive partly from the effects of starvation on the
brain and can perpetuate the illness. Several treatments and
their combinations have been tested for binge eating disorder,
with possible efficacy in the short term. New forms of treatment
delivery have also been tested for bulimia nervosa and binge
eating disorder with promising results. Progress has been made
in treatment of adolescent anorexia nervosa, although not for
the adult expression of this disorder.
Contributors
All authors contributed to the search and selection of the
literature and to the writing of the Seminar.
Conflicts of interest
JT has written several books on eating disorders for which she
receives royalties. AMC has received honoraria as speaker for
Meddley and Janssen-Cilag pharmaceutical industries, and has
participated in multicentre trials supported by Abbott and
Janssen-Cilag (without grants) between 2001 and 2007. NZ
declares that she has no conflicts of interest.
Acknowledgments
We thank the anonymous reviewers for their comments on early
drafts of this Seminar. JT was partly funded by a UK
Department of Health National Institute for Health Research

(NIHR) Programme Grant for Applied Research (reference
number RP-PG-0606-1043) and receives support from the NIHR
Specialist Biomedical Research Centre for Mental Health award
to the South London and Maudsley NHS Foundation Trust and
the Institute of Psychiatry, King's College London. The views
expressed herein are not necessarily those of the Department of
Health or NIHR. AMC was funded by CAPES (Coordenação de
Aperfeiçoamento de Pessoal de Nível Superior), Ministry of
Education, Brazil, with a post-doctoral grant at the Institute of
Psychiatry, King's College London, during 2008 (during the
writing and review process of this Seminar). NZ is partly
funded by the US National Institutes of Health (K23-MH-
070418).
Sidebar
Search strategy and selection criteria
We searched the Cochrane Library, Medline, and Embase up to
March, 2009. We used the search terms: "anorexia nervosa",
"bulimia nervosa", "binge eating disorder", and "eating
disorders" in combination with the terms "treatment", "biology",
"outcome", "epidemiology", "comorbidity", "personality",
"osteoporosis", "medical", "neuropsychology", "neuroimaging",
"psychotherapy", and "pharmacotherapy". We manually
searched the main eating disorder specialist journals and
reference lists of articles identified by this search strategy.
Several review articles or books are included because they
provide comprehensive overviews that are beyond the scope of
this Seminar. We largely selected publications in the past 6
years, but did not exclude commonly referenced and highly
regarded older publications, or more recent ones published
during the review process and that we considered of relevance
to the scope of the Seminar. Whenever possible we have cited
systematic reviews on a topic.

Panel: Common symptoms in eating disorders
Behaviours
Restrictive behaviour
* Cutting back on amount of food eaten
* Strict rules about eating (eg, time of day, specific
macronutrient content)
* Prolonged fasting (greater than 8 waking hours)
* Ritualised behaviour associated with the purchase,
preparation, and consumption of food
* Little variety in foods (eg, extreme vegan diets, avoidance of
fat, etc)
* Avoidance of social eating
* Secret eating
* Social competitiveness around eating
Binge eating
* Eating an amount of food in a discrete time that is considered
excessive in view of the situational context (objective)
* Eating an amount of food that is not excessive in view of the
context but is considered large by the individual because of
associated feelings of loss of control over eating (subjective)
Associated features of binge eating

* Eating more rapidly than normal
* Eating until uncomfortably full
* Eating large amounts when not hungry
* Eating alone because of embarrassment
* Feeling disgusted, depressed, or very guilty because of eating
Purgative behaviour
* Self-induced vomiting; spitting
* Misuse of laxatives, diuretics, diet pills, etc
Excessive exercise
* Intense, highly driven exercising of a compulsive nature
* The drive to exercise is associated with impaired social or
physical function, or both
Drinking
* Limited drinking (<0.5 L per day)
* Excess drinking (>1.5 L per day)
Body checking
* Repeated weighing
* Pinching or measuring the size of body parts (eg,
circumference of wrist)

* Repeatedly checking the protrusion of specific bones
* Checking that specific clothes fit
* Mirror gazing
* Comparison with others' bodies
Body avoidance
* Avoidance of behaviours above (eg, refusal to weigh,
avoidance of mirrors, wearing bulky clothes)
Psychopathology
Body image disturbance
* Weight and shape concerns (eg, preoccupation with weight,
shape, or both)
* Overvaluation of shape and weight in determination of self-
worth
* Minimisation or denial of symptom severity
* Disturbance in the way body is experienced
* Intense fear of weight gain, even though underweight
Physical symptoms
* Weight loss or failure of growth with associated features of
starvation-eg, amenorrhoea
* Absence of at least three consecutive menstrual cycles
(women)

* Reduced libido
* Reduction in waking erections (men)
* Reduced beard growth in men
* Sensitivity to cold
* Weakness, fatigue, etc
This panel outlines the most common symptoms of eating
disorder. A range of symptoms caused by starvation are also
present in anorexia nervosa, which are not all detailed here. All
these symptoms are not usually volunteered by the patient and
often have to be gently elicited or are noted by informants.
Article 2
Endocrinología y Nutrición (English Edition)
March 2015, Vol.62(3):111–
113, doi:10.1016/j.endoen.2015.01.002
Editorial
Current perspective of eating disorders ☆
Panorama actual de los trastornos de la conducta alimentaria
Josefina Castro-Fornieles
Show more
Eating disorders (EDs) are a group of conditions associated with
highly persistent changes in feeding-related behavior which

cause severe physical and psychological and functioning
consequences. The most common EDs include anorexia nervosa
(AN), bulimia nervosa (BN), and binge eating disorder, which
usually start in adolescence or early adulthood. The most recent
classifications of mental disorders, such as the DSM-5,1 include
within EDs other disorders more typical of childhood such as
avoidant/restrictive food intake disorder. AN is defined as self-
imposed weight loss associated with an exaggerated evaluation
of self weight or body figure; its severity is established based
on the body mass index. BN consists of the occurrence of
regular and frequent binge episodes associated with behavior to
compensate for the potential weight increase such as vomiting
or the use of laxatives. Changes related to the overvaluation of
figure and weight also occur. Binge eating disorder is
characterized, like BN, by regular binge episodes, but patients
have no compensatory behaviors and therefore eventually have
overweight and obesity. They also show no changes related to
body image. Avoidant/restrictive food intake disorder, usually
occurring at younger ages, consists of a decreased intake for
different causes, usually psychological, which leads to a weight
loss that may be extreme, but there is no impaired body image
or fear of weight increase. The grouping of EDs in a different
way, including those with no overvaluation of weight and
figure, is a conceptual change that implies that this is not a
necessary symptom, and this has led to a protracted discussion
among experts.2 All these EDs are disorders that deserve to be
given greater attention due to their high prevalence, and also
because in many cases they are not adequately and timely
diagnosed. In the general population, the approximate lifetime
prevalence rates of AN, BN, and binge eating disorder in
women are 1%, 2%, 3.5%, respectively.3 The numbers for each
disorder may vary depending on the use of more or less strict
diagnostic criteria.4Obesity is not included among the
psychiatric disorders because it is considered that genetic,
physiological, behavioral, and environmental factors that may
vary between the individuals who suffer from it contribute to its

etiology. There is however a significant association between
obesity and some mental disorders such as binge eating
disorder. EDs involve a significant interference with social,
work, family, and personal functioning, and also markedly
affect quality of life. On the other hand, their endocrine,
biochemical, bone, cerebral, and cardiological complications,
amongst others, are very marked, and may eventually be severe.
The high mortality, especially in AN, is also relevant. Women
with AN have a 5.2-fold greater chance of premature death from
any cause, and an 18.1-fold greater chance of dying from
suicide than women aged 15–34 years in the general
population.5
As regards the etiology of these disorders, several social,
cultural, psychological, and genetic factors are considered to be
involved.6 In developed countries, social and cultural pressure
to be thin and have an ideal body cannot be underestimated,
because this increases the number of subjects who place
themselves at risk by going on diets and changing their behavior
in other ways in order to lose weight. Psychological aspects
such as low self-esteem, high perfectionism in the case of AN,
or impulsiveness in BN may also be relevant. Adverse
experiences such as school, family, or social abuse in childhood
and adolescence, either physical, emotional, or sexual, increase
vulnerability to different psychiatric disorders, including EDs.
Neurobiology and the different hormones regulating hunger and
body weight are also altered.7 For instance, there are reports of
structural and functional abnormalities in cerebral
neuroimaging, serotonergic and dopaminergic changes in
cerebrospinal fluid, or the dysregulation of hormones such as
leptin or ghrelin, among many others,8 which may vary
depending on the specific ED. These changes may be reversed
in most cases, especially in adolescents, if treated early. By
contrast, while the disorder lasts, such changes may be involved
in its maintenance and especially in the long-term physical
consequences.

On the other hand, there is a high heritability rate in EDs
affecting aspects such as the body mass index and regarding the
rapid development of an ED after some trigger such as going on
a diet or suffering a stressful life event. Epidemiological studies
suggest a greater risk of AN in first degree relatives of patients,
and heritability is up to 80% according to some twin studies.
However, genetic studies have not been able to find definitive
and reproducible results,9 and its genetic base appears to be
related to different biological and psychopathological variables.
Thus, an association has been found with specific genes which
are relevant in weight regulation, and also with other genes
related to different neurotransmission mechanisms such as
dopaminergic and serotonergic pathways, which may influence
symptoms such as mood, impulsiveness, addictive behavior,
binge eating, or perfectionism.10 and11 It therefore appears that
the answer with regard to ED etiology is an interaction of
genetically determined individual characteristics and
environmental pressures that lead to risk behaviors such as diet
or vomiting. Epigenetic changes in DNA structure not coded in
its sequence, but implying durable changes in genetic
expression and which may be transmitted to future generations
also appear to be relevant. This may occur, for example, after
periods with a severe lack of food (during wars or droughts) or
at times of significant stress.12
As regards treatment, it should preferably be conducted,
whenever possible, on an outpatient basis or in a day hospital,
in order to interfere as little as possible with the general
functioning of patients, many of whom are adolescents. Hospital
admission should be reserved for cases where medical or
psychological risk exists or which have not responded to less
intensive treatment. A joint approach by different professionals
taking into account the nutritional, medical, and psychological
aspects is required.13Nutritional recovery and management and
correction of any biological changes are indispensable. The

most successful psychological approach in controlled studies
has been cognitive-behavioral therapy; in adolescents, a family
approach should be added. Drug treatment may be helpful
administered concomitantly with the psychological approach,
but evidence of its efficacy is variable depending on the
ED.14Results in AN are not encouraging, although selective
serotonin reuptake inhibitors may help improve the symptoms of
depression, perfectionism, or irritability. They do not help in
recovering weight, but may contribute to prevent recurrence.
Studies with antipsychotics have not been able to demonstrate
their efficacy, although they appear to be helpful in cases
refractory to treatment and clear thinking and behavior
disturbances. In BN, selective serotonin reuptake inhibitors and
some antiepileptics such as topiramate have been shown to be
effective in different controlled studies. In binge eating
disorder, in addition to the drugs mentioned for BN, other drugs
such as orlistat, which helps to reduce weight in these patients,
have also been used. Long-term follow-up is required to
maintain improvement and prevent recurrence. The prognosis of
these disorders is often not good: some ED chronically persists
in approximately 20% of cases, and 30% continue to have some
symptoms despite improvement. In patients receiving early
treatment during adolescence, the prognosis appears to be
better.15
To sum up, EDs are common disorders if the different diagnoses
they encompass are considered, and may be associated with
severe complications. Mutually interacting biological and
psychological factors appear to be involved in their etiology.
The early diagnosis of EDs is important to increase the chances
of improvement with treatment, which should necessarily
address the different symptoms, as much the physical as the
psychiatric and psychological.
Conflicts of interest

Article 1 of neurocongnitive disorders
DSM-5 and Neurocognitive Disorders
Joseph R. Simpson, MD, PhD
+Author Affiliations
Dr. Simpson is Staff Psychiatrist, Los Angeles County Jail
Mental Health Services, and Clinical Associate Professor,
Department of Psychiatry and Behavioral Sciences, University
of Southern California Keck School of Medicine, Los Angeles,
CA.Address correspondence to: Joseph R. Simpson, MD,
PhD, P.O. Box 818, Hermosa Beach, CA 90254. E-
mail: [email protected]
Next Section
Abstract
The newest edition of the Diagnostic and Statistical Manual of
Mental Disorders (DSM-5) introduces several changes in the
diagnostic criteria for dementia and other cognitive disorders.
Some of these changes may prove helpful for clinical and
forensic practitioners, particularly when evaluating less severe
cognitive impairments. The most substantial change is that the
cognitive disorder-not otherwise specified category found in
prior editions has been eliminated. Those disorders that do not
cause sufficient impairment to qualify for a diagnosis of
dementia are now defined as neurocognitive disorders and
placed on a spectrum with the more severe conditions. The
concept of social cognition is also introduced as one of the core
functional domains that can be affected by a neurocognitive
disorder. This concept may be particularly significant in the
evaluation of patients with non-Alzheimer's dementias, such as
frontotemporal dementia. With the aging of the population and

the increasing recognition of the possibility of long-lasting
cognitive deficits after traumatic brain injury, the need for
assessment of cognitive disorders in medicolegal contexts is
certain to increase. Forensic psychiatrists who perform these
evaluations should understand the conceptualization of
Neurocognitive Disorders as presented in DSM-5 and how it
differs from prior diagnostic systems.
The importance of dementia in the field of forensic psychiatry
cannot be exaggerated. It affects numerous core areas of civil
and criminal forensic practice, such as testamentary capacity,
capacity to consent to medical treatment, competence to stand
trial, and criminal responsibility, to name but a few. For many
practicing forensic psychiatrists and psychologists, diagnosing
dementia, determining its severity, and reaching a conclusion
about its effect on the medicolegal capacity in question is a
regular component of their work. As the average age of the
population continues to increase in most industrialized
countries, the demand for mental health professionals who have
the expertise in dementia to address medicolegal concerns is
certain to grow.
In addition to dementia, another type of acquired cognitive
disorder, cognitive impairment after brain injury, is also
becoming more and more relevant in the forensic arena. The
population of people who have sustained brain trauma at some
point in their lives is increasing. Part of the increase is related
to 21st century military conflicts, where tactics such as placing
improvised explosive devices under passing vehicles have
produced a higher proportion of brain injuries than in previous
wars. In addition, the survival rate for both military and civilian
brain trauma has increased relative to earlier eras when medical
technologies were less advanced.1,–,3
Neurologists, neuropsychologists, and psychiatrists have also
begun to examine the potential cumulative effects on cognition

of less drastic but repeated brain injuries. Persistent cognitive
impairment resulting from repeated concussions (i.e., mild
traumatic brain injuries) has been linked to chronic traumatic
encephalopathy (CTE), a neuropathological finding associated
with a dementing condition long known in boxers (dementia
pugilistica) and now thought to have affected some professional
athletes.4
Previous SectionNext Section
Changes Introduced by DSM-5
The Diagnostic and Statistical Manual of Mental Disorder, Fifth
Edition (DSM-5),5 contains revisions of the diagnostic criteria
and nomenclature for dementia and other cognitive disorders.
The name of the diagnostic category has been changed; the
section entitled delirium, dementia and amnestic and other
cognitive disorders in the fourth edition and subsequent text
revision (DSM-IV6 and DSM-IV-TR7) is now “neurocognitive
disorders,” or NCDs. The dementias, if the clinician prefers, can
still be referred to by their traditional names (e.g., Alzheimer's
dementia, vascular dementia, dementia due to Huntington's
disease). All the diagnostic entities found in the prior section
are subsumed under the new NCD rubric, and therefore
cognitive impairments that are not severe enough to qualify for
a diagnosis of dementia are now also defined as belonging to
the category of NCDs. They are no longer referred to by the
descriptor not otherwise specified (NOS) found in DSM-IV.
Under the previous classification system, cognitive impairments
not meeting the criteria for dementia were labeled cognitive
disorder NOS, or perhaps age-related cognitive decline. The
non-DSM term mild cognitive impairment (MCI) has also been
in widespread use in the elderly population, despite its limited
clinical value. Patients identified as having MCI are known to
progress to dementia at a higher rate than age-matched patients

without MCI, but there are currently no therapeutic
interventions to delay or prevent progression, nor are there any
reliable predictors of which patients with MCI will develop
dementia.8
In the new system, cognitive impairments that do not reach the
threshold for a diagnosis of dementia are termed mild NCDs,
whereas the dementias constitute nearly all of the major NCDs.
The diagnostic criteria for mild NCD include:
Evidence of modest cognitive decline from a previous level of
performance in one or more cognitive domains (complex
attention, executive function, learning and memory, language,
perceptual motor, or social cognition) based on:
Concern of the individual, a knowledgeable informant, or the
clinician that there has been a mild decline in cognitive
function; and
A modest impairment in cognitive performance, preferably
documented by standardized neuropsychological testing or, in
its absence, another quantified clinical assessment.
The cognitive deficits do not interfere with capacity for
independence in everyday activities (i.e., complex instrumental
activities of daily living such as paying bills or managing
medications are preserved, but greater effort, compensatory
strategies, or accommodation may be required [Ref. 5, p 605].
The concept of a continuum between mild and major NCDs is
explicitly noted. “Major and mild NCDs exist on a spectrum of
cognitive and functional impairment” (Ref. 5, p 607). “The
distinction between major and mild NCD is inherently arbitrary,
and the disorders exist along a continuum. Precise thresholds
are therefore difficult to determine” (Ref. 5, p 608).

The use of standardized neuropsychological testing is
specifically discussed in the context of distinguishing between
major and mild NCDs. Evidence of impairment on standardized
testing is Criterion A2 for both types of NCDs (substantial for
major, modest for minor NCD), although other quantified
clinical assessments can be used when standardized testing is
not practical. It is noted that standardized testing is particularly
important when evaluating patients with suspected mild NCD,
and suggested cutoffs are provided: “For major NCD,
performance is typically 2 or more standard deviations below
appropriate norms (3rd percentile or below). For mild NCD,
performance typically lies in the 1–2 standard deviation range
(between the 3rd and 16th percentiles)” (Ref. 5, p 607).
The mild-major continuum will undoubtedly take some getting
used to. Under the new schema, any cause of dementia can also
produce mild NCD. Thus, both major and mild NCD due to
Alzheimer's disease are diagnosable conditions. Clinicians may
find it awkward to apply the Alzheimer's label to patients who
do not meet criteria for dementia, as Alzheimer's has heretofore
been essentially synonymous with senile dementia. This type of
usage may be less confusing for mild NCD due to, for example,
Parkinson's or Huntington's disease, in which other symptoms
are often much more prominent than the cognitive impairments,
particularly early in the course of illness.
Potentially adding to the confusion, the term mild has been
retained as a specifier of severity for the major NCDs, along
with moderate and severe. So, for example, in DSM-5 we find
this sentence: “Apathy is common in mild and mild major NCD”
(Ref. 5, p. 607). It seems unwieldy that the same adjective,
mild, can be used either in reference to an NCD not severe
enough to qualify as a dementia or when describing the severity
of a particular clinical case of dementia (i.e., a major NCD). In
other words, a patient can have mild NCD (not a dementia),

mild major NCD, moderate major NCD, or severe major NCD
(these latter three are all dementias). In theory, a patient might
even progress through each of these stages over time. Granted,
the mild major usage is not much different from the use of the
mild specifier in major depressive disorder, but it seems to risk
confusion among providers as well as consumers and their
family members nonetheless.
Etiology of Neurocognitive Disorders
A further potential source of confusion or ambiguity of the NCD
conceptualization is that for several of the most common
dementia syndromes, the clinician is expected to qualify the
diagnosis with the descriptor probable or possible. This is the
case for those NCDs that lack a gold standard premortem
diagnostic test: specifically, Alzheimer's disease,
frontotemporal lobar degeneration (Pick's disease in DSM-IV
and DSM-IV-TR), Lewy body disease, vascular disease, and
Parkinson's disease. In cases of NCD due to traumatic brain
injury (TBI), HIV infection, prion disease, or Huntington's
disease, the probable and possible specifiers are not required, as
the causative factor can be definitively identified during life.
There is no disputing the causative nature of TBI in some cases
of major NCD. Although there is no close correlation between
the severity of the TBI and the resultant cognitive impairment,
the probability of developing a major NCD is undoubtedly
greater with moderate and severe TBI than it is with mild TBI.
On the other hand, the most common cause of mild NCD, and
also the most likely to lead to eventual civil litigation in such
cases, is TBI.
Head injuries are extremely common in society. Even though
most of them either produce no brain injury at all or cause only
transient impairment, the sheer number of events means that
NCD due to TBI is far from rare. DSM-5 cites 1.7 million TBIs

annually in the United States, with “1.4 million emergency
department visits, 275,000 hospitalizations, and 52,000 deaths”
(Ref. 5, p. 625). These numbers were taken from the U.S.
Centers for Disease Control and Prevention's 2010
publication9 on TBI in the United States, which includes a
wealth of information on the demographics of TBI victims and
the causes of TBI.
In DSM-5, not all brain injuries can be considered potentially
causative of NCD. The diagnostic criteria for NCD due to TBI
require that the TBI be associated with at least one of four
features: loss of consciousness, posttraumatic amnesia,
disorientation and confusion, or neurological signs, such as
neuroimaging findings, seizures, visual field cuts, anosmia, or
hemiparesis (Ref. 5, p 624). Furthermore, the NCD must have
its onset either immediately after the TBI or after recovery of
consciousness and must persist past the acute postinjury period.
Thus, trauma that produced no cognitive or neurological
changes at the time of the incident cannot produce an NCD
under this scheme.
Diagnostic Criteria for Neurocognitive Disorders
There have also been some significant changes in the diagnostic
criteria for the various NCDs. The criteria for delirium have
been reworded to some degree, but overall, they are fairly
similar to the previous criteria. One notable difference is the
addition of attenuated delirium syndrome, an example of the
diagnosis, other specified delirium. In this syndrome, “the
severity of cognitive impairment falls short of that required for
the diagnosis” (Ref. 5, p 602) or only some of the criteria for
delirium are met.
In DSM-5, the amnestic disorders, whose appearance in the title
of the section in previous editions implied a certain importance,
have all but disappeared. In fact the only reference to these

disorders is on the introduction page, which states:[T]he major
NCD definition is somewhat broader than the termdementia, in
that individuals with substantial decline in a single domain can
receive this diagnosis, most notably the DSM-IV category of
“Amnestic Disorder,” which would now be diagnosed as major
NCD due to another medical condition and for which the
term dementia would not be used [Ref. 5, p 591].
The diagnostic criteria for the major NCD category is where the
substantial differences from the criteria for dementia in DSM-
IV are found. In the new system, memory impairment is no
longer a requirement in the diagnosis of a major NCD.
Impairment in only one cognitive domain is enough to qualify
for a diagnosis of a major NCD, except in the case of major
NCD due to Alzheimer's disease, where two domains are still
required, one of which must be memory impairment. This
change may be useful, given the growing recognition that a
significant percentage of people with NCDs, particularly those
with conditions such as frontotemporal dementia, have a
relatively intact memory, at least until later in the course of the
illness.
New descriptions of the cognitive domains affected by NCDs
are also introduced in DMS-5. In DSM-IV, the cognitive
disturbances that could be seen in dementia (in addition to
memory impairment) were all indeed cognitive: aphasia,
apraxia, agnosia, and impaired executive functioning. DSM-5
includes these concepts in somewhat reworded form, and adds
the domain of social cognition. Table 1 of the chapter (Ref. 5,
pp 593–5) summarizes the six cognitive domains (complex
attention, executive function, learning and memory, language,
perceptual motor, and social cognition) and lists examples of
signs and symptoms and possible methods of assessment.

Implications for Forensic Psychiatry
What effects might the new conceptualization of neurocognitive
disorders have on the practice of forensic psychiatry? One
potential change for the better is that the severe, disabling
cognitive disorders (the dementias) may more clearly be viewed
as lying on a continuum with the less severe disorders that do
not reach the threshold for a diagnosis of dementia. Separating
the universe of cognitive disorders into dementia and cognitive
disorder NOS ran the risk of obscuring commonalities between
the two. Cognitive disorder NOS, like all NOS diagnoses, also
could carry the implication that the professional making the
diagnosis in reality does not know very much about what is
going on with the patient. From a medicolegal perspective, the
new classification system may prove useful in emphasizing that
mild NCDs differ from major NCDs only in degree, not in kind.
For patients with neurodegenerative diseases, meeting criteria
for only mild NCD will in most cases unfortunately be nothing
more than a transitional state on the inexorable path to a major
NCD. However, in the case of cognitive disorders due to static
insult(s), most commonly TBI, but possibly other events, such
as stroke, anoxia due to cardiac arrest, acute toxic exposure, or
medication overdose, the new diagnostic entity may have
significant clinical and forensic implications. For example, the
criteria for NCD due to TBI specified in DSM-5 could help
researchers establish a more scientific ground for conditions
that have been in some ways controversial, such as
postconcussional syndrome and the aforementioned CTE,
neither of which is mentioned in DSM-5.4,10,11
From a medicolegal perspective, a diagnosis of mild NCD
sounds more definitive and thus may carry more weight in the
courtroom than the former cognitive disorder NOS. Only time
will tell how widespread the use of the mild NCD diagnostic
category in the courtroom will become and how persuasive

testimony about the impact of mild NCD on the legal issue at
hand will be.
The recognition that some patients with dementia have
relatively intact memory is likely to be important in both civil
and criminal forensic matters. Previously, normal-range memory
performance on neuropsychological tests in a subject thought to
have dementia might lead the evaluator to instead lean toward a
diagnosis of mood disorder or personality disorder. Under the
new criteria, a diagnosis of dementia can be made without overt
memory impairment (except in cases of Alzheimer's), with
potential implications for the forensic opinion on many legal
questions, such as undue influence, competence to stand trial,
and criminal responsibility. It can be anticipated that patients
whose dementia manifests in impaired judgment and executive
function, but whose memory is intact, will now be identified
more easily, and the impact of their impaired condition on their
legal capacities will be better appreciated, with the requirement
for formal memory deficits removed.
In addition to the inclusion of social cognition as one of the six
domains potentially impaired by an NCD, forensic practitioners
will be encouraged to note that legal involvement is specifically
mentioned as one of the potential sequelae of frontotemporal
NCD (Ref. 5, p 617). Behavioral and personality changes,
including criminal acts and violations of social norms, are not
uncommon in frontotemporal dementia (FTD). For example, a
recent article in The Journal described several examples of
aberrant and criminal behavior in a series of subjects who were
subsequently found to have FTD. These included repetitive
shoplifting despite the ability to pay, attempted child
molestation, and hit-and-run.12 The relatively early age at onset
and often, preserved memory and other abilities in FTD can
make these types of cases challenging to explain to family
members, victims, and courts as being due to organic disease
rather than willful bad behavior. The new language concerning

this diagnosis may help in explaining FTD and its effects to
those involved.
For legal questions such as negligence, malpractice, personal
injury, or workers' compensation, where the presence of a
diagnosable impairment (and its causation) is the primary focus,
a forensic expert applying DSM-5 to diagnose mild NCD should
be straightforwardly helpful to the finder of fact. A diagnosis of
mild NCD is likely to be more difficult to discount in a legal
context than the more nebulous cognitive disorder NOS. On the
other side of the coin, applying DSM-5 criteria for NCD due to
TBI could prevent those who lack sufficient symptoms (e.g.,
who do not demonstrate impairments on objective testing),
whose initial injury did not have any of the required clinical
features necessary to produce an NCD, or whose symptoms
developed after an interval of documented normal function,
from successfully claiming that their current difficulties are the
result of the alleged brain trauma.
The factors become more complicated when the question is the
impact of mild NCD on other functional or legal capabilities.
Can mild NCD render someone incompetent or incapacitated?
Would someone with mild NCD be more susceptible to undue
influence? By definition, mild NCD does not interfere with
capacity for independence in everyday activities, but does this
lack of interference extend to drawing up a will or to refusing a
life-saving medical procedure?
One could envision an attorney making the argument that
Criterion B for mild NCD (“the cognitive deficits do not
interfere with capacity for independence in everyday activities
… such as paying bills or managing medications …”) (Ref. 5, p
605) extends to the cognitive capacities at issue: for example,
testamentary capacity. After all, if the testator is still
cognitively capable of paying his bills, how could he at the
same time lack knowledge of his assets (or heirs and other

aspects of his finances)?
A similar case could be made for competence to stand trial.
Given the functional independence (by definition) of a
defendant with mild NCD, it might be challenging to establish
that the diagnosis prevents him from having “sufficient present
ability to consult with his lawyer with a reasonable degree of
rational understanding” or a “rational as well as factual
understanding of the proceedings against him,” the standard for
competence to stand trial prescribed by the U.S. Supreme Court
inDusky v. United States.13 (A complex case involving, for
example, sophisticated financial crimes, might be an exception,
where mild NCD could be sufficient to render the defendant
incompetent.)
Conclusion
With the aging of the population, and the aftermath of 12 years
of combat for U.S. military personnel, a clear understanding of
the spectrum of cognitive disorders and of their diagnosis and
management has never been more important for health care
professionals. Forensic experts will undoubtedly encounter
more and more cases involving traumatic brain injury and
neurodegenerative disease in the years ahead.
The conceptualization in DSM-5 of mild neurocognitive
disorder, and the elimination of the diagnosis of cognitive
disorder, not otherwise specified, may be helpful to the forensic
practitioner tasked with examining a person who is in the early
stages of a dementing illness, or who has experienced a
traumatic brain injury, and may help in the explanation of his
condition and impairments to a finder of fact. Other potential
benefits of the new system include the removal of the
requirement of memory loss for a diagnosis of dementia, and the

introduction of social cognition as a specified functional
domain. However, the actual effect of these changes on fact
finders who hear expert testimony in civil and criminal matters
is not yet known, and it will undoubtedly take some time before
the implications of the changes in DMS-5 that affect the
forensic evaluation of neurocognitive disorders are fully
appreciated.
Footnotes
Disclosures of financial or other potential conflicts of interest:
None.
© 2014 American Academy of Psychiatry and
Cite ......
J Am Acad Psychiatry Law 42:2:159-164 (June 2014)
Copyright © 2015 by the American Academy of Psychiatry and
the Law.
Article 2
Defining Neurocognitive Disorders
McDonald, William M, MD. The American Journal of Geriatric
Psychiatry19.11 (Nov 2011): 909-14.
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Researchers are questioning the boundary between normal
cognition and subtle problems that are a prelude to dementia. In
the 1980s, "normal cognitive decline" had several pseudonyms
including age-associated memory impairment, age-consistent
memory impairment, and late-life forgetfulness. The difficulty
was that normal cognitive decline was poorly defined and the
diagnoses of clinically significant age-related memory loss
lacked reliability when applied clinically.1 Many potential
cognitive problems were dismissed as "within expectations for
âge" or "senior moments."
Recently the understanding of what is "normal" cognition in the
elderly individuals has been refined. The syndrome of mild
cognitive impairment (MCI) was first described 20 years ago
and considerable data supports the validity of MCI. MCI is of
interest because subtypes of MCI have been shown to be
predictive of the later development of Alzheimer disease (AD)
and other dementing illnesses.2 In fact, the probability of
conversion from MCI to dementia is estimated to be
approximately 15%.3 Estimates of the prevalence of MCI are
approximately 5% to as high as 29%3 and climbing with the
aging of the population.
MCl is defined as cognitive decline greater than expected for an
individual's age and educational level that does not interfere
notably with activities of daily life.4 The definition of MCI has
been further characterized by Petersen5 and the classification
proposed by an international working group on MCI. This

workgroup defined four subgroups: amnestic MCI single
cognitive domain, multiple cognitive domains (memory plus one
or more nonmemory domains), single nonamnestic (one
nonmemory domain), and nonamnestic/multiple cognitive
domains (more than one nonmemory domain).6 This
classification system has been adopted by the National Institute
of Health Alzheimer's Disease Research Centers (ADRCs) and
provides a common definition for research and clinical care.
Amnestic and nonamnestic MCI subgroups have distinct
etiologies and paths of cognitive decline. Recently the
diagnostic categories of MCI have been expanded to include
both neuropsychiatrie features as well as performance on
complex functional activities. These changes in the
classification of MCI are intended to incorporate data that
supports the subtle changes in complex activities of daily living
that often are the first signs of MCI.7 Complex activities or
instrumental activities of daily living include financial
management, housework, using a telephone, using public
transportation, and shopping for groceries. Neuropsychiatrie
syndromes (apathy, depression, anxiety, irritabüity) have also
been shown to be common feature of MCI8 and are associated
with an increased likelihood of developing AD.9
In this issue of the Journal, Goldberg et al.10 describe an
efficient, sensitive screening tool for testing the functional
capacity of older adults using a performance-based scale that
distinguishes adults with normal cognitive/functional capacity
from adults with MCI and AD. Physicians who specialize in
geriatrics typically screen for cognitive impairments using the
Mini-Mental State Examination11 or the Montreal Cognitive
Assessment.12 Unfortunately these tests are not sensitive to
assessing difficulties in performing complex functional tasks.
Testing functional capacity during an office visit can be
challenging and dependent on self-report from the caregiver and
patient, which are often unreliable.

The study by Goldberg et al. validates a short form of the
University of California, San Diego, Performance-Based Skills
Assessment (UPSA).13 Performance-based tasks require the
patient to execute everyday living skills to assess their abilities
compared to a normative control group. The longer version of
the UPSA is a valid measure of functional status in MCI.14
There are several advantages to the brief version of the UPSA.
The brief version assesses instrumental activities of daily living
in several domains but does not require the types of props used
in the longer version (i.e., materials to assess performance on
household tasks) and can be completed in an office visit with
minimal patient fatigue.
The investigators found the UPSA short form detects functional
impairment in patients with MCI and AD in about 10 to 15
minutes. The UPSA short form could therefore be used to screen
for functional impairments in older patients who do not show
memory problems on the Mini-Mental State Examination,
Montreal Cognitive Assessment, or other office based screens
but perhaps have subjective complaints or concerns raised by
family members. This type of early screening is important
clinically and in developing community-based research studies.
Once identified as screening positive for MCI, the challenge is
to determine the appropriate treatment based on long-term
outcome and identified risk factors. Up to 40% of patients
meeting MCI criteria are diagnosed with normal cognitive
function on longitudinal follow-up and a significant minority
will have stable cognitive function without progression to
dementia.15'16 The conversion rates from MCI to AD are highly
variable and there is a need to further refine the criteria and
evaluate the longitudinal followup of subjects diagnosed with
MCI.5 The diagnostic accuracy of subgroups of MCI will
depend on longitudinal studies that demonstrate that MCI
clinical criteria are associated with a pathological state and

progression of cognitive and functional problems. This has
practical implications including what physicians should tell
their patients when the patient meets criteria for a diagnosis of
MCI.
Four papers in the Journal describe very different approaches to
further refining the subgroups of MCI related to outcomes. In a
comprehensive latent class analysis of 1,655 subjects enrolled
in 29 National Institutes of Health AD Centers, Hanfelt et al.17
define seven empirically based subgroups of MCI based on
memory and functional and neuropsychiatrie features: three are
primarily cognitive (either memory problems alone, memory
problems with other affected cognitive domains, or a
nonamnestic subtype), three demonstrate prominent functional
and neuropsychiatrie disturbances (two of these subgroups had
prominent cognitive deficits and the third showed relatively
normal cognitive performance), and one subgroup was described
with minimal impairment. This study reaffirmed that MCI is a
heterogeneous syndrome and defines subtypes of MCI according
to a common etiology.
Hanfelt et al. found that patients with cardiovascular disease
(CVD) were more likely to be in two of the subgroups with
prominent functional deficits and neuropsychiatrie symptoms.
The investigators hypothesize that CVD is related to
neuropsychiatrie symptoms based on previous research that
CVD is associated with deficits in neuropsychiatrie syndromes
including depression and apathy. Further they hypothesized that
the patients in these CVD subgroups would be more likely to
progress to a vascular dementia.
Identifying subtypes of MCI with risk factors for specific
dementias is important in establishing the trajectory for patients
diagnosed early in the dementing process who could benefit
from specific interventions. Recently a consensus conference
organized by the American Heart Association/ American Stroke

Association acknowledged the importance of vascular risk
factors in cognitive impairment and dementia. The members of
this conference recognized the importance of public health
initiatives to target treatment of patients with CVD to decrease
the conversion rate from MCI to AD.18-19
The data from these 29 Alzheimer disease research centers is
particularly important to future research in this area. These
centers are part of the National Alzheimer Disease Coordinating
(ADC) Center in Seattle, Washington, which is a National
Institute on Aging (NIA)-funded center that facilitates
collaborative research among NIA-funded ADCs that
contributed patient data to this study. Nationally funded centers
such as the ADC are crucial to this research and can organize
the resources to follow these patients longitudinally.
A different approach to identifying at-risk patients was
employed by Duff et al.,20 who investigated a
neuropsychological probe to determine vulnerability to later
dementia. These investigators took advantage of the fact that
demented patients benefit less from practice effects (i.e.,
subjects improve when taking a test for the second time) than
matched normal controls. In this prospective study, the
investigators found that amnestic MCI patients who do not show
benefit over 1 week from practice effects were significantly
worse on measures of immediate memory, delayed memory,
language, and overall cognition when they were retested a year
later.
The investigators state that identifying a subgroup of amnestic
MCI patients with a more malignant course could help
clinicians focus resources on this subgroup and also help
researchers studying MCI enrich patient samples with the
subgroup of patients who are more likely to dement. If
replicated in a larger sample, this type of testing would be a
costeffective, practical, and efficient means for clinicians and

researchers to further categorize patients with amnestic MCI.
Yeh et al.21 explore MCI in patients in remission from late-life
depression capitalizing on the fact that mood disorders in late-
life are associated with both cognitive impairment and a higher
rate of conversion to a dementing syndrome.22 As the
investigators note, depression in elders is often accompanied by
deficits in all major cognitive domains, including memory,
executive function, and informationprocessing speed. And,
although many of the cognitive problems clear with the
successful treatment of the mood disorder, often there are
residual deficits.23
The investigators evaluated consecutive outpatients at a
geriatric center in a university teaching hospital who were older
than 59 years, had no evidence of dementia or significant
functional problems in ADLs, and met criteria for major
depressive episode currently in remission. They replicated
earlier studies of cognitive impairment in remitted patients with
late-life depression finding that more than half of the patients in
this study met criteria for MCI (52.3%): 28.5% with amnestic
MCI and 23.8% with nonamnestic MCI. The amnestic MCI
patients had a later age of onset and increased ventricular
atrophy on magnetic resonance scans; whereas, the nonamnestic
MCI group had a significantly higher stroke risk. Late-life
depression, ventricular atrophy, and amnestic MCI are all
associated with AD and the investigators hypothesize that the
amnestic MCI group is the subgroup with the highest risk of
converting to AD. In comparison, the nonamnestic MCI group
had a higher stroke risk and would be more likely to develop a
vascular depression.
This finding is similar to the finding by Hanfelt et al. that CVD
was associated with deficits in functional and neuropsychiatrie
domains and not associated with primary cognitive or amnestic
forms of MCI. Also, similar to Hanfelt et al., these investigators

hypothesize that the patients meeting nonamnestic MCI criteria
will be more likely to develop a vascular form of dementia.
Long-term follow-up of the subjects in Leh et al. will provide
valuable data in determining which of these subjects dement and
the nature of their dementing illness. As Leh et al. point out,
understanding the consequences of the residual cognitive
problems in older patients in remission from a major depression
will guide treatment interventions.
Duara et al.24 move the bar even closer to normal cognition in
defining a group of subjects with preMCI. The criteria for pre-
MCI are symptomatic cognitive and subtle functional
impairment by history, without cognitive deficits confirmed on
formal neuropsychological testing. The investigators find that
more than 90% of patients meeting criteria for preMCI showed
neuropathology consistent with AD at autopsy and these
patients have a conversion rate between normal controls and
patients with MCI.25
In a very ambitious study, the investigators compare the
longitudinal course of 275 subjects with preMCI, no cognitive
impairment (NCI), nonamnestic MCI, amnestic MCI, or mild
dementia over 2-3 years of follow-up and evaluated on clinical,
imaging, and neuropsychological characteristics. At baseline,
the pre-MCI subjects can be distinguished from NCI subjects
with subtle impairments on language and executive function
diagnosed by an experienced clinician interviewing the patient.
These deficits were not apparent on neuropsychological testing
but the patients did show higher apathy scores as well as
smaller left hippocampal volumes. In support of pre-MCI as a
harbinger for dementia, 28.6% of the pre-MCI subjects
progressed to a formal diagnosis of MCI or dementia compared
to 4.1% of corrvmunity-dwelling elders. Compared to MCI
patients, there were significantly fewer pre-MCI patients who
progressed to dementia over the 2-3 year follow-up. Pre-MCI
was therefore on the border of normal cognition and MCI.

In further support of the pre-MCI classification, the latent class
analysis by Hanfelt et al.17 also identified one of the seven
subgroups, which they termed "minimally impaired" and this
group met some of the criteria for pre-MCI. They defined the
munimally impaired subgroup as individuals who "exhibited
preserved cognitive functioning across all domains according to
the ... neuropsychological test battery and yet, the clinicians
making a consensus diagnosis agreed that these individuals
should not be characterized as such" based on a review of all
available clinical information.
The primary purpose in subtyping MCI patients and identifying
them in the prodromal period of their illness is to provide
therapies that can affect the course of the illness by treating the
neurodegenerative process. To date, there are no FDA-approved
medications to treat MCI.26 Nonpharmacological interventions
(e.g., physical activity and cognitive exercise) have shown some
promise but need further clinical trials.27
In this context, James et al. explore an interesting hypothesis
that the extent of movement covered during daily functioning is
associated with more rapid cognitive decline in older adults and
increased risk of incident MCI and AD. The investigators found
that cognitive decline and the development of MCI and AD
increased in patients followed over 4 years who had restricted
life space movements (e.g., a person who had not been to an
area beyond their home environment in the previous week was
more likely to develop MCI than a person who traveled out of
town).
Although the investigators could not exclude a restricted life
space as an early sign of impending dementia, they
hypothesized that patients who travel have more "environmental
complexity," which has been theorized to protect against
cognitive impairments in later Ufe. If this is true, then exposing

MCI patients to more complex challenges may be therapeutic.
Conversely, restricting their environment (e.g., moving them
into an institutional setting) to provide support may increase
their cognitive and functional decline. If this study is
replicated, this research could have implications for the
recommendations to families caring for loved ones who are
showing early signs of dementia.
Clearly MCI is a heterogeneous disorder with some MCI
patients developing dementia while others remain stable or
improve over time. The early identification of which MCI
patients will progress to AD or other dementia syndromes has
important clinical implications and may help public health
interventions target specific populations at risk.
Further support for the importance of MCI as a clinical
syndrome is the inclusion of "minor Neurocognitive Disorders
(NCDs)" in the proposed criteria from the NCD Work Group of
the American Psychiatric Association's Diagnostic and
Statistical Manual of Mental Disorders Task Force.28 The
minor NCDs are distinguished from the major NCDs including
AD and Lewy Body disease. The definition of minor NCDs is
inclusive of both MCI and pre-MCI as described earlier and
encompasses both mild impairments in younger individuals and
impairments that may be transient, static, and reversible.
Updated criteria on the work done by the NCD Work Group is
available at www.dsm5.org.
Future research is needed to define clinical biomarkers, genetic
screens and link clinical syndromes with the later development
of dementia.29'30 An increased likelihood of developing
dementia is associated with apolipoprotein E4 allele carrier
status,31 MRI volumetric measurements of the hippocampus,32
cerebral hypometabolism on fluorodeoxyglucose positron
emission tomography in areas known to affected in AD,33
elevated t /aß ratios in the cerebrospinal fluid,34 elevated

fibrillary amyloid levels in the neocortex on positron emission
tomography scans,35 and abnormal activation patterns on
functional MRI.36 These potential biomarkers should be applied
to evaluate the risk of MCI patients developing dementia.
The importance of identifying the earliest symptoms of
cognitive impairment and the subgroups of patients who will
progress to dementing illnesses has become increasingly
important in developing effective therapies.37 The most
effective strategies will be novel treatments that intervene early
in the neurodegenerative cascade leading to cell death and
obvious clinical symptoms.38 The difficulty with therapeutic
strategies such as the Cholinesterase inhibitors is that these
medications treat the result of the neurodegenerative process
rather than addressing the etiology. Clearly the most effective
approach will be to target interventions in the prodromal period
to the specific neurodegenerative process.
Defining "normal" memory is becoming increasingly important
as the field understands the trajectory for individuals who fall
off the expected age-associated memory loss and effective
treatments are developed to interrupt the neurodegenerative
process and improve outcomes. Until then, the next time you
walk into a room and cannot remember why you went there you
should be consoled by the words of the immortal Yogi Berra
who said, "If you don't know where you are going, you will
wind up somewhere else," The articles in this month's Journal
are evidence that we do know where we are going.
References
References
1. Smith G, Ivnik RJ,
Cite.....

McDonald, W. M., M.D. (2011). Defining neurocognitive
disorders. The American Journal of Geriatric
Psychiatry, 19(11), 909-14. Retrieved from
4
Article 3
Major and Mild Neurocognitive Disorder
Anonymous. Psychiatric News48.10 (May 17, 2013): 12.
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DSM-5 SELF-EXAM
The diagnosis of dementia is subsumed under the newly named
entity major neurocognitive disorder (NCD), although the term
dementia is not precluded from use in the etiologic subtypes
where that term is standard. Further, DSM-5 now recognizes a
less severe level of cognitive impairment, mild NCD, which can
also be a focus of care.
Mild NCD is a new disorder that permits the diagnosis of less
disabling syndromes that may nonetheless be the focus of
concern and treatment. While the threshold between minor and
major is inherently arbitrary, there are important reasons to
consider these two levels of impairment separately. The major
NCD syndrome provides consistency with the rest of medicine
and with prior editions of this manual and necessarily remains

distinct to capture the care needs for this group. While the mild
NCD syndrome is new to DSM-5, its presence is consistent with
its use in other fields of medicine, where it is a significant
focus of care and research, notably on Alzheimer's disease,
cerebrovascular disorders, HIV, and traumatic brain injury.
These questions are from DSM-5 Self-Exam Questions: Test
Questions for the Diagnostic Criteria, which may be preordered
at http://www.appi.org/ Sea rchCenter/Pages/Search Detail.
aspx?ltemld= 62467 from American Psychiatric Publishing. The
answers and rationales are posted at http://www.
psychnews.org/pdfs/DSM-5_Self_ Examination_QandA_5.pdf.
The questions were developed under the leadership of Philip
Muskin, M.D., a professor of clinical psychiatry at Columbia
University College of Physicians and Surgeons. The book,
available in August, contains 500 questions for all the
categories of psychiatric disorders and includes Section III.
1. In DSM-IV, the severity threshold criterion for the diagnosis
of dementia was "cognitive decline sufficient to interfere with
social and occupational functioning." What replaced this
criterion in DSM-5 in the diagnosis of major neurocognitive
disorder?
a) impairment in occupational functioning
b) impairment in social functioning
c) impairment in completing selfcare activities
d) impairment in objective measures of cognitive function
e) both impairment on objective measures of cognitive function
and impairment in independent completion of daily activities as
an effect of this cognitive impairment.

2. In DSM-5, on what criterion does the distinction between
mild neurocognitive disorder and major neurocognitive disorder
depend?
a) whether or not the individual is concerned about a decline in
cognitive function
b) the presence of impairment on cognitive testing
c) whether or not the cognitive impairment is sufficient to
interfere with independent completion of activities of daily
living
d) co-occurrence with delirium
e) co-occurrence with another Axis I psychiatric disorder.
3. Expressed as a percentile score, what is the severity of
cognitive impairment on objective testing (relative to
appropriate norms) required to support a diagnosis of major
neurocognitive disorder?
a) below the 60th percentile
b) below the 50th percentile
c) below the 25th percentile
d) below the 16th percentile
e) below the 3rd percentile.
Copyright American Psychiatric Publishing, Inc. May 17, 2013
Cite....

Major and mild neurocognitive disorder. (2013). Psychiatric
News, 48(10), 12. Retrieved from
14
EDITORIAL
Emotion in Eating Disorders
Janet Treasure*
Section of Eating Disorders, Division of Psychological
Medicine, Institute of Psychiatry, King’s College, London, SE5
8AF, UK
*Correspondence
Janet Treasure, PhD FRCP FRCPysch, Section of Eating
Disorders, Division of Psychological Medicine, Institute of
Psychiatry, King’s College, London, SE5 8AF, UK.
Email: [email protected]
Published online in Wiley Online Library
(wileyonlinelibrary.com) DOI: 10.1002/erv.2211
In contrast to the interest that has been shown in understanding
and treatment of the behaviours, physical consequences and
thoughts, emotions have been somewhat neglected. Perhaps, this
neglect mirrors the emotional avoidance and attachment
difficulties
that are characteristic of people with eating disorders and that
can distort introspection and self-report. Figure 1 is a schematic
representation of the emotional brain based on Panksepp’s
model

(Panksepp, 2011) of three interacting processes. The primary
process lies within the evolutionary oldest parts of the brain and
represents the affective consciousness from sensory,
homeostatic
and emotional inputs. The secondary process involves learning
and memory that contribute to emotional habits. Finally, there is
the tertiary process of cognitive control. How does what we
know
about eating disorder fit within this model? I selectively look at
the literature in order to set the scene for the papers in this
edition
that follow.
Eating disorders may result from abnormal functioning in each
of
these three processes. First, there appears to be enhanced
sensitivity to
punishment in the primary process whereas the response to
reward
is attenuated in anorexia nervosa and exaggerated in bulimic
disor-
ders (Harrison, Treasure, & Smillie, 2011). Anxiety,
internalising
traits and threat sensitivity can emerge before the onset of the
eating disorder (Adambegan et al., 2012) in particular social
anxiety
(Swinbourne et al., 2012). These traits are also seen in family
members (Lilenfeld et al., 1998), which suggest that they may
in part
be genetically or epigenetically determined. Anomalies in the
secondary process may arise from particular experiences that
account for how and why negative emotional reactions to food
weight and social stimuli are learned (Treasure, Cardi and Kan,
2012; Treasure, Corfield, & Cardi, 2012). Many eating disorder
behaviours represent cognitive control of the tertiary system.
Functional differences in the dorsal cognitive system (dorsal

caudate,
hippocampus, parietal dorsolateral prefrontal and anterior
cingulate)
are present in both the ill and recovered state in anorexia
nervosa
(Wagner et al., 2007; Zastrow et al., 2009). These are associated
with
altered dopamine and serotonin function (Bailer & Kaye, 2011).
In this edition, anomalies between the top down control and the
experiential bottom level in eating disorders are described.
Emotional inhibition suggestive of high levels of control are
reported in anorexia nervosa (Claes et al., 2012; Davies, Swan,
Schmidt, & Tchanturia, 2011; Espeset, Gulliksen, Nordbo,
Skarderud, & Holte, 2012; Joos et al., 2012), whereas in binge
eating disorder, top down control is reduced (Danner, Evers,
Stok, van Elburg, & de Ridder, 2012). At the experiential level,
cues relating to food and shape are associated with increased
activation in limbic and cortical areas in people with eating
disor-
ders, whereas activation to more standard emotional cues is
similar to what is found in healthy controls. Eating disorder
behaviours are linked with emotional experiences. Unlike
healthy
controls, fasting improved mood in people with bulimia
nervosa (Moreno-Dominguez, Rodriguez-Ruiz, Fernandez-
Santaella,
Ortega-Roldan, & Cepeda-Benito, 2012). In a subclinical group,
decreased emotional expression mediated the relationship
between
an invalidating early environment and eating disorder symptoms
(Haslam, Arcelus, Farrow, & Meyer, 2012). Treatments focused
on
improving emotional regulation can produce change (Abbate-
Daga

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