Sleep, eating, and sexual dysfunction

SLEEP DISORDERS

Normal sleep

 Awake (eyes open)  alert, active mental concentration (waves = highest frequency, lowest
amplitude); awake (eyes closed   waves)
 2 states of sleep
o Non-REM (NREM)
 NREM sleep divided into: N1, N2, N3
 N1 (5%) – light sleep ( waves)
 N2 (45%) – deeper sleep, when bruxism occurs (sleep spindles and K cpx)
 N3 (25%) – deepest NREM sleep (slow wave sleep;  waves = lowest frequency,
highest amplitude); HR and BP fall; linked w circadian-endocrine system
activation
 Sleepwalking, night terrors, and bedwetting occur
 BZDs reduce N3 and REM sleep  therefore good for night terrors and
sleepwalk.
o REM (25%; q90mins, with duration lasting longer through night)
 Loss of motor tone, increased O2 use, increase HR and BP (increased ACh)
Extraocular movements due to PPRF activation.
 Dreaming, nightmares, and penile/clitoral tumescence occur
 May serve memory processing function.
 Depression: increases total REM sleep but decreases REM latency
 EtOH, BZDs, and NA reduces REM sleep (“good quality sleep”)
o These alternate cyclically (60 -90 mins), interrupted by arousals (normal to wake up),
regulated by circadian rhythm (biological rhythm that is approximately but not 24 h;
endogenously generated even in absence of environment factors)
 Driven by SCN of hypothalamus (SCN required for entrainment to light)
 Circadian rhythm controls nocturnal release of ACTH, prolactin, melatonin, and
NA.
 Absence of light (retina)/environment (non-phobic zeitgeber e.g. exercise,
meals)  intergeniculate leaflet of ventral part of LGN of thalamus  SCN 
NA release  pineal gland  melatonin
 Light inhibits melatonin release form pineal gland (so peak at night).
 Melatonin is absent at birth (post-natal rapid increase, peaks 1-3y, then
falls in puberty, stabilises, falls in elderly)
o Sleep-wake cycle: sleep pressure modulated by adenosine which is accumulated in
forebrain the longer we stay awake. While the Circadian drive opposes it (for
wakefulness).
 Duration of sleep
o Neonates – up to 16 h, 50% REM sleep: reduced to 25% quickly
o Child – stable sleep pattern w excess deep sleep (N3) around 10 h
o Teens – sleep clock drifts later; longer duration of sleep = 8.5 – 9.5 h
o Adults – 7 to 8 h sleep; sleep onset advances (earlier) again
o Older adults – depth of slow wave sleep and total REM sleep decline = more
morningness; sleep more fragmented; compounded by daytime naps + more time in bed
+ lack of light exposure + health issues.
 Sleep, eating, and sexual dysfunction

 EEG – often with chin EMG to demonstrate loss of muscle tone at most stable muscle in REM
sleep.

Assessment

 Hx
o Description + impact (e.g. on emotion, cognition, somatic)
o Onset and development (can be childhood; morning/evening; FHx)
o Enquire about SHIFT WORK including early/late starts
o Physical + psychological factors disturbing sleep
o Meds (for sleep, psych disorders, and other medical disorders)
o Sleeping arrangements
o 24 h sleep/wake schedule including weekends
 Sleep questionnaires
 Actigraphy (confirms that you are actually sleeping for 2 weeks before MSLT)
 Polysomonography + EEG ($$$)
 Video-telemetry/polysom
 MSLT (multiple sleep latency test)/MWT (measure of wakefulness test)
o MSLT: objective measure of propensity to sleep 4 chances to sleep – 10am, 2pm, 4pm,
6pm)
 Indications: evaluate narcolepsy or hypersomnia
 MSL (mean sleep latency = time to fall asleep) of 8 min  definitely abnormal
(can be seen in shift workers and chronic sleep deprivation).
 If shift worker = requires sleep saturation 2 weeks before taking test
 12 – 30 mins  ? if significant
 If narcolepsy = 2X more sleep + naps at least to Dx
 MLS < 8 mins + > 2 SOREMPs = sleep-onset REM periods
o MWT: measure to stay awake in sleep-inducing environment
 Indicated in determining if previous Tx successful e.g. CPAP.
 4X trial of 40 mins to simply sit still and do nothing that could intentionally keep
them awake. 1st trial often 1.5 – 3 h after normal wake-up time (w breakfast 1h
before 1st trial; lunch after 2nd trial). Each trial is 2 h apart.
 Average = 30 minutes
 If stay awake for > 40 mins for all 4 sessions = insomnia

Insomnias

 Difficulty initiating, maintaining sleep or waking up too early or chronically non-restorative sleep
THAT persists despite adequate chance for sleep AND at least 1 impariment (emotional,
cognitive, or somatic). It doesn’t present as daytime sleepiness.
1. Cognitive (affects frontal lobe) difficulty concentrating, memory problems, errors
2. Emotion  irritable, low mood (pervasive)
3. Somatic  more sensitive to pain (processing), heart disease, more susceptible to
infections, GI Sx
 N.B. insomnia is a co-morbidity in all major psych disorders and neurodegenerative disorders
 Common (1/3 adults complain about it, but subjective  only 6% meets Dx criteria). RF for
premature death.
 80% are due to anxiety and depression
1. But insomnia is also a risk factor for 1st and recurrent episodes of depression
 Sleep, eating, and sexual dysfunction

2. Insomnia and fatigue MC residual Sx after Tx of depression

3. Better outcome if sleep AND mood disorder BOTH treated adequately
 Most of the rest are 2o to medical conditions (esp. PD), chronic pain, and substance misuse.
Remaining fraction (<10%) is primary insomnia – to distinguish these cases, R/O presence of an
underlying psych or medical disorders (e.g. restless leg syndrome, lymphoma).
 Path: “Spielman model”
1. Premorbid personality trait = “on the go” type of person = guilty of sleeping
2. Stress pushes over clinical threshold of unable to sleep
3. Focuses a lot on the negative cognition  effort to sleep become issue  self-induced
high arousal (any noise disturb them)  perpetuate
 Hx: ask about factors affecting sleep such as shift working, medication, EtOH, caffeine, etc.
 Ix: sleep diary, corroboration from sleeping partners.
 Tx:
1. Treat associated disorder e.g. sedative use for depression w insomnia
2. Sleep routine
 Stimulus control  go to bed only when sleepy, use bed for sleeping or sex. Put
out lights immediately, get up if awake for > 20 mins.  aim: sleep within 10-15
min once on bed.
 Sleep restriction set bedtime and wakeup time. Adhere closely. Avoid naps.
Sleep at regular time and avoid daytime naps.
3. Sleep hygiene  appropriate length of time in bed at night (as above), pay attention to
health practices (e.g. caffeine and EtOH  use warm milk instead) and stimuli (e.g.
noise, light, heat, exercise* = reduce it) that affect sleep, ensure bright light exposure
during the day.
 *Evening exercise better than night exercise to aid daytime alertness and
encourage deep non-REM sleepat night.
4. Relaxation therapy  CBT, biofeedback routine to reduce arousal. Wind down 90
minutes before, practise relaxation in bed
5. CBT-I (insomnia)
 5-8X sessions. Sleep hygiene (above) + sleep restriction (only time this is NOT
used is already sleepy during the day + epilepsy  as both will lead to RTA!!) +
stimulus control
 Strategies to reduce cognitive arousal and effort; intrusive thoughts, racing
mind, trying to sleep.
 Relaxation training
 Cognitive therapy  alter dysfunctional belief and attitudes about sleep.
6. Pharmacotherapy
 Hypnotics  short-acting BZDs and related drugs. Effective in ST and widely
used. But can cause daytime drowsiness. Avoided long term due to dependence
 Antidepressants: amitriptyline, trazodone, mirtazapine
 OTC: anti-H, tryptophan, melatonin
 Problems:
 ST effectiveness + cognitive/psychomotor impairment
 Falls in elderly esp. at night (esp. Z drugs put to deep sleep)
 May trigger parasomnias, laters sleep architecture
 Daytime hangover effect
 Tolerance and dependence + withdrawal effects (BENZOs)
 Sleep, eating, and sexual dysfunction

 Reinforce feeling of lack of control = negative cognitive effect… very

important self-perpetuating factor
7. Melatonin (naturally occurring hormone regulating circadian rhythm) – only for ST Tx (no
longer than 3 weeks) of insomnia in those > 55.

Excessive daytime sleepiness (hypersomnia)

 Excessive daytime sleepiness caused by:

1. Insufficient sleep
2. Fragmented sleep (e.g. interrupted by RLS)
3. Primary disorder of excessive daytime sleepiness
 PSYCH: depression, bipolar, neurasthenia = CFS
 MED: narcolepsy, epilepsy, head injury, structural brain disease, Klein-Levin
syndrome, OSA, chronic disease and PAIN
 OTHER: drug S/E – Rx or illicit (SEDATIVES)
 Delayed sleep syndrome
 CNS hypersomnia
4. Head injury
 Dx can only be made if R/O other sleep disorders

R/O: narcolepsy, RLS, OSA

 In narcolepsy – there are repeated attacks of daytime somnolence, usually leading irresistibly to
sleep… onset: 20s, associated w cataplexy (abrupt loss of tone w/o LOC), hypnaGOgic
hallucinations (on falling asleep = “GO”), and sleep paralysis (cannot move when awake)
1. Autoimmune origin (98% have DR15 variant of HLA-DR2)
2. Path = loss of hypothalamic hypocretin-producing neurons
3. Tx: stimulants (modafinil, amps); clomipramine for the cataplexy

Restless leg syndrome

 Sensorimotor disorder characterised by intense discomfort, mainly in the leg, during evening,
when at rest. Produces irresistible urge to move legs.
 May be accompanied by periodic leg movements in sleep, perceived by bed partners as kicks
(70%) that occur in cycles of 20-40s.
 Important cause of chronically disturbed sleep (causes both insomnia and daytime sleepiness)
 Dx = clinical.
 Path = disturbed supraspinal pain modulation involving BG and/or descending dopaminergic
pathways. Defect in DA-Fe stores/transport (Fe is a co-factor for hydroxylation of tyrosine
hydroxylase = enzyme involved in RDS in DA synthesis). Fe-deficiency is commonly found in 2o
RLS – (anaemia, pregnancy, ESRD renal dz). AD inheritance w anticipation in 50%.
 Tx:
1. Avoid caffeine, chocolate, MSG, aerobic exercise after 7 pm, limit use of centrally acting
stimulants (decongestants, nicotine, anti-H, appetite suppressants), avoid AD (TCAs/SSRI
except bupropion and nefazodone), avoid anti-HTN (CCB) and anti-emetics
(metoclopramide)
2. Apply counterstimuli e..g shock, socks, stretch, hot baths/showers, ice pack
3. MILD: no Tx, avoid triggers, codeine
4. MOD: codeine + pregabalin/gabapentine (alpha-2 ligands)
 Sleep, eating, and sexual dysfunction

5. Severe: DA agonists = pramipexole, ropinirole, or rotigotine patch (decrease dose after

7 days).

OSA

 Epworth sleepiness scale = patients rate sleepiness level in normal daytime situation (0 = never,
1 = low chance, 2 = moderate chance, 3 = high chance of dozing)
 Situations include: sitting and reading, theatre/meeting (sit there inactive) watching TV,
passenger in car, lying down to rest, sitting and talking, sitting quietly after lunch (w/o EtoH), in
car while stopped in traffic
 Scores: 0 – 8 is normal; 9 -12 mild; 13 – 16 moderate; > 16 severe sleepiness

Parasomnias

 Abnormal episodic events during sleep (entry, during, arousal from). Examples: sleepwalking,
nightmares. Can be normal (developmentally) v.s. emotional/dreaming/ANS functioning.
1. NORMAL development in children. In adults  emotional stress
2. Basic drive states emerge with parasomnias e.g. aggression, locomotion, eating, sexual
 DDx odd nocturnal behaviours = epilepsy, REM behaviour disorders
 See paeds psych

SLEEP-WAKE CYCLE DISORDERS

 Delayed sleep phase syndrome (MC)

1. YOUNG patient
2. Usually habitual sleep times delayed > 2 hours, relative to conventional or socially
acceptable times. Patients have difficulty initiating sleep and prefer late wake-up times
3. Once sleep ensures, sleep is reported to be normal.
4. Attempts to fall asleep earlier is unsuccessful  school dropout, unemployment, EtOH +
drug abuse (esp. CANNABIS) to try to help sleep…
5. Tx:
 Patient has to be motivated
 Acknowledged difficulty in falling asleep
 Start w sleep hygiene; address light exposure
 Use sleep diaries and actigraphy (e.g. watch) over 7 days to establish window of
sleep onset time in relation to age-apt bed times and morning wake-up time
 Can also record phase delay of other circadian rhythms such as nadir of
temperature or dim light melatonin onset (DLMO)
 Chronotherapy over 1 week
 Shift sleep time 3h every day until desired timing.
 Morning bright light therapy
 Use 3h light pulse in morning to advance the clock.
 Avoid light in evening (delay onset of sleep)
 Exogenous melatonin must be apt time
 E.g. if want to sleep at 4 am, melatonin @ 2am.
 ?Kids give 0.5 h before sleep
 On stopping, will revert to previous sleep-wake cycle
 Sleep, eating, and sexual dysfunction

 Advanced sleep phase syndrome

1. OLDER adults
2. Retired + EtOH
3. Sleep pressure EARLY at 8 – 9 pm  try to stay awake but when they sleep, they fall into
a deeper sleep than when they do  wakes up 4-5 am
 Irregular sleep wake rhythm disorder
1. Neurodegenerative disorder
 Non-24 h sleep wake cycle disorder
1. Individual clock fail to sync to 24 h day.
2. Seen in the totally blind and also autism, Angelman, Rett.
3. Hard to Dx  need motivation
 SHIFT WORK disorder
 JET LAG
 Circadian sleep-wake disorder not otherwise specified
 Sleep, eating, and sexual dysfunction

EATING DISORDERS

General

 Onset: 7 -13. CORE features: preoccupation (intense fear of) about weight gain, changing body
shape, and unrealistic goals of idealised clothing size/lack of insight
 2 main diseases = anorexia and bulimia. Many patients (50%) do not meet all criteria for AN or
BN, and are labelled EDNOS (eating disorder not otherwise specified in DSMIV) v.s. other weird
disorders that don’t fit (“Otherwise specified feeding/eating disorder = OSFED).

Eating disorders in men

 1:6 cases.
 Dieting often for specific goals e.g. athletic performance, to avoid teasing
 M are more sensitive about shape waist UP (v.s. women = opposite)
 M start dieting from higher weight and feel fat at relatively higher weights than woman
 M less likely seek Dx evaluation due to perceived stigma.

ANOREXIA NERVOSA

Clinical features

 Core features above

 Other elements:
1. Self-induced LoW, induced primarily by restriction of food intake
2. Weight > 15% below normal (BMI < 17.5)
3. Irrational fear of fatness/intense drive for thinness
4. Body image distortion and excessive reliance on weight or shape for self-esteem
5. Amenorrhoea (if post-menarche and not using OCP). Part of wider endocrine disturbance
that includes elevated cortisol + GH
6. 2 subtypes:
 ANR = AN restrictive
 Over-evaluation  strict diet + weight-control AND aberrant rewards &
social reinforcement (emotional numbing later or euphoria initially) 
starvation syndrome (rumination/preoccupation about food & eating +
obsessionality, rigidity, social withdrawal, hunger)
 Paradox: the more they starve, the more distorted body image they
perceive
 ANBP = AN binge-purge (behaviour in last 3 months)
 Over-evaluation  strict diet + weight-control  LIFE EVENT +
ASSOCIATED MOOD CHANGE  binge eating (  compensatory
vomiting/laxative misuse) OR low weight ( starvation syndrome)
 Additional features:
1. Range of bodily SiSx which become more pronounced as weight loss progresses
 Physical Sx – sensitivity of cold, GI Sx (constipation, bloating), dizziness,
amenorrhoea, poor sleep
 Physical Si - emaciation, cold extremities, dry skin (sometimes orange =
hypercarotenaemia), lanugo downy hair on back, forearms, and cheeks, atrophic
secondary sexual characteristics, bradycardia, postural hypotension,
arrhythmias, peripheral oedema, proximal myopathy, FTT in kiddos
 Sleep, eating, and sexual dysfunction

 Medical Cx can be serious and life-theratening, esp. if the effects of starvation

are exacerbated by metabolic consequence of vomiting, or diuretic, or laxative
abuse.
 Abnormalities on Ix:
 Low LH, FSH, E2, T3. Increased GH, cortisol
 Hypoglycaemia, hypokalaemia/natraemia, metabolic alkalosis
 ECG = prolonged QTc (serious)
 Osteopenia and osteoporosis
 Low WBC and platelets
 Hypercholesterolaemia
 Delayed gastric emptying, acute gastric dilatation (due to over-rapid
refeeding)

Cardiac Cx
 Increased risk = severe/rapid weight loss,
pure f, ipepac, physical dz, age.
 ECG = beware QTc > 450 ms
 Abnormalities and their signs
o Small heart + fatigue  HF  SOB,
lying, cyanosis, oedema
o Mitral valve prolapse  C/P
o Bradycardia, low BP, orthostatic
hypotension  syncope, poor
peripheral perfusion
o Hypothermia > cold peripheries,
blue nails
o Arrhythmias  palpitations
GI Cx
 Gastroparesis up to 6 weeks on refeeding.
 Abdo pain = diffuse, non-tender; “chronic”
IBS
 Regulx, heartburn, dysphagia
 Constipation in 1st 3 weeks on refeeding
 Reflex hypofunctioning of colon & cathartic
colon (TTx = educate, reassure, fluid, fibre,
lactulose/glycerine suppository e.g. Movicol)
 RARE but dangerous = acute gastric
dilatation (1st few days of refeed/bingeing =
severe pain + bloating + succusion splash +
loss of bowel sounds + vomiting 
circulatory failure

Osteoporosis (silent but severe; often 35 y+) Childbearing

 Multifactorial = low weight, low E, low
intake
 Severity depends partly on age of onset of
eating dz; may not be reversible due to age.
 Can cause wedge #, vertebral collapse
 Assessment = DEXA scan (can be
motivational to see results); repeat if
abnormal q2y
 Tx (encourage weight regain)
o PPx/Rx = Ca2+, vitamin D, weight
regain (beware of exercise).
o OCP, HRT = no clear evidence, ?role
of E2 patch.
o Bisphosphonates reserved for
older patients; resorptive agents
e.g. tetraparatide more effective.
 Fertility usually preserved even after years w
no periods
 Only safe after weigh restoration
 Underweight W have underweight babies (LT
risks)
 OB risk lowered if BMI > 19.5
 Mothers w ongoing eating concerns need
help to ensure mealtime concerns don’t
affect baby
 Many become excellent and happy mothers
(some feel having kids help w their eating
disorder)
o Learn to be in touch w their bodily
needs during preg
o Learn from kids straightforward
attitude to food.

2. Use of diuretics, laxative, excess exercise or self-induced vomiting to enhance LoW

3. Core psych features become paradoxically worse as weight is lost  could be dude to 5-
HT dysfunction. This disorder is thus self-perpetuating – reinforced by the fact that
 Sleep, eating, and sexual dysfunction

achieving a lower weight has certain rewards (it enhance feelings of self-control, result
in perceived approval from peers, avoid sexual devt or gain parental attention)
4. Depressive and obsessional Sx
5. If the onset is before puberty – 2o sexual development delayed
6. Depression, fatigue, and irritability as LoW becomes pronounced
7. Social withdrawal and narrowing of interests

Aetiology and epidemiology

 Most RF shard w bulimia

 Risk factors are:
1. Bio
 10:1 females in clinical sample (6:1 in community)
 Western societies
 Adolescence = average onset = 15-16 y (1% F 12-18).
 FHx – eating disorder, depression, substance misuse (BN), premorbid obesity
(BN), premorbid: early menarche (BN)
 Genetics esp. AN (very heritable similar to BAD, schizo).
 Altered 5-HT and DA function, exacerbated by weight loss.
 Dysfunctional cortico-striatal circuitry  compulsions
 Aberrance in activity and volume of caudate and OFC seen in AN, OCD,
addictions. “Want it but can’t have it”.
2. Psycho
 Premorbid characteristics = low self-esteem, perfectionism (AN) vs impulsivity
(BN), anxiety.
 (V.S. normal = many things improve self-confidence)
 Self-perpetuating (compulsive nature = central maintenance + barrier to
recovery). Altered introception  allows starvation to occur w lack of concern
of consequences (insula not working). Aberrant reward processes.
3. Social
 Premorbid experiences = adverse parenting (low contact, high expectations,
arguments), sexual abuse, family dieting, critical comments on
eating/weight/shape, pressure to be slim
 Certain groups = ballet dancers, models, jockeys, gymnasts
 Familial risk DOES NOT seem to be genetic in origin (v.s. other psych disorders)

DDx

 Classic pt unmistakable but early stages must be DDx form causes of LoW
 Psych DDx – depression (severe), substance misuse, OCD, body dysmorphic disorder
 Organic DDx – malabsorption, IBD, hypopituitarism, cancer
 How to distinguish?
1. CORE psych Sx of AN
2. R/O the other causes

Assessment

 Establish Dx  Hx + collateral; NO physical tests

 Assessment
 Sleep, eating, and sexual dysfunction

o Physical state (not necessary but helpful in AN > BN as patients w AN have range of
abnormalities, many secondary to disturbed eating habits… in BN there are only minor
abnormalities EXCEPT vomiting + laxative misuse = electrolyte disturbance)
o Psych state (+ attitude to Tx  must know how they feel)
o Social circumstances

Tx (NICE 2004)

 Setting:
1. Most ADULTS should be managed on OPD basis (psych Tx = CBT-E + risk assessment)
2. Inpatient Tx = specialised setting w careful physical monitoring.
 I/p and day patient if not improved or at hi-risk
 I/p admission predicts poor outcome in TEENS
3. Family interventions that directly address eating disorder should be offered to
CHILDREN and TEENS (educate parents to gradually control child eating)
4. Wider environment (schools, GP, families; socio-cultural pressures; assertive outreach)
 Objectives are to: (1) alter person’s attitude to weight and body shape via psych Tx, (2) help
them increase weight, (3) detect and Tx medical Cx
 2+3 can be achieved successfully in ST. Component 1 is difficult and often resistant
 Principles are:
1. Establish good therapeutic R/S – many reluctant to accept Tx. Help them gain insight and
maintain motivation thereafter. Agree on goals, at what rate, and if exercise apt?
2. Encourage weight gain to break cycle and overcome starvation. Behavioural strats e.g.
contingent rewards promote this
3. CBT changes attitudes to change attitudes and preoccupations. Transdiagnostic CBT is a
modified CBT used. But in most adolescent patients, family therapy helps.
4. AD or anti-Q do not have established role, but used to Tx co-morbid disorders (c.f. BN)
5. Monitor physical condition: K+ check regularly. Multivitamins and supplements.
 Inpatient Tx:
1. If LoW intractable and severe (BMI < 14) or serious death risk (medical cx or suicide) 
admit to specialist unit (for 8-12 weeks): medical ward for refeeding and psych ward if
psychiatric risk (e.g. suicide)
2. This is to manage medical complications.
3. Feed but avoid refeeding syndrome (see below)
4. Allow intensive psych Tx.
5. Compulsory admission RARELY used and considered only if life-threatening. Forced
refeeding sometimes used but is controversial.
 Refeeding syndrome – due to sudden feeding when the body has depleted stores of P, Mg, K.
When the patient is refed suddenly, the insulin release depletes the already depleted stores,
amplifying cardiac problems. Avoid by:
1. ID high-risk: chronic/severe underweight, not eaten for 1 wk, frequent (more than daily)
binge, purging, or lax.
2. Measure electrolytes and correct electrolyte abnormalities BEFORE refeeding.
3. Measuring electrolytes before refeeding. Monitor serum P + electrolytes every alternate
day for 1st week THEN q1wk.
4. Start at 1200 kcal/d and gradually increased q3-5d (slow increase of 300-400 cal) until
1kg gain/week
5. Monitor for tachycardia and oedema.
 Sleep, eating, and sexual dysfunction

MARSIPAN for severe AN (assessment)

Physical = CV, muscle power (SUSS test: can Postural drop < 20 mmHg
they rise from squatting, can they sit up QTc > 450 msec (also ST and T changes)
from lying flat  proximal myopathy) K+ <2.5, Phos < 7 + U&Es (low K+ in eating disorders
BMI < 13- 14 plus RATE of weight lost more signifies low total body K+ and hypoK+ can recur
important (BMI graphing), escalating risk soon after discharge w fatal results… so give K+
Wgt lost >> 1kg/wk supplement.
CK, BM, Mg, LFTs, FBC (bloods may be normal despite
soon dying)
Criteria for inpatient admission
 LOW BMI < 14 / > 30% BW loss
 Rapid weight lost > 1 kg/wk
 Physical deterioration putting health at immediate risk (e.g. severe binge-purging)
 Marked physical co-morbidity complicates Tx (e.g. DM  binge drink sweet drinks = hyper,
misuse insulin = hypos)
 Serious depressive Sx/suicidal risk
 Failure to progress w day or OPD Tx
Do not discharge patients at high risk w/o specialist consultation.

Criteria for day patient Tx

 BMI > 14
 Motivated to change
 Failure of less intensive Tx
 Medically stable
Pros Cons
1. Save lives 1. Traumatic past I/P experiences
2. Intensive support w eating 2. Removal of own control  agentless
3. Specialist CBT and Tx of comorbidity 3. Contamination and competition
4. Time out from social stressors and 4. Consolidation of AN identity (other AN
demands girls) + isolation from social normality
5. Life saving for selected pt 5. Institutionalisation
6. Stepped care 6. $$$
7. Concentration of resoruces around the
sickest (least movable) at expense of
outreach and early intervention
PSYCHIATRIC issues
 Admit to specialist eating disorder unit (SEDU)
 Regular liason w psychiatrist
 Be aware of sabotaging behaviour such as falsifying weight, water drinking, exercise
 Use only experienced and trained nurses to observe (pass NG tube, monitor)
 If staff (e.g. agency) inexperienced in management of AN are recruited, provide a concise
management plan to follow
 Consider MHA Section if patient fails to improve.
o When refuse + concern re: not giving Tx = life-threatening
Sleep, eating, and sexual dysfunction
 Sleep, eating, and sexual dysfunction

Prognosis

 Variable outcome.
 20% good outcome w short-lived disorder and full recovery.
 Another 10-20% develop chronic and intractable disorder
 The rest progress to another eating disorder/ relapse/ residual features
 AN = highest mortality rate of all psych disorders.
 Mortality rate 10X increase in 1st 10 years of illness (10-20% in LT F/U). This is 12X higher than
general population, 2X more than other psych inpatients. Death usually due to complications of
starvation (60% direct effect of illness)… only 27% by suicide.
 Poor outcome associated w long duration prior to pt; onset in adulthood; severe LoW;
vomiting.
 Sleep, eating, and sexual dysfunction

BULIMIA NERVOSA

Clinical features

 Uncontrolled (“loss of control”) eating binges (excessive  1000-4000 kcal and repetitive 
recurrent > 2/wk)
1. At first due to diet-induced hunger  then become a means to deal w emotions.
 Then they feel bad about it (regret or shame)
 Then they self-induced vomit/laxatives/diuretics (“purging”) to negate calorific effects of the
binge.
 With “Core Sx” of eating disorders = irrational fear of fatness, distortion of body image.
 1 X per week.
 Must not meet Dx criteria for AN. Bulimics normally have OK weight due to the compensation –
if body weight reduced, then some physical features of AN can be present (described above)
 Two subtypes = purging (80%) and compensation e.g. restrict/exercise (20%)
 Small number of woman have BPD who DSH (often cut) and misuse EtOH or drugs.
 Physical signs of BN:
1. Russell’s sign (calluses on knuckles)
2. Pitted teeth (gastric erosion)
3. Salivary gland enlargement
4. Metabolic disturbances (metabolic alkalosis)
5. Hoarse voice (oesophagitis)
6. Laxative use = pigmentary changes of colon + colonic motility problems + electrolytes
disturbances
7. Diuretic use = electrolyte changes and renal dysfunction

Aetiology and epidemiology

 2% women aged 16-35 (but only 10% seek help)

 RF shared w AN (as described above).
 Genetic predisposition that overlaps w anxiety
1. Genetic contribution to BN is controversial; some studies suggest large heritability of
over 80%...

DDx

 AN w bulimic features must be R/O (anorexia trumps bulimia, diagnostically, although in reality
this could be EDNOS)
 Sporadic bingeing in other psych disorders e.g. atypical depression
 Medical causes of vomiting
 Binge eating disorder = recurrent binges occur but without extreme weight control behaviour.
This leads to obesity (25% of medical obesity). Unlike BN, it is characterised only by bingeing and
relentless grazing. Pt: often gradual in 30s-40s.

Tx (NICE for BN and EDNOS)

 More effective and better evaluated than AN. Take a stepped care approach, depending on
severity of problem and pt wishes.
 Sleep, eating, and sexual dysfunction

1. Pre-requisite (while awaiting CBT): self-help manuals and Tx of depression e.g. CBT-BN,
CBT-E
2. 1st-line: adolescence with BN should be treated w CBT adapted as necessary (family,
development) i.e. modified CBT effective in 60-70%  majority remain well 5 y later.
CBT aims to help patient: (1) understand link between bingeing, vomiting, and dieting;
(2) regulate their diet and break vicious cycle between the 3 behaviours; and (3)
preoccupation w body shape.
3. IPT also works but takes longer (IPT works by emphasising R/S problems)
4. 2nd-line: HIGH DOSE (60-80 mg/day) SSRI = fluoxetine (best evidence) reduce f of
bingeing and vomiting. Disorder often relapses on stopping… (AD anti-bulimic effects are
NOT sustained as it doesn’t involve them LEARNING).
 Only use if CBT failed or CO-MORBID with severe depression (alongside with BN-
CBT).
 Can’t use in AN = worsen (anti-bulimic = won’t eat).
 Fluoxetine best safety profile.

Prognosis

 BN probably better than that of AN (mortality certainly lower).

 People who have had BN for average of 5 years  30-50% still have eating disorder (BN or
atypical eating disorder) 5-10 y later.
 Poor prognostic factors include: (1) premorbid childhood obesity, (2) low self-esteem, and (3)
personality disturbance.

OSFED

Atypical AN

 All of the criteria for AN met except despite significant weight loss, the individual weight is
within or above the normal range

Subthreshold BN

 All of criteria for BN met, except that the binge-eating and compensatory behaviours < 1X /week
or < 3 m

Subthreshold binge-eating disorder

 Low frequency or limited duration

Binge-eating disorder

 Later onset. M = F and older (+ often depressed)

 Recurrent episodes of binge eating > weekly > 3 m.
 Causes impairment and/or distress
 No compensatory behaviours
o 50% binge eat before dieting begins
o Around 65% obese
 No over-evaluation of control of eating, weight, and shape.
Sleep, eating, and sexual dysfunction
 Sleep, eating, and sexual dysfunction

PSYCHOSEXUAL DYSFUNCTION

General

 Common consequence of psych disorders OR their Tx. E.g. loss of libido in depression, and
ejaculatory failure due to anti-Q
 Sexual dysfunction may contribute to psych disorder. E.g. anxiety exacerbated by man worrying
about his impotence
 Each of the components of sex can go awry = desire, physiological arousal, and orgasm.
1. Sexual desire disorders  lack of; excess
2. Failure of genital response  ED (impotence); vaginal dryness
3. Orgasmic dysfunction  premature ejaculation; anorgasmia
4. Other  vaginismus (involuntary spasm of vaginal musculature); dyspareunia

Sexual dysfunction

 Each type of dysfunction may be due to psych or medical causes, or both.

1. Painful intercourse, loss of sexual desire, and impaired orgasm more common in women
2. The main problems for men are impotence and premature ejaculation.
 Assessment
1. Ask explicitly – many people are glad to be asked (their first chance to get help)
2. Respond to cues e.g. depressed patients w no pleasure from life  ask if affects interest
in sex. If no cue  “I need to ask some questions about your sex life to help me
understand your problem”. Use terminology apt to person’s age and culture
3. Questions to ask
 Nature and f of sex? Particular problem present?
 Changing interest (note: increased libido in mania usually NOT a p/c)
 Men:
 ED – any problems getting or keeping erection; lose erections in
morning or masturbating (= organic cause)
 Worry about sexual performance (performance anxiety  impotence)
 Ejaculatory function – do you cum too quickly, how long after
penetration, do you feel anxious about this? Common in inexperience,
anxious men.
 Women:
 Do you have pain on intercourse – when, where? Dyspareunia and
vaginal dryness have psych and gyn causes.
 Do you feel anxious or tense about sex? Extreme anxiety  vaginismus
 Sexual development:
 Estimate age of puberty – voice break, periods start? Delay in sex devt
can lead to psych effects or indicate an abnormality e.g. Turner’s
 When did you first masturbate? First intercourse? Altered by cultural
and individual differences
 Sexual orientation and preference
 What is their orientation? Any preferences or fetishes – detailed
questioning indicated if patient views it as problem, or forensic context.
If so, what and have they gotten into trouble?
 Other issues:
 Current psych disorders (depression and most other psych disorders)
 Sleep, eating, and sexual dysfunction

 General health (diabetes, vascular dz; do physical O/E)

 Current meds (H2 antagonists, thiazides, anti-HTN, AD, antipsychotics)
 ED
1. Inability to reach erection or sustained erection long enough for intercourse
2. Most are 2o – i.e. full erection possible at one time but now can’t. 1o ED is rare and due
to neuro or circulatory problems.
3. Common causes are: anxiety, EtOH, unwanted S/E from Rx meds, diabetes, vascular dz
4. Tx: combine PSYCH + physical
 PDE-V inhibitors e.g. sildenafil – it is possible to Rx this for “PSYCH” impotence
on the NHS (but restricted in specialist centres and those suffering severe
distress from such impotence).
 Dyspareunia
1. Pain on sex. Can be due to impaired lubrication w vaginal secretions (from anxiety or
inadequate arousal), or from physical scarring (childbirth)
2. Pain on penetration may be due to pelvic pathology
3. If it is secondary to psych  Tx: sexual therapy

 Psych Tx of sexual dysfunction: Some may respond to reassurance or self-help manuals. Other
requires sex therapy by psych or therapists. This is a behavioural method and is effective if
purely psych. Principles:
1. Tx couple together
2. Educate about sex and factors affecting it
3. Encourage open discussion of feelings and decrease anxiety and embarrassment
4. Use graded exposure (couple gradually build sexual R/S, setting aide time and commit to
series of steps… non-genital sensate focus  genital focus  intercourse).
5. Additional methods used for specific forms of dysfunction e.g. dilators for vaginismus or
squeeze technique for premature ejaculation
6. Lack of sexual desire has worst prognosis.

Other sexual disorders (sexual desire and sexual identity)

 In ICD-10, they are grouped w PDs. Forensic psych may be asked to report psych status of sex
offenders. Homosexuality is NOT a psych condition anymore.
 Gender identity disorders
o Gender dysphoric disorder = transsexualism  M wishes to live as F. Seeks hormonal
and surgical Tx to match body of their subjective gender. Sexual orientation variable and
sexual desire often low. They suffer great distress, and depression is common
o Transvestism = urge to dress in clothes of opposite sex. If accompanied by sexual arousal
around it = fetishstic transvestism. There is NO desire to change sex. Transvestites are
often married and X-dressed secretly. NO specific Tx.
 Paraphilias = disorders of sexual preference (wide range of object, can be dysfunctional and
over-dependent = fetish; usually a male disorder)
o Paedophilia – sexual interest in prepubescent children  Tx: antiandrogens
(cyproterone acetate, goserelin) reduces libido and reoffending rates. Jail if offend.
o Exhibitionism – expose genitals to strangers. Type 1 = inhibited = feels urge to show
flaccid penis and feel guilty. Type 2 = disinhibited = aggressive men who exposes erect
penis and masturbate then or later. Type 2 associated w actual sexual assault. Tx =
behavioural. SSRIs have limited evidence base…