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(From left to right) Dr BobGrove, Professor Dame CarolBlack, Professor ManselAylward, Dr Debbie Cohen,Professor Gordon Waddell andProfessor Peter White
Swedish research exchange10 March 2009University research helping to remove the barriers people face when returning towork has been shared with policy makers at a leading conference in Stockholm.
Professor Mansel Aylward CB, Director of the Centre for Psychosocial andDisability Research in the School of Psychology, headed a British team ofacademics to the first conference of the new Social Council of Sweden at theMinistry of Health and Social Affairs in Stockholm.
Professor Aylward, Dr Debbie Cohen and Professor Gordon Waddell outlined keypieces of University research helping to explain and address the obstacles peopleface in the UK when returning to work.
In his keynote address, Professor Aylward chronicled the development of“Pathways to Work” in the UK and drew upon research undertaken by his team atCardiff which further explored obstacles to return to work and interventions toaddress them..
Professor Aylward said: “The first conference of the new Social Council of Sweden, at the invitation of the SwedishGovernment, was an opportunity to share our research knowledge with academics, researchers, healthcareprofessionals and senior government advisors, officials and politicians - including Sweden’s Secretary for Healthand Social Affairs, Bettina Kashefi , on what works.
“We hope our presentations will provide the scientific and research knowledge to inform the SwedishGovernment’s plans for Welfare reform.”
The Conference was also addressed by other key UK academics. Dr Bob Grove of The Sainsbury Centre, King’sCollege London gave an update on the evaluation of the ‘Pathways to Work’ project; Professor Peter White ofBart’s and the London School of Medicine discussed Symptoms Defined Illness and their handling in occupationalrehabilitation and Professor Dame Carol Black, UK National Director for Health, Work and Well-being, outlined thefindings of a review of the health of Britain's working age population: Working for a healthier tomorrow.
Professor Aylward and his team from Cardiff also spent a day at the Karolinska Institute. Meeting with ProfessorAlexanderson, who chairs the Swedish Social, it was an opportunity to explore joint research opportunities.Professor Aylward added: “The visit to the Karolinska Institute allowed us to discuss and set out the basis forcollaboration between the Karolinska Institute and Cardiff University. We hope this will lead to joint research in thearea of health and work.”
Related linksCentre for Psychosocial and Disability Research
Department for Work and Pensions
What helps occupational rehabilitation when the doctor cannot explain the symptoms?
Peter White
Agenda
Symptom defined illnesses (SDIs)The example of chronic fatigue
syndromeBiopsychosocial management is bestPrevention is even better
Kroenke, et. al., AJM, 1989Kroenke, et. al., AJM, 1989
Abdominal Pain
Abdominal Pain
3-YearIncidence
(%)
3-YearIncidence
(%)
00
22
1010
44
66
88
ChestpainChestpain
FatigueFatigue
DizzinessDizziness
HeadacheHeadache
EdemaEdema
Back PainBack Pain
DysphagiaDysphagia
InsomniaInsomnia
NumbnessNumbness
SymptomsSymptoms
Organic CauseOrganic Cause
Prevalence of unexplained symptoms in hospital clinicsClinic Prevalence % Chest Cardiology Gastroenterology Rheumatology Neurology Dental Gynaecology
59 56 60 58 55 49 57
Total
56
Symptom defined illnesses
Tension headaches,Atypical facial and chest painsFibromyalgia (chronic widespread pain)Other chronic pain disordersIrritable bowel syndromeMultiple chemical sensitivityChronic (postviral) fatigue syndrome (ME)
How common is CFS?
0.2 - 2.6 % population or primary care
Risk (OR) of depressive illness with chronic physical disorders
CFS 7.2Fibromyalgia 3.4Peptic ulcers 2.8COPD 2.7Migraine 2.6Back pain 2.3Cancer 2.3MS 2.3
UK costs of CFS
118,000 on incapacity benefit19,000 on disability living allowance+ Cost of medical and social care+ Loss of employment
Outcome is poor without treatment
Systematic review of longitudinal studies
5 % (range 0 - 31) recovered by follow up39 % (range 8 - 63) some improvement
Cairns R, Hotopf M, Occup Med 2005
Use the biopsychosocial model
The biopsychosocial model “takes into account the patient, the social content in which he lives and ... the physician role and the health care system.”
George Engel, 1977
Management is biopsychosocial
• Biological e.g. medication, physical rehabilitation
• Psychologicale.g. CBT
Social
Remove the barriers to recovery -
Relationships .. at work or homeIatrogenic .. bad healthcare advice Benefit gap .. financial incentives
The lost art of rehabilitation
We have forgotten not only how to rehabilitate patients, but that we need to do so for the patient to make a full recovery.
Graded exercise therapy for CFS
Exercise = “an activity requiring physical effort”
Percentage improved with GET
0
10
20
30
40
50
60
70
UK UK UK NZ Austral
GETControl
Percentage improved with CBT
0
10
20
30
40
50
60
70
80
UK UK NL NL UK
CBTControlControl
But do these treatments help patients return to work?
“Only cognitive behavior therapy, rehabilitation, and exercise therapy interventions were associated with restoring the ability to work.”
- Even without occupation as the aim.
Systematic review: SD Ross et al, Arch Intern Med 2004
Predictions of non-response to GET
• High psychological distress• Membership of a self-help group• Sickness benefit
R Bentall et al, 2002
Social risks
“If you have to prove you are ill, you can’t get well.” (N Hadler, 1996)
“ME is an incurable disease.”(UK doctor, 2008)
Does the BPS approach work?
• CFS• Low back pain• IBS• Depressive illness• (Cardiac disease)• (DM)
Preventing SDIs
Patients with infectious mononucleosis– Brief rehabilitation, with graded return to
activities– Compared to leaflet
By 6 months, 26% had abnormal fatigue after rehab, compared to 50% of controls.
B Candy et al, 2004
What is chronic fatigue syndrome; and what is ME?
Peter WhiteBart’s and the London
AgendaWhat is CFS?
ICD-10Research criteriaClinical criteriaOne functional somatic syndrome versus heterogeneity
What is ME?Original epidemic MEDiagnostic labels affect prognosis
Is it physical or mental? It’s both
Does the ICD-10 help us?
No -At least five ways to classify CFS
Myalgic Encephalomyelitis
G93.3 in Neurology chapter of ICD-10Postviral fatigue syndrome,
Includes: benign myalgic encephalomyelitisChronic fatigue syndrome, postviral
Neurasthenia
F48 in ICD-10 mental disorders chapterNeurasthenia
Excludes postviral fatigue syndrome Includes fatigue syndrome
Other ways to classify CFS
F45.1 Undifferentiated somatoform disorder
F45.3 Somatoform autonomic dysfunctionIncludes: Da Costa syndrome, Neurocirculatory asthenia
F45.9 Somatoform disorder, unspecified
Other ways to classify CFS
R53.82 Chronic fatigue, unspecified Includes:Chronic fatigue syndrome NOS
R54 Senile asthenia!
7 research criteria
• CDC 1988• Australian 1990• Oxford 1991 • London ME 1993• CDC revised 1994• CDC revised 2003• Brighton (post-vaccine) Collaboration, 2007
CDC (international) definition of CFS
• 6/12 of persistent/relapsing unexplained fatigue
• of new onset• not the result of on-going exertion• not substantially relieved by rest
CDC CFS
4 associated symptoms: sore throat tender lymph glands myalgiaarthralgianew headaches unrefreshing sleep post-exertion malaise poor memory or concentration
CDC definition of CFS
• Substantial disability
• Medical and psychiatric exclusions
No empirical support
• Population study of Swedish twins (31,000): CFS-like illness; no CDC specificitySullivan et al, 2005, Kato et al…
• Population study of 1,468 pairs of 8-17 year oldsCDC not delineated Fowler et al, 2005
• CDC population studies in Wichita & Georgia:For every patient with CDC CFS, 2-8 times more with
disabling fatigue.
3 clinical criteria
• Canadian 2003 • RCPCH 2004• NICE 2007
Canadian criteria for ME
• Fatigue• Post-exertional fatigue/malaise• Sleep dysfunction• Pain
Any 2 of:“confusion, impairment of concentration and short-term memory consolidation, disorientation, difficulty with information processing, categorizing and word retrieval, and perceptual and sensory disturbances – e.g. spatial instability and disorientation and inability to focus vision. Ataxia, muscle weakness and fasciculations are common. There may be overload phenomena: cognitive, sensory – e.g. photophobia and hypersensitivity to noise - and/or emotional overload, which may lead to “crash”periods and/or anxiety.”
“At Least One Symptom from Two of the Following:__ a. Autonomic Manifestations: orthostatic intolerance - neurallymediated hypotension (NMH), postural orthostatic tachycardia syndrome (POTS), delayed postural hypotension; light-headedness; extreme pallor; nausea and irritable bowel syndrome; urinary frequency and bladder dysfunction; palpitations with or without cardiac arrhythmias; exertional dyspnea.__ b. Neuroendocrine Manifestations: loss of thermostatic stability – subnormal body temperature and marked diurnal fluctuation, sweating episodes, recurrent feelings of feverishness and cold extremities; intolerance of extremes of heat and cold; marked weight change - anorexia or abnormal appetite; loss of adaptability and worsening of symptoms with stress.__ c. Immune Manifestations: tender lymph nodes, recurrent sore throat, recurrent flulike symptoms, general malaise, new sensitivities to food, medications and/or chemicals.”
NICE
4 months of fatigue with:– new or specific onset (not life long)– persistent and/or recurrent– unexplained– substantial reduction in activity- characterised by post-exertional
malaise/fatigue
NICE 2
One of: - The 8 CDC symptoms plus:- general malaise or ‘flu-like’ symptoms- dizziness and/or nausea- palpitations in the absence of identified
cardiac pathology- Normal exclusions
RCPCH• “..generalised fatigue causing significant
impairment for 6/12 months for which no alternative explanation has been found...”
• “..the fatigue is likely to be associated with other ‘classical’ symptoms (..) such as difficulty in concentrating and disturbed sleep patterns and is classically exacerbated by effort (both mental and physical).”
One functional somatic syndrome
CFS patients have close comorbidity with:• Irritable bowel syndrome• Fibromyalgia• Regional pain disordersAre they all part of the same disorder,
presenting to different specialists?YES - Wessely and Sharpe, Lancet 1999NO – White, 2004
CFS studies with symptoms and demographics
• 744 clinic patients: 68% neurasthenia, 32% somatoform disorderHickie et al, 1995 & 2001
All studies since have found heterogeneity
Is the CFS endophenotype heterogeneous?
Analysis
• Latent Class Analysis (LCA) • 121 chronically fatigued women• 38 healthy matched controls
Five ill sub-groups
1. Obese & hypnoeic2. Obese, hypnoeic & stressed3. Insomnia & pain (myalgia)4. Polysymptomatic, depressed5. Polysymptomatic, depressed, stressed,
insomniac and menopausalVollmer-Conna et al, 2006
External validation of groups
• 5 groups: demographic and clinical• 2 groups; gene expression• 3 groups: gene polymorphisms• Replication in Georgian sample
Should we give up the diagnosis of CFS/ME?
A working hypothesis:CFS/ME may be the final common pathway
from several different diseases with the same clinical presentation
It has utility, particularly for treatment
To lump or split?
• Population study of Swedish twins (31,000):
Two latent comorbid traits1 dominated by mood disorders2 all other disorders (FM, CFS, IBS, headaches)
“neither lumpers nor splitters are correct”Kato et al (in press)
GPRD study
• 4,388 patients with CFS/ME/PVFS• IBS and healthy matched controls• Both ill groups - more premorbid mood and
other functional disorders• But triggering infections differentiated
them.Gallagher et al, submitted
What is ME?
• Myalgic encephalomyelitis• First described in a 1956 Lancet editorial
describing epidemics of fatigue with neurological symptoms and signs – the author later regretted doing this.
Royal Free epidemic of 1955 (Ramsay)
74% “showed objective evidence of involvement of the central nervous system”
- “heavy involvement of the cranial nerves”- “Objective evidence of brain stem and
spinal cord involvement..”- “Paralysis of the face occurred in just under
20%..”
ME
• April 1978 conference - at the RSM!• Organic incurable neurological disease• What message does this give our patients?
The effect of a doctor’s “ME”label on prognosis
• “ME” lasted longer than “CFS”.• “ME” patients had more consultations both
in general and specifically for fatigue.• No differences before diagnosis
Conclusions
• CFS/ME exists, but is hard to define• Broad based definitions are best• Both heterogeneity and comorbidity should
be addressed• Beware what you mean when you give a
diagnosis
Robert Kendell: “The distinction between mental and physical illness”“Not only is the distinction between mental
and physical illness ill-founded and incompatible with contemporary understanding of disease, it is also damaging to the long-term interests of patients themselves.”
BJ Psych 2001
Kendell again
“..if we do continue to refer to ‘mental’ and ‘physical’ illnesses we should preface both with ‘so-called’, to remind ourselves and our audience that these are archaic and deeply misleading terms.”
BJ Psych 2001
What is CFS, and what is ME?
Peter WhiteBergen, October 20th 2009
Agenda
What is CFS?
What is ME?
Define your phenotype……
XMRV and CFS
How you define CFS will determine what you find
Does the ICD-10 help?
No -At least six ways to classify CFS
Myalgic Encephalomyelitis
G93.3 in Neurology chapter of ICD-10Postviral fatigue syndrome,
Includes: benign myalgic encephalomyelitisChronic fatigue syndrome, postviral
Neurasthenia
F48 in ICD-10 mental disorders chapterNeurasthenia
Excludes postviral fatigue syndrome Includes fatigue syndrome
Other ways to classify CFS
F45.1 Undifferentiated somatoform disorder
F45.3 Somatoform autonomic dysfunctionIncludes: Da Costa syndrome, Neurocirculatory asthenia
F45.9 Somatoform disorder, unspecified
Other ways to classify CFS
R53.82 Chronic fatigue, unspecified Includes:Chronic fatigue syndrome NOS
R54 Senile asthenia!
Can we use research criteria?
7 to choose from
7 research criteria
• CDC 1988• Australian 1990• Oxford 1991 • London ME 1993• CDC revised 1994• CDC revised 2003• Brighton (post-vaccine) Collaboration, 2007
CDC (international) definition of CFS
• 6/12 of persistent/relapsing unexplained fatigue
• of new onset• not the result of on-going exertion• not substantially relieved by rest
CDC CFS
4 associated symptoms: sore throat tender lymph glands myalgiaarthralgianew headaches unrefreshing sleep post-exertion malaise poor memory or concentration
CDC definition of CFS
• Substantial disability
• Medical and psychiatric exclusions
Recent audit of my clinic
• 250 new patients seen• 54 (22%) - alternative psychiatric diagnosis• 47 (19%) - alternative medical diagnosis
Risk of major depressive illness with chronic physical disorders
CFS 7.2Fibromyalgia 3.4Peptic ulcers 2.8COPD 2.7Migraine 2.6Back pain 2.3Cancer 2.3MS 2.3
SB Patten et al, 2005 (n = 115,071)
No empirical support for CDC criteria
Swedish twin population study(n = 31,000):
CFS-like illness; no CDC specificitySullivan et al, 2005, Kato et al, 2008
CDC population studies in USA:For every patient with CDC CFS, 2-8
times more with disabling fatigue.
3 clinical criteria
• Canadian 2003 • RCPCH 2004• NICE 2007
Canadian criteria for ME
• Fatigue• Post-exertional fatigue/malaise• Sleep dysfunction• Pain
Any 2 of:“confusion, impairment of concentration and short-term memory consolidation, disorientation, difficulty with information processing, categorizing and word retrieval, and perceptual and sensory disturbances – e.g. spatial instability and disorientation and inability to focus vision. Ataxia, muscle weakness and fasciculations are common. There may be overload phenomena: cognitive, sensory – e.g. photophobia and hypersensitivity to noise - and/or emotional overload, which may lead to “crash” periods and/or anxiety.”
“At Least One Symptom from Two of the Following:__ a. Autonomic Manifestations: orthostatic intolerance - neurally mediated hypotension (NMH), postural orthostatic tachycardia syndrome (POTS), delayed postural hypotension; light-headedness; extreme pallor; nausea and irritable bowel syndrome; urinary frequency and bladder dysfunction; palpitations with or without cardiac arrhythmias; exertional dyspnoea.__ b. Neuroendocrine Manifestations: loss of thermostatic stability – subnormal body temperature and marked diurnal fluctuation, sweating episodes, recurrent feelings of feverishness and cold extremities; intolerance of extremes of heat and cold; marked weight change - anorexia or abnormal appetite; loss of adaptability and worsening of symptoms with stress.__ c. Immune Manifestations: tender lymph nodes, recurrent sore throat, recurrent flulike symptoms, general malaise, new sensitivities to food, medications and/or chemicals.”
NICE
4 months of fatigue with:– new or specific onset (not life long)– persistent and/or recurrent– unexplained– substantial reduction in activity- characterised by post-exertional
malaise/fatigue
NICE 2
One of: - The 8 CDC symptoms plus:- general malaise or ‘flu-like’ symptoms- dizziness and/or nausea- palpitations in the absence of identified
cardiac pathology- Normal exclusions
CDC criteria give you reliability, but not validity.
Always measure comorbid conditions.
Is the CFS heterogeneous?
The measures, US style!
Medical and drug historyHormones ++Immune tests +PolysomnographyGene polymorphismsGene expression
SymptomsDisabilityIQPsychiatric exam
Analysis
• Principal components analysis (PCA) • Latent Class Analysis (LCA) • 121 chronically fatigued women• 38 healthy matched controls
Vollmer-Conna U et al, 2006
Five endophenotypes
1. Obese & hypnoeic2. Obese, hypnoeic & stressed3. Insomnia & pain (myalgia)4. Symptomatic, depressed5. Symptomatic, depressed, insomnia,
stressed and menopausal
External validation of endophenotypes
• 5 groups: demographic and clinical• 3 groups; gene expression• 3 groups: SNPs• Replication in Georgian sample
Aslakson E et al, 2009
One functional somatic syndrome
CFS patients have close comorbidity with:• Irritable bowel syndrome• Fibromyalgia• Regional pain disordersAre they all part of the same disorder,
presenting to different specialists?YES - Wessely and Sharpe, Lancet 1999NO – Wessely and White, 2004
UK GPRD study
• 4,388 patients with CFS/ME/PVFS• IBS and healthy matched controls• Both ill groups - more premorbid mood and
other functional disorders• But triggering infections differentiated
them.Gallagher A et al, 2009
Common factors predispose to all functional somatic syndromes
Uncommon triggers differentiate functional somatic syndromes
What is ME?
• Myalgic encephalomyelitis• First described in a 1956 Lancet editorial
describing epidemics of fatigue with neurological symptoms and signs.
Royal Free hospital epidemic of 1955
(M Ramsay)
74% “showed objective evidence of involvement of the central nervous system”
- “heavy involvement of the cranial nerves”- “Objective evidence of brain stem and
spinal cord involvement..”- “Paralysis of the face occurred in just under
20%..”
When did ME become endemic?
1978 conference - at the UK RSMEpidemic “ME” became endemicOrganic incurable neurological diseaseWhat message does this give our patients?
The effect of a doctor’s “ME” label on prognosis
• “ME” lasted longer than “CFS”.• “ME” patients had more consultations both
in general and specifically for fatigue.• No differences before diagnosis
Hamilton WT et al, 2005
Conclusions
• CFS exists, but is hard to define• Make sure it’s not something else• Watch out for comorbid disorders• Beware what you mean when you give a
diagnosis
What causes CFS/ME, and does this determine treatment?
Peter WhiteBergen, October 20th 2009
Agenda
What causes it?PredisposingTriggers
What maintains it?Perpetuating
Do these determine treatments?
Predisposing risk markers
FemaleAge – puberty to retirement (39)Previous functional somatic
syndromes (Previous mood disorders)(Childhood traumas)
Stress as antecedents
• 3 – 8 times risk of childhood traumaC Heim et al, 2006 & 2008 (retrospective)
• 1.6 risk of feeling stressed, measured 25 years previously (case control)
6 x risk of feeling stressed compared to co-twinK Kato et al, 2006 (prospective)
Genes
• Gene expression highly variable and not replicated.
• Glucocorticoid receptor SNP x 3 riskRajeevan M et al, 2007
• Sub-groups associated with MA and GR SNPsSmith A et al, 2006
Predisposing activity
Childhood inactivity?Childhood and adult overactivity?Retrospective perception of
overactivity/super fit and healthy?
Activity and birth cohorts
Underactive childhood (1970 BC)Overactive childhood (1946 BC)Overactive adulthood (1946 BC)None of the above (1958 BC)
Triggering risk markers
Certain infections: e.g. EBV, Coxiella Burnetii, Hepatitis A, Parvo? Giardiasis?
Stressful events or difficulties?Not: immunisations
Maintaining risk markers
Older age, mood disorders, illness beliefs, inactivity, sleep problems, search for legitimacy, benefits, diagnostic label
Not: immune or viral measures
The biopsychosocial and biomedical models
Biomedical model is “the reduction of illness to measurable biological parameters”
Edward Shorter, 2003Biopsychosocial model “takes into account
the patient, the social content in which he lives and ... the physician role and the health care system.”George Engel, 1977
Does knowledge of causes determine treatment?
Yes – and no
Treatment of CFS
Cognitive behaviour therapy Graded exercise therapy
D Chambers et al, 2006J Malouf et al, 2008
Initial infection
Rest or “boom & bust
Bodily adaptation
Sleep problems
Fatigue
Beliefs
What changes with GET?
• Physical fitness and strength
• Exercise capacity
• Perception of effort
Physiological changes with GET
• 13 % increase in peak VO2• 27 % increase in strength
Not associated with feeling better
• Reduced sub-max heart rate response to exerciseAssociated with 18 % increase in treadmill time
Sense of effort normalises with GET
Graded Exercise Therapy
Graded Exposure Therapy
(Physical reconditioning)
It changes the brain more than the body
Beliefs and behaviour change with GET
15 % believed physical deconditioning was the cause of CFS before, compared to 81 % after treatment.
= BCT
Conclusion
CFS is multifactorialBiological, psychological and socialHeterogeneous and homogeneousRehabilitation works, but not as we know it.
The distinction between mental and physical illness
“The distinction between mental and physical illness is ill-founded and incompatible with contemporary understanding of disease”
Robert Kendell, BJ Psych 2001
Robert Kendell again
“..if we do continue to refer to ‘mental’ and ‘physical’ illnesses we should preface both with ‘so-called’, to remind ourselves and our audience that these are archaic and deeply misleading terms.”
Treatments for chronic fatigue syndrome
Peter WhiteBergen, 2009
Agenda
• Trials of graded exercise therapy• Trials of cognitive behaviour therapy • How do they work?• What we don’t know – PACE trial
How do you treat it?
• By helping the patient remove the barriers to their recovery….
• 5 systematic reviews all conclude that behavioural treatments work with little or no harm
Graded exercise therapy
Percentage improved with GET
0
10
20
30
40
50
60
70
UK UK UK NZ Austral
GETControl
Wearden A et al, 1998
• 33% dropped out (<12% in other trials)• Only 5 sessions in 3/12 • Higher initial intensity of exercise• Physiological improvement before
increasing exercise
Graded Exercise Therapy
Exercise = “an activity requiring physical effort”
Graded Exercise Therapy
• Explanation/education• Assess physical capacity• Establish baseline activity• Individualised home exercise• Duration then intensity• Target heart rates• Feedback and explanation
Cognitive behaviour therapy
Trials of CBT
• 10 randomised trials• Excluding 2 not aimed to help recovery• Excluding 2 not using CB therapists• Excluding Lenny Jason’s trial
Percentage improved with CBT
0
10
20
30
40
50
60
70
80
UK UK NL NL UK
CBTControlControl
CBT for CFS
(a) Assessment of illness beliefs and coping strategies
(b) Structuring of daily rest, sleep and activity, with a gradual return to normal activity
(c) Challenging unhelpful beliefs about symptoms and activity
Do effects last?
Yes
2 years after GET
5 years after CBT
Those who stop self-management relapse?
Are they cures?
In some - Yes
23% recovered immediately after CBT
25 % recovered 5 years after CBT
(compared to 5 % without treatment)
Fears of behavioural approaches
• 50% report being worse after graded exercise therapy in a patient charity survey
• CBT means “it’s all in my mind”
What’s the problem?“..when it comes to ICD10 G93.3 Myalgic
Encephalomyelitis, the somatoform psychiatrists are fundamentally wrong. Meanwhile the "fatigue" clinics will ….. be fiddling with ME patients - testing them with nothing other than psychological interventions that do not address the underlying biomedical abnormalities in people with Myalgic Encephalomyelitis.”
Banishing fears of behavioural approaches
• Those reporting harm with GET had not received appropriately supervised graded exercise therapy, and diagnosis uncertain.
• CBT is associated with 5 mls increase in grey matter in the brain and normalisation of HPA axis.
What we don’t know
• Why do some not improve?• Is pacing as effective?• How about therapy AND good medical care?• Mediators• Moderators
Pacing, graded Activity and Cognitive behaviour therapy: a
randomised Evaluation
White PD, Sharpe MC, Chalder T, (PIs)
Aims
• Efficacy and adverse effects• Health economics and societal costs• Moderators• Mediators
Problems and solutions
How to define the illnessOxford criteria – widest generalisationStratify by CDC and ME – most different
ModeratorsStratify by comorbid major depression
What are the outcomes?Both symptoms and disability
Inclusion criteria
Chalder Fatigue Questionnaire score is 6 or more
SF-36 physical function sub-scale score is 65 or less
> 17 years old
Exclusion criteria
• Medical exclusions• Risk of self harm and other exclusionary
psychiatric diagnoses, assessed by SCID• Those unable to do therapies e.g. language
problems
Treatments
• Manualised• Each based on different model
– 1st session 90 minutes and subsequent sessions up to 50 mins
– 14 + 1 booster follow up session at 36 weeks– Some by telephone if necessary
Integrity of therapy
• Group and individual supervision• Manuals – patients and therapists• Pilot patients• Measuring competency• Listening and rating tapes throughout trial• What happens when some-one leaves • Measures of treatment adherence
Primary Outcomes
• Summary stats on fatigue and disability• Clinically significant?
Fatigue (50% reduction in fatigue or a score of 3 or less)
SF-36 (a score of 75 or 50% increase from baseline)
Secondary outcomes
• Other CFS criteria & symptoms (ME)• Clinical Global Impression change score• Adverse effects• Activity and fitness• Mood• Sleep• Economic
Adverse Events
• Serious adverse events (SAEs)• Serious adverse reactions (SARs)• Non serious adverse events• Follow up after adverse events• Policy for deteriorating participants
What PM thought about PACE
“As will all serious illnesses, it is important that patients, their families and the healthcare professionals looking after them have the best scientific information available and the PACE trial has been designed to help them decide for themselves what treatment is likely to be best from them.”
www.number-10.gov.uk/output/Page14656.asp
Recruitment problems
• New centre • Extending trial• Publicity• Prime Minister’s support!
Other trial difficulties
• Departures from protocol• Additional therapy during & after the trial• Absence of a therapist (holidays, sick leave,
maternity cover)• Recruitment and training of new therapists
Treatment issues
• Ownership• Non-specific therapist effects• Ensuring equipoise• Doctors!
• 641 patients• 3% drop out from follow up• 6% drop out from treatment• Follow up ends in December• Results autumn 2010?
Conclusions
• Individually delivered CBT and GET are the best evidence based treatments
• We should offer them to all our patients• Which treatment for which patient?• Can we do them more quickly?• Can we do better?
PeterWhite,CFS:neurological,psychologicalorboth?
THEBRITISHNEUROPSYCHIATRYASSOCIATIONwww.bnpa.org.uk
NeurologyandPsychiatrySpRsTeachingWeekend12to14December2008StAnne’sCollege–OxfordWoodstockRoad,OX26HS
THEESSENTIALSOFNEUROPSYCHIATRYTheBritishNeuropsychiatryAssociation
NeurologyandPsychiatrySpRsTeachingWeekend12to14December2008StAnne’sCollege,Oxford
NeurologyandPsychiatrySpRsTeachingWeekend.Handbook.www.bnpa.org.uk
WelcomeIntroductionNeurologistsandpsychiatristsbothcareforpatientswithdisordersofthebrainand its functions, yet there is remarkably little common training in the twodisciplines.Thereisoftenbothaculturalandphysicaldividebetweenthe ‘careofthebrain’andthe ‘careofthemind’.Theaimofthisweekend,thefirstof itskind, is to bring together roughly equal numbers of neurology and psychiatrytrainees, for a course that will cover the more basic aspects of assessment –history taking and examination – in the two specialties, review the use of thecommonapproachestoinvestigation,andthencoveraseriesofmajortopicsinneuropsychiatry, particularly in areas that tend to be neglected, such as‘functional’orsomatoformdisordersanddisordersofsleep.Weaimtoinspireaswell as instruct, so we have leavened the mix with some talks that will giveglimpses of exciting current research on mind and brain. We hope that themeetingasawholewillbeinformalandhighlyinteractive.Thisanewventure for theBritishNeuropsychiatryAssociationwhichexists tofoster education in the middle ground between these disciplines. Our mainactivity is to hold an annual two‐day meeting, in February, which, uniquely,attractspsychiatrists,psychologistsandneurologists.Ifyouenjoythisweekend,whynot join theBNPA, and come toour2009meeting (5‐6thFebruaryat theInstituteofChildhealth)?We are very grateful to UCB and Biogen for substantial support fromunrestrictededucationalgrantswhichhavekeptdownthecostofthemeeting.AdamZemanBNPAChairman
TheBritishNeuropsychiatryAssociationNeurologyandPsychiatrySpRsTeachingWeekend
12to14December2008StAnne’sCollege,Oxford
NeurologyandPsychiatrySpRsTeachingWeekend.Handbook.www.bnpa.org.uk
Chronicfatiguesyndrome:neurological,psychologicalorboth?
PeterWhite,ProfessorofPsychologicalMedicine,BartsandtheLondonMedicalSchool
[email protected] isacommonsymptominboththecommunityandprimarycare.Whenasked,between10and20percentofpeopleinthecommunitywillreportfeelingabnormally tired at any one time. At the same time, fatigue is continuouslydistributedwithinthecommunity,withnopointofrarity.Thereforeanycut‐offis arbitrary and the prevalence will vary by how the question is asked, thesymptom volunteered, and its context. Between 1.5% and 6.5% of Europeanpatients will consult their general practitioner with a primary complaint offatigueeveryyear,theincidencevaryingbyageandpopulation.Fatigueismorecommonly reported andpresented to general practitioners bywomen and themiddle‐aged,and ismostcloselyassociatedwithmooddisordersandreportedstress.ItdoesnotseemtovarybyethnicityintheUK,butthereisanintriguingparadoxinthatitisreportedmorecommonlybythoseinhighincomecountries,yetispresentedtomedicalcaremoreofteninlowincomecountries.Prolongedorchronic fatigue is significantly lesscommonthan thesymptomoffatigueanditisonlyinthelast10yearsthatconsensushasemergedabouttheexistence of a chronic fatigue syndrome (CFS), also called myalgicencephalomyelitis (ME). CFS is now accepted as a valid diagnosis by medicalauthoritiesintheUK,intheUnitedStatesofAmerica,aswellasinternationally.Aboutonethirdofpatientspresentingtotheirdoctorwithsixmonthsoffatiguewill meet criteria for a chronic fatigue syndrome. The other two thirds havefatiguesecondarytoanothercondition,mostcommonlymoodandprimarysleepdisorders. Its primary symptom is fatigue, both physical and mental, whichparticularly follows exertion.Other symptoms agreed in consensual guidelinesinclude poor concentration and memory, sleep disturbance, headache, sorethroat, tender lymphglands,muscleand jointpain.Thereare several criterionbaseddefinitionsofCFS.Thesedefinitionswerederivedbyconsensusandhavenotbeensupportedbyempiricalstudies,andcontinuetoberefined.Theirutilitystems fromproviding reliable criteria for research studies, rather than clinicaluse. The prevalence of CFS is between 2.5 % and 0.4 % depending on thedefinition used and whether comorbid mood disorders are excluded (that is
mood disorders that are not thought to be the primary diagnoses). It ismostcommoninwomen,themiddle‐aged,andethnicminorities(unlikefatigue)–atleastinEnglishspeakingcountries.ThediagnosisandclassificationofCFSThe clinical taxonomy for CFS is amess. The ICD‐10 classification defines CFSwithin both the neurology chapter and mental health chapters. Myalgicencephalomyelitis, the alternative name for CFS, is classified as a neurologicaldisease (G93.3)(a.k.a. post‐viral CFS), whereas neurasthenia (a.k.a. CFS nototherwise specified) is classifiedwithinmentalhealth (F48). (Incidentally, thismess is not specific to CFS, since there are several conditions within theneurology chapter of ICD‐10 that are also classified in the mental andbehavioural disorders chapter. For instance, Alzheimer’s disease is classifiedwithin neurology, whereas dementia due to Alzheimer’s disease is classifiedunder mental health. My personal view is that it is high time that all mentalhealth disorders and neurological diseases affecting the brain were classifiedwithin the same chapter, simply called diseases/disorders of the brain andnervous system.) There is also a current debate between “lumpers” and“splitters” about the nosology of “functional” somatic syndromes (symptomdefined conditions), such as CFS, IBS and “fibromyalgia”. Some argue that thecloseassociationsbetweenthesyndromes(thosewithCFSarealsomorelikelyto have fibromyalgia and/or IBS) argues in favour of their being differentmanifestations of one over‐arching functional somatic syndrome (the“lumpers”).Othersarguethatthesesyndromesarebestunderstoodbyexploringtheir heterogeneity (the “splitters”). There is evidence to support botharguments,buttwolargeandrecentepidemiologicalstudiessuggestthatchronicunexplained fatigue, for one, is both associated with and separate from other“functional” somatic syndromes. In particular, predisposing risk factors aresharedwhereastriggeringfactorsaredifferent.CFSisnotaneasydiagnosistomake,sincemisdiagnosisiscommoninpatientsdiagnosedashavingCFS.ArecentauditofmyCFSclinicrevealedthat4outof10newpatients(n=250)assesseddidnothaveCFS,andthatwasafterathirdofreferrals had already been rejected as not being CFS. The most commonmisdiagnoses were mood disorders, especially depressive disorders, andprimarysleepdisorders,particularlysleepapnoea.Othermisdiagnosesincludedcoeliacdiseaseandautoimmuneconditions.Alternativeneurologicaldiagnosesweremadein2%.AetiologyandpathophysiologyThe aetiology of CFS is unknown, but there is evidence that different riskmarkersareassociatedwithpredisposition, triggering,andmaintenanceof theillness. Predisposing risk markers include female sex, middle age, mooddisorders(especiallydepressivedisorders),othersymptomdefinedsyndromes,such as irritable bowel syndrome, and possibly either sedentary behaviour orexcessive activity. As might be expected CFS patients are more likely to haveattended their GP, than healthymatched controls, even up to 15 years before
onset,but recentwork shows that thosewith IBS (andnoCFS)have the sametendency.Triggeringriskmarkersarelesswellestablished,butthereissufficientevidencetosupportcertaininfectionsasaetiological factorsnotonlyforfatiguebutalsoCFS,with thebest replicatedevidence supportinga role forEpstein‐Barrvirusinfection, which triggers CFS in 10% of those infected. Maintaining orperpetuating risk markers are most important in determining treatmentprogrammes, since reversingmaintaining factors should lead to improvement.Reasonablywellestablishedfactorsincludemooddisorders,suchasdysthymia,illness beliefs such as believing the whole condition is physical, pervasiveinactivity,avoidantcoping,membershipofapatientsupportgroup,andbeinginreceiptofordisputeaboutfinancialbenefits.Few pathophysiological findings in CFS have been replicated in independentstudies. Those that have been include down‐regulated hypothalamic‐pituitary‐adrenal axis, physical deconditioning, and discrepant reports betweenperception of symptoms and disability and their objective tests. The latterfindingisnowsupportedbyfunctionalbrainscanningstudiessuggestingalteredbrainactivitywithspecifictasks.Thediscrepancybetweensubjectivestatesandobjectivetestshasbeenfoundbeforeinothersymptomdefinedsyndromes,suchas“fibromyalgia”,andmayberelatedtoenhancedinteroception(theperceptionof visceral phenomena), a concept first described by Charles Sherrington in1904.Onehypothesiscurrentlybeingtestedisthatthecommonpredispositionto“functional”somaticsyndromesiscausedbyenhancedinteroception.Recentworksuggeststhatthesefactorsmaybereversedbyrehabilitation.PrognosisWithout treatment the prognosis of CFS is poor with a systematic review ofoutcomesfindingthemedianfullrecoveryratewas5%(range0–31%)andthemedian proportion of patients who improved of 39.5% (range 8–63%). Beingyounger,havinglessfatiguebaseline,asenseofcontroloversymptomsandnotattributingillnesstoaphysicalcausewereallassociatedwithabetteroutcome.Theprognosisisconsiderablybetteraftertreatment.TreatmentTheNICEguidelines, published in2007,werebasedonanupdated systematicreview.Theessenceofspecialistcareisrehabilitation,providedonanindividualbasiswithanappropriatelyqualifiedandtrainedtherapist.Thetwoapproacheswiththegreatestevidenceofefficacyarecognitivebehaviourtherapy(CBT)andgradedexercisetherapy(GET).Approximately60%ofpatientsreportsignificantimprovementwiththeseapproachesandabout25%reportfullrecovery,whichlasts. No pharmacological treatments are recommended (antidepressants areineffective),but symptomaticpharmacotherapy for specific symptoms (suchaspain) or comorbid conditions (such as depressive illness) can be helpfulcomplementarytreatments.
These rehabilitation approaches have not received universal approval frompatient charities, with concerns that patients may be harmed by exercisetherapiesorthatCBTimplyingthattheconditionispsychological.IsCFSneurologicalorpsychological?This is a nonsensical question when one considers the neuroscience ofconsciousness and recent advances in functional brain physiology. Thephilosopher, John Searle, stated the answer to this Cartesian dualism that stillbedevilswesternmedicine. “Consciousstatesarecausedbyneurophysiologicalmechanisms,andarerealisedinneurophysiologicalsystems.”Thereforeitisnotpossible to have a psychological process or event without a neurologicalmediatingprocess.Itisneitherofthemindorbody;itisboth.FatiguesecondarytoneurologicaldiseasesFatigueiscommonlyassociatedwithchronicmedicaldisorders,butitshouldbedifferentiatedfromfatiguability.Fatiguabilityistheonsetofaphysicalsensationof fatigue and weakness after exertion and is commonly reported withneurologicaldiseasessuchasmultiplesclerosisandmyopathies.Apartfrommeasuresofdiseaseactivity,otherassociationsofsecondaryfatiguein general that have been repeatedly found include sleep disturbance, mooddisorders, inactivity and physical deconditioning. Studies of fatigue associatedwith multiple sclerosis are instructive and exemplary. As in all studies ofsecondary fatigue,measures of the severity or pathophysiology of the diseaseitselfareassociatedwithfatigue.Somecytokinesareassociated,butothersarenot. Associations vary depending on the fatigue measure, confirming themultidimensional nature of fatigue, but all measures are associated withdepression. Objectively confirmed sleep disturbance is also associated withfatigue. Fatigue associated with MS therefore requires biopsychosocialmanagement.Therehavebeenanumberofstudiesofvarious treatmentsaimedatreversingthe associations of secondary fatigue in general, in the hope they would helpfatiguedirectly,withvariableresults.AswithCFS,themostconsistentevidenceofefficacyhasbeenwithgradedexerciseprogrammesandCBT.BibliographyAttarianHP,BrownKM,DuntleySP,etal.Therelationshipofsleepdisturbancesandfatigueinmultiplesclerosis.Arch.Neurol.61(2004),525–8.Baker R, Shaw EJ. Diagnosis andmanagement of chronic fatigue syndrome ormyalgicencephalomyelitis(orencephalopathy):summaryofNICEguidance.BMJ2007doi:10.1136/bmj.39302.509005.AEChambersD,BagnallA‐M,HempelS,ForbesC. Interventions for the treatment,management and rehabilitation of patients with chronic fatigue
syndrome/myalgicencephalomyelitis:anupdatedsystematicreview.JRSocMed2006;99:506‐20.CleareAJ.Theneuroendocrinologyofchronicfatiguesyndrome.Endocr.Rev.24(2003),236–52.FlacheneckerP,Bihler I,WeberF,etal.,CytokinemRNAexpression inpatientswithmultiplesclerosisandfatigue.Mult.Scler.10(2004),165–9.FulcherKY,WhitePD.Strengthandphysiologicalresponsetoexerciseinpatientswith the chronic fatigue syndrome. J. Neurol. Neurosurg. Psychiatry69 (2000),302–7.JoyceJ,HotopfM,WesselyS.Theprognosisofchronicfatigueandchronicfatiguesyndrome:asystematicreview.Q.J.Med.90(1997),223–33.KroenckeDC,LynchSG,DenneyDR.Fatigueinmultiplesclerosis:relationshiptodepression,disability,anddiseasepattern.Mult.Scler.6(2000),131–6.LyallM,PeakmanM,WesselyS.Asystematicreviewandcriticalevaluationoftheimmunologyofchronicfatiguesyndrome.J.Psychosom.Res.55(2003),79–90.National Institute for Health and Clinical Excellence. Clinical guideline CG53.Chronic fatigue syndrome/myalgic encephalomyelitis (or encephalopathy):diagnosisandmanagement.London,NICE,2007.http://guidance.nice.org.uk/CG53.Reevesv WC et al. Identification of ambiguities in the 1994 chronic fatiguesyndrome research case definition and recommendations for resolution. BMCHealthServRes3(2003),25.Romani A, Bergamaschi R, Candeloro E, et al., Fatigue inmultiple sclerosis:multidimensional assessment and response to symptomatic treatment. Mult.Scler.10(2004),462–8.M.C.Tartaglia,S.Narayanan,S.J.Francis,etal.,Therelationshipbetweendiffuseaxonaldamageandfatigueinmultiplesclerosis.Arch.Neurol.61(2004),201–7.Wessely SC, Hotopf M, Sharpe M. Chronic Fatigue and its Syndromes (Oxford:OxfordUniversityPress,1998).WesselyS,NimnuanC,SharpeM.Functionalsomaticsyndromes:oneormany?Lancet354(1999),936–9.WesselyS,WhitePD.Indebate:thereisonlyonefunctionalsomaticsyndrome.Br.J.Psychiatry185(2004),95–6.WhitePD,ThomasJM,KangroHO,etal.,Predictionsandassociationsoffatiguesyndromes and mood disorders that occur after infectious mononucleosis.
Lancet358(2001),1946–54.WhitePD,SharpeMC,ChalderT,DeCesareJC,WalwynR;onbehalfofthePACEtrialgroup.ProtocolforthePACEtrial:arandomisedcontrolledtrialofadaptivepacing, cognitive behaviour therapy, and graded exercise, as supplements tostandardisedspecialistmedicalcareversusstandardisedspecialistmedicalcarealoneforpatientswiththechronicfatiguesyndrome/myalgicencephalomyelitisorencephalopathy.BMCNeurol2007;7:6.
Cognitive and behavioural
treatments for functional somatic
syndromes
Peter White & Kate Harri
London 2012
Agenda
• Do these treatments work?
• Do treatments help occupation?
• An example of CBT for pain
• Predictors
• Mediators
Risk markers for prolonged CFS
Fatigue, symptoms, mood disorders,
physical illness beliefs, pervasive
inactivity, sleep problems
Risk markers for prolonged whiplash
- Unexpectedness
- low education, female
Pain, symptoms, ↓ROM, passivity,
psychol. Distress
SJ Kamper et al, 2007
Risk markers for musculoskeletal
pain in primary care
- Pain, past history, multiple sites
- Passivity, psychol. distress
- ↓ROM and disability
- Social adversity
CD Mallen et al, 2007
Initial infection
Rest or “boom & bust
Bodily adaptation
Sleep problems
Fatigue
Beliefs
Biopsychosocial model of CFS
CBT for pain disorders
Effect sizes versus waiting list controls
Pain 0.40
Depression 0.36
Activity 0.46
Social function 0.60
RTW ????
S Morley et al, Pain, 1999
CBT & GET for CFS
Effect sizes for function
CBT 0.36
GET 0.39
RTW ????
BD Castell et al, 2011
CBT for fibromyalgia
Effect sizes
Pain 0.47
Function 0.42
RTW ????
JA Glombiewski et al, 2010
GET for fibromyalgia
Effect sizes
Pain 0.31
HRQOL 0.40
RTW ????
W Hauser et al, 2010
RTW after MDT for CWP: women JS Skouen et al, 2006
Physical function
30
4
0
50
6
0
70
Ph
ysic
al F
un
ctio
n S
core
Time
SMC GET APT CBT
Main treatment phase Follow up phase
Remission in PACE
0
5
10
15
20
25
APT CBT GET SMC
%age
%age
Healthcare cost-effectiveness
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
0 5000 10000 15000 20000 25000 30000 35000 40000 45000 50000 55000 60000
QALY threshold (£)
Pro
bab
ilit
y t
hat
inte
rven
tio
n i
s m
ost
co
st-
eff
ecti
ve
SMC
CBT
GET
APT
Informal Care and Lost Employment in PACE
APT CBT GET SMC
Informal care hours per week 11.0 8.0 7.7 11.4
Informal care cost (£s) 6196 4008 4073 6507
Lost employment % 86 84 86 89
Lost employment cost (£s) 14,865 13,958 14,638 14,157
P McCrone et al, 2012
Societal cost-effectiveness
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
0 5000 10000 15000 20000 25000 30000 35000 40000 45000 50000 55000 60000
QALY threshold (£)
Pro
ba
bilit
y t
ha
t in
terv
en
tio
n is
mo
st
co
st-
eff
ec
tiv
e
CBT
GET
SMC
APT
CBT & GET have moderate
efficacy but only modest effects
in helping RTW after FSS
What moderates response to
behavioural treatments?
Moderators of non-response to GET or
CBT for CFS
• Membership of a self-help group
• Severity of fatigue
• Sickness benefit
• High combined mood score
• Involvement in legal proceedings to achieve
disability benefits
• Not duration of illness!
R Bentall et al, 2002
J Prins et al, 2003
Moderators of non-response to CBT
for pain
• More pain and pain sites
• Depression
• Rumination
• Catastrophising
• Life difficulties
JA Turner et al, 2007
Disability insurance claims:
return to work
Diagnosis %
CFS/ME 14
Depression 18
Low back pain 22
Swiss Re, 2001
FSS insurance claims
1. Interpersonal clash at work
Domestic responsibilities
2. Never referred for treatment
No CBT/GET available locally
Already received “CBT” and/or “GET”
3. Dr X – “mitochondrial disease”
Prof Y – “Fibro is incurable… and [X] will never
return to work”
Social risks
“If you have to prove you are ill, you can’t get
well.” (N Hadler, 1996)
“ME is an incurable disease.”
What mediates response to
behavioural treatments?
Mediators of response to GET or CBT
for CFS
• Treatment dose (number of sessions)
• Reduction in symptom focusing
• Reduction in fear avoidance
Not increased activity
Not increased fitness
Not change in cognitions
Not change in mood
Mediators of response to CBT for pain
• Treatment dose
• Increased perceived pain control
• Reduction in serious pain beliefs
• Reduced catastrophising
• Increased self-efficacy
Conclusion
• Biopsychosocial model best fit for FSS
• Rehabilitation based treatments are moderately helpful, but are not aimed to help RTW
• Their effect on occupation is mild to moderate
• Targets for more effective rehab include attitudes & beliefs of doctors, employers, and patients, as much as developing more vocationally targeted treatments.
ME or CFS: Belief or science?
Peter White
Barts and the London
RCPsych Liaison Psychiatry Conference
29/02/12 - 02/03/12
My most recent new patient
50, single woman
Unwell since aged 21 – mumps
Diagnosed “ME” aged 30
“Classical ME” aged 40
“ME has ruined my life – no career,
no relationship, no children
History of many years exhaustion,
poor sleep, low self-esteem, low
mood, anxiety, fear of falling when
away from home, “brain fog” (71
symptoms)
Serious suicide attempt aged 45
Treatments - B12, 5 sessions of
occupational therapy, 75 mg
venlafaxine, CAM
MSE - miserable, anxious, constant
suicidal thoughts, poor eye contact,
derealisation, depersonalisation
Pulse 100 bpm, tremor
Beck depression 51/63
HADS depression 18/21
HADS anxiety 18/21
Diagnosis of severe and chronic
major depressive disorder, with
panic attacks with agoraphobia,
with derealisation
“But I need treatment for my ME; I
am not mad; I won’t go and see a
psychiatrist.”
“Tragic tale of woman with
chronic fatigue syndrome 'too
tired' to eat”
Derby Telegraph
Monday
“She had battled for years with chronic fatigue syndrome.. (no Rx 5 years)
“A post mortem examination showed she weighed 3st 2lbs when she died..
“Mr O said L's loss of appetite was caused by a lack of energy, but medics said she had anorexia.
“Why did they insist on the "anorexia" label? It is well documented that people with severe ME become too tired and weak to eat..
The right diagnosis
40% of patients attending a CFS clinic did
not have CFS.
J Newton et al, 2010
49% of patients attending a CFS clinic did
not have CFS.
Devasahayam et al, 2012
CFS
(N=1,423)
Co-morbid depression 32%
Co-morbid anxiety 32%
Irritable Bowel Syndrome 29%
Fibromyalgia/Chronic
Widespread Pain
28%
Migraine 21%
Chronic Regional Pain Disorder 3%
Co-morbid medical conditions
RPE on a light cycle test (sedentary controls)
Perception of effort with exercise
• Sleep disturbance
• Mood (both depression and anxiety)
• Aerobic fitness and strength
• Somatic focusing
• Introversion
• Emotionality
Subjective more than objective
A global discrepancy between the subjective and objective:
• Effort with exercise versus work done
• Reported disability versus physical activity
• Cognition: symptoms versus tests
• Insomnia versus polysomnography
Beliefs are associated with outcome
• Physical illness
• Viral illness
• Exercise is dangerous or damaging
• Family and partner’s beliefs
Predictions of non-response to GET
• Membership of a self-help group
• Sickness benefit
• High combined HADS score
R Bentall et al, 2002
Prediction of non-response to CBT
• Involvement in legal proceedings to achieve disability benefits
J Prins et al, 2003
The effect of a doctor’s “ME” label on prognosis
• “ME” lasted longer than “CFS”.
• “ME” patients had more consultations both in general and specifically for fatigue.
• No differences before diagnosis
Beliefs of doctors determine behaviour
• 32 single woman, attended with mother
• Unwell with ME since 18
• ME “caused by Lyme disease”
Beliefs of doctors determine behaviour
• 32 single woman, attended with mother
• Unwell with ME since 18
• ME “caused by Lyme disease”
• Hearing voices since 18
• Passivity experiences
• Thought broadcast
• Abulia
Beliefs of doctors determine behaviour
• Spoke with mother
• Confirmed “voices”, but also convinced of Lyme disease
Beliefs of doctors determine behaviour
• Spoke with mother
• Confirmed “voices”, but also convinced of Lyme disease
• St Elsewhere’s week later for CSF and antibiotics, in spite of my diagnosis of schizophrenia
• In spite of my calling GP urgently
Beliefs of doctors determine behaviour
• One year later, I was copied into a letter from a psychiatrist..
Beliefs of doctors determine behaviour
• One year later, I was copied into a letter from a psychiatrist..
• “I agree she has a schizophrenia like illness, but I understand she has Lyme disease, which is the likely underlying cause, and I would advise re-referral to a Lyme disease specialist.”
Doctor’s attitudes to MUS patients
188 GP patients
• Rejecting (most common)
• Colluding
• Empowering (least common, most useful)
P Salmon et al, BMJ, 1999
Can the science help us?
• Predisposition - female, childhood trauma, other FSS,
depression
• Precipitated by various stressors – especially infection
(glandular fever, meningitis etc), life events
• Perpetuated by behavioural and psychological factors, and their
physiological consequences on fitness, sleep, and HPA axis
CFS: What do we know?
R Gracely et al, 2002
Brain activation in fibromyalgia - case
control
CBT is associated with increased grey matter
De Lange F et al, 2008
Bart’s Pilot Study Results
White et al. 2004
* * * * *
CBT is associated with improved HPA
Roberts A et al, 2008
Initial infection
Rest or “boom & bust
Bodily adaptation
Sleep problems
Fatigue
Beliefs
Yes, it’s the biopsychosocial model
Liaison psychiatrists to the rescue!
• Liaison psychiatrists are what is left of general physicians, physicians themselves being super-specialised.
• We need to have the confidence to combine the science with our therapeutic skills to explain, empower and engage with our patients.
• Beliefs can change; science will help, since “knowledge is power”.