Beyond Psychiatric diagnosis. Sami Timimi

Transcription

1 Beyond Psychiatric diagnosis Sami Timimi

2 A game of semantics What is ADHD? What is diabetes? This kid can t concentrate and is hyperactive, what is causing that? How do you know its ADHD?

3 Why are we waiting? Robins and Guze (1970) predicts laboratory studies, including chemical, physiological, radiological, anatomical, and psychological tests. Kendler (1980) overview confirmed that early biological studies failed to establish the construct validity of schizophrenia and other diagnoses. Andreasen (1995) promises future riches through molecular genetics, neurochemistry, neuroanatomy, neurophysiology and neuro-imaging, but concedes that the long-hoped-for laboratory tests anticipated by Robins and Guze (1970) had not materialised. Goodyer (2011) If I was to stand up in the 21st century and describe diabetes as the only disorder by which you could present with polydipsia, polyuria and weight loss I am not quite sure what the audience would think. If I was then to proceed in describing on the basis of randomised controlled trials where I would select the individuals who may have polydipsia, polyuria and weight loss without any kind of pathophysiological test.. I think I might be in a lot of trouble as a scientist, possibly as a clinician. But I can do that in psychiatry

4 Aetiology No markers. No cause identified. Cause implied in PTSD, but trauma common. Depression excludes bereavement but not other losses. Genetics rejecting categories.

5 Breaking News "This is really exciting because it gives us the first direct genetic link to ADHD. Now we can say with confidence that ADHD is a genetic disease and that the brains of children with this condition develop differently to those of other children," she said.

6 What did they really find? Found 14% with ADHD have deleted or replicated genes (Copy Number Variants - CNVs), as do 7% controls (leaves 7%). 36% in those with Intellectual Disability. 11% ADHD with no intellectual disability (leaves 4%). Average IQ in ADHD group 86 (leaves?0%). If have CNVs 1 in 25 chance of ADHD. Conclusion: strong association between low IQ and increased CNVs. Probably none with ADHD per se. Elevated risk of increased CNVs associated with, autism, schizophrenia, ADHD, bi-polar (not depression/ anxiety) mainly accounted for by IQ.

7 Genetics Assumed high heritability based on twin studies. Ignores EEA. Many research teams have searched for genes that may be involved. They haven t turned up any prime candidates yet, only dozens, maybe hundreds of bit players (Hughes, 2012) First Genome Wide Association Studies (GWAS) on autism implicated two regions with mild effects.. subsequent GWAS failed to turn up any parts of the genome with statistical significance (Williams, 2012). The recent 'breakthroughs' proposing a common genetic pathways in psychiatric disorders (Cross-Disorder Group of the Psychiatric Genomics Consortium, 2013 ) was only able to explain between 1 and 2% of the variance in any of the target disorders (ADHD, ASD, Bipolar Disorder, Major Depressive Disorder, and Schizophrenia). Given the sample size they used (over 30,000) the findings have no clinical significance.

8 Neuroimaging in ADHD NICE note the lack of consistency found in neuroimaging studies and conclude that the following brain regions may be implicated: left prefrontal cortex, left thalamus, right paracentral lobule; frontal, temporal, and parietal lobes; the striatum; splenium of the corpus callosum; right caudate; total cerebral volume; right cerebral volume; and portions of the cerebellum. The guidelines also notes It was not possible to include or exclude the role of medication in the observed changes to brain volume and structure (NICE, 2008). Non medicated v age matched control not yet done. maturational delay of several years in a series of ADHD patients as compared with controls. Brain maturation did catch up with controls after a lag of 2 to 3 years (Shaw et al, 2007; Nakao et al, 2011).

9 Neuroimaging in autism Lack of consistently replicated findings. e.g. studies documented an increase in cerebellar volume, smaller than average, and no significant differences. sample heterogeneity (such differences reflecting IQ differences) regular problem. Technical challenges: Brain connectivity theory replicated by head movement. Until its biological basis is found, any attempts to use brain imaging to diagnose autism will be futile Lange (2012).

10 Validity Fails to uncover features that distinguish natural boundaries. Rules regularly broken (e.g. bereavement even when symptoms of depression fulfilled) High co-morbidity. Circular thinking. Descriptors fail to explain. Poor correspondence with impairment.

11 DSM 5 Psychotherapy is the only form of treatment which, at least to some extent, appears to create the illness it treats Jerome Frank (Frank, 1961). Reliability: To say that we've solved the reliability problem is just not true It's been improved. But if you're in a situation with a general clinician it's certainly not very good. There's still a real problem, and it's not clear how to solve the problem" Robert Spitzer, lead editor of DSM III (Spiegel, 2005). Validity: There is no definition of a mental disorder. It s bullshit. I mean, you just can t define it these concepts are virtually impossible to define precisely with bright lines at the boundaries. Allen Francis, lead editor of DSM IV (Greenberg, 2010). Creates illnesses Reliability poor Its bullshit

12 Reliability Rosenhan s 1973 study highlighted reliability. DSM-III claim improved reliability. Field studies, no uniformly high reliability. Reliability no different to pre-dsm-iii in clinical settings. DSM 5 field trials no condition achieved a convincing level of reliability. Your diagnosis depends on who you see more than what you have.

13 Prognosis No improvement in long term outcomes. Big increase in numbers on long term disability due to mental illness. Many diagnoses conceived as life-long chronic disorders. Stigma increased by illness like any other illness model. Internal stigma associated with worse outcomes.

14 Public policy impact Epidemiology finds high rates of mental illness. Lower rates of treatment interpreted as unsatisfactory case detection. Campaigns such as Defeat Depression did not improve outcomes, but increased medicalisation. Australia increase in knowledge accompanied increase in rates of major depression and decrease in quality of life. Poor knowledge - a protective factor. Psycho-education for depression in schools increased likelihood of depressive thoughts. Developed societies have poorest levels of mental well-being.

15 Treatment Matching treatment to diagnosis minimal impact on outcome. The technical model brought splenectomy, insulin coma, lobotomy and neuroleptics. Common factors more important in predicting outcome: extra-therapeutic and quality of alliance. Drug treatment. Same drug used across categories. Evidence Supported Treatments (EST) approach comes down to who has the will and the money.

16 Predicting outcomes Patient/Extratherapeutic/Factors/(87%)/ Feedback/Effects/ //15A31%/ Treatment/Effects/ ///13%// Alliance/Effects/ ///////38A54%// Model/Technique....8%. Duncan, B. (2010). On becoming a better therapist. Washington DC: American Psychological Association Therapist/Effects/ /////////46A69%/ Model/Technique/Delivered:/ Expectancy/Model/Technique/Delivered:/ Expectancy/Allegiance/ Rationale/Ritual/(General/Effects)/ //////////////30A?%/ /

17 Diagnostic Paradigm Social position Cultural issues Focus on technology of diagnosis and treatment relationships Ethics and values

18 Post-technological paradigm Training priorities Use of drugs and therapy Discourse centred on: -values/ethics -meanings/contexts -relationships/power Appropriate research Service models

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20 Partners for Change Outcome Management Systems (PCOMS) Norway couples therapy. Feedback v TAU; Both persons reliable or sig. change 50.5% v. 22.6%. FU v TAU-34.2% v. 18.4% Feedback sep./ divorce rate. 2 independent US based studies. Feedback group doubled controls (10.4 vs. 5.1 points)

21 PCOMS in real clinical settings Community Health and Counselling Services in Maine: Number of patients seen for more than one year from 655 (pre-pcoms) to 321 (post-pcoms). Number patients seen more than two years from 227 (pre-pcoms) to 94 (post-pcoms). No Shows down by 30%. Southwest Behavioral Health Services, Arizona: Average length of an episode of care in children s services from 315 days to 188. Length of stay in adult 322 days to 158. No shows down by 47%. Center for Family Service, Florida.. Using 40% fewer sessions to achieve program goals. No shows down by 25%.

22 OO-CAMHS CORE principles CONSULTATION: pay attention to extra-therapeutic factors OUTCOME: Monitor outcome session-by-session. If no change by session 5, review with patient and MDT. RELATIONSHIP: Monitor the alliance session-bysession. ETHICS OF CARE: Develop a whole team ethos. Teams are the drivers of change.

23 Data comparison April-Oct OO-CAMHS team 104 patients Over 2 years: 9% Over 1 year: 28% Non-OO-CAMHS team 168 patients Over 2 years: 34% Over 1 year: 58% Tier 4: 1% (1 pt.) Tier 4: 9% (15 pt.) DNA: 7% Cancellation: 11% DNA: 11% Cancellation: 10%

24 Whole service implementation

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