Thursday 16 May 2013

The DSM-5 and the Complexities and Capitalizing of Classification


Well it’s not actually a journal article but as everyone and their dog has an opinion on the launch of DSM-5 next week I thought I would pitch in as well.

First why bother with classification at all? We have classification because it is useful for communication and ultimately inevitable. The reason that it is inevitable is that once you recognize that some people share something in common that other people do not have – low mood or forgetfulness for example – you are creating a classificatory system. The other choices are everyone is unique (not that useful because it means you can’t apply lessons from one person to another) or that everyone is the same (again not that useful).

So given that we have to have a system of classification in medicine what should it look like? There are three choices – classification by symptoms, by course of the disorder or by aetiology.

Until the mid-19th century most disorders in medicine were classified by symptoms – so a reading of medical textbooks from the 1700s would have several chapters on different types of fever. This changed as more knowledge was gained about how the body worked and links were made between pathology and symptoms in life. For most medical disciplines the classification changed from symptoms to aetiology so that physicians today don’t diagnosis central crushing chest pain disorder (a symptom), they diagnosis a myocardial infarction (an aetiology). Classification by course of a disorder has been tried in medicine but is never really that successful as it can only be done retrospectively.

The reason that classification never shifted from symptoms to aetiologies in psychiatry is that the brain is the most complex organ in the human body (whose workings we still don’t fully understand), which is enclosed in a bony box (the skull), making it hard to study (unlike the heart or pancreas for example). So in psychiatry, with a few exceptions, we are still stuck with a symptomatic classification of disorders. The trouble with symptomatic classifications is that they are not really that powerful in helping decisions about treatment or prognosis – hence the focus on formulations in training psychiatrists which attempt to take a wider view of the aetiology and impact of disorders.

Which brings us to DSM-5  This is a classification by symptoms from a particularly U.S. point of view. The two big criticisms of DSM-5 are that it medicalizes what should be normal and that, while it pretends to be biomedical, the evidence for the biological basis for most disorders is lacking.

In my opinion there is considerable merit in the argument about DSM-5 being an attempt to medicalize the normal – a sort of “psychiatric mission creep”. The suspicion here is of the influence of pharmaceutical companies on the designers of DSM-5 to create new markets.

There are many examples of undeclared conflicts of interest, particularly in U.S. academic psychiatry, influencing the research agenda and the interpretation of research. The other financial conflict concerns the American Psychiatric Association who publishes the DSM. The drafting of DSM-5 has missed most deadlines except the final publication and launch date, leading to the suspicion that the APA is in poor financial straits and needs the DSM to come out now in order to collects the money it makes from its sales. 

The second argument about the DSM-5 is that it does not reflect biological reality and the comparison is often made with the rest of medicine. However, many disorders in medicine are equally subjective (pain for example) or their cause is obscure (headaches or migraines anyone?). Also disorders in other areas of medicine regularly undergo reclassification (epilepsy or acute coronary events come to mind).

Critics often condemn the “medical model” when what they really are referring to is a reductionist biological model that equates all disease with biological pathology. However, anyone who spends any time on a medical ward round or out-patient clinic will quickly discover that the “medical model” actually means integrating biology, psychology and sociology in a complete package.

So in psychiatry we are still left with a predominantly symptomatic classification to understand people who present with distress. Our focus should be on improving and defending services for such people and, as good clinicians, integrating psychology and biology to do something helpful.

The role of classificatory symptoms is often exaggerated – the best quote I have heard about them is that “they are like lines of longitude and latitude – nothing like them exists in the real world – but they are helpful in finding your way around”.

Monday 13 May 2013

Screening to Assess who is at Risk for Suicide Falls Short - Screening to Assess Depression Likely More Constructive in Managing the Risk of Suicide

Annals of Internal Medicine; Published first online April 23, 2013

Suicide and how to prevent it is a hot topic. From the evidence that we have, investing in primary care to improve the detection and treatment of depression would appear to be the place where you get the biggest bang for your buck. Depression is clearly related to suicide, so you would think that screening for suicide in primary care might be helpful in suicide prevention.

However, a recent systematic review of “Screening for and Treatment of Suicide Risk Relevant to Primary Care” in the Annals of Internal Medicine concluded that screening in primary care was of limited usefulness. The authors searched for English language studies only (again!) up to December 2012 which looked at two questions:

“What are the benefits and accuracy of screening instruments in primary care?”

“What is the effectiveness of suicide prevention interventions in primary care or mental health settings?”

Addressing the first question, the authors found five studies which showed no clear short term benefits (within two weeks) of screening and that the accuracy of screening instruments was poor. It should be noted that while the authors talk about screening, this is not screening as it would be applied to other disorders in medicine. In other disorders screening refers to the time between biological onset (say the presence of cancerous cells) and developing symptoms (for example breast lumps).

For screening to be effective, treatment given before symptoms develop needs to be more effective than treatment given after symptoms appear. Clearly if people respond positively to questions about suicide then “symptoms” have already developed, so what the authors are really talking about here is case finding rather than screening. Perhaps more effort should be put into screening people for depression rather than suicide specifically.

The second part of this review looked at interventions in both primary care and mental health settings that might reduce suicide risk. As one of the authors of a study included in this review I was interested to see their conclusions. What the authors found were 49 trials looking at reducing suicidal risk.

Psychotherapies reduced suicide attempts in adults but had little effect on suicidal ideas whereas interventions which tried to enhance usual care had little effect on suicide risk. Nearly all the studies were not done in primary care and recruited patients at high risk of suicide from general hospitals (usually people who presented with self-harm to the emergency department) so the results cannot really inform what to do with people detected as being suicidal in primary care.

So what next? Risk assessment tools do not predict who will commit suicide or repeat self-harm. What are needed are better risk management systems rather than yet another risk assessment form. Screening for depression and offering brief effective treatments – possibly computerized therapies – that can be used in primary care may prove to be a more useful strategy than simply screening to find “suicidal” people.

Wednesday 8 May 2013

Childhood Trauma and Abuse is the Smoking of Psychiatry

Annals of Internal Medicine 2013; 158(3): 179-190

Childhood trauma and abuse is the smoking of psychiatry. As a risk factor for mental illness it is comparable to how smoking a pack of cigarettes per day increases the risk of lung cancer and heart disease.

As an adult psychiatrist I see the consequences of poor starts to life and do my best to manage the consequences. However, doing my best often isn’t that effective or proves to be only a temporary solution. So the real question at hand is - what if we could do something to prevent child abuse from happening?

This is the question addressed in a systematic review published in the Annals of Internal Medicine in February this year. The authors update the US preventive services task force recommendations from 2004 on the prevention of child abuse and neglect. They reviewed the literature up until the middle of 2012 and found 11 randomised controlled trials which tested different interventions to prevent child abuse.

However, they only included English language studies and didn’t search outside MEDLINE, PsycINFO or the Cochrane Central Register of Controlled Trials which means non-English language studies were likely to be missed. (It seems strange that systematic reviewers ignore non-English language studies – is the implication that they are somehow less “good” than English language papers or that we can’t learn from “foreign” countries?).

The authors found one study in a paediatric clinic (although in other countries this would more likely be a family physician practice) which sought to identify and then refer those children up to age 5 at high risk of abuse and neglect. The program found that the intervention produced a significant reduction in child protective service reports up to four years after the child was seen. The evidence was less clear cut for various forms of home visits by nurses or “trained laypersons” up to three years after birth.

The conclusion of the review is that risk assessment and behavioural interventions in paediatric clinics reduced abuse and neglect for young children, but the evidence is inconsistent for home visitation programs. Plus, of course, it’s clear that additional research is needed.

This seems to be one of those areas where there is the choice between focusing on those at high risk or trying to address abuse at a population level – the classic Geoffrey Rose problem first articulated over salt and hypertension. Providing leadership through the development of infant mental health services may be one way forward.

Monday 6 May 2013

Antipsychotics Not the Answer for Treatment Resistant Depression

PLOS Med 2013; 10(3): e1001403

The so called atypical antipsychotics are no more effective than the older ones but the neuromuscular adverse effects have been replaced by metabolic ones.

One exception to this broad generalization is their use as an adjunctive treatment for treating depression, although there is a suspicion that this is a sign of “indication creep” for drugs which may be coming off patent. To address this, a systematic review raises its head in the March PLOS Medicine on-line Journal.

The authors identified 14 trials (all funded by drug manufacturers) where patients with depression who were “treatment resistant” were randomized to receive either an antipsycotic or placebo. The trials were short term studies ranging from 4 to 12 weeks and included aripriprazole, an olanzapine/fluoxetine combination, quetiapine and risperidone.

All four drugs had significant effects on remission and response (except the olanzapine/fluoxetine combination which did not affect response rates). However the effect was small with a mean difference of about 2.5 on the Montgomery-Asberg Depression Rating Scale. Additionally, on measures of quality of life the drugs had no or very small effect (with the exception of risperidone which had a small to moderate effect). Numbers needed to treat for remission compared to placebo were 9 for aripiprazole, quetiapine and risperidone and 19 for the olanzapine/fluoxetine combination.

Treatment was associated with weight gain, akathisia, sedation and abnormal metabolic laboratory results.

So would I have an antipsychotic if I had treatment resistant depression? Probably not and if I did I'd want to stop it pretty quickly.

Friday 3 May 2013

Association between Depression and Hospital Outcomes among Older Men

Canadian Medical Association Journal; 185.2 (Feb. 5, 2013) p117. 

It is a little known fact that the Canadian Medical Association Journal ranks at number 8 in the list of the world’s top medical journals as judged by impact factor. So to emphasize yet again that there is no health without mental health and the global nature of healthcare, in February the Journal published a cohort study of over 5400 Australian men.

These men were over 65 years old and were enrolled in the “Health in Men study” where they were assessed for depression at baseline on the Geriatric Depression Scale.  Two years later of the 339 men who scored more than 7 on the rating scale 152 (44.8%) had at least one non-psychiatric emergency hospital admission compared to 1164 of 5072 (22.9%) non depressed men.
The depressive symptoms also predicted whether these men were admitted to hospital (for non-psychiatric conditions), the number of admissions and the total length of stay. The system of separating mental health care from other aspects of health care is anachronistic and can no longer be supported by the evidence. Once funders recognize that taking into account the whole person improves quality and reduces costs this separation will increasingly be seen to be out of date and a sign of organizational stigma.

Thursday 2 May 2013

Discrimination against Depression

Lancet 2013; 381(9860)55-62

Maintaining the theme of having “global” in the title of every paper it publishes The Lancet produced a paper in January on discrimination experienced by people with depression around the world. The authors surveyed 1082 selected people with depression in 35 countries and found that four out of five experienced some form of discrimination.

The most common areas where people reported discrimination was by family members, friendships, marriage or divorce and keeping a job. Three quarters of people wished to conceal their depression from other people (in the medical profession I would suspect this figure would be higher).

It’s not entirely clear what the point of this paper is as the participants were not randomly selected but were approached by local research staff so the numbers are hard to generalize and should be taken with a pinch of salt. Nor did the authors report discrimination by country which would have been interesting to see how they stack up and might have generated ideas about how to address stigma.

Perhaps for clinicians reading this the take home message is to ask the question “Have you ever been discriminated against because of your depression or do you anticipate any discrimination”. I would guess the most likely areas this would apply would be at work or at the hands of the health system where discrimination against people with mental illness is rife.

Wednesday 1 May 2013

Putting Alzheimer’s on Ice?

New England Journal of Medicine 2013; 368:107-116
Iceland is not renowned for its contribution to medical science, being a small country in between the North Atlantic and the Arctic Ocean. However, that seems about to change as an Icelandic team scored two major papers and an editorial in the New England Journal of Medicine in January. The fuss was all about TREM2 which is a receptor on brain cells which is involved in clearing away damaged tissue and inflammation associated with the damage.
What the Icelandic team has shown is that people with later onset dementia have a higher risk of the gene that codes for this receptor having a mutation. The mutation results in less TREM2 and therefore more brain inflammation.
All very interesting but clearly not the whole picture as the prevalence of the abnormal gene that codes for TREM2 in the general population is less than 1% so it cannot account for the 20% plus rate of Alzheimer’s in the older population. Also the odds ratio for the increased risk was less than 3 so hardly a massive rise. So not much in this for jobbing clinicians but watch this space for the development of drugs acting at the TREM2 receptor…