Getting over our fear of neurobiological psychiatry

by Grace Boey

11641-mainWhat does the brain have to do with mental illness? The answer is – perhaps – a lot. Psychiatric drugs that affect brain chemistry have met with increasing success and acceptance over the past few decades, giving credence to the idea that fixing the brain might fix our mental problems. Growing amounts of research also suggest that many psychiatric conditions are linked to the brain. Though nothing as dramatic as a single “depressive switch” has been found, independent studies suggest that dysregulation of the cortical-limbic system plays a large role in major depression. It’s also been hypothesized that schizophrenia is a misconnection syndrome, or an underlying problem in the ability of different brain regions to send messages back and forth efficiently and accurately.

Yet, overly brain-based approaches to mental disorder face large amounts of backlash. For one, studies like the ones above are far from conclusive. Also, history has given us good reason to be suspicious of brain-based psychiatric theories and treatments (lobotomy, anyone?). Psychoactive drugs alone are often inadequate for treating mental illness, and most patients respond best to a combination of medication and psychotherapy.

Perhaps the biggest setback to neurobiological views of psychiatry is the following intuition: that we aren’t just our brains. A person can’t simply be reduced or equated to her brain, and to do so would dehumanize the patient. Viewing clinical psychiatry as a brain-fixing exercise ignores the fact that patients are people with feelings, stories and personal problems that have brought them to the doctor’s office in the first place. We can't just pump patients full of drugs, and then tell them to go home. The importance of this seems to be confirmed in the superior efficacy, in so many cases, of psychotherapy over drugs.

So, what are we supposed to do with all this neuropsychiatric research? It hardly seems that we should just ignore it. At the same time, we want to recognize that a patient can’t – and shouldn’t – be treated as just a brain. Lots of lip service is paid to how neuroscience and psychology are supposed to “work together hand in hand”, yet tugging intuitions on mental illness make it hard to articulate just why or how this harmony is supposed to occur. The current patchwork, “whatever works best” approach to psychiatric treatment betrays a widespread lack of grounding principles for the concept of mental disorder. As Thomas Insel, director of the National Institute of Mental Health (NIMH) puts it, “Patients with mental disorders deserve better.”

Symptoms versus causes

One big reason for all the confusion is this: psychiatry often focuses disproportionately on mental symptoms, rather than underlying causes (or, pathologies). Take, for example, The American Psychiatric Association’s (APA) Diagnostic and Statistical Manual of Mental Disorders (DSM), which is perhaps the most widely used diagnostic standard by clinical practitioners and insurance companies in America. DSM defines and categorizes mental disorders solely according to what symptoms are displayed, and determining whether someone has a mental disorder usually involves checking items off a list. According to DSM-IV, for someone to be considered depressed, she must simply meet at least 5 of a list of 9 symptoms – persistent depressed mood, diminished interest or pleasure in activities, weight loss, insomnia, agitation, fatigue, feelings of worthlessness, inability to concentrate, and recurrent thoughts of death.

Why is such an approach problematic? In the rest of clinical medicine, we know that different diseases or disorders can produce identical symptoms (one only needs to watch an episode of House to get an inkling of this). Consequently, symptom-based treatment rarely gets to the root of the problem. For example, coughing is a symptom that can reflect anything from the common cold to tuberculosis. The diagnoses and treatments for the cold and tuberculosis are obviously very different, and we don’t think of them as being similar illnesses. What happens in the body of someone with tuberculosis is completely different from that of someone with a cold.

On April 29 2013, NIMH released (through Insel’s blog) a scathing critique of DSM. The statement affirmed what many had been complaining about for decades – that DSM lacked a valid way of defining disorders, concentrated entirely on symptoms, and held psychiatry back from catching up with the rest of clinical medicine. The way we carve up the vast field of mental disorders is wrong, or at least counterproductive. Here is an excerpt:

While DSM has been described as a “Bible” for the field, it is, at best, a dictionary … The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment.

If the way we identify and classify mental disorders is mistaken, then it’s no wonder we’ve got problems developing effective treatments – both pharmacological and psychotherapeutic – for specific disorders. It’s no surprise either that we’ve had problems identifying neurobiological commonalities between patients with the same disorders. We’re pretty much just groping around in the dark.

NIMH proposes a new research approach, the Research Domain Criteria (RDoC):

RDoC is a framework for collecting the data needed for a new nosology. … The diagnostic system has to be based on the emerging research data, not on the current symptom-based categories. Imagine deciding that EKGs were not useful because many patients with chest pain did not have EKG changes. This is what we have been doing for decades when we reject a biomarker because it does not detect a DSM category. We need to begin collecting the genetic, imaging, physiologic, and cognitive data to see how all the data – not just the symptoms – cluster and how these clusters relate to treatment response.

… Going forward, we will be supporting research projects that look across current categories – or sub-divide current categories – to begin to develop a better system. … Clinical trials might study all patients in a mood clinic rather than those meeting strict major depressive disorder criteria. Studies of biomarkers for “depression” might begin by looking across many disorders with anhedonia or emotional appraisal bias or psychomotor retardation to understand the circuitry underlying these symptoms.

Such an approach would effectively help psychiatry catch up with the rest of clinical medicine. Nancy Andreasen, Chair of Psychiatry at the University of Iowa’s College of Medicine, cites the need to conform to medical research’s iterative process of discovery:

In the absence of a pathological marker, the current definitions of mental illnesses are syndromal and are based on a convergence of signs, symptoms, outcome, and patterns of familial aggregation.

Finding the neural mechanisms of mental illnesses must be an iterative process; syndromal clinical definitions (or the phenomeno-type) are progressively tested, refined, and redefined through the measurement of neurobiological aspects (or the bio-type). This process is not fundamentally different from that used to study other diseases. The diagnosis of diabetes, for example, has evolved from the observation of glucosuria to multiple subdivisions based on age of onset, severity of symptoms and complications, degree of islet cell movement, and genetic factors.

Judging disorder with the mental, defining disease with the brain

So far, so good for the psychiatric revolution. But how does the “symptoms versus causes” debate affect the principles behind our concept of mental illness? In particular, what role can the brain play in psychiatry, and what roles can’t it play?

If we are to follow the NIMH’s lead, then mental disorders will ideally be defined and demarcated by patterns in brain structure and activity. Yet there’s strong reason to think that psychological functions will have priority in judging the presence of disorder. We’ll never be able to judge, just by looking at someone’s brain, whether there is a disorder at hand or not. Even if we perfect our identification and mapping of various mental disorders onto the brain, neurobiological correlations – or even causations – do nothing to change the fact that we had identified symptoms as disorderly to begin with. Major depression and schizophrenia were identified long before we developed any real capacity to study the brain. If not for the devastating mental symptoms of Alzheimer’s disease, we wouldn’t think anything of the plaques and tangles it causes in the brains of its sufferers; we would simply look at such brains as having benign growths as opposed to being disorderly. It is simply not the case that we go around identifying deviant brain states, and then identifying them as mental disorders.

Derek Bolton, Professor of Philosophy and Psychopathology at the Institute of Psychiatry, Kings’ College London notes:

Structural neuroimaging studies are able to detect signs of neural abnormality or damage, such as atrophy … However … whether a brain structural abnormality matters in relation to psychological functioning can only be judged in these terms, in terms of the associated psychological functioning, not in terms of the physical characteristics of the brain as such. Structural abnormality of the brain does not necessarily imply abnormality in psychological functioning, and still less does the former capture what is mean by the latter.

Functional neuroimaging studies of people with some specified psychological condition indicate what neural areas and paths of connectivity are implicated in that condition. This methodology applies in the same way whether the condition in question is normal or abnormal … Analogous to the point just made about structural neuroimaging … whether a specified kind of psychological functioning is normal or abnormal is a matter to be judged in these terms, in terms of psychological or behavioural functioning, not in terms of the brain activity involved. By all means it is the case that if we are assuming that a specific psychological condition is a disorder then we may say in a derivative sense that the brain activity involved in producing it is disordered, but the inferential logic runs this way round, not the other: we do not see from the functional neuroimages that the brain activity (or the areas involved in the brain activity) are disordered, and then infer that the associated psychological functioning is a disorder.

It’s important to note that this issue crops up for physical disorders as well. Physical abnormalities are only considered disorders in virtue of their bad effects on the individual. Yet these effects are still distinct from the underlying disorders themselves – the inflammation of the bronchi that defines bronchitis is distinct from the chest pains, wheezing and excess phlegm that it causes. And insofar as pain is a mental state, then a significant number of physical disorders are disorders almost solely in virtue of a mental symptom – such as arthritis. Conversely, there are many clearly deviant physical conditions that aren’t seen as disorders, like polydactylism (an excess of toes or fingers). Having six toes on one foot is an anomaly, not a disease.

Principles behind integrated treatment

The kind of picture we have now is this: the psychological domain still has a role in judging the presence of mental disorder, while the disease is ultimately defined and identified in the brain. But our work here isn’t done – psychology and neuroscience still compete in providing treatment for the mentally ill.

One worry with holding the view sketched so far is that it puts one in the company of those who think psychiatry should be considered a subfield of neurology. This view is often seen as implying that psychiatric methods must mirror neurological methods; that is to say, psychiatrists should focus on treating brains, and the patient’s psychological states should only be important in giving symptomatic clues to the underlying disorder. Once a diagnosis is made, medicine for the brain is prescribed, and psychotherapy is inappropriate. The patient is, essentially, a brain to be fixed.

Such an objection has several problems. First and foremost, psychologically-based treatments like counselling, psychotherapy and cognitive behavioural therapy (CBT) are capable of altering the brain itself. CBT for major depression seems to affect clinical recovery by modulating the functioning of specific sites in limbic and cortical regions. Effective CBT for phobia corresponds with a decrease in limbic and paralimbic activity, and effective CBT for OCD is associated with decreased metabolism in right caudate nucleus.

If that’s still too impersonal, then consider this next point. Many mental disorders seem to follow a diathesis-stress model, where a mental illness manifests when someone with the predisposition for it (or, ‘diathesis’) interacts with a stressor from life experience. Someone with a genetic predisposition to major depression, for example, may only develop the condition after a trigger event such as a bad relationship or the death of a loved one. This is why depression seems to be influenced by such a large number of factors, including psychological, social, environmental and genetic ones.

If this is so, then there’s a very real sense in which a therapist needs to engage with the patient as a person, and address his qualitative emotions and personal problems in order to help him clinically. Psychotherapy might help a mentally-troubled individual tremendously by helping him cope with the stressor that originally triggered her symptoms, allowing her to move on from an episode. Such therapy can also help a patient develop healthier psychological habits that prevent him from relapsing into bad states. Where the diathesis-stress model is applicable, overcoming personal problems is essential to clinical recovery. It’s hard to say that anyone is just paying lip service to psychotherapy here.

As it turns out, there is a principled way that psychiatric treatment can be an integration of psychotherapy and pharmacology (or other neurological treatments). Depending on the individual’s condition and needs, either one or a combination may be the best clinically valid course of treatment. In order to help a patient, a psychiatrist will often have to understand him as a person as well as a brain in order to treat him effectively. And even in cases where only pharmacological or neurological treatment is suitable, dehumanization of the patient is just as likely to occur as the impersonal treatment of someone with a broken leg. Doctors, in general, sympathize with broken legs, even though sympathy does nothing to heal a broken bone. Likewise, good psychiatrists sympathize with their patients in simple virtue of their mental and personal hardship, not because sympathy is needed for treatment. The claim that the neurobiological view of psychiatry is necessarily dehumanizing, then, is a straw man – one that we shouldn't be afraid of.

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