Arianna’s dream was to become a researcher. “My older brother has been sick and suffering a lot, and I want to help him and also help stop suffering in the world.” She often said these words to herself, as a way to remember that keeping her promise alive meant hard work, keeping up with great grades, and maintaining her extracurricular activities. Arianna wanted to be sure she was doing all the right things to get ready for college and in preparation for graduate school.

At age 15; however, Arianna suddenly developed some unusual and disturbing symptoms, including auditory hallucinations, visual hallucinations and disorganized behavior. She also became disinhibited with impulsive behavior and developed a rash that puzzled everyone and swollen joints in both upper and lower extremities. Due to the sudden onset of Arianna’s behavior and experiences, she was taken to the emergency department, admitted to an inpatient psychiatric unit, and diagnosed with Schizoaffective Disorder.

Arianna was later discharged on Lithium and Haldol, with an appointment to the outpatient clinic. Saul, the outpatient child psychiatrist and Laura, a social worker and the outpatient adolescent therapist, completed a thorough initial evaluation, and after the intake, started talking about Arianna’s presentation. It was an enigma, and they wondered if something else, other than Schizophrenia or Schizoaffective Disorder, might be the more appropriate, correct explanation for Arianna’s psychotic symptoms.  Saul and Laura did not simply accept the paper report of the carrying diagnosis. They persevered in the diagnostic workup, coordinated with the rest of the pediatric team involved, and completed additional testing, until eventually, their suspicion was confirmed. Arianna’s psychotic symptoms were not due to Schizophrenia or Schizoaffective disorder. Arianna had a condition known as Anti-NMDA receptor encephalitis.

Anti-NMDA receptor encephalitis is an autoimmune disease that occurs when antibodies produced by an individual’s own immune system attack the NMDA receptors, abundant in the brain. NMDA receptors are proteins that control the passage of electrical impulses in the brain. This condition affects mostly young children, particularly, young female adolescents, like Arianna, and often the main symptoms are psychiatric in nature, just as in Arianna’s case.

An accepted and basic definition by the medical literature of differential diagnosis is “the distinguishing of a disease or condition from others presenting with similar signs and symptoms.” It simply means that before confirming any diagnosis, say, Major Depressive Disorder, for example, other conditions need to be identified as a possible cause of the presenting symptoms.

Many of us are familiar with the concept of differential diagnosis and most of us may also be aware of its shortcomings as a process. A differential diagnosis means you already have a diagnosis, and you simply want to differentiate this diagnosis with other similar conditions. It is a process that comes from the medical model—the pathologizing culture—and it follows a reactive way of thinking.  In general medicine, such a thought process may be justified.

For example, consider a 43 year-old female presenting with severe chest pain. It makes sense to think about Myocardial Infarction (MI), also known as a heart attack, as the most likely possible cause and then think about a differential diagnosis. While only six percent of chest pain may be due to a life-threatening condition, physicians are trained and, rightly so, to think about the worst-case scenario, like an MI, until proven otherwise. If this is missed, or if not diagnosed and treated in a timely manner, a myocardial infarction can be fatal within a matter of hours. In mental health, on the other hand, there is rarely a case where differing a diagnosis may lead to devastating consequences within a matter of hours.

The opposite has been found to be true. Making a mental health diagnosis may have an ever-lasting impact on anyone, and especially in these times where stigma has been one of the major barriers to seeking mental health treatment. We as mental health professionals, in particular, and health professionals in general, need to adopt a different thought process, thinking about and diagnosing mental illness, and in order for us to do so, I would like to invite you to break away from the typical “medical model.”

Therefore, friends and colleagues, I would like to take a stand and invite you to do the same. Break away from the traditional “medical model” and think about understanding mental illness with a totally different framework that reflects the sophistication and complexity of human life (the brain, mind and behavior) and the complexity of our field of mental health. In order for us to do this, instead of differential diagnosis, I suggest that we start with understanding the complaints and the signs and symptoms with which our clients and patients present. We need to take some time to look at the circumstances and the context of each symptom, and I would like to call this;

“Symptom Contextualization”

The above case, about Arianna, illustrates how classic symptom presentation of what many would quickly attribute to Schizophrenia or Schizoaffective Disorder may actually be explained by a different entity or diagnosis. This case also sets a framework to start discussing the meaning of symptoms in mental health, the process of putting them into context, and the concept of “symptom contextualization.”

Should we really be rendering diagnosis and providing treatment without a thorough understanding of the presenting symptoms and complaints?

When I teach and supervise clinicians, including social workers, nurses and other medical staff and health practitioners, I often ask myself: “How do I explain the need to understand the meaning, the circumstances, the causes and functions of the presenting symptoms before “pulling the trigger” on quickly providing a mental health diagnosis. Typically, I introduce the concept of “symptom contextualization” by asking for a definition and insist on something clearly expressed. Some then define it as “looking at the circumstances of the symptoms,” others as, “looking at the context of the symptoms,” but almost everyone says something that is close enough to my thinking behind the concept. And they all add how this is a much needed concept to force them to take one step back to think through the client’s and patient’s symptoms, putting the clinical presentation into context, in order to properly formulate the related problem and adequately provide a solution (or problem solve).

So, in order to further illustrate and emphasize the importance of “symptom contextualization” I will ask those I teach:

“What does it mean when someone is laughing to himself or herself;

what does “laughing to oneself,” mean?

Without hesitation, almost everyone is quick to say, “psychosis,” or “schizophrenia,” and often stop there. However, as I challenge them to continue looking, to continue thinking, we always end up discussing 7-8 additional contexts that support “laughing to self.”

This article is only an introduction to the concept of symptom contextualization. In a subsequent article, I am going to discuss the secrets of successfully contextualizing psychotic symptoms. Meanwhile, I would invite you to tell me:

• How important is it for you to learn more about symptom contextualization?
• Tell me about a time when you or someone you worked with (no names please) may have misinterpreted a symptom because it was not well contextualized.
• Give one way in which this will be helpful to your practice.
• Are you able to put each of the major psychotic symptoms into context?

I hope you start thinking about ways to break away from the “medical model” when making diagnosis in mental health. I hope I was able to make it clear that while this “medical model” has its place in general medicine, it may do more damage than good to our patients and clients we serve in the field of mental health. The “medical model” mindset may increase stigma, hampering the delivery of appropriate mental health treatment, which in turn will continue to complicate our efforts to adopt the preventive measures required in mental health. I hope you are now ready to take the steps to start applying the concept of symptom contextualization in your practice.

References:

1. Goldsmith CA, Rogers DP. The case for autoimmunity in the etiology of schizophrenia. Pharmacotherapy. 2008;28:730–741
2. Ching KH, Burbelo PD, Carlson PJ, et al. High levels of anti-GAD65 and anti-Ro52 autoantibodies in a patient with major depressive disorder showing psychomotor disturbance. J Neuroimmunol. 2010;222:87–89.
3. Nemeroff CB, Simon JS, Haggerty JJ, Jr, et al. Antithyroid antibodies in depressed patients. Am J Psychiatry. 1985;142:840–843
4. Roos RP, Davis K, Meltzer HY. Immunoglobulin studies in patients with psychiatric diseases. Arch Gen Psychiatry. 1985;42:124–128
5. Diamond B, Huerta PT, Mina-Osorio P, et al. Losing your nerves? Maybe it’s the antibodies. Nat Rev Immunol. 2009;9:449–456
6. Moscato EH, Jain A, Peng X, et al. Mechanisms underlying autoimmune synaptic encephalitis leading to disorders of memory, behavior and cognition: insights from molecular, cellular and synaptic studies. Eur J Neurosci. 2010;32:298–309
7. Kayser MS, Kohler CG, Dalmau J. Psychiatric manifestations of paraneoplastic disorders. Am J Psychiatry. 2010;167:1039–1050.
8. Tuzun E, Dalmau J. Limbic encephalitis and variants: classification, diagnosis, and treatment. Neurologist. 2007;13:261–271
9. Dalmau J, Gleichman AJ, Hughes EG, et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol. 2008;7:1091–1098
10. Florance NR, Davis RL, Lam C, et al. Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis in children and adolescents. Ann Neurol. 2009;66:11–18
11. Sebire G. In search of lost time from “demonic possession” to anti-N-methyl-D-aspartate receptor encephalitis. Ann Neurol. 2010;67:141–142. author reply 142–143.
12. Brey RL, Holliday SL, Saklad AR, et al. Neuropsychiatric syndromes in lupus: prevalence using standardized definitions. Neurology. 2002;58:1214–1220.
13. Bonfa E, Golombek SJ, Kaufman LD, et al. Association between lupus psychosis and anti-ribosomal P protein antibodies. N Engl J Med. 1987;317:265–271
14. Matus S, Burgos PV, Bravo-Zehnder M, et al. Antiribosomal-P autoantibodies from psychiatric lupus target a novel neuronal surface protein causing calcium influx and apoptosis. J Exp Med. 2007;204:3221–3234.