This post is part of a series of guest posts on GPS by the graduate students in my Psychopathology course. As part of their work for the course, each student had to demonstrate mastery of the skill of “Educating the Public about Mental Health.” To that end, each student has to prepare three 1,000ish word posts on a particular class of mental disorders, with one of those focusing on changes made from the DSM-IV to the DSM-5.
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Distinguishing Dissociative Identity Disorder and Schizophrenia by Kelley R. Bailey
I remember the first time I saw the movie Sybil with Sally Fields. It creeped me out. It was the portrayal of abuse that happened to Sybil as a little girl that freaked me out. That scene with her mother giving her ice enemas while she tied little Sybil to the piano and played and played banging on the keys screaming at Sybil to hold it. Creeeeee-py! For years I thought multiple personalities were just a form of schizophrenia and that trauma was related to both and that both were creepy. I thought the movie was the way “crazy” people acted, all crazy people had schizophrenia, and a schizophrenic was a person with multiple personalities because of the abuse that happened to them as a little kid. It was the homeless man wandering the streets talking to himself. It was all those people in the psych ward at hospitals. It was all those people who believed in ghosts or who talked in tongues and danced with snakes. The movie totally shaped my perception of mental disorders generally, but multiple personality disorder and schizophrenia in particular.
The book Sybil came out in 1973 and instantly shot to the top of the best seller list, selling over 6 million copies. I guess the public liked creepy. Within a few years of publication, cases of multiple personality — now known as dissociative identity disorder — rapidly jumped from less than 100 diagnoses total to thousands in the United State alone. Although Sybil’s diagnosis of DID is disputed today, it did catapult the recognition of the disorder into a mental health category into the Diagnostic and Statistical Manual (DSM). The first comprehensive articles began to appear in psychiatric literature in 1980, largely thanks to the publication of the book Sybil and the subsequent movie.
The disorder no longer creeps me out, as a matter of fact I’ve become highly interested in the brain, how it works, and how there remains the possibility, given the right scenario, that we have no control over our thoughts. I guess that’s why I’ve chosen the field of counseling. It gives me the opportunity to understand or try to understand the workings of the brain and how it affects us so deeply, and dissociative identity disorder (DID) has all the intriguing aspects of the brain, personality, and disfunction. Attempting to understand DID not only causes confusion for general public, but for the mental health field as well. Some doubt even it’s existence, others doubt the cause, but one leading etiology has emerged – trauma and specifically posttraumatic disorder, which in turn manifest into DID. The posttraumatic model (PTM) states the dissociation is a defense response to childhood trauma, specifically severe sexual and physical abuse, often repeated abuses. This model is easily understood, in that a child who has been traumatized by repeated physical or sexual abuse dissociates from the event as a defensive mechanism from the trauma. PTM holds that DID is a form or variant of post-traumatic stress disorder (PTSD) and is a coping reaction to the childhood trauma. (It is important at this point to note that there is a growing number of researchers who posit a different model – an sociocultural model to explain DID and that they are increasing in influence.)
Because of the link with trauma, people often confuse DID and schizophrenia. Often dissociative identity disorder is mistaken as schizophrenia, but it doesn’t generally go the other way (people mistaking dissociative identity disorder for schizophrenia). Importantly, though, the two are categorically different both behaviorally (see this link for a breakdown of those differences) and at the biological level, in both brain function and structure.
In schizophrenia there is an augmentation in the ventricular system that has been seen in 45 to 50 out of 60 studies conducted using computed tomography (CT) scanning. What does that mean? Basically the ventricular system holds our cerebrospinal fluid (CSF), which protects our brains from impact, acts as a shock absorbers for the central nervous system, and feeds the brain with nutrients while at the same removing “junk” from the brain. It’s unknown if enlarged ventricles of the brain cause schizophrenia (that old chicken and the egg problem), but it can be an indicator. You’d think an enlarged ventricle system with all it’s benefits wouldn’t be harmful but apparently that’s not the case, at least as far as researchers can tell. Presently the only thing enlargement of the ventricles does tells us is if there is disease. It is also helpful in studying and differentiating mental disorders, but that’s about it.
On the biochemical level, excessive dopamine is linked to schizophrenic symptoms. Antipsychotic drugs used to treat schizophrenia unequivocally block dopamine, which helps decrease the positive symptoms. It is also known that when people take amphetamines or cocaine, which are drugs that increase dopamine transmission, they have an increased probability of experiencing psychosis. As in, when dopamine is supplemented in the brain you can literally make someone psychotic (or a while, at least).
Markedly different biological makers occur in patients with DID, in particular in the amygdalar and hippocampal volumes. The amygdala regulates our fight/flight response and it also plays a role in storing memories that are associated with an emotional event among other functions. One of the tasks of the hippocampus is long term memory storage.
When the amygdala is removed, animals become indifferent to stimuli that would have otherwise have caused fear and sexual responses. If the hippocampus is damaged, a person cannot build new memories, and lives instead in a strange world where everything they experience just fades away, even while older memories from the time before the damage are untouched. We can see some connection with these areas and the presentation of DID. In persons with dissociative identity disorder, we generally see smaller hippocampal and amygdalar volumes. The hippocampus and amygdala are needed for activating our feelings of fear or the need to get out of a situation. Both have been shown to be smaller in those with PTSD as well. This makes sense, as the majority of patients with DID also have a diagnosis of PTSD. Again, research is unclear if smaller regions indicate a propensity for developing PTSD or if trauma is the culprit in decreased volumes of both the hippocampus and amygdala. This is significant in that there is a strong correlation of trauma and dissociative identity disorder. Studies are emerging suggesting the volume of the hippocampus and amygdala, if smaller to begin with, may indicate a person could be at risk for development of PTSD or DID should trauma occur.
So what do we do? First recognize the differences. Gaining a correct diagnosis early can mean a much more effective treatment plan and productive life for the patient. Practitioners, even if not working with this population extensively, need to have a broad understanding of the two for recognition and referral. Dissociative identity disorder and schizophrenia are classified differently in the DSM, present differently, have different etiologies, and the two are functionally and structurally different in the brain. There are many other areas to discuss on the dissimilarities between these two disorders other than what was presented here, but the brain differences highlight the structural and some functional disparities between the two. Seeing the varying areas of the brain which are impacted within each disorder is another means of dispelling public opinion on the similarities of schizophrenia and dissociative identity disorder.
