By E. FULLER TORREY, MD
Sandra Steingard, MD, a psychiatrist practicing in Vermont, recently posted a blog criticizing the concept of anosognosia on the website of Robert Whitaker, “Mad in America.” Dr. Steingard made some important points but ultimately does not appear to understand the biology of anosognosia.
Anosognosia is a condition in which a subset of persons with schizophrenia (and bipolar disorder with psychotic features) are unable (not just unwilling) to understand they are sick because of damage to the parts of the brain which we use to think about ourselves. It is also referred to as a lack of insight or lack of awareness. As “The Anatomical Basis of Schizophrenia" reported, there are now at least 15 imaging studies that demonstrate how the brains of people with schizophrenia who have anosognosia differ anatomically from the brains of people with schizophrenia who are aware of their own illness and thus do not have anosognosia."
Dr. Steingrad asserts that anosognosia does exist for some neurological patients with strokes but that, for patients with schizophrenia, anosognosia is merely “conjecture,” not fact. As proof, she says imaging studies of schizophrenia do not look the same as imaging studies of strokes. But, of course, they do not, because anosognosia in individuals with schizophrenia involves multiple brain regions and especially includes the white matter connecting tracts between these regions. Thus, on a brain scan, anosognosia in schizophrenia looks different from anosognosia when caused by a stroke, which involves well-defined brain areas such as the inferior parietal lobule.
Second, Dr. Steingard doubts the validity of anosognosia in schizophrenia because brain scans cannot be used to verify it. She is correct that brain scans cannot be used diagnostically, but that does not invalidate the existence of anosognosia. Because of the anatomy of schizophrenia, it is not yet possible to diagnose schizophrenia, or patients who have anosognosia, using a brain scan as a diagnostic tool. Statistically significant group differences for such measures as the volume of the dorsal prefrontal cortex can easily be measured, but you cannot use the volume of the dorsal prefrontal cortex to predict whether any individual patient has or does not have anosognosia. Many factors in addition to schizophrenia may affect the volume of the dorsal prefrontal cortex, including genetic differences, anoxia at birth, nutrition in childhood, etc.
Anosognosia and denial
In addition, Dr. Steingrad seems confused by the differences between anosognosia and denial. Anosognosia is caused by damage to the brain caused by the schizophrenia disease process. Denial is a thought mechanism we all use to not pay attention to something we would prefer not to be true. Nobody ever said that there are not “brain changes” underlying denial; there are of course neurochemical and neuroelectrical brain changes underlying every thought we have. Brain changes occur in all individuals all the time. But, it is brain damage caused by the schizophrenia disease process that causes the anosognosia found in some patients with this condition.
The brain damage found in schizophrenia is well-established. In 2002, I published a summary of 65 studies showing such damage in individuals with schizophrenia who had never been treated with any antipsychotic medication. Since that time, the number of such studies has multiplied. Within the last month, for example, a meta-analysis was published on 33 imaging studies looking at brain volumes in 771 patients with schizophrenia who had never been treated. It reported significant decreases in total brain volume, as well as, the volume of the gray matter, white matter, hippocampus, thalamus, and caudate (Haijma et al, Brain volumes in schizophrenia: A meta-analysis of over 18,000 subjects, Schizophrenia Bulletin, advance access). Another just-published study, using diffusion tensor imaging (DTI) to assess specific white matter connecting tracts in 20 patients with schizophrenia who had never been treated, reported abnormalities in the white matter tracts previously suspected of being abnormal in schizophrenia (Guo et al., Right lateralized white matter abnormalities in first-episode, drug naïve paranoid schizophrenia, Neuroscience Letters, advance access). In short, any mental health professional who doubts schizophrenia is a brain disease is probably restricting their scientific reading to the National Geographic.
The difference between anosognosia and denial can therefore be summarized as follows: A woman with schizophrenia sits daily in Lafayette Park, across from the White House, believing she is married to the President and waiting for him to call her to come over. She believes he has to wait to acknowledge her because of the interference of Israeli secret agents. She is very patient and, at night, sleeps on the streets, where she is regularly abused. When offered medication, she adamantly refuses it, saying there is nothing wrong with her. This is anosognosia. Another woman, trained as a mental health professional, briefly examines some scientific data and concludes it is wrong because it conflicts with her deeply held social belief system. This is denial.
The new antipsychiatry
It is significant that Dr. Steingard chose to put her blog on Robert Whitaker’s “Mad in America” website. This site has become one of the new antipsychiatry centers. Whitaker is correct in criticizing the pharmaceutical industry, the overuse of psychiatric medications by physicians and the psychiatric profession for being financially in the pocket of the pharmaceutical industry. However, Whitaker is dead wrong in alleging that schizophrenia is caused by the antipsychotic drugs used to treat it (see Anatomy of a Non-Epidemic). Like other antipsychiatrists, he ignores the many studies that have demonstrated brain damage in individuals with schizophrenia before they had ever taken any psychiatric medication.
This is the new anti-biological antipsychiatry. In his book, Mad in America, Whitaker described schizophrenia as a term “loosely applied to people with widely disparate emotional problems.” Whitaker cites approvingly the work of Dr. Loren Mosher, who described schizophrenia as merely “disturbed and disturbing behavior.” And he includes on his website, the lectures of Dr. Peter Breggin who described schizophrenia as “a psychospiritual overwhelm” and “a failure of nerve.” For the treatment of schizophrenia, Whitaker recommends “love and food and understanding, not drugs.” This anti-medication bias is shared by almost all of the new antipsychiatrists.
Laypersons such as Robert Whitaker can be partially excused for their lack of understanding regarding the biological underpinnings of schizophrenia. They are not trained to do so. Mental health professionals who deny that schizophrenia is a brain disease have no such excuse, however, and are simply demonstrating their ignorance.
Make no mistake: The concept of anosognosia is deeply disturbing to antipsychiatrists. If we believe the woman with schizophrenia sitting in Lafayette Park is merely exercising her civil rights to live as she chooses, that is a comforting thought, and we should defend her right to do so. If, on the other hand, we believe she has brain damage secondary to her schizophrenia, which impairs her right to choose (i.e., that her behavior is determined by her delusions, and she is not truly free to choose at all), then that is an uncomfortable thought. And if there is medication available that might diminish her delusions so she would be truly free to choose her behavior, what should we do? Many antipsychiatrists have embraced the “recovery movement,” but treating such a person with medication is the one thing that might make recovery possible. Isn’t this what the “recovery movement” should be about?