By David Tuller, DrPH
Last week I wrote a post on some of the signs used to diagnose people with “functional neurological disorder” (FND)—the phrase that has largely supplanted “conversion disorder” to describe neurological symptoms with no identified organic cause. In that post, I should have been clearer that I do not question whether people experience these symptoms. There is obviously a large group of patients with extremely disabling conditions that remain undiagnosed and in many cases likely cannot be diagnosed through current medical technologies.
My concern is the longstanding insistence of psychiatrists and neurologists that these patients have no physiological dysfunctions that could account for the symptoms, and that the symptoms were therefore psychologically induced–whatever exactly that would mean. The relatively recent adoption of the more neutral-sounding FND does not wipe out this history. As with conversion disorder, the newer category has vague and expansive boundaries, making it possible for clinicians to define more or less anything they have trouble diagnosing as FND.
The term “medically unexplained symptoms” (MUS) raises similar concerns. Many people have symptoms that remain unexplained. To take that as de facto evidence that they are unexplainable and by definition psychogenic is a leap of logic that ignores the possibility of future scientific and medical advances. Like FND, MUS might be a useful descriptive term of certain phenomena in some contexts. But it is problematic when MUS becomes a diagnosis used to shunt people into psychotherapy after a primary care consultation, as happens in the UK through the expanding program known as Improving Access to Psychological Therapies.
In addition to rebranding conversion disorder as FND, psychiatrists and neurologists have in recent years taken to analogizing these complaints to “software” as opposed to “hardware” problems. That is, major cerebral structures are viewed as comparable to “hardware,” and the communications and other functions linking regions of the brain represent the “software.” And if software is the problem, the optimal solution would be to replace or reprogram it. Following this analogy, I guess emotions and cognitions and beliefs would be considered parts of the malfunctioning “software.”
Despite the popularity of the hardware/software meme among FND experts, this binary presentation of the science turns out to be pretty inaccurate. According to a review of relevant research published last March in the journal NeuroImage: Clinical, unexplained neurological complaints are in fact associated with measurable “hardware” abnormalities across a number of regions of the brain. These findings would appear to contradict many previous claims.
The paper is called “Structural alterations in functional neurological disorder and related conditions: a software and hardware problem?” The authors conclude that the answer is yes. As they write, “While the framing of FND as a ‘software’ problem is well-received, this conceptualization may require more nuanced considerations…Emerging structural neuroimaging findings point towards a parallel “hardware” related neurobiology in some FND populations.”
The authors also note that “it remains unclear whether structural abnormalities relate to predisposing vulnerabilities or consequences of the disorder.” In other words, they don’t have much idea what is causing which or how best to interpret the findings.
From a field that has spent a century or more vehemently denying any organic basis for complaints with no known organic explanation, this acknowledgement of “hardware” problems is rather remarkable. Leading voices in the FND domain should pursue major efforts to disseminate this news to patients, given its significance. Yet the high-profile and widely read *neurosymptoms.org* website—created by a co-author of the “hardware” review—continues to describe FND in strictly binary terms that apparently no longer fit the emerging science.
*[In this sentence and another mention of this website below, I initially wrote “neurosymptoms.com” instead of “neurosymptoms.org.” I apologize for the error.]
In a page on “causes,” the site includes this statement: “If you were a computer its [sic] like having a software problem rather than a hardware problem. If you have a software bug on your computer, it might keep crashing or work really slowly. You wouldn’t solve that problem by opening up the computer and looking at the components. You wouldn’t see anything if you did an x-ray of that computer…You’d have to solve it by reprogramming the computer, working out which programs were causing the problem.” The phrase “its [sic] like having a software problem rather than a hardware problem” is highlighted as a “pull-quote” on the page.
According to the recent “hardware” review, however, investigators have so far found quite a lot on that metaphorical computer x-ray. So perhaps looking at the “components” and not just the “bugs” in the “software” makes sense after all—contrary to the standard pronouncements of psychiatrists and neurologists as well as the current statement on neurosymptoms.org.
A commentary last month in JAMA Neurology raises similar concerns. In the essay, Harvard neurologist Matthew Burke reports that there is a “silent epidemic” of people with FND–and he highlights the (now arguably inoperative) hardware/software analogy. He cites the range of neuroimaging studies that provide “physiological explanations for once mysterious links between regions implicated in emotional processing and the generation of “physical” symptoms (eg, pain, fatigue, weakness)” but does not specifically mention the reported findings of structural abnormalities.
Then he writes the following:
“Despite the growing scientific literature, there has been minimal shift in physician attitudes toward these patients. Physicians seem quite comfortable with the idea of structural brain lesions causing psychological symptoms, such as a frontal lobe stroke causing depression or a temporal lobe tumor causing delusions. However, the reverse causality of psychological factors (borne of the same substrates—neurotransmitters, neurons, and synaptic connections) leading to neurological or systemic symptoms is often hastily dismissed and remains highly stigmatized. Thus, many physicians either simply ignore these kinds of symptoms or wrongfully assume that patients are malingering.”
Burke comes across as a sympathetic clinician concerned about the well-being of patients, and his point about unacceptable or questionable physician attitudes is well taken. But perhaps it should not be surprising that many physicians ignore or misinterpret “these kinds of symptoms.” For more than a century, psychiatrists and neurologists have promoted the dogma that unexplained neurological complaints resulted from the unconscious conversion of anxieties and psychological distress into somatic manifestations, not from pathophysiological processes.
And Burke himself continues to insist on the primacy of “psychological factors” in FND. Yet the neuroimaging studies he cites document apparent associations. They do not and could not document his theorized “reverse causality of psychological factors.” (He acknowledges that these “psychological factors” are “borne of” biochemical substrates, but he leaves it at that; perhaps more analysis of that point would have been warranted.)
Given the long list of recognized diseases formerly attributed to “psychological factors,” the source of Burke’s confidence that such entities are “leading to” neurological symptoms is unclear. He could be right that there is a silent epidemic of people with misunderstood neurological disorders. But his analysis seems blind to the historical role that psychiatry and neurology have played in creating this misunderstanding in the first place with their entrenched practice of slapping dismissive psychiatric labels on patients that confound them.
(If these two disciplines actually want to demonstrate that they are moving beyond their biases, perhaps they should terminate the phrase “psychogenic non-epileptic seizures.” After all, the “hardware” review included reports of “reduced inferior frontal gyrus” and “altered orbitofrontal CTH [cortical thickness]” in these patients. For multiple reasons, it is hard to justify the continued use of the word “psychogenic” in this context.)