Functional neurological disorders involve symptoms such as tremors, tingling and numbness, weakness, loss of balance, paralysis, hearing and vision problems and many other symptoms that have not had a pinpointed physiological cause. It is a newer term that encompasses many symptoms and also includes conversion disorder. In these cases, mainstream medicine uses the testing that they have available (blood tests, imaging technology, etc) and finds there is no known organic cause that can be part of the diagnosis.
Anxiety and depression have both been associated with medically unexplained symptoms  and psychotherapy has shown efficacy in many with somatoform problems . Functional neurological disorders can also co-exist with actual diseases rather than just existing by themselves; a lot of factors are supposed to be considered and investigated when making this diagnosis . Between 10-30% of patients seen by neurologists have symptoms that are not currently explainable in terms of physical disease . This shows just how important it is to understand this problem.
This area of research is considered very complex and researchers do not want the amount of disability or distress caused by functional neurological disorders to be underestimated or ignored, especially considering the distress and disability involved is similar to those with actual diagnosed diseases . The terminology used when presenting the possibility to patients is also being carefully crafted in order to not offend them .
“Functional symptoms were previously called “hysterical”, but the term’s derogatory connotations and the ever widening meaning of the word (for example, mass hysteria, hysterical personality) make it inappropriate.5 Functional problems are sometimes called “psychogenic” or attributed to “conversion”. However, in the ICD-10 the term “psychogenic” is defined quite narrowly as signifying an association with recent trauma,11 and the term “conversion” evokes an aetiological mechanism for which we have no evidence. These models are too simplistic in most cases .”
Before presenting my criticisms in how the functional neurological category can be misleading in some cases, I will state that yes, this is a real category of neurological disorders and the field has complex, genuine, and interesting research. Some researchers in this domain are adopting a biopsychosocial view of FNDs that takes a multifaceted approach looking at common pathways in nervous system dysfunction rather than viewing the problem as being “only psychological.” Here are other important things to note:
“Functional neurological symptoms refer to neurological symptoms that are not explained by disease. They may also be called psychogenic, non-organic, somatoform, dissociative or conversion symptoms. The most common functional neurological symptoms are non-epileptic attacks and functional weakness.”
1. “Psychosomatic” can be easily confused with the term somatoform. However, psychosomatic phenomena is not the exact same same thing as somatoform/functional neurological symptoms. Psychosomatic would involve physical illnesses that are caused or made worse by mental factors; this would include mental factors that affect the expression and course of a diagnosed physiological disease. Somatic/functional neurological symptoms would be when there is no diagnosed physiological disease and both the symptoms and the cause are all considered psychological.
2. There was past discussion about the somatoform disorder classification and how it was not optimal for diagnostic reasons [8-9].
“In the taxonomies (Diagnostic and Statistical Manual of Mental Disorder, 4th edition (DSM-IV),10 International Statistical Classification of Diseases, 10th revision (ICD-10)11) functional symptoms can be classified as manifestations of somatoform disorders (physical symptoms which suggest a general medical condition) or dissociative disorders (disruption of the usually integrated functions of consciousness, memory, identity, or perception). However, many functional neurological symptoms (like amnesia or seizures) fulfil diagnostic criteria for both categories. Perhaps because of this, the present clinical criteria in the ICD and DSM systems do not perform well diagnostically if relied upon alone.12 What is more, the term “somatoform” does not imply a positive explanation for the symptom, and there have been increasing criticisms of the somatoform classification with more emphasis being placed on symptomatology.13
With DSM–V on the horizon, discussion again has started about the classification of somatoform disorders (Wise & Birket-Smith, 2002). It has been argued that somatoform disorders are not psychiatric disorders in a strict sense. Indeed, it is not very clear that unexplained physical symptoms are caused by psychological factors. It is clear, however, that there is a strong relationship with anxiety and depression, given that half of the patients in general practice with anxiety or depression suffer from a somatoform disorder as well. The relationship could be due to anxiety and depression causing (awareness of) physical symptoms, or physical symptoms causing anxiety and depression, or there may be a more complex relationship such as a circular causality. Furthermore, a third factor, such as consulting behaviour, could be related to both. In addition to patients with comorbid disorders, many more patients suffer from a somatoform disorder without anxiety or depression. From our study it is evident that both somatoform disorders and anxiety and depression come with substantial functional impairment and that the combination is even worse. A somatoform presentation seems to result from a complex interplay of perception and attribution of symptoms, resulting in unproductive illness behaviour. It has been demonstrated repeatedly that a cognitive–behavioural approach can be effective in alleviating this burden (Kroenke & Swindle, 2000). The inclusion of a well-defined category of somatoform disorders in DSM–V is needed to facilitate further research on the effective treatment of such patients.”
Now after an update, it is called somatic symptom disorder rather than somatoform disorder. Somatic symptom disorders can involve a wide range of symptoms involved with the whole body in addition to the excessive worry caused by the perceived symptoms, whereas functional neurological disorders are those that more specifically have symptoms that mimic neurologically based problems.
“A somatic symptom disorder formerly known as a somatoform disorder, is any mental disorder which manifests as physical symptoms that suggest illness or injury, but which cannot be explained fully by a general medical condition or by the direct effect of a substance, and are not attributable to another mental disorder (e.g., panic disorder).
In the newest version of DSM-5 (2013) somatic symptom disorders are recognized under the term Somatic Symptom and Related Disorders:
-Somatic Symptom Disorder: This will take over many of what was formerly known as Somatization Disorders, and Hypochondriasis
-Factitious disorder: Can be either imposed on ones self, or to someone else (Formally known as Factitious Disorder by proxy).
-Illness anxiety disorder: A somatic symptom disorder involving persistent and excessive worry about developing a serious illness. This disorder has recently gone under review and has been altered into three different classifications.
-Somatoform disorder Not Otherwise Specified (NOS)
Included among these disorders are false pregnancy, psychogenic urinary retention, and mass psychogenic illness (so-called mass hysteria).
Somatization disorder as a mental disorder was recognized in the DSM-IV-TR classification system, but in the latest version DSM-5, it was combined with undifferentiated somatoform disorder to become somatic symptom disorder, a diagnosis which no longer requires a specific number of somatic symptoms.”
The classifications and distinctions can be quite confusing for anyone unfamiliar with this part of psychiatry and neurology, but it is worth reading about over time if you want to understand how it is being used.
Here, I will present a syllogism example that can identify specific flawed reasoning where it may exist in the mind of a neurologist, psychiatrist, or other doctor.
⁃ Somatic and functional neurological disorders often involve co-existence with anxiety, depression, and other psychiatric factors as initiating causes of physically felt symptoms in the absence of a known organic cause.
⁃ This person I am evaluating (and based on our testing abilities) has unexplained physically-felt symptoms and they also have anxiety, depression, and/or other psychiatric symptoms.
⁃ Therefore, the anxiety, depression, and/or other psychiatric underpinnings must be the cause of the physical symptoms the patient describes.
Is there anything wrong with these premises and the conclusion when considering all of the possible factors and interpretations? The answer is yes. Some researchers have pointed out that it is difficult to know what caused what (physical symptoms resulting in psychological symptoms, or the other way around) but the issue here is when causation is automatically assumed by a doctor. “Your stress is causing the symptoms you perceive.” This would be a good example of correlation does not imply causation. Another key question to ask is “What is within conventional medicine’s testing abilities and is it adequate enough for the extent of the problem?” While certain diseases and structural problems can be ruled out, they do not account for all possible explanations. For example, mitochondrial dysfunction is not routinely tested for and it can cause both psychological and physical symptoms . Moreover, there are rare diseases and biochemical abnormalities that may exist that are not screened for in routine conventional testing . This includes but is not limited to the following: methylation testing, genetic polymorphism screenings, mitochondrial testing, cytokine measurements, xenobiotic exposure evaluations, brain autoantibodies, CSF pressure (in cases of IIHWOP) and more. While some of these are still not understood for their potential role in associations or clinical usage for functional neurological and somatic symptoms, it is important that it is investigated so we understand if some type of exposure or biochemical factor (heavy metals, metabolism, etc) may have had impact on nervous system function. While our measuring capabilities may not be perfect or complete, they can help us go a step forward if they are considered. I must also mention the fact that at one point ulcerative colitis was considered “psychosomatic” until the actual immune factors were identified. This is due to the fact unknown etiology often sparks psychological theories.
These psychological theories can cause problems especially in situations where something physical actually is involved, but remains to be found and properly investigated. I found an article that was very interesting and discussed how secondary neuronal damage can have psychiatric manifestions. These researchers found important overlaps in brain insult symptoms and neuropsychiatric symptoms.
“However, 40% of neuropsychiatric signs and symptoms were found to be commonly shared by traumatic, infectious, toxic, oncogenic, and degenerative brain insults, suggesting that the same or similar brain regions/structures can be possibly affected by different acute and chronic brain insults.”
They also discussed limitations to our imaging technology on picking up certain changes in the brain.
“A neuropsychiatric disorder should have its morphological alter-ations in the brain. Any brain insult can certainly cause histo-morphological, biochemical, or molecular biological alterations in some parts of the brain, such as the limbic system, basal ganglia system, the brainstem, the basal forebrain, the cerebellum, and the cerebral cortex. Unfortunately, these alterations at the cellular and molecular level are usually not easy to detect by using traditional diagnostic imaging techniques (e.g., ultrasound, X-rays, CT, and MRI), because tiny morphological changes (such as neuronal cell death or loss) in deep brain structures (such as the limbic system and basal ganglia system) can be often covered by other normal neural tissue layers of the brain. Much of the neuronal damage in deep brain structures can be seen only under a microscope after death (13).”
Some of the symptoms they also looked at in this analysis also included somatic symptoms:
“Somatoform disorders are a group of neuropsychiatric disorders characterized by physical symptoms that suggest physical illness or injury. However, the cause for the symptoms cannot be fully explained by a general physical illness because physical exami-nations and clinical lab tests do not indicate the presence of a physical illness (101). This has led to the hypothesis that the physical symptoms of these patients’ experience may be from a neuropsychiatric source associated with brain damage (102). They may be relevant to the damage to some parts of the cerebral cortex (such as dorsolateral prefrontal, insular, rostral anterior cingulate, premotor, parietal cortices, and parahippocampal gyrus) (103, 104). Because the cerebral cortex controls sensory–motor coupling, sensory feed-back system, and somatic sensation, cortical damage may cause increased sensitivity to internal physical sensations and pain. The increased sensitivity to somatic feelings may predispose patients to produce somatoform symptoms (105, 106).”
“If a patient has neuropsychiatric signs and symptoms of unknown origin, physicians and psychiatrists should be aware that potential neuronal damage can possibly exist in the patient’s brain and not simply conclude that the patient has a psychological problem associated with social/environmental factors. Necessary treatment aimed at slowing down the process of neuronal damage and attenuating individual symptoms or clusters of neuropsy-chiatric and neurological disorders may help improve recovery of neurobehavioral functions. The clinical symptom-comparing approach used in the present study to identify the same clin-ical manifestations may be a useful tool for investigating the causes of neuropsychiatric disorders and other complex diseases of unknown origin.”
So yes, even somatoform symptoms may possibly be rooted in unseen neuronal damage.
Furthermore, a 2005 systematic review concluded that there was a misdiagnosis rate of 5% for FNDs (conversion disorder) since 1970. Is this number entirely accurate? That can depend on interpretation/inclusion and exclusion criteria, but it is still important to note nonetheless. It is being said that functional disorders should be based on positive signs and strict criteria rather than only being based on (some) negative test results (exclusionary diagnosis) . This could be misleading if further needed tests end up showing association with a real illness. Rare diseases can be misdiagnosed as psychiatric and psychological and this must be taken into consideration. Functional neurological disorders could co-exist with an organic illness as well and one existing does not automatically discredit the other.
Pertinently, Harvard Ph.D. student Jennifer Brea is a director of a documentary titled Unrest; she is another person who has suffered at the hands of false assumption. She has chronic fatigue syndrome (myalgic encephalomyelitis) and was diagnosed by a neurologist with the psychiatric conversion disorder. Conversion disorder is grouped with functional neurological disorders. There has been controversy surrounding the conversion disorder diagnosis based on oversimplification .
“One of the most common conditions bringing patients to neurologists, FND involves a constellation of neurologic symptoms — including weakness, tremors, walking difficulties, convulsions, pain and fatigue — not explained by traditional neurologic diagnoses. This condition has also been called conversion disorder, reflecting one theory that patients were converting emotional distress into physical symptoms, but Perez notes that this now appears to be an oversimplified view of a complex neuropsychiatric condition. The research team hopes that advancing the neurobiological understanding of FND will increase awareness and decrease the stigma — including skepticism about the reality of patients’ symptoms — often associated with this condition.
Previous functional MRI studies have suggested that a group of brain structures forming part of what is called the salience network — which are involved in detecting important bodily and environmental stimuli, as well as integrating emotional, cognitive and sensory-motor experiences — showed increased activity in FND patients during a variety of behavioral and emotion-processing tasks. The current study is one of the first to examine structural relationships between components of the salience network and the physical and mental health of patients with FND.”
Even if this somehow was the case for her (unlikely), it would still not disprove all neurobiological cause.
Furthermore, the neurologist who diagnosed her claimed there was some “past trauma” she does not remember. There is no evidence for this statement and it is presented as unfalsifiable. An ethical skeptic has to ask “Is this considered proof by non-falsifiability?”
Jennifer also had a history of viral infection and was given prescriptions accordingly. Yet, this was not considered or accepted as a possible sign of an etiological event.
An NIH researcher, Brian Walitt, is another example of a researcher who has assumed that fibromyalgia and chronic fatigue syndrome are somatoform. In the following 2015 paper this statement is made:
“The discordance between the severity of subjective experience and that of objective impairment is the hallmark of somatoform illnesses, such as fibromyalgia and chronic fatigue syndrome.”
To claim that CFS/ME and fibromyalgia are somatoform is a bit of stretch; this broad of a conclusion cannot be made considering the state of evidence and what is currently unknown. It wasn’t until recently that it was discovered that cytokine signature was associated with chronic fatigue syndrome. The reason this information wasn’t being collected on patients in clinical practice is because the tests aren’t offered, and as Montoya (one of the researchers) says regarding what is offered by mainstream medicine, “those tests aren’t measuring the right things.”
This evidence alone disproves the notion that chronic fatigue syndrome patients have a disease of purely “psychological origin.” What is more likely is that chronic fatigue syndrome is a disease involving multiple etiological links and pathways varying in subgroups. For example, CFS/ME has also been connected to intracranial hypertension without papilledema in some CFS patients. If the investigators involved in this study had not looked into this, what would our current state of knowledge be? Each investigator that asks the right question leads us further and further down the knowledge development process. We cannot assume answers before questions are even asked.
What needs to be both understood and avoided is pro-innovation bias, the argument from ignorance, probabilistic fallacy, and the availability heuristic.
Pro-innovation bias is “the tendency to have an excessive optimism towards technology or science’s ability to shed light into a subject or advance understanding, while often failing to identify its limitations and weaknesses, and habitually dismissing all other methods (The Ethical Skeptic, n.d.).” Simply put, any excessive optimism or confidence in our current understanding of this issue may be overplayed. In turn, this can lead to conclusions that were made too quickly before more biological bases could even be discovered or explored.
The argument from ignorance asserts that a proposition is true because it has not yet been proven false, or is false because it has not been shown to have any evidence. A functional neurological disorder diagnosis could in many cases be based on an argument from ignorance. A proposition regarding somatic/functional neurological symptoms may be assumed to be true (because it has not been proven false). This is also because the alternative explanations have not yet been found due to scientific obscurity.
Additionally, this situation can relate to the probabilistic fallacy and availability heuristic. The probability fallacy involves “the presumption that one holds enough data to determine what is probable and improbable in a field of a set of data” and the availability heuristic involves “adjudicating an answer to a question according to only the information which is available at the time (The Ethical Skeptic, n.d.).” Although current and past symptom history is considered in functional neurological disorder diagnoses, this diagnostic “answer” may still only be serving the overall information known at the time in the field of science and medicine.
Provisional Knowledge – the contrivance of a series of purposed provisional arguments, into a stack of probable explanations wherein we ignore the increasing unlikelihood of our conclusions and simply consider the stack of plurality to be proscribed; and eventually by Neuhaus’s Law, prescribed (The Ethical Skeptic, n.d.)
We also have to play close attention to psychologism. This is “when psychology plays the sole or central role in underpinning facts or explaining a non-psychological fact or principle expressed as constituting accepted knowledge. Suffers from the weakness that psychological principles enjoy a perch which can never be falsified, therefore they are at risk of standing as pseudoscience (The Ethical Skeptic, n.d).” Michael Loughlin, a senior philosophy lecturer at Manchester Metropolitan University has explored this problem in regards to how ambiguities in diagnostic terms and psychological inference can be fallacious when perceiving and categorizing symptoms since they can have possible underlying (and unseen) physical causes.
An important issue here is that assumptions are being used for specious proclamations and it is harming patients. An example of this in the case of a patient with chronic fatigue syndrome, Karina Hansen, a danish woman who was taken forcibly from her loving parents and forced to undergo psychiatric treatment for an assumed functional neurological disorder. Another example is of a case study where a woman with prion disease died after she was originally diagnosed with conversion disorder and major depression. Below will be the case history (if you find this too long you can scroll down and skip over it or look at the provided link to the PDF).
“Ms. A was a 49-year-old Caucasian woman who had never married and who had been a communications product engineer. Before onset of her symptoms, she had never seen a psychiatrist, never been diagnosed with a psychiatric disorder, and never been treated with a psychotropic medication. Her medical history was notable only for a febrile illness that may have been an encephalitis of uncertain etiology after a trip to South America when she was in her 20s. There was no family history of psychiatric illness, epilepsy, or neurological or neurodegenerative disorders.
Ms. A had grown up as the youngest of three children. She described her relationship with her two brothers as an adult as “distant.” Her relationship with her parents was reported to have been “good,” although additional details were lacking, and both parents were deceased. She had no history of physical or sexual abuse, but she felt that she had been excessively teased by her brothers while growing up, which left residual resentment even late into her adult life. She did not date frequently in either her teens or 20s. She had a number of heterosexual romantic relationships but described these as superficial and brief. She noted that she had always been sexually interested in women, but until just before the onset of the symptoms leading to hospitalization, she had never had a same-sex romantic relationship. The revelation of her homosexuality to her family was poorly received. She described it as “cold,” and she felt criticized and ashamed. Ms. A had begun her employment with a communications company as a telephone operator and had advanced over the next 20 years until she became a high-level manager in research and development.
Ultimately, she was recruited into an upper-level management position with a competitor in the field. She traveled frequently to Europe as part of her new job. During this transition in her career, she met a woman with whom she hoped to have a fulfilling romantic relationship and thus estranged herself from her family. In the context of these psychosocial stressors and after a flight from Europe, she developed an acute onset of lower-back pain while lifting her laptop computer out of an overhead bin. Soon after she saw a chiropractor for lower-back pain; upon examination, the practitioner noted some weakness of the lower extremities. She received no benefit from the chiropractic visits and began to note the onset of new symptoms. These included a tremor “all over [her] body” and weakness in “big muscle groups.” This made ambulation difficult and was the beginning of a slow deterioration in gait. She made an appointment with her primary care physician.
A workup included magnetic resonance imaging (MRI) of her spine, which showed a mild lumbar right-paramedian bulge that was judged to be inadequate to explain her symptoms. Her laboratory tests included a CBC, a full metabolic panel, including liver function tests—all of which were found to be within normal ranges—a measurement of erythrocyte sedimentation rate (4), and a rheumatoid factor check (negative result). These results were obtained almost 2 months after Ms. A’s original lower-back strain. Ms. A’s medical and emotional needs became overly burdensome to her partner, which led to the end of their romantic relationship. Ms. A continued to experience weakness in her lower extremities and ambulation difficulties.
Her physician ordered an MRI of the brain, which was normal except for evidence of chronic sinusitis in the left maxillary sinus. An MRI of her cervical spine was also performed, and the results were found to be normal. Additionally, a lumbar puncture was performed as the diagnostic considerations expanded to include multiple sclerosis, encephalitis, neurosyphilis, subacute sclerosing panencephalitis, and acute idiopathic polyneuritis. Results of tests regarding CSF glucose, cell cytology, protein, gram stain, immunoglobulin M, immunoglobulin G, fluorescent treponemal antibody absorption, and immunoglobin banding were all negative. Despite reassurance that these symptoms would likely remit, Ms. A continued to experience more weakness and ataxia. She was seen by another internist and diagnosed with atypical multiple sclerosis.
She was given a trial of methylprednisolone sodium succinate and noted a brief period of symptom improvement. She was seen by a neurologist 1 month later, and an EEG was ordered. Again, the result was unrevealing. Five months after her initial symptoms, Ms. A complained of diplopia, difficulty swallowing, and frequency of urination in addition to her symptoms of leg weakness, tremor, and gait difficulties. She saw another neurologist whose differential diagnosis included Creutzfeldt-Jacob disease. She was then seen by an associate of a national authority on prion disease, who felt that Creutzfeldt-Jakob disease was a “low-probability” diagnosis, but a measurement of blood mercury level was recommended, which was also found to be negative. At this point Ms. A’s treating physician began to seriously consider that these symptoms might have a psychological component, which led to a psychiatric evaluation. About 6 months from the onset of her symptoms, Ms. A completed a neurocognitive and psychological battery of tests.
The results were as follows: score of 30/30 on the Mini-Mental State Examination (MMSE), a score of 33/33 on the Blessed Dementia Scale (5), and a Sensory Perceptual Screening (6)examination performed without errors. She completed the Wechsler Memory Scale—Revised (7). Her score fell within the average to high-average range, and she was judged to have high-average intellectual abilities. Also of note was that her receptive and expressive language abilities were found to be intact, her conversational speech was fluid and nonphasic, her digit repetition was high average, her oral calculations were average, and her attention and concentration were normal. The only abnormal finding in this test battery was on the MMPI-2, which showed elevated depression.
Although Ms. A complained of weakness and an unstable gait, results of formal neurologic examinations continued to be completely normal. In addition, Ms. A’s complaints of waxing and waning strength and difficulty walking were difficult to explain. At this time, she was given axis I diagnoses of major depression and conversion disorder. Ms. A was given fluoxetine for depression and buspirone for anxiety. She was thereafter discharged to a residential psychiatric facility. Nearly 8 months after the first appearance of lower-back strain, Ms. A was seen by a specialist in dissociative disorders and psychosomatic illness. He hypnotized Ms. A and noted that she was highly hypnotizable and that, under hypnosis, her symptoms improved. She continued to decompensate and was transferred from the residential facility to a skilled nursing facility secondary to functional deterioration and an inability to complete activities of daily living without assistance.
This deterioration continued until Ms. A was again hospitalized, this time on the Behavioral Medicine Unit at Stanford University Hospital. At that time, she was confined to a wheelchair. She complained of waxing and waning dysarthria and difficulty swallowing, an ataxic-like gait, and tremors that would move over her entire body, which she would refer to as “convulsions.” She also had occasional complaints of diplopia, for which she would compensate by closing one eye, and frequent squinting. She continued to experience subjective weakness in her lower extremities, which varied in degree, although it was always present. At this time, both Ms. A and her family agreed that her mood was normal. Her score on the MMSE at admission was 24/30; she appeared to be poorly motivated to complete the test. Her insight was judged to be good, and she was reported to say that she was motivated to determine the cause of her disability so she could return to work. She admitted that being ill had brought her family back to her and that her ex-lover was again in frequent contact, both of which pleased her deeply. Upon examination her tremors were noted to wax and wane depending on the content of her conversation.
Her diagnoses at admission were conversion disorder and major depression, single episode, moderate, nonpsychotic, and in remission with a regimen of fluoxetine and buspirone. Psychological testing was ordered, as was a follow-up neurology consultation. Upon completion of neurological and psychometric evaluations, Ms. A’s primary diagnosis remained conversion disorder. Supporting this diagnosis were fluctuating and at times bizarre symptoms: waxing and waning memory deficits, an inability to ambulate without assistance despite adequate strength, back pain, eye squinting, and tremor, but no evidence of spasticity or cerebellar abnormalities.
There was also some concern over factitious elements, such as a new complaint of life-long auditory and visual hallucinations. Ultimately, it was decided to proceed with a behaviorally oriented rehabilitation program. This involved aggressive physical therapy, occupational therapy, and participation in groups and activities, with the focus on treating Ms. A’s functional disability. Furthermore, with the intent of both confirming and treating the conversion disorder, it was explained to Ms. A that in the setting of such an intensive rehabilitation program, her functional ability should improve if it was simply related to an underlying medical etiology, such as the apparent severe muscle deconditioning she had experienced.
It was also explained to Ms. A that if she did not improve after undergoing such an intensive rehabilitation program, it would be owing to either a lack of participation or motivation on her part or because her condition was purely the result of a psychological disturbance. That is to say, improvement would confirm a medical etiology. This behavioral approach to treating conversion disorder was based on a review of the literature and the apparent success of the use of this “double-bind” model (3).
The neurology service was consulted soon after Ms. A was hospitalized. They found her to have normal conjugate eye movements without nystagmus, although she complained of diplopia. Her palate lifted symmetrically, her gag reflex was intact, and a fluctuating dysarthria in her speech was described as “clear” at times. She was noted to have decreased muscle bulk on the anterior tibialis muscles bilaterally and a slight contracture of the left Achilles tendon, both attributed to deconditioning. Her muscle strength was intact, with bilaterally symmetric deep tendon reflexes. She had intermittent tremors of her trunk and extremities, both at rest and with movement, without an apparent pattern. She had no cerebellar abnormalities; e.g., heel-to-shin and finger-to-nose movements were intact. While standing Ms. A was unable to place her left heel to the floor, was unsteady, and was unable to stand unassisted. She appeared to be cognitively intact, although her affect ranged from tearful to “flattened.” Noting her prior workup and neurologic evaluations, the neurology service assessed the observed tremors and other symptoms as highly elaborated and “functional” in nature.
There was noted a lack of cooperation with the funduscopic examination, which was complicated by Ms. A’s frequent blinking. The neurology service emphasized that at that time there was no evidence of nervous system disease, concurred with a diagnosis of conversion disorder, and recommended continued behaviorally based treatments. With great encouragement, Ms. A was at times able to ambulate somewhat better and at other times was only able to ambulate with two-person support. Her speech would fluctuate in terms of intelligibility, her tremors would wax and wane, and her ability to perform on the MMSE would change as well. Some of the variability was clearly associated with anxiety about issues and concerns expressed in the content of her speech. She clearly responded to decreased nursing attention with vocalizations but not always with words, sometimes moaning plaintively.
While eating she was observed to throw her head back, causing her to choke on her food; however, with consistent reinforcement, she would keep her chin down while chewing and have no difficulty. Because of concerns over her apparent swallowing difficulties, a videofluoroscopic study was performed and an occupational therapy swallowing examination completed. Both showed normal swallowing reflexes but noted that she would tilt her head back and choke at times. This was considered to be volitional behavior.
There were also attempts at managing her condition with psychotropic medication. Ms. A had had a good response to fluoxetine for her depression, and this treatment was continued and the dose increased. The buspirone therapy was continued, and olanzapine was added at a dose up to 10 mg, given at night, mostly for episodes of agitation and concern that Ms. A was at times psychotic. None of these medication changes appeared to change her course of illness. Approximately 6 weeks after Ms. A’s admission, the psychiatry service noted waxing and waning primitive reflexes. In addition, she began to exhibit progressively more disinhibited behavior, such as throwing food and smearing it on her face, along with choking sounds. She developed an exaggerated startle response to innocuous stimuli. Another MRI and EEG were performed, and again the neurology service was consulted. Ms. A had an essentially normal examination.
The service noted slurred speech but felt it was functional and that no evidence of dysarthria was present. Ms. A knew the date but appeared to be disoriented to place. The neurology service did not note any disconjugate gaze but raised questions about subtle right nasolabial fold flattening, oral dyskinesias, and uncoordinated tongue movements. There also was a concern over a subtle right lower-extremity rigidity that had not been noted previously. Additionally, mild, right-greater-than-left intention tremor was noted. Ms. A’s repeat MRI of the head resulted in a normal scan without evidence of ventricular enlargement or expanded sulci. The neurology team noted that the buspirone may have caused her tremor, referring to it as tardive dyskinesia, and thought both fluoxetine and olanzapine may have contributed to it as well. They recommended simplification of the medication regimen. Earlier in her hospitalization, Ms. A had been administered an MMPI-2. The results of the entire neuropsychological battery were now considered to be invalid because of her excessive endorsement of symptoms.
In addition, a Rorschach test given Ms. A was deemed unscorable. She tended to tell long, convoluted stories about the inkblots and could not be redirected. She used what appeared to be neologisms (e.g., “torcle bug” and “buldar”), but when she was questioned, she would laugh and say that she had made them up by combining words. Ms. A was dysarthric and difficult to understand. She tended to avoid responding to questions with direct answers and appeared to be somewhat disinhibited; e.g., she asked the female examiner out on a date.
Given the lack of information gained from administration of these tests, the examiner requested copies of the raw data from Ms. A’s previous neuropsychological testing. Her MMPI-2 results, taken 4 months earlier, were notable only for depression and lacked the expected elevation in somatic preoccupation, denial, repression, and endorsement of neurological symptoms that is often found in individuals with conversion disorder.
Subsequently, psychological testing was readministered, and this time it was considered to be valid. Ms. A was given the shorter Millon Clinical Multiaxial Inventory—III (8), the Rorschach test, and the Thematic Apperception Test. The results of the Millon Clinical Multiaxial Inventory—III were considered to be valid, but Ms. A appeared to answer it with a bias toward magnifying her symptoms, as it indicated the presence of a significant mental disorder. Her profile suggested a personality disorder with narcissistic, avoidant, and paranoid features. Her Rorschach test results had 19 scorable responses and, this time, was notable for linear responses and an absence of neologisms. Ms. A exhibited considerable effort and demonstrated complexity in her thought process, as well as an ability to synthesize information. She had some difficulty with perceptual accuracy and demonstrated a tendency to become easily disorganized.
Ms. A continued to fare poorly, her grooming was very poor, and her ability to perform simple activities of daily living was severely impaired. Despite aggressive behavioral strategies to treat a presumptive conversion disorder, no progress was seen. Repeated neurologic consultations were inconclusive. An MRI and EEG showed no abnormality. After exhaustive review of Ms. A’s care, strategies to improve her function, and attempts to define a possible medical etiology, it was reluctantly agreed that no progress had been made in the prior 6 weeks of intensive therapies. Plans were made to have her moved to a skilled nursing facility. Ms. A’s response to this proposed move was dramatic. There was an increase in nonverbal vocalizations, choking, disinhibited outbursts, difficulty following directions, and tearfulness. She began to look more abulic, with more frequent and severe difficulties with chewing and swallowing. With the expected discharge date looming, another EEG was ordered. It was decided to place a nasogastric tube for feeding. However, less than 24 hours after insertion, it was taken out by Ms. A. Another was placed, with a similar result. Faced with the difficulties of having Ms. A undergo even a minor procedure for the presumed conversion disorder, her unwillingness to allow the nasogastric tube to remain in place, and ambivalence about proceeding to percutaneous endoscopic gastrostomy placement in an individual with a psychosomatic illness, we decided to initiate another trial of oral feedings. That day Ms. A ate both lunch and dinner without significant difficulty.
Ms. A was found later that night in cardiopulmonary arrest. It occurred almost 90 minutes after dinner, which had been observed by nursing staff and described as uneventful. After dinner that night, Ms. A had been heard choking; although her oropharynx had been examined and was found to be clear of food and debris. She was found cyanotic approximately 30 minutes later, without respiration or pulse. Suction performed during cardiopulmonary resuscitation revealed small bits of food—apparent evidence of aspiration. Ms. A was presumed to have asphyxiated because of an obstructed airway. It was thought possible at the time that Ms. A may have moved some food into her chair and later put it into her mouth and choked, suffering asphyxiation, cardiopulmonary collapse, and near-death. She was resuscitated and sent to the intensive care unit, where about 36 hours later she was declared brain dead by EEG. Ironically, the EEG ordered earlier in the week was read at the same time as the EEG from the ICU. The former was noted to be abnormal and interpreted as showing excessive theta activity in bilateral temporal areas that was consistent with an encephalopathy. The EEG report specifically mentioned the possibility of a rapid neurodegenerative process in the differential. Ms. A was removed from life support after a lengthy meeting with her family, and she expired shortly thereafter.
The family granted permission for an unrestricted autopsy. On general autopsy, Ms. A was found to have acute and organizing bronchopneumonia, with fragments of vegetable material in the bronchus consistent with prior aspiration. The results of gross examination of the external brain and coronal sections was found to be entirely normal, with no evidence of inflammation, neoplasm, atrophy, or white matter changes.
However, microscopic examination revealed changes indicative of prion disease; namely, sections of the frontal, hippocampal, and occipital cortices showed moderate neuronal loss, reactive astrocytosis, and variably sized vacuoles within the neuropil, also know as spongiform change (Figure 1A). No kuru-type plaques were seen; no inflammation was observed. The underlying white matter showed patchy myelin loss and spongiform change. In addition, many of the sections revealed evidence of acute ischemic/hypoxic injury, with shrunken neurons displaying hyperchromatic, indistinct nuclei and eosinophilic cytoplasm (Figure 1B). Sections of the midbrain and brainstem also showed spongiform change, as well as neuronal dropout and gliosis in the substantia nigra and olivary nuclei. A section of the cerebellum showed a normal-appearing granular cell layer, loss and acute ischemic/hypoxic injury of the Purkinje neurons, and mild spongiform change in the molecular layer. The underlying cerebellar white matter had mild spongiform change, and the dentate nucleus showed gliosis and neuronal loss.
In compliance with an ongoing surveillance program sponsored by the American Association of Neuropathologists and the Centers for Disease Control and Prevention, tissue was sent for immunodiagnostic studies to collaborators at the newly formed National Prion Disease Pathology Surveillance Center in Cleveland. Western immunoblot analysis revealed the presence of the pathogenic, protease-resistant isoform of prion protein, which confirmed the diagnosis of prion disease (Figure 2). Of interest, this sensitive detection method (9) discerned the protease-resistant isoform of prion protein, as evidenced by the unique three-band pattern revealed after digestion with proteinase K in the comparison tissue from another patient with Creutzfeldt-Jakob disease (lane 1) and in the frontal cortex from Ms. A (lane 4). It found no protease-resistant isoform of prion protein in the cerebellar tissue (lane 3). This might suggest a sampling or technical error or that levels of the prion protein in the cerebellum were possibly too low for detection.”
Conclusions from this presented case study:
“A remarkable aspect of this case was the nearly unani- mous opinion by the neurology and psychiatry services that this patient’s presentation was conversion disorder and was not organic until after she had coded and was in the intensive care unit. This case provides an excellent teaching example of why the physician needs to sustain a suspension of belief or disbelief and seriously consider in every patient whether an entirely psychological or entirely biological explanation will identify the current diagnosis and appropriate interventions.
The belief that this patient had a conversion disorder also appeared to dissuade the consulting neurologists from reconsidering some of their findings. Signs such as an apparent dyskinesia of the tongue, a flattened affect, at least one frontal release sign, functional evidence of disin- hibition, and loss of appropriate social behaviors may have been minimized by the consulting service.
This case report is, to the best of our knowledge, the first report in the literature of a patient, who, upon death, was diagnosed with Creutzfeldt-Jakob disease and who had symptoms that were thought to represent a primary diag- nosis of a psychosomatic illness. This report also contains, to our knowledge, the first serial psychometric examina- tion of a patient with Creutzfeldt-Jakob disease. Despite the use of different psychometric instruments, there was a clear pattern of development of impaired defenses and primitive personality characteristics that were associated with clinical decline and progression of the disease.
In addition to the visible effects of the neurodegenera- tive process on motor control and cerebellar function, we argued that the neurodegeneration of frontal cortices and subcortical structures affected
Ms. A’s personality and possibly created a vulnerability for the elaboration of symptoms concordant with pathologic illness behavior. More subtle effects that may have affected interhemi- spheric communication, dominance, or interference of parietal motor control may have contributed to this bio- logic vulnerability as well (35, 36). This case provides a small window into the neurobiology of personality and perhaps into conversion itself. It also reveals the power of our biases and the intersection of neurobiology and psy- chological models of psychiatric illness.”
While I understand that psychological explanations may seem sexy and tempting to psychiatrists and even some neurologists, I still highly recommend suspending judgement before making declarations and using them to justify medical kidnappings and erroneous diagnoses.
In closing, some major points to outline are (1) yes, functional neurological disorders and somatic symptoms are real and need as much research as possible on the topic, (2) professionals in the field of psychiatry and neurology need to openly discuss the limits to some of their neurological disorder diagnoses especially concerning functional neurological disorders and somatic symptoms, (3) while the criteria is very specific and researchers call for positive diagnoses rather than just diagnoses based on exclusion, they can still be falsely made when it is assumed that science and medicine already have the needed resources to identify every single pathophysiological/biochemical problem related to symptoms of disease, and (4) the diagnostic manual needs to include a disclaimer that states that a functional neurological disorder diagnosis may in fact be innacurate because our testing methods/detection capabilities are not complete and science may advance the field in such a way that contradicts the diagnosis. The diagnosis can be highly misleading and proves to be so once science sheds light on misunderstood and unexplored issues.
Similarly to this issue of assumption, I have also outlined the psychiatric fallacy wherein psychiatrists use fallacious reasoning and fail to properly investigate or identify potential biological causes of commonly diagnosed mental disorders . It is up to the patient population and ethical scientists and skeptics to weigh the current state of evidence and openly discuss their questions, concerns, findings, and observations. The below image will also visually demonstrate an important concept of the knowledge development process.
The larger circle contains smaller circle sections tha relate to a specific time frame of information and knowledge. As each section moves outward, we see that the circle gets bigger and years add together. The 20 year circle contains the smaller 10 year circle within it, the 30 year circle contains the 10 and 20 year circles within it, the 40 year circle contains the 10, 20, and 30 year circles within it, and this continues to go on and on. Each circle contains knowledge from different years combined within it based on the time and the extent of development. We cannot assume that our circle represents the entire whole and that the circle will not grow in size over time as new information is collected. When people within each time frame assume their section has all of the answers, they are suffering from myopia. Each section has critical importance and plays a part in the entire circle’s growth, size, and intelligence.