Conversion Disorder in Neuro-Ophthalmology
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Patients with non-organic disease may present to ophthalmologists with afferent (visual loss) or efferent (double vision) complaints. Ophthalmologist should carefully document the eye findings and if nonorganic disease is suspected careful attention to proving that the vision is better than claimed is essential for diagnosing nonorganic disease. A normal structural eye examination is not sufficient to make the diagnosis of nonorganic visual loss and formal visual field testing is recommended for patients with unexplained visual loss. The presence of a tunnel field should be confirmed on 1 and 2 meter confrontation testing. A funnel field implies an organic etiology as does the presence of bitemporal or homonymous hemianopsia or central/cecocentral scotomas (which are uncommon nonorganic presentations). Electrophysiology (VEP and ERG) may be necessary to help with the diagnosis of nonorganic visual loss but an abnormal VEP does not prove organic disease. We prefer the term “nonorganic visual loss” to describe these patients because the DSM V has specific criteria for the differential diagnosis including CD. Although most patients do not require psychiatric evaluation, we recommend that patients with psychiatric co-morbidities or exacerbating psychological risk factors be considered for referral to psychiatry in order to make a DSM V diagnosis and be treated with available and appropriate pharmacologic and non-pharmacologic psychotherapy if indicated.
Disease
Conversion disorder (CD), is a non-organic neurological symptom disorder with a specific Diagnostic and Statistical Manual (DSM) recognized category of psychiatric disorder. Patients with CD report various unexplained symptoms and signs that affect the sensory and/or motor function that cannot be explained by organic pathology (i.e., non-organic) (1). Most cases of CD are associated with significant psychological stress, triggers, or conflict (2) although patients may deny or be unaware of these psychologic conditions. CD may significantly impair the patient’s ability to function and vary in severity and complexity (3). Compared to similar but distinct DSM disorders (e.g., malingering, or factitious disorders), patients with CD are not consciously aware of their disease and thus cannot voluntarily control their symptoms at will and are not feigning their distress or symptoms (4). For example, “a woman who believes it is not acceptable to have violent feelings may suddenly feel numbness in her arms after becoming so angry that she wanted to hit someone. Instead of allowing herself to have violent thoughts about hitting someone, she experiences the physical symptoms of numbness in her arms” (5). This monograph is focused on the neuro-ophthalmic manifestations of CD.
Etiology
Although the exact etiology or pathogenesis of CD is not known, CD is often found to be associated with recent psychological trauma, stressors, or conflicts (6). The symptoms are thought to be a manifestation of the patient’s unconscious internal conflict “converting” to a somatic manifestation (1). There are also psychological theories that CD is a result of immature coping mechanisms learned in childhood to suppress emotions in difficult situations with a possible recurrence of these symptoms when faced with similar situations later in life (3). There has been evidence that the symptoms have biologically plausible mechanisms of expression through impaired communications between the amygdala and supplementary motor area causing excessive cortical arousal (7). Patients with CD may have slight impairments on neuropsychological tests as a result of these biological factors (1). Regardless of mechanism however, patients with CD may present to ophthalmology with afferent (e.g., visual loss, eye pain, positive or negative visual phenomenon) or efferent (e.g., double vision, oscillopsia, extraocular motility or lid spasms) complaints that can mimic organic neuro-ophthalmic pathology.
Epidemiology
The prevalence of CD within general hospital settings has been reported to be as low as 5% and as high as 25%8. In one study of patients referred for neurology outpatient appointments, 30% have been reported to have CD (9). Although CD is reportedly more common in females compared to males (2:1 up to 10:1) it can affect either gender, any age, and any racial group (1). In the past, the outdated and somewhat pejorative term “hysteria” was sometimes applied to women, many of whom had either organic disease or other DSM disorders including CD. The root word “hyster-“ from the Greek word for uterus implied that only females could be affected by “hysteria” and thus this diagnosis was stricken from the DSM in 1980. We prefer the non-judgmental term “nonorganic” and, if appropriate, the term “CD” for patients meeting DSM criteria.
Risk Factors
Although there are some proposed sociodemographic risk factors that are common in patients with CD, the diagnosis can occur in any patient regardless of demographic background. Some proposed associations of CD include (1):
• Rural residence
• Lack of education
• Lower socioeconomic status
• History of sexual or physical abuse
• Younger age
• Female
History
When nonorganic neuro-ophthalmic disease (including CD) is suspected, it is important to make the patient feel comfortable enough to share their story in addition to their symptoms (3). Allow the patient to list all symptoms they have been experiencing recently (3). Ask about recent triggering events or stressor in the patient’s life. Patients may benefit from full psychiatric histories and evaluation if the ophthalmologist is unable or unwilling to explore all of the DSM V criteria and alternative DSM V diagnoses (3).
Physical examination
Monocular or bilateral but asymmetric unexplained visual acuity loss:
• Starting at the 20/10 or better (rather than 20/20 )line and moving up the chart might be more helpful rather than the conventional way of checking visual acuity (starting at the claimed level of vision). Some patients with non-organic visual loss are suggestible and may be reassured or “coaxed” in to seeing better than the claimed level of visual acuity.
• A 4 BD vertical prism can be placed over the “good” or “better” seeing eye. The patient should be informed about the nature of a prism (e.g., “This is a prism, it bends the light and will make the image appear double. I am going to test your “good” eye first). For example, in a patient with 20/20 in the right eye (OD) and 20/200 in the left eye (OS), a single letter (e.g., “E”) from the Snellen line just at or below visual acuity of the better (OD) seeing eye (e.g., 20/40 line) could be displayed with the occlude over the “bad” eye (OS) The patient should then report what they see. If the patient reports seeing “two letter E’s” with the prism OD then not only does this prove the non-organic nature of the visual acuity loss (an organic response would be only one letter E if the vision truly is 20/200 OS) but amazingly we now have documentation of 20/40 vision in both eyes (OD and OS) without even directly testing the vision OS.
Visual field testing
• Patients with nonorganic visual loss often report a constricted (“tunnel”) visual field. A confrontation field test can define how many degrees of constriction is patient under monocular viewing conditions. Patients who show a tunnel field (i.e., the visual field constriction remains unchanged despite increasing the test distance) when checked at 1 and 2 meters suggests nonorganic vision loss. The organic response of a constricted visual field is a funnel configuration and not a tunnel configuration. This means that the organic visual field constriction must expand at 2 meter testing when compared to 1 meter testing.
• Patients with non-organic visual field constriction may be tested with saccades into the claimed “blind” visual field. This is a good test for non-organic constriction or any visual field defect because the patient typically does not recognize this test as testing their visual function. The idea can be reinforced by the clinician by stating that the test is of “eye movements”. Sometimes the patient can be distracted from the intent of the testing by asking if there is “pain with eye movement testing” (patients often respond that there is pain with eye movement). If the patient can make an accurate saccade and see the visual target (e.g, the examiner’s finger) in the documented “blind” visual field then this establishes the nonorganic nature of the visual field loss.
• Although visual field constriction (tunnel visual field) is the most common nonorganic visual field presentation, formal visual field test (e.g., Humphrey perimeter) may show a variety of possible visual defects in nonorganic disease (e.g., generalized depression, clover leaf type, or even hemianopic field loss). Bitemporal hemianopsia, homonymous hemianopsia, or central/cecocentral visual field defects are not common nonorganic presentations and clinicians should be cautious in making the diagnosis of nonorganic visual loss with these specific visual field defects. For patients with strictly monocular visual field defects, because of the overlapping nature of the visual fields between the two eyes, the visual field test can be repeated with both eyes open. If the repeat testing under binocular conditions shows persistence of the visual field defect with both eyes open this is consistent with a nonorganic cause.
Pupil exam
• The pupil examination is an objective confirmation of organic disease and should be normal in nonorganic visual loss.
• The presence of light near dissociation in bilateral cases or a relative afferent pupillary defect in unilateral or bilateral or asymmetric cases is evidence of organic disease.
• Patients with CD should have intact pupillary light reflexes (3).
Example testing for severe bilateral visual loss. These tests are only valid for complete or near complete blindness (hand motion or worse visual acuity) and are not appropriate tests for minimal, mild or even moderate visual loss.
• Patients with severe visual loss can be observed in the office before the examination even begins. From the onset of the patient encounter, the ophthalmic technician should be asked if the patient had difficulty getting to the exam chair without assistance or other vision directing behaviors in the waiting room.
• Optokinetic test: Patients claiming complete or near complete bilateral blindness can be tested for the optokinetic nystagmus response (OKN). Holding the OK rotating drum with black and white alternating vertical strips in front of the patient’s eyes the drum is slowly rotated in front of the patient’s eyes. If nystagmus is generated this is evidence of nonorganic response. In unilateral visual loss, the OKN drum can be rotated initially with both eyes open and then the clinician can cover the “good” eye while simultaneously continuing to rotate the drum before the fellow “bad” eye. If the examiner notes optokinetic nystagmus, this indicates that the patient’s afferent system for the OKN response is detecting the stripes and is evidence of nonorganic disease (3).
• Signature test: Have the patient sign a paper. If the hand motor function is normal a patient who produces no signature or a distorted signature compared with baseline, then the test is positive for nonorganic disease. A truly organically blind patient can still sign their name without difficulty (3).
• Fingertip test: Ask the patient to touch the tips of their index fingers together. A positive test is when a patient has difficulty completing this task when viewing with the blind eye(s). A truly blind patient can use their proprioception to complete this task assuming motor function is normal (3).
• Mirror test: Hold a mirror in front of the patient and have the patient open their eyes. As the examiner moves the mirror, observe if the patient tracks themselves in the mirror. If so, the test is positive and indicates that the patient is not truly blind (3).
In some patients, additional electrophysiological tests like pattern visual evoked potential (VEP) and full field or multifocal electroretinogram (ERG) may be used to adjudicate the functioning of the retina and posterior visual pathways. A normal pattern VEP and ERG in conjunction with a normal ocular exam can help to confirm the diagnosis of nonorganic visual loss. Unfortunately, the VEP can be defeated by patients who defocus the image or look away from the target during testing and thus an abnormal VEP does not prove organic disease. Nevertheless, patients with abnormal electrophysiology should be considered organic until proven to be nonorganic.
See also Eyewiki on Functional vision loss (12): https://eyewiki.org/Functional_Visual_Loss
Signs and Symptoms
The signs and symptoms of CD are variable and no one characteristic presentation is predictive of CD. Patients with CD may present with severe, debilitating, and sudden illness or mild, non-debilitating or chronic symptoms. Although there is often an association of CD with a psychiatric stressor, trigger, or even prior DSM V diagnosis, some patients with CD have no psychologic triggers, stress, or risk factors. Unfortunately, some patients with CD deny or are unaware of their prior stress, triggers, or risk factors and thus the CD is an unconscious manifestation of their psychological conflict. There may be high concern or paradoxically an inappropriate lack of concern for the presence or severity of their symptoms. Often with recognition and treatment of the underlying CD risk factors (stress reduction, pharmacotherapy for defined DSM indications) there can be improvement of the somatic manifestations (e.g., improved vision).
Some common manifestations of CD include partial or complete blindness, psychogenic nonepileptic seizures (PNES), unexplained sensory loss, motor tics, pseudodementia, pseudodystonia, and pseudoparalysis (1). Non-organic visual disturbances are especially common in CD and can present with blurry vision, unusual eye movements, double vision, eye pain, positive/negative visual phenomenae or nonorganic visual field defects (4).
DSM criteria for diagnosis
According to the DSM V, the diagnostic criteria for CD include (10):
• One or more symptoms of altered voluntary motor or sensory function
• Clinical findings that show evidence of incompatibility between the symptoms and recognized neurological or medical conditions
• Symptoms or deficit that are not better explained by another medical or mental disorder
• Symptoms or deficit that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation. Compared to the prior DSM iterations, it is no longer required to have comorbidities and “la belle indifference” for diagnosis, but the presence of these findings will support the diagnosis (3).
CD can be defined by criteria and thus is not truly a diagnosis of exclusion (6). However, ophthalmic providers should consider alternative organic disease prior to making the diagnosis of nonorganic visual loss. The diagnosis of nonorganic visual loss requires not only that the eye exam be normal (or incompatible with the type or severity of the visual loss) but also that the patient sees better than claimed. Documenting normal (or inconsistent) visual performance is sometimes a time consuming and challenging task. Clinicians should carefully document any inconsistencies on the exam (3). Patients with CD commonly have comorbid neurological disorders which may complicate the evaluation and may not provide a single (e.g., nonorganic) unifying diagnosis (i.e., nonorganic overlay) (10).
In addition, the DSM V criteria require that other psychiatric DSM V diagnoses be considered in the differential diagnosis. These include the following:
1. Factitious disorder: the patient may intentionally lie or fake symptoms without clear motivation (as in malingering) (11).
• Falsification of physical or psychological signs or symptoms, or induction of injury or disease, associated with identified deception (10).
• The individual presents himself or herself to others as ill, impaired, or injured (10).
• The deceptive behavior is evident even in the absence of obvious external rewards (10).
• The behavior is not better explained by another mental disorder, such as delusional disorder or another psychotic disorder (10)
2. Malingering: intentional feigning of symptoms for a secondary gain (11).
• While there are no diagnostic criteria, malingering should be strongly suspected if any combination of the following is noted (10):
• Medicolegal context of presentation (e.g., the individual is referred by an attorney to the clinician for examination, or the individual self-refers while litigation or criminal charges are pending).
• Marked discrepancy between the individual’s claimed stress or disability and the objective findings and observations.
• Lack of cooperation during the diagnostic evaluation and in complying with the prescribed treatment regimen.
• The presence of antisocial personality disorder.
3. Somatic symptom disorder: while similar to CD in that the symptoms cannot be linked to organic cause; patients are preoccupied with the symptoms and have excessive distress (11).
• One or more somatic symptoms that are distressing or result in significant disruption of daily life(10).
• Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated health concerns as manifested by at least one of the following (10):
• Disproportionate and persistent thoughts about the seriousness of one’s symptoms.
• Persistently high level of anxiety about health or symptoms.
• Excessive time and energy devoted to these symptoms or health concerns.
• Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically more than 6 months) (10).
Management
Successful treatment is dependent upon a strong therapeutic alliance between the patient and the provider (13). Many patients with conversion disorder will not be able to understand their unconscious psychological stress (1). Successful resolution of symptoms can only occur once patients have recognized the connection between their psychological and physical symptoms (1). Suggestions for a successful treatment include:
• Refrain from informing the patient of the diagnosis at the first meeting with the patient (1).
• Reassure the patient that despite the lack of organic sources, the symptoms the patient is experiencing are very real (14).
• Provide common examples (queasy stomach when public speaking) (13).
• Emphasize that because there is no structural damage, symptoms are potentially reversible (3).
• Discuss with the patient that accepting and understanding the diagnosis often leads to reversal of the symptoms. By accepting the diagnosis of conversion disorder, the patient will be able to properly engage with rehabilitation and will prevent further psychological stress from wondering what is wrong (3).
• Over the long term, patients should be taught to recognize potential triggers and appropriately react to prevent relapse (13).
Psychotherapy and physical therapy have also been proven to be helpful in the treatment of CD (14). In addition, medication for any underlying DSM V psychiatric comorbidities such as depression and anxiety will aid in the treatment of CD (14). Vision rehabilitation can be offered to those who present with vision loss.
Medical follow up
Documentation at follow-up appointments is important to show improvement as well as to look for co-existent organic disease (12). Referrals to neurology, psychiatry, or physical therapy may be appropriate depending on the co-morbidities and in order to establish the diagnosis of CD by DSM V criteria (4).
Prognosis
Generally, the visual prognosis for CD is good, with >90% having symptom resolution in one month and with up to 75% patients having no recurrence (2). Prognosis improves if the patient has the following factors (2):
• Sudden onset of symptoms
• Short duration of symptoms
• Early identifiable stressor
• No ongoing litigation
• Good premorbid functioning
• Lack of comorbid psychiatric disorders.
References
1. Ali S, Jabeen S, Pate RJ, et al. Conversion Disorder— Mind versus Body: A Review. Innov Clin Neurosci. 2015;12(5-6):27-33.
2. Blitzstein SM. Recognizing and treating conversion disorder. Virtual Mentor VM. 2008;10(3):158-160. doi:10.1001/virtualmentor.2008.10.3.cprl1-0803
3. Peeling JL, Muzio MR. Conversion Disorder. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2019. http://www.ncbi.nlm.nih.gov/books/NBK551567/. Accessed December 27, 2019.
4. Bezerra DM, Bezerra EM, Junior AJS, Amorim MAS, Miranda DB de. Postoperative visual loss due to conversion disorder after spine surgery: a case report. Braz J Anesthesiol Engl Ed. 2018;68(1):91-95. doi:10.1016/j.bjane.2015.03.005
5. Conversion disorder: MedlinePlus Medical Encyclopedia. https://medlineplus.gov/ency/article/000954.htm. Accessed December 27, 2019.
6. Somatoform Disorder: Overview, Somatization Disorder, Factitious Disorders and Malingering. November 2019. https://emedicine.medscape.com/article/918628-overview. Accessed December 27, 2019.
7. Harvey SB, Stanton BR, David AS. Conversion disorder: towards a neurobiological understanding. Neuropsychiatr Dis Treat. 2006;2(1):13-20.
8. Feinstein A. Conversion disorder: advances in our understanding. CMAJ Can Med Assoc J Assoc Medicale Can. 2011;183(8):915-920. doi:10.1503/cmaj.110490
9. Carson AJ, Best S, Postma K, Stone J, Warlow C, Sharpe M. The outcome of neurology outpatients with medically unexplained symptoms: a prospective cohort study. J Neurol Neurosurg Psychiatry. 2003;74(7):897-900. doi:10.1136/jnnp.74.7.897
10. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-5. 5th ed. Arlington, VA: American Psychiatric Publishing; 2013.
11. Owens C, Dein S. Conversion disorder: the modern hysteria. Adv Psychiatr Treat. 2006;12(2):152-157. doi:10.1192/apt.12.2.152
12. Functional Visual Loss - EyeWiki. https://eyewiki.aao.org/Functional_Visual_Loss. Accessed December 27, 2019.
13. Mulugeta S, Tesfay K, Frank R, Gruber-Frank C. Acute loss of vision in a young woman: A case report on psychogenic blindness. Ethiop J Health Sci. 2015;25(1):99-104-104. doi:10.4314/ejhs.v25i1.13
14. Stonnington CM, Barry JJ, Fisher RS. Conversion disorder. Am J Psychiatry. 2006;163(9):1510-1517. doi:10.1176/ajp.2006.163.9.1510
