When Stress-Sensitive Stiffness Was Diagnosed as Conversion Disorder
FND Nope
Moderator
A published case report describes a 52-year-old woman whose progressive lower-limb stiffness, muscle spasms and gait disturbance were eventually diagnosed as conversion disorder. Her symptoms had an important feature that could easily appear to support a functional explanation: she reported that they became worse with stress and fatigue. The diagnosis did not hold. Further neurological investigation eventually identified markedly elevated anti-GAD antibodies and characteristic abnormalities on electromyography, supporting a diagnosis of stiff-person syndrome (SPS).
The case is particularly interesting because stress and fatigue genuinely exacerbated her symptoms despite the eventual diagnosis of stiff-person syndrome. The case therefore illustrates that stress sensitivity, by itself, cannot distinguish a functional or psychogenic presentation from neurological disease.
Progressive stiffness and loss of mobility
The patient's symptoms had been present for approximately one year when she was referred to the reporting clinic. She described rigidity and muscle spasms affecting her lower limbs. The stiffness began distally and progressively moved proximally, eventually becoming severe enough to interfere with walking and climbing stairs. By the time of the later assessment, she had become wheelchair-dependent.
She specifically reported that stress and fatigue appeared to worsen her symptoms. During the preceding year she had undergone investigations and assessments in several different settings, including rheumatology, orthopaedics and psychiatry. According to the case report, various diagnoses had been considered before she was ultimately diagnosed with conversion disorder and treated with antidepressants.
Her medical history was also notable for Hashimoto's thyroiditis and hypertension. At the time described in the report, her medications included sertraline, levothyroxine, atenolol and pregabalin.
Neurological examination
On neurological examination, movement of the lower limbs was restricted in all directions, with rigidity involving both distal and proximal muscles. Deep tendon reflexes were reported as normal in the upper and lower limbs, while plantar responses were flexor bilaterally.
Routine investigations did not immediately reveal an explanation. Creatine kinase, complete blood count, erythrocyte sedimentation rate, C-reactive protein and rheumatoid factor were reported as normal. Thyroid function testing, antithyroglobulin antibodies and thyroid-stimulating hormone receptor antibodies were also normal.
The investigation changes direction
More specific testing produced a very different picture. Her anti-thyroid peroxidase antibody level was elevated at 75 IU, compared with a stated normal range of 0–34 IU. More importantly, serum anti-glutamic acid decarboxylase (anti-GAD) antibodies were reported at 72, with the laboratory's normal value stated as less than 1.
Electromyography provided further objective evidence. The authors reported continuous motor-unit discharge and simultaneous co-contraction in the lower extremities. These findings, together with the clinical presentation and anti-GAD result, supported stiff-person syndrome rather than conversion disorder.
Because SPS can occasionally occur as a paraneoplastic neurological syndrome, the clinicians also investigated for malignancy. Tumour markers and paraneoplastic testing were reported as normal, while mammography and CT imaging of the chest, abdomen and pelvis did not identify an occult cancer.
Response to treatment
The patient was treated with intravenous immunoglobulin (IVIG), reported as a total dose of 2 g/kg over five days. The authors described significant improvement beginning during the admission, with improvement still evident at the two-month follow-up.
The response does not by itself establish the diagnosis, but in this case it followed a diagnostic work-up that had already identified both strongly elevated anti-GAD antibodies and electrophysiological abnormalities consistent with SPS.
Stress was real. The explanation was wrong.
Perhaps the most useful part of this case is that there is no need to dispute the patient's report that stress worsened her symptoms. Stiff-person syndrome can itself be sensitive to emotional stress and other stimuli. The presence of a stress-symptom relationship therefore did not distinguish conversion disorder from neurological disease in this patient.
This matters because observations can be completely genuine while the interpretation attached to them is wrong. A symptom changing with stress does not demonstrate that the symptom originates from a functional or psychogenic mechanism. Stress can modify the expression of neurological disease as well.
Nor does this case establish that every unusual gait, episode of stiffness or stress-responsive neurological symptom represents SPS. Stiff-person syndrome is rare, and diagnosing it incorrectly creates its own problems. Modern research has documented substantial overdiagnosis of SPS as well as missed SPS, with functional neurological disorders among the common alternative diagnoses in patients incorrectly thought to have stiff-person spectrum disorders. The lesson therefore cuts both ways: neither label should substitute for evidence.
The authors' own warning
The authors explicitly discussed the danger of overdiagnosing psychogenic gait disorders and thereby missing an organic neurological disorder. Their conclusion was that stiff-person syndrome and other movement disorders should be considered when an unusual gait leads clinicians toward conversion disorder, particularly because delayed diagnosis can result in prolonged neurological disability.
“Psychogenic gait disorders are common and are the major manifestations in patients with psychogenic movement disorders. But it may be over diagnosed and missed the organic problems.”
The wording is awkward, but the point is straightforward. This patient spent approximately a year with a conversion disorder diagnosis while a rare neurological disease continued to progress. By the time SPS was identified, she had gone from progressive leg stiffness and difficulty climbing stairs to requiring a wheelchair.
Why this case matters
This is not simply another example of an initial diagnosis later being replaced. It demonstrates a more specific diagnostic problem: a feature that may appear compatible with a functional explanation can also occur in an established neurological disease. Stress sensitivity did not protect the conversion diagnosis from falsification, and it did not make the later biological findings less important.
The eventual diagnosis rested on a combination of the clinical pattern, markedly abnormal anti-GAD antibodies and characteristic electrophysiological findings. Once those findings emerged, the earlier interpretation had to give way to the evidence.
That is how a diagnosis should work. Clinical observations generate and support hypotheses, but those hypotheses must remain revisable when stronger evidence appears.
Source
Stiff person case misdiagnosed as conversion disorder: A case report, published in Caspian Journal of Internal Medicine, 2017.
For broader context on the difficulty of distinguishing stiff-person spectrum disorders from other conditions, including FND, see Stiff-person spectrum disorder diagnosis, misdiagnosis, and suggested diagnostic criteria. In that Mayo Clinic cohort, misdiagnosis of SPSD was itself common, reinforcing the need for objective clinical, serological and electrophysiological evidence rather than assuming that diagnostic error runs in only one direction.
