Abnormal somatosensory evoked potentials in a child with motor conversion disorder: A case report.

A 12‐year‐old female child complained of bilaterally limited lower limb activity for 4 days before admission to the pediatric neurology department. She could not walk alone, but she could maintain a squatting posture for 10 min when using the toilet and was also observed to raise her legs inadvertently. She had suffered trauma to her right hand at 4 years old, and the activity of the hand remained slightly limited as of the current admission. The girl's parents both had mental retardation; therefore, she was in the care of her grandfather and had little contact with her parents. Before the onset of the disease, she had been required to start school, at which time her stress level increased.

The patient had restricted movement of the joints in both lower extremities, with normal touch, blunted pain, and significant lower limb weakness (muscle strength I–II). Upper limb muscle tone and strength were normal. There were no sensory deficits. The abdominal wall reflex was normal. The Achilles tendon reflex and the knee reflex were absent. Pathological reflexes were absent. No other pathological results were found on examination.

Blood work (routine blood test, liver and kidney function, cardiac biomarkers, muscle enzymes, coagulation test, ammonia test, pyruvate‐blood test, lactic acid) showed normally, and viral markers (IgM antibodies to enterovirus, Epstein–Barr virus, coxsackievirus, adenovirus, cytomegalovirus, rubella virus, simple Herpes virus) were negative. Plain and enhanced spinal magnetic resonance imaging (MRI) showed no abnormalities. Nerve conduction in the lower limbs was normal. Somatosensory evoked potential (SSEP) detection was first performed on the third day after disease onset in our hospital outpatient clinic. The cathode was located between the medial malleolus and the Achilles tendon, where stimulation caused big toe abduction. The anode was placed 3 cm distal to the cathode and delivered constant current pulses of 100 msec, applied at 3 Hz, with a stimulus intensity of 8 mA; the data were sampled every 100 msec for analysis, and each run represented the average of two hundred stimuli. Cortical waves (P40) were recorded over the scalp at Cz and referenced to Fz. Spinal waves [cauda equina (CE)] were recorded over the L5 spinous process and popliteal fossa (PF) waves were recorded over posterior tibial nerve at PF, referenced to another surface electrode placed 3–4 cm away. In order to ensure that the results were correct, each recording was repeated more than two times. We used a Nihon Kohden Neuropack MEB‐9200K for recording. When the bilateral tibial nerves were stimulated, cortical P40 waves were bilaterally absent, and bilateral CE waves and PF waves with normal latencies (17.9 ms for the right tibial nerve CE, 17.5 ms for the left tibial nerve CE, 8.75 ms for the right tibial nerve PF, 8.75 ms for the left tibial nerve PF) were elicited (Fig. 1a,b).

Fig 1

Bilateral posterior tibial nerve somatosensory evoked potential (SSEP). (a) SSEP lower limb stimulate right tibial (3rd day of the disease course). (b) SSEP lower limb stimulate left tibial (3rd day of the disease course). (c) SSEP lower limb stimulate right tibial (11th day of the disease course). (d) SSEP lower limb stimulate left tibial (11th day of the disease course). CE, cauda equina; PF, popliteal fossa; L5, L5 spinous process; Ref, reference.

A neurological and psychiatric joint consultation arrived at a diagnosis of motor conversion disorder which might be triggered by anxiety regarding starting school. After 4 days of hospitalization with psychological counseling and B vitamin supplementation, she gradually walked. On the 11th day of the disease course, she could walk on her own. Then, we re‐examined SSEPs. Bilateral cortical P40 waves, CE waves, and PF waves were normal latencies (36.4 ms for the right tibial nerve P40, 36.4 ms for the left tibial nerve P40, 18 ms for the right tibial nerve CE, 17.9 ms for the left tibial nerve CE, 8.35 ms for the right tibial nerve PF, 8.25 ms for the left tibial nerve PF) (Fig. 1c,d). At a 7‐month telephone follow‐up, the patient was attending school and she had no physical symptoms such as limb weakness.

We reviewed the literature on conversion disorder patients with SSEP abnormalities , , , and our case. The present case and the reviewed cases indicate functional neurological disorder may have abnormal SSEP and provide some clues regarding the mechanism of conversion disorder. We speculated that the possible mechanism of the loss of cortical SSEP was the same as Yazici et al. and Vuilleumier's, indicating that top‐down inhibition works at the thalamus level. But the case had two limitations; first, she did not undergo brain MRI, and second, vitamin B level testing was not available in our hospital and vitamin B deficiency could be considered a differential because she was treated with supplementation. SSEP testing is less expensive and easier to perform than neuroimaging. Further studies on SSEP may clarify the neurobiological markers of conversion disorder and provide an improved reference for diagnosis and treatment.

Disclosure statement

The authors have no competing interests to declare.

Ethics approval and consent to participate

The ethics committee of West China Second University Hospital judged that there was no need to review this case.

Consent for publication

Written informed consent was obtained via her grandfather's oral consent for the publication of this case report.

Availability of data and materials

All data generated or analyzed during this study are included in this published article.