Conversion disorders (CD) are frequently related to the locomotor system (paresis, abnormal movements) but also to the somatosensory system (positive and negative symptoms) or visual system (tunnel vision, blindness).1 2 CD is classified within the group of “somatoform disorders” in the Diagnostic and Statistical Manual of Mental Disorders-IV and its definition implies that the patient has no voluntary control over the production of symptoms (unlike factitious disorder or malingering). The reported rate of misdiagnosis of conversion symptoms has, on average, been 4% since 1970.1 Psychogenic paralysis (PP) is generally a diagnostic challenge for the neurologist, usually leading to an expensive work-up to exclude organic lesions.

There are several theories explaining CD. There are, however, few methods that are able to highlight the mechanisms underlying this disorder.1 2 Some reports suggest that functional brain imaging3 and neurophysiological studies may prove to be a useful approach. We report a case of PP where changes in transcranial magnetic stimulation (TMS) were found.

A 25-year-old married healthy woman was referred to the neurology department with a 3 day history of mild headaches and gradual left lower limb weakness which progressed to affect the left upper limb. She had no pain but mentioned numbness in both lower limbs. She suffered from urinary retention, and catheterisation was performed. Two days later it was possible to remove the catherisation without any complications.

The previous year she had suffered generalised arthralgia but no definite diagnosis was made after extensive investigation. She had no personal or family history of psychiatric or neurological disorders, in particular migraine, and she was not taking any CNS medications.

On neurological examination she was calm, showing no concern for her disability, cranial nerve examination was unremarkable, the right limbs had normal power but the left limbs showed marked paresis, with the left lower limb showing no movement (even after noxious stimuli). Pinprick hypoaesthesia was discovered with a T8 midline sharp sensory level and anaesthesia in the left lower limb. In addition, frequent errors for positional sense were observed in the left toes. Reflexes were weak but symmetric, and plantar response was flexor on the right side but seemed absent on the left.

On admission the medical staff noticed normal left body movements when the patient was distracted. The patient underwent a psychiatric interview and the diagnosis of presumed PP was confirmed. Immediately, the patient assumed that she had suffered stressful events at the time of symptoms onset (familial conflicts) and 30 min later she started walking with no support.

A number of investigations were performed. Brain and spinal cord MRI were normal. CSF analysis was unremarkable. Nerve conduction studies, and visual and somatosensory evoked potentials were normal. TMS showed a clearly asymmetric corticomotor threshold (minimum intensity able to evoke ⩾50% responses with more than 50 μV of amplitude in 10 consecutive stimuli), which was higher on the right hemisphere (table 1). Moreover, the motor evoked potential (MEP) recorded in the left abductor hallucis had a very small amplitude. Central conduction times (using Kimurás formula to calculate peripheral conduction time) were normal (table 1).

The very positive reaction to the psychiatry intervention and the absence of any secondary gain favoured the diagnosis of CD. Escitalopram was started and the patient was referred to the psychiatry outpatient clinic. She remained well on follow-up, with no neurological symptoms.

One month after admission TMS was repeated. MEP amplitudes and abnormal right hemisphere corticomotor threshold became normal (table 1).

Motor evoked potentials have been suggested to be useful in the diagnosis of PP, as they are normal in these patients. In our patient, central conduction time was normal in both the lower and upper limbs, and symmetric. In contrast, the corticomotor threshold was clearly asymmetric, being increased in the right hemisphere. This abnormal asymmetry normalised on the second study. Either cortical or lower motor neuron (LMN) inexcitability could explain the finding of abnormal threshold; however, as the mean amplitude of the F waves was symmetric between both sides, decreased cortical excitability is the most probable cause for this observation. This would support the very small MEP (0.2 mV) in the left abductor hallucis in the first study which increased in size by 10-fold on the second evaluation. In general, mean amplitudes for MEP and F waves were smaller in the first study; this can derive from decreased LMN excitability related to resting.4 There is no evidence that escitalopram itself might account for this change.

To our knowledge, no previous study has investigated volitional modulation of TMS cortical threshold. In this case, the highly increased corticomotor threshold, with preservation of LMN excitability, suggests the presence of inhibitory activation over the motor cortex as the main physiological counterpart for her paresis. Brain functional imaging studies have supported the fact that in PP there is increased motor and premotor cortex inhibition driven by hyperactivation in the orbitofrontal and frontal cingulated regions.5 Possibly, this can represent a protective mechanism modulated by the primary limbic affective system.6 Indeed, positron emission tomography in three patients with hysteria disclosed hypofunction of the left dorsolateral prefrontal cortex during volitional movement of the symptomatic limb.

Conclusions from a single case require caution. However, this report indicates that further studies using TMS in PP and conversion disorders to address corticomotor excitability merit development.