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Psychogenic aphonia: spectacular recovery after motor cortex transcranial magnetic stimulation
  1. N Chastan1,
  2. D Parain1,
  3. E Vérin2,
  4. J Weber1,
  5. M A Faure3,
  6. J-P Marie4
  1. 1
    Department of Neurophysiology, Rouen University Hospital, University of Rouen, France
  2. 2
    Department of Physiology, Rouen University Hospital & UPRES-EA 3830-GRHV, University of Rouen, France
  3. 3
    Phonatrician, Paris, France
  4. 4
    Department of Otolaryngology, Rouen University Hospital, & UPRES-EA 3830-GRHV, University of Rouen, France
  1. Professor J-P Marie, CHU de Rouen, Service d’ORL, Dévé 1er étage, 1 rue de Germont, 76031 Rouen cedex, France; jean-paul.marie{at}chu-rouen.fr

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Psychogenic aphonia is a disabling conversion disorder with no standard psychotherapeutic1 or speech-therapeutic treatment.2 We present here a case report describing a promising new treatment for this disorder based on repetitive transcranial magnetic stimulation (rTMS).

A left-handed 18-year-old woman developed a sudden total loss of normal speech production which was preceded by hoarseness. Coughing and syllabic “trillo” phonation were normal, indicating normal articulatory ability. An otolaryngological examination noted a normal larynx with no sign of lesion or vocal cord palsy, and videostroboscopic examination showed no vocal-cord adduction except during coughing. Neurological examination and brain MRI were normal. The patient reported moderate familial conflict and academic problems. Psychological evaluation revealed chronic anxiety. Thirty sessions of speech therapy produce no improvement. The conversion disorder persisted for 20 months. As a final treatment, two rTMS sessions of 150 s duration (50 stimuli delivered at 0.33 Hz, and maximal intensity of 2.5 Tesla) were attempted with a circular coil (P/N 9784-00). The first magnetic stimulation was applied to the left prefrontal cortex with no effect. One week later, a second rTMS session was applied to the right motor cortex with a dramatic and immediate improvement, leading to a normal speech within a few days, and still normal at 6 months’ follow-up. We attributed the clinical improvement to the rTMS, and not to a placebo effect (lack of effect with prefrontal cortex rTMS), or the natural course of the illness.

Functional MRI studies have demonstrated a reversible decreased activation of contralateral primary motor3 or somatosensory cortex4 in conversion disorder patients, with motor and sensory symptoms respectively. An abnormal activation of the orbitofrontal and anterior cingulate cortex has also been observed.5 The physiopathology of conversion symptoms could be explained by an active inhibition of these two prefrontal areas on primary motor areas.5 6

The modulation of cortical excitability by rTMS could be a powerful new therapy for conversion disorders. In the past, patients with non-organic limb paralysis have been treated with 15 Hz rTMS sessions of motor cortex for 5–12 weeks,7 with variable benefits. Here, we hypothesise that they have activated the depressed motor cortex with excitatory high-frequency rTMS. On the contrary, in our aphonic patient, recovery was total with only one session of low-frequency rTMS. We have possibly blocked the active inhibition of the motor cortex with inhibitory low-frequency rTMS.

This spectacular effect could also be explained by an important laryngeal muscular activation produced by the motor cortex stimulation and not by the prefrontal cortex stimulation.

Motor cortex rTMS could be a therapeutic option for psychogenic aphonia, and perhaps for other motor conversion disorders. To our knowledge, this is the first description of psychogenic aphonia rTMS treatment. The potential benefit of such treatment should be evaluated in a randomised controlled trial versus placebo.

REFERENCES

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Footnotes

  • See Editorial Commentary, p 4

  • Competing interests: None.

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