Paroxetine for Treatment of Somatization Disorder

The patient was a married 38-year-old woman with somatization disorder. Over the previous 16 years, she had been treated unsuccessfully by various doctors who had prescribed acetaminophens and minor tranquilizers for joint pain. The patient was hospitalized in our neurological unit, since she could not move by herself. She remained in bed because of worsening pains. There were no pathological findings in the joints or muscles on neurological and orthopedic examinations. She fulfilled DSM-IV criteria for somatization disorder. She was treated with mianserin 30 mg/day but complained of drowsiness and increasing pains in the knees. Mianserin was replaced by paroxetine 10 mg daily. After 2 weeks on paroxetine, the dosage was increased to 20 mg/day and she spontaneously began standing up. After 3 weeks, she could sit down and stand up because of improvement in joint pain. Because she complained of sleep disturbance, diazepam 6 mg/day was added. After 6 weeks, the dose of paroxetine was titrated to 40 mg/day and she could walk slowly with less pain in her knees. Because she complained of sleepiness in the daytime, diazepam was tapered to 4 mg/day. After 8 weeks, she could climb and descend stairs. She was discharged 9 weeks after paroxetine treatment and has been maintained on 30 mg/day of paroxetine and 4 mg/day of diazepam while receiving outpatient rehabilitation.

To our knowledge, this is the first reported case of a patient successfully treated for somatization disorder with paroxetine. Treatment with paroxetine is effective in improving depression, obsessive-compulsive disorder, and panic disorder.² The two antidepressants that were given to the patient have different actions on monoaminergic neurotransmission; that is, blockade of presynaptic alpha-2-adrenergic receptors and serotonin antagonism (mianserin)³ and selective serotonin reuptake inhibition (paroxetine).² In our case, clinical symptoms improved when paroxetine was given to a patient showing poor response or resistance to mianserin. Diazepam 6 mg/day was given, but the dose was reduced after the patient complained of daytime sleepiness. Her past history showed that minor tranquilizers had not been effective for the symptoms. After approximately 2 weeks of paroxetine administration, somatodendritic 5-HT_1A and terminal 5-HT_1B/1D serotonin autoreceptors become desensitized, which leads to more serotonin being released with each action potential.⁴ This effect is thought to be central to the therapeutic efficacy of paroxetine. In this case, the onset of clinical efficacy was observed after 2 to 3 weeks of paroxetine treatment. These findings suggested that this patient's symptoms should be regarded as a feature of an underlying serotonergic spectrum disorder including obsessive-compulsive disorder. However, only double-blind placebo-controlled studies could confirm the validity of this clinical observation.