Paroxetine for treatment of somatization disorder.

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Back to table of contents Previous article Next article LetterFull AccessParoxetine for Treatment of Somatization DisorderGaku Okugawa, M.D., Ph.D., Ayaka Yagi, M.D., Hirofumi Kusaka, M.D., Ph.D., and Toshihiko Kinoshita, M.D., Ph.D., Gaku OkugawaSearch for more papers by this author, M.D., Ph.D., Ayaka YagiSearch for more papers by this author, M.D., Hirofumi KusakaSearch for more papers by this author, M.D., Ph.D., and Toshihiko KinoshitaSearch for more papers by this author, M.D., Ph.D., Departments of Neuropsychiatry (g.o., t.k.) and Neurology (a.y., h.k.), Kansai Medical University, Osaka, JapanPublished Online:1 Nov 2002AboutSectionsView EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail SIR: Somatization disorder is characterized by recurring, multiple, clinically significant somatic complaints. A somatic complaint is considered to be clinically significant if it results in medical treatment causing significant impairment in social, occupational, or other important areas of function.1 Treatment modalities have not been well studied. A MEDLINE search in the spring of 2002 did not reveal any citations on the use of paroxetine in somatization disorder. We here describe the successful treatment with paroxetine of somatization disorder in a 38-year-old woman.Case ReportThe 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.CommentTo 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-HT1A and terminal 5-HT1B/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.References1 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision. Washington, DC, American Psychiatric Association, 2000Google Scholar2 Gunasekara NS, Noble S, Benfield P: Paroxetine: an update of its pharmacology and therapeutic use in depression and a review of its use in other disorders. Drugs 1998; 55:85-120Crossref, Medline, Google Scholar3 Brogden RN, Heel RC, Speight TM, et al: Mianserin: a review of its pharmacological properties and therapeutic efficacy in depressive illness. Drugs 1978; 16:273-301Crossref, Medline, Google Scholar4 Chaput Y, Montigny C, Blier P: Presynaptic and postsynaptic modifications of the serotonin system by long-term administration of antidepressant treatments: an in vivo electrophysiologic study in the rat. Neuropsychopharmacology 1991; 5:219-229Medline, Google Scholar FiguresReferencesCited byDetailsCited BySomatization Disorder: A Practical Review1 September 2004 | The Canadian Journal of Psychiatry, Vol. 49, No. 10 Volume 14Issue 4 November 2002Pages 464-465 Metrics History Published online 1 November 2002 Published in print 1 November 2002