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Exacerbation of Psychogenic Movement Disorder by Interferon Treatment of Hepatitis C

TO THE EDITOR: There are a number of neuropsychiatric side effects caused by interferon (IFN) treatment, such as fatigue syndrome, major depressive episodes, suicidal ideation, and mania.¹ IFN treatment can also worsen preexisting psychiatric and psychosomatic disorders.²

We report the case of a 63-year-old patient who presented to our joint hepatological-psychiatric outpatient clinic for IFN treatment of chronic hepatitis C virus (HCV) infection.

Case Report
The patient reported a 25-year history of chronic psychogenic gait disorder and personality disorder. The first signs of psychogenic movement disorder (PMD) had presented in the context of the diagnosis of the HCV infection in 1980, with fluctuating/intermittent symptoms. After a myocardial infarction in 1993, the patient developed a more severe chronic PMD, present at all times, also presenting with paroxysmal weakness of the entire lower body. Since 1994, there have been repeated hospitalizations on psychosomatic and psychiatric wards, without significant improvement of the PMD.

We started the patient on citalopram 20 mg/day for 4 months before the IFN treatment to prevent the possible development of depressive symptoms.³ Three months after the start of the IFN treatment, the patient developed worsening of the PMD, requiring use of a wheelchair at home, resulting in his referral to our hospital for psychiatric admission. On various occasions, he had spent hours lying in the same position until somebody helped him to get up.

On his admission, we saw a patient in a wheelchair. When helped into the upright position, he displayed a severe movement disorder, with sudden weakness of one or both legs. The patient showed effortful swaying of the trunk to counterbalance the weakness of the legs present at all times when standing or walking. He showed states of weakness of the whole body, accompanied by total incapacity to move without the help of others. On physical exam, the patient displayed an athletic body constitution and no consistent neurological deficits. Upon psychiatric exploration, we found a minor depressive syndrome (score of 17 on the Hamilton Rating Scale for Depression), in spite of his antidepressant pretreatment. We confirmed a combined personality disorder showing histrionic, narcissistic, and obsessive-compulsive traits (by means of the Structured Clinical Interview for DSM-IV [SCID II] and the Minnesota Multiphasic Personality Inventory [MMPI]), which had been administered on previous hospitalizations. We switched antidepressant therapy to escitalopram and increased the dosage to 20 mg/day. We added psychotherapeutic treatment in single and group settings. The patient was weaned from the wheelchair and achieved considerable improvement of the PMD. We saw full remission of depressive symptoms, and continued the IFN treatment.

Discussion

Mechanisms for direct effects of IFN on the CNS, such as decrease of tryptophan availability, central serotonergic deficit, increase of cortisol after activation of the hypothalamic-pituitary-adrenal axis, and induction of cytokines have been described elsewhere.⁴ These effects are known to play a role in the pathophysiology of depression. We have also discussed emotional stress or a breakdown of defense mechanisms as psychological factors for the exacerbation of the PMD. Learning about the diagnosis of chronic HCV infection is a major stressful life-event that may have contributed to the onset of the PMD in our patient in 1980.⁵ The treatment of the HCV may reactivate the burden related to knowing about the disease. We conclude that IFN treatment may impart the risk of worsening PMD by inducing stress, by biological effects leading to depression, and by reduction of patients’ abilities to cope with intra- and interpersonal conflicts by use of defense mechanisms. We therefore recommend intensified psychotherapeutic support and antidepressant pharmacotherapy in these instances.

REFERENCES

1. Dieperink E, Willenbring M, Ho SB: Neuropsychiatric symptoms associated with hepatitis C and interferon: a review. Am J Psychiatry 2000; 157:867–876[Abstract/Free Full Text]
2. Renault PF, Hoofnagle JH, Park Y, et al: Psychiatric complications of long-term interferon therapy. Arch Intern Med 1987; 147:1577–1580[Abstract]
3. Schaefer M, Schwaiger M, Garkisch AS, et al: Prevention of interferon–associated depression in psychiatric risk patients with chronic hepatitis C. J Hepatol 2005; 42:793–798[CrossRef][Medline]
4. Capuron L, Raison CL, Musselman DL, et al: Association of exaggerated HPA-axis response to the initial injection of interferon with development of depression during interferon therapy. Am J Psychiatry 2003; 160:1342–1345[Abstract/Free Full Text]
5. Castera L, Constant A, Bernard PH, et al: Psychological impact of chronic hepatitis C: comparison with other stressful life events and chronic diseases. World J Gastroenterol 2006; 12:1545–1550[Medline]

Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Articles & Searches Download to citation manager Citing Articles via Google Scholar Articles by Mundt, A. P. Articles by Ströhle, A. Search for Related Content PubMed Citation Articles by Mundt, A. P. Articles by Ströhle, A. Other Neuropsychiatric Disorders Syndromes Secondary to General Medical Disorders

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