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Transient Psychosis With Psychogenic Polydipsia in Schizotypal Patient Taking Fluoxetine

Key Words: Letter • Letters

TO THE EDITOR: Several cases of transient psychosis with fluoxetine were previously reported,^1–3 with possible increased risk to patients with paranoid symptoms.³ We report the case of a patient with schizotypal personality disorder who developed transient psychosis with polydipsia after treatment with fluoxetine.

Case Report

Ms. A., a 40-year-old white, married woman with no prior psychosis, had a history of odd speech and behavior, unusual beliefs (that crystals had magic power and that she knew the cure for AIDS), and a lack of friends sufficient to establish diagnosis of schizotypal personality disorder. She had a history of preoccupation with an herbal diet and "clearance of her body" by drinking water, but no history of polydipsia.

Three months before hospital admission, she developed a new-onset major depression. She had obsessive preoccupations about marital problems and about having been sexually abused as a child, depressed mood, feelings of worthlessness and hopelessness, anhedonia, decreased energy level, and suicidal ideation. The patient was started on fluoxetine (20 mg/day) by an outpatient psychiatrist. After 11 weeks on fluoxetine, Ms. A.'s mood symptoms had improved, but she became preoccupied with "doing things in certain order" and progressively more psychotic, believing that she must protect herself from "negative forces" by placing tissues throughout the house. She experienced command auditory hallucinations to "clean her body" by drinking more water. In addition, she placed tape over electrical outlets, because she felt that electricity "may interact with water in her body." One week after the onset of psychotic symptoms (and 1 week before hospital admission), she discontinued the fluoxetine.

Electrolyte imbalance from polydipsia resulted in seizures, and she was admitted to the hospital neurology service. Serum biochemistry was as follows: Na 122 mmol/L (135–146), K 3.1 (3.5–5.0), bicarbonate 23 (22–33), blood urea nitrogen 4 (7–18), and osmolality 297 (280–296); urine osmolality was 141 (50–1,200). Normal values are in parentheses. No neurological pathology was found. The patient was placed on fluid restriction, with prompt resolution of hyponatremia.

During the psychiatric consultation on the day following admission, the patient denied hearing voices and displayed some insight in reporting that "her behavior was strange." However, she remained delusional, believing that she must "protect herself" by putting tape on the walls and ceiling of the ward. We started haloperidol 5 mg/day for 3 days and then 10 mg/day. The psychosis gradually resolved after 2 weeks' treatment with haloperidol and 3 weeks off fluoxetine.

After discharge from the hospital, the patient returned completely to her baseline functioning. She was placed on fluoxetine again 2 months later and remained asymptomatic over 1 year, without neuroleptics. After 1 year, she had another psychotic break following a severe argument with her husband. This episode was not accompanied by polydipsia, was very brief, and was self-limited. The patient recompensated after 3 days in the psychiatric hospital without neuroleptic treatment.

Discussion

This case describes the emergence of psychosis and psychogenic polydipsia following fluoxetine administration. We ruled out SIADH (syndrome of inappropriate secretion of antidiuretic hormone) because urine osmolality was much lower than plasma osmolality. We ruled out psychosis due to delirium, as the patient's sensorium was clear and psychotic symptoms persisted after prompt resolution of hyponatremia. It is unlikely that the psychosis was a manifestation of a first episode of schizophrenia. The clinical course with complete return to baseline functioning and lack of psychotic symptoms for a year without further neuroleptic treatment; the brief, self-limited nature of another psychotic episode following a precipitating event; and the absence of the family history of schizophrenia are rather consistent with transient psychosis in a patient with schizotypal features. This case is suggestive of psychosis induced by fluoxetine. The fact that the patient tolerated the rechallenge with fluoxetine does not exclude this possibility. Slow resolution of psychotic symptoms during the first psychotic episode after 2 weeks' treatment with haloperidol and 3 weeks off fluoxetine is consistent with the long half-life of fluoxetine: up to 16 days for its active metabolite.

Cases of fluoxetine-induced paranoid exacerbations in schizophrenia and schizoaffective disorder have been reported.⁴ Some of previously reported cases of psychosis with fluoxetine and other selective serotonin reuptake inhibitors included a history of paranoid symptomatology.³ A 5HT-3 receptor-mediated, selective fluoxetine-induced hyperdopaminergia was suggested to be a mechanism of paranoid exacerbations in these patients and schizophrenic patients.³ This is to our knowledge the first report of psychosis following fluoxetine administration in a schizotypal patient. A central dopaminergic dysfunction similar to such of schizophrenic patients has been demonstrated in patients with schizotypal personality disorder.⁵ Possibly, schizotypal patients are vulnerable to the psychotogenic effects of fluoxetine similar to patients with schizophrenia. We suggest that the fluoxetine might have exacerbated our patient's belief in "clearance of her body" with drinking water by making this hallucination a more florid psychotic experience.

Disturbance of sodium retention was noted in patients with affective disorders.⁶ Fluoxetine may decrease seizure threshold.⁷ Both of these factors might have contributed to the dramatic consequences of polydipsia in our patient.

This case calls for clinical attention to possible induction of psychosis by fluoxetine in patients with schizotypal features.

REFERENCES

1. Mandalos GE, Szarek BL: Dose-related paranoid reaction associated with fluoxetine. J Nerv Ment Dis 1990; 178:57–58[Medline]
2. Hersh CB, Sokol MS, Pfeffer CR: Transient psychosis with fluoxetine (letter). Am Acad Child Adolesc Psychiatry 1991; 30:851–852[Medline]
3. Lauterbach EC: Serotonin reuptake inhibitors, paranoia, and the ventral basal ganglia. Clin Neuropharmacol 1991; 14:547–555[Medline]
4. Bacher NM, Ruskin P: Addition of fluoxetine to treatment of schizophrenic patients (letter). Am J Psychiatry 1991; 148:274–275
5. Siever LJ, Amin F, Coccaro EF, et al: CSF Homovanillic acid in schizotypal personality disorder. Am J Psychiatry 1993; 150:149–151[Abstract/Free Full Text]
6. Crammer JL: Drinking, thirst and water intoxication. Br J Psychiatry 1991; 159:83–89[Abstract/Free Full Text]
7. Levinson ML, Lipsy RJ, Fuller DK: Adverse effects and drug interactions associated with fluoxetine therapy. DICP: Annals of Psychotherapy 1991; 25:657–661

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 Gutkovich, Z. Articles by Bogdonoff, L. Search for Related Content PubMed Citation Articles by Gutkovich, Z. Articles by Bogdonoff, L. Schizophrenia Spectrum Disorders

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