Cognitive impairment in the elderly is an increasingproblem. Up to 48% of the general population >85

years old may suffer from some kind of dementia.1 Drug-related effects are an important contributor to this problem.2

Drugs may cause delirium, which is characterized by im-paired consciousness, cognition, or perception, but theycan also cause impairments similar to those observed withAlzheimer disease (e.g., decreased memory, learning, think-ing, or problem-solving abilities). We report the case of awoman who developed amnesia after starting fluoxetinefor depression.

Case Report

An 87-year-old white woman had a history of atrial fibrillation, coro-nary artery disease, gastroesophageal reflux disease, hypertension, aller-gic rhinitis, and glucose intolerance. She was living at an assisted-livingfacility where she was able to manage her own medications. On Decem-ber 13, 2002, she presented to her physician reporting impaired memoryand not being able to remember her medication schedule. She had beenseen at the emergency department (ED) the previous night stating thatshe was "not being able to think well." The ED physician noted her to beoriented to person, place, and date. Cranial nerves II through XII wereintact. Studies were done to rule out electrolyte or metabolic distur-bances, subdural hematoma or other intracranial processes, digoxin toxi-city, and urinary tract infection. Computed tomography (CT) of the headrevealed mild age-related volume loss and chronic ischemic white-matterchanges. Laboratory evaluation showed a normal complete blood cell

count and urinalysis, sodium 131 mEq/L, potassium 4.0 mEq/L, glucose96 mg/dL, blood urea nitrogen 18 mg/dL, creatinine 1.2 mg/dL, anddigoxin concentration 1.2 ng/mL. The international normalized ratio(INR) was therapeutic at 2.2.

The next day at the clinic visit, she was alert. Her social skills were ac-ceptable, and she was able to comprehend the content and importance ofthe conversation. A medication review revealed she was taking the fol-lowing drugs: warfarin 2.5 mg once daily except 5 mg on Fridays,isosorbide dinitrate 40 mg twice daily, spironolactone 50 mg/d, digoxin0.25 mg/d, furosemide 20 mg/d, rabeprazole 20 mg/d, loratadine 10mg/d, fluticasone nasal spray 2 puffs/d, triamcinolone oral inhaler 2puffs twice daily, albuterol oral inhaler as needed, enalapril 5 mg/d, andfluoxetine 20 mg/d. The most recent addition to this regimen was fluoxe-tine, begun October 11, 2002, for treatment of fatigue and apathy at-tributed to depression. Initial dosing began with 10 mg/d for 2 weeks,then increasing to 20 mg/d. On November 5 and 19, the patient reportedimprovements in mood. The family noted a slight decrease in her cogni-tive functioning starting in early November, as evidenced by repeateddonations to the same charitable organizations and including her formerlast name on correspondence and when paying bills.

During a December 6 visit with her physician, the patient was diag-nosed with a urinary tract infection and received a prescription for cipro-floxacin 250 mg twice daily for 5 days. At the December 13 visit, fluox-etine was discontinued because the physician believed that this was thepossible cause for the woman’s memory loss. Five days later, her memo-ry had declined further. She was unable to answer any questions abouther medications. She was oriented to person, but not to place or time. Aformal Mini-Mental State Exam (MMSE) was not done at this time. Shewas visibly upset about her condition and repeatedly was asking whythis was happening to her.

The patient was admitted to the hospital and evaluated by a neurolo-gist. Examination confirmed that she was oriented only to her name.Formal MMSE was attempted, but the patient was unable to follow theclinician’s directions. She demonstrated no memory of the past. SheAuthor information provided at the end of the text.

Memory Loss in a Patient Treated with Fluoxetine

Jacqueline D Joss, Robert M Burton, and Cecilia A Keller

OBJECTIVE: To report a case of severe memory loss in an elderly patient after initiation of fluoxetine.

CASE SUMMARY: An 87-year-old white woman was started on fluoxetine for depression, and the dose was titrated to 20 mg/d. Shedeveloped progressive memory loss over the next 6 weeks for which she ultimately was hospitalized. Other potential causes for hermemory loss were ruled out. After fluoxetine was discontinued, the patient’s memory improved significantly over the next 2 months.An objective causality assessment indicated a possible relationship between the memory loss and fluoxetine in this patient.

DISCUSSION: Our report documents a case of severe reversible memory deterioration after initiating fluoxetine. Fluoxetine has afavorable adverse effect profile when compared with older classes of antidepressants. Postmarketing studies and isolated casereports, however, suggest that fluoxetine may harm memory in some patients. Some selective serotonin-reuptake inhibitors (SSRIs)appear to cause memory loss more frequently than others.

CONCLUSIONS: Clinicians should be aware of the possible effects of fluoxetine (and possibly other SSRIs) on memory.

KEY WORDS: fluoxetine, memory loss, selective serotonin-reuptake inhibitors.

Ann Pharmacother 2003;37:1800-3.

Published Online, 29 Oct 2003, www.theannals.com, DOI 10.1345/aph.1D154

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could converse, spell, and perform simple arithmetic. While the patientcould follow 3-point commands, she scored 0 out of 3 for short-termmemory. There was no evidence of expressive or receptive aphasia.Physical examination was unremarkable. Vitamin B12 and folate levelswere normal. Magnetic resonance imagery of the brain revealed mildvolume loss commensurate with age and mild to moderate nonspecificpunctate areas of deep and subcortical white-matter hyperintensities. Val-proic acid was given for 2 days, then discontinued after an electroen-cephalogram ruled out a seizure disorder.

The patient was discharged to her son’s care after 2 days. On Decem-ber 31, she saw the same neurologist and scored 19/30 on the FolsteinMMSE. She had problems with orientation, but scored well on languageand recall. Her family noted an improvement. Ten days later, the patienthad improved even further. She was oriented to person, place, and time,but still needed help with medications from her family. After discussingthe risks and benefits with the woman’s physician, the family chose todiscontinue furosemide and warfarin to minimize the complexity of hermedication regimen. One month later, her memory had further im-proved. She scored 26/30 on the MMSE. She missed 1 item of short-term recall and the correct day of the week. The score was maintained 2weeks later.

Discussion

This case reveals a patient with significant reversiblememory impairment that appears to be related to drug ther-apy. Fluoxetine and ciprofloxacin were the only 2 newmedications during the time in question. Fluoxetine and itsactive metabolite both have half-lives of several days.3 Thefamily noted a decline in memory starting about 2 weeksafter drug initiation and the symptoms peaked 5 days afterfluoxetine was discontinued, resulting in admission to thehospital at a time when one would expect the drug concen-tration to be at steady-state. Symptoms improved 2 weeksafter the drug was discontinued. The patient’s mental statuscontinued to improve over 2 months following the discon-tinuation of fluoxetine. This time course correlates wellwith the half-life of the drug.

In contrast, ciprofloxacin has a shorter half-life (3–5 h)in adults. Reported adverse central nervous system symp-toms related to ciprofloxacin include nervousness, agita-tion, insomnia, anxiety, nightmares, and paranoia.4 Whilememory loss has been reported in postmarketing data,causality with ciprofloxacin cannot be firmly established(personal communication, Robert Harrison BS, Bayer Phar-maceuticals Corporation, February 28, 2003). One case re-port indicated ciprofloxacin as a possible cause of disorien-tation, emotional lability, and hallucinations 3 hours after asingle dose of 250 mg for a urinary tract infection in a 53-year-old woman recovering from sigmoidectomy.5 The pa-tient recovered fully within 24 hours. In our case, symp-toms preceded the use of ciprofloxacin and persisted forseveral weeks, making ciprofloxacin an unlikely cause.

While not formally evaluated before her acute episode,the patient may have had some age-associated memoryimpairment at baseline. This mild form of memory lossusually does not affect functional social activity.6 The pa-tient was relatively independent before the reported events.Since her low mood was the reason for prescribing of flu-oxetine, pseudodementia, a memory problem resultingfrom depression, was considered in the differential diagno-sis. The onset of the memory loss tends to be more abrupt

than in dementia and to plateau at a mild level of impair-ment.6 Treatment for this form of dementia is aggressiveantidepressant therapy. Our patient had reported a subjec-tive improvement in mood in the visits preceding thememory loss, and her memory loss improved after the an-tidepressant was discontinued. These factors make pseudo-dementia an unlikely diagnosis.

Transient global amnesia is a disorder affecting middle-aged and older persons.7 This diagnosis was considered bythe neurologist. People are usually alert when an episodeof transient global amnesia occurs. The spells are charac-terized by amnesia of present events and the recent past.The patient usually can perform high-level intellectual ac-tivity and language functions. Typical episodes last no morethan a few hours, after which no abnormal mental functionis apparent, except for a memory gap for the attack itself. Inour patient, the memory gap lasted for several days.

Transient memory loss can be caused by a transient is-chemic event. Our patient had evidence of mild chronic is-chemic changes on CT scan. Memory loss duration was,however, longer than would be expected. Minor intracra-nial bleeding must be considered, as the patient was onwarfarin. Fluoxetine can inhibit the metabolism of war-farin. In this patient, the CT scan showed no acute changesand the INR was within the therapeutic range when theevent occurred.

We review 5 case reports citing fluoxetine as the causeof impaired memory. In each case, cognitive function re-turned to baseline after fluoxetine discontinuation or dosereduction. A 60-year-old woman with recurrent depressionpresented with forgetfulness, learning difficulties, and im-paired concentration for 9 months during fluoxetine therapy.8

Another report documented memory loss in a young womanwhen the fluoxetine dose was increased from 40 to 60mg/d.9 A 14-year-old boy with major depression developedsymptoms of decreasing attention, hyperactive behavior,poor concentration, distractibility, and poor memory afterstarting fluoxetine.10 An objective assessment revealed sig-nificant improvement in visual, verbal, and general memo-ry after the drug was discontinued, despite a deteriorationin mood. A 73-year-old man with major depression devel-oped very rapid cognitive impairment when fluoxetine 20mg/d was added to his existing treatment of alprazolam 0.5mg at bedtime.11 Another report described dose-relatedshort-term and procedural memory loss due to fluoxetinein a 51-year-old brain-injured patient.12

As cognitive impairment occurs in depression, effectivetreatment may improve analytical thinking and memory.Antidepressants may cause impaired cognition, therebyblunting the effect of therapy. This adverse effect of antide-pressants may be missed, especially in the elderly, where ahigher frequency of baseline cognitive impairment is pre-sent.1 Older patients are at greater risk of developing drug-in-duced delirium or dementia because of existing imbalancesin neurotransmittors (e.g., acetylcholine) and age-relatedchanges in drug clearance. Memory dysfunction has beenreported with tricyclic antidepressants (TCAs).13,14 Selec-tive serotonin-reuptake inhibitors (SSRIs) have a more fa-

Case Reports

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vorable adverse effect profile than TCAs, and their use hasbecome common in the treatment of depression. A reviewof 19 randomized clinical trials totaling 3183 patients com-paring fluoxetine, TCAs, and placebo did not list the oc-currence of amnesia.15 No significant impairment of cogni-tion was seen in a single-dose study of fluoxetine in 90healthy volunteers.16

Several trials have documented improved memory indepressed patients treated with fluoxetine, which is likely afunction of treatment response. A 6-week study comparingfluoxetine and trazodone in 38 unipolar depressed patientsdemonstrated an equal improvement of memory betweenthe drugs, and it paralleled the improvement in depressionduring the trial.17 Fluoxetine 10 mg/d was compared withamitriptyline 25 mg/d in 37 elderly patients with depres-sion and Alzheimer disease.18 These investigators reporteda significant improvement in the MMSE scores in bothtreatment groups after the 45-day study period. Ten pa-tients in the amitriptyline group withdrew because of con-fusion and disorientation.

Comparative trials between SSRIs have shown variableeffects. A 1-year trial compared fluoxetine with paroxetinein 242 elderly depressed patients.19 Besides significant im-provement in depressive symptoms, equal and significantimprovement was noted in global cognitive function, wordlearning, and attention skills. Other investigators detected apositive effect produced by paroxetine on cognition in 29depressed elderly patients, some with baseline decreasedcognitive function.20 A 3-way, placebo-controlled, cross-over study of sertraline and paroxetine in healthy volunteersfound that paroxetine induced long-term memory impair-ment, while sertraline improved performance on a verbalfluency task.21 A 3-week trial in elderly volunteers demon-strated a decline in delayed verbal recall and paired-associ-ate learning scores with paroxetine, while the same scoreswere improved with sertraline.22 Other studies in healthyvolunteers revealed increased memory consolidation withcitalopram23 and no effect on psychomotor performance orcognition with fluvoxamine.24,25

Eli Lilly reports fluoxetine-associated amnesia as "fre-quent" (i.e., occurring in at least 1/100 patients based ondata from US clinical trials of 10 782 pts.).3 Fluvoxaminedata are similar.26 Placebo rates and severity of memorydysfunction are not available from this source. Other SSRIsappear to have a lower incidence of amnesia; the paroxe-tine prescribing information lists amnesia as occurring "in-frequently" (i.e., 1/100–1/1000)27; amnesia is not listed forsertraline28 and citalopram.29

The SSRIs are structurally diverse and have clear varia-tions in their pharmacodynamic profiles.30 Sertraline andcitalopram are the most selective for the inhibition of sero-tonin reuptake relative to norepinephrine, while fluoxetineis the least discriminatory. Various mechanisms have beenproposed by which these agents affect cognition. A studydemonstrated that depressed patients assigned to amitripty-line did not perform as well as those on fluoxetine on averbal learning task after 3 weeks.31 Serum anticholinergicactivity was higher in the amitriptyline group. The authors

concluded that blockade of muscarinic receptors impairedworking memory formation.

Paroxetine has significant anticholinergic properties, pos-sibly causing increased memory problems.30 Sertraline in-hibits dopamine reuptake, thereby acting as an indirectdopamine agonist. Dopamine deficiency in the prefrontalcortex is associated with the cognitive impairment ofschizophrenia and Parkinson’s disease. Correcting dopaminelevels appears to improve these symptoms. One report pos-tulated that dopamine enhances cognition by enhancing theincoming neural signals relative to background “noise,” thuspromoting the firing frequency of innervated neurons.32 Us-ing bromocriptine (a dopamine agonist) and fenfluramine (aserotonin agonist), the researchers demonstrated facilitatedmemory with bromocriptine and delayed memory with fen-fluramine, suggesting an interaction between dopamine andserotonin in the modulation of cognitive behavior.

Fluoxetine binds to the 5-HT2C receptor. Activation ofthis receptor has been associated with impaired cognition.Sertraline and fluvoxamine bind at the sigma1 binding site,which is implicated in the regulation of dopaminergictransmission. The significance of this observation is notclear, since it has not yet been established whether the SSRIsare agonists or antagonists at this site.30

Use of the Naranjo probability scale showed a possiblerelationship between memory loss and fluoxetine in ourpatient.33 The use of ciprofloxacin complicates the causalityassessment. Based on the literature review, pharmacokinet-ics of the 2 drugs, and timing and duration of the symp-toms, fluoxetine is the more likely cause. From the litera-ture reviewed, it can be concluded that the SSRIs maycause memory loss. These agents may thereby blunt theimprovement of cognitive function that is often seen withsuccessful therapy of depression. Further research is need-ed to fully explain the differences between the agents andhow these adverse events may be prevented.

Summary

We report a case of significant memory impairment pos-sibly caused by fluoxetine. Several case reports supportthis finding, and manufacturer data indicate an incidenceof ≥1%. Other SSRIs may also rarely cause memory loss,while sertraline appears to have memory-enhancing effectsin some patients. As more exposure data are collected onthe newer SSRIs, further differences may emerge. Clini-cians should be aware of these potential effects on cogni-tion when evaluating patients for adverse events or whenchoosing an SSRI for patients with preexisting dementia.

Jacqueline D Joss PharmD, Clinical Pharmacy Specialist, Am-bulatory Services, Good Samaritan Regional Medical Center, Cor-vallis, ORRobert M Burton MD PhD, Physician in Internal Medicine, Samar-itan Internal Medicine, Good Samaritan Regional Medical CenterCecilia A Keller MD, Board-Certified Adult Neurologist, Neurolo-gy Department, The Corvallis Clinic, CorvallisReprints: Jacqueline D Joss PharmD, 3615 NW Samaritan Dr.,Ste. 103, Corvallis, OR 97330-3763, FAX 541/768-6662, jjoss@samhealth.org

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JD Joss et al.

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The assistance of Anna Mihok BS, Murray Memorial Library, and Aly Ottomeier BSCPhT, Pharmacy Administration, Good Samaritan Regional Medical Center, is ac-knowledged.

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2. Gray SL, Lai KV, Larson EB. Drug-induced cognition disorders in theelderly. Incidence, prevention and management. Drug Safety 1999;21:101-22.

3. Package insert. Prozac (fluoxetine). Indianapolis: Eli Lilly, February 2001.4. Package insert. Cipro (ciprofloxacin). West Haven, CT: Bayer Corpora-

tion, May 2002.5. Segev S, Alkan M. Transient mental impairment associated with quinolone

therapy (abstract). Rev Infect Dis 1988;10(suppl 1):S262.6. Sacktor NC, Mayeux R. Symptoms of neurologic disorders. In: Bussy

RK, ed. Merritt’s textbook of neurology. Baltimore: Williams & Wilkins,1995:1-8.

7. Victor M, Ropper AH. Dementia and the amnesic (Korsakoff) syndrome.In: Principles of neurology. New York: McGraw-Hill, 2001:444-63.

8. Mirow S. Cognitive dysfunction associated with fluoxetine (letter). Am JPsychiatry 1991;148:948-9.

9. Bradley SJ, Kulik L. Fluoxetine and memory impairment. J Am AcadAdolesc Psychiatry 1993;32:1078-9.

10. Bangs ME, Petti TA, Janus MD. Fluoxetine-induced memory impair-ment in an adolescent. J Am Acad Child Adolesc Psychiatry 1994;33:1303-6.

11. Singh R, Gupta A, Singh B. Acute organic brain syndrome after fluoxe-tine treatment (letter). Am J Psychiatry 1995;152:295-6.

12. Hall T, Barrera RD, Randon M. Reversible memory loss following treat-ment with fluoxetine: a case study. Behav Intervent 2000;15:217-24.

13. Legg JF, Stiff MP. Drug-related test patterns of depressed patients. Psy-chopharmacology (Berl) 1976;50(2):205-10.

14. Schatzberg AF, Cole JO, Blumer DP. Speech blockade: a tricyclic sideeffect. Am J Psychiatry 1978;135:600-1.

15. Pande AC, Sayler ME. Adverse events and treatment discontinuations influoxetine clinical trial. Int Clin Psychopharmacol 1993;8:267-9.

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17. Fudge JL, Perry PJ, Garvey MJ, Kelly MW. A comparison of the effectsof fluoxetine and trazodone on the cognitive functioning of depressedoutpatients. J Affect Disord 1990;18:275-80.

18. Taragano FE, Lyketsos CG, Mangone CA, Allegri RF, Comesana-DiazE. A double-blind, randomized, fixed-dose trial of fluoxetine vs. amitrip-tyline in the treatment of major depression complicating Alzheimer’sdisease. Psychosomatics 1997;38:246-52.

19. Cassano GB, Puca F, Scapicchio PL, Trabucchi M, for the Italian StudyGroup on Depression in Elderly Patients. Paroxetine and fluoxetine ef-fects on mood and cognitive functions in depressed nondemented elderlypatients. J Clin Psychiatry 2002;63:396-402.

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23. Harmer CJ, Bhagwagar Z, Cowen PJ, Goodwin GM. Acute administra-tion of citalopram facilitates memory consolidation in healthy volun-teers. Psychopharmacology 2002;163:106-10.

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25. Linnoila M, Stapletin JM, George DT, Lane E, Eckardt MJ. Effects offluvoxamine, alone and in combination with ethanol, on psychomotorand cognitive performance and on autonomic nervous system reactivityin healthy volunteers. J Clin Psychopharmacol 1993;13:175-80.

26. Package insert. Fluvoxamine maleate tablets. Morgantown, WV: MylanPharmaceuticals, October 2000.

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28. Package insert. Zoloft (sertraline). New York: Pfizer, October 2002.29. Package insert. Celexa (citalopram). St. Louis: Forest Laboratories, Au-

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EXTRACTO

OBJETIVO: Reportar un caso con pérdida severa de memoria en unpaciente envejeciente después de comenzar el uso de fluoxetina.

RESUMEN DEL CASO: Una mujer de 87 años comenzó una terapia defluoxetina 20 mg diario para depresión. Después de 6 semanas, lapaciente desarrolló pérdida de memoria progresiva para lo cual fuehospitalizada. Otras causas potenciales fueron eliminadas. Al cabo de 2meses, la paciente mejoró significativamente al descontinuar elmedicamento. Una evaluación objetiva de causalidades de este efectoclasificó la reacción como un posible evento adverso al medicamento.

DISCUSIÓN: Nuestro reporte documenta un caso severo reversible en eldeterioro de la memoria después de iniciar el uso de fluoxetina. Estemedicamento tiene un perfil de efecto secundario favorable si secompara con los antidepresivos antiguos. Sin embargo, estudios despuésdel mercadeo y reportes de casos aislados sugieren que fluoxetina podriaperjudicar la memoria en algunos pacientes. Algunos inhibidores delretomado de serotonina (SSRIs por sus siglas en inglés) parecen causarpérdida de memoria unos más frecuentemente que otros. La literaturaevaluada es incluída.

CONCLUSIONES: Los clínicos deben estar conscientes de los posiblesefectos adversos de fluoxetina en la memoria y posiblemente otrosinhibidores del retomado de serotonina.

Wilma M Guzmán-Santos

RÉSUMÉ

OBJECTIF: Décrire un cas de perte de mémoire sévère chez une personneâgée suite à la prise de la fluoxétine.

RÉSUMÉ DU CAS: Il s’agit d’une femme âgée de 87 ans chez qui on adébuté de la fluoxétine pour une dépression. La posologie a été titrée à20 mg par jour. Elle a présenté une perte de mémoire progressive surune période de 6 semaines pour laquelle elle a été hospitalisée. Lesautres causes potentielles de perte de mémoire ont été éliminées. Suite àl’arrêt de la fluoxétine, la mémoire de la patiente s’est améliorée sur unepériode de 2 mois.

DISCUSSION: Ce cas documente une cause réversible de perte de mémoiresuite à la prise de la fluoxétine chez une personne âgée. La fluoxétine aun profil d’effets indésirables favorable lorsque comparé auxantidépresseurs de première génération. Les études de surveillance et lescas isolés cependant suggèrent que la fluoxétine peut avoir un effet auniveau de la mémoire chez certains patients. Certains inhibiteurssélectifs de la recapture de la sérotonine semblent provoquer des pertesde mémoire plus fréquemment que d’autres.

CONCLUSIONS: Les professionnels de la santé devraient porter uneattention particulière d’une perte de mémoire possible lors de la prise dela fluoxétine.

Louise Mallet

Case Reports

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