she was admitted to outpatient service with complaints of social isolation , insomnia , reluctance and occasional cryings that started one year ago with increasing frequency . she attempted suicide for 4 times within the last four months and she was complaining basically about the problems in her family . she did not receive regular treatment in the past and she had not suffered from a medical illness in the past . in the psychiatric assessment , she was appearing at her chronological age . after anamnesis and psychiatric assessment , depression and cluster b personality disorder were diagnosed and the patient was admitted to mood disorder clinic . olanzapine ( 10 mg 1x1 ) and mirtazapine ( 30 mg 1x1 ) treatment was started . with this treatment partial remission after 23 days of hospitalization she was discharged to be followed up on an ambulatory basis . after 15 days in the outpatient clinic , based on her anamnesis , her symptoms of reluctance , social isolation , cries and anhedonia aggravated . duloxetine 60 mg / day was added to the treatment . in this examination , she did not define any physical complaint . fifteen days later , in the second visit , she was having difficulty in walking with rigidity , restlessness and tremor in her hands . in the examination , cogwheel rigidity , patient s symptoms could not be explained with the use of any drug other than duloxetine . duloxetine and the other drugs were ceased due to patient s disturbance and then biperiden ( 2 mg bid ) treatment was started . at the third visit pathophysiology of parkinsonism resulting from ssri and snri group drugs is still not clearly understood . it is reported that it can be derived from the interaction between serotonin and norepinephrine in the cortex and basal ganglia and might be related with dopamine function . it has been suggested that drugs may cause eps with a change in postsynaptic transmission of dopamine receptors resulting in pathophysiological changes in basal ganglions . another proposed vision of developing parkinsonism with drugs is that it might be associated with a predisposition to parkinson s disease . drug interactions are another mechanism that is related with the etiology of eps associated with ssris and snris . duloxetine is metabolized by the enzymes cytochrome 1a2 and 2d6 and especially inhibition of cyp 1a2 increases duloxetine level markedly . duloxetine causes drug interactions by inhibiting the enzymes cyp 1a2 mildly and cyp 2d6 moderately . in our case , the patient was receiving duloxetine and olanzapine . olanzapine is the molecule that is , metabolized mostly by cyp 1a2 and then by cyp 2d6   . due to mild inhibition of cyp 1a2 by duloxetine , we think that eps in our patient is not related with the drug interactions but with the molecule itself . although case reports of eps secondary to duloxetine are rare , according to fda adverse event reporting system ( aers ) incidence of eps induced by duloxetine is higher than that induced by sertraline , escitalopram , fluoxetine and bupropion . when we have reviewed the cases of eps caused by antidepressants , we have seen that eps were observed more often when there were predisposing factors such as psychomotor disorder , extrapyramidal symptoms that developed secondary to another drug use in the past , different kinds of drug applications at the same time , insufficiency of cytochrome enzymes , simultaneous parkinson s disease , recent cessation of monoamine oxidase inhibitors . some studies have demonstrated that the presence of a1 allele in the polymorphism of d2 dopamine receptor gene taq 1a is a risk factor for eps . ageing and female sex are also risk factors for antidepressant- induced eps . no family history for parkinson s disease , simultaneous onset of movement disorder and duloxetine treatment did not provide supportive evidence about drug induced parkinsonism in this 45-year - old women . in cases of antidepressant induced eps , dose of drug can be reduced or it can be ceased or replaced by another antidepressant . in some cases , eps emerged by adding duloxetine to the patient s current antipsychotic treatment and due to her complaints severity treatment was ceased . it should be remembered that antidepressant associated eps can occur at any time of the treatment .
in literature , there are more than hundred cases of extrapyramidal symptoms ( eps ) associated with selective serotonin reuptake intibitors ( ssri ) whereas eps case reports associated with serotonin noradrenaline reuptake inhibitors ( snri ) are in a relatively small number . 
 a snri group drug duloxetine that is used for indication of major depression since 2004 is a double acting antidepressant that acts by blocking serotonin and noradrenaline reuptake . 
 side effects of duloxetine on extrapyramidal system are not expected due to low affinity to d2 receptors . in this case , 
 report manifestations of parkinsonism developed in a patient who used duloxetine for major depression are presented . since any 
 duloxetine induced eps case has not reported so far , we have thought that this case can contribute to the literature .