2 stimuli. Moreover, the patient complained of intermittenl paraesthesias and dysaesthesias particularly in both arms and left sided headaches. An ophthalmologist was con- sulted the same day and diagnosed a left-sided acute optic neuritis with paracentral scotoma. We immediately started an intravenous pulse treatment with methyl-prednisolone (initially 1 g for 3 days, then oral dose reduction step by step with 10 days). Simultaneously, neurological and cardiologic was initiated to assess inﬂammatory or ischemic brain disorders within 5 days. Thorough electrophysiological investigations including visual evoked potentials, cMRT, clinical laboratory, and cerebral spinal ﬂuid analysis did not indicate an inﬂammatory brain disorder or ischemia. Blood coagulation tests were within normal range. Neu- rosonography showed physiological extra- and intracranial vessels. Echocardiographic investigations (TTE and TEE) conﬁrmed a very small PFO which had probably no clinical relevance, but low-dose Aspirin (100 mg) was recommended. Gynecological assessment revealed normal ﬁndings apart from left sided lactation; prolactin was not increased. The patient responded well to steroid pulse therapy but temporarily tended towards increased blood glucose levels and ankle edema occurred. Blood glucose normalized after cessation of steroid treatment and edema disappeared after small doses of frusemide. 3. Discussion and Conclusion The patient presented is the ﬁrst case in the literature suﬀer- ing simultaneously from the trias of marked mydriasis, optic neuritis, and galactorrhea. The exact mechanism of action remains speculative, but some eﬀects have been already observed experimentally or clinically. Mydriasis obviously can be explained via 5-HT1a-receptor stimulation [10]. Optic neuritis may be caused by several drugs such as isoniazid or ethambutol, but only in very rare cases follow- ing administration of SSRIs [11]. Acute allergic reactions occurred after the administration of escitalopram and may, therefore, serve as a suitable pathophysiological model although the course was much more delayed and less severe in our patient [12]. Experimental data using arthritis models in rats discuss a proinﬂammatory role of central serotonin which indicates an aggravating eﬀect of SSRIs with regard to the inﬂammation cascade [13]. This experimen- tal ﬁndings were only partially conﬁrmed by population- based determinations of C-reactive protein (CRP), which revealed increased CRP levels only after use of tricyclic antidepressants but not after intake of SSRIs [14]. However, the results are equivocal, as ﬂuoxetine obviously ameliorates neuropathic or inﬂammatory pain conditions [15]. Mydriasis, possibly due to brain activating properties of serotonin, has been conﬁrmed in healthy volunteers [16]. Galactorrhea occurred in patients during treatment tricyclics (imipramine) or SSRI (escitalopram) without depending on increased prolactin levels [17]. Euprolactinemic galac- torrhea is discussed as the result of indirect inhibition of tuberoinfundibular dopaminergic neurons. On the contrary, hyperprolactinemia and subsequent galactorrhea has also been observed during treatment with citalopram [8]. Case Reports in Medicine In conclusion, the exact underlying toxicological mech- anism of optic neuritis in our patient, however, remains to be elucidated. With regard to galactorrhea, altered hypotha- lamic dopamine availability may be responsible for the side eﬀect. A general CNS-stimulating eﬀect of serotonin may be the cause of mydriasis following intake of SSRIs. 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