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Cystic cavities associated with old cerebral infarction or hemorrhage may cause mood disorders as well as cognitive impairments. Here we report a patient who has a linear cystic lesion in the left cerebral hemisphere adjacent to lateral ventricle with neurocognitive impairment and mood disorder comorbidity. A 28-year-old female patient was admitted to our clinic with inability to think with the right side of her brain, numbness at the right side of the head and neck, anhedonia, forgetfulness. 4 months ago, she was admitted to a neurology outpatient clinic with complaints of numbness and painful contractions at the right side of her neck. She was told to have a normal state based on MRI scan and she was referred to psychiatry for evaluation. The patient was hospitalized in our unit. She had no history of any physical illness. In the first psychiatric examination she had a depressive mood, an anxious affect, passive suicidal thoughts, slowed thinking and decreased attention. Results of routine biochemical tests, complete blood count and thyroid hormone profile were within normal range. Trişuoperazine 1 mg/day, Venlafaxine 75 mg/day and alprazolam 1.5 mg/day were administered to the patient. During next visit, it was seen that she had difficulty in making simple mathematical calculations. It was learned from the patient and her relatives that she had no difficulties in making such calculations before. It was also learned that her depressive complaints were not alleviated despite a 4-month old treatment and she had periods of sleep disturbances and agitations. She was started on lamotrigine 25 mg/day that was increased over the next three weeks to 200 mg/day, with an excellent clinical response. Benton visual retention test and neurocognitive battery and neurology consultation were planned. MRI showed a cystic cavity (old hemorrhage or infarct) in the left cerebral hemisphere adjacent to lateral ventricle. Neurology requested cranial MRI, CT and EEG. Patient’s EEG was normal. MRI and CT findings were consistent with the former results. Neuropsychiatric battery revealed mild subcortical (frontal) memory impairment but recalling was preserved. Benton visual retention test suggested an organic pathology. Neurological examination was normal and neurology requested a second neuropsychiatric battery. The second neuropsychiatric battery was performed two weeks later and results were consistent with her age and educational status. Therefore, no additional recommendations were made by neurology. Patient whose depressive symptoms, numbness, sleep disturbances and cognitive functions improved was discharged with venlafaxine 75 mg/day, trişuoperazine 1 mg/day and lamotrigine 200 mg/day. Benign intracranial lesions detected during treatment or investigation may disrupt cognition in a progressive manner even in young and middle aged patients and may cause additional psychiatric symptoms that may be resistant to therapy. In our case, a benign cranial lesion was detected during investigation and was thought to cause neurocognitive changes and mood symptoms. Also, an excellent response to an antiepileptic like lamotrigine suggested cellular destruction.