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SECONDARY CAUSES OF depression should be considered in patients with atypical presentations. Careful consideration of these secondary causes could result in early identification and initiation of appropriate treatment to prevent further complications. We report a middle aged man who presented initially with depression, but was found to have craniopharyngioma on evaluation. Persistent loss of libido led to further evaluation and identification of craniopharyngioma and associated pituitary dysfunction.

A 40-year-old man presented with a 3-month history of pervasive sad mood, anhedonia, fatigability, depressive cognitions, decreased sleep and appetite and loss of libido. Physical examination and hemogram were normal. Mental status examination was corroborative. He was diagnosed with major depressive disorder (DSM-IV) and started on sertraline 100 mg/day.

The patient showed significant improvement in mood symptoms over the next 2 months but continued to have loss of libido. On further clarification, he also complained of decreased facial hair growth. His endocrine profile indicated low luteinizing hormone (0.29 mIU/mL; normal, 1.5–9.3); low testosterone (24.94 ng/dL; normal, 241–827) and high prolactin (19.05 ng/mL; normal, 2.1–17.7). Cortisol (14.12 μg/dL; normal, 5–25), T3 (190 ng/dL; normal, 70–200), T4 (10.2 μg/dL; normal, 5–13) and thyroid-stimulating hormone (TSH; 0.854 μIU/mL; normal, 0.3–4.5) were normal. On magnetic resonance imaging (MRI) of the brain, a 2.5 cm × 1.5 cm × 1.8 cm, well-defined, lobulated, suprasellar mass lesion with cystic and calcified components was seen. The lesion was seen extending into the sella and compressing the pituitary. Laterally, the lesion was limited within the suprasellar cistern. Ventricles were normal. MRI features were suggestive of craniopharyngioma. Perimetry examination of visual fields by an ophthalmologist was normal. Because the craniopharyngioma was small and did not compress the optic nerve, conservative management with regular follow up was advised by the neurosurgeon. We revised the diagnosis to depression secondary to general medical condition (DSM-IV).

He was started on hormone treatment with testosterone 1 g/3 months, thyroxine 100 μg/day, prednisolone 7.5 mg/day, vitamin D3 (cholecalciferol) 60000 units/month by an endocrinologist in view of the abnormal hormone profile and symptoms. Sertraline was stopped because the patient did not have mood symptoms. The patient reported improvement in libido over the next 2 months. At end of 2 years of follow up, he was maintaining remission. A repeat scan after 1 year indicated marginal increase in tumor mass (3.6 cm × 2 cm × 1.8 cm) but there was no compression of the optic nerve. Informed consent for publication was obtained from the patient.

The present case emphasizes the importance of physical symptoms in identifying secondary causes of depression. Persistent loss of libido even after the remission of mood symptoms prompted further evaluation. Craniopharyngioma is associated with different psychiatric manifestations such as mania,[1] paranoia[2] and depression.[3] Associated hypothalamic–pituitary abnormality is a contributing factor.[4] One limitation of the present report is that we did not use a rating scale for the measurement of the severity of depression. A second limitation is that diagnosis of craniopharyngioma was based on MRI. Although histopathology would have confirmed the diagnosis, this was not done because the patient was managed conservatively. Third, we did not measure free T3 and T4, which would have given a full picture of thyroid dysfunction. Because total T3 and total T4 can be affected by protein levels and protein-binding ability, measurement of TSH, free T4 and free T3 is recommended for a patient in whom thyroid dysfunction is suspected. Although depression as a reaction to loss of libido in this patient was a possibility, improvement in depressive symptoms following treatment with persistent loss of libido made it unlikely. Finally, although the present patient was managed conservatively, treatment decisions regarding surgery must be made on an individual basis because craniopharyngioma has a tendency to become adherent to surrounding structures and compress the optic nerves/chiasm. The present case highlights the importance of assessing physical symptoms in a person with depressive disorder. Persistence of physical symptoms despite improvement in mood symptoms can be an important clinical indicator of possible underlying organic etiology.

References

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  2. References
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    Prusty G, Subramanya, Hemalatha V, Narayanan HS. Craniopharyngioma presenting as mania. Indian J. Psychiatry 1982; 24: 305306.
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    Murray P, Halimi S, Bouchartat J. Paranoid reaction and craniopharyngioma of the third ventricle. Association in the evolution and regression of these two pathologies. Ann. Med. Psychol. 1982; 140: 931940.
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    Spence SA, Taylor DG, Hirsch SR. Depressive disorder due to craniopharyngioma. J. R. Soc. Med. 1995; 88: 637638.
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    Musselman DL, Nemeroff CB. Depression and endocrine disorders: Focus on the thyroid and adrenal system. Br. J. Psychiatry Suppl. 1996; 30: 123128.