Pituitary is a common terrain for the appearance of tumoral changes, representing the origin of about 15% of all intracranial tumors [13]. These tumors are, for the most part, histologically benign, as they arise from hormone secreting cells in the anterior lobe. Therefore, the aim of the paper is to specify the clinical and paraclinical clinical onset characteristics, the evolutionary peculiarities, as well as the metabolic complications secondary to the prolactin hypersecretion. The effects of prolactin-secreting pituitary tumors may occur as a result of mass effects of tumors or even hyperprolactinaemia. Because microadenomas are intrathecal, visual defects may not occur, but headaches occur more often (50%) than normal (27%) [1, 6]. A large tumor that extends beyond the limbs of the turkey can cause headaches and vision defects. The classical presentation is bitemporal hemianopsia due to the compression of the optic chiasm from a tumor that extends to the upper level. If chiasma is prefixed or if the tumor extends posteriorly, compression of a single optical system results in visual field defects similar. The lateral extension in the cavernous sinus can lead to the illness of the oculomotor function involving the cranial nerves III, IV and VI and the branches V1 and V2 of the cranial nerve V, alone or in combinations.
Forward signaling by EphB1/EphB2 interacting with ephrin-B ligands at the optic chiasm is required to form the ipsilateral projection
