What causes intermittent headaches?

In real life, intermittent headaches are a relatively common physical and brain disease. Suffering from intermittent headaches is not only very harmful to the health of the body, but also easily causes severe pain in the head and easily causes some head complications. There are many reasons for intermittent headaches. This is a symptom caused by tumors in the brain, which can easily lead to blood supply hormones and cause intermittent headaches.

What causes intermittent headaches?

Causes of intermittent headaches

Non-functioning pituitary adenomas are actually a group of heterogeneous tumors, most of which have division function (mostly gonadotropin), but their secretion function is low and does not cause an increase in blood hormone levels. This type of tumor is called silent adenoma.

Some non-functioning adenomas may have no secretory function and their cellular origin is unclear, which is called naked cell tumor or featureless cell adenoma.

Pathogenesis

There have been two theories in the study of the pathogenesis of pituitary tumors, namely the pituitary cell defect theory and the hypothalamic regulation disorder theory. It is now basically agreed that the development of pituitary tumors can be divided into two stages: the initial stage and the promotion stage.

In the initial stage, defects in pituitary cells themselves are the main cause of the disease, while in the promotion stage, factors such as hypothalamic regulation disorders play a major role. That is, a pituitary cell mutates, leading to the activation of oncogenes and/or the inactivation of tumor suppressor genes. Then, under the promotion of internal and external factors, the monoclonal mutant cells continue to proliferate and gradually develop into pituitary tumors.

1. Intrinsic defects of pituitary tumor cells

The use of molecular biological techniques has now made it clear that most functional and non-functional adenomas are monoclonal, originating from the unrestricted proliferation of a single mutant cell. The causes of mutation are activation of oncogenes and/or inactivation of tumor suppressor genes.

The main oncogenes that have been identified include gsp, gip, ras, hst and PTTG, and the tumor suppressor genes include MEN-1, p53, Nm23 and CDKN2A. The gsp gene was found in 40% of GH tumors, 10% of non-functioning adenomas, and 6% of ACTH tumors.

The activation of the gsp gene and the gip2 gene inhibits the activity of endogenous GTPase, so that the α-subunit of the Gs protein and the Gi2 protein are continuously activated. The latter two can be regarded as the products of the gsp oncogene and the gip2 oncogene, respectively.

These two oncogene products can directly cause the activation of nuclear transcription factors such as AP-1, CREB and Pit-1, increasing hormone secretion and initiating tumor growth.

In addition, the activation of oncogenes will lead to an increase in intracellular cAMP levels, which can stimulate cyclin (cell cycle protein) DL and 3 to produce cdk2 and cdk4, the latter two of which can promote cells to enter the S phase from the G1 phase.