Galactorrhea can take place as a result of dysregulation of certain hormones. Hormonal causes most frequently associated with galactorrhea are hyperprolactinemia and thyroid conditions with elevated levels of thyroid-stimulating hormone (TSH) or thyrotropin-releasing hormone (TRH). No obvious cause is found in about 50% of cases.

Lactation requires the presence of prolactin, and the evaluation of galactorrhea includes eliciting a history for various medications or foods (methyldopa, opioids, antipsychotics, serotonin reuptake inhibitors, as well as licorice) and for behavioral causes (stress, and breast and chest wall stimulation), as well as evaluation for pregnancy, pituitary adenomas (with overproduction of prolactin or compression of the pituitary stalk), and hypothyroidism. Adenomas of the anterior pituitary are most often prolactinomas. Overproduction of prolactin leads to cessation of menstrual periods and infertility, which may be a diagnostic clue. Galactorrhea may also be caused by hormonal imbalances owing to birth control pills.

Galactorrhea is also a side effect associated with the use of the second-generation H receptor antagonist cimetidine (Tagamet). Galactorrhea can also be caused by antipsychotics that cause hyperprolactinemia by blocking dopamine receptors responsible for control of prolactin release. Of these, risperidone is the most notorious for causing this complication. Case reports suggest proton-pump inhibitors have been shown to cause galactorrhea.

Neonatal milk or witch's milk is milk secreted from the breasts of approximately 5% of newborn infants. It is considered a normal variation and no treatment or testing is necessary. In folklore, witch's milk was believed to be a source of nourishment for witches' familiar spirits.

Prolactin secretion in the pituitary is normally suppressed by the brain chemical dopamine. Drugs that block the effects of dopamine at the pituitary or deplete dopamine stores in the brain may cause the pituitary to secrete prolactin. These drugs include the major tranquillizers (phenothiazines), trifluoperazine (Stelazine), and haloperidol (Haldol); antipsychotic medications, such as risperidone and quetiapine; metoclopramide (Reglan), domperidone, cisapride used to treat gastro-oesophageal reflux; medication-induced nausea (such as cancer drugs); and, less often, alpha-methyldopa and reserpine, used to control hypertension; and estrogens and TRH. The sleep drug ramelteon (Rozerem) also increases the risk of hyperprolactinaemia. A benzodiazepine analog, etizolam, can also increase the risk of hyperprolactinaemia. In particular, the dopamine antagonists metoclopramide and domperidone are both powerful prolactin stimulators and have been used to stimulate breast milk secretion for decades. However, since prolactin is antagonized by dopamine and the body depends on the two being in balance, the risk of prolactin stimulation is generally present with all drugs that deplete dopamine, either directly or as a rebound effect.

Physiological (i.e., non-pathological) causes include: pregnancy, breastfeeding, and mental stress.

The following are some of the possible medical causes of galactorrhea hyperprolactinemia that are listed by the Diseases Database: pregnancy, breastfeeding, sexual intercourse, shingles, prolactin secreting pituitary tumor, along with many others.

Hyperprolactinemia occurs more commonly in women. The prevalence of hyperprolactinemia ranges from 0.4% in an unselected normal adult population (10,000 normal Japanese adults working at a single factory) to as high as 9 to 17% in women with reproductive disorders. Its prevalence was found to be 5% in a family planning clinic population, 9% in a population of women with adult-onset amenorrhea, and 17% among women with polycystic ovary syndrome.

Hyperprolactinemia can cause reduced estrogen production in women and reduced testosterone production in men. Although estrogen/testosterone production may be restored after treatment for hyperprolactinemia, even a year or two without estrogen/testosterone can compromise bone strength, and patients should protect themselves from osteoporosis by increasing exercise and calcium intake through diet or supplementation, and by avoiding smoking. Patients may want to have bone density measurements to assess the effect of estrogen/testosterone deficiency on bone density. They may also want to discuss testosterone/estrogen replacement therapy with their physician.

Autopsy studies indicate that 6-25% of the U. S. population have small pituitary tumors. Forty percent of these pituitary tumors produce prolactin, but most are not considered clinically significant. Clinically significant pituitary tumors affect the health of approximately 14 out of 100,000 people. In non-selective surgical series, this tumor accounts for approximately 25-30% of all pituitary adenomas. Some growth hormone (GH)–producing tumors also co-secrete prolactin. Microprolactinomas are much more common than macroprolactinomas.

Hyperprolactinemic SAHA syndrome is a cutaneous condition characterized by lateral hairiness, oligomenorrhea, and sometimes acne, seborrhea, FAGA I, and even galactorrhea.

Multiple endocrine neoplasia or MEN is part of a group of disorders that affect the body's network of hormone-producing glands (the endocrine system). Hormones are chemical messengers that travel through the bloodstream and regulate the function of cells and tissues throughout the body. Multiple endocrine neoplasia involves tumors in at least two endocrine glands; tumors can also develop in other organs and tissues. These growths can be noncancerous (benign) or cancerous (malignant). If the tumors become cancerous, some cases can be life-threatening.

The two major forms of multiple endocrine neoplasia are called type 1 and type 2. These two types are often confused because of their similar names. However, type 1 and type 2 are distinguished by the genes involved, the types of hormones made, and the characteristic signs and symptoms.

These disorders greatly increase the risk of developing multiple cancerous and noncancerous tumors in glands such as the parathyroid, pituitary, and pancreas. Multiple endocrine neoplasia occurs when tumors are found in at least two of the three main endocrine glands (parathyroid, pituitary, and pancreatico-duodenum). Tumors can also develop in organs and tissues other than endocrine glands. If the tumors become cancerous, some cases can be life-threatening. The disorder affects 1 in 30,000 people.

Although many different types of hormone-producing tumors are associated with multiple endocrine neoplasia, tumors of the parathyroid gland, pituitary gland, and pancreas are most frequent in multiple endocrine neoplasia type 1. MEN1-associated overactivity of these three endocrine organs are briefly described here:

- Overactivity of the parathyroid gland (hyperparathyroidism) is the most common sign of this disorder. Hyperparathyroidism disrupts the normal balance of calcium in the blood, which can lead to kidney stones, thinning of the bones (osteoporosis), high blood pressure (hypertension), loss of appetite, nausea, weakness, fatigue, and depression.

- Neoplasia in the pituitary gland can manifest as prolactinomas whereby too much prolactin is secreted, suppressing the release of gonadotropins, causing a decrease in sex hormones such as testosterone. Pituitary tumor in MEN1 can be large and cause signs by compressing adjacent tissues.

- Pancreatic tumors associated with MEN-1 usually form in the beta cells of the islets of Langerhans, causing over-secretion of insulin, resulting in low blood glucose levels (hypoglycemia). However, many other tumors of the pancreatic Islets of Langerhans can occur in MEN-1. One of these, involving the alpha cells, causes over-secretion of glucagon, resulting in a classic triad of high blood glucose levels (hyperglycemia), a rash called necrolytic migratory erythema, and weight loss. Another is a tumor of the non-beta islet cells, known as a gastrinoma, which causes the over-secretion of the hormone gastrin, resulting in the over-production of acid by the acid-producing cells of the stomach (parietal cells) and a constellation of sequelae known as Zollinger-Ellison syndrome. Zollinger-Ellison syndrome may include severe gastric ulcers, abdominal pain, loss of appetite, chronic diarrhea, malnutrition, and subsequent weight loss. Other non-beta islet cell tumors associated with MEN1 are discussed below.

In a diagnostic workup individuals with a combination of endocrine neoplasias suggestive of the "MEN1 syndrome" are recommended to have a mutational analysis of the MEN1 gene if additional diagnostic criteria are sufficiently met, mainly including:

- age <40 years

- positive family history

- multifocal or recurrent neoplasia

- two or more organ systems affected

Although the causes of craniopharyngioma is unknown, it can occur in both children and adults, with a peak in incidence at 9 to 14 years of age. There are approximately 120 cases diagnosed each year in the United States in patients under the age of 19 years old. In fact, more than 50% of all patients with craniopharyngioma are under the age of 18 years. There is no clear association of the tumor with a particular gender or race. It is not really known what causes craniopharyngiomas, but they do not appear to "run in families" or to be directly inherited from the parents.

The disease can remit spontaneously or become chronic, with exacerbations and remissions. In some persons, it can progress to pulmonary fibrosis and death. About half of cases resolve without treatment or can be cured within 12–36 months, and most within five years. Some cases, however, may persist several decades. Two-thirds of people with the condition achieve a remission within 10 years of the diagnosis. When the heart is involved, the prognosis is generally less favourable, though corticosteroids appear effective in improving AV conduction. The prognosis tends to be less favourable in African Americans than in white Americans.

Some 1990s studies indicated that persons with sarcoidosis appear to be at significantly increased risk for cancer, in particular lung cancer, lymphomas, and cancer in other organs known to be affected in sarcoidosis. In sarcoidosis-lymphoma syndrome, sarcoidosis is followed by the development of a lymphoproliferative disorder such as non-Hodgkin lymphoma. This may be attributed to the underlying immunological abnormalities that occur during the sarcoidosis disease process. Sarcoidosis can also follow cancer or occur concurrently with cancer. There have been reports of hairy cell leukemia, acute myeloid leukemia, and acute myeloblastic leukemia associated with sarcoidosis.

Sometimes, sarcoidosis, even untreated, can be complicated by opportunistic infections.

Foroozen divides the causes of chiasmal syndromes into intrinsic and extrinsic causes. Intrinsic implies thickening of the chiasm itself and extrinsic implies compression by another structure. Other less common causes of chiasmal syndrome are metabolic, toxic, traumatic or infectious in nature.

Intrinsic etiologies include gliomas and multiple sclerosis. Gliomas of the optic chiasm are usually derived from astrocytes. These tumors are slow growing and more often found children. However, they have a worse prognosis, especially if they have extended into the hypothalamus. They are frequently associated with neurofibromatosis type 1 (NF-1). Their treatment involves the resection of the optic nerve. The supposed artifactual nature of Wilbrand's knee has implications for the degree of resection that can be obtained, namely by cutting the optic nerve immediately at the junction with the chiasm without fear of potentially resulting visual field deficits.

The vast majority of chiasmal syndromes are compressive. Ruben et al. describe several compressive etiologies, which are important to understand if they are to be successfully managed. The usual suspects are pituitary adenomas, craniopharyngiomas, and meningiomas.

Pituitary tumors are the most common cause of chiasmal syndromes. Visual field defects may be one of the first signs of non-functional pituitary tumor. These are much less frequent than functional adenomas. Systemic hormonal aberrations such as Cushing’s syndrome, galactorrhea and acromegaly usually predate the compressive signs. Pituitary tumors often encroach upon the middle chiasm from below. Pituitary apoplexy is one of the few acute chiasmal syndromes. It can lead to sudden visual loss as the hemorrhagic adenoma rapidly enlarges.

The embryonic remnants of Rathke’s pouch may undergo neoplastic change called a craniopharyngioma. These tumors may develop at any time but two age groups are most at risk. One peak occurs during the first twenty years of life and the other occurs between fifty and seventy years of age. Craniopharyngiomas generally approach the optic chiasm from behind and above. Extension of craniopharyngiomas into the third ventricle may cause hydrocephalus.

Meningiomas can develop from the arachnoid layer. Tuberculum sellae and sphenoid planum meningiomas usually compress the optic chiasm from below. If the meningioma arises from the diaphragma sellae the posterior chiasm is damaged. Medial sphenoid ridge types can push on the chiasm from the side. Olfactory groove subfrontal types can reach the chiasm from above. Meningiomas are also associated with neurofibromatosis type 1. Women are more prone to develop meningiomas.

The heritability of sarcoidosis varies according to ethnicity. About 20% of African Americans with sarcoidosis have a family member with the condition, whereas the same figure for European Americans is about 5%. Additionally, in African Americans, who seem to experience more severe and chronic disease, siblings and parents of sarcoidosis cases have about a 2.5-fold increased risk for developing the disease. Investigations of genetic susceptibility yielded many candidate genes, but only few were confirmed by further investigations and no reliable genetic markers are known. Currently, the most interesting candidate gene is "BTNL2"; several "HLA-DR" risk alleles are also being investigated. In persistent sarcoidosis, the HLA haplotype "HLA-B7-DR15" are either cooperating in disease or another gene between these two loci is associated. In nonpersistent disease, there is a strong genetic association with HLA DR3-DQ2. Cardiac sarcoid has been connected to TNFA variants.

They are classified by histology as benign; however, as with many brain tumors, their treatment can be difficult, and significant morbidities are associated with both the tumor and treatment.

- Headache (obstructive hydrocephalus)

- Hypersomnia

- Myxedema

- post surgical weight gain

- Polydipsia

- Polyuria (diabetes insipidus)

- Vision loss (bitemporal hemianopia)

- Vomiting

- often occurs post treatment

- Growth hormone (GH) insufficiency, caused by the reduction in growth hormone (GH) production. Symptoms include:

- Stunted growth and delayed puberty (in children)

- General fatigue, loss of muscle mass and tone (in adults)

- Pituitary insufficiency

- often occurs to some degree because craniopharyngiomas develop in the area of the pituitary stalk, which can affect the function of the pituitary gland.

- Reduction in prolactin production. This is very uncommon and occurs with severe pituitary insufficiency.

- Large pituitary tumors can paradoxically elevate blood prolactin levels due to the "stalk effect." This elevation occurs as a result of the compression of the pituitary stalk, which interferes with the brain's control of prolactin production.

- In premenopausal women, elevated prolactin can lead to reduction or loss of menstrual periods and/or breast milk production (galactorrhea).

- With stalk effect, prolactin levels are usually only slightly elevated, as opposed to prolactinomas in which the prolactin level is usually very high.

- Diabetes insipidus. This occurs due to the absence of a posterior pituitary hormone called antidiuretic hormone (ADH). Symptoms include:

- Excessive thirst

- Excessive urination

- Adrenal insufficiency. This occurs because of a reduction in ACTH production, a reduction in cortisol. In severe cases, it can be fatal. Symptoms include:

- Fatigue

- Low blood pressure

- Electrolyte abnormalities

Chiasmal syndrome is the set of signs and symptoms that are associated with lesions of the optic chiasm, manifesting as various impairments of the sufferer's visual field according to the location of the lesion along the optic nerve. Pituitary adenomas are the most common cause; however, chiasmal syndrome may be caused by cancer, or associated with other medical conditions such as multiple sclerosis and neurofibromatosis.