In terms of management, unless the syndrome results in other medical problems, treatment for endocrine dysfunction associated with pituitary malfunction is symptomatic and thus supportive;however, in some cases, surgery may be needed.

Empty sella syndrome (abbreviated ESS) is where the pituitary gland shrinks or becomes flattened, filling the sella turcica with cerebrospinal fluid on imaging instead of the normal pituitary. ESS can be found in the diagnostic workup of pituitary disorders, or as an incidental finding when imaging the brain.

Hormonal suppressive therapy with luteinizing hormone receptor agonists like leuprolide can be used to treat the seizure component, and are effective in most patients.

Surgery is offered if there is failure of medical therapy or rapid growth of lesion, with specific options including stereotactic thermocoagulation, gamma knife radiosurgery, and physical resection by transsphenoidal microsurgery. Surgical response is typically better when the seizure focus has been found by EEG to originate in or near the mass. The specific location of the lesion relative to the pituitary and infundibulum and the amount of hormonal disturbance at presentation can help predict risk of hypopituitarism following surgery.

It was shown through various testing that administration of Bromocriptine can improve field of vision defects and lower prolactin levels. It was also found that when using corticosteroids, there was a decrease in size of the gland, and relieved compression on the dura mater. These corticosteroids were also found to have an immunosuppressive effect which helped with reducing the autoimmune reaction of the gland.

The prognosis for hypophysitis was variable for each individual. The depending factors for hypophysitis included the advancement of the mass on the Sella Turcica, percentage of fibrosis, and the body's response to corticosteroids. Through the use of Corticosteroids, the vision defects tend to recover when the gland size began to decrease. The prognoses of the limited number of reported cases were usually good.

The first priority in suspected or confirmed pituitary apoplexy is stabilization of the circulatory system. Cortisol deficiency can cause severe low blood pressure. Depending on the severity of the illness, admission to a high dependency unit (HDU) may be required.

Treatment for acute adrenal insufficiency requires the administration of intravenous saline or dextrose solution; volumes of over two liters may be required in an adult. This is followed by the administration of hydrocortisone, which is pharmaceutical grade cortisol, intravenously or into a muscle. The drug dexamethasone has similar properties, but its use is not recommended unless it is required to reduce swelling in the brain around the area of hemorrhage. Some are well enough not to require immediate cortisol replacement; in this case, blood levels of cortisol are determined at 9:00 AM (as cortisol levels vary over the day). A level below 550 nmol/l indicates a need for replacement.

The decision on whether to surgically decompress the pituitary gland is complex and mainly dependent on the severity of visual loss and visual field defects. If visual acuity is severely reduced, there are large or worsening visual field defects, or the level of consciousness falls consistently, professional guidelines recommend that surgery is performed. Most commonly, operations on the pituitary gland are performed through transsphenoidal surgery. In this procedure, surgical instruments are passed through the nose towards the sphenoid bone, which is opened to give access to the cavity that contains the pituitary gland. Surgery is most likely to improve vision if there was some remaining vision before surgery, and if surgery is undertaken within a week of the onset of symptoms.

Those with relatively mild visual field loss or double vision only may be managed conservatively, with close observation of the level of consciousness, visual fields, and results of routine blood tests. If there is any deterioration, or expected spontaneous improvement does not occur, surgical intervention may still be indicated. If the apoplexy occurred in a prolactin-secreting tumor, this may respond to dopamine agonist treatment.

After recovery, people who have had pituitary apoplexy require follow-up by an endocrinologist to monitor for long-term consequences. MRI scans are performed 3–6 months after the initial episode and subsequently on an annual basis. If after surgery some tumor tissue remains, this may respond to medication, further surgery, or radiation therapy with a "gamma knife".

In larger case series, the mortality was 1.6% overall. In the group of patients who were unwell enough to require surgery, the mortality was 1.9%, with no deaths in those who could be treated conservatively.

After an episode of pituitary apoplexy, 80% of people develop hypopituitarism and require some form of hormone replacement therapy. The most common problem is growth hormone deficiency, which is often left untreated but may cause decreased muscle mass and strength, obesity and fatigue. 60–80% require hydrocortisone replacement (either permanently or when unwell), 50–60% need thyroid hormone replacement, and 60–80% of men require testosterone supplements. Finally, 10–25% develop diabetes insipidus, the inability to retain fluid in the kidneys due to a lack of the pituitary antidiuretic hormone. This may be treated with the drug desmopressin, which can be applied as a nose spray or taken by mouth.

The primary goal in treatment of IIH is the prevention of visual loss and blindness, as well as symptom control. IIH is treated mainly through the reduction of CSF pressure and, where applicable, weight loss. IIH may resolve after initial treatment, may go into spontaneous remission (although it can still relapse at a later stage), or may continue chronically.

Tuber cinereum hamartoma (also known as hypothalamic hamartoma) is a benign tumor in which a disorganized collection of neurons and glia accumulate at the tuber cinereum of the hypothalamus on the floor of the third ventricle. It is a congenital malformation, included on the spectrum of gray matter heterotopias. Formation occurs during embryogenesis, typically between days 33 and 41 of gestation. Size of the tumor varies from one to three centimeters in diameter, with the mean being closer to the low end of this range. It is estimated to occur at a frequency of one in one million individuals.

The best-studied medical treatment for intracranial hypertension is acetazolamide (Diamox), which acts by inhibiting the enzyme carbonic anhydrase, and it reduces CSF production by six to 57 percent. It can cause the symptoms of hypokalemia (low blood potassium levels), which include muscle weakness and tingling in the fingers. Acetazolamide cannot be used in pregnancy, since it has been shown to cause embryonic abnormalities in animal studies. Also, in human beings it has been shown to cause metabolic acidosis as well as disruptions in the blood electrolyte levels of newborn babies. The diuretic furosemide is sometimes used for a treatment if acetazolamide is not tolerated, but this drug sometimes has little effect on the ICP.

Various analgesics (painkillers) may be used in controlling the headaches of intracranial hypertension. In addition to conventional agents such as paracetamol, a low dose of the antidepressant amitriptyline or the anticonvulsant topiramate have shown some additional benefit for pain relief.

The use of steroids in the attempt to reduce the ICP is controversial. These may be used in severe papilledema, but otherwise their use is discouraged.

A pineal gland cyst is a usually benign (non-malignant) cyst in the pineal gland, a small endocrine gland in the brain. Historically, these fluid-filled bodies appeared on of magnetic resonance imaging (MRI) brain scans, but were more frequent at death, seen in of autopsies. A 2007 study by Pu "et al". found a frequency of 23% in brain scans (with a mean diameter of 4.3 mm).

It was once believed that smaller cysts (less than 5.0 mm) were usually asymptomatic, but for larger cysts (greater than 5.0 mm), symptoms could include headache, unexpected seizures, visual disturbances, memory loss, cognitive decline, muscle fasciculations, nausea, weakness, fatigue, light sensitivity, tinnitus, circadian rhythm dysfunction, or hydrocephalus if the cyst impinged on the superior colliculi or caused obstruction of the cerebral aqueduct. Newer research shows that the size of the cyst does not necessarily correlate to the presence of symptoms. In some cases, it will need to be removed before life-threatening situations occur.

Despite the pineal gland being in the center of the brain, due to recent advancements in endoscopic medicine, endoscopic brain surgery to drain and/or remove the cyst can be done with the patient spending 1-3 nights in the hospital, and being fully recovered in weeks, rather than a year, as is the case with open-skull brain surgery.

The National Organization for Rare Disorders states that pineal cysts larger than 5.0 mm are "rare findings" and are possibly symptomatic. If narrowing of the cerebral aqueduct occurs, many neurological symptoms may exist, including headaches, vertigo, nausea, muscle fasciculations, eye sensitivity, and ataxia. Continued monitoring of the cyst might be recommended to monitor its growth, and surgery may be necessary.

In a small population of people with larger, symptomatic cysts, the following comorbid conditions have been noted: Pseudotumor cerebri (elevated intracranial pressure), empy sella, hormonal disturbances, flattened optic discs, chiari malformation, sjogren's, POTS, dysautonomia, PCOS.

Stafne defect is uncommon, and has been reported to develop anywhere between the ages of 11 and 30 years old, (although the defect is developmental, it does not seem to be present form birth, implying that the lesion develops at a later age). Usually the defect is unilateral (on one side only) and most commonly occurs in men.

Tetracosactide given intravenously, is a corticosteroid that causes the brain to produce additional spinal fluid to replace the volume of the lost CSF and alleviate symptoms, and has been used to treat CSF leaks.

In two small studies of two patients and another with one patient suffering from recurrent CSF leaks where repeated blood patches failed to form clots and relieve symptoms, the patients received temporary but complete resolution of symptoms with an epidural saline infusion. The saline infusion temporarily restores the volume necessary for a patient to avoid SIH until the leak can be repaired properly. Intrathecal saline infusion is used in urgent cases such as intractable pain or decreased consciousness.

The gene TGFBR2 has been implicated in several connective tissue disorders including Marfan syndrome, arterial tortuosity, and thoracic aortic aneurysm. A study of patients with SCSFLS demonstrated no mutations in this gene. Minor features of Marfan syndrome has been found in 20% of CSF leak patients. Abnormal findings of fibrillin-1 has been documented in these CSF-leak patients, but only one patient demonstrated a fibrillin-1 defect consistent with Marfan syndrome.

A 1994 community-based study indicated that two out of every 100,000 people suffered from SCSFLS, while a 2004 emergency room-based study indicated five per 100,000. SCSFLS generally affects the young and middle aged; the average age for onset is 42.3 years, but onset can range from ages 22 to 61. In an 11-year study women were found to be twice as likely to be affected as men.

Studies have shown that SCSFLS runs in families and it is suspected that genetic similarity in families includes weakness in the dura mater, which leads to SCSFLS. Large scale population-based studies have not yet been conducted. While a majority of SCSFLS cases continue to be undiagnosed or misdiagnosed, an actual increase in occurrence is unlikely.

The Stafne defect (also termed Stafne's idiopathic bone cavity, Stafne bone cavity, Stafne bone cyst (misnomer), lingual mandibular salivary gland depression, lingual mandibular cortical defect, latent bone cyst, or static bone cyst) is a depression of the mandible on the lingual surface (the side nearest the tongue). The Stafne defect is thought to be a normal anatomical variant, as the depression is created by ectopic salivary gland tissue associated with the submandibular gland and does not represent a pathologic lesion as such.

A ten-patient study conducted by Pareja et al. found that all patients diagnosed with CPH were responsive to indomethacin and were able to completely control their symptoms. Doses of the drug ranged from 25 mg per day to 150 mg per day with a median dose of 75 mg per 24-hour period.

Almost all cases of CPH respond positively and effectively to indometacin, but as much as 25 percent of patients discontinued use of the drug due to adverse side effects, namely complications in the gastrointestinal tract.

According to a case study by Milanlioglu et al., 100mg of lamotrigine, an antiepileptic drug, administered twice daily alleviated all painful symptoms. No side effects were noted after two months of treatment. Dosage of lamotrigine was decreased to 50mg a day after the first two months, and no symptoms or side-effects were recorded after a three-month followup.

Use of topiramate has also been found to be an effective treatment for CPH, but cluster headache medications have been found to have little effect.

Treatment options depend on the type of tumor and on its size:

- Prolactinomas are most often treated with cabergoline or quinagolide (both dopamine agonists), which decrease tumor size as well as alleviates symptoms, followed by serial imaging to detect any increase in size. Treatment where the tumor is large can be with radiation therapy or surgery, and patients generally respond well. Efforts have been made to use a progesterone antagonist for the treatment of prolactinomas, but so far have not proved successful.

- Somatotrophic adenomas respond to octreotide, a long-acting somatostatin analog, in many but not all cases according to a review of the medical literature. Unlike prolactinomas, thyrotrophic adenomas characteristically respond poorly to dopamine agonist treatment.

- Surgery is a common treatment for pituitary tumors. The normal approach is Trans-sphenoidal adenectomy, which usually can remove the tumor without affecting the brain or optic nerves.

- Danazol is a steroid compound that has been labelled as an "Anterior pituitary suppressant".

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.

GH treatment is not recommended for children who are not growing despite having normal levels of growth hormone, and in the UK it is not licensed for this use. Children requiring treatment usually receive daily injections of growth hormone. Most pediatric endocrinologists monitor growth and adjust dose every 3–6 months and many of these visits involve blood tests and x-rays. Treatment is usually extended as long as the child is growing, and lifelong continuation may be recommended for those most severely deficient. Nearly painless insulin syringes, pen injectors, or a needle-free delivery system reduce the discomfort. Injection sites include the biceps, thigh, buttocks, and stomach. Injection sites should be rotated daily to avoid lipoatrophy. Treatment is expensive, costing as much as US $10,000 to $40,000 a year in the USA.

GH deficiency is treated by replacing GH with daily injections under the skin or into muscle. Until 1985, growth hormone for treatment was obtained by extraction from human pituitary glands collected at autopsy. Since 1985, recombinant human growth hormone (rHGH) is a recombinant form of human GH produced by genetically engineered bacteria, manufactured by recombinant DNA technology. In both children and adults, costs of treatment in terms of money, effort, and the impact on day-to-day life, are substantial.

Initial treatment is similar to atrophic rhinitis, namely keeping the nasal mucosa moist with saline or oil-based lubricants and treating pain and infection as they arise; adding menthol to lubricants may be helpful in ENS, as may be use of a cool mist humidifer at home. For people with anxiety, depression, or who are obsessed with the feeling that they can't breathe, psychiatric or psychological care may be helpful.

In some people, surgery to restore missing or reduced turbinates may be beneficial.

A 2015 meta-analysis identified 128 people treated with surgery from eight studies that were useful to pool, with an age range of 18 to 64, most of whom had been suffering ENS symptoms for many years. The most common surgical approach was creating a pocket under the mucosa and implanting material - the amount and location were based on the judgement of the surgeon. In about half the cases a filler such as noncellular dermis, a medical-grade porous high-density polyethylene, or silastic was used and in about 40% cartilage taken from the person or from a cow was used. In a few cases hyaluronic acid was injected and in a few others tricalcium phosphate was used. There were no complications caused by the surgery, although one person was over-corrected and developed chronic rhinosinusitis and two people were under-corrected. The hyaluronic acid was completely resorbed in the three people who received it at the one year follow up, and in six people some of the implant came out, but this did not affect the result as enough remained. About 21% of the people had no or marginal improvement but the rest reported significant relief of their symptoms. Since none of the studies used placebo or blinding there may be a strong placebo effect or bias in reporting.

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.

Carcinomas that metastasize into the pituitary gland are uncommon and typically seen in the elderly, with lung and breast cancers being the most prevalent, In breast cancer patients, metastases to the pituitary gland occur in approximately 6-8% of cases.

Symptomatic pituitary metastases account for only 7% of reported cases. In those who are symptomatic Diabetes insipidus often occurs with rates approximately 29-71%. Other commonly reported symptoms include anterior pituitary dysfunction, visual field defects, headache/pain, and ophthalmoplegia.

Empty nose syndrome has been observed to affect a small proportion of people who have undergone surgery to the nose or sinuses, particularly those who have undergone turbinectomy (a procedure that removes some of the bones in the nasal passage). The incidence of ENS is variable and has not yet been quantified, but it is considered rare.

Untreated, the condition can cause significant and longterm physical and emotional distress in some people; some of the initial presentations on the condition described people who committed suicide. It is difficult to determine what treatments are safe and effective, and to what extent, in part because the diagnosis itself is unclear.

Although CPH is often compared to cluster headaches, it is much less prevalent, occurring in only 1–3% of those who experience cluster headaches. CPH occurs roughly in 1 in 50,000 people, while cluster headaches are comparatively more common and are found in 1 in 1000 people.

Cluster headaches occur primarily in men, while CPH is more commonly diagnosed in women. The female to male ratio of diagnosed patients can range anywhere from 1.6:1 to 2.36:1. Symptoms may begin to appear at any age, but onset usually occurs in adulthood with a mean starting age within the thirties.