Cingulate herniation
In cingulate or subfalcine herniation, the most common type, the innermost part of the frontal lobe is scraped under part of the falx cerebri, the dura mater at the top of the head between the two hemispheres of the brain. Cingulate herniation can be caused when one hemisphere swells and pushes the cingulate gyrus by the falx cerebri. This does not put as much pressure on the brainstem as the other types of herniation, but it may interfere with blood vessels in the frontal lobes that are close to the site of injury (anterior cerebral artery), or it may progress to central herniation. Interference with the blood supply can cause dangerous increases in ICP that can lead to more dangerous forms of herniation. Symptoms for cingulate herniation are not well defined. Usually occurring in addition to uncal herniation, cingulate herniation may present with abnormal posturing and coma. Cingulate herniation is frequently believed to be a precursor to other types of herniation. Transcalvarial herniation
In transcalvarial herniation, the brain squeezes through a fracture or a surgical site in the skull. Also called "external herniation", this type of herniation may occur during craniectomy, surgery in which a flap of skull is removed, the protruding brain region preventing the piece of skull from being replaced during the operation. Upward herniation
Increased pressure in the posterior fossa can cause the cerebellum to move up through the tentorial opening in upward, or cerebellar herniation. The midbrain is pushed through the tentorial notch upward.
Among patients presenting with Zollinger-Ellison syndrome, 20 to 60% have MEN 1. A severe secretory diarrhea can develop and cause fluid and electrolyte depletion with non–β-cell tumors. This complex, referred to as the watery diarrhea, hypokalemia and achlorhydria syndrome (VIPoma) has been ascribed to vasoactive intestinal polypeptide, although other intestinal hormones or secretagogues (including prostaglandins) may contribute. Hypersecretion of glucagon, somatostatin, chromogranin, or calcitonin, ectopic secretion of ACTH resulting in Cushings syndrome, and hypersecretion of somatotropin–releasing hormone (causing acromegaly) sometimes occur in non–β-cell tumors. All of these are rare in MEN 1.Nonfunctioning pancreatic tumors also occur in patients with MEN 1 and may be the most common type of pancreatoduodenal tumor in MEN 1. The size of the nonfunctioning tumor correlates with risk of metastasis and death. Pituitary
Pituitary tumors occur in 15 to 42% of MEN 1 patients. From 25 to 90% are prolactinomas. About 25% of pituitary tumors secrete growth hormone or growth hormone and prolactin. Excess prolactin may cause galactorrhea, and excess growth hormone causes acromegaly clinically indistinguishable from sporadically occurring acromegaly. About 3% of tumors secrete ACTH, producing Cushings disease. Most of the remainder are nonfunctional. Local tumor expansion may cause visual disturbance, headache, and hypopituitarism. Pituitary tumors in MEN 1 patients appear to be larger and behave more aggressively than sporadic pituitary tumors. Other manifestations
Adenomas of adrenal glands occurs occasionally in MEN 1 patients. Hormone secretion is rarely altered as a result, and the significance of these abnormalities is uncertain.