Genetics
The most frequent genetic mutations (~50%) involved in meningiomata are inactivation mutations in the neurofibromatosis 2 gene (merlin) on chromosome 22q.TRAF7 mutations are present in about one-fourth of meningiomata. Mutations in the TRAF7, KLF4, AKT1, and SMO genes are commonly expressed in benign skull-base meningiomata. Mutations in NF2 are commonly expressed in meningiomata located in the cerebral and cerebellar hemispheres. Pathophysiology
Meningiomata arise from arachnoidal cap cells, most of which are near the vicinity of the venous sinuses, and this is the site of greatest prevalence for meningioma formation. Some subtypes may arise from the pial cap cells that migrate during the development together with blood vessels into the brain parenchyma. They most frequently are attached to the dura over the superior parasagittal surface of frontal and parietal lobes, along the sphenoid ridge, in the olfactory grooves, the sylvian region, superior cerebellum along the falx cerebri, cerebellopontine angle, and the spinal cord. The tumor is usually gray, well-circumscribed, and takes on the form of the space it occupies. They usually are dome-shaped, with the base lying on the dura. Locations
Parasagittal/falcine (25%)
Convexity (surface of the brain) (19%)
Sphenoid ridge (17%)
Suprasellar (9%)
Posterior fossa (8%)
Olfactory groove (8%)
Middle fossa/Meckels cave (4%)
Tentorial (3%)
Peri-torcular (3%)
Intraparenchymal (rare)Other uncommon locations are the lateral ventricle, foramen magnum, and the orbit/optic nerve sheath. Meningiomata also may occur as a spinal tumor, more often in women than in men. This occurs more often in Western countries than Asian.Histologically, meningioma cells are relatively uniform, with a tendency to encircle one another, forming whorls and psammoma bodies (laminated calcific concretions).
It typically begins with blood accumulating in the pericardial sac posterior to the heart, and eventually expands to surround the entire heart. The fluid build-up then causes pressure within the pericardial sac to increase. If the pressure becomes greater than the intracardiac pressure of the heart, compression of the adjacent cardiac chambers can occur. This compression, called cardiac tamponade, is often associated with hemopericardium and can be fatal if not diagnosed and treated promptly. Early signs of this compression include right atrial inversion during ventricular systole followed by diastolic compression of the right ventricular outflow tract.There have also been cases reported in which hemopericardium was noted as an initial manifestation of essential thrombocythemia. Diagnosis
Hemopericardium can be diagnosed using echocardiography, a cardiac ultrasound. Chest X-rays are also often taken when hemopericardium is suspected and would reveal an enlarged heart. Other observable signs include rapid heart rate, jugular venous distension, low blood pressure, and pulsus paradoxus. Treatment
When discovered, hemopericardium is usually treated by pericardiocentesis, a procedure wherein a needle is used to remove the fluid from the pericardial sac. This procedure typically utilizes an 8-cm, 18-gauge needle that is inserted between the xiphoid process and the left costal margin until it enters the pericardial sac, when it can then be used to drain the fluid from the sac. A catheter is often left in the pericardium to continue draining any remaining fluid after the initial procedure. The catheter can be removed when the hemopericardium no longer persists.