PhysicalThe physical findings mirror the aforementioned symptoms and include signs due to raised intracranial pressure, involvement of cranial nerves, compression of the underlying parenchyma, and involvement of bone and subcutaneous tissues by the meningioma. Raised intracranial pressure leads to papilledema, decreased mentation and, ultimately, to brain herniation. Involvement of the cranial nerves may lead to anosmia, visual field defects, optic atrophy, diplopia, decreased facial sensation, facial paresis, decreased hearing, deviation of the uvula, and hemiatrophy of the tongue. Compression of the underlying parenchyma may give rise to pyramidal signs that are exemplified by pronator drift, hyperreflexia, positive Hoffman sign, and presence of the Babinsi sign. Parietal!lobe syndrome may occur if the parietal lobes are compressed.o Compression of the dominant "usually left# parietal lobe may give rise to $erstmann syndrome% agraphia, acalculia, right!left disorientation, and finger agnosia.o Compression of the nondominant "usually right# parietal lobe leads to tactile and visual extinction and neglect of the contralateral side.o Compression of the occipital lobes leads to a congruent homonymous hemianopsia. &pinal meningiomas may give rise to a Bro'n!&e(uard syndrome "ie, contralateral decreased pain sensation, ipsilateral 'eaness, decrease in position sense#, sphincteric 'eaness and, ultimately, complete (uadriparesis or paraparesis.Causes&ee the list belo'% Trauma and viruses have been investigated as possible causative agents for development of meningiomas. Ho'ever, no definitive proof has yet been found. The role of inflammation "eg, posttraumatic insult# resulting in the upregulation of C)*!+ has been investigated in the tumorogenesis of meningiomas.,-. )n the other hand, the role of radiation in the genesis of meningiomas has been sho'n.o Patients sub/ected to lo'!dose irradiation for tinea capitis may develop multiple meningiomas decades later in the field of irradiation.o High!dose cranial irradiation may induce meningiomas after a short latency period. $enetic causes have been implicated in the development of meningiomas.o The best!characteri0ed and most common genetic alteration is the loss of the 12+ gene "NF2# on chromosome ++(,3. . NF2 encodes a tumor suppressor no'n as merlin "or sch'annomin#.o )f interest, the meningioma locus is close to but probably different from the gene responsible for 12+.o 4p to 567 of sporadic meningiomas 'ere found to harbor NF2mutations.o )ther cytogenetic alterations are chromosomal loss of 8p, 9p, 5(, and 8:(.o ;oss of chromosome 86 is associated 'ith increased tumor grade, shortened time to recurrence, and shortened survival.o Progression to anaplastic meningioma has been associated 'ith involvement of chromosomal site 8!binding protein, has been identified as a potential biomarer in patients 'ho have a high ris of recurrent meningioma.,8+. &everal findings suggest an association bet'een hormones and the ris for meningiomas, including increased incidence in 'omen versus men and the presence of estrogen, progesterone, and androgen receptors on some of these tumors. Ho'ever, the exact nature of this relationship and its implication on the management of meningiomas remain under investigation. ?hether cell phone use increases the ris of meningiomas "and of brain tumors in general# remains of great interest, especially 'ith the recent tremendous increase in the use of these devices 'orld'ide. >t present, the available data do not support such an association@ ho'ever, all published studies have relatively small sample si0es and a short period of follo'!up.,89.Aifferential Aiagnoses