Meningioma Clinical Presentation: History, Physical, Causes

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Meningioma

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Presentation

History

Meningiomas produce their symptoms by several mechanisms. They may cause symptoms by irritating the underlying cortex, compressing the brain or the cranial nerves, producing hyperostosis^[4]and/or invading the overlying soft tissues, or inducing vascular injuries to the brain.^[5]The signs and symptoms secondary to meningiomas may appear or become exacerbated during pregnancy but usually abate or improve in the postpartum period.

Irritation: By irritating the underlying cortex, meningiomas can cause seizures. New-onset seizures in adults justify neuroimaging (eg, MRI) to exclude the possibility of an intracranial neoplasm.
Compression: Localized or nonspecific headaches are common. Compression of the underlying brain can give rise to focal or more generalized cerebral dysfunction, as evinced by focal weakness, dysphasia, apathy, and/or somnolence.

Stereotypic symptoms: Meningiomas in specific locations may give rise to the stereotyped symptoms listed in the Table. These stereotypical symptoms are not pathognomonic of meningiomas in these locations; they may occur with other conditions or lesions. Conversely, meningiomas in these locations may remain asymptomatic or produce other unlisted symptoms. Table. Symptoms and Signs Associated with Meningiomas in Specific Locations

Table. (Open Table in a new window)

Location	Symptoms
Parasagittal	Monoparesis of the contralateral leg
Subfrontal	Change in mentation, apathy or disinhibited behavior, urinary incontinence
Olfactory groove	Anosmia with possible ipsilateral optic atrophy and contralateral papilledema (this triad termed Kennedy-Foster syndrome)
Cavernous sinus	Multiple cranial nerve deficits (II, III, IV, V, VI), leading to decreased vision and diplopia with associated facial numbness
Occipital lobe	Contralateral hemianopsia
Cerebellopontine angle	Decreased hearing with possible facial weakness and facial numbness
Spinal cord	Localized spinal pain, Brown-Sequard (hemispinal cord) syndrome
Optic nerve	Exophthalmos, monocular loss of vision or blindness, ipsilateral dilated pupil that does not react to direct light stimulation but might contract on consensual light stimulation; often, monocular optic nerve swelling with optociliary shunt vessels
Sphenoid wing	Seizures; multiple cranial nerve palsies if the superior orbital fissure involved
Tentorial	May protrude within supratentorial and infratentorial compartments, producing symptoms by compressing specific structures within these 2 compartments^[6]
Foramen magnum	Paraparesis, sphincteric troubles, tongue atrophy associated with fasciculation

Vascular: This presentation, although rare, should be considered. Meningiomas of the skull base may narrow and even occlude important cerebral arteries, possibly presenting either as transient ischemic attack (TIA)–like episodes or as stroke.
Miscellaneous
- Intraventricular meningiomas may present with obstructive hydrocephalus.
- Meningiomas in the vicinity of the sella turcica may produce panhypopituitarism.
- Meningiomas that compress the visual pathways produce various visual field defects, depending on their location.
- Rarely, chordoid meningiomas can present with hematologic disturbances, namely Castleman syndrome.^[7]

Physical

The 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 Babinski sign. Parietal-lobe syndrome may occur if the parietal lobes are compressed.
- Compression of the dominant (usually left) parietal lobe may give rise to Gerstmann syndrome: agraphia, acalculia, right-left disorientation, and finger agnosia.
- Compression of the nondominant (usually right) parietal lobe leads to tactile and visual extinction and neglect of the contralateral side.
- Compression of the occipital lobes leads to a congruent homonymous hemianopsia.
Spinal meningiomas may give rise to a Brown-Sequard syndrome (ie, contralateral decreased pain sensation, ipsilateral weakness, decrease in position sense), sphincteric weakness and, ultimately, complete quadriparesis or paraparesis.

Causes

Trauma and viruses have been investigated as possible causative agents for development of meningiomas. However, no definitive proof has yet been found.

The role of inflammation (eg, posttraumatic insult) resulting in the upregulation of COX-2 has been investigated in the tumorogenesis of meningiomas.^[8]

On the other hand, the role of radiation in the genesis of meningiomas has been shown.

Patients subjected to low-dose irradiation for tinea capitis may develop multiple meningiomas decades later in the field of irradiation.
High-dose cranial irradiation may induce meningiomas after a short latency period.

Genetic causes have been implicated in the development of meningiomas.

The best-characterized and most common genetic alteration is the loss of the NF2 gene (NF2) on chromosome 22q^[9]. NF2 encodes a tumor suppressor known as merlin (or schwannomin).
Of interest, the meningioma locus is close to but probably different from the gene responsible for NF2.
Up to 60% of sporadic meningiomas were found to harbor NF2 mutations.
Other cytogenetic alterations are chromosomal loss of 1p, 3p, 6q, and 14q.
Loss of chromosome 10 is associated with increased tumor grade, shortened time to recurrence, and shortened survival.
Progression to anaplastic meningioma has been associated with involvement of chromosomal site 17q.
The following events were found to be associated with higher grades of meningiomas: loss of the tumor suppressor in lung cancer-1 gene (TSLC-1), loss of progesterone receptors, increased expression of cyclooxygenase 2 and ornithine decarboxylase.
Monosomy of chromosome 7 is a rare cytogenetic change. However, it is frequently reported in radiation-induced meningiomas.
The invasive potential of meningioma cells seems to be reflected by a balance between the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs).
The most consistent chromosomal abnormality isolated in meningiomas is on the long arm of chromosome 22.
Meningiomas can also be associated with different genetic syndromes, namely Gorlin^[10]and Rubinstein-Taybi syndromes^[11].
IMP3, an oncofetal RNA-binding protein, has been identified as a potential biomarker in patients who have a high risk of recurrent meningioma.^[12]

Several findings suggest an association between hormones and the risk for meningiomas, including increased incidence in women versus men and the presence of estrogen, progesterone, and androgen receptors on some of these tumors. However, the exact nature of this relationship and its implication on the management of meningiomas remain under investigation.

According to a systematic review of the literature, individuals who are overweight or obese and those who do not engage in physical activity have an increased risk for meningioma. With normal weight used as the reference group, being overweight (BMI, 25 to 29.9) was associated with a 20% increased risk for meningioma, and obesity (BMI, 30 or more) was associated with a 50% increased risk. In contrast, being overweight or obese was not related to glioma.^{[13, 14]}

Whether cell phone use increases the risk of meningiomas (and of brain tumors in general) remains of great interest, especially with the recent tremendous increase in the use of these devices worldwide. At present, the available data do not support such an association; however, all published studies have relatively small sample sizes and a short period of follow-up.^[15]

Differential Diagnoses

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Media Gallery

Case 1: MRI of a meningioma on plaque.
Case 1: Bone-window CT reveals calcification of the meningioma.
Case 1: Surgical view of the tumor. The dura is opened, and the meningioma can be seen extending en plaque over the surface of the brain.
Case 1: Bone flap seen along the removed meningioma in toto.
Case 2: Gadolinium-enhanced MRI of a meningioma invading the overlying dura and bone. Compare with appearance in Case 1.
Case 2: Bone-window CT scan reveals the skull involvement. Note the absence of tumoral calcification.
Case 2: Intraoperative view shows the skull involvement.
Case 2: Bone flap was removed. Note tumoral breach of the dura. The dura and overlying skull were removed surgically. Duraplasty and cranioplasty were performed
Case 2: Surgical specimen. Complete resection was achieved.
Case 3: Tentorial meningioma. A, Contrast-enhanced CT scan shows the enhancing meningioma. Transverse T1-weighted MRIs shows isointensity of the tumor compared with the surrounding brain (B) and its homogenous enhancement (C). Coronal (D), coronal enhanced (E), and sagittal enhanced (F) T1-weighted MRIs. Posterior circulation angiograms show tumoral blush (arrow in G) and the Bernasconi-Cassinari artery (arrow in H).
Case 3: Tentorial meningioma. Gadolinium-enhanced T1-weighted MRI immediately (A) and 2 years after surgery (B-D). Transverse images show posterior (arrow in B) and anterior (arrow in C) recurrence involving the tentorium. Sagittal images show posterior (D) and anterior (E) recurrence involving the tentorium. Lower vignette reveals complete excision of the recurrence after a second operation.
Case 3: Tentorial meningioma A, Pathology showed syncytial meningioma. Note hypercellularity and minimal whorling (hematoxylin-eosin, original magnification X400). B, MRI performed 4 years after the first operation reveals a recurrence over the posterior tentorium. C, Two-dimensional planning for stereotactic radiosurgery. Three recurrences lie in the plane of the tentorium on a single line. D, Three-dimensional planning for stereotactic radiosurgery. Three arcs were used to irradiate the largest recurrence.
Case 4: Recurrent subcutaneous meningioma. A, Patient underwent surgery for a parieto-occipital meningioma in 1978. She was lost to follow-up until 1996, when this transverse T2-weighted MRI was obtained. Arrow indicates surgical bed of the resected meningioma. B, Although the initial surgical bed is tumor-free, sagittal T2-weighted MRI shows a large subcutaneous recurrence. C, Lower transverse section also shows recurrence. Note variegated appearance of the tumor. D, Transverse section at a lower level. Postoperative sagittal (E) and transverse (F, G) enhanced T1-weighted MRI shows gross total removal of the tumor. H and I, Tumoral recurrence 3 months after surgery, at the same level as in G and F, respectively. Patient received repeat surgery for subtotal removal of the tumor; a pediculated subcutaneous flap was used to close the surgical defect. After surgery, patient received conventional radiotherapy.
Case 5: Bilateral olfactory meningioma invading the facial sinuses. Coronal (A), transverse (B), and sagittal (C) gadolinium-enhanced T1-weighted MRI shows bilateral olfactory meningiomas, and the falx dividing the tumor in 2. Arrow indicates tumor invasion of the sinuses. D, Postoperative enhanced T1-weighted MRI shows that the tumor was completely removed by means of craniotomy and a transfacial approach. E, Tumor was first approached intracranially. Enhanced T1-weighted MRI reveals complete excision of the intracranial component. Arrow indicates residual in the sinuses. F, Residual was completely excised by means a transfacial approach performed with the otolaryngology team.
Case 6: Subfrontal meningioma in a patient with abnormal behavior. A, Contrast-enhanced CT scan clearly shows bilateral subfrontal meningioma. B, Transverse T1-weighted MRI of same lesion. C, Intense gadolinium enhancement of the tumor. Coronal (D) and sagittal (E) gadolinium-enhanced T1-weighted MRIs. F, Anterior circulation angiogram reveals posterior displacement of the anterior cerebral artery by tumor. G, Postoperative MRI shows complete removal of the tumor. H-I, Pathology slides (hematoxylin-eosin; original magnification X100 in H, X400 in I) show syncytial meningioma with well-identified whorls and no psammoma bodies.
Case 7: Parasagittal meningioma invading the superior sagittal sinus (SSS). A, Sagittal T1-weighted MRI shows a meningioma (arrow). B, T2-weighted MRI. Note midline shift and tumoral invasion of the skull (arrow). C, Transverse T2-weighted MRI. D, Angiogram shows invasion of the SSS, which remains patent. Sagittal (E, G), transverse (F) postoperative T1-weighted MRI. H, Gadolinium-enhanced postoperative T1-weighted MRI shows residual tumor, which was intentionally left to preserve patency of the SSS. I, Pathology slide (hematoxylin-eosin, original magnification X100) shows a highly vascular syncytial meningioma.
Pathology slides (hematoxylin-eosin; original magnification X400 in A-B, X100 in C-D). A, Fibroblastic meningioma (arrowheads) abutting the dura (arrow). B, Psammomatous meningioma (arrow indicates psammoma body). C, Meningothelial meningioma, tumor in case 4. E, Meningioma with marked vascularity (arrowheads indicate meningioma cluster; arrow, vessel wall).
Case 4: Pathology slides (hematoxylin-eosin, original magnification X400). A, Meningioma with malignant features, as evinced by prominent nucleoli (yellow dot) and mitoses (arrows). B, Intranuclear cytoplasmic intrusion (pseudoinclusion).
This is an extra-axial tumor. Glioblastoma multiforme (GBM) and astrocytoma are intraparenchymal tumors, and GBM enhances in a variegated fashion. Acoustic schwannomas are seen in the posterior fossa but not in this location. Fibrous dysplasia involves the skull but does not cause this amount of compression.
Surgery on a 46-year-old female with a 2-cm, dural-based enhancing tumor along the left frontal convexity. The lesion was presumed to be a meningioma and showed serial enlargement on MRI, prompting the procedure. Pathology confirmed the tumor to be a WHO grade I meningioma. Video courtesy of Anand I. Rughani, MD, and Jeffrey E. Florman, MD.
Meningioma resection in the tuberculum sellae. Video courtesy of Anand I. Rughani, MD, and Jeffrey E. Florman, MD.

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Table.

Location	Symptoms
Parasagittal	Monoparesis of the contralateral leg
Subfrontal	Change in mentation, apathy or disinhibited behavior, urinary incontinence
Olfactory groove	Anosmia with possible ipsilateral optic atrophy and contralateral papilledema (this triad termed Kennedy-Foster syndrome)
Cavernous sinus	Multiple cranial nerve deficits (II, III, IV, V, VI), leading to decreased vision and diplopia with associated facial numbness
Occipital lobe	Contralateral hemianopsia
Cerebellopontine angle	Decreased hearing with possible facial weakness and facial numbness
Spinal cord	Localized spinal pain, Brown-Sequard (hemispinal cord) syndrome
Optic nerve	Exophthalmos, monocular loss of vision or blindness, ipsilateral dilated pupil that does not react to direct light stimulation but might contract on consensual light stimulation; often, monocular optic nerve swelling with optociliary shunt vessels
Sphenoid wing	Seizures; multiple cranial nerve palsies if the superior orbital fissure involved
Tentorial	May protrude within supratentorial and infratentorial compartments, producing symptoms by compressing specific structures within these 2 compartments^[6]
Foramen magnum	Paraparesis, sphincteric troubles, tongue atrophy associated with fasciculation

Table. Summary of the 2007 WHO Grading Scheme for Meningiomas

WHO Grade	Histological Subtype	Histological Features
I	Meningothelial, fibroblastic, transitional, angiomatous, microcystic, secretory, lymphoplasmacytic metaplastic, psammomatous	Does not fulfill criteria for grade II or III
II (Atypical)	Chordoid, clear cell	4 or more mitotic cells per 10 hpf and/or 3 or more of the following: increased cellularity, small cells, necrosis, prominent nucleoli, sheeting, and/or brain invasion in an otherwise Grade I tumor
III (Anaplastic)	Papillary, rhabdoid^[22]	20 or more mitoses per 10 hpf and/or obviously malignant cytological characteristics such that tumor cell resembles carcinoma, sarcoma, or melanoma

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Author

Georges Haddad, MD Clinical Assistant Professor, Department of Medicine, Division of Vascular Surgery, American University of Beirut, Lebanon

Georges Haddad, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Ali Turkmani, MD Staff Physician, Department of Neurosurgery, American University Hospital

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Nicholas Lorenzo, MD, MHA, CPE Founding Editor-in-Chief, eMedicine Neurology; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc

Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American Academy of Neurology

Disclosure: Nothing to disclose.

Chief Editor

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS is a member of the following medical societies: American College of International Physicians, American Heart Association, American Stroke Association, American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners Institute, National Association of Managed Care Physicians, American College of Physicians, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, Royal Society of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Jorge C Kattah, MD Head, Associate Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria

Jorge C Kattah, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences

Disclosure: Nothing to disclose.

Frederick M Vincent, Sr, MD Clinical Professor, Department of Neurology and Ophthalmology, Michigan State University Colleges of Human and Osteopathic Medicine

Frederick M Vincent, Sr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners Institute, American College of Legal Medicine, American College of Physicians

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthors Tarafa Baghdadi, MD and Roukoz B Chamoun, MD to the development and writing of this article.

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