Republic of the Philippines

Region I Medical Center

Dagupan, City Pangasinan
Department of Surgery

Written Case Presentation:

Meningioma

Submitted by:
Bam Deepak B.
4th year medicine
Virgin Milagrosa University foundation
 Republic of the Philippines
Department of Health
Regional Health Office No. 1
REGION 1 MEDICAL CENTER
Dagupan City

A CASE OF MENINGIOMA

GENERAL DATA

This is the case of patient P. E, a 53 year old, Female, married , Filipino, Roman Catholic,
born Dec 31, 1965 and currently residing at san Fabian , Pangasinan was admitted for the first
time in Region I Medical Center on march 17, 2019 at around 3: 15 o’clock in the afternoon.
The Informant for the medical history was the Patient herself and the Reliability is
Excellent (100%).

CHIEF COMPLAINT: “left sided weakness”

HISTORY OF PRESENT ILLNESS:

4 month prior to admission patient had left sided weakness associated with progressive
headache more on right frontal area no sought consult no medication was taken ,persistence of
symptoms with increase headache 1 episode of seizure on dec 2018 charaterized by stiffning of
extremities followed by upward gaze as described by daughter then patient sought consult at
medical department of R1mc patient then , Admitted at medical ward with initial impression of
CVB bleed with medication of CITICHOLINE 500MG TID IV , OMEPRAZOLE 40MG IV OD ,
LACTULOSE 30CC ODHS, ATORVASTATIN 40MG ODHS , plain cranial CT-scan was requested , it
shows extra-axial lobulated isodense mass in the right frontoparietal region as described .
contrast -enhanced study is advised for the further evaluation related marked mass effect with
subfalcine herniation from right to left with non-communicating hydrocephalus then patient was
transferred to surgery further evaluation and management under neurosurgery.

PAST MEDICAL HISTORY:

The patient was known case of hypertension on losartan 50mgtab day as a maintenance
dosage.
No previous history of surgery nor blood transfusions.

FAMILY HISTORY:

Her Father died at the age of 67 years old due to cerebrovascular accident, there is history
of highblood pressure on father side. No history cancer nor history of diabetes and other
heredofamilial diseases noted .

PERSONAL, SOCIAL AND ENVIRONMENTAL HISTORY:

Patient is a sales lady, non-smoker and non-alcoholic beverage drinker, no known

allergies to food and drug and denied use of illegal drug. Patient is living with her 56 years old
husband and 3 children .

REVIEW OF SYSTEMS:

Constitutional: no weight loss; no loss of appetite; no fever; no chills

Neurologic: no syncope, no seizures, no sensory problems / numbness / tingling sensations
noted, no scotoma, no vertigo, no tremors nor involuntary movements noted.
EENT: No blurring of vision, no diplopia, no eye pain, no problems in hearing, no sore throat, no
epistaxis, no eye discharge, no nose discharge, no ear discharge
CARDIOVASCULAR: No chest pain or discomfort noted, no orthopnea, no palpitations
RESPIRATORY: No cough, no hemoptysis, no difficulty of breathing
GIT: No dysphagia, no odynophagia, no flatulence/burping, no nausea, no vomiting, no change
in bowel movement
GUT: No dysuria, no incontinence
FEMALE REPRODUCTIVE: no dysmenorrhea, no
MUSCULOSKELETAL: no joint pain; no redness or swelling noted, no decrease in the range of
motion
IMMUNOLOGIC: no easy bruising or bleeding, no urticarial/allergy
PSYCHIATRIC: No insomnia, no mania or mood swings, no psychotropic drugs

PHYSICAL EXAMINATION
GENERAL SURVEY:
The patient was seen to be conscious, coherent, oriented to time, place and person and not in
cardiopulmonary distress.

VITAL SIGNS:
Cardiac Rate: 82 bpm, O2 saturation: 99%
Respiratory Rate: 17 cpm Temperature: 36.6°C
Blood Pressure: 100/70 mmHg

SKIN: no pallor, no cyanosis, no jaundice, no lesions, no rashes, no petechial / ecchymosis, there

is tumor at the plantar area with blood and pus discharge.

HEENT: The head is upright, midline, no unusual facie observed, pink palpebral conjunctiva,
anicteric sclerae, auricles are equal and size and appearance

LYMPH NODES: no cervical lymphadenopathies noted.

CHEST AND LUNGS: The chest is symmetrical in appearance with clear breath sounds on both
lung fields. With good air entry, no tactile fremitus, resonant both lungs
HEART: Normal heart rate and regular rhythm, adynamic precordium, no murmurs

ABDOMEN: Soft, flat not distended with normoactive bowel sounds. No direct or rebound
tenderness noted.
EXTREMITIES: There were no deformities seen in the extremities, there is limitation in motion
noted. there is 1/5 Muscle strength in left side of extremities.

NEUROLOGIC:
Neurologic Exam

Cerebrum: Patient is conscious, coherent and cooperative and oriented to time, place and person.

Cranial nerve , GCS 15/15

 I – can smell coffee

 II, III – pupils equally reactive to light
 III, IV, VI – intact extra occular muscles
 V – Intact corneal reflex, bilateral intact masseter muscle contraction
 VII – (-) facial asymmetry
 VIII – can hear, bilateral
 IX, X – intact gag reflex
 XI – can shrug shoulders, bilateral
 XII - tongue midline on protrusion

 Sensory System:

Pain Sensation: Can distinguish sharp from dull.

Light touch: Responds to light touch

Vibration: Can sense vibration and position sense

 Motor:

 RIGHT UPPER 5+/5  LEFT UPPER 1+/5

 RIGHT LOWER 5+/5  LEFT LOWER 1+/5

The patient has visible muscle contraction.

  Cerebellum: No abnormal gait no ataxia, No nystagmus; can do heel to shin test;
can do rapid alternating movements; can do finger to nose test, no
dysdiadokinesia, no involuntary movements noted.

 Reflexes :Joint reflexes intact, symmetric, normoreflexive, brisk, negative

Babinski, Meningeal Signs: Negative Kernig’s and Brudzinki’s signs.

Deep tendon reflex

GCS 15, no sensory deviations, intact cranial nerves

Cranial nerves:
LABORATORY:
Blood Typing: “o” Rh positive
CBC

WBC 6.7
Neutrophil 62.3
Lymphocyte 24.5
Monocyte 7.3
Eosinophil 5.9
Basophils 00
Erythrocyte 5.0
Hemoglobin 139
Platelate 284

CLINICAL CHEMISTRY

Result Ref range

Urea 2.3 2.9- 8.2

Sodium 146.30 mmol/l 135-148

Potassium 3.95 mmol/l 3.50-5.30

Chloride 106.10 mmol/l 98-107

Ionized calcium 1.27 mmol/l 1.13-1.32

Creatinine 38 mmol/l 35-71

Cholesterol 5.10 mmol/l 3.89-5.83

Triglyceride 1.77mmol/L 0.45-1.58

HDL 1.18mmol/l 1.09-2.28

LDL 3.12mmol/l 0-3.37

Fasting blood sugar 4.77mmol/l 3.89-5.83

Coagulation test :

Protime :

Control – 10.2 seconds

Patient- 9.15 seconds

% activity – 127%

INR-0.89

APTT:

Control -28.0 seconds

Patient -21.1 seconds

Ratio – 0.76

URINALYSIS

Physical examination

Color Light Yellow

Transpirancy turbid

Chemical examination

blood Negative

bilirubin Negative

urobilinogen Normal
 ketones Negative

protein Negative

nitrite Negative

glucose Negative

pH 6.5

Specific gavity 1.025

leucocyte Negative

Urine flow cytometry

RBC 19/ uL

Pus cell 3/uL

Epithelial cells 7/uL

Hyaline cast 1/uL

bacteria 291

CHEST AP SITTING VIEW :

No definitive active lung infiltrate is seen.
Cardiac silhouette is magnified. Aorta is not unusual.
Diaphragm and both costophrenic sulci are unremarkable.
Lateral curvature of the thoracic spine convex to left peaking at the level of T8 which may still
secondary to position although mild levoscoliosis.
Cranial CT- Scan non-contrast – There is extra axial lobulated isodense mass measuring 82.5X
43.7X48.6 mm in right frontoparietal region, with marked perilesional edema , compressing the
right lateral and 3rd ventricles with consequent dilation of left lateral ventricle . adjacent cortical
sulci and right sylvian fissure are affected.
Rest of the parenchyma is normal with well-defined gray -white matter interface.
No evidence of intracerebral hemorrhage.
Midline structure are shifted towards the left by about 10.5 mm which subfalcine herniation.
Remainder of cortical sulci , cistern and left fissures are not unsual .
Cerebellum and posterior fossa structure are unremarkable.
Orbits, paranasal sinuses and petromastoids are intact.
No evidence fracture in bony calvaria.
CT-Angiogram of head/neck – in correlation with the previous plain and contrast ct-scan of
head dated march 18. 2019, present study again show an avidly enhancing multilobulatd extr -
axial mass with no significant change in size and appearance and no change in it’s surrounding
edema. The mass is predominantly supplied by cortical branches of the anterior cerebral
artery.

The anterior cerebral artery artery shows no sign of narrowing and anterior communicating
artery is patent. however, both are displaced toward left by aforementioned mass.
The middle cerebral arteries arise normally from internal carotids on each side and form normal
insular loop however, the right is displaced inferiorly toward the left by the mass. there is no
circumscribed vascular narrowing or dilatation.
The vessel lumen shows homogenous signal intensity.
The visualized segments of vertebral arteries are normal in caliber and shows no evidence of
dilatation nor luminal defects. The basilar artery shows normal course and caliber and divides
into normal sized posterior cerebral arteries. posterior communicating are undisturbed on both
sides. No segments show concolution or circumscribed dilation.

Dierential diagnosis/diagnostic considerations of meningioma

1. multiple meningiomas: suggests neurofibromatosis 2 (NF2)
2. pleomorphic xanthoastrocytoma (PXA) (p.635): may mimic meningiomas since they tend to
be peripherally located and may have a dural tail
3. Rosai-Dorfman disease: especially if extracranial lesions are also identified. A connective
tissue disorder with sinus histiocytosis and massive painless lymphadenopathy (most have
cervical lymphadenopathy). Usually in young adults. Isolated intracranial involvement is rare.
MRI: duralbased
enhancing mass with signal characteristics similar to meningioma, may have dural tail.
Most common intracranial locations: cerebral convexities, parasagittal, suprasellar, cavernous
sinus. Pathology: dense fibrocollagenous connective tissue with spindle cells and lymphocytic
infiltration, stains for CD68 & S-100. Histiocytic proliferation without malignancy. Foamy
histiocytes are characteristic. Surgery and immunosuppressive therapy not e ect ive. Low-dose
XRTmay be the best option.

IMPRESSION: Falx meningioma

Course in the ward :

o DAT
o Omeprazole 40mg IV OD
o Dexamethasone 4mg IV q6
o Atorvastatin 40 mg/tab ODHS
o Amlodipine 10mg/tab OD
o Citicholine 500mg/tab TID
o Lactulose syrup 30ml ODHS
o Mannitol 100 cc q6
o Furosemide 20mg q8
o Paracetamol 1gm iv q6
o Diazepam 5mg iv PRN for seizure
o Patient was CP cleared and OR notified from Anesthesia
o NPO prior to OR
o Tramadol 50mg iv q6
o Tranexamic acid 1gm iv q8
o Oxacillin 1gm iv q8
o Cefuroxime 750 mg iv q8
o Vitamin k 1amp iv q8
o Other medication continue omeprazole , dexamethasone and mannitol iv
INTRAOPERATIVE FINDINGS:

Picture taken during Operation

Date of Operation: 4/2/19
Dr. Florendo/Dr. Dalisay/Dr.Ong
1. Patient was on Supine Position head turning to the left .
2.Performing Asepsis/Antisepsis ( hair shaving )
3.total Sterile Drapes
4. right temporo-Parieal craniotomy
5.tumor attached to Falx hard , firm at the periphery suckable . tumor excised at peripheral
portion using bipolar and Cautery loop.
6.thin residual tumor at the falx bulk approximated bone flap reteryl.
7. Scalp closed by vicryl and proline.

OPERATION DONE: Craniotomy, Excision A Falx Meningioma right, Fronto-parietal.

HISTHOPATHOLOGY : Meningioma , WHO grade I ( MENINGIOTHELIA )

FINAL DIAGNOSIS : FALX MENINGIOMA , RIGHT FRONTO-PARIETAL , WHO grade I (

MENINGIOTHELIA )
 CASE DISCUSSION

INTRODUCTION
Meningiomas are the most common benign intracranial tumor. They originate from
arachnoid cap cells, which are cells within the thin, spider web-like membrane that covers the
brain and spinal cord. The arachnoid is one of three protective layers, collectively known as the
meninges, surrounding the brain and the spinal cord. The meninges also include the dura
mater and pia mater. Although the majority of meningiomas are benign, these tumors can
grow slowly until they are very large if left undiscovered and, in some locations, can be severely
disabling and life-threatening. Most patients develop a single meningioma; however, some
patients may develop several tumors growing simultaneously in other parts of the brain
or spinal cord.

Some meningiomas are found along the dural lining in the venous sinuses of the brain and skull
base, locations where arachnoid cap cells are most abundant. The following subtypes are based
on the location of the tumor.

 Cavernous Sinus Meningioma: Occurs near the area that drains deoxygenated blood to the
heart from the brain.
 Cerebellopontine Angle Meningioma: Located near the margin of the cerebellum; acoustic
neuromas (vestibular schwannoma) typically are found in this area.
 Cerebral Convexity Meningioma: Located on the upper surface of the brain cerebral convexity.
 Foramen Magnum Meningioma: Located near the opening at the base of the skull through
which the lower portion of the brainstem passes.
 Intraorbital Meningioma: Located in or around eye sockets.
 Intraventricular Meningioma: Located in the chambers through which cerebrospinal fluid is
carried throughout the brain.
 Olfactory Groove Meningioma: Located along the nerves connecting the nose to the brain.
 Parasagittal/Falx Meningioma: Located adjacent to the dural fold that separates the two brain
hemispheres
 Petrous Ridge Meningioma: Portion of the temporal bone (which supports the temple) that
contain sections of the organs that facilitate hearing.
 Posterior Fossa Meningioma: Occurs near the back of the brain.
 Sphenoid Meningioma: Located near the sphenoid bone behind the eyes.
 Spinal Meningioma: Located in the spine, in some cases against the spinal cord.
 Suprasellar Meningioma: Located near the area of the skull where the pituitary gland is found.
 Tentorium Meningioma: Located near where the brain connects to the brainstem, an area
known as the tentorium cerebelli.
Parasagittal and falx meningiomas
Up to 50% invade the superior sagittal sinus (SSS). Grouped based on location along AP direction
of SSS as:
1. anterior (ethmoidal plate to coronal suture): 33%. Most often present with H/A and mental
status changes
2. middle (between coronal and lambdoidal sutures): 50%. Most often present as Jacksonian
seizure and progressive monoplegia
3. posterior (lambdoidal suture to torcular Herophili): 20%. Most often present with H/A, visual
symptoms, focal seizures, or mental status changes
Classification systems for the extent of SSS invasion include one by Bon nal and Brotchi,9 and a
more recent one by Sindou et al.10 shown in 􀀀Fig. 42.1.
Parasagittal meningiomas may originate at the level of the motor strip, and a common initial
manifestation of these is a contralateral foot drop.
Fig. 42.1 Grading system for meningioma invasion ofthe superior sagittal sinus Modified from
Sindou MP et al., J Neurosurg,
Shown: schematic coronal section through superior sagittal sinus (SSS).
Type I= attachment to lateral wall of sinus
Type II= invasion of lateral recess
Type III= invasion of lateral wall
Type IV= invasion of lateral wall and roof
Type V= total sinus occlusion, contralateral wall
spared
Type VI= total sinus occlusion, invasion of all walls

Pathology
Four critical histopathological variables:
1. grade
2. histological subtype
3. proliferation indices
4. brain invasion
There are a number of pathologic classification systems,15,16 (p 465),17 and transitional forms
between the major types exist. More than one histological pattern may be seen in a given tumor.
The WHO 2000 classification is shown in below
1. meningiomas with low risk of both recurrence and/or aggressive growth (WHO grade III)
a) meningothelial or meningotheliomatous, AKA syncytial: the most common. Sheets of
polygonal cells. Some use the term angiomatous for meningotheliomatous variety with closely
packed blood vessels
b) fibrous or fibroblastic: cells separated by connective tissue stroma. Consistency is more
rubbery
than meningotheliomatous or transitional
c) transitional: intermediate between meningotheliomatous and fibrous. Cells tend to be spindle
shaped, but areas of typical meningotheliomatous cells occur. Whorls, some of which are
calcified (psammoma bodies)
d) psammomatous: calcified meningothelial whorls
e) angiomatous
f) microcystic: AKA“humid” or vacuolated meningioma. The characteristic dilated extracellular
spaces are usually empty, but occasionally contain substance that stains positive for PAS
(glycoprotein) or contain fat. The cysts may coalesce and form grossly or radiologically visible
cysts and may resemble astrocytomas
g) secretory
h) lymphoplasmacyte-rich
2. meningiomas with greater recurrence risk and/or aggressive growth include
a) atypical meningioma: increased mitotic activity (1–2 mitotic figure/high-powered field),
increased cellularity, focal areas of necrosis, giant cells. Cellular pleomorphism is not unusual but
is not significant in and of itself. Increasing atypia appears to correlate with increasing
aggressiveness
b) rhabdoid meningiomas: usually have malignant features and behave aggressively. Behavior in
the absence of malignant features is undetermined19
c) malignant meningiomas: AKA anaplastic, papillary or sarcomatous. Characterized by frequent
mitotic figures, cortical invasion, rapid recurrence even after apparent total removal, and, rarely,
metastases (see below). Frequent mitotic figures (≥ 4 mitoses per high-power field) or the
presence of papillary features are strong predictors of malignancy. May be more common in
younger patients

Prevalence and Incidence

According to the Brain Science Foundation and the American Society of Clinical Oncology,
meningiomas account for about 34 percent of all primary brain tumors and most often occur in
people between the ages of 30 and 70. Malignant meningiomas account for about two to three
percent of all meningiomas.

Types and Classification

The World Health Organization (WHO) classification of brain tumors is the most widely utilized
tool in grading tumor types. The WHO classification scheme recognizes 15 variations of
meningiomas according to their cell type as seen under a microscope. These variations are
called meningioma subtypes; the technical term for these cell variations is histological
subtypes.

World Health Organization (WHO) Meningioma Classifications

WHO Grade I — Benign WHO Grade II — Atypical WHO Grade III — Malignant

Meningiothelial Chordoid Papillary

Fibrous (fibroblastic) Clear Cell Rhabdoid

Transitional (mixed) Atypical Anaplastic

Psammomatous

Angiomatous

Microcystic

Secretory

Lymphoplasmacyte-rich

Metaplastic

Atypical meningiomas (which account for seven to eight percent of meningioma cases) exhibit
increased tissue and cell abnormalities. These tumors grow at a faster rate than benign
meningiomas and can invade the brain. Atypical meningiomas have a higher likelihood of
recurrence than benign meningiomas.

Malignant meningiomas show increased cellular abnormalities, and grow at a faster rate than
benign and atypical meningiomas. Malignant meningiomas are the most likely to invade the
brain, spread to other organs in the body and recur more often than the other two types.

Risk Factors
As noted earlier, meningiomas most often occur in people between the ages of 30 and 70.
Children are not as likely as adults to develop meningioma.
 Women are more than two times as likely as men to develop a meningioma. Malignant
meningioma diagnoses are three times as likely in men. Spinal meningiomas occur 10 times
more frequently in women than in men.

Exposure to ionizing radiation, especially high doses, has been associated with a higher
incidence of intracranial tumors, particularly meningiomas. There also is evidence indicating a
connection between meningiomas and low doses of radiation. The most well-known case
involves children in Israel who were given radiation for scale ringworm between 1948 and
1960. Within the U.S., dental X-rays are the most common form of exposure to ionizing
radiation. A number of studies have linked the number of full mouth dental radiographs to
increased risk of meningioma.

The genetic disorder Neurofibromatosis type 2 (NF2) is believed to put people at a higher risk
of developing meningioma. Patients with NF2 also may be more likely to develop malignant or
multiple meningiomas.

Per the Brain Science Foundation, a number of studies have suggested a correlation between
meningiomas and hormones. Such findings include the following:

 Increased occurrence of meningioma in women

 The detection of such hormones as estrogen, progesterone and androgen in some
meningiomas
 A link between breast cancer and meningioma
 A connection between meningioma growth, menstrual cycles and pregnancy

Researchers are beginning to explore the possible connection between meningioma risk and
the use of oral contraceptives and hormone-replacement therapy procedures.

Symptoms
Because meningiomas commonly are slow-growing tumors, they often do not cause noticeable
symptoms until they are quite large. Some meningiomas may remain asymptomatic for a
patient's lifetime or be detected unexpectedly when a patient has a brain scan for unrelated
symptoms. Presenting signs and symptoms depend on the size and location of the tumor.
Symptoms of meningiomas may include any of the following:

 Headaches
 Seizures
 Change in personality or behavior
 Progressive focal neurologic deficit
 Confusion
 Drowsiness
 Hearing loss or ringing in the ears
 Muscle weakness
 Nausea or vomiting
 Visual disorders

Symptoms can be related more specifically to the location of the meningioma. Examples include
the following:

 Falx and Parasagittal: Impaired levels of brain functioning such as reasoning and memory. If
located in the middle section, it would likely cause leg weakness/numbness or seizures.
 Convexity: May cause seizures, headaches and neurological deficits.
 Sphenoid: Vision problems, loss of sensation in the face or facial numbness and seizures
 Olfactory Groove: Loss of smell due to compression of the nerves that run between the brain
and the nose. If the tumor grows large enough, vision problems may occur due to compression
of the optic nerve.
 Suprasellar: Vision problems due to compression of the optic nerves/chiasm.
 Posterior Fossa: Facial symptoms or loss of hearing due to compression of cranial nerves,
unsteady gait and problems with coordination.
 Intraventricular: May block the flow of cerebrospinal fluid, resulting in (obstructive
hydrocephalus), potentially leading to headaches, lightheadedness and changes in mental
function.
 Intraorbital: Buildup of pressure in the eyes, leading to a bulging appearance and potential loss
of vision.
 Spinal: Back pain or pain in the limbs caused by compression of the nerves which run into the
spinal cord.
 


Diagnosis
It can be difficult to diagnose meningiomas for several reasons. Because the majority of
meningiomas are slow-growing tumors and primarily affect adults, symptoms may be so subtle
that the patient and/or doctor may attribute them to the normal signs of aging. Adding to the
confusion is that some of the symptoms associated with meningiomas can also be due to other
medical conditions. Misdiagnosis is not uncommon and, in fact, may take several years to
diagnosis correctly.

When a patient presents slowly increasing signs of mental dysfunction, new seizures or
persistent headaches or if there is evidence of pressure inside the skull (e.g. vomiting, swelling
of the optic nerve head in the back of the eye), the first step should be a thorough neurological
evaluation, followed by radiological studies, if needed.

Sophisticated imaging techniques can help diagnose meningiomas. Diagnostic tools

include computed tomography (CT or CAT scan) and magnetic resonance imaging (MRI).
Intraoperative MRI also is used during surgery to guide tissue biopsies and tumor
removal. Magnetic resonance spectroscopy (MRS) is used to examine the tumor's chemical
profile and determine the nature of the lesions seen on the MRI.

Sometimes, the only way to make a definitive diagnosis of the meningioma is through a biopsy.
The neurosurgeon performs the biopsy, and the pathologist makes the final diagnosis,
determining whether the tumor appears benign or malignant, and grading it accordingly.

Treatment Options
Surgery
Meningiomas primarily are benign tumors, frequently with defined borders and often enabling
complete surgical removal, which offers the best chance for a cure. The neurosurgeon opens
the skull through a craniotomy to enable full access to the meningioma. The goal of surgery is
to remove the meningioma completely, including the fibers that attach it to the coverings of
the brain and bone. However, complete removal can carry potential risks that may be
significant, especially when the tumor has invaded brain tissue or surrounding veins.

Although the goal of surgery is to remove the tumor, the first priority is to preserve or improve
the patient's neurological functions. With patients for whom total removal of the tumor carries
significant risk of morbidity (any side effect that can cause decreased quality of life), it may be
better to leave some of the tumor in place and observe future growth with regular imaging
studies. In such cases, the patient will be observed over a period of time with regular
examinations and MRIs, while for other patients, radiation therapy may be deemed the best
approach. It is common for patients to undergo preoperative embolization of the tumor to
ensure safety during the surgical procedure. The embolization procedure is similar to a cerebral
angiogram except that the surgeon fills the blood vessels in the tumor with glue to stop blood
supply to the tumor.

Today, surgeons are able to offer safe and effective treatments for tumors in locations such as
the skull base that were historically considered inaccessible. Additionally, improved imaging has
 allowed for the identification of miniscule areas of residual or recurrent tumor. Lesions growing
along the skull base are not well served by the rudimentary Simpson grading system with
respect to their recurrence potential.

Simpson classification of extent of meningioma resection

Simpson
grade Definition

Macroscopically complete removal including excision of the dural

I attachment and of any abnormal bone.

Macroscopically complete removal with coagulation of the dural attachment

II but without removal of underlying bone.

Macroscopically complete removal of the intradural tumor, without

III resection of the dural attachment or underlying bone.

IV Subtotal resection.

V Simple decompression, with or without biopsy.

Observation
Observation over a period of time may be the appropriate course of action in patients who
meet the following criteria:

 Patients with few symptoms and little or no swelling in the adjacent brain areas
 Patients with mild or minimal symptoms who have a long history of tumors without much
negative effect on their quality of life
 Older patients with very slow-progressing symptoms
 Patients for whom treatment carries a significant risk
 Patients who choose not to have surgery after being offered alternate treatment options

Radiation Therapy
Radiation therapy uses high-energy X-rays to kill cancer cells and abnormal brain cells, and to
shrink tumors. Radiation therapy may be an option if the tumor cannot be treated effectively
through surgery.

 Standard External Beam Radiotherapy uses a variety of radiation beams to create a conformal
coverage of the tumor while limiting the dose to surrounding normal structures. The risk of
 long-term radiation injury with modern delivery methods is very low. Newer techniques of
delivery aside from 3-dimensional conformal radiotherapy (3DCRT) include intensity-
modulated radiotherapy (IMRT).

 Proton Beam Treatment employs a specific type of radiation in which protons, a form of
radioactivity, are directed specifically to the tumor. The advantage is that less tissue
surrounding the tumor incurs damage.

 Stereotactic Radiosurgery (such as Gamma Knife, Novalis and Cyberknife) is a technique that
focuses the radiation with many different beams on the target tissue. This treatment tends to
incur less damage to tissues adjacent to the tumor. Currently, there is no data to suggest one
delivery system is superior to another in terms of clinical outcome. Each has its advantages and
disadvantages.

Chemotherapy
Chemotherapy is rarely used to treat meningioma, except in atypical or malignant subtypes that
cannot be adequately treated with surgery and/or radiation therapy.
Outcome
In adults, the patient's age at the time of diagnosis is one of the most powerful predictors of
outcome. In general, the younger the adult, the better his or her prognosis tends to be.

There generally is a better outcome if the entire tumor is surgically removed. However, this is
not always possible due to the location of the tumor.

Reference –
Schwartz's Principles of Surgery,
10th Edition
Neurosurgery
Mark S. Green berg, MD
NCCN guideline for meningioma.
https://www.aans.org/Patients/Neurosurgical-Conditions-and-
Treatments/Meningiomashttps://academic.oup.com/nop/article/3/2/120/1752207