(group i – without cavernous sinus invo lvement & group ii –with cavernous sinus...

A COMPARATIVE ANALYS

THE CLINICO-RADIOLOGICAL FEATURE

OUTCOME AND RECURRENCE

SUBGROUPS OF MEDIAL

(GROUP I – WITHOUT

GROUP II –WITH CAVERNOUS SINUS

Thesis submitted in partial fulfilment of the rules and regulations

for MCh (Neurosurgery) Degree of Sree Chitra

Tirunal Institute for Medical Sciences and Technology

Dr.

DEPARTMENT OF NEUROS

SREE CHITRA TIRUNAL

SCIENCES & TECHNOLOG

THIRUVANANTHAPURAM

A COMPARATIVE ANALYSIS OF

RADIOLOGICAL FEATURES, SURGICAL

COME AND RECURRENCE RATE OF TWO DIFFEREN

MEDIAL SPHENOID WING MENINGIOMAS

WITHOUT CAVERNOUS SINUS INVOLVEMENT &

WITH CAVERNOUS SINUS INVOLVEMENT)


for MCh (Neurosurgery) Degree of Sree Chitra


By

Dr. Dipendra Kumar Pradhan

October 2013

DEPARTMENT OF NEUROSURGERY

SREE CHITRA TIRUNAL INSTITUTE FOR MEDICA

SCIENCES & TECHNOLOGY

THIRUVANANTHAPURAM, KERELA – 695011

S, SURGICAL

RATE OF TWO DIFFERENT

IOMAS-

LVEMENT &



INSTITUTE FOR MEDICAL

“A comparative analysis of the

surgical outcome and recurrence rate of

subgroups of medial

without cavernous sinus involvement &

Group II –with cavernous sinus involvement

Submitted by

Programme :

Month & year of submission :

A comparative analysis of the clinico-radiological features,

ome and recurrence rate of two different

subgroups of medial sphenoid wing meningiomas (Group I

cavernous sinus involvement &

with cavernous sinus involvement).”

Submitted by : Dr. Dipendra Kumar Pradhan

Programme : MCh Neurosurgery

ubmission : October, 2013

radiological features,

two different

Group I –

Dipendra Kumar Pradhan

CERTIFICATE

This is to certify that the thesis entitled “A comparative analysis

of the clinico-radiological features, surgical outcome and recurrence

rate of two different subgroups of medial sphenoid wing meningiomas,

(Group I – without cavernous sinus involvement and Group II –with

cavernous sinus involvement) ” is a bonafide work of Dr. Dipendra

Kumar Pradhan and was conducted in the Department of

Neurosurgery, Sree Chitra Tirunal Institute for Medical Sciences &

Technology, Thiruvananthapuram (SCTIMST), under my guidance and

supervision.

Dr. Suresh Nair N.

Professor and Head

Department of Neurosurgery

SCTIMST, Thiruvananthapuram,

Kerala.

DECLARATION

This thesis titled “A comparative analysis of the clinico-

radiological features, surgical outcome and recurrence rate of two

different subgroups of medial sphenoid wing meningiomas (Group I –

without cavernous sinus involvement and Group II –with cavernous

sinus involvement) ”, is a consolidated report based on a bonafide study

of the period from January 2000 to December 2011, done by me under

the Department of Neurosurgery, Sree Chitra Tirunal Institute for

Medical Sciences & Technology, Thiruvananthapuram.

This thesis is submitted to SCTIMST in partial fulfillment of rules

and regulations of MCh Neurosurgery examination.

Dr. Dipendra Kumar Pradhan

Department of Neurosurgery,

SCTIMST, Thiruvananthapuram,

Kerala.

ACKNOWLEDGEMENT

I express my earnest gratitude to my esteemed teacher, Dr. Suresh Nair,

Professor and Head of the Department of Neurosurgery, whose guidance has

been invaluable and I am extremely grateful and indebted for his contributions

and suggestions during the entire work. To me he remains a mentor and a

source of inspiration throughout.

I owe a deep sense of gratitude to Dr. Girish Menon, Professor,

Department of Neurosurgery, SCTIMST, for his invaluable advice,

encouragement and guidance, without which this work would not have been

possible.

I express my gratitude to Dr. Mathew Abraham, Associate professor,

Department of Neurosurgery, SCTIMST, whose ever-available help and

guidance during the course of the study were invaluable.

I am deeply indebted to Dr. Easwer H. V, Dr. Krishna kumar. K, Dr.

Gopalakrishnan C.V., Dr. George Vilanilam, Dr. Jayanand Sudhir B, my

seniors and colleagues, and I thank them for their constant encouragement and

support.

I am thankful to Mr. Thampi N.G., Senior Medical records officer and Head,

Department of Medical Records, for his support in retrieving old medical

records during the entire study.

It is also my bounden duty to record my debt to the scholars and

authors whose works I have consulted for necessary materials in preparing

this dissertation.

Last but not the least, I owe a deep sense of gratitude to all my patients

without whom this work would not have been possible.

INDEX

Page No.

INTRODUCTION 1 - 3

REVIEW OF LITERATURE 4 - 34

AIM OF THE STUDY 35

MATERIALS AND METHODS 36 - 39

RESULTS 40 - 59

DISCUSSION 60 - 72

CONCLUSION 73

REFERENCES 74 - 88

PROFORMA

ABBREVIATIONS

ANNEXURE 1- Master chart for Group I & II

Introduction

1

INTRODUCTION

Meningiomas constitute approximately 13% to 19% of all primary

intracranial tumours and are the most common tumours of the sphenoid wing

in the anterior skull base, accounting for approximately 20% of supratentorial

meningiomas(1,2).

Cushing and Eisenhardt in 1938,(3) were the first to describe sphenoid

wing meningiomas in detail, distinguishing between globoid tumours with a

nodular shape and en plaque tumours. The globoid tumours were categorized

into 3 groups: 1) medial 2) middle and 3) lateral as per the anatomical

orientation of the lesser sphenoid wing —a medial third, representing the

medial posterior-to-anterior projecting segment most adjacent to the anterior

clinoid process; a middle third is the medial to lateral segment and the lateral

third is the anterior to posterior segment, joining with the temporal squamosa.

Meningiomas arising in the medial third of the sphenoid wing present

more challenges for neurosurgeons, given its proximity to the optic nerve, the

cranial nerves entering the superior orbital fissure and cavernous sinus and its

relation to internal carotid artery and its branches.

The middle and lateral third sphenoid wing meningiomas, as per the

present day concept, do not have distinct radiographic, microsurgical

characteristics or surgical outcome to warrant a separate grouping and are

Introduction

2

therefore clubbed into single entity, Stephen M. Russell et al(4). Their clinical

presentation and outcome of treatment is different from the medial group.

Till date, there are few studies analyzing and comparing the clinico-

radiological features, surgical outcomes and recurrences in patients

undergoing surgery for medial sphenoid wing meningiomas (SWM). This is

understandably so, due to rarity of this tumour location and also lack of

precise definition of this group of tumours. After Cushing and Eisenhardt in

1938,(3) Al-mefty(5) attempted to subclassify medial (clinoidal) sphenoid wing

meningiomas into three groups- Group I arising from dura proximal to

arachnoid ensheathment of supraclinoid ICA, Group II arising distal to

arachnoid ensheathment of ICA and Group III arising from optic foramen dura.

Group I and Group II had surgical relevance, as tumours in Group I had poor

arachnoid plane of dissection with the ICA, and therefore had increasing risk

of complications. Though, this concept has stood the test of time and being

followed by many, this theory is presently being challenged and refuted by

some comtemporary researchers(4,6,7,8). They have proposed that chronicity of

tumour compression, intrinsic tumour characteristics and invasiveness and

repeated surgery are the main determinants for poor dissection plane from

ICA.

Other important determinant for higher morbidity, mortality, and

recurrence rates observed in these medial group tumours compared with

meningiomas in other locations of sphenoid wing is the infiltration of

cavernous sinus which can be evaluated in pre operative imaging and also

Introduction

3

during surgery. Despite an improved orientation by understanding the

microsurgical anatomy and by advances in standard operative technique, the

surgical resection of cavernous sinus meningiomas remains a significant

challenge and is associated with high surgical morbidity (9,10,11,12,13,14,15). Unlike

in the past with aggressive approach to cavernous sinus

meningiomas (14,16,17,18,19), many authors have now confirmed the beneficial

outcome with subtotal excision and adjuvant radiotherapy (4,6,8,20).

We have also observed that, in this category of medial sphenoid wing

meningiomas, cavernous sinus infiltration is important determinant of surgical

morbidity like cranial nerve dysfunction involving the extraocular movements,

infarcts, poorer visual outcome and gross tumour residue and recurrence.

Recently, two authors viz. Makoto Nakamura et al.(6) in 2006 and Stephen M.

Russell et al.(4) have contributed to highlight the differences of medial SWM

between those with and without cavernous sinus infiltration.

Here, we also attempt to present our analysis of 72 cases of medial

SWM operated in our institute, in the period January 2000 to December 2011,

in the backdrop of cavernous sinus infiltration; with 43 cases in Group I

(without cavernous sinus infiltration) and 29 patients in Group II (with

cavernous sinus infiltration) .

Review of Literature

4

REVIEW OF LITERATURE

Historical Background

The first report detailing a successful craniotomy for the removal of an

intracranial meningioma appeared in The Lancet in 1881. In this article, Sir

William McEwen,(21) a Glasgow surgeon, reported on the operation he

performed on July 27, 1879, on a 14-year-old girl experiencing swelling at the

upper and inner portion of the left orbital cavity. Francesco Durante is known

for the successful removal of a left olfactory groove meningioma, performed

on June 1, 1884 (22,23). The neoplasms currently referred to as meningiomas

were referred to with a wide range of names in older medical literature,

depending on the source. Various descriptors included ‘fungoid tumours,

fungus of the dura mater, epithelioma, psammoma, dural sarcoma, dural

endothelioma, fibrosarcoma, angio endothelioma, arachnoidal fibroboastoma,

endotheliosis of the meninges, meningeal fibroblastoma , meningoblastoma ,

mestothelioma of the meninges and sarcoma of the dura’.(24)

Harvey Cushing is pre-eminent in the history of meningioma surgery.

Cushing proposed the term meningothelioma in an effort to describe these

tumours according to the tissue involved. Later, Cushing opted for the term

meningioma. In 1922, he reported on 85 cases of meningioma(25). Then, in

1938, Cushing and Eisenhardt published Meningiomas : Their Classification,

Regional Behaviour, Life History, and Surgical End Results, in which they

reported in detail the cases of 313 patients encountered between 1903 and


5

1932 (3). In 1922 Cushing wrote: “There is today nothing in the whole realm of

surgery more gratifying than the successful removal of a meningioma with

subsequent perfect functional recovery.” (25)

Epidemiology

Incidence

Meningiomas constitute approximately 13%–19% of all primary

intracranial tumours(2) and accounting for approximately 20% of supratentorial

meningiomas(1,2,26). The distribution of intracranial meningioma’s is

approximately as follows: convexity (35%), parasagittal (20%), sphenoid ridge

(20%), intraventricular (5%), tuberculum sellae (3%), infratentorial (13%),

and others (4%)(1,2). The incidence of clinically significant meningiomas is

approximately 2.3/ 100,000 population, and about 5.5/100,000 population

when autopsy data are included(26). Age-specific incidence rates are given in

the graph below, revealing an increasing risk with age (27,28). The male:female

ratio ranges from 1:1.4 to 1:2.1, but it is widely accepted to be approximately

1:2 (1, 2).

0

5

10

15

20

age specific incidence of meningiomas

per 100,000 population

age specific incidence of

meningiomas per 100,000

population


6

Sphenoid wing Meningioma

Anatomy of Sphenoid Bone (Os sphenoidale)

Ossification : Until the seventh or eighth month of fetal life the body of

the sphenoid consists of two parts, viz. Presphenoid in front of the

tuberculum sellae, with which the small wings are continuous and

postsphenoid, comprising the sella turcica and dorsum sellae, which are

associated with great wings, and pterygoid processes. The greater part of the

bone is ossified in cartilage. There are fourteen centers in all, six for the

presphenoid and eight for the postsphenoid.

The sphenoid bone (Fig. no. 1) is an unpaired bone situated in front of

the temporal bone and basilar part of the occipital bone. Its shape somewhat

resembles that of a butterfly or bat with its wings extended. It is divided into

the following parts:

• a median portion, known as the body of sphenoid bone, containing

the sella turcica which houses the pituitary gland

• two greater wings and two lesser wings

• Pterygoid processes of the sphenoides which project from it posteriorly

• Two sphenoidal conchae are situated at the anterior and posterior part of

the body.


7

Figure no. 1- A sphenoid bone , superior view.

Lesser wing of sphenoid

The main features of the lesser wing are the optic canal, the anterior

clinoid process, and the superior orbital fissure.

Surfaces

Superior surface: is flat, and supports part of the frontal lobe of the brain.

Inferior surface: forms the back part of the roof of the orbit, and the upper

boundary of the superior orbital fissure.

Borders

The anterior border is serrated for articulation with the frontal bone.

The posterior border, smooth and rounded, is received into the lateral fissure

of the brain.


8

Medial end of this border forms the anterior clinoid process, which

gives attachment to the tentorium cerebelli. It is sometimes joined to the

middle clinoid process by a spicule of bone, and when this occurs the

termination of the groove for the internal carotid artery is converted into a

foramen (carotico-clinoid).

The lesser wing is connected to the body by two roots. Between the

two roots is the optic foramen, for the transmission of the optic

nerve and ophthalmic artery.

Greater sphenoid wing

Cerebral surface

It forms part of the middle cranial fossa, It has a number of foramina in it:

• Foramen rotundum: transmits the maxillary nerve.

• Foramen ovale : transmits the mandibular nerve, the accessory meningeal

artery, and sometimes the lesser petrosal nerve.

• Sphenoidal emissary foramen: transmits a small vein from the cavernous

sinus.

• Foramen spinosum: transmits the middle meningeal vessels and

a recurrent branch from the mandibular nerve.

Lateral surface

The lateral surface is convex, and divided by a transverse ridge,

the infratemporal crest, into two portions:

• Superior temporal surface, forms a part of the temporal fossa, and gives

attachment to the temporalis.


9

• Inferior temporal surface, enters into the formation of the infratemporal

fossa, and, together with the infratemporal crest, serves as an attachment

to the lateral pterygoid muscle

Orbital surface

The orbital surface of the great wing is smooth and quadrilateral in shape,

forms the posterior part of the lateral wall of the orbit.

Margin

• Its medial half forms the anterior boundary of the foramen lacerum, and

presents the posterior aperture of the pterygoid canal for the passage of

the corresponding nerve and artery.

• Its lateral half articulates, by means of a synchondrosis, with the petrous

portion of the temporal.

Cavernous sinus

The cavernous sinus (Fig.no. 2) is one of the dural venous sinuses, located on either

side of the pituitary fossa and body of the sphenoid bone between the endosteal and

visceral layers of the dura.

Figure no.2- cavernous sinus anatomy.


10

Vascular connections

It receives blood from:

• Inferior ophthalmic vein

• Superficial middle cerebral vein

• Inferior cerebral veins

• Sphenoparietal sinus and occasionally

o central retinal vein

o frontal tributary of the middle meningeal vein

Drainage of the cavernous sinus is via:

• Superior petrosal sinus to the transverse sinus

• Inferior petrosal sinus directly to the jugular bulb

• Venous plexus on the internal carotid artery to the pterygoid plexus

• Emissary veins passing through sphenoidal foramen, foramen ovale,

foramen lacerum

• Facial vein through superior ophthalmic vein and angular vein or

pterygoid venous plexus or deep facial vein

• Superior sagittal sinus through middle cerebral vein and superior

anastomotic vein.

Depending on relative pressures, the superior ophthalmic veins either

drain into or drain the cavernous sinus. Additionally the cavernous sinuses

connect to each other via the intercavernous sinuses.


11

Nerves

The cavernous sinus transmits multiple cranial nerves to the superior

orbital fissure, these are:

• In the lateral wall from superior to inferior:

o Oculomotor nerve (CN III)

o Trochlear nerve (CN IV)

o Trigeminal nerve (CN V) ophthalmic and maxillary divisions.

• Traversing the sinus lateral to the ICA

o Abducens nerve (CN VI)

Artery

The internal carotid artery enters the posterior inferior aspect of the

sinus, and bends upon itself as the carotid siphon (cavernous segment - C4).

Two branches arise from this segment: meningohypophyseal

trunk and inferolateral trunk. The artery is surrounded by a plexus of

sympathetic nerves from the superior cervical ganglion.

Classifications of sphenoid wing meningioma

Cushing and Eisenhardt

In 1938, Cushing and Eisenhardt(3) reported the first surgical

experience with meningiomas of the sphenoid ridge. They divided sphenoid

ridge meningiomas into four categories:


12

1) Tumours of the deep or clinoidal third, 2) middle-ridge tumours, 3) en

plaque pterional tumours, and 4) global pterional tumours.

In this classification scheme the lesser sphenoid wing is divided into thirds,

with changes in the orientation of the wing roughly demarcating the

boundaries of these segments—

1) Medial third, which represents the medial posterior-to-anterior projecting

segment most adjacent to the anterior clinoid process

2) Middle third, which runs medial to lateral

3) Lateral third, which runs anterior to posterior, eventually joining with the

temporal squamosa.

Al-Mefty’s classification of clinoidal meningioma

Anatomical basis for classification

Al-Mefty(5) classified clinoidal meningiomas into three categories based

on the anatomic site of origin and degree of surgical difficulty. As the carotid

artery emerges from the cavernous sinus inferomedial to the anterior clinoid, it

enters the subdural space to be vested in the carotid cistern. The arachnoid

does not follow the internal carotid artery into the cavernous sinus space, nor

is it attached to the anterior clinoid process. A 1- mm or 2-mm segment of

naked internal carotid artery lies between the investment of the carotid cistern

and the dura of the cavernous sinus(29). This segment is not to be confused

with the extradural segment which lies between the two rings anchoring the

carotid artery as it exits the cavernous sinus space.(30)


13

Group I

The meningioma's origin is proximal to the end of the carotid cistern,

inferior and medial to anterior clinoid process, the tumor enwraps the carotid

artery, directly adhering to the adventitia in the absence of an intervening

arachnoid membrane. This anatomic arrangement accounts for the surgeon’s

inability to dissect the tumour from the ICA and MCA branches. (Fig. no. 3)

Fig. no. 3- Artist's drawing of a Group I meningioma. The tumor encases the carotid artery

and its branches, with direct attachment to the adventitia. The optic nerve maintains an

arachnoid plane from the chiasmatic cistern.

Group II

Tumours of Group II originate from the superior and/ or lateral aspect

of the anterior clinoid above the segment of the carotid invested in the carotid

cistern. Thus, as the tumour grows, an arachnoid membrane of the carotid

cistern and distally of the sylvian cistern separates the tumour from the arterial

adventitia. (Fig. no.4)


14

Fig. no 4 -Group II meningioma: An arachnoid membrane of the carotid cistern separates the

tumor from the adventitia, rendering dissection possible. The optic nerve maintains an

arachnoid membrane from the chiasmatic cistern.

Group III

Tumours in Group III originate at the optic foramen, extending into the

optic canal and the tip of the anterior clinoid process. The arachnoid

membrane investing the carotid artery is present. Because this tumor arises

proximal to the chiasmatic cistern, there may be no arachnoid investment

between the optic nerve and the tumour. (Fig. no. 5)

Figure no. 5- Group III meningioma: Artist's drawing showing the tumor originating in the

optic foramen. The tumor is small, separated from the carotid by the carotid cistern, but it

extends into the optic canal.


15

Abdel– Aziz et al.(8) proposed classification of medial or clinoidal

meningiomas with respect to cavernous sinus involvement into 3 subtypes

(Fig. no. 6):

a) Clinoido-cavernous

b) Spheno-cavernous

c) Sphenoclinoido-cavernous meningiomas

Figure no.6 - Inner sphenoid wing and clinoidal meningiomas classified according to their

extension into the cavernous sinus. A, clinoido-cavernous, B, spheno-cavernous, and C,

spheno-clinoido-cavernous.(8)


16

Makoto Nakamura et al. (6) classified sphenoid wing meningioma:

(Fig. no. 7)

I – Medial SWM without CS involvement

II – Medial SWM with CS involvement

III – Middle SWM

IV – Lateral SWM

Figure no. 7

Arterial supply to sphenoid wing meningioma

Meningiomas of the medial sphenoid ridge are usually fed by direct

(sometimes intracavernous) branches of the internal carotid, or the ascending

pharyngeal artery, and sometimes a recurrent branch of the ophthalmic artery

passing through the superior orbital fissure.


17

Lateral tumours derive much of their blood supply from the superficial

temporal and middle meningeal arteries. Additional feeding vessels may

include the anterior meningeal and other branches of the ethmoidal arteries.

Clinical Presentation of Sphenoid wing meningioma

Clinical signs and symptoms reflect tumor location and growth pattern.

Tumours of the lateral sphenoid wing will often become relatively large before

the development of a focal deficit such as hemiparesis or aphasia. Tumours of

the medial sphenoid ridge commonly cause early and more specific

symptoms due to the proximity of the optic apparatus and cavernous sinus.

Patients with sphenoorbital meningiomas typically present with

exophthalmos, deterioration of visual acuity and field cuts, and diplopia.

Tumour growth in the cavernous sinus or superior orbital fissure may lead to

ocular palsies. Intraorbital tumor growth characteristically causes diplopia

due to restriction of ocular movements rather than oculomotor nerve paresis.

Involvement of the cavernous sinus will also sometimes result in sensory loss

in the distribution of the ophthalmic and eventually other division of the

trigeminal nerve.

Extracranial tumor growth and hyperostosis can cause cosmetic

disturbances. Seizures are relatively frequent. Uncinate fits and gustatory and

olfactory hallucinations point to the temporal lobe as their origin, as well as

complex-partial and generalized tonic-clonic seizures. Finally, the number of

patients with more or less asymptomatic meningiomas diagnosed during the

course of a workup (for headache or vertigo) is increasing.


18

Risk factors

Ionizing radiation

At present, the primary environmental risk factor identified for

meningioma is exposure to ionizing radiation (IR) with risks from six fold to

tenfold. (33, 34,35,36) In one of the most well-known studies of ionizing radiation

and meningioma risk, children who were given radiation therapy for scalp

ringworm in Israel between 1948 and 1960 (the Tinea Capitis Cohort), were

observed to have a relative risk of almost 10 for meningioma.(37) Radiation

therapy for intra-cranial tumours has also been linked to meningioma risk.(35)

Hormones

An association between hormones and meningioma risk has been

suggested by a number of findings(38,39,40,41,42) including the increased

incidence of the disease in women versus men (2:1), the presence of

estrogen, progesterone, and androgen receptors on some meningiomas, an

association between breast cancer and meningiomas, and indications that

meningiomas change in size during the luteal phase of the menstrual cycle

and pregnancy and the regression of multiple meningiomas in a patient

following cessation of estrogen agonist therapy.(41, 42)


19

Hormone Receptors

Estrogen

The prevalence and function of estrogen receptors in meningiomas

remains a controversial topic. Data from ‘Brigham and Women’s Hospital’

indicates that differences exist in the prevalence of estrogen receptor isoforms

alpha and beta, with 44% of meningiomas expressing ER-alpha mRNA and

68% expressing ER-beta mRNA.(43) These receptors have been more

extensively characterized for breast cancer but no such data exist for

meningioma response.(44)

Progesterone

The majority of meningiomas (40–100%) possess progesterone

receptors (PR). Hsu et al(40) observed that benign meningiomas were more

likely than malignant to be PR positive (96% versus 40%), with PR status

being inversely related to mitotic index and grade and therefore associated

with better prognosis.

Androgen

Approximately 50% of meningiomas have been noted to express

androgen receptors, with tumours from women exhibiting a higher rate than

tumours from men. Data suggest that androgen expression positivity rates

vary positively with stage(45). As for estrogen receptors and PR, little is known

regarding the usefulness of these receptors relative to clinical prediction and

treatment.


20

Other receptors

Preferential immunoreactive staining for the sst2A subtype

somatostatin receptor has been shown in meningiomas. (46) The dopamine D1

(but not D2) receptor has also been demonstrated in meningiomas.

Meningiomas are also positive for prostaglandins, most notably prostaglandin

E2. (47) Several growth factors have been shown to stimulate meningiomas,

including epidermal growth factor, fibroblast growth factor, and PDGF.

Breast cancer and meningioma

Schoenberg and associates(48), were the first to suggest that the

concomitant occurrence of breast cancer and meningioma was higher than

could be expected from pure coincidence. A number of explanations have

been proposed for this association including common risk factors (age at

menopause or use of OCP) or shared genetic predisposition.

Head trauma

Since the time of Harvey Cushing, head trauma has been suggested

as a risk factor for meningioma, although the results across studies are not

consistent. Although several small case control studies from the early 1980s

report an increased risk of meningioma associated with head trauma for both

males (OR 1.9, P < 0.01) and females (OR 2.0, P <0.01), other studies report

no such association.(49,50)


21

Cell phone use

At present, little evidence exists for an association between the two.

Newly reported data from the large Interphone study replicated earlier

negative findings even for the highest exposed groups (>10 years of heavy

exposure).[51] Of note, Swedish investigators of the Interphone study recently

reported a significant association between one type of benign brain tumor,

acoustic neuroma, and long-term cell phone use (OR 3.9; 95% CI, 1.6- 9.5)

[52].

Occupation/diet/allergy

An international case/control study found no association between diet

and meningioma.(53) Although a number of studies which examined the

relationship between glial brain tumours and allergic disease such as asthma

and eczema have found evidence for an association, little evidence has been

found for such an association for meningioma. (54,55) A study of innate immune

genes did not find strong evidence of risk imparted by variants in such

genes. (56)

Viruses

In work reported by Inoue (57), Inoue-Melnick virus (IMV), a DNA virus

linked to subacute myelo-opticoneuropathy, was isolated from six of seven

human meningioma-derived cell cultures but was not isolated from six other

brain tumor cell cultures. Of 26 patients with meningioma, 22 (84.6%) were

positive for the IMV antibody. Rachlin and Rosenblum stated that “although


22

there is strong biochemical evidence associating DNA tumor viruses with

human meningiomas, the role of the virus in the development of the tumor

remains undefined.”(58)

Venous thrombosis

Sawaya and Ramo(59) demonstrated a higher rate of venous

thrombosis of the legs in patients with meningiomas than in those with

glioblastomas or brain metastasis. Using 125 I-fibrinogen leg scans, they

found that the incidence of thrombosis was 72% for meningioma patients,

60% for glioblastoma patients, and 20% for patients with brain metastasis.

Family history of meningioma

Malmer et al(60) and Hemminki et al(61) using data from the Swedish

and Norwegian Registry Databases, reveal an increased risk with increasing

numbers of affected first degree relatives with meningioma, indicating a

familial risk for meningioma tumours.

Molecular Genetics

Loss of heterozygosity at chromosome 22 with inactivation of the NF-2

gene, is the earliest and best characterized genetic change association with

meningiomas, (62) and is affected in the majority of NF-2–related tumours and

more than 50% of sporadic meningiomas. (63,64) DAL-1 on chromosome 18p,

have been found in the majority of atypical and malignant meningioma

specimens.(65) Deletions in chromosomes 1p ,10q and 14q appear to correlate

in several studies with a higher histologic grade and/or rate of recurrence. (66)


23

Progression to atypical meningioma is associated with telomerase

activation,(67) and loss of progesterone receptor expression,(68) MIB-1 labeling

indices, VEGFR expression, quantitative staining of proliferating cell nuclear

antigen and expression of Janus tyrosine kinase and signal transducer and

activator of transcription proteins. (69,70,71)

Histopathology

The 2007 WHO classification of tumours of the CNS lists meningiomas

under the heading “Tumours of the meninges” and the subheading “Tumours

of meningothelial cells.” WHO recognizes three grades based on pathologic

criteria and the risk of recurrence and aggressive growth as follows: (72)

WHO Grade I WHO Grade II

Meningothelial meningioma Atypical meningioma

Fibrous (fibroblastic) meningioma Clear cell meningioma

Transitional (mixed) meningioma Chordoid meningioma

Psammomatous meningioma

Metaplastic meningioma WHO Grade III

Angiomatous meningioma Rhabdoid meningioma

Microcystic meningioma Papillary meningioma

Secretory meningioma Anaplastic (malignant)

Lymphoplasmacyte-rich meningioma


24

Common histological variants are:

Meningothelial meningioma (Fig.no. 8)

Distinctive features of meningothelial meningiomas include intranuclear

cytoplasmic pseudo inclusions, in which an invaginated cytoplasmic remnant

occupies the interior of the nucleus and displaces the nuclear chromatin.

Another useful feature is the presence of so-called Orphan Annie's eye nucleii

with central clearing and peripheral margination of the chromatin.

Figure no. 8- A. Squash preparation of a meningothelial meningioma showing the typical

whorl formation. B. Meningothelial meningioma with typical intranuclear inclusions.

Fibrous (fibroblastic) meningioma

Uncommon in pure form, this meningioma variant consists of spindle

cells forming parallel, storiform and interlacing bundles in a collagen-rich

matrix. Whorl formation and psammoma bodies are infrequent.

Transitional (mixed) meningioma

Feature the coexistence of meningothelial and fibrous patterns as well

as transitions between these patterns.


25

Atypical meningioma

A meningioma with increased mitotic activity (4 or more mitoses per 10

high-power), or three or more of the following histologic features: increased

cellularity, small cells with a high nuclear: cytoplasmic ratio, prominent

nucleoli, uninterrupted patternless or sheet-like growth, and foci of

‘spontaneous’ or ‘geographic’ necrosis. Atypical meningiomas often have

moderately high MIB-1 labelling indices.

Immunohistochemistry

The test for epithelial membrane antigen (EMA) is positive in 80% of

meningiomas. The results of S-100 staining are quite variable. Meningiomas

also express markers for fibroblasts (vimentin). Syncytial and transitional

meningiomas express E-cadherin. Another use of immunohistochemistry lies

in differentiating atypical meningiomas from similar but pathologically distinct

tumours, such as secretory meningioma from metastatic carcinoma. (71)

Radiology

Plain radiographs: reveal three characteristic findings in meningioma

patients, hyperostosis, increased vascular markings, and calcification.

CT scan: On non–contrast-enhanced CT, meningiomas are typically

isodense to slightly hyperdense compared with contiguous brain parenchyma.

Calcification may be seen. Meningiomas usually enhance homogeneously

and intensely and is usually broadly based against a bony structure or dural


26

margin. A common bony manifestation is hyperostosis. The amount of edema

surrounding a meningioma is variable. The dura mater adjacent to the

attachment of a meningioma may enhance on CT or MRI after the

administration of a contrast agent, so-called dural tails. Histologically, in dural

tail, although only connective tissue and vascular tissue proliferation were

seen, in some cases meningioma cell nests were also identified. (73)

MRI: On T1-weighted MRI, 60% of meningiomas are isointense and 30% are

mildly hypointense compared with gray matter. On T2-weighted images, the

tumours are isointense (50%) or mildly to moderately hyperintense (40%).

Hyperintensity on T2-weighted images suggests higher water content,

denoting a meningothelial meningioma, a vascular meningioma, or an

aggressive meningioma. However, it is suggestive of an easily suckable tumor

during surgery. Meningiomas usually enhance intensely and uniformly after

the injection of gadolinium, with typical dural tail enhancement.

Angiography may be an adjunct in the preoperative assessment of some

meningiomas. It enables the surgeon to assess the vascularity and vascular

supply of the tumour, and the presence of tumour encroachment on vascular

structures. Angiography will also allow for a test occlusion of the carotid artery

if injury or sacrifice of this vessel is a possibility. Preoperative embolization is

used as an adjunct in some centers to reduce intraoperative blood loss, (74,75)

although in a comparative study no advantage of preoperative embolization

could be demonstrated. (74)


27

Scintigraphy: Somatostatin receptor scintigraphy using 111In octreotide is

an extremely sensitive test for meningiomas. It can be used preoperatively

when the diagnosis is not straightforward. In the postoperative period,

somatostatin receptor scintigraphy can be helpful in differentiating contrast

uptake from residual tumour and that from nonspecific. (76)

Natural History

The authors of several studies have described the natural history of

meningiomas, and they based their findings on samples ranging from 17 to 70

tumours. Because of small sample sizes and the variety of the methods used

to measure the tumor growth, information regarding the tumor growth rate and

prognostic factors were inconclusive. One study from Cleveland Clinic ,

Ohio,(72) included 273 conservatively managed meningiomas in 244 patients.

Intracranial meningioma growth was observed in 44.0% by the linear diameter

measurement and in 74.0% by the volumetry within 4 years.

The following factors were found to be significant based on at least 2

methods of study: young age (≤ 60 years), lack of calcification, hyperintensity

on T2-weighted MR imaging, large size (> 25-mm diameter), and edema.

Patients with these positive factors may need to be observed more closely. (77)


28

Treatment Options

Surgical Therapy and Recurrence

The only definitive cure for meningioma is complete surgical resection.

In 1957. Simpson(78) introduced a five-grade classification of the surgical

removal of meningiomas. (Table no. 1) In Simpson’s series of 265

meningiomas, 55 (21%) had recurrence. The rates of tumor recurrence

according to the extent of resection were: grade I, 9%; grade II, 19%; grade

III, 29%; grade IV, 44%. Other studies appearing subsequently, with at least

10 years’ follow-up, found similar recurrence rates. In one study, convexity

meningiomas undergone grade 0 resection showed no recurrence at mean

follow-up period 5 years and 8 months.(80)

In 1992, Kobayashi and associates(79) revised the Simpson grading

system from a microsurgical perspective by introducing a classification system

based on the extent of microscopic resection. (Table no. 2)

The anatomic location of a meningioma influences its rate of

recurrence. Highest recurrence rates (>20%) are with sphenoid wing

meningiomas, followed by those with parasagittal meningiomas (8% to 24%),

convexity and suprasellar meningiomas is 5% to 10% depending on the grade

of resection.(81)


29

Table no. 1- Simpson Grading System

Grade Description

I Macroscopically complete tumor removal with excision of the

tumor’s dural attachment and any abnormal bone

II Macroscopically complete tumor removal with coagulation of its

dural attachment

III Macroscopically complete removal of the intradural tumor without

resection or coagulation of its dural attachment or extradural

extensions

IV Subtotal removal of the tumor

V Simple decompresssion of the tumor

(Adapted from Simpson D. The recurrence of intracranial meningiomas

after surgical treatment. J Neurol Neurosurg Psychiatry. 1957;20:22). (78)

Table no. 2- Modified Shinshu Grade or Okudera- Kobayashi Grade

Grade Description

I Complete microscopic removal of tumor and dural attachment with

any abnormal bone

II Complete microscopic removal of tumor with diathermy coagulation

of its dural attachment

IIIA Complete microscopic removal of intradural and extradural tumor

without resection or coagulation of its dural attachment

IIIB Complete microscopic removal of intradural tumor without

resection or coagulation of its dural attachment or of any extradural

extensions

IVA Intentional subtotal removal to preserve cranial nerves or blood

vessels with complete

microscopic removal of dural attachment


30

IVB Partial removal, leaving tumor of <10% in volume

V Partial removal, leaving tumor of >10% in volume, or

decompression with or without biopsy.

Adapted from Kobayashi K, Okudera H, Tanaka Y. Surgical considerations on skull

base meningioma. Paper presented at the First International Skull Base Congress,

June 18, 1992, Hanover, Germany. (79)

Non surgical treatment

Nonsurgical therapies are used for recurrent or incompletely resected

meningiomas.

Radiation therapy/ Radiosurgery

Radiosurgery has proved to be an effective adjuvant therapy in

controlling growth of meningiomas and plays an important role in

meningiomas involving CS. Tumour growth control rate after Gamma knife of

CS meningiomas ranged from 91% to 96.5% at 5 years and 82% to 94% at 10

years(82,83,84,85,86,87). In terms of long-term control, however, the clinical

recurrence rate after 15 years with subtotal resection and radiation therapy is

75%, and the rate of complications is 56%.(87) Radiation induced complications

and the possibility of radiation-induced malignancy or tumor progression are

concerning issues. (88 -93) Guthrie and associates, (94) concluded that “while

surgical excision is the treatment of choice, radiation therapy should be

considered in following scenarios:


31

(1) After surgery for a malignant meningioma,

(2) Following incomplete resection of a meningioma for which the risk of

resection of an eventual recurrence is judged to be excessive,

(3) For patients with multiple recurrent tumours for whom the surgeon judges

repeat surgery to be too risky, and

(4) As a sole therapy of a progressively symptomatic patient with a

meningioma judged by the surgeon to be inoperable.

Hormonal Therapy

The presence of hormonal receptors in meningiomas has prompted

research into hormonal manipulation as treatment. The oral progesterone

agonist megestrol acetate (Megace) was used in a small trial of nine patients

with no observed response. (95)

The SWOG completed a study of mifepristone for unresectable

meningiomas (198 total patients of whom 160 were evaluated).(96) The results

did not support a role for Mifepristone compared with placebo (median PFS

was 10 months in Mifeprisrone arm and 12 months in the placebo arm).

In addition, SWOG reported a Phase II trial of 21 patients with

meningioma treated with oral tamoxifen, an estrogen receptor antagonist (97).

One patient achieved a partial response, two patients had a minor response,

and six patients had stable disease for longer than 6 months.


32

Biotherapy and Chemotherapy

Recombinant interferon-alpha has been found to inhibit the growth of

cultured human meningioma cell lines in vitro. (98,99) In the largest report, six

patients with recurrent unresectable and previously irradiated meningiomas

were treated. One patient had an objective response and four patients had

stable disease for longer than 6 months.

In a clinical trial with hydroxyurea by Schrell et al.(100) involving four

patients, another by Newton et al (101) involving 40 patients, and a third trial by

Mason et al (102) involving 20 patients suggested in vivo efficacy( > 80% with

stable disease for a median of 20 to 30 months).

A recent trial of chronic oral temozolomide for surgical and

radiotherapy refractory meningiomas failed to demonstrate activity in 16

patients (103) Trapidil, a drug with known antagonistic action against PDGF,

showed a dose-dependent inhibition of meningioma cell proliferation. (104)

In another small trial of 16 patients, those with recurrent meningiomas

shown to overexpress somatostatin receptors by octreotide scintigraphy were

treated with monthly long-acting somatostatin.(105) Thirty-one percent of

patients demonstrated a partial imaging-documented response, and 44%

achieved PFS at 6 months with minimal toxicity. Animal trials are being

conducted to assess the possible use of a growth hormone receptor

antagonist (pegvisomant) as a medical treatment for meningiomas.(106)


33

Recurrence

Besides surgical grade of resection, as mentioned above, other factors

determining recurrence are pathology, cellular and molecular criteria,

hormonal receptor status and radiological imaging. Benign meningiomas

have recurrence rates of about 7–25%, atypical meningiomas of 29–52% of

cases and anaplastic meningiomas at rates of 50–94%. (107)

Pathological features associated with a significantly higher rate of

recurrence are invasion of the dura or brain infiltration, papillary or

hemangiopericytic pattern and lack of progesterone receptors. Cellular criteria

include the presence of mitoses (>20/10 high power fields), increased

cellularity, nuclear polymorphism, focal necrosis, high levels of expression of

VEGF and high MIB-1 labeling index. (40,68,69,71,81) Moller and Braendstrup,

(108) however, found that proliferating cell nuclear antigen and Ki-67 are of

minor value as predictors of the recurrence of benign meningiomas.

Multivariate analysis in Nakasu and coworkers (109) study of 101 patients

revealed that only the shape of the tumor was significant; “mushrooming” and

lobulated meningiomas were more likely to recur than round ones.

Surgical Outcome

Complications after surgery are related to lack of proper understanding

of the anatomy of medial sphenoid wing and its relation to the arteries, optic

nerve and cranial nerves in cavernous sinus and superior orbital fissure. The


34

surgical morbidity/ mortality was higher in those with a radical and aggressive

resection, especially in cavernous sinus region (83,97,98). This has lead to

some authors in recent times (4,6,7,110,111,112) to follow a conservative strategy

with or without radiosurgery.

Summary of the outcome of surgery and the mortality rate of medial

sphenoid wing meningiomas in chronological order are given in table no.13

and discussed under relevant headings later on.

Aim of the Study

35

AIM OF THE STUDY

A comparative analysis of the clinico -radiological features, surgical

outcome and recurrence rate of two different subgroups of medial sphenoid

wing meningiomas (SWM), viz.

Group I – without cavernous sinus involvement and

Group II – with cavernous sinus involvement.

Materials and Methods

36

MATERIALS AND METHODS

A retrospective study was conducted from period of January 2000 to

December 2011 on sphenoid wing meningiomas operated in our Department

of Neurosurgery, Sree Chitra Tirunal Institute For Medical Science and

Technology, Trivandrum. Out of a total of 168 cases of sphenoid wing

meningiomas (SWM) operated, 72 cases were medial SWM (others included

17 cases of middle, 63 pterional, and 17 sphenoorbital meningiomas). We

further subclassified the 72 cases of medial SWM into two groups (Group I-

without cavernous sinus involvement and Group II – with cavernous sinus

involvement), from data obtained from pre operative radiological records and

operative findings.

Data collection

The list of patients having undergone surgery for SWM were obtained

from the operation theatre records, followed by study of individual files from

the medical records department. Clinical and radiological presentation, study

of operative notes for approaches and findings, and HPR were reviewed.

Follow up details were obtained by personally calling patients to our OPD and

assessing the present status, while few have been interviewed through

telephonic conversation.

Radiology

Preoperative evaluation of most of our patients included initial CT scan

with contrast and followed by MRI studies, T1 and T2-weighted sequences


37

with gadolinium contrast. Some patients operated on emergency basis or

during the first quarter of study period underwent only C T scan with contrast.

Digital Substraction Angiogram (DSA) of four cerebral vessels with cross

compression study were performed for most cases with encasement of ICA

(cavernous / supraclinoid). The purpose of doing DSA was to define the

arterial supply to the tumour bulk, nature of compression of ICA (narrowing,

obliteration, displacement) and adequacy of cross circulation to distal ICA

through alternate arterial territory. It also served to determine our

aggressiveness of tumour decompression around prominent vessels to avoid

inadvertent injury. Pre-operative embolization of feeders were not done in

any of our cases.

Surgery

Perioperative Management and recent surgical technique used:

Antiepileptic prophylaxis of oral Phenytoin sodium 100 mg thrice daily

was started at least 1 week prior to surgery, else, loading dose of parentral

Phenytoin sodium 17mg/kg was administered. Those with allergy to Phenytoin

were started on alternate AED as per discussion with our Epileptologist. Pre

operative antibiotics of Ceftriazone 1gm and Amikacin 500mg were given in 2

doses at 12 and 2 hours prior to surgery. Intraoperative anti oedema

measures (i/v Mannitol, 1gm/kg, and hyperventilation) were carried out prior to

dural opening to make the brain lax, lumbar drainage of CSF was not done in

any of our cases.


38

Position - The patient was placed supine and head end elevated to promote

venous return. The head was rotated 30 to 40 degrees to the opposite side

and extended slightly to allow the brain to fall away from the cranial base

minimizing retraction. The head was fixed in position using the Mayfield head

clamp.

Craniotomy- Majority of patient underwent standard frontotemporal

craniotomy, only three cases (1 in group I and 2 in group II) underwent FTOZ

during the mentioned period of study.

Extradural work- The steps included dissection of the pre temporal and

subfrontal dura away from the sphenoid wing. The dural fold at the level of the

meningio-orbital artery was cut to allow disconnection of the dura propria of

the temporal lobe from its attachment to the frontal dura. The dura propria of

temporal lobe was further mobilized by interdural dissection over the

cavernous sinus to complete the process of convexitization. This process of

exposing the anterior clinoid process itself lead to significant devascularization

of the tumor. Then, the anterior clinoidectomy was done with high speed

diamond drill and copious irrigation with saline. The optic canal was

decompressed by removing the optic strut and the optic roof as required. We

attempted to achieve maximum bony work extradurally in most of the cases.

Intradural exposure- The sylvian fissure was routinely opened from the level

of the limen insulae toward its proximal point to help visualize the MCA and

ICA. Once this was achieved, debulking of the tumor was started with

intermittent dissection of the tumor away from the adjacent brain and blood


39

vessels. The dura at the base of the skull and over the clinoid region was

totally removed. The dural defect was reconstructed with either fascia lata or

pericranium and was reinforced with fibrin glue. The clinoidal space was

obliterated with subcutaneous fat from thigh/abdomen.

Postoperative - All patients were cared for in a neuro ICU for 1 to 2 days

before returning to the ward. DVT prophylaxis was started with LMW heparin

from day 2, provided post operative CT scan showed satisfactory hemostasis,

for those with motor deficits, bedridden/immobile patient and obese females

beyond 3rd decade of life. In uneventful cases, patients were usually

discharged by 7 to 10 days. First follow up visit was at 6 weeks, then at

3months, 6 months and yearly thereafter.

Statistical Analysis

Data of both tumor groups were compared using the Chi Square test

with 1 degree of freedom (for comparison of percentages) and unpaired t test

for comparison of two mean values. A P value was calculated for each

comparison using two-tailed analysis with significance assumed at the 0.05

level.

Patient characteristics

Patients were divided into two groups

sinus involvement) and Group II (with cavernous sinus i

consisted of 43 patients and Group II of 29 patients

presentation in Group I was

38.4 years (range 28-51yr) with standard deviation of 8.9 and 8.3

respectively. Sex ratio was skewed towards females

Group I and 1.9:1 in Group

and 19/29 females in Group

Figure no.9

We also observed a

occurrence in both the groups

was the dominant hemisphere in


40

RESULTS

Patients were divided into two groups – Group I (without cavernous

sinus involvement) and Group II (with cavernous sinus involvement)

consisted of 43 patients and Group II of 29 patients. (Fig. no. 9) Mean age

I was 48.7 years (range 31–65yr) and Group II was

51yr) with standard deviation of 8.9 and 8.3

respectively. Sex ratio was skewed towards females, F: M ratio of 2.07: 1 in

Group I and 1.9:1 in Group II (or 29/43 females, 67.4%, affected in Group I

/29 females in Group II, 65.5%).

- Group I and Group II tumour distribution.

We also observed a predilection towards left side for tumour

groups (I & II, 58.1% and 55.2% respectively). L

misphere in all our patients. In Group I, 1 patient had


Group I (43 patients)

Group II (29 patients)

Results

cavernous

nvolvement). Group I

Mean age at

and Group II was

51yr) with standard deviation of 8.9 and 8.3,

M ratio of 2.07: 1 in

affected in Group I

for tumour

). Left side

1 patient had

Group I (43 patients)

Group II (29 patients)

Results

41

undergone initial surgery for same tumour at alternate centre and presented

to us with residue/recurrence, whereas, in Group II, there were 3 such

patients.

Clinical presentation

The most common presenting symptoms were headache (74.4% in

Group I and 89.7% in Group II, p =0.109), visual disturbances (58.1% in

Group I and 58.6% in Group II, p=0.968), seizures (16.3% in Group I and

20.7% in Group II, p= 0.633) and behavioural problems/ memory

disturbances. The symptoms presented to us at admission are tabulated in

Table no. 3. There was no preceding history of exposure to radiation or

trauma in any of the cases.

Group II patients were more likely to present with raised ICP

complications (9.3% in group I and 37.9% in group II, p = 0.003) and

dysphasia/apahasia (3 patients (10.3%) in group II and none in group I, p=

0.031). 3 patients were stuporous (GCS <8/15) at presentation in group II (2

had generalized seizures and were in post ictal state and 1 presented with

raised ICP and signs of herniation).

Results

42

TABLE no. 3 : Presenting complaints in Group I and II of medial

sphenoid wing meningiomas.

Clinical

presentation

GROUP 1,

n=43 (%)

GROUP 2,

n =29 (%)

Chi

square,

P- value

Headache 31 (74.4) 26 (89.7) 2.57 0.109

Raised ICP 4 (9.3) 11 (37.9) 8.61 0.003

Visual deterioration 25 (58.1) 17 (58.6) 0.00 0.968

Focal Seizures 4 (9.3) 1 (3.4) 0.92 0.338

Generalised

seizures

7 (16.3) 6 (20.7) 0.23 0.633

Stuporous

(GCS<8/15)

0 3 (10.3) 4.64 0.031

Proptosis 0 1 (3.4) 1.5 0.220

Hemiparesis 2 (4.7) 4 (13.8) 1.89 0.169

Dysphasia/aphasia 0 3 (10.3) 4.64 0.031

Behavioural

problems

8 (18.6) 5 (17.2) 0.02 0.883

Incidental 1 (2.3) 0 0.68 0.408

memory difficulties

(subjective)

10 (23.3) 4 (13.8) 0.99 0.320

Previous surgery

elsewhere

1 (2.3) 3 (10.3) 2.12 0.145

Neurocutaneous

markers

2 (4.7) 0 1.39 0.239

Results

43

Tumour characteristics

Tumour size was categorized into 3 sizes : <2cm, 2-4 cm and >4cm. Its

distribution is depicted in the graph below. (Fig no.10) Hyperostosis of

sphenoid wing and orbit were more common in Group II, 23/29 patients

(79.3%) compared to 23/43 patients (53.5%) in Group I, p= 0.025. Two

patients in group II showed erosion into the orbit and out of which, one

presented with proptosis. Three patients in group I (7%) and one patient in

group II (3.4%) had cystic component, p = 0.521. Tumour calcification was

noted in 5 patients (11.6%) and 2 patients (6.9%) in groups I and II,

respectively, p= 0.506.

Figure no. 10- Distribution of three categories of tumour sizes (<2cm, 2 -4 cm and

>4cm ), hyperostosis, cystic component and calcification in Group I and II medial

SWM.

0

10

20

30

40

50

60

70

80

90

Medial group I Medial group II

Tumour size <2cm

Tumour size 2-4 cm

Tumour size > 4cm

Column1

hyperostosis p=0.025

cystic

calcification

Results

44

Surgery

Gross total resection (Simpson Grade I + II) was achieved in 31

patients (72.1%) in Group I and 12 patients (41.2%) in Group II tumours

(Table no.4, Fig no. 11). To confirm the gross radicality of tumour resection in

each tumour groups, operative records findings and postoperative imaging

(CT scan with and without contrast) were analyzed in all cases. The rate of

subtotal excision or Simpson’s grade III/ IV excision was higher in group II,

58.8% vs 27.9 % in group I).

Figure no. 11- Distribution of Simpson’s Grades of tumour resection in Group I and II

medial SWM.

0

10

20

30

40

50

60

70

80

medial SWM group I medial SWM group II

SIMPSON I

SIMPSON II

SIMPSONIII

SIMPSON IV

Gross total

resection(Simpson's I + II)

Table no. 4 : Simpson’s Grades of tumour resection

Simpson

I

Simpson

II

Simpson III Simpson IV GTR

(I +II)

Group I 27.9% 44.2% 9.3% 18.6% 72.1%

Group II 6.8% 34.4% 31.2% 27.6% 41.2%

Rec. tumour 0 0 0 100% 0

Results

45

Figure no. 12- A 51 years old female with medial SWM (Group I) presented with

seizures and headache, a) MRI brain axial with gadolinium contrast, b) coronal

contrast, c) T2WI coronal d) Pre operative CT brain axial with contrast showing relative

sparing of cavernous sinus and was confirmed during surgery, e) & f) post surgery CT

with contrast showing no residue. Simpson’s grade I excision was done after

convexitization of dura.

a) b) c)

f) e) d)

Results

46

Figure no. 13- A 43 years old female with medial SWM (group II), presented with no

PL and 3rd

CN paresis in right eye. a), b) MRI brain T1W axial and coronal with

gadolinium contrast, c) CT brain axial contrast showing involvement of right cavernous

sinus with encasement of cavernous and supraclinoid ICA. d) &e) DSA with right ICA

injection showing opening of carotid siphon and upward displacement of M1 MCA and

genu with narrowing of supraclinoid ICA. f) post surgery CT brain showing residue

over cavernous region.

a) b) c)

f) e) d)

Results

47

The arachnoid plane of dissection from carotid vessels and

surrounding brain parenchyma was good in 55% of cases in either groups, but

poor in 44% of cases, rest of the cases had heterogenous/ patchy plane of

dissection. Encasement of the ICA and its branches, taken as encircling >270

degrees, was observed in 39.5% in Group I and 62% in Group II tumours,

significantly higher in Group II tumours (p= 0.029).

Optic canal was deroofed in 9 patients (20.9%) in group I and 5 patients

(17.2%) in group II , p=0.698. (Table no. 5)

Table no. 5- Intraoperative observations

Characteristics GROUP 1,

n=43 (%)

GROUP 2, n

=29 (%)

Chi

square

P-

value

Arachnoid plane with

ICA, MCA- Good

20 (55.6) 16 (55.2) 0.00 0.975

Poor 16 (44.4) 13 (44.8)

Intermediate 7 0

ICA encircled(> 270 deg) 17 (39.5) 18 (62) 4.74 0.029

MCA encasement na na

Orbital involvement 0 4 (13.8) 6.28 0.012

Optic canal deroofed 9 (20.9) 5 (17.2) 0.15 0.698

Results

48

Histology

Histological grading was done as per WHO classification of CNS

tumours 2007(72). It revealed that the most common subtype was

meningothelial and transitional types. Many specimens showed a mixed

picture or dual histopathological characteristics, mainly meningothelial and

transitional types. (Table no.6)

Table no. 6- Histopathological distribution.

Histology type Group I , n=43 (%) Gr II , n=29 (%)

Meningothelial 19 (44) 18 (62)

Fibroblastic 3 (7) 1 (3)

Transitional 22 (51) 20 (69)

Psammomatous 2 (5) 0

Angiomatous 4 (9) 0

Atypical 6 (14) 3 (10)

Rhabdoid 1 (2) 0

WHO grade I 35 (82) 26 (90)

WHO grade II 7 (16) 3 (10)

WHO grade III 1 (2) 0

WHO grade II tumours were seen in 7 cases (16%) in groups I and 3

cases (10%) in Group II. Group I consisted of 6 atypical type and 1 clear cell

histology. Group II had all 3 atypical meningiomas. WHO grade III

meningioma was seen in one patient of Group I (rhabdoid pathology).

Results

49

Visual outcomes

We defined a change in visual acuity (VA) as a worsening or

improvement of single line of Snellen acuity or from light-inspection to hand

movement, from hand-movement to figures-counting.

In group I, 16 (37.2%) patients presented with preoperative VA

impairment and 9 (20.9%) patients with visual field defect. This included 5

patients with no PL (perception of light) and 2 with HM (only perception of

hand movement) at presentation. 24 patients (56%) showed stable vision/

unchanged to pre operative status at time of discharge, 10 showed

improvement (23%) and 7 reported worsening (16%). Amongst the 7 reported

cases of worsening of vision, there were 2 new cases with no PL ( these were

the 2 cases with only HM before surgery) and 1 case of only PL.

In group II (29 patients), 11 (37.9%) presented with acuity loss and 6

(20.7%) presented with field defect. This included 4 patients with no PL and 1

with only HM at presentation. Visual acuity remained unchanged in 18 (62%),

2 (7%) showed improvement and 6 (21%) actually worsened after surgery

including 1 additional case with no PL (Table no. 7).

We want to highlight that, most of these above patients showed

improvement in vision subjectively and also by confrontation testing during

each subsequent follow up visits, though, we do not have formal visual acuity

and field charting for most of these patients. We have observed that, no

improvement occurred amongst those with no PL, either at presentation or

Results

50

after surgery. Comparing the visual outcome between these two groups, none

of the values were significant.

Table no. 7- Visual outcome in Group I and II.

Characteristics GROUP 1,

n=43 (%)

GROUP 2, n

=29 (%)

Chi square P- value

Pre surgery vision

Acuity loss 16 (37.2) 11 (37.9) 0.00 0.951

No PL 5 4

Only PL /HM 2 1

Visual Field defect 9 (20.9) 6 (20.7) 0.00 0.980

Post surgery vision-

Stable/unchanged 24 (56) 18 (62) 0.081 0.7762

improved 10 (23) 2 (7) 2.263 0.1325

worsened 7 (16)

(2 new

cases of no

PL + 1 with

only PL)

6 (21)

(1 new case

of no PL)

0.07 0.8691

Cranial nerves involvement

In Group I, one patient presented with partial ptosis (CN III), otherwise,

extraocular movements were normal in rest of the cases. But, new

postoperative CN III paresis was seen in 9 cases (20.9%), p = 0.012, and CN

VI paresis in 2 cases (4.7%) and Frozen eye on same side in 1 cases (2.3%)

(Table no. 8). In Group II, 4 (13.8 %) cases already presented with a CN III

deficit and 2 (6.9%) with CN VI paresis and 1 (3.4%) with CN V sensory

Results

51

deficit. 14 of 29 (48.3%) patients had a new or worsening postoperative CN

III paresis which was significant between the two groups, p = 0.015. In group

II, 4 (13.8%) cases had a new postoperative CN IV paresis and CN VI paresis

each.

Most of the isolated post operative cases of CN III and CN VI deficit

showed improvement on long term follow up, but the 6 patients with frozen

eye (2 from group I and 4 from group II) remained status quo.

Table no. 8- Pre and Post surgery extraocular cranial nerves status.

Group 1, n=43

(%)

Group 2, n

=29 (%)

Chi square P value

Pre operative deficits

Cranial nerve 3rd 1 (2.3) 4 (13.8) 6.28 0.012

4th 0 0 - -

5th 0 1 (3.4) 1.50 0.220

6th 0 2 (6.9) 3.05 0.081

Post surgery

deficits (new/

worsening)

3rd 9 (20.9) 14 (48.3) 5.96 0.015

4th 1 (2.3) 4 (13.8) 1.89 0.169

5th Na Na na Na

6th 2 (4.7) 4 (13.8) 1.89 0.169

Frozen eye 1 (2.3) 4 (13.8) 1.89 0.169

Results

52

Residue and Recurrence Rate

All our patients underwent post surgery CT scan brain (plain and

contrast) on day 1. Residue present was descriptively noted, but volumetric

measurement was not done. In our present analysis, residue was seen in 8

(18.6%) cases in group I and 15 (51.7%) cases in group II.

Group I: Radiological residue in CT scan was seen in 8 (18.6%) cases

and recurrence with tumour growth was observed in 4 (9.3%) out of 8 cases.

The time to recurrence varied considerably ranging from 1 to 8 years.

Amongst these 4 cases, only 1 case underwent resurgery for its recurrence

but then, the procedure was abandoned due to intraoperative cardiac event.

Patient was resuscitated and stabilized and later referred for RT.

Group II: Radiological residue in CT scan, on day 1, was found in 15

(51.7%) cases, (p =0.003). Increase in size of residue/recurrence was noted

in 8 (27.5%), 4 (13.8%) underwent repeat surgery. The time period to

recurrence ranged from 2 to 12 years but majority (6/8 cases) after 4th year.

The criteria for repeat surgery for recurrence were symptomatic patients and

significant increase in tumour size.

Following are the summary of 4 patients in group II subjected to repeat

surgery for recurrence:

Case 1, Female patient in 5th decade underwent repeat surgery after 12years

with Simpson’s grade IV excision. She was referred for SRS for residue but

patient refused. She is presently on 4th year of follow up after 2nd surgery

Results

53

with minimal increase in size of residue. She developed MCA stroke twice in

2007 and 2011 and is recovering.

Case 2, Patient presented with recurrence after 4 years and grade IV excision

done followed by RT. At last follow up, 8 years after 2nd surgery, there was

no recurrence.

Case 3, Patient presented with recurrence after 2 years and grade IV excision

done followed by RT. Patient is currently stable with small residue.

Case 4, Patient was earlier operated elsewhere and came with recurrence

after 2 years, underwent Grade I excision and is doing well.

Postoperative Radiotherapy

Post surgery radiotherapy (RT) were received by 5 patients in Group I

and 6 patients in Group II. Our policy for administering RT were, those cases

with gross tumour residue, recurrence with high risk of repeat surgery, WHO

grade II and III tumours and finally consenting patient.

In group I, 5 (11.6 %) cases underwent RT (4 cases of atypical

meningioma and 1 case of Rhabdoid histology). Remaining, 3 out of 8 cases

of WHO grade II pathology, refused to undergo any form of adjuvant therapy.

Though we had 8 residual Simpson’s grade IV excision cases in Group I,

initially, we followed up all these cases : 1 case showed resolution of tumour

in repeat imaging after 1 year, 4 showed increase in size/recurrence and 3

cases had a stable disease. Amongst the 4 recurrent cases in Group I, only 1

case underwent RT. (The fate of 5 irradiated patients in Group I were: 1 died

Results

54

due to medical reasons after over a year, 3 have shown no recurrence/

increase in size and 1 case in which surgery was abandoned due to

intraoperative MI has a stable residual tumour after RT).

In group II, 6 (20.7%) cases underwent RT- it included 2 out of 3

cases with atypical meningioma, the 3rd patient with atypical histopathology,

though planned for RT, developed cardiac arrest at 6 weeks of follow up and

died. Amongst the 15 (51.7%) cases of residual tumour in Group II, 8

(27.5%) showed increase in size, and out of which, 4 cases (13.8%)

underwent repeat surgery based on symptomatology . They all underwent

Simpson’s Grade IV excision and were subjected to RT post surgery. Those

not irradiated but with residual tumour i.e 11 (37.9%) cases were under

follow up and having stable tumour size.

All of 6 (20.7%) irradiated cases, in Group II, showed stable residual

tumour at last follow up, except one (who was earlier operated 3 times

outside our institute and received RT, he died after 6 months as a sequel of

ICA injury and massive infarct).

KPS and mortality

The clinical outcome was measured by Karnofsky Performance Score

(KPS). Group I - 43 cases were followed up for mean 3.95 years (range 1 to

11 years). At admission, mean KPS was 75.11 (range 40 to 90). The mean

score improved to 84.2 at the time of discharge, with KPS > 90 in 18 (41.8%)

cases . At last follow up, the calculated mean KPS was 90.7, with 33 (78.5%)

Results

55

cases having KPS >90. (Table no. 9). 5 (11.6%) cases presented with KPS

50-60 due to severe frontal lobe signs and raised ICP features. The latter

group of 5 cases showed marked improvement after surgery. There was 1

death at a follow up period of one year in group I. This case was a 57 years

old female patient who underwent Simpson’s grade II excision with atypical

meningioma. At the time of discharge, her KPS was 90 and was subjected to

RT. She died a year later due medical reasons (Table no. 9).

Table no. 9- Karnofsky Performance score (KPS) in GROUP I

(mean=3.95 years follow up).

KPS score Pre op. KPS,

no. (%)

Post op KPS at

discharge, no. (%)

KPS at last follow

up, no.42 (%)

100 0 1 (2.3) 12 (28.5)

90 4 (9.3) 17 (39.5) 21 (50)

80 20 (46.5) 24 (55.8) 9 (21.4)

70 14 (32.6) 1 (2.3) 0

60 4 (4.7) 0 0

50 1 (2.3) 0 0

40 0 0 0

10-30 O 0 0

Mean KPS 75.11 84.2 90.7

Group II - 29 cases were followed up for a mean of 4.7 years (range 1-

12 years). At admission, mean KPS was 67.2 ( range 10-30 to 80). 3 patients

presented with KPS 30- 40, amongst which 2 were in post ictal phase, and 1

with raised ICP with evidence of herniation. Amongst these 3 cases, one died

Results

56

on day 10th due to sequel of vascular injury, others improved and was

discharged with KPS of 60 to 70.

Two perioperative deaths were noted in group II- first case developed

right MCA territory infarct and succumbed to its sequel on the 10th post

operative day. Another case was recovering well after surgery, but

succumbed on the 5th day after surgery due to pulmonary embolism.

The mean KPS at discharge was 57.35, only 5 cases (17.2%) had >90

KPS at discharge. The mean KPS at last follow up was 84.54 and KPS

exceeding > 90 was noted in 15(68.1%) cases.

Table no. 10- Karnofsky Performance score in GROUP II (mean=4.7years

follow up).

KPS score Pre operative

KPS - no. (%)

Post op KPS at

discharge, no. (%)

KPS at last follow

up (no. 22 (%)

100 0 0 0

90 0 5 (17.2) 15 (68.1)

80 12 (41.3) 11 (37.9) 2 (9)

70 13 (44.8) 7 (24.1) 5 (22.7)

60 2 (6.8) 2 (6.9) 0

50 0 1 (3.7) 1 (left MCA stroke

after 5 years of

surgery)

40 1 (3.4) 1 (3.7) 0

10-30 2 (6.8) 0 0

Mean KPS 67.2 57.35 84.54

Results

57

Two deaths occurred at 6weeks and 6 months of follow up in group II.

The first patient died of cardiac arrest at 6 weeks and other patient

succumbed to sequel of right supraclinoidal ICA injury at 6 months.

Morbidity

Besides visual and cranial nerves involvement, arterial infarcts,

dysphasia / apahasia, meningitis and seizures were frequently observed

morbidities. List of other morbidites are given in the Table no. 11.

Group II patients experienced higher motor deficits due to infarct, 6

(20.7%) cases in group II versus 2 cases (4.7%) in group I, p= 0.014. The 2

cases in group I had small perforator infarct and its deficits improved with

time and physiotherapy. Amongst the 6 patients with infarct in group II, 1 had

ICA injury intraoperative, and 1 each with MCA and PCA territory infarct,

remaining 3 cases had small perforator infarct. Patient with MCA infract died

on 10th post operative day and one with ICA infract succumbed 6 months

later as a part of its sequel. 2 additional patients developed right MCA stroke

4 and 6 years post surgery in group II which was unrelated to surgery.

Post surgery meningitis was noted in 6 (20.7%) cases in group II and

none in group I, p=0.002. Seizures in 2 (4.7%) in group I vs 6 (20.7%) in

group II, p = 0.034. CSF rhinorrhoea was noted in 2 (4.7%) cases in group I

and 1 (3.4%) case in group II. The 2 cases in group I were treated

conservatively, whereas 1 case in group II underwent Theco- peritoneal

shunting.

Results

58

Table no. 11- Morbidity after surgery in group 1 and group 2

GROUP 1,

n=43 (%)

GROUP 2, n =29

(%)

Chi

square

P value

Hemiparesis (new/

worsening)

2 (4.7) 7 (24.1) 6.01 0.014

Infarct 2 (4.7)

(perforators)

6 (20.7) (1 ICA,

1MCA, 1PCA, 3

perforators)

4.51 0.034

CSF rhinorrrhoea 2 (4.7) 1 (3.4) 0.06 0.802

Seizures 2 (4.7) 6 (20.7) 4.51 0.034

Meningitis 0 6 (20.7) 9.71 0.002

DVT 1 (2.3) 1 (3.4) 0.08 0.776

SJS 1 (2.3) 0 0.68 0.408

Behavioural problem 1 (2.3) 4 (13.8) 3.52 0.060

Patient follow up

Follow-up data included clinical examinations and imaging (contrast-

enhanced MR images /CT scans) at 6weeks, 3 months, 6months and yearly

thereafter (Table no. 12).

Results

59

43 patients in group I were followed up for mean of 3.95 years (range 1 to 11

years) and 14 (32.5%) patients had >4 years of follow up. Out of 43 patients,

5 cases lost follow up, as given in table no. 12.

Out of 29 patients in group II, 2 died in perioperative period and 2 died

within one year period and the remaining were followed up for mean of 4.7

years ( range 1 to 12 years), 3 patients were lost to follow up.

Table no.12 – Patient follow up data given as frequency.

Group I (n=43) Group II (n=29)

Follow up

duration in

years

No. of

patient

No. lost

to follow

up

thereafter

Rec of

tumour

Death No of

patient

No. lost

to follow

up

thereafter

Rec of

tumour

Death

<1 years 3 1 0 3 1 1 2

>1-2 years 16 2 0 1 5 2 0

>2-4 years 10 0 0 6 0 1

>4-7 years 9 0 2 5 0 2

>7-10

years

3 2 1 6 0 2

>10 years 2 0 1 2 0 2

Discussion

60

DISCUSSION

Classification of Medial Sphenoid Wing Meningiomas

The initial classification on sphenoid wing meningiomas by Cushing

and Eisenhardt (3) has stood the test of time and remains mostly valid, but

now, numerous authors have sought a revision that incorporates information

and experiences gained from the contemporary use of multiplanar MRI

microsurgical technique and surgical outcome.

Then, almost after five decades, Al-Mefty (5) reported 24 patients with

clinoidal meningiomas, and subclassified the tumours into three groups: a)

medial ridge tumours with marked attachment to the carotid tree because of

no intervening arachnoid membrane, b) medial ridge tumours without marked

attachment to carotid tree secondary to an intervening arachnoid membrane

being present, and c) small tumours solely within the optic canal.

Recently, many of the contemporary authors like Kaye AH (121), Lee JH

(20), Samii M (122), Stephen M. Russell (4), Makoto Nakamura (6), have put forth

their reservations on the above Al-mefty’s classification(5) for the following

reasons. First, Group 3 tumours (optic canal meningiomas) do not involve the

carotid tree and, therefore, should not be included when evaluating medial

ridge (clinoidal) meningiomas. Secondly, these authors unanimously agree

that, amongst those tumours that are markedly attached to the intracranial

vessels without an apparent intervening arachnoid layer, not all originate

proximal to the carotid artery’s arachnoid ensheathment (i.e. Group 1 tumours

Discussion

61

in Almefty’s classification). They are of the view that, though in a small

minority of patients this is true, other factors like chronicity of tumour

compression, tumour consistency, invasiveness of the tumour, and cases with

a previous resection are probably more important determinants of resectability

and unfavourable plane of dessection. Even in Al-Mefty’s series (5), 4 out of

the 24 patients had previous resection.

In this study, we also agree with the above authors that, recurrence,

chronicity and intrinsic tumour behaviour are the deciding factors for

favourable arachnoid plane or interface with vessels which can be witnessed

only at the time of surgery. This is further proven by the fact that some

tumours show variable dissection plane even with the MCA vessels. In our

series, the main factors leading to subtotal tumor resection was CS

involvement and poor plane of dissection from major arteries especially in

recurrent cases (all underwent Simpson’s grade IV excision). Al-mefty’s grade

III tumours with optic foramen origin are of smaller size with predominantly

early visual disturbances. This particular group of tumour was excluded from

our present study.

Hereby, we classified the medial SWM according to pre and post

operative evidences of CS involvement. Stephen M. Russsell et al. (4) and

Nakamura et al. (6) have confirmed the clinical utility and treatment strategy of

this subdivision. Treatment for tumours without CS extension is gross total

removal, whereas, for tumours with CS extension, often, only the intradural

Discussion

62

tumour is removed with the residual part infiltrating the CS usually managed

conservatively or irradiated.

Cavernous Sinus Involvement

The surgical management of patients with meningiomas involving the

CS has been continuously debated and remains controversial. More

aggressive and radical intracavernous tumor removal was proposed by

Sekhar et al., (16,17,18) De Monte et al.,(14) and Dolenc et al.,(19) along with the

encased ICA, with or without saphenous vein graft reconstruction.(16,18)

Surgical morbidity associated with aggressive resection of

meningiomas involving the CS remains high. (7,9,10,11,12,13,14,15,118) There are

several reasons for this high morbidity. First, disruption of the fine blood

supply of the ocular CNs may occur during dissection of CS meningiomas.

(123,124) Second, dissection of the meningioma from the CNs may be

impossible because of the poor arachnoidal plane and tumour infiltration of

the nerves. (125) Finally, meningiomas may infiltrate the adventitia of the C4

segment of the ICA. (126, 127)

DeMonte et al. (14) reported 41 patients with histologically benign

meningiomas involving the CS who underwent aggressive surgery. Although

total removal was achieved in 76% of cases, 10% experienced recurrence 5

years after surgery. Pre-existing CN deficits improved in only 14% of the

patients, remained unchanged in 80%, and worsened permanently in 6%.

Discussion

63

De Jesus et al. (15) evaluated the tumour recurrence and progression in

119 patients with meningiomas involving the CS. During a relatively short

mean follow-up period of 33.8 months, they found recurrences in 10% of

completely resected tumours and 15% of incompletely resected tumours. The

data on most common complications of CS surgery, i.e. impairment of

extraocular muscles or loss of trigeminal nerve function was not mentioned.

Abdel-Aziz et al.,(8) in 2004, reported 38 patients with large SWM

involving the CS. In 22 of 24 patients, total microscopic excision was achieved

in tumours that involved only the lateral compartment of the CS (modified

Hirsch Grades 0 and 1) (128). (Modified Hirsch grades are as follows: HG 0,

tumour touches and rests on the ICA without encasement; HG 1, tumour

partially encases the ICA; HG 2, tumour completely encases, without

narrowing the ICA; HG 3 tumour completely encases and narrows the ICA;

and HG 4, tumour completely encases and obliterates the ICA).(128)

All 14 of 38 patients who had tumours that encased the CS of the ICA

(Hirsch Grades 2–4) underwent incomplete resection. Among 38 patients,

mortality was 0%, late CN deficits remained in 6 (16%), late KPS exceeded 90

in 34 patients (90%) and 4 patients (10.5%) developed a recurrence or

regrowth. Of 20 patients who were treated with either linear accelerator-based

SRS or fractionated conformal RT, 11 had residual tumour with a moderate to

high proliferative index, 4 had atypical tumours and 1 had angioblastic

meningioma, 2 had regrowth, and 2 had recurrent tumours. In 18 (90%) of the

20 patients who underwent radiation, tumour size was reduced or controlled.

Discussion

64

We also agree with their conclusions that residual tumour in the medial

compartment (HG 2–4) may be managed by observation or radiotherapy,

depending on cellular atypia, proliferative index, patient’s age, and clinica

status.

In Nakamura et al. (6) analysis of medial SWM with CS involvement,

indeed showed a high recurrence rate of 27.5% after surgery. This difference

in recurrence could be due to less radical approach of authors considering

that only 14.5% underwent GTR, in addition, this study had a significantly

longer follow up period of 79.04 months. IIIrd CN paresis was the presenting

complaint in 19 patients (27.5%) and additional 6 patients (12%) developed

new IIIrd CN paresis. 10 (14.5%) presented with IVth CN paresis with 2 new

cases after surgery and 9 (13%) presented with VI th CN paresis with 2 new

cases after surgery. Also to note here is that, 6 (12%) patients in this cohort

showed IIIrd CN improvement, 2 showed IVth CN but none showed VIth CN

improvement after surgery.

In similar study by Stephen M Russell et al.,(4) 11 out of 35 patients with

CS involvement was followed for a mean of 12.8 years, out of which 10 cases

(90%) underwent grade III/IV excision. Recurrence was seen in 3 (9%) and

IIIrd CN deficit seen in 1 patient (9%). Conventional EBRT was used for 5

patients (3 with recurrence and other 2 who had undergone Grade IV

excision). After receiving radiation, no tumor progression occurred in these

five patients (average follow-up, 7.1 yr). None of the patients had atypical or

malignant meningiomas. Therefore, the authors concluded that GTR of medial

Discussion

65

ridge meningiomas invading the CS, which was present in 11 (31%) of their

patients, is not warranted.

In our analysis, 29 of 72 patients of medial SWM with CS involvement,

we could achieve a GTR of 41.2% through meticulous interdural dissection

and stripping off the outer layer of CS. Those infiltrating the CS with vessels

encasement was left untouched. Residue was noted in 15 (51.7%) and the

majority were followed up regularly in yearly basis. 6 (20.7%) cases showed

enlargement of residue and became symptomatic with time lag ranging from 2

to 12 years (majority after 4 years), out of which 4 underwent repeat surgery (

Simpson’s grade IV). EBRT was given to 6 patients in group II, which

included all 4 with recurrence and repeat surgery and 2 patients with atypical

histology. Except for one patient who died due to sequel of ICA injury and

infarct after 6 months, others have shown a stable residual tumour after RT.

We also experienced significantly higher post surgical CN deficits: 14

cases (48.3%) with new/worsening IIIrd CN paresis, 4 (13.8%) of IVth CN

and VIth CN paresis each. 4 cases (13.8%) developed unilateral complete

ophthalmoplegia (frozen eye), 2(6.9%) out of which had frozen eye as

presentation before surgery. Our cranial neuropathy was higher amongst

contemporary studies because of our initial attempt to remove tumour

completely. Michael E. Sughrue et al.,(129) reported partial IIIrd CN palsY in

approximately 20% of medial-third tumor cases. Abdel-Aziz and colleagues

(8) reported cranial neuropathies in 16% of their cases, and Langevin and

colleagues (130) noted diplopia in 15.8% of patients.

Discussion

66

In our view, a more aggressive approach to meningiomas involving the

CS will lead to more surgical morbidity. A multidisciplinary approach using

tailored surgical resection and salvage postoperative RT can maximize tumor

control and minimize patient morbidity.

Extent of resection and recurrence rate of Medial SWM

The rate of recurrence for medial SWM is regarded as one of the

highest for intracranial meningiomas. Mirimanoff et al.(131) reported a

recurrence rate or tumour progression in 34% at 5 years and 54% at 10 years

for medial SWM compared to 3% and 25% at 5 and 10 years for convexity

meningiomas.

Analyzing the recurrence among different tumour locations at the

cranial base, Mathiesen et al. (132) also observed the highest recurrence rate

among clinoidal/medial SWM, with 60 to 100% at 10 years and 72 to 100% at

25 years after surgery, depending on the Simpson grade of resection. Basso

and Carrizo(133) reported a recurrence rate of 26.92% among 26 inner third

meningiomas at 10 years after surgery. Nakamura et al.(6) reported recurrence

in 7.7% of Group I tumours and 27.5% of Group II tumours during a mean

follow-up period of 69.3 months (5.8 yr). Nakamura et al.(6) could achieve

92.3% GTR in group I and 14.5% in group II tumours.

In our study, recurrence with tumour progression was observed in 4

cases (9.3%) of group I and 8 cases (27.5%) of group II at a mean follow up

of 3.95 years and 4.7 years, respectively. Here, it is to note that, all the

Discussion

67

recurrences occurred in those with residual tumours after first surgery [i.e , 4

of 8 residual cases (50%)in Group I and 8 of 15 residual cases (53.3%) in

Group II]. We could achieve GTR of 72.1% in group I and 41.2 % in group II.

Our policy regarding adjuvant therapy in WHO grade I meningiomas

was to follow up with serial imaging yearly regardless of grade of resection.

Patients were subjected to RT only after recurrence with progression, repeat

surgery and WHO grade II- III tumours.

Stephen M Russell et al. (4) achieved only 9 % GTR in group II tumours,

yet, recurrence rate was significantly lower at 9% because they subjected

their patients with subtotal resection to early RT.

Thus, it is widely evident from various studies that RT/SRS in cases

with subtotal resection of CS involvement, confirms to better outcome.

Visual Outcome in Medial Sphenoid Wing Meningiomas

The past views regarding postoperative visual recovery in patients with

clinoidal meningiomas have been quite pessimistic. (5) Poor visual outcome

was previously attributed to an ischemic mechanism, and visual deficits were

considered mostly irreversible. (5,134) Only few data exists concerning visual

function after resection of these tumours.

Al-Mefty et al. (5) reported 24 of 28 patients with clinoidal meningiomas

who presented with visual disturbances. Visual impairment improved in only

six (25%) patients after tumour removal.

Discussion

68

Risi et al(118) in their report on 34 patients with meningiomas involving

the anterior clinoid process, 32% of 20 patients with preoperative visual

impairment had postoperative improvement in their vision. Benjamin V et

al.(135) reported in their series of 20 surgically treated medial SWM,

improvement of vision in 50% of patients who were not blind before surgery.

Lee et al. (20) have done an extensive study on visual outcome in

clinoidal meningiomas. They proposed at least three possible mechanisms of

preoperative optic nerve injury- ischemia, compression, and demyelination.

Favorable results were reported in a recent series of 15 patients who

underwent surgery of clinoidal meningiomas with use of a cranial base

technique consisting of extradural anterior clinoidectomy coupled with optic

canal unroofing and optic sheath opening. Six of eight (75%) patients with

preoperative visual impairment experienced a significant improvement with a

follow-up period ranging from 6 to 60 months (mean, 37.2 months).

Nakamura et a.l (6), in their series of 108 medial SWM with 39 in group

I and 69 in group II, noted immediate postoperative improvement of visual

function in 56%, and vision remaining unchanged in 44% with Group 1

tumours who were not blind before surgery. Outcome of visual function was

less favourable in Group 2 tumours with vision improvement in 30%, stable in

60% and worsening in 10% of patients. Only 10% of patients who underwent

surgical resection of a recurrent Group 2 tumour showed immediate visual

improvement. Nakamura et al.(6) have questioned the necessity for extradural

extensive cranial base approach in Lee et al.(20) series for a favourable visual

Discussion

69

outcome. Nakamura et al. used this extradural cranial base approach only for

those with intraosseous involvement. (6)

Stephen M Russell(4) reported that among the 30 patients with

preoperative visual loss, 22 patients (73%) improved, six (20%) were

unchanged, and two (7%) worsened. Here also, the authors were very

sceptical regarding extensive extradural cranial base approach and were

selective in their approach.

We have noted a similar pattern of preoperative visual acuity loss and

field defect before surgery, in either of the groups I and II. Approximately, 37%

presented with acuity loss and 20 % with field defect. Post surgery, in group I,

vision remained unchanged in 56 %, improved in 23% and worsened in 16 %.

Whereas, in group II, vision remained stable in 62%, improved in 7% and

worsened in 21%.

Our approach to this category of tumour was decided on individual

basis considering radiological, clinical, age and general condition of patient.

14.6% (4 patients) underwent FTOZ and rest were subjected to standard

fronto-temporal craniotomy with sphenoid ridge drilling with or without anterior

clinoidectomy. Optic canal was deroofed in 20.9% (9 patients) in group I and

17.2% (5 patients) in group II. It is to be highlighted here, that most of our

patients presented with poor visual acuity and larger size of tumour (tumour

size >2cm in 74.5% in group I and 68.8% in group II) which probably explains

our poor visual outcome.

Discussion

70

Morbidity and mortality

Cushing and Eisenhardt (3) noted that “the crux of the removal lies in

freeing the growth from its entanglement with the vessels at the carotid

bifurcation,” and he cautioned surgeons about the hazards of entering the

carotid field.

Aggressive resection of tumour invading the CS is associated with new

and permanent CN palsies, cavernous ICA injury, and CSF leak. These risks

outweigh the benefits of GTR.

Injury to the vessels of the anterior circulation has been the major

cause of operative morbidity and mortality in past surgical series. Bonnal et

al., 1980 (10), had a surgical mortality of 43% and Fohanno and Bitar in 1986

had 27% mortality(117). Since then, more recent reports have shown lower

rates of operative morbidity and mortality, as approach became more

conservative and better understanding of the anatomy. (20,118,119)

Lee et al. in 2001 (20), reported a 87% GTR with no mortality in 15

patients with global medial ridge tumours. Other peer reviewed series in

chronological event are given in the table no.13 and shows decreasing trend

of mortality.

We in our study of 72 patients, had no perioperative mortality in group I

tumours, 1 died a year later due to medical reasons. In Group II, we

experienced 2 cases of intraoperative injury to MCA and ICA each. One case

succumbed to its sequel at 10th day and other at 6 months. One more death

Discussion

71

occurred on the 5th post operative day due to pulmonary embolism. Literature

shows that efforts to remove adherent tumour from encased vessels in the

past had met with rates of vascular injury exceeding 20% (136). Our 2 cases of

major arterial injury accounted for 6.89%. Small vessel/ perforator infarct with

hemiparesis occurred in 2 cases (4.7%) in group I and 4 cases (13.55%) in

group II. These patients improved in long term and was independent for

activities of daily living.

The outcome in our patients was measured with Karnofsky’s

Performance Score (KPS) at the time of discharge and at last follow up

(ranging 1 to 12 years). In group I, mean KPS at discharge was 84.2 and at

last follow up 90.7. In group II, mean pre surgical KPS was 67.2, at discharge

57.35 (increased morbidity was due to infarct, meningitis, behavioural

problems, metabolic disturbances, etc) and mean KPS improved significantly

to 84.54 at last follow up.

We believe that aggressive GTR of medial SWM invading the

cavernous sinus is not warranted, especially in older patients. In summary, a

multidisciplinary approach using both pragmatic surgical resection and

salvage postoperative radiation treatment can maximize tumour control while

minimizing patient morbidity.

Discussion

72

Table no 13: Summary of studies of medial SWM in the peer-reviewed literature

Series (ref

no.)

No. of

patients

Size CS

involve

ment

%

F/U mortality GTR Improved

vision

Rec.

Cushing and

Eisenhardt,

1938 (3)

13 na 7 yr 15% 31% 8% 36%

Ugrumov et al.,

1979 (113)

17 na Na 23% 0% Na Na

Konovalov et

al., 1979 (114)

70 na Na 19% 85% Na Na

Ojemann, 1980

(115)

13 na 11.3yr 0% 0% 15% 31%

Bonnal et al.,

1980 (10)

7 na 1-8 yr 43% 29% 17% 25%

Pompili et al.,

1982 (116)

9 na 7yr 4% 50% 48% 12%

Fohanno and

Bitar, 1986

(117)

18 na na 27% Na Na 25%

Al-Mefty, 1990

(5)

24 na 38 4.8yr 8% 89% 8% 4%

Risi et al., 1994

(118)

34 na 1.9yr 6% 59% 32% 21%

Day, 2000

(119)

6 <5cm 3

months

0% 66% Na Na

Goel, 2000

(120)

60 85%

>3cm

0 na 5 70 25.5 na

Lee et al., 2001

(20)

14 3.7cm 13 3.1yr 0% 87% 75% 0%

Abdel-Aziz et

al., 2004 (8)

38 >3cm 100 8yr 0% 58% Na 11%

Nakumura et al

2006 (6)

108 na 64 6.59yr 0% Gr I

92.3%

Gr II

14.5%

56%

30%

7.7%

27.5%

Stephen M

Russell et al

2008 (4)

35 4.5cm 31.4 12.8 0% 69% 63% 9%

Behari, 2008

(110)

20 6.12 90 na 5 45% 15% na

Bassiouni,

2009 (111)

106 na 29 6.9

years

1.9 58 40.4 10.2

Our study

2012-13

72 >2cm

74.5%

Gr I no.

43

Gr II

no. 29

3.95yr,

4.7yr

0%

6.9%

Gr I

72.1%

Gr II

41.2%

23%

7%

9.3%

27.5%

Conclusion

73

CONCLUSION

The surgical treatment of medial SWM still remains a challenge for

neurosurgeons. The major determining factors for subtotal resection are the

CS infiltration, repeat surgery for recurrence and vascular encasement. Group

II tumours though can be managed aggressively, it may be associated with

increased morbidity like permanent cranial nerve deficits of extraocular

movements, infarct and poorer KPS.

It is also observed that, many residual tumours remain stable for many

years and some even reduce in size/ disappear, depending upon the tumour

grade and growth pattern and hence, can be closely followed up. SRS can be

offered as an adjuvant therapy in cases of subtotal resection in view of recent

literature with favourable results, though long term outcome data is awaited.

In Group I tumours, GTR should be ideally attempted in all cases with

acceptable results, therefore, it is important to accurately identify these two

subgroups for optimal treatment.

There are several limitations to our study in view of shorter follow up

period, smaller sample size and fewer cases in the SRT/SRS arm.

Nevertheless, this study attempts to highlight the importance of classifying

medial SWM into two subgroups with respect to cavernous sinus involvement,

as the surgical approach, complication rates, recurrence and prognosis is

different between the two subgroups.

References

74

REFERENCES

01. Rachlin JR, Rosenblum ML. Etiology and biology of meningiomas. In:

Al-Mefty O, editor. Meningiomas. New York: Raven Press, 1991; 27–

35.

02. DeMonte F, Al Mefty O. Meningiomas. In: Kaye AH, Laws ER Jr,

editors. Brain Tumours. New York: Churchill Livingstone, 1995; 675–

704

03. Cushing H, E.L., : Meningiomas: Their Classification, Regional

Behaviour, Life History, and Surgical End Results. . Springfield, IL,

Charles C Thomas, 1938.

04. Stephen M. Russell, Medial sphenoid ridge meningiomas:

classification, microsurgical anatomy, operative nuances, and

long-term surgical outcome in 35 consecutive patients 2008

Mar;62(3 Suppl 1):38-50; discussion 50, Neurosurgery

05. Al-Mefty O: Clinoidal meningiomas. J Neurosurg 73:840–849, 1990.

06. Nakamura M, Roser F, Jacobs C, Vorkapic P, Samii M: Medial

sphenoid wing meningiomas: Clinical outcome and recurrence rate.

Neurosurgery 58:626-639, discussion 626-639, 2006

07. O’Sullivan MG, van Loveren HR, Tew JM Jr: The surgical resectability

of meningiomas of the cavernous sinus. Neurosurgery 40:238–244,

1997

08. Abdel-Aziz KM, Froelich SC, Dagnew E, Jean W, Breneman JC,

Zuccarello M, van Loveren HR, Tew JM Jr: Large sphenoid wing

meningiomas involving the cavernous sinus: Conservative surgical

strategies for better functional outcomes. Neurosurgery 54:1375–1384,

2004

References

75

09. Biglan AW, Sekhar LN, Cheng KP, Wright DC: A protocol for

measuring ophthalmic morbidity and recovery after cranial base

surgery. Skull Base Surg 4:26–31, 1994

10. Bonnal J, Thibaut A, Brotchi J, Born J: Invading meningiomas of the

sphenoid ridge. J Neurosurg 53:587–599, 1980

11. Cusimano M, Sekhar LN, Sen CN, Pomonis S, Wright DC, Biglan A,

Jannetta P: The results of surgery for benign tumours of the cavernous

sinus. Neurosurgery37:1–10, 1995

12. Klink D, Sampath P, Miller NR, Brem H, Long DM: Long-term visual

outcome after nonradical microsurgery in patients with parasellar and

cavernous sinus meningiomas. Neurosurgery 47:24–31, 2000

13. Knosp E, Perneczky A, Koos WT, Fries G, Matula C: Meningiomas of

the space of the cavernous sinus. Neurosurgery 38:434–442, 1996

14. DeMonte F, Smith HK, Al-Mefty O: Outcome of aggressive removal of

cavernous sinus meningiomas. J Neurosurg 81:245–251, 1994

15. De Jesus O, Sekhar LN, Parikh HK, Wright DC, Wagner DP: Long-term

follow-up of patients with meningiomas involving the cavernous sinus:

Recurrence, progression, and quality of life. Neurosurgery 39:915–919,

1996.

16. Sekhar LN, Moller AR: Operative management of tumours involving the

cavernous sinus. J Neurosurg 64:879–889, 1986

17. Sekhar LN, Patel S, Cusimano M, Wright DC, Sen CN, Bank WO:

Surgical treatment of meningiomas involving the cavernous sinus:

Evolving ideas based on a ten year experience. Acta Neurochir Suppl

65:58–62, 1996.

18. Sekhar LN, Sen CN, Jho HD: Saphenous vein graft bypass of the

cavernous internal carotid artery. J Neurosurg 72:35–41, 1990

References

76

19. Dolenc VV, Kregar T, Ferluga M, Fettich M, Mozrina A: Treatment of

tumours invading the cavernous sinus, in Dolenc VV (ed): The

Cavernous Sinus: A Multidisciplinary Approach to Vascular and

Tumorous Lesions. Vienna, Springer-Verlag, 1987, pp 377–391

20. Lee JH, Jeun SS, Evans J, Kosmorsky G: Surgical management of

clinoidal meningiomas. Neurosurgery 48:1012–1021, 2001

21. Macewen W: Intra-cranial lesions, illustrating some points in connexion

with the localization of cerebral affections and the advantages of

antiseptic trephining. Lancet 2:581-582, 1881

22. Durante F: Contribution to endocranial surgery. Lancet 2:654-655,

1887.

23. Tomasello F, Germano A: Francesco Durante: the history of

intracranial meningiomas and beyond. Neurosurgery 59:389-396,

2006

24. Bakay, : The history of surgery of meningiomas. Schmidek HH, ed.

Meningiomas and Their Surgical Management, , Philadelphia: WB

Saunders; 1991. 173

25. Cushing, H., The meningiomas (Dural Endotheliomas): Their Source

and favoured seats of origin. Brain, 1922. 45(2): p. 282-316

26. Kurland LT, Schoenberg BS, Annegers JF et al. The incidence of

primary intracranial neoplasms in Rochester, Minnesota. Ann N Y Acad

Sci 1982;381:6–16

27. Claus EB, Bondy ML, Schildkraut JM, Wiemels JL, Wrensch M, Black

PM: Epidemiology of intracranial meningioma. Neurosurgery 57:1088–

1095, 2005

28. Jukich PJ, McCarthy BJ, Surawicz TS, Freels S, Davis FG: Trends in

incidence of primary brain tumours in the United States, 1985–1994.

Neuro-oncol 3:141– 151, 2001.

References

77

29. Yasargil MG: Microneurosurgery. Stuttgart: Georg Thieme Verlag,

1984, Vol 1, pp 26-32

30. Dolenc VV: Anatomy and Surgery of the Cavernous Sinus. Wien:

Springer-Veflag, 1989

31. Bannal J, Thibaut A, Brotchi j, Born J. Invading meningiomas of the

sphenoid ridge.] Neurosurg 1980;53(5):587-599

32. Brotchi j, Pirotte B. Sphenoid wing meningiomas. In: Sekhar LN,

Fessler RG, eds. Atlas of Neurosurgical Techniques: Brain. New York,

NY:: Thieme; 2006:623-632

33. Hijiya, N., et al., Cumulative incidence of secondary neoplasms as a

first event after childhood acute lymphoblastic leukemia. JAMA, 2007.

297(11): p. 1207-15.

34. Preston, D.L., et al., Tumours of the nervous system and pituitary gland

associated with atomic bomb radiation exposure. J Natl Cancer Inst,

2002. 94(20): p. 1555-63.

35. Ron, E., et al., Tumours of the brain and nervous system after

radiotherapy in childhood. N Engl J Med, 1988. 319(16): p. 1033-9.

36. Sadetzki, S., et al., Genotyping of patients with sporadic and radiation-

associated meningiomas. Cancer Epidemiol Biomarkers Prev, 2005.

14(4): p. 969-76.

37. Sadetzki, S., et al., Radiation-induced meningioma: a descriptive study

of 253 cases. J Neurosurg, 2002. 97(5): p. 1078-82

38. Black PM, Carroll R, Zhang J: The molecular biology of hormone and

growth factor receptors in meningiomas. Acta Neurochir Suppl

65:50–53, 1996

References

78

39. Blitshteyn S, Crook J, Jaeckle KA: Is there an association between

meningioma and hormone replacement therapy? A study of women at

the Mayo Clinic Jacksonville. From the Society for Neuro-Oncology

Meetings Abstracts 2004

40. Hsu DW, Efird JT, Hedley-Whyte ET: Progesterone and estrogen

receptors in meningiomas: Prognostic considerations. J Neurosurg

86:113–120, 1997.

41. Claus, E.B., et al., Exogenous hormone use and meningioma risk.

Cancer, 2007. 110(3): p. 471-476.

42. Vadivelu, S., L. Sharer, and M. Schulder, Regression of multiple

intracranial meningiomas after cessation of long-term progesterone

agonist therapy. J Neurosurg, 2010. 112(5): p. 920-4

43. Carroll RS, Zhang J, Black PM: Expression of estrogen receptors alpha

and beta in human meningiomas. J Neuro-oncol 42:109–116, 1999

44. Goodwin JW, Crowley J, Eyre HJ, Stafford B, Jaeckle KA, Townsend

JJ: A phase II evaluation of tamoxifen in unresectable or refractory

meningioma: A Southwest Oncology Group study. J Neuro-oncol

15:75–77, 1993.

45. Chen J, Chen G: Expression of androgen receptor in meningiomas. J

Tongji Med Univ 21:140–142, 2002

46. Schulz S, Pauli SU, Schulz S, et al: Immunohistochemical

determination of five somatostatin receptors in meningioma reveals

frequent overexpression of somatostatin receptor subtype sst2A. Clin

Cancer Res 2000; 6:1865-1874

47. Kokoglu E, Tuter Y, Sandikci KS, et al: Prostaglandin E2 levels in

human brain tumor tissues and arachidonic acid levels in the plasma

membrane of human brain tumours. Cancer Lett 1998; 132:17-21.

References

79

48. Schoenberg BS, Christine BW, Whisnant JP: Nervous system

neoplasms and primary malignancies of other sites: the unique

association between meningiomas and breast

cancer. Neurology 1975; 25:705-712.

49. Annegers, J.F., et al., Head trauma and subsequent brain tumours.

Neurosurgery, 1979. 4(3): p. 203-6.

50. Eskandary, H., et al., Incidental findings in brain computed tomography

scans of 3000 head trauma patients. Surg Neurol, 2005. 63(6): p. 550-

3; discussion 553.

51. Brain tumour risk in relation to mobile telephone use: results of the

interphone international casecontrol study. International Journal of

Epidemiology, 2010. 39(3): p. 675-694.

52. Lohn S: Mobile phone use and risk of intracranial tumours. Karolinska

Institute, Stockholm, Sweden, 2004

53. Terry, M.B., et al., An international case-control study of adult diet and

brain tumor risk: a histology-specific analysis by food group. Ann

Epidemiol, 2009. 19(3): p. 161-71

54. Wigertz, A., et al., Allergic conditions and brain tumor risk. Am J

Epidemiol, 2007. 166(8): p. 941-50.

55. Brenner, A.V., et al., History of allergies and autoimmune diseases and

risk of brain tumours in adults. Int J Cancer, 2002. 99(2): p. 252-9.

56. Rajaraman, P., et al., Risk of meningioma and common variation in

genes related to innate immunity. Cancer Epidemiol Biomarkers Prev,

2010. 19(5): p. 1356-61.

57. Inoue YK: Inoue-Melnick virus and associated diseases in man: recent

advances. Prog Med Virol 1991; 38:167-179

References

80

58. Rachlin JR, Rosenblum ML: Etiology and biology of meningiomas.

In: Al-Mefty O, ed. Meningiomas, New York: Raven Press; 1991:27

59. Sawaya R, Rämö OJ: Systemic and thromboembolic effects of

meningiomas. In: Al-Mefty O, ed. Meningiomas, New York: Raven

Press; 1991:137

60. Malmer, B., R. Henriksson, and H. Gronberg, Familial brain tumours-

genetics or environment? A nationwide cohort study of cancer risk in

spouses and first-degree relatives of brain tumour patients. Int J

Cancer, 2003. 106(2): p. 260-3.

61. Hemminki, K., et al., Familial risks in nervous-system tumours: a

histology-specific analysis from Sweden and Norway. Lancet Oncol,

2009. 10(5): p. 481-8.

62. Perry A, Gutmann DH, Reifenberger G: Molecular pathogenesis of

meningiomas. J Neurooncol 70: 183-202, 2004

63. Harada T, Irving RM, Xuereb JH, Barton DE, Hardy DG, Moffat DA,

Maher ER: Molecular genetic investigation of the neurofibromatosis

type 2 tumor suppressor gene in sporadic meningioma. J Neurosurg

84:847-851, 1996.

64. Antinheimo J, Sankila R, Carpén O, Pukkala E, Sainio M, Jääskeläinen

J: Population-based analysis of sporadic and type 2 neurofibromatosis-

associated meningiomas and schwannomas. Neurology 54:71–78,

2000

65. Perry A, Cai DX, Scheithauer BW, Swanson PE, Lohse CM, Newsham

IF, Weaver A, Gutmann DH: Merlin, DAL-1, and progesterone receptor

expression in clinicopathologic subsets of meningioma: a correlative

immunohistochemical study of 175 cases. J Neuropathol Exp Neurol

59:872-879, 2000

References

81

66. Zang KD: Meningioma: a cytogenetic model of a complex benign

human tumor, including data on 394 karyotyped cases. Cytogenet Cell

Genet 93: 207-220, 2001

67. Simon M, Bostrom JP, Hartmann C: Molecular genetics of

meningiomas: from basic research to potential nclinical applications.

Neurosurgery 60:787- 798, 2007.

68. Wen PY, Drappatz J: Novel therapies for meningiomas. Expert Rev

Neurother 6:1447-1464, 2006.

69. Yamasaki F, Yoshioka H, Hama S, Sugiyama K, Arita K, Kurisu K:

Recurrence of meningiomas. Influence of vascular endothelial growth

factor expression. Cancer 89:1102–1110, 2000

70. Magrassi L, De-Fraga C, Conti L, Butti G, Infuso L, Govoni S, et al:

Expression of the JAK and STAT superfamilies in human

meningiomas. J Neurosurg 91:440–446, 1999

71. The Lancet Neurology, volume 5, Riemenschneider MJ, Perry A,

Reifenberger G: Histological classification and molecular genetics of

meningiomas, pp 1045–1054, copyright 2006, with permission from

Elsevier

72. Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, Jouvet A,

Scheithauer BW, Kleihues(2007). The 2007 WHO Classification of

Tumours of the Central Nervous System Acta Neuropathol 2007

Aug;114(2):97-109

73. Nakau, H., et al., Pathologic significance of meningeal enhancement

("flare sign") of meningiomas on MRI. Surg Neurol, 1997. 48(6): p.

584-90; discussion 590-1

74. Bendszus M, Rao G, Burger R, et al. Is there a benefit of preoperative

meningioma embolization? Neurosurgery 2000;47(6):1306-1311,

discussion 1311-1312

References

82

75. Dowd CF, Halbach VV, Higashida RT. Meningiomas: the role of

preoperative angiography and embolization. Neurosurg Focus

2003;15(1):E10

76. Klutmann, S., et al., Somatostatin receptor scintigraphy in postsurgical

follow-up examinations of meningioma. J Nucl Med, 1998. 39(11): p.

1913-7

77. Soichi Oya, M.D., Ph.D., Seon-Hwan Kim, M.D., Ph.D., Burak Sade,

M.D., and Joung H. Lee, M.D: Natural history of intracranial

meningiomas. J Neurosurg 114:1250–1256, 2011

78. Simpson D: The recurrence of intracranial meningiomas after surgical

treatment. J Neurol Neurosurg Psychiatry 1957; 20:22-39

79. Kobayashi K, Okudera H, Tanaka Y. Surgical considerations on skull

base meningioma. Paper presented at the First International Skull

Base Congress, June 18, 1992, Hanover, Germany

80. Kinjo T, Al-Mefty O, Kanaan I: Grade zero removal of supratentorial

convexity meningiomas. Neurosurgery 1993; 33:394-399

81. Yamasaki F, Yoshioka H, Hama S, etal: Recurrenceof

meningiomas. Cancer 2000; 89:1102-1110

82. Iwai Y, Yamanaka K, Yasui T, et al: Gamma Knife surgery for skull

base meningiomas. The effectiveness of low-dose treatment. Surg

Neurol 1999; 52:40-44.

83. Roche PH, Pellet W, Fuentes S, et al: Gamma Knife radiosurgical

management of petroclival meningiomas: results and indications. Acta

Neurochir (Wien) 2003; 145:883-888.

84. Stafford SL, Pollack BE, Foote RL, et al: Meningioma radiosurgery:

tumor control, outcomes, and complications among 190 consecutive

patients. Neurosurgery 2001; 49:1029-1037.

References

83

85. Zachenhofer I, Wolfsberger S, Aichholzer M, et al: Gamma-Knife

radiosurgery for cranial base meningiomas: experience of tumor

control, clinical course, and morbidity in a follow-up of more than 8

years. Neurosurgery 2006; 58:28-36.

86. Noel G, Bollet MA, Calugaru V, et al: Functional outcome of patients

with benign meningiomas treated by 3D conformal irradiation with a

combination of photons and protons. Int J Radiat Oncol Biol

Phys 2005; 62:1412-1422.

87. Mathiesen T, Kihlström L, Karlsson B, Lindquist C: Potenital

complications following radiotherapy for meningiomas. Surg

Neurol 2003; 60:193-200.

88. Kaido T, Hoshida T, Uranishi R, et al: Radiosurgery-induced brain

tumor. Case report. J Neurosurg 2001; 95:710-713.

89. Klenishcmidt-Demasters BK, Kang JS, Lillehei KO: The burden of

radiation-induced central nervous system tumours: a single

institutions's experience. J Neuropathol Exp Neurol 2006; 65:204-216.

90. Sheehan J, Yen CP, Steiner L: Gamma Knife surgery-induced

meningioma. Report of two cases and review of the literature. J

Neurosurg 2006; 105:325-329.

91. Yu JS, Yong WH, Wilson D, Black KL: Glioblastoma induction after

radiosurgery for meningioma. Lancet 2000; 356:1576-1577.

92. Milker-Zabel S, Zabel-du Bois A, Huber P, et al: Fractionated

stereotactic radiation therapy in the management of benign cavernous

sinus meningiomas: long-term experience and review of the

literature. Strahlenther Onkol 2006; 182:635-640.

93. Rowe J, Grainger A, Walton L, et al: Risk of malignancy after Gamma

Knife stereotactic radiosurgery. Neurosurgery 2007; 60:60-66.

References

84

94. Guthrie BL, Carabell SC, Laws Jr ER: Radiation therapy for intracranial

meningiomas. In: Al Mefty O, ed. Meningiomas, New York: Raven

Press; 1991:255

95. Grunberg SM, Weiss M: Lack of efficacy of megestrol acetate in the

treatment of unresectable meningioma. J Neurooncol 8: 61–65, 1990

96. Grunberg SM, Weiss MH, Spitz IM, Ahmadi J, Sadun A, Russell CA, et

al: Treatment of unresectable meningiomas with the antiprogesterone

agent mifepristone. J Neurosurg 74:861–866, 1991

97. Goodwin JW, Crowley J, Eyre HJ, Stafford B, Jaeckle KA, Townsend

JJ: A phase II evaluation of tamoxifen unresectable or refractory

meningiomas: a Southwest Oncology Group Study. J Neurooncol

15:73–77, 1993

98. Kaba SE, DeMonte F, Bruner JM, Kyritsis AP, Jaeckle KA, Levin V, et

al: The treatment of recurrent unresectable and malignant

meningiomas with interferon alpha-2B. Neurosurgery 40: 271–275,

1997

99. Wöber-Bringöl Ç, Wöber C, Marosi C, Prayer D: Interferon-alfa- 2b for

meningioma. Lancet 345:331, 1995

100. Schrell UMH, Rittig MG, Anders M, Koch UH, Marschalek R,

Kiesewetter F, et al: Hydroxyurea for the treatment of unresectable and

recurrent meningiomas. II. Decrease in the size of meningiomas in

patients treated with hydroxyurea. J Neurosurg 86:845–852, 1997

101. Newton HB, Slivka MA, Stevens C: Hydroxyurea chemotherapy for

unresectable or residual meningioma. J Neurooncol 49: 165–170, 2000

102. Mason WP, Gentili F, Macdonald DR, Hariharan S, Cruz CR, Abrey LE:

Stabilization of disease progression by hydroxyurea in patients with

recurrent or unresectable meningioma. J Neurosurg 97:341–346, 2002

References

85

103. Chamberlain MC, Tsao-Wei D, Groshen S: Temozolomide for

treatment resistant recurrent meningioma. Neurology 62: 1210–1212,

2004

104. Todo T, Adams EF, Fahlbusch R: Inhibitory effect of trapidil on human

meningioma cell proliferation via interruption of autocrine growth

stimulation. J Neurosurg 1993; 78:463-469.

105. Chamberlain MC, Glantz MJ, Fadul CE: Recurrent meningioma:

salvage therapy with sandostatin. Neurology 69:969–973, 2007

106. McCutcheon IE, Flyvberg A, Hill H, et al: Antitumor activity of the

growth hormone receptor antagonist pegvisomant against human

meningiomas in nude mice. J Neurosurg 2001; 94:487-492.

107. Korshunov A, Shishkina L, Golanov A (2003). Immunohistochemical

analysis of p16INK4a, p14ARF, p18INK4c, p21CIP1, p27KIP1 and

p73 expression in 271 meningiomas correlation with tumor grade and

clinical outcome. Int J Cancer 104: 728-734

108. Moller ML, Braendstrup O: No prediction of recurrence of meningiomas

by PCNA and Ki-67 immunohistochemistry. J

Neurooncol 1997; 34:241-246

109. Nakasu S, Nakasu Y, Nakajima M, et al: Preoperative identification of

meningiomas that are highly likely to recur. J Neurosurg 1999; 90:455-

462

110. Behari S, Giri PJ, Shukla D, Jain VK, Banerji D: Surgical strategies for

giant medial sphenoid wing meningiomas: A new scoring system for

predicting extent of resection. Acta Neurochir (Wien) 150:865-877,

discussion 877, 2008

References

86

111. Klink DF, Sampath P, Miller NR, Brem H, Long DM: Long-term visual

outcome after nonradical microsurgery patients with parasellar and

cavernous sinus meningiomas. Neurosurgery 47:24-31, discussion 31-

22, 2000

112. Sindou M, Wydh E, Jouanneau E, Nebbal M, Lieutaud T: Longterm

follow-up of meningiomas of the cavernous sinus after surgical

treatment alone. J Neurosurg 107:937-944, 2007

113. Ugrumov VM, Ignatyeva GE, Olushin VE, Tigliev GS, Polenov AL:

Parasellar meningiomas: Diagnosis and possibility of surgical treatment

according to the place of original growth. Acta Neurochir Suppl (Wien)

28:373–374, 1979

114. Konovalov AN, Fedorov SN, Faller TO, Sokolov AF, Tcherepanov AN:

Experience in the treatment of the parasellar meningiomas. Acta

Neurochir Suppl (Wien) 28:371–372, 1979.

115. Ojemann RG: Meningiomas of the basal parapituitary region: Technical

considerations. Clin Neurosurg 27:233–262, 1980.

116. Pompili A, Derome PJ, Visot A, Guiot G: Hyperostosing meningiomas

of the sphenoid ridge—clinical features, surgical therapy, and long-term

observations: Review of 49 cases. Surg Neurol 17:411–416, 1982.

117. Fohanno D, Bitar A: Sphenoidal ridge meningioma. Adv Tech Stand

Neurosurg 14:137–174, 1986.

118. Risi P, Uske A, de Tribolet N: Meningiomas involving the anterior

clinoid process. Br J Neurosurg 8:295–305, 1994

119. Day JD: Cranial base surgical techniques for large sphenocavernous

meningiomas: Technical note. Neurosurgery 46:754–760, 2000

120. Goel A, Gupta S, Desai K: New grading system to predict resectability

of anterior clinoid meningiomas. Neurol Med Chir (Tokyo) 40:610-616;

discussion 616-617, 2000

References

87

121. Kaye AH: Surgical management of clinoidal meningiomas.

Neurosurgery 48:1019–1020, 2001

122. Samii M, Tatagiba M: Surgical management of clinoidal meningiomas.

Neurosurgery 48:1020, 2001

123. Knosp E, Müller G, Perneczky A: The blood supply of the cranial

nerves in the lateral wall of the cavernous sinus, in Dolenc VV (eds):

The Cavernous Sinus. Berlin, Springer-Verlag, 1987, pp 60–68.

124. Krisht A, Barnett DW, Barrow DL, Bonner G: The blood supply of the

intracavernous cranial nerves: An anatomic study. Neurosurgery

34:275– 279, 1994

125. Larsen JJ, van Loveren HR, Balko MG, Tew JM Jr: Evidence of

meningioma infiltration into cranial nerves: Clinical implications for

cavernous sinus meningiomas. J Neurosurg 83:596–599, 1995

126. Kotapka MJ, Kalia KK, Martinez AJ, Sekhar LN: Infiltration of the

carotid artery by cavernous sinus meningiomas. J Neurosurg 81:252–

255, 1994

127. Shaffrey ME, Dolenc VV, Lanzino GL, Wolcott WP, Shaffrey CI:

Invasion of the internal carotid artery by cavernous sinus meningiomas.

Surg Neurol 52:167–71, 1999.

128. Hirsch WL, Sekhar LN, Lanzino G, Pomonis S, Sen CN: Meningiomas

involving the cavernous sinus: Value of imaging for predicting surgical

complications. AJR Am J Roentgenol 160:1083–1088, 1993

129. Michael E. Sughrue, M.D Modern surgical outcomes following surgery

for sphenoid wing meningiomas, Clinical article; Journal of

Neurosurgery Jul 2013 / Vol. 119 / No. 1, Pages 86-93

130. Langevin CJ, Hanasono MM, Riina HA, Stieg PE, Spinelli HM: Lateral

transzygomatic approach to sphenoid wing meningiomas.

Neurosurgery 67 (2 Suppl Operative):377–384, 2010

References

88

131. Mirimanoff RO, Dosoretz DE, Linggood RM, Ojemann RG, Martuza RL:

Meningioma: Analysis of recurrence and progression following

neurosurgical resection. J Neurosurg 62:18–24, 1985

132. Mathiesen T, Lindquist C, Kihlstrom L, Karlsson B: Recurrence of

cranial base meningiomas. Neurosurgery 39:2–7, 1996

133. Basso A, Carrizo A: Sphenoid ridge meningiomas, in Schmidek HH

(ed): Operative Neurosurgical Techniques: Indications, Methods, and

Results. Philadelphia, W.B. Saunders, 2000, pp 316–324

134. DeMonte F: Surgical treatment of anterior basal meningiomas. J

Neurooncol 29:239–248, 1996

135. Benjamin V, McCormack B: Surgical management of tuberculum sellae

and sphenoid ridge meningiomas, in Schmidek HH (ed): Operative

Neurosurgical Techniques: Indications, Methods, and Results.

Philadelphia, W.B. Saunders, 2000, pp 305–315

136. Kattner KA, Fukushima T: Management of vascular invasion during

radical resection of medial sphenoid wing meningiomas. Skull Base

11:99–104, 2001

Sree Chitra Tirunal Institute for Medical Sciences &

Technology

Proforma for patients with sphenoid wing meningiomas

A. GENERAL INFORMATION:

1.Name 2. age

3. Sex (Male/Female)

4. hospital no.

5. address

6. Contact no.

8.Date of admission 9. Date of discharge/death

B. PRESENTATION AND HISTORY:

1. Memory disturbances (recent /past)

2. Behavioural problems (yes/no)

3. Headache (yes/no)(mild, moderate, severe)

4. Raised ICP

5. Seizure (SPS, CPS, GTCS)

6. Focal deficit (motor/ sensory/cranial nerves)

7. Visual deficit (acuity, field/none)

8. Incidentally detected (yes/no)

10. Duration of symptoms……………………. 11. History of radiation exposure (yes/no)

12. History of trauma (yes/no) 13. Family history- (meningioma/others tumours)

14. Syndromic association

C. EXAMINATION :

1. neurocutaneous markers

2. motor deficits

3. Cranial nerves involvement (yes /no)

4. Visual deficit (acuity - ……………. / field defect- ……………………………………….)

D. IMAGING:

1. CT scan: 1a. NECT: hypodense/Isodense/Hyperdense/Mixed/ Calcification

1b.CECT: homogenous/ Heterogenous/ Non- enhancing

1c. Bone changes: Normal/ Hyperostosis/ Bone erosion

2. MRI : 2a. T1WI: Hypontense/isointense/ Hyperintense

2b. T2WI: Hypontense/ Isointense/Hyperintense

2c. contrast: Homogenous/ Heterogenous/ Cystic changes

3. MRS (if done) 4.DWI-

5.Size of lesion-…………………………………

7. DSA : a. Feeders- ECA/ICA/ both/none

b. ICA involvement- narrowing/irregularity/displacement/total occlusion

c. Cross circulation (good/poor)

E. LOCATION:

Medial (clinoidal)/ middle/ lateral (pterional)/ en-plaque

F.SURGERY / Date:

1. Simpson’s grade of excision : grade I / II/ III/ IV/ V

2. Craniotomy: frontotemporal/ FTOZ/FTZ

3. Drilling of sphenoid bone : extradural / intradural

4. Hyperostosis (clinoid/ lesser wing/greater wing/ convexity/ orbital roof/lateral wall)

5. Vascularity (intraoperative)- (mild/mod/high)

6. Plane of dissection (Arachnoid plane) of tumour (good/ patchy/ poor all around)

7. Vascular injury intraoperative (yes/no)

8. Intraoperative finding of major blood vessel (encasement/displaced)

9. Optic canal de-roofed (yes/no)

10. Intraoperative finding of Cavernous sinus involvement (yes/no)

G. COMPLICATIONS post operative: CLINICAL:

1. Motor weakness (improved/ static/ worsening)

2.Visual deficit (acuity: improved/ static/ worsening )

(field : improved/ static/ worsening)

3. cranial nerves involvement ( yes/no)

3a. 3rd

CN (partial/complete)

3b. 4th

CN

3c. 5th

CN (sensory/ motor)

3d. 6th

CN (unilateral/ bilateral) 3e. other cranial nerves

4. Behavioural problems (yes/no) 5. DVT/PE (yes/no)

6. Meningitis (yes/no) 7. CSF rhinorrhoea- (yes/no)

8. Seizures 9. Horner’s syndrome (yes/no)

H. RADIOLOGICAL COMPLICATION:

1. Infarct : none/ small (perforators)/ large arterial territory)

2. Hematoma: no mass effect/mass effect/none

3.Residue (yes/no)

4.Recurrence-(yes/no) 5.Time to recurrence-

I.HISTOPATHOLOGY

1. WHO Grade I/ Grade II/Grade III 2. Specify HPR-

J. ADJUVANT THERAPY

1.Radiotherapy- EBRT/ Conformal RT/ SRT/SRS

K. FOLLOW UP- Karnofsky Performance Score /vision

1. At discharge / 6 weeks /6 months / 1 year / 2 year / total duration

L. MORTALITY(yes/no)

1. perioperative/ follow up (time period)

M . RESURGERY : Yes/ No

ABBREVIATIONS

1) CNS - Central Nervous System

2) CN - Cranial nerve

3) CS - Cavernous sinus

4) CT - Computerised Tomogram

5) D/s - Discharge

6) EBRT - External Beam Radiotherapy

7) F/U - Follow Up.

8) GCS - Glassgow Coma Scale

9) GTR - Gross Total Resection

10) HM - Hand movement

11) HPR - Histopathological Report

12) HSE - Herpes Simplex Encephalitis

13) ICU - Intensive care unit

14) IFN α - Interferon α

15) ICA - Internal cerebral artery

16) KPS - Karnofsky performance score

17) MCA - Middle cerebral artery

18) MRI - Magnetic Resonance Imaging

19) MSWM - Medial sphenoid wing meningioma

20) OCP - Oral contraceptive pills

21) OR - Odds Ratio

22) PDGFR - Platelet growth derived Growth Factor Receptor

23) PFS - Progression free survival

24) PL - Perception of light

25) PR - Progesterone receptor

26) RT - Radiotherapy

27) SRS - Stereotactic radiosurgery

28) VEGFR - Vascular endothelial growth factor receptor

Na

me

Ag

e

f / m

Ho

sp

ital n

o.

Rrig

ht/ le

ft

du

ratio

n o

f sym

p in

mo

nth

s

He

ad

ach

e

Ra

ise

d IC

T

S

z (

foca

l / g

en

)

GC

S

Be

ha

vio

ura

l pro

ble

ms

Me

mo

ry

mo

tor

de

ficit

pre

op

. vis

ion

acu

ity

field

cu

t

po

st o

p v

isio

n s

tatu

s

pre

op

CN

de

ficits

po

st o

p n

ew

CN

de

ficits

Siz

e(1

- 2

)

(>2

-4)

(>4

cm

)

ca

lci

Hyp

ero

sto

sis

DS

A-C

ross c

irc.

CS

invo

lv.

su

rge

ry -

FT

Sim

pso

n's

gra

de

OC

de

ro

ofe

d

en

ca

se

me

nt

go

od

ara

ch

no

id p

lan

e

infa

rct

co

mp

lica

tion

s

HP

R

RT

Pre

op

KP

S

KP

S a

t d

/s

La

st K

PS

F/ U

du

ratio

n in

ye

ars

mo

rta

lity

Re

sid

ue

Re

cu

rre

nce

Tim

e to

re

c. in

ye

ars

Re

su

rge

ry

rem

ark

s

Mohammed KP 44 m 293885 L 12 0 0 G 13/15 0 0 1 0 0 U none none 0 0 1 0 1 na 1 1 IV 0 1 0 perf H M,T 0 40 60 70 4 0 1 1 2 0 follow up

Nirmala A 36 f 290212 R 6 1 0 0 0 0 0 no PL 0 cnbt 3rd 3rd 0 0 1 1 1 1 1 1 IV 0 1 0 ICA H M,T 1 70 40 died 1 1 1 3x 4x ICA injury, death <6months

Saharban K 24 f 305468 L 12 1 0 0 0 0 0 PL 0 died 3rd 3rd 0 1 0 0 1 na 1 1 IV 1 1 1 0 Sz, DVT M,T 0 70 died 0 0 1 0 - - 0 died on 5th POD, PE

Lisamma Samuel 44 f 254850 L 12 1 1 G 0 0 0 no PL 0 U, no PL none none 0 0 1 0 1 1 1 1 IV 1 1 1 0 0 M 0 70 80 90 6 0 1 0 0 0 Improved, left eye no PL

Murugan M 26 m 257899 L 1 1 0 0 0 0 0 no PL 0 U ,no PL none none 0 1 0 0 1 na 1 1 IV 0 1 0 perf H T 0 70 70 S ,50 7 0 1 0 0 Left MCA infarct in dec 2010

Syamala T 42 f 286688 R 12 1 1 0 0 0 0 0 0 U none 3rd 0 1 0 0 1 1 1 1 I 1 1 1 0 0 T 0 70 80 90 4 0 0 0 0 follow up

Rajalakshmi R 51 f 344061 L 8 1 0 0 0 1 0 0 0 U none none 0 1 0 0 1 na 1 1 II 0 1 1 0 0 M,T 0 80 90 90 1 0 0 0 0 improved

Lalithambika T 43 f 336512 R 6 0 0 G 1 0 0 1 0 U none none 1 0 0 0 1 1 1 I 1 1 1 0 Sz, B T 0 70 80 90 2 0 0 0 0 0 psychiatry problem

Rajan V 42 m 342334 L 1 0 0 F 0 0 0 0 0 U none 3rd 0 1 0 0 1 1 1 1 IV 0 1 0 0 Sz atyp 1 80 80 90 1 0 1 0 0 0 post RT, small residue

Shylaja 36 f 236279 R 8 1 1 0 0 0 0 0 1 I none 3rd 1 0 0 0 0 1 1 FTOZ IV 0 1 0 perf H, B M,T 0 60 70 70 5 0 1 1 2 0 follow up

Lilly Prascal 47 f 9702888 R 12 0 0 0 0 0 0 no PL 0 U, no PL none none 0 1 0 0 1 1 1 1 I 0 0 1 0 0 M,F,T 0 80 80 S, 70 16 0 1 1 12 1 stroke in 2007, sept.2011, f/u

Manoj kG 33 m 283880 L 4 1 1 0 0 0 0 1 1 W, no PL none none 0 1 0 0 0 0 1 1 II 0 0 1 0 B M,T 0 70 70 80 4 0 0 0 0 follow up

Subaida ashraf 41 f 275341 L 3 1 0 0 0 0 0 1 0 W none none 1 0 0 0 1 1 1 II 0 0 1 0 MN M 0 70 80 90 4 0 1 0 0 follow up

Jyoti Das 26 f 303649 L 6 1 0 0 0 0 0 0 0 U frozen frozen 1 0 0 0 1 na 1 1 II 1 1 1 0 0 T 0 80 90 90 1 0 1 0 0 residue, referred for SRS , no F/U

Shiny Thomas 31 f 265844 R 24 1 0 0 0 0 0 1 1 W, I 6th none 0 1 0 1 1 na 1 1 I 0 0 1 0 0 M,T 0 80 90 90 5 0 0 0 0 0 seizures

Nadasha Ravi 50 m 320408 L 6 1 0 0 0 0 0 0 0 U none 3rd 0 1 0 0 1 1 1 1 II 0 1 1 0 0 M,T 0 80 80 90 2 0 0 0 0 0 improved

padmanabhan 45 m 317900 R 2 1 0 0 0 0 0 0 0 W none 3rd 0 1 0 0 0 1 1 FTOZ II 0 1 0 0 0 M,T 1 80 70 90 3 0 0 1 2 1 first SX in KMC , mangalore

Santhamma 58 f 218285 R 8 1 0 0 0 0 0 0 0 U none none 1 0 0 0 1 1 1 1 II 0 0 0 0 B M 0 80 80 90 9 0 0 0 0 0 improved

Stella D 42 f 214102 L 1 1 1 0 1 1 1 1 0 W 7th umn frozen 0 0 1 0 0 0 1 1 II 0 0 0 0 Sz, MN T 0 70 80 90 8 0 1 0 0 0 improved

Asokan Pillai B 43 m 206695 L 4 1 1 0 4/15 0 cnbt cnbt cnbt cnbt cnbt 0 0 1 0 1 1 II 0 1 0 PCA H M,T 0 30 60 90 10 0 0 0 0 0 improved, left Pca infarct Razeeda Jamal TA 31 f 197264 L 3 1 0 0 0 0 0 0 0 U none 3rd 1 0 0 0 1 1 1 1 II 0 0 1 0 CSF rhi M 0 80 80 90 10 0 0 0 0 0 improved, TP shunt for CSF rhin

Sudhakaran P 53 m 190741 L 1 1 1 0 0 0 0 0 W none 3rd 1 0 0 0 0 na 1 1 II 0 0 1 0 0 M 0 80 80 70 10 0 0 0 0 0 HSE in 2005, memory

Lalithaambika PU 44 f 181908 R 36 1 0 G 0 0 1 1 1 U none frozen 0 0 1 0 1 1 1 FTOZ IV 0 1 0 0 Sz, Mn T 1 70 80 70 12 0 1 1 4 1 F/U

Mary Bennet V 46 f 253000 L 3 1 1 0 0 0 0 0 0 U none none 1 0 0 0 0 na 1 1 II 0 0 1 0 0 M 1 80 90 90 7 0 0 1 2 1 residue stable

Geetha S 20 f 253635 R 3 1 1 G 0 0 0 1 1 W frozen frozen 0 1 0 0 1 na 1 1 IV 0 1 0 0 Sz atyp 1 70 70 90 1 0 1 1 0 no follow up

Nalini Kv 61 f 282120 R 12 1 0 0

mmse

11/30 1 1 0 cnbt cnbt U none none 0 1 0 0 1 0 1 1 II 0 0 0 0 MN T 0 60 70 90 5 0 1 0 0 improved

Karrupaiah 62 m 279117 R 1 1 0 0 1 0 1 1 0 U none 3rd 0 0 1 0 1 1 1 1 II 0 1 1 perf H, MN atyp 0 70 70 70 6wk 1 1 0 0 cardiac arrest at 6weeks

Chellamma R 41 f 269479 L 6 1 1 0

mmse

14/30 0 0 0 0 1 U none none 0 0 1 0 1 1 1 1 I 0 0 1 0 0 F 0 70 90 0 6wk 0 0 0 0 no follow up

Jayabal R 54 m 263858 R 3 1 1 F 5/15. 0 0 1 cnbt cnbt died cnbt died 0 0 1 0 1 na 1 1 II 0 1 0 MCA H M,T 0 30 died 0 0 1 1 0 0 0 died, right MCA infarct, POD 10th

MN - Meningitis U - Unchanged M - Meningiothelial meningioma Atyp - Atypical Meningioma G - Generalized seizure

Sz - Seizure I - Improved T - Transitional meningioma HM - Hand movement F - Focal seizure

B - Behavioural problem W - Worsened F - Fibroblastic Meningioma PL - Perception of light S - Stroke

H - Hemiparesis

Medial Sphenoid Wing Meningioma with cavernous sinus involvement (Group II) n = 29

Na

me

Ag

e

se

x

Ho

sp

ita

l n

o.

sid

e (

rig

ht/le

ft)

du

ratio

n o

f sym

p. In

mo

nth

s

He

ad

ach

e

Ra

ise

d IC

T

Sz (

foca

l /g

en

)

Be

ha

vio

ura

l p

rob

lem

s

Me

mo

ry

mo

tor

de

ficit

Pre

op

. vis

ion

/acu

ity

fie

ld d

eficit

po

st o

p. vis

ion

sta

tus

pre

op

CN

de

ficits

po

st o

p n

ew

CN

de

ficits

Siz

e(1

- 2

)

(>2

-4)

(>4

cm

)

ca

lcific

atio

n

Hyp

ero

sto

sis

DS

A-C

ross c

irc.

CS

in

vo

lve

me

nt

su

rge

ry-

FT

Sim

so

n's

gra

de

Op

tic c

an

al d

e r

oo

fed

ICA

en

gu

lfm

en

t

go

od

ara

ch

no

id p

lan

e

co

mp

lica

tio

n

HP

R

RT

KP

S a

t d

/s

La

st K

PS

F/ U

du

ratio

n in

ye

ars

Mo

rta

lity

Re

sid

ue

Tim

e to

re

cu

rre

nce

Re

su

rge

ry

Re

ma

rks

Krishna Kutty Nair 62 m 291238 R 3 1 0 G 0 0 0 0 1 U none none 0 1 0 0 0 0 0 1 I 0 0 1 0 T 0 90 90 3 0 0 0 0 improved

Thankam TP 55 f 318095 R 3 1 0 0 0 0 0 0 0 U none none 1 0 0 1 0 0 0 1 II 0 0 0 0 F,T 0 90 100 1 0 0 0 0 improved

NisaruddinK 40 m 322083 L 4 1 0 F 0 0 0 0 0 U none none 0 1 0 0 0 0 0 1 I 0 0 1 0 M,T 0 80 90 2 0 0 0 0 improved

Ramu N 57 m 321938 L 12 0 0 0 0 0 0 no pl 0 U, no PL none 6th 0 0 1 0 0 1 0 1 III 0 1 0 0 F,T 0 80 100 2 0 1 0 0 follow up

Sajimon KK 36 m 274757 L 1 1 0 G 0 0 0 0 0 U none none 0 1 0 0 1 1 0 1 I 0 0 1 0 M,T 0 100 100 5 0 0 0 0 improved

Mohanan PI 40 m 233355 R 6 0 0 0 0 0 0 no PL 0 U, no PL none none 0 1 0 0 0 1 0 1 II 0 0 0 0 M 0 90 90 4 0 0 0 0 no PL

Fathima K 37 f 254342 R 2 1 0 0 0 0 0 0 0 U none none 0 1 0 0 0 0 0 1 II 0 0 0 0 P 0 90 90 2 0 0 0 0 lost follow up

Ponnama TC 51 f 249005 L 4 1 0 0 0 0 0 no PL 0 U, no PL none none 0 0 1 0 0 0 0 1 II 0 0 0 0 M 0 80 80 6 0 0 0 0 no PL

pennama Daniel 52 f 319920 R 3 1 1 0 1 1 0 1 0 W, only PL none none 0 1 0 0 0 0 0 1 III 0 1 0 0 M 0 80 80 1 0 0 0 0 follow up

Rema M 26 f 340066 L 6 1 0 0 0 0 0 no PL 0 U, no PL none none 0 1 0 0 0 1 0 1 II 0 0 0 0 M 0 80 80 1 0 0 0 0 folow up, no PL

Marykutty T 59 f 281587 L 3 0 0 0 0 0 0 1 1 I none none 1 0 0 0 0 0 0 1 II 0 1 0 0 T 0 80 90 2 0 0 0 0 improved

Omana G 42 f 239878 L 2 1 0 G 0 0 0 0 0 W none 3rd 1 0 0 0 0 1 0 1 II 0 1 0 0 Atyp 0 80 90 7 0 0 0 0 status quo,

Suma Jacob 39 f 236501 R 2 0 0 0 0 0 0 1 1 I none none 0 1 0 0 0 1 0 1 I 0 0 1 0 T 0 90 90 7 0 0 0 0 improved

Jessy Anith 41 f 337795 L 4 1 1 0 0 0 0 1 0 W none 3rd 0 1 0 0 1 1 0 FTOZ II 0 0 0 0 Atyp 0 80 90 1.6 0 0 0 0 improved

Jayalatha Satheesh 31 f 280128 R 6 1 0 G 0 0 0 1 0 U none none 0 1 0 0 0 0 0 1 II 0 0 0 0 M,T 0 90 100 4 0 0 0 0 improved

Ratha V 62 f 280675 L 1 0 0 G 0 0 0 0 0 U none none 0 1 0 0 1 1 0 1 I 1 0 1 0 M,T 0 90 100 1 0 0 0 0 lost follow up

Thulasi bai P 51 f 311013 R 12 1 0 G 0 0 0 0 0 U none 3,4,6CN 0 1 0 0 1 0 0 1 I 0 0 0 0 M,F 0 90 100 2 0 0 0 0 improved

Murugeswaran 44 m 310856 R 3 1 1 0 0 1 0 0 U 3rd I 0 1 0 0 1 0 0 1 I 0 0 1 0 A 0 90 90 2 0 0 0 0 improved

Badarnisha 57 f 307725 R 2 1 0 0 0 0 0 no PL 0 U, no PL none none 0 0 1 0 1 1 0 1 II 0 0 0 0 Atyp 1 90 90 0.5 1 0 0 no follow up, death < 1yr

Rosamma Mathai 48 f 357591 L 24 1 0 0 0 0 0 0 0 U none 3rd 1 0 0 0 1 0 0 0 I 1 0 1 CSF rhinor T 0 80 90 2 0 0 0 0 improved

Subhagan B 50 m 288998 L 6 1 0 0 1 1 0 1 1 W, HM none none 1 0 0 0 0 1 0 1 III 1 1 1 DVT M,T 0 80 100 4 0 0 0 0 left eye HM

Selvamam A 58 f 284317 R 12 1 0 0 0 1 1 0 0 U 7 umn none 0 0 1 0 1 1 0 1 II 0 0 1 0 M,T 0 80 100 4 0 0 0 0 improved

Naga Lakshmi 51 f 344700 L 2 1 0 0 0 0 0 0 0 U none none 0 1 0 0 1 1 0 1 II 0 0 1 0 T 0 90 90 1 0 0 0 0 improved

Mini Ninan 40 f 320481 L 12 1 0 0 0 0 0 0 1 W, noPL none none 0 1 0 1 0 0 1 II 0 1 1 0 M,A 0 80 80 3 0 0 0 0 no PL

Irulayee M 41 f 334054 L 18 1 0 0 1 0 0 0 0 U none 3rd 0 0 1 1 0 1 0 1 IV 0 1 0 seizures M,T 0 80 90 2 0 0 1yr 0 RT

Soosamma Jacob 48 f 335958 R 6 1 0 0 0 0 0 0 1 I none 3rd 1 0 0 0 0 1 0 1 II 0 0 0 motor T 0 70 90 2 0 0 0 0 improved

Mungeswaran 44 m 310856 R 3 1 1 0 1 1 0 0 0 U none none 0 1 0 1 1 0 0 1 IV 0 1 0 0 A 0 80 90 2 0 1 0 0 improved

Kamimozhi 31 f 313100 L 1 1 0 0 0 1 0 0 0 U none none 1 0 0 0 0 1 0 1 IV 0 0 0 0 M 0 90 100 3 0 1 0 0 status quo

Pareed T A 32 m 248512 L 6 0 0 G 1 1 0 0 0 W none 3rd 1 0 0 1 1 1 0 1 II 0 1 0 0 M,T 0 80 80 6 0 0 6yr 0 follow up

Muthuval K 57 f 191773 L 2 1 0 G 0 0 0 HM 0 I none 3rd 1 0 0 0 1 1 0 1 II 1 1 1 0 M 0 90 90 8 0 0 0 0 improved

Komalavathy KG 59 f 197951 L 6 1 0 F 1 1 0 0 0 I none none 0 1 0 0 1 1 0 1 I 0 0 1 CSF rhinor P 0 90 80 11 0 0 8yr 0 follow up

Kumaran M 54 m 261350 L 6 1 0 F 1 1 1 1 0 I none none 0 1 0 0 1 1 0 1 IV 1 1 0 0 M 0 80 80 5 0 1 1yr 0 follow up, seizures

Habeeba N 45 f 276100 L 2 1 0 0 0 0 0 0 0 W none none 1 0 0 0 0 0 0 1 IV 1 1 0 0 T 0 80 90 5 0 1 0 0 seizures

Sarasa K 44 f 186752 L 2 1 0 0 0 0 0 1 1 I none none 1 0 0 0 1 1 0 1 I 1 0 1 0 T 0 80 80 11 0 0 0 0 psychiatry problems

Sarojini KK 52 f 194512 R 6 1 0 0 0 0 0 HM 0 W, noPL none none 0 1 0 1 1 0 0 1 II 1 0 1 0 T 0 80 90 8 0 0 0 0 no follow up

Esthappan T 62 m 228499 R 3 1 0 0 0 0 0 1 1 I none none 0 1 0 0 1 1 0 1 II 1 1 1 0 Atyp 1 80 80 8 0 0 3yr 1 2nd sx abandoned due to MI

Ameer M 54 m 228184 L 12 0 0 0 1 1 0 0 0 U none none 0 1 0 0 1 1 0 1 II 0 0 1 0 T,A 0 80 100 6 0 0 0 0 first op in 1991, improved

Jolly Ponnachan 47 f 288091 R 4 1 1 0 0 0 0 0 0 U none none 0 0 1 0 1 1 0 1 I 0 0 0 0 Atyp 1 90 90 3 0 0 0 0 improved

Prabha Sreenivas 54 f 263775 L 3 1 0 0 0 0 0 0 0 U none none 0 1 0 0 0 1 0 1 II 0 0 0 0 Atyp 1 80 100 5 0 0 0 0 improved

Balakrishnan K 54 m 307520 L 4 0 0 F 0 0 0 0 0 U none 3rd 0 1 0 0 1 1 0 1 III 0 1 1 0 T 0 90 100 2 0 0 0 0 improved

Sumathi KP 43 f 306276 R 6 1 0 0 0 0 0 0 0 U none none 0 1 0 0 1 1 0 1 IV 0 1 0 0 R 1 80 90 3 0 1 0 0 no residue in repeat scan

Narayanaswamy 65 m 305320 R 24 0 0 0 0 0 0 0 1 U none none 0 1 0 0 0 0 0 1 IV 0 1 1 motor M,T 0 80 90 2 0 1 0 0 incidental, BPPV subsided

Latha P V 44 f 291947 L 3 1 0 0 0 0 0 1 0 U none none 0 1 0 0 1 1 0 1 IV 0 1 1 seizures M 0 80 90 4 0 1 0 0 follow up

U - Unchanged M - Meningiothelial meningioma Atyp - Atypical Meningioma G - Generalized seizure

I - Improved T - Transitional meningioma HM - Hand movement F - Focal seizure

W - Worsened F - Fibroblastic Meningioma PL - Perception of light

Medial Sphenoid Wing Meningioma without cavernous sinus involvement (Group I) n = 43

(group i – without cavernous sinus invo lvement & group ii –with cavernous sinus...

Documents