NEURO-OPHTHALMIC MANIFESTATIONS OF INTRACRANIAL TUMOURS – A CLINICAL PROFILE
Dissertation Submitted for
M.S.Degree(Branch III) Ophthalmology
April 2014.
THE TAMILNADU DR.M.G.R.MEDICAL UNIVERSITY
CHENNAI
CERTIFICATE
This is to certify that this dissertation entitled “NEURO-
OPHTHALMIC MANIFESTATIONS OF INTRACRANIAL
TUMOURS-A CLINICAL PROFILE” is a bonafide work done by Dr.
R.Dhivya under our guidance and supervision in the Neuro-ophthalmology department of Aravind Eye Hospital and Post Graduate Institute of
Ophthalmology, Madurai during the period of her post graduate training in
Ophthalmology for May 2011 – April 2014.
Dr. S.Mahesh kumar Dr.Kowsalya Guide Co-Guide Head of The Department Consultant Neuro-ophthalmology Neuro-ophthalmology Aravind Eye Hospital, Aravind Eye Hospital, Madurai. Madurai
Dr.M.Srinivasan Director, Aravind Eye Hospital, Madurai. .
DECLARATION
I, Dr.R.Dhivya, hereby declare that this dissertation entitled, “NEURO-
OPHTHALMIC MANIFESTATIONS OF INTRACRANIAL
TUMOURS-A CLINICAL PROFILE”, is being submitted in partial fulfilment for the award of M.S. in Ophthalmology Degree by the Tamil
Nadu DR. MGR Medical University in the examination to be held in April
2014.
I declare that this dissertation is my original work and has not formed the basis for the award of any other degree or diploma awarded to me previously.
Dr.R.Dhivya, Aravind Eye Hospital, Madurai.
ACKNOWLEDGEMENT First and foremost I am thankful to Almighty for always being with me and guiding me throughout my life.
I would like to express my heartfelt gratitude to my beloved parents for the dreams they have dreamt and the hardships they have been through to make me stand where I am today. I also thank my husband and my sister who had been supporting me throughout my tougher times.
I take this opportunity to pay respect and homage to
Dr.G.Venkatasamy, our founder.
I am privileged to have on my side Dr.P.Namperumalsamy,
Chairman emeritus and Director of Research, Dr.G.Natchiar, Director emeritus and chief of Department of Neuro-ophthalmology,
Dr.M.Srinivasan, Director emeritus and other scholars at Aravind eye care system who had been a great source of inspiration to us.
I am very grateful to Dr.R.D.Ravindran, Chairman of Aravind Eye care system for having created an environment enriched with all the facilities for learning and gaining knowledge.
Words cannot express my deep sense of gratitude and heartfelt thanks to my mentor and guide Dr.S.Mahesh kumar, Professor Department of
Neuro-ophthalmology who with his able guidance, optimistic attitude and constant encouragement gave me all the confidence and determination to complete my dissertation.
My sincere thanks to Dr.N.Venkatesh Prajna, Director of
Academics, who offered his guidance and support throughout my residency period.
I take the privilege to express my gratitude and humble regards to
Dr.Kowsalya, consultant in Neuro-ophthalmology for her valuable guidance, timely suggestions during my study.
I am grateful to Bio-Statistician, for her guidance in statistical analysis of this study.
My very sincere thanks to Mrs.Kumaragurupari, Senior Librarian for her immediate responses in providing all the articles and academic support required in the completion of this thesis.
I would like to thank the para medical staffs of Neuro-ophthalmology department for their support.
I would fail in my duty if I didn’t thank the countless patients who have been the learning ground for my study and my residency.
CONTENTS PART - I
S. No Title Page No
1. Review of literature 1
Introduction
2. Anatomy of Optic Chiasm 3
3. Chiasmal syndrome 4
4. Pituitary adenoma 7
5. Acoustic neuroma 23
6. Meningioma 28
7. Craniopharyngioma 34
8. Mid Brain and Pineal gland tumours 36
9. Malignant Brain tumours and Secondaries 38
PART - II
Sl.No. Title Page No.
10. Aims & Objectives 41
11. Materials and Methods 42
12. Analysis & Results 46
13. Discussion 71
14. Limitations 75
15. Conclusion 76
16. Bibliography
17. Proforma
18. Master Chart
INTRODUCTION
Intracranial tumors are serious and life-threatening because of its invasive and infiltrative character in the limited space of the intracranial cavity. Primary Brain tumour is one of the major reasons for seeking neurological consultations worldwide. The clinical features and management option depends upon the site, size and type of the tumour1.The clinical features in patients with intracranial tumour may be caused by the influence on hormone secretion/depression or their mass related pressure effect on the surrounding structures or due to development of hydrocephalus1. Some
Intracranial tumours present with ophthalmic abnormalities; these abnormalities could result from their effect on the visual pathway, ocular nerves and orbito-ocular tissues2. Neuro-ophthalmic signs and symptoms of intracranial tumours are visual loss, headache,vomiting, giddiness, double vision, nerve palsies, pupillary abnormalities, ptosis, proptosis,visual field defects and optic nerve head changes like optic atrophy, papilloedema etc.
Visual signs and symptoms form major presentation in certain types of brain tumours and may be of great help in early diagnosis when initial signs are unspecific.
The most common Intracranial tumours that presents with ophthalmic features are Pituitary adenoma, Meningioma, Acoustic schwannoma,
Craniopharyngioma,Glioma, metastatic tumours1 etc.
Patients with intracranial tumours can present with various symptoms like
1. Defective vision
2. Defective visual field/colour vision
3. Headache
4. Vomiting
5. Giddiness/Fainting
6. Seizures
7. Tinnitus
8. Hard of hearing
9. Transient obscuration of vision
10. Double vision etc…,
The major cause for visual field defect is due to compression of optic chiasm known as chiasmal syndrome1.Pituitary adenomas are the most common cause for chiasmal syndrome.
ANATOMY OF OPTIC CHIASM
The optic chiasm is at the junction of two optic nerves. The nasal fibers of each optic nerve decussate (cross) across the chiasm to the opposite side while the temporal fibers are uncrossed to form the optic tract of the same side. This allows the right half of the visual field to end up on the left side of the brain and the left half of the visual field to locate to the left side of the Brain.
At the optic chiasm, 53% of the fibres from the nasal retina cross the midline to join the uncrossed temporal fibers. These nasal fibers carry information from the temporal visual field. Similarly, the temporal fibres carry information from the nasal field.
Optic chiasm is clinically very important because many important structures are located around it. The Pituitary gland is situated below the optic chiasm in the sella turcica. The sella turcica is covered in front by tuberculum sellae and behind by the dorsum sellae. The supraclinoid branches of the internal carotid artery flank the chiasm. The cavernous sinuses are located lateral and inferior to the chiasm. The frontal lobe of the
Brain lies above the chiasm and behind the optic chiasm lies the third ventricles.
CHIASMAL SYNDROME
Compression of fibres of optic chiasm leads to chiasmal syndrome.
Chiasmal syndrome is divided into anterior, middle and posterior.
Anterior chiasmal syndrome involves the junction of the optic nerve and optic chiasm. Middle chiasmal syndrome involves the decussating fibers in the body of the optic chiasm while posterior chiasmal syndrome involves the distal fibers. The classic anterior chiasmal lesion produces central scotoma, and contralateral superotemporal field defect. This is known as
Junctional scotoma6.
Compression of Middle fibres of optic chiasm involve the uncrossed temporal fibres result in a nasal or binasal hemianopia. Lesions in the body of the chiasm most commonly damage the crossing nasal fibers. This leads to a bitemporal hemianopia. Posterior chiasmal syndrome affects the macular fibres which cross more posteriorly. This leads to paracentral bitemporal field defect. Posterior chiasmal compression may also involve the optic tract and cause a contralateral homonymous hemianopia.
Longstanding damage to optic nerve fibres can lead to Optic disc pallor. If the lateral uncrossed fibers are spared then, the pallor appears in a bow-tie configuration6.
In this type of lesion the fibres affected are retinal ganglion cells nasal to the macula in the papillomacular bundle. Compressive lesions often cause headache and may compress the third ventricle leading to hydrocephalus.
The major cause of chiasmal syndrome is compressive lesions like pituitatry adenomas, craniopharyngiomas and meningiomas 5.
Non functional pituitary adenomas can present with visual field defects which may be the earliest manifestation.Field defects are rare in functional pituitary tumours6.
Other causes of chiasmal syndrome are
Ø Gliomas,
Ø Trauma
Ø Metabolic
Ø Toxic
Ø Infectious (very rare)
Gliomas of optic chiasmis commonly associated with
Neurofibromatosis type1.
A : Lesion in right optic nerve – right complete blindness
B : Lesion in Optic chiasm – Bitemporal Hemianopia
C:Lesion in optic tract – Incongruous Homonymous hemianopia
D:Lesion of optic radiation in parietal lobe – Superior quadrantanopia
E:Lesion in visual cortex – Congruous homonymous hemianopia sparing the macula.
Lesion involving the tip of the visual cortex causes congruous homonymous macular defct. Pupillary reflexes are normal and optic atrophy do not occur following visual cortex lesion.
PITUITARY TUMOURS
CLINICAL ANATOMY:
The pituitary gland is known as the master endocrine gland which is of a size of pea situated in a bony cavity called the sella turcica and covered by diaphragm sellae above. Sella turcica is located in the body of the sphenoid bone in the middle cranial fossa.It has three lobes: anterior, intermediate, and posterior. The pituitary gland is connected to hypothalamus by the median eminence by infundibulum or pituitary stalk.
Posteriorly is the dorsum sellae which is continuous with the clivus, inferoposteriorly. The dorsum sellae is terminated laterally by the posterior clinoid process7.
The pituitary gland is situated between the paired cavernous sinuses.
Because of this, lateral extension of pituitary adenoma can cause compression of nerves in cavernous sinus and can present with multiple cranial nerve palsies. Pituitary adenoma is the most common tumour of pituitary gland. Other tumours are pituitary adenocarcinoma and metastasis to the pituitary gland,the most common site of primary tumour being the
Breast.
PITUITARY ADENOMAS
Pituitary adenoma is the most common Benign tumour arising from the pituitary gland. They constituite about 10% of all intracranial tumours and 50 to 80% of pituitary tumours2.
CLASSIFICATION:
Classification of pituitary adenomas is based on their size and hormone secretion7.
A) Based on the size, it is classified in to
1. Microadenoma< 10mm in diameter
2. Macroadenoma> 10mm in diameter
B) Based on hormone secretion,it is classified in to
1. Secretory
2. Non secretory
C) Based on histology,it is classified in to
1. Chromophobic
2. Chromophilic
a) Acidophilic
b) Basophilic
This is on a basis of whether the adenoma take up the stain
(Eosin/Hematoxlin) or Not. Micro adenomas are usually Functional, that is they secrete hormones and present with endocrine effects. Macro adenomas are usually Non-secretory tumours and they present with mass effects. Most ophthalmologists come across macro adenomas with pressure effect on
Optic chiasm. Patients with Micro adenomas usually do not have ophthalmic features and they are referred by Physician or Endocrinologists for visual field and fundus evaluation .
FUNCTIONAL PITUITARY TUMOURS7:
Type of Hormone Secreted Hitological Pathology Functional Classification Adenoma Prolactinoma Prolactin Acidophilic Galactorrhea,hypogonadism,
(Most common) amenorrhoea,infertility,
impotence
Somatotrophic Growth hormone(GH) Acidophilic Gigantism in children and adenoma Acromegaly in adults
Corticotrophic Adrenocorticotrophic Basophilic Cushing’s disease adenoma hormone (ACTH)
Gonadotrophic Leutinizing Basophilic Asymptomatic adenoma hormone(LH),
Follicle stimulating
hormone(FSH)
Thyrotrophic Thyroid stimulating Basophilic Usually Asymptomatic,may adenoma (Rare) hormone(TSH) cause hyperthyroidism
This is MRI study of a patient with small 5*5mm poorly low signal enhancing lesion involving the pituitary gland suggestive of Pituitary microadenoma.
Her serum prolactin levels were elevated and she had galactorrhoea and infertility. She was referred to us for visual field evaluation,which was normal.
OPHTHALMIC MANIFESTATIONS OF PITUITARY ADENOMA
1. DEFECTIVE VISION :
Patients with pituitary macroadenoma can present with defective
visual acuity ranging from 6/9 to loss of light perception. This is due
to damage to optic nerve fibres because of compression.
2. DEFECTIVE COLOUR VISION:
Patients may present with normal colour vision, if the damage to optic
nerve fibres are not significant, that is in the early stage. When the
tumour enlarges and compresses the optic chiasm,this causes defect in
colour vision, contrast sensitivity, defect in red colour desaturation.
3. VISUAL FIELD DEFECT8:
The most common visual field defect in pituitary adenoma is
Bitemporal Hemianopia involving the superior field first. This is due
to pressure effect on optic chiasm. Other less common field defects
are Junctional scotoma (central scotoma in one eye and temporal field
defect in other eye),Homonymous hemianopia, generalized field
constriction etc…,
4. LOSS OF DEPTH PERCEPTION :
Patients with total bitemporal hemianopia may develope complete loss
of depth perception. This phenomena is known as "post-fixational
blindness”. This is due to overlap of both the non seen temporal
hemifield at the time of convergence.
5. EXTRAOCULAR MUSCLE PARESIS:
Extraocular muscle palsy is a rare presentation of pituitary adenoma.This may be due to lateral extension of the tumour to the cavernous sinus and affect III, IV, V, or VI cranial nerves and produces partial or total Cavernous sinus syndrome. The most common cranial nerve affected is oculomotor nerve with or without pupillary involvement. This results in Binocular double vision. In case of Rapidly worsening vision and diplopia with extraocular muscle paresis Pituitary apoplexy should be ruled out.
6. NYSTAGMUS:
Optic chiasmal syndrome may produce Seesaw nystagmus, due to damage to interstitial nucleus of cajal. This is a rare type of nystagmus in which one eye intorts and elevates and the other eye depresses and extorts. This type of nystagmusis also found in suprasellar tumours like
Craniopharyngioma
7. FUNDUS CHANGES:
Most of the cases show normal optic discs in fundus examination. If altered, it can be a Temporal pallor or diffuse Primary optic atrophy in case of chronic compression of the tumour. If only nasal part of macular fibres are affected, then only the nasal and temporal part of the optic disc will be affected. This is known as “Bow-Tie” atrophy9. One of the very rare features of Pituitary adenoma is Papilledema, this is due to the extension of suprachiasmal tumour to the Third ventricle, obstructing the cerebrospinal fluid outflow.
Optic disc of a patient with a pituitary adenoma showing atrophy of the nasal
and temporal areas and relative sparing of the superior and inferior areas of
the disc (Bow-Tie atrophy).
Fundus picture of a patient with pituitary adenoma with chronic compression
showing Primary Optic Atrophy
8. PITUITARY APOPLEXY:
It is a life threatening complication of pituitary adenoma and is due to
acute infarction or hemorrhage of Pituitary gland,leading to sudden onset
of headache, worsening of visual acuity, altered sensorium, extra ocular
movement restriction and hormone imbalance18.Pituitary apoplexy can
lead to stroke due to extravasation of the hemorrhage in the
subarachnoid space.The life-threatening emergency as a result of
pituitary apoplexy is adrenal crisis, as well as other acute endocrine
abnormalities. The diagnosis is confirmed by MRI. Because this is a true
medical emergency, corticosteroids have to be started immediately and
severe cases should undergo immediate surgical decompression of sella
turcica.
DIAGNOSTIC TESTS :
1. VISUAL FIELD TESTING:Automated static or kinetic perimetry
are used to assess the visual fields. In a patient with a history
suspicious pituitary disease, visual field testing confirms the presence
of a compressive optic chiasmal lesion. Visual fields are also
commonly documented prior and following neurosurgical intervention
to assess the prognosis.
Humphrey 24-2 visual field showing Bitemporal hemianopia.
2. NEUROIMAGING:
Pituitary gland is best seen on contrast enhanced coronal sections.
Magnetic Resonance imaging is the investigation of choice for sellar and
parasellar lesions to determine their location, size and extension to
adjacent tissues12.
Computed Tomography (CT)
Microadenomas may present as less enhancing lesions within the substance of the pituitary gland, whereas macroadenomas are more variable in their appearance.
Magnetic Resonance Imaging (MRI)
Microadenomas are best seen on unenhanced T1-weighted coronal or sagittal scans. They are seen as hypointense areas within the substance of the relatively hyperintense pituitary gland13. With gadolinium contrast enhancement,these lesions remain less intense compared to the normal gland and will enhance late.
On T2-weighted images, the adenoma is more indistinct, as it appears iso-intense or slightly hyperintense in comparison with the surrounding gland.
Macroadenomasare more obviously seen, as they extend beyond the anatomical borders of the sella. The homogenicity of the images suggests the relative solidity of the tumour
3. LABORATORY TESTING:
Complete endocrine workup is mandatory for assessing the functional
status of the pituitary adenoma16.The lab investigations vary according
to the clinical presentation. For example, the most sensitive test for
acromegaly is the failure to supress Growth hormone in response to
oral glucose load.
MANAGEMENT:
Management of pituitary adenomas need multidisciplinary approach by
Ophthalmologist, Endocrinologist, Neurosurgeon and ENT surgeon.
Management depends on the type of the tumor, its secretory function, its size. And its impact on the patient's visual acuity. The main Goals of treatment include good visual outcome and reversal of hormonal imbalance.
The most common treatment modality is surgical approach. Some functional tumours can be treated medically. The main indication of surgery in case of pituitary adenoma is visual field loss and other features of compression.
Radiotherapy (external beam or gamma-knife) is considered as second-line of treatment modality11.
MEDICAL TREATMENT :
PROLACTINOMAS:
The primary modality of treatment for Prolactinoma is Medical treatment. Dopamine agonists (Bromocriptine or Cabergoline) normalize prolactin level as well as reduces the tumor size. Although both
Bromocriptine and Cabergoline has same mechanism of action, the first line drug in treatment of prolactinoma is Bromocriptine.It binds to D2 dopamine receptor and suppresses prolactin secretion. Bromocriptine is used safely in pregnancy.The major side effects of Bromocriptine are gastrointestinal, cardiovascular, or neurological symptoms.
Cabergoline is a newer drug that also binds to D2 dopamine receptors.
It has less incidence of side effects when compared to bromocriptine.
ACROMEGALY:
Somatostatin analogues like Octreotide, Lanreotide and growth hormone receptor agonists, Pegvisomant are used to treat growth hormone secreting tumours. Octreotide has the maximum effect on tumor size reduction.
SURGICAL INDICATIONS:
The following are some of the indications for surgical debulking of a pituitary adenoma19
§ Pituitary macroadenoma with chiasmal syndrome
§ Patients with prolactinoma who do not respond to medical therapy
§ Patients with prolactinomas who cannot tolerate the side effects of the
drugs
§ Patients with prolactinomas who had cystic features on MRI (80% of
tumour volume on T2 sequences) that were unlikely to shrink sufficiently
with medical management alone
§ Pituitary macroadenoma with cavernous sinus involvement
§ Pituitary apoplexy
The most preferred route of surgical excision is endoscopic debulking (trans- sphenoidal/trans-frontal) of the tumour, because of smaller incision and faster post operative recovery. Prognosis of pituitary adenoma depends on pre-treatment visual acuity, visual fields, age of the patient, duration of symptoms, size of the tumour and presence of optic atrophy. Patients undergoing radiotherapy show slower recovery.
COMPLICATIONS:
1. Tumour recurrence
2. Pituitary apoplexy
3. Secondary empty sella syndrome
4. Radionecrosis
5. Chiasmal traction from adhesion
ACOUSTIC NEUROMA
Acoustic neuroma is a slow growing benign tumour involving the myelin forming cells of eighth cranial nerve(vestibulocochlear nerve).In earlier stage, it is asymptomatic,later most common symptoms are sensorineural hearing loss ,tinnitus, vertigo, gait disturbance,disturbance in balance and equilibrium26.As the tumour size increases it produces pressure effect on Brainstem and involve other cranial nerves.
ORIGIN AND EXTENSION:
The Acoustic neuroma arises from the vestibulocochlear nerve inside the internal auditory canal. The tumour enlarges and occupies the cerebellopontine angle. In this site the tumour compresses the trigeminal nerve, facial nerve, and further increase in size affects the glossopharyngeal and vagus nerve. The tumour may obstruct the cerebrospinal fluid outflow and may cause raised intracranial tension.
CLINICAL SIGNS:
Reduced corneal sensation on affected side
Ø Lagophthalmos
Ø Exposure keratopathy
Ø Blepharospasm
Ø Ipsilateral cerebellar signs
Ø Cranial nerves involvement (5,7,8,9,10,11,12th cranial nerves)
Ø Brun’s nystagmus(Peripheral nystagmus on looking away from the
lesion and central nystagmus on looking towards the lesion)
The peripheral nystagmus is of high frequency and low amplitude, central nystagmus is of low frequency and high amplitude 27.
Ø Fundus changes: Papilloedema due to raised intracranial tension and
Secondary optic atrophy is a late feature.
INVESTIGATIONS:
Magnetic resonance imaging with Gadolinium enhancement is the gold standard investigation of choice.
Contrast enhanced CT Scan can detect tumour of greater than 2cm diameter.
Audiometry should be done to quantify the amount of sensorineural hearing loss.
NEUROFIBROMATOSIS TYPE 2:
Bilateral acoustic neuroma is one of the diagnostic criteria for NF Type 2.
Bilateral Acoustic neuroma with multiple meningiomas with obstructive hydrocephalus in a case of Neurofibromatosis type 2.
TREATMENT:
Surgical removal of the tumour is the definitive treatment for Acoustic neuroma, but surgery is very difficult to perform due to the location of the tumour adjacent to the vital tissues29. It needs a combined management by
Neurosurgeon and Otorhinolaryngologist.
Surgery will not reverse the damage occured to the vestibulocochlear and facial nerve and so hearing impairement and facial weakness will not recover after the surgical excision of the tumour 30.At the time of tumour removal,a part of vestibular nerve is also removed and surgery itself causes increased risk of facial nerve injury and so it is monitored during the surgery.
The various approaches of tumour removal are28
Translabrynthine approach
Middle cranial fossa approach
Sub occipital retrosigmoid approach.
The choice depends upon the size of the tumour, preoperative vestibular nerve damage, patient’s age and comorbidity and also depends on patient’s and surgeon’s preference.
RADIOTHERAPY:
The main ways by which radiation can be given are
Gamma knife radiosurgery
Cyber knife radiosurgery
Fractionated stereotactic radiotherapy
The main indications of radiotherapy are tumour size reduction in case of large tumours and residual or recurrent small tumour post surgery 31.
The major adverse effect following radiation are development of secondary tumour or conversion of benign tumour to malignant.
PROGNOSIS AND FOLLOW UP:
In general Acoustic neuroma has good prognosis, but there is a minimal chance of tumour recurrence, so frequent followup with
Gadolinium enhanced MRI is essential.
MENINGIOMAS
Meningiomas are derived from any of the three layers of meninges
(the duramater, arachnoid or the pia mater).Intra cranial meningiomas constitute around 20% of all the primary brain tumours 20.They mostly affect in the middle and late decades of life. Multiple intracranial meningiomas are more common in patients with Neurofibromatosis23.Meningiomas can arise from any part of the brain,of which convexity and parasagittal meningiomas are more common. The signs and symptoms differ according to the location of the tumour.
SUPRASELLAR MENINGIOMAS:
The tumour arises from the arachnoid granulations overlying the dura of tuberculum sellae and its adjacent tissues.Painless gradually progressing vision loss is the most common symptom22.The signs are bilateral optic nerve dysfunction presenting as visual loss, defective colour vision,field defects and optic atrophy. Very rarely, a very large tumour can produce mass effect and increases the intracranial tension and produces papilloedema and may also presents with pyramidal signs and altered sensorium.
CONVEXITY MENINGIOMAS:
The tumours are most commonly located in frontal and parietal lobes.The clinical features vary depending upon the location of the tumour.
FRONTAL LOBE SIGNS:
These are mostly neurological signs like22
· Lack of impulse,absence of inhibition
· Inappropriate laughter
· Sudden changes in social behavior
· Jacksonian seizure
· Forced grasp reflex
· Motor aphasia(if left frontal brocca’s area is affected)
· Raised intracranial tension leading to papilloedema
· Visual loss,field defects
· Conjugate deviation of the eye away from the side of lesion
· Inability to voluntarily close the eyelids(reflex closure retained)
PARIETAL LOBE SIGNS:
· Astereognosis (inability to recognize objects by sensory touch)
· Acalculia, Agraphia, Alexia (inability to read written words)
· Agnosia (inability to name objects)
· Non dominant parietal lobe lesions lead to Hemineglect
· Distortion of images
· Defective stereopsis
· Contralateral inferior quadrantanopia
· Papilloedema or optic atrophy.
TEMPORAL LOBE:
· Headache
· Complex formed visual hallucinations
· Contralateral superior quadrantanopia
· Seizures
· Papilloedema
OCCIPITAL LOBE:
· Contralateral homonymous hemianopia
· Unformed visual hallucinations that can mimic aura of migraine and
may cause delay in diagnosis
· Visual agnosia22 (V/A, fields-normal but cannot recognise or name the
object, if however the object is presented using different sensory
modality (sound/touch),the patient can immediately recognize & name
it)
· Raised intracranial tension leading to cranial nerve palsies and
papilloedema.
PARASAGITTAL MENINGIOMAS:
· This develop in the space between the superior sagittal sinus
and falx cerebri anywhere from anterior to posterior.
· Anteriorly located tumours produce symptoms of frontal lobe
involvement
· Posteriorly located tumours produce symptoms of parietal and
occipital lobe involvement.
OLFACTORY GROOVE MENINGIOMAS:
In this type the tumour originates from arachnoid cells adjacent to the olfactory groove and crista galli. It starts as a midline tumour and extends asymmetrically to one side.This leads to features of compressive optic neuropathy on ipsilateral side and features of raised intracranial tension on contralateral side due to mass effect and this entity is known as FOSTER
KENNEDY SYNDROME22 characterized by a triad of
· Anosmia
· Optic atrophy on ipsilateral side
· Contralateral papilloedema
SPHENOID WING MENINGIOMAS:
Meningiomas can arise from
a) Outer third of sphenoid wing (greater wing)
b) Middle third (lesser wing)
c) Inner third (clinoid type)
It can extend upto superior orbital fissure and can cause limitation of extraocular motility and proptosis.
Meningiomas can also involve middle cranial fossa, posterior cranial fossa, optic nerve sheath, orbit, cerebello-pontineangle, clivus, foramen magnum, ventricles, cavernous sinus and tentorium cerebelli.
INVESTIGATIONS:
High resolution CT or Gadollinium enhanced MRI are the modality of choice.
TREATMENT:
Surgical excision is the first line of treatment25
CRANIOPHARYNGIOMAS
The tumour arises from remnants of rathke’s pouch. They are mostly located in the suprasellar cistern and they compress the anterior visual sensory system. It predominantly affects children 32. Symptoms differ from children and adults.
The clinical features when the tumour affects children are increased intracranial tension, hydrocephalus, endocrine disturbance, signs and symptoms of hypothalamus involvement, papilloedema and rapid progression to secondary optic atrophy32.
In adults,the features are
· Fluctuating visual loss due to the cystic nature of the tumour
and variable compression effect due to spontaneous changes in
size of the cyst
· Endocrine disturbances like loss of secondary sexual
characteristics, lethargy, polyphagia, polydipsia, hyperthermia.
· Primary optic atrophy due to direct compression of visual
pathway
· Oculomotor nerve palsy due to extension of the tumour
· See saw nystagmus22- one eye elevates and intorts while the
other eye depresses and extorts.This is due to compression of
the diencephalon in the region of the interstitial nucleus of
cajal.
· The various imaging features are erosion of clinoid process and
dorsum sellae, cystic spaces in tumour, suprasellar
calcification,widening of sutures and enlarged pituitary fossa.
Treatment : surgical resection with treating the endocrine
abnormalities. Prognosis is excellent.
CT Scan showing large cystic lesion with marginal calcification and enhancement involving the suprasellar region and compressing optic chiasm with bilateral primary optic atrophy,the mass measuring 3.3x3.0x2.6cms
MID BRAIN AND PINEAL GLAND TUMOURS
These tumours are located in dorsal midbrain.
Clinical features:
· Vertical conjugate gaze palsy
· Normal horizontal gaze
· Convergence palsy
· Convergence retraction nystagmus22
· Mid dilated sluggishly reacting pupil
· Light near dissociation
· Hearing affected if inferior colliculus is involved
· Cerebellar signs
· Nuclear third nerve palsy
· Benedict’s syndrome if red nucleus is involved
· Raised ICT and abducent nerve palsy
Radiotherapy is the treatment of choice because the tumour cannot be
approached surgically because of its location to vital structures.
PONTINE TUMOURS
The most common tumour involving the pons is pontine glioma.
The clinical features of pontine involvement are 34
· Horizontal gaze palsy (inability to look in the direction of affected
side)
· Conjugate gaze deviation (eyes deviated to opposite side of lesion)
· Dissociated nystagmus (increase in intensity of nystagmus when the
patient attempts to look towards the side of the lesion)
· Multiple cranial nerve palsies
· Normal vertical gaze
· Cerebellar signs
· Hemiparesis, Sensory disturbances
MALIGNANT BRAIN TUMOURS
A primary malignant Brain tumour arises from the cells within the brain tissue. It can be broadly classified in to four grades depending upon their severity. Grade 1 and 2 are low grade malignant tumours while grade 3 and
4 are high grade tumours. The higher the grade of malignancy, the more the aggressiveness and spread of the tumour34.
MEDULLOBLASTOMA:
These are high grade malignant tumours of cerebellum. This mostly affects children and are rare in adults.The other common malignant tumour in children is Astrocytoma of cerebellum.
GLIOMAS:
Gliomas are primary malignant brain tumours that originate from glial cells.The various types are
· ASTROCYTOMA: Originating from astrocytes,which can be either
low grade or high grade.The high grade astrocytoma is known as
anaplastic astrocytoma.
· GLIOBLASTOMA MULTIFORME:This is the most common high
grade malignant brain tumour in adults. This tumour grows rapidly
and can be fatal22.
· OLIGODENDROGLIOMA
· EPENDYMOMA
SECONDARY BRAIN TUMOURS
These are also known as metastatic Brain tumours. The common sites
of primary are Lung, Breast, Colon, Kidney and Skin (melanoma) 33.
CLINICAL FEATURES:
· Generalised illness, lethargy
· Loss of appetite and body weight
· Seizures
· Decreased coordination, clumsiness, fall
· Memory loss, poor judgement
· Headache,Vomiting
· Personality changes
· Speech difficulties
· Vision loss or double vision
A thorough neurological and systemic workup is mandatory.
The treatment is mainly palliative. The primary tumour must be
treated. The various modalities of treating metastasis are radiotherapy,
chemotherapy, stereotactic radiosurgery and supportive palliative
care.
AIMS AND OBJECTIVES
Ø To study the various Neuro-ophthalmic features of intracranial
tumours.
Ø To correlate the ocular manifestations and site of the intracranial
tumour.
Ø To study the behavior and natural course of the Brain tumour.
Ø To study the prognosis of each tumour after treatment.
MATERIALS AND METHODS
A prospective observational case study on the various Neuro- ophthalmic manifestations of intracranial tumours and its visual prognosis to treatment.
A prospective study of 192 consecutive patients who were proven to have Brain tumour clinically and radiologically from a period of june 2011 to june 2013 for a period of 2 years who presented to the Department of
Neuro-ophthalmology, Aravind eye hospital, Madurai.
INCLUSION CRITERIA:
· History suggestive of symptoms of raised intracranial tension
· Reduced BCVA in one or either eye
· Relative afferent pupillary defect
· Defective colour vision
· Field defects
· Fundus changes- Normal/Temporal pallor/Optic atrophy /
Papilloedema
· Extraocular movement restriction
EXCLUSION CRITERIA:
· Unconscious patients
· Patients operated previously for some neurological disease
· Other neurological diseases
CLINICAL EVALUATION:
A series of 192 patients who presented to our Neuro-ophthalmology department with clinically and radiologically proven diagnosis of intracranial tumour were included in our study and all these patients underwent a thorough ophthalmological and neurological evaluation.
The patient’s particulars like name, age, sex, address were documented in a proforma specially designed for the study, and was filled by the examining doctor.
A detailed history of each and every symptom the patient has was taken, like the onset, duration, progression, associated factors, aggravating and relieving factors were documented.
The patients were also enquired about history of any prior visual loss, history of trauma/ systemic illness/ surgical or medical intervention/ family history of Brain tumours, as which could influence the diagnosis.
Each one of the patient included in our study has to undergo routine
· Visual acuity by means of snellen’s chart
· Refraction
· Pupillary reaction to carefully look for RAPD, sluggish pupil, dilated
fixed pupil or normal pupil
· General ophthalmic examination by torch light and slit lamp.
· Intraocular pressure measurement for patients above 40 years by non -
contact tonometry method
· Fundus examination by direct ophthalmoscope and slit lamp
biomicroscopy using +90 dioptre lens and Indirect ophthalmoscopy.
· Extraocular movement examination using torch light
· Hess and diplopia charting when needed
· Corneal sensation evaluation
· Colour vision evaluated by Ishihara’s colour vision chart
· Central fields tested either by Bjerrum’s screen or Humphrey's visual
field analyser.
· Patients were carefully examined for any nystagmus, if present, the
type, intensity, amplitude, frequency of the nystagmus were
documented.
· A Complete neurological evaluation was done to every patient
including general consciousness status, cranial nerve examination,
motor system evaluation (superficial and deep tendon reflexes),
sensory system, cerebellar signs including gait, balance, Rombergism,
Diadechokinesia, finger nose testing and other system examinations
were done.
· Neuroimaging was done in all patients either CT/MRI with or without
contrast depending upon the need and affordability of the individual
patients.
Patient’s visual acuity, pupillary reaction, colour vision, fields and
fundus were assessed during follow up examinations at one month and
three months.
ANALYSIS
Analysis of collected data was done based on the following
1. Incidence 2. Age and sex distribution 3. Various symptoms 4. Onset of symptoms – Acute/Subacute/Chronic 5. Presenting Best Corrected Visual Acuity – a. No PL/PL/HM/1/60 b. 5/60 – 1/60 c. 6/6 – 6/60 6. Anterior segment involvement including cranial nerves affected 7. Colour vision – Normal/Defective/Inconclusive because of poor vision. 8. Central fields 9. Nystagmus – Absent/Present 10. Fundus status – Normal/Abnormal 11. Central nervous system – Normal/Abnormal 12. Radiological findings 13. Treatment - Observation/ Surgery/ Radiotherapy/ Chemotherapy/ Combination of treatment. 14. Visual Acuity at follow up – Static/ Improved/ Deteriorated 15. Fundus status at follow up
RESULTS
Based on the inclusion and exclusion criteria 192 cases were taken up for the study.
DEMOGRAPHICS
TABLE 1 : INCIDENCE
Total number of Neuro-ophthalmology 20,579
cases in the study period
Number of patients with Intracranial 192
tumours
From this table 1 it can be seen that Intracranial tumours with Neuro- ophthalmic manifestations constituited 0.93% of Neuro-ophthalmology cases within the specified period of study.
TABLETABLE 2 : AGE DISTRIBUTION OF CASES
N Mininimum ageage Maximum Mean Standard Median age age Deviation
Age 192 3 75 41.97 16.005 43 (in years)
CHART -1
AgAAgege andand SSexex DiDDististributiontributionibution of PatientPatiPatientsents withith Brainrain Tumours
23 23 25 22 21 20 20 20
15 13 11 Male 9 9 10 6 6 Female 4 5 3 2
N o. o f pat i e n ts w th brain tu m ours 0 1 -10 11 -2021 - 30 31 -4041 -5051 -6061 -7071 -80 AgAgee Group (in yrs)
Majority of tthehe ppaattienntsts in the study beelolongongedngeedd to thhee age grorouupp 30-50
years.(n=87)
TABLE 3 : GENDER
Frequency PercPercentage
Male 104 54.2
Female 88 45.8
Total 192 100.0
CHART -2
GENDER
45.8% 54.2% Males FeFemmalesles
TABLE 4 : COMPLAINTS/SYMPTOMS
COUNT PERCENTAGE PERCENTAGE OF RESPONSES OF CASES Defective vision 156 58.6 81.3 Headache 48 18.0 25.0 Vomiting 8 3.0 4.2 Tinnitus 2 0.8 1.0 Hard of hearing 6 2.3 3.1 Giddiness 13 4.9 6.8 Fits 2 0.8 1.0 Double vision 9 3.4 4.7 Fever 1 0.4 0.5 Transient 8 3.0 4.2 obscuration of vision Drooping of upper 5 1.9 2.6 lid(ptosis) Others 8 3.0 4.2 Total responses 266 100.0 138.5
0 missing cases,192 valid cases.
From this table 4 it is clear that a single patient may present with multiple symptoms and out of which the most common presenting symptom of a patient with Brain tumour is Defective vision, followed by Headache and Giddiness.
TABLE 5 : ONSET OF SYMPTOMS
ONSET FREQUENCY PERCENTAGE
Acute 1 0.5
Subacute 120 62.5
Chronic 71 37.0
Total 192 100.0
Out of 192 patients, only one patient presented to us with sudden onset of symptoms. In majority of cases, the onset is subacute.
TABLE 6 : BCVA
BCVA FREQUENCY PERCENTAGE
6/6 – 6/60 98 51.0
5/60 – 1/60 45 23.4
<1/60 49 25.5
TOTAL 192 100.0
TABLETABLE 7: ANTERIOR SEGMENT
FFREQREQUENCY PERCENTAGE Normal 151 78.6 CranialNerves 35 18.3 involvement Ptosis 1 0.5 Proptosis 2 1.0 Lagophthalmos 3 1.6 Total 192 100.0
The mooststst commmmonon antanterioorr segmeennt finding iiss ininvvoolvevementent of exextrtraoccuullaarr movements.
CHART - 3
ANTERINTERIOORR SEGMENT
NORMAL
18.2 CCRRANIAL NNERVERVESES INVOLVEMENT PTOSIS
PROPTOSIS 78.6 LAGOPHTHALMALMOS
TABLE 8 : PUPIL
FREQUENCY PERCENTAGE
Normal 97 50.5
RAPD 82 42.7
Dilated fixed pupil 12 6.3
Sluggish pupil 1 0.5
Total 192 100.0
Relative afferent pupillary defect is the most common pupillary abnormality in patients with Intracranial tumours.
TABLE 9 : COLOUR VISION
FREQUENCY PERCENTAGE
Normal 58 30.2
Defective 81 42.2
Inconclusive 53 27.6
Total 192 100.0
TABLE 10 : EXTRA OCULAR MOVEMENTS
FREQUENCY PERCENTAGE
Full 160 83.3
Abduction restricted 10 5.2
Adduction restricted 3 1.6
Combined movement 19 9.9 restriction Total 192 100.0
TABLE 11 : CRANIAL NERVES AFFECTED
NERVE AFFECTED FREQUENCY PERCENTAGE OF CASES Optic nerve 134 69.8 Oculomotor nerve 15 42.8 Trochlear nerve 6 17.1 Trigeminal nerve 13 37.1 Abducent nerve 22 62.8 Facial nerve 3 8.6 Vestibulocochlear nerve 16 8.3 Vagus nerve 1 2.8
Multiple cranial nerves are involved in 19 patients.
TTABLEABLE 12 : NYSTAGMUS
FREQUENCY PERCENTAGE
Present 16 8.3
Absent 176 911.7.7
Total 192 100.0
CHART - 4 NYSTAGMUS TYPE
12.5% (n=2) CONVERGENCE RETRACTION
25% (n=4) SEESAW
56.3%56.3% PENDULAR (n=9)n=9)
JERKY 6.3% (n=1)
0 10 20 30 40 50 60
TABLE 13 : CENTRAL FIELDS
FREQUENCY PERCENTAGE
Normal 83 43.3
Generalized constriction 11 5.7
Bitemporal defect 39 20.3
Homonymous hemianopia 2 1.0
Enlargement of blind spot 3 1.6
Central/centrocaecal scotoma 1 0.5
Cannot be plotted because of low 52 27.1 visual acuity Tubular field 1 0.5
Total 192 100.0
CHHARTART – 5 FUNDUS CHANGES
40
34.9% 35
30 27.6%
25 17.2% 20 1616.1% 15
10
3.1% 5 1% 0 TEMPORAL POA SOA PAPILLOEDEMA DISC NORMALNORMAL PALLOR HYPEREMIA
POA – Primaryary ooptptic atatrophy
SOA – SeSeccoonndadaryry opoptic attrroopphyhy
The funduundusndus chahanngesges vvaarriesies aacccorording to thehe looccatationion andnd sizzee of tthehe ttuumour.
Sellar and supra sellar tumouursrs present with either nnorormalal funndus/dus/ Temporal pallor/POA.
PostePosterior fossossaa tumoursurs preresseenntt with papilloedema.
TABLE 14 : CENTRAL NERVOUS SYSTEM
FREQUENCY PERCENTAGE
Normal 182 94.9
Altered sensorium 2 1.0
Gait disturbance 5 2.6
Hemiparesis 1 0.5
Rombergism 2 1.0
CHART -6 TYPE OF TUMOUR
PITUITARY ADENOMA,46.9% MENINGIOMA,24% ACOUSTIC NEUROMA,8.3% CRANIOPHARYNGIOMA,7.3 GLIOMA,5.7% MALIGNANT,5.7% SECONDARIES,2.1%
TABLE 15 : TREATMENT
FREQUENCY PERCENTAGE
Medical 17 8.9
Surgical 153 79.7
Radiotherapy 8 4.2
Chemotherapy 2 1.0
Gamma Knife 1 0.5 Radiosurgery Surgery followed by 7 3.6 Radiotherapy Radiotherapy and 4 2.1 Chemotherapy Total 192 100.0
TABLE 16
TUMOUR FREQUENCY(PERCENTAGE) PITUITARY ADENOMA 90(46.87%) Pituitary microadenoma 1(1.1) Pituitary macroadenoma 67(74.4) Pituitary apoplexy 4(4.4) Functional tumour 10(11.1) With cavernous sinus extension 8(8.9) MENINGIOMA 46(23.95%) Suprasellarplanumsphenoidale 16(34.8) meningioma Anterior clenoid meningioma 2(4.3) With sellar extension 4(8.7) Cribriform plate/skull base 4(8.7) Anterior convexity meningioma 6(13.0) Optic nerve sheath 2(4.3) Parasellar meningioma 3(6.5) Posterior fossa meningioma 5(10.9) Clivo-cavernous meningioma 1(2.2) Petro-clival meningioma with pontine 1(2.2) compression Multiple meningiomatosis 2(4.3) SCHWANOMMA 16(8.33%) Acoustic neuroma(unilateral) 12(75)
Acoustic neuroma(bilateral) 2(12.5) Trigeminal schwanomma 1(6.3) TUMOUR FREQUENCY(PERCENTAGE) Middle cranial fossa schwanomma 1(6.3) CRANIOPHARYNGIOMA 14(7.29%) GLIOMA 11(5.73%) Tectalglioma 2(18.2) Brainstem glioma 2(18.2) Oligodendroglioma 1(9.1) Optic nerve glioma 2(18.2) Opticochiasmatic hypothalamic glioma 3(27.3) Cerebral glioma 1(9.1) MALIGNANT TUMOURS 11(5.72%) Glioblastoma multiforme 4(36.4) Chondrosarcoma 1(9.1) Spheno-ethmoidal malignancy 1(9.1) High grade astrocytoma 2(18.2) Gliosarcoma(cerebri) 1(9.1) Medulloblastoma 2(18.2) SECONDARIES 4(2.08%) Primary in Lungs 2(50) Primary in Breast 1(25) Primary in Nasopharynx 1(25) TOTAL 192
TABLE 17 : TUMOURS IN PAEDIATRIC AGE GROUP
TUMOUR FREQUENCY PERCENTAGE
Craniopharyngioma 7 53.8
Glioma 4 30.8
Malignant tumour 2 15.4
Total 13 100.0
The malignant tumour that presented to us in paediatric age group was
Medulloblastoma.
The types of Glioma are Optico-chiasmatic hypothalamic glioma (3 patients), Brainstem glioma (1 patient)
TABLTABLEE 1188 : FOLLOW UP BCVA
FREQUENCY PERCENTAGE
Lost to follow up 61 31.8
6/6 – 6/60 71 37
5/60 – 1/60 33 17.2
< 1/60 27 14.1
Total 192 100.0
In this stududy,y,6611 pattiienntts llosost ttoo foollllow up
CCHAHARRT – 7 FOLLOW UP FUNDUS
35 31.8% 30 25% 24.5% 25
20
15
10 8.9% 6.3% 5 1.6% 1.6% 0.5% 0
TABLE 19 : BCVA Vs FOLLOWUP BCVA CROSS TABULATION
(p<0.001)
BCVA FOLLOW UP BCVA TOTAL
6/6 – 6/60 5/60 – 1/60 <1/60
6/6 – 6/60 Frequency 65 3 68 % within followup 91.5% 9.1% 51.9% BCVA 5/60 – 1/60 Frequency 4 30 1 35 % within followup 5.6% 90.9% 3.7% 26.7% BCVA <1/60 Frequency 2 26 28 % within followup 2.8% 96.3% 21.4% BCVA TOTAL Frequency 71 33 27 131 % within followup 100% 100% 100% 100% BCVA
There was a statistically significant association between BCVA at presentation and follow up BCVA (p<0.001).Thus the visual prognosis depends upon the vision at presentation.
CHART - 8
BCBCVA AT PRESENTATATITIOONN AND AT FOLFOFOLLOLOWWUPUUPP 100 90 80 n=71 70 n=68 60 50 BCVABCVA AT PRESENTATIONPRESENTATION nn=35=35 FOLLOWFOLLOWUP BCVABCVA 40 n = 33 n = 28 30 n =27 20 10 0 6/6 -6/60 5/60 -1/60 <1/60
CHART - 9
Coommparismpparisarisonon of Preseseentntiningg andand Foollllowowupup BCVA in Pituitary Adenoma
40 36 36
35
30 22 25 21
20 Presenting BCVA 11 15 10 N o . of Pa t i e nts Followup 10 BCVA 5
0 6/6 -6/60 5/60 -1/60 <1/60 Visual Acuity
The moostst ccoommmmonon presentation of sellar tumours likelike pituitatarryy adennooma iiss ddeeffeectctive visvisioonn//ddeeffectiveve field of visioon.n. The optic nneerrvvee fibreses are damaagedged andnd ccaannnotnot be rreepaired even afafter tretreaatmenent. So,the visuvisual prognosis is poopoor inin pituitary tumoours.urs.
TABLE 20 :TYPE OF TUMOUR Vs PRESENTING BCVA CROSS
TABULATION (p= 0.206)
TYPE OF TUMOUR BCVA TOTAL 6/6 –6/60 5/60 - 1/60 < 1/60 Pituitary adenoma Frequency 48 25 17 90 % within type of tumour 53.3% 27.8% 18.9% 100% Meningioma Frequency 21 9 16 46 % within type of tumour 45.7% 19.6% 34.8% 100% Acoustic neuroma Frequency 12 2 2 16 % within type of tumour 75% 12.5% 12.5% 100% Craniopharyngioma Frequency 7 1 6 14 % within type of tumour 50% 7.1% 42.9% 100% Glioma Frequency 3 4 4 11 % within type of tumour 27.3% 36.4% 36.4% 100% Malignant tumour Frequency 6 3 2 11 % within type of tumour 54.5% 27.3% 18.2% 100% Secondaries Frequency 1 1 2 4 % within type of tumour 25% 25% 50% 100% TOTAL Frequency 98 45 49 192 % within type of tumour 51% 23.4% 25.5% 100%
Table 21 : TYPE OF TUMOUR Vs AGE IN YEARS,CROSS
TABULATION (p<0.001)
Type of Tumour Age in Years Total
1- 11-20 21-30 31-40 41-50 51-60 61-70 71-80
10
Pituitary adenoma 2 8 22 18 28 8 4 90 Meningioma 6 11 15 11 1 2 46 Acoustic neuroma 5 4 5 1 1 16 Craniopharyngioma 3 5 2 1 2 1 14 Glioma 4 2 2 3 11 Malignant tumour 1 3 1 1 3 2 11 Secondaries 1 1 1 1 4 TOTAL 8 12 24 43 44 42 13 6 192
TABLE 22: TYPE OF TUMOUR Vs GENDER,CROSS
TABULATION(p=0.096)
TYPE OF TUMOUR GENDER TOTAL
MALE FEMALE
Pituitary adenoma 45 45 90
Meningioma 22 24 46
Acoustic neuroma 7 9 16
Craniopharyngioma 12 2 14
Glioma 8 3 11
Malignant tumour 8 3 11
Secondaries 2 2 4
TOTAL 104 88 192
There was a significant association between type of tumour and age group (p<0.001),but there was no association between gender and type of tumour (p=0.096)
DISCUSSION
Intracranial tumours can present with varied manifestations,
Ophthalmic signs and symptoms may be the first presenting feature before diagnosing Brain tumours. So, Ophthalmologists should evaluate the patient meticulously and thoroughly.
The mean age group is 41.97 years, and this constituites the economically and physically active population. This mean age is younger than those recorded in other studies, 43.5years in a study conducted in
Bangkok4 and 50.6 years in a study conducted in Romania 2. The signs and symptoms of intracranial tumours are usually nonspecific and slowly evolving, this may be responsible for previous consultations before final referral to Neuro-ophthalmology clinic.
Neuro imaging has become mandatory for diagnosis and treatment plan in cases of Brain tumours.
The location, size and involvement of the visual pathway and oculomotor nerves determine to a greater extent in ophthalmic involvement in Brain tumours.
Pituitary microadenoma and other functional pituitary tumours do not have ophthalmic features as early presentations. So, they mostly consult the
Endocrinologist for their problem and we, Ophthalmologists get referral from them to rule out visual involvement.
Defective vision is the most common ophthalmic symptom in our study.81.3% of cases presented with defective vision in this study. In a study conducted in Africa by Onakpoyo et al1.., they reported defective vision in
52% of their patients. The difference may be related to the difference in the pattern of Brain tumours studied, that is in our study Pituitary adenoma and
Meningiomas constituited 70.9% of all tumours. The location of these tumours predispose to compression of optic nerve, optic chiasm and optic tract leading to defective visual acuity and defective field of vision.
Ocular cranial nerve involvement was reported in 18.2% of our patients which was responsible for double vision. This is somewhat similar to 12.5% reported in onakpoyo et al, and also higher than the 10% reported in Kenya.
The third cranial nerve involvement is most common in Pituitary adenomas. Sixth cranial nerve may be involved in raised intracranial tension as a false localizing sign.
Optic nerve head changes like temporal pallor, optic atrophy and papilloedema were found in 83.9% of our patients. Papilloedema was found in 17.2% of our cases and primary optic atrophy in 27.6% of our patients.
This emphasizes the importance of ophthalmoscopy in routine neurological evaluation.
Field defects were found in 29.7% of our patients, while the fields was unable to plot in 27.1% of cases because of low visual acuity. The most common field defect is Bitemporal defect(20.3%) followed by Generalised constriction(5.7%) in our study. This is because Pituitary adenoma and
Meningiomas are the two common tumours in our study which presents with the above field defect. This is similar to the study conducted in prasat eye institute Bangkok4,which says 16.8% of their patients presented with
Bitemporal field defect.
Nystagmus was present in 8.3% of our patients which was noted significantly higher than other studies;1.3% in the Bangkok 5year
prospective study. In our study, pendular nystagmus is the most common type (56.3%),followed by seesaw nystagmus (25%)
The wide spectrum of clinical syndromes including endocrinological cardiovascular, neurological, ophthalmological, determine the need of a multidisciplinary management between different specialists. Early diagnosis is very important in order to establish a proper therapeutic plan and achieve the best prognosis for these patients.
LIMITATIONS OF OUR STUDY
Ø 61 patients lost follow up. So correct analysis between individual patients
vision and fundus could not be analysed before and after treatment for
patients who lost follow up.
Ø For some patients MRI was not done because of the cost factor, patients
were not affordable and so CT was done. This could have missed some
micro details like extension of the tumour and the tissues involved.
Ø HFA could not be done in all patients again because patients were not
affordable. For those patients Bjerrum’s central field testing was done.
CONCLUSION
1. The mean age of patients affected by Brain tumour was 41.97 years,with
maximum in age group of 30-50 years.
2. There is a slight Male prepondance.
3. Defective vision is the most common presentation followed by Headache
and Giddiness.
4. Multiple cranial nervers were affected in 19 patients.
5. Nystagmus was present in 8.3%, out of which pendular nystagmus is the
most common type followed by seesaw nystagmus.
6. Field defect was found in 56.8% of cases.
7. Sellar and suprasellar tumours compress the visual pathway and the most
common presentation is Temporal pallor followed by Primary optic
atrophy, while posterior fossa tumours present with papilloedema and in
late case secondary optic atrophy.
8. Central nervous system disturbances like altered sensorium, gait
disturbance and Rombergism were seen in some patients of posterior
fossa tumours.
9. Pituitary adenomas constitute 46.9% of all tumours, followed by
meningiomas 24%
10. Pituitary macroadenoma presents with ocular features as it compresses
the visual pathway.
11. The visual prognosis is poor in case of pituitary macroadenomas.
12. Bilateral acoustic neuromas and multiple meningiomatosis are associated
with Neurofibromatosis.
13. Malignant tumours are fast growing and the symptoms rapidly progresses
and the patient deteriorates fastly and it could be fatal.
14. The most common primary site in Brain secondaries is Bronchogenic
carcinoma, followed by carcinoma Breast in females.
Usually detection of Intracranial tumours occurs in advanced stages when
the presence of the tumor has caused unexplained symptoms. Improved
diagnostic techniques are allowing Intracranial tumours to be detected at
increasingly earlier stages, but cases are still seen with Neuro-
ophthalmological symptoms as the presenting symptoms.
PITUITARY ADENOMA WITH CAVERNOUS SINUS EXTENSION
This patient with pituitary adenoma with lateral extension to left cavernous sinus, presented with left pupil involving complete third nerve palsy.
PITUITARY ADENOMA WITH CAVERNOUS SINUS EXTENSION
PLANUMSPHENOIDALE SUPRASELLAR MENGIOMA
MRI showing hetrogenously enhancing mixed signal intensity sellar mass lesion with suprasellar extension measuring about 2.45*2.51*2.10cm suggestive of Pituitary macroadenoma with chronic hemorrhagic apoplexy.
ANTERIOR CONVEXITY MENINGIOMA
CT scan showing large frontal lobe Meningioma with midline shift the same patient presented to us with bilateral papilloedema,
ACOUSTIC NEUROMA
Hetrogenously enhancing mass in right cerebellopontine angle, Acoustic neuroma
NEUROFIBROMATOSIS TYPE 2
MRI Brain with gadolinium enhancement showing bilateral acoustic neuroma, intraventricular ependymoma and spinal neuroma. This patient presented with bilateral papilloedema, gait disturbance and Rombergism positive.
TRIGEMINAL SCHWANNOMA
NEUROFIBROMATOSIS TYPE 1 CAFÉ- AU- LAIT SPOT
This patient presented to us with chronic headache, MRI showing fusiform homogenous swelling in right optic nerve suggestive of optic nerve glioma, high grade cerebellar astrocytoma with MR Spectroscopy showing high choline and decreased NAA levels Clinically, the patient had multiple café au lait spots all over his body.
GLIOMAS Tectalglioma with obstructive hydrocephalus
BRAINSTEM GLIOMA
OPTICO CHIASMATIC HYPOTHALAMIC GLIOMA
GLIOBLASTOMA MULTIFORME
High grade malignant tumour, this patient presented with sudden onset headache, vomiting and altered sensorium and papilloedema. this patient was on chemotherapy, and she lost her life within 25 days of diagnosis.
MEDULLOBLASTOMA
Medulloblastoma with obstructive hydrocephalus and MR spectroscopy showed increased choline levels.
ADENOID CYSTIC CARCINOMA OF SPHENOID SINUS
SECONDARIES IN BRAIN WITH PRIMARY BRONCHOGENIC CARCINOMA
Multiple brain secondaries with secondary deposits in right orbital apex
PRIMARY BRONCHOGENIC CARCINOMA
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PROFORMA
OCULAR MANIFESTATIONS OF INTRA CRANIAL TUMOURS
STUDY NO.
Name ………………………………………………… Date………………………….
Age MR No. .
Gender M-Male, F-Female
Address ………………………………………………………………………..
…………………………………………………………………………
…………………………………………………………………………..
Phone number ……………………………………………………………….
Diagnosis …………………………………………………………………….
CHIEF COMPLAINTS / DURATION
Headache
Defective vision 1-Present Complaints
Double vision 2-Absent
Vomiting 1-<1month Duration
Giddiness 2-1month to 1year
Tinnitus 3->1year
Fits
Vertigo
Hearing
Transient obscuration of vision
Drooping of upper lid
Others ……………………………………………………………………………………
Onset : 1-Acute,2- Subacute,3- Chronic
Course: 1-Progressive,2-Stationary
OCULAR EXAMINATION:
RE LE
BCVA 1- 6/6 to 6/60
2- 5/60 to 1/60
3- <1/60
LIDS 1-Normal
2-nerves affected
3-Ptosis
4-Proptosis
5-Lagophthalmos
PUPIL : RE LE
A) Anisocoria B) Direct 1-Present C) Indirect 2-Absent, D) RAPD 1- Normal 2- RAPD, 3- Dilated fixed pupil
4- sluggish pupil 5- others
EOM: 1-Abduction restricted,
2-Adduction Restricted,
3-multiple movements restricted,
4-full
Others if any
Nystagmus: 0-Absent
1-Present (1-jerky,2- pendular,3-rotatory,4- upbeat,5-downbeat,6- seesaw,7-convergence retraction,8-others)
CLINICAL INVESTIGATIONS:
RE LE
Colour vision 1 –Normal, 2 – Defective
Red colour desaturation 1 – 100%
Brightness sensitivity 2 - <100% 3-Cannot makeout
Corneal reflex 1 –Central, 2- Deviated
FUNDUS:
Normal 1 –yes, 2 - No
Disc edema
Hyperemia 1- Present
Pale disc 2- Absent
Dilated & Tortuous vessels
Splincter hemorrhage
Primary Optic atrophy
Secondary Optic atrophy
Others …………………………………………………………………….
Macula 1- Normal, 2- Abnormal
CENTRAL FIELDS: RE LE
Normal 1-Yes, 2-No
Bitemporal defect
Centrocaecalscotoma 1-Present
Enlargement of Blind spot 2-Absent
Hemianopia
General constriction
Homonymous Hemianopia
Cannot be ploted
NEUROLOGICAL EXAMINATION:
Higher functions
Cranial nerves 1 -Normal
Sensory/Motor system 2 -Affected
Gait
Rombergism 1 –Present, 2-Absent
X-Ray:
CT/MRI Scan:
Treatment: a)Medical 1-Yes b)Surgical 2 –No
HPE:
1st Follow up: Date:
RE LE
BCVA 1- 6/6 to 6/60
2- 5/60 to 1/60
3- <1/60
Colour vision 1 –Normal, 2 –Defective,
3-cannot makeout
FUNDUS:
Normal 1-Yes, 2-No
Disc edema
Hyperemia 1- Present
Pale disc 2- Absent
Dilated &Tortuous vessels
Splincter hemorrhage
Primary Optic atrophy
Secondary Optic atrphy
CENTRAL FIELDS: Normal 1-Yes, 2-No Bitemporal defect
Centrocaecalscotoma 1-Present, 2-Absent Enlargement of Blind spot
Homonymous Hemianopia
General constriction
Cannot be ploted
2nd Follow up: Date:
BCVA 1- 6/6 to 6/60 2- 5/60 to 1/60
3- <1/60 Colour vision 1 –Normal, 2 –Defective, 3- cannot makeout FUNDUS: Normal 1-Yes, 2-No
Disc Edema
Hyperemia 1-Present
Pale disc 2-Absent
Dilated vessels
Splincter Hemorrhage
Primary Optic atrophy
Secondary Optic atrophy
CENTRAL FIELDS:
Normal 1-Yes, 2- No
Bitemporal defect 1 -Present
Centrocaecalscotoma 2 -Absent
Enlargement of Blind spot
Homonymous Hemianopia
General constriction
Hemianopia
Cannot be ploted
ABBREVATIONS
BCVA – Best Corrected Visual Acuity
V/A – Visual Acuity
PL – Perception of Light
HM – Hand Movements
RAPD – Relative Afferent Pupillary Defect
CT – Computed Tomography
MRI – Magnetic Resonance Imaging
HFA – Humphrey Field Analysis
NF – Neurofibromatosis
ICT – Intracranial Tension
POA – Primary Optic Atrophy
SOA – Secondary Optic Atrophy
KEY TO EXCEL SHEET
Gender- 1.Male
2.Female
Complaints: Dv-defective vision
H-headache
V-vomiting 1-present
T-tinnitus blank/no entry-
absent Hoh-hard of hearing
G-giddiness
F-fits
Dip-diplopia/double vision
Fv-fever
Tov-transient obscuration of vision
Pto-ptosis/drooping of upper lid
O-others
Onset : 1- acute,2-subacute,3-chronic
BCVA : 0-lost to follow up, 1-6/6-6/60,2- 5/60 to 1/60, 3- <1/60
Pupil : 1-normal, 2-RAPD, 3-dilated fixed pupil, 4-sluggish pupil,
5-others
Nerves affected : N-normal,number specified – specific cranial
nerve
Involved
Anterior segment : 1-normal, 2-nerve affected, 3-ptosis, 4-proptosis,
5-lagophthalmous
Nystagmus : 0-absent, 1-present. If present, then 1-jerky, 2-
pendular,3-rotatory,4-upbeat,5-downbeat,6-
seesaw,7-convergence retraction,8-others
Extraocular movements(EOM) : 1,abduction restricted,2-adduction restricted,3- multiple
movements restricted,4-full
Colour vision : 1-normal,2-defective,3-cannot be taken
Central fields : 1-generalised constriction,2-bitemporal defect,3-
homonymous hemianopia,4-binasal defect,5-
enlargement of blind spot,6-central/centrocaecal
scotoma,7-others,8-cannot be ploted,9-tubular
field,10-normal
Fundus : 0-lost to follow up,1-temporal pallor,2- primary
optic
atrophy,3-secondary optic atrophy,4-
papilloedema,5-resolving papilloedema,6-disc
hyperemia,7-others,8-normal
CNS : 1-normal,2-altered sensorium,3-motor/sensory
defect,4-gait disturbance,5-hemiparesis,6-
rombergism,7-both gait disturbance &rombergism
Treatment : 1-medical,2-surgical,3-radiotherapy,4- chemotherapy,5-
gammaknife radiosurgery,6-surgery &
radiotherapy,7-radiotherapy& chemotherapy,8-
others
Diagnosis : p1(1)-pituitary microadenoma, p2(2)-pituitary
macroadenoma,p3(3)-pituitary apoplexy,pf(4)-
functional pituitary tumour,PN(5)-nonfunctional
pituitary tumour,PC(6)- with cavernous sinus
extension,7-other pituitary tumours.
M1(8)-Suprasellarplanumsphenoidale
meningioma,M2(9)-anterior clenoid
meningioma,M3(10)-suprasellar meningioma with
sellar extension,M4(11)-cribriform plate/skull
base meningioma,M5(12)-anterior convexity
meningioma,M6(13)-optic nerve sheath
meningioma,M7(14)-parasellar
meningioma,M8(15)-posterior fossa
meningioma,M9(16)-clivo-cavernous
meningioma,M10(17)-petro-clival meningioma
with pontine extension,M11(18)-multiple
meningiomatosis,19-Other type of meningiomas
A1(20)-unilateral acoustic neuroma,A2(21)- bilateral acoustic neuroma,TS(22)-trigeminal schwanoma,MS(23)-middle cranial fossa schwanoma,24-other schwanomas
C(25)-craniopharyngiomas
PG(26)-pontineglioma,TG(27)- tectalglioma,BG(28)-brainstem glioma,CG(29)- cerebellar glioma,OG(30)- oligodendroglioma,ONG(31)optic nerve glioma,OCHG(32)-opticochiasmatic hypothalamic glioma,AG(33)-anterior convexity glioma
GBM(34)-glioblastomamultiforme,ACC(35)- adenoid cystic carcinoma,CS(36)- chondrosarcoma,SM(37)-spheno- ethmoidalmalignancy,AS(38)-high grade
astrocytoma, GS(39)-gliosarcoma,MB(40)- medulloblastoma,41-other malignant tumours
SL(42)-secondary brain tumour with primary in lungs,SB(43)-Primary in breast,SN(44)-primary in nasopharynx,45-multiple meningiomas.
MASTER CHART sno mrno name age gender dv h v t hoh g f dip fv tov pto o onset bcva pupil Nerlayer sno mrno name antseg nystag nystagpre eom cv cf fundus cns diagnosis diag rx follbcva follfund tumour 1 3236809 SURYA NARAYANA 33 1 1 3 1 1 5,7 1 3236809 SURYA NARAYANA 2 0 4 1 10 3 1 A1 20 2 1 3 3 2 3213538 SANTHANA LAKSHMI 36 2 1 3 1 1 LAGOPHTHALMOUS 2 3213538 SANTHANA LAKSHMI 5 0 4 1 10 3 1 A1 20 2 1 3 3 3 3150029 SEDHURAM 48 1 1 2 1 1 N 3 3150029 SEDHURAM 1 0 4 1 5 4 1 A1 20 2 1 5 3 4 3390536 DHANA MARY 29 2 1 1 1 2 1 1 5,8,10 4 3390536 DHANA MARY 2 1 2 4 1 10 4 7 A2 21 2 0 0 3 5 3412767 THANGAMMAL 55 2 1 1 1 2 1 1 5,6,8 5 3412767 THANGAMMAL 2 1 2 4 1 10 4 1 A1 20 2 0 0 3 6 3397876 KESI 27 2 1 1 2 3 2 5,8 6 3397876 KESI 2 0 4 3 8 3 1 A2 21 2 0 0 3 7 3385459 SULAIKA BEEVI 49 2 1 1 2 1 1 5,8 7 3385459 SULAIKA BEEVI 2 0 4 1 10 4 4 A1 20 2 1 5 3 8 3342394 RAMAN 45 1 1 1 2 3 1 5,6,8 8 3342394 RAMAN 2 0 1 1 10 4 4 A1 20 2 0 0 3 9 3551290 TAMILMANI 45 2 1 1 1 2 1 1 LAGOPHTHALMOUS 9 3551290 TAMILMANI 5 1 2 4 1 10 4 4 A1 20 2 1 5 3 10 3526970 MAHENDRAN 32 1 1 1 1 1 2 1 1 N 10 3526970 MAHENDRAN 1 1 2 4 1 5 4 4 A1 20 2 1 5 3 11 3479852 MEENAKSHI 29 2 1 1 2 1 1 6 11 3479852 MEENAKSHI 2 1 2 1 1 10 4 1 A1 20 2 1 5 3 12 1273457 PANDISELVI 30 2 1 1 1 2 1 1 LAGOPHTHALMOUS 12 1273457 PANDISELVI 5 0 4 1 10 4 1 A1 20 2 1 5 3 13 1315516 ESHWARAMMA 65 2 1 1 2 1 1 N 13 1315516 ESHWARAMMA 1 0 4 1 10 4 4 A1 20 2 1 5 3 14 1322148 SIVASANKARA REDDY 48 1 1 1 2 2 1 N 14 1322148 SIVASANKARA REDDY 1 0 4 1 10 4 1 A1 20 2 2 5 3 15 1158068 ARIYARAJ 26 1 1 2 2 2 3,4,6 15 1158068 ARIYARAJ 2 0 3 3 8 2 1 MS 23 2 0 0 3 16 3275899 BALAGURU 35 1 1 2 1 1 5,6,7 16 3275899 BALAGURU 2 0 1 1 10 8 1 TS 22 2 0 0 3 17 3195550 SYED RAFINISHA 49 1 1 2 3 3 PROP 17 3195550 SYED RAFINISHA 4 0 3 3 8 2 1 M3 10 2 3 2 2 18 3191830 RAMESH 35 1 1 2 1 1 N 18 3191830 RAMESH 1 0 4 2 10 6 1 M5 12 2 1 6 2 19 3230765 KALAIYARASI 40 2 1 3 1 2 N 19 3230765 KALAIYARASI 1 0 3 2 1 6 1 M6 13 1 1 4 2 20 3098448 RAMU 57 1 1 3 3 2 N 20 3098448 RAMU 1 0 3 2 10 2 1 M7 14 2 1 1 2 21 3265986 MUTHU 48 2 1 2 1 1 N 21 3265986 MUTHU 1 0 4 2 2 1 1 M3 10 2 0 0 2 22 3267193 KANNAN 45 1 1 3 2 2 N 22 3267193 KANNAN 1 0 4 3 8 2 1 M1 8 2 0 0 2 23 3279135 JEYA BHARATHY 60 1 1 1 2 3 2 N 23 3279135 JEYA BHARATHY 1 0 4 3 8 4 1 M4 11 2 0 0 2 24 3177878 NAJIBUNISHA 45 2 1 3 1 2 N 24 3177878 NAJIBUNISHA 1 0 4 2 10 1 1 M4 11 6 1 1 2 25 3289999 VETRISELVI 34 2 1 1 2 1 1 N 25 3289999 VETRISELVI 1 0 4 1 10 4 1 M8 15 2 1 4 2 26 3311518 PARVATHY 45 2 1 2 1 2 N 26 3311518 PARVATHY 1 0 4 2 10 2 1 M1 8 2 0 0 2 27 3316771 ANANTHI 28 2 1 1 2 1 1 6 27 3316771 ANANTHI 2 0 2 1 5 4 2 M5 12 2 1 5 2 28 3299793 CHELLAMMA 40 2 1 1 1 3 1 1 6 28 3299793 CHELLAMMA 2 0 2 1 10 4 1 M5 12 2 1 5 2 29 3141416 AMIRTHAM 60 2 1 3 2 2 N 29 3141416 AMIRTHAM 1 0 4 2 10 1 1 M1 8 2 1 1 2 30 3337372 POTHAMMAL 45 2 1 3 1 1 N 30 3337372 POTHAMMAL 1 0 4 2 1 1 1 M1 8 2 1 1 2 31 3358789 PETCHI 50 2 1 2 1 1 N 31 3358789 PETCHI 1 0 4 2 10 2 1 M1 8 1 1 2 2 32 3305428 ELANGOVAN 40 1 1 3 2 2 N 32 3305428 ELANGOVAN 1 0 4 3 8 1 1 M2 9 2 2 1 2 33 3402961 MANIVANNAN 52 1 1 2 1 3 3,4,6 33 3402961 MANIVANNAN 2 0 3 1 10 8 1 M7 14 2 0 0 2 sno mrno name age gender dv h v t hoh g f dip fv tov pto o onset bcva pupil nerlayer sno mrno name antseg nystag nystagpre eom cv cf fundus cns diagnosis diag rx follbcva follfund tumour 34 3390536 DHANA MARY 29 2 1 1 1 2 1 1 5,8,10 34 3390536 DHANA MARY 2 1 2 4 1 10 4 7 M 45 2 0 0 2 35 3411878 SALUHA BEEVI 45 2 1 1 2 1 1 N 35 3411878 SALUHA BEEVI 1 0 4 1 10 4 1 M4 11 2 0 0 2 36 3459945 SASI REKHA 63 2 1 2 3 2 N 36 3459945 SASI REKHA 1 0 4 3 8 2 1 M1 8 2 3 2 2 37 3241504 SOUNDARAPANDIAN 43 1 1 2 2 2 N 37 3241504 SOUNDARAPANDIAN 1 0 4 2 10 2 1 M1 8 2 2 2 2 38 3242302 SAROJAMMA 50 2 1 3 3 2 N 38 3242302 SAROJAMMA 1 0 4 3 8 2 1 M2 9 2 0 0 2 39 3397876 KESI 27 2 1 1 2 3 2 5,8 39 3397876 KESI 2 0 4 3 8 3 1 M8 15 2 0 0 2 40 3375298 RAJA GANDHI 57 1 1 1 2 1 1 5 40 3375298 RAJA GANDHI 2 0 4 1 10 8 1 M8 15 2 0 0 2 41 3375880 SHANMUGAM 45 1 1 3 2 1 N 41 3375880 SHANMUGAM 1 0 4 1 2 1 1 M1 8 2 0 0 2 42 3291595 MOHAN RAJ 42 1 1 3 3 2 PROP 42 3291595 MOHAN RAJ 4 0 4 3 8 2 1 M6 13 2 3 2 2 43 3596346 MATHIYALAGAN 25 1 1 3 3 2 N 43 3596346 MATHIYALAGAN 1 0 4 3 8 2 1 M1 8 2 3 2 2 44 3611919 JANITA ANTHONY RANI 33 2 1 3 3 2 N 44 3611919 JANITA ANTHONY RANI 1 0 4 3 8 2 1 M1 8 2 3 2 2 45 3558333 SIVAKAMI 39 2 1 1 2 1 1 N 45 3558333 SIVAKAMI 1 0 4 2 10 4 1 M8 15 2 0 0 2 46 3484895 SYED ABUDAHIR 37 1 1 1 2 1 1 N 46 3484895 SYED ABUDAHIR 1 0 4 1 10 4 1 M8 15 2 1 5 2 47 3490339 VASUKI 52 2 1 3 3 1 N 47 3490339 VASUKI 1 0 4 3 8 2 1 M1 8 2 3 2 2 48 3501338 MUTHUKALAI 55 1 1 2 3 3 3,4,6 48 3501338 MUTHUKALAI 2 0 3 3 8 8 1 M4 11 2 0 0 2 49 3500419 BANDARU BASKARA RAO 74 1 1 3 3 2 N 49 3500419 BANDARU BASKARA RAO 1 0 4 3 8 2 1 M9 16 2 0 0 2 50 3475494 PERANANTHAN 40 1 1 2 1 1 N 50 3475494 PERANANTHAN 1 0 4 1 1 4 1 M5 12 2 1 5 2 51 3474731 MAHALINGAM 43 1 1 2 1 3 3 51 3474731 MAHALINGAM 2 0 3 1 10 8 1 M3 10 1 1 8 2 52 2944754 MURUGESHWARI 22 2 1 2 1 2 N 52 2944754 MURUGESHWARI 1 0 4 2 10 1 1 M1 8 2 1 1 2 53 1823988 SHANTHI 45 2 1 2 1 1 5,6 53 1823988 SHANTHI 2 0 1 1 10 8 1 M10 17 3 1 8 2 54 3333232 JEYAM 52 2 1 3 3 2 N 54 3333232 JEYAM 1 0 4 3 8 2 1 M1 8 2 3 2 2 55 1252075 PERIYASAMY 42 1 1 2 1 2 N 55 1252075 PERIYASAMY 1 0 4 2 10 1 1 M5 12 1 1 1 2 56 1346223 SEBASTHIAMMAL 55 2 1 1 2 3 1 N 56 1346223 SEBASTHIAMMAL 1 0 4 3 8 4 1 M5 12 2 0 0 2 57 1204027 ABBURI MALAKONDIAH 55 1 1 2 2 2 N 57 1204027 ABBURI MALAKONDIAH 1 0 4 3 8 2 1 M1 8 2 2 2 2 58 1141526 MUTHU 75 1 1 2 2 1 6 58 1141526 MUTHU 2 0 1 1 10 8 1 M7 14 2 2 1 2 59 1272154 KAVITHA 27 2 1 1 1 2 2 1 N 59 1272154 KAVITHA 1 0 4 3 8 4 1 M11 18 1 2 4 2 60 3417424 VALLI 37 2 1 3 3 2 N 60 3417424 VALLI 1 0 4 3 8 2 1 M1 8 2 3 2 2 61 1121180 MOULALI 52 1 1 3 3 2 N 61 1121180 MOULALI 1 0 4 3 8 2 1 M1 8 2 3 2 2 62 834204 BASHA 40 1 1 3 2 1 N 62 834204 BASHA 1 0 4 2 1 1 1 M3 10 2 2 1 2 63 3160198 PACKIAM 45 2 1 3 2 2 N 63 3160198 PACKIAM 1 0 4 3 8 2 1 P2 2 2 2 2 1 64 3199522 JOTHIRAJAN 53 1 1 3 3 2 N 64 3199522 JOTHIRAJAN 1 0 4 2 1 2 1 P2 2 2 0 0 1 65 3199608 BARAK ALI 33 1 1 3 1 2 N 65 3199608 BARAK ALI 1 0 4 2 2 8 1 P2 2 2 1 2 1 66 3169720 SUBBULAKSHMI 42 2 1 2 2 2 N 66 3169720 SUBBULAKSHMI 1 0 4 2 6 2 1 PF 4 1 2 1 1 sno mrno name age gender dv h v t hoh g f dip fv tov pto o onset bcva pupil nerlayer sno mrno name antseg nystag nystagpre eom cv cf fundus cns diagnosis diag rx follbcva follfund tumour 67 3096822 VELUSAMY 51 1 1 3 2 1 N 67 3096822 VELUSAMY 1 0 4 1 2 2 1 P2 2 2 1 2 1 68 3233150 BABU JOSEPH 52 1 1 3 1 2 N 68 3233150 BABU JOSEPH 1 0 4 2 2 1 1 P2 2 2 1 8 1 69 3095186 KABAR SINGH 21 1 1 1 2 1 2 N 69 3095186 KABAR SINGH 1 0 4 2 2 1 1 P2 2 2 0 0 1 70 3130746 SARADHA SHARMA 32 2 1 2 1 2 N 70 3130746 SARADHA SHARMA 1 0 4 1 10 8 1 PF 4 1 1 8 1 71 3141079 ACHAMMAL 68 2 1 3 2 1 N 71 3141079 ACHAMMAL 1 0 4 2 1 1 1 P2 2 2 2 2 1 72 3237027 DEVASENA 37 2 1 3 1 1 N 72 3237027 DEVASENA 1 0 4 1 10 8 1 PF 4 1 1 8 1 73 3237165 RAMANUJAM 75 1 1 2 1 3 3,4,6 73 3237165 RAMANUJAM 2 0 3 1 10 1 1 PC 6 1 1 1 1 74 3246047 PARAMESHWARI 47 2 1 2 3 1 N 74 3246047 PARAMESHWARI 1 0 4 3 2 2 1 P2 2 2 0 0 1 75 3248489 PIRUNTHAVAN 36 1 1 2 2 1 N 75 3248489 PIRUNTHAVAN 1 0 4 1 2 1 1 P2 2 2 0 0 1 76 3248897 SRINIVASAN 46 1 1 3 1 2 N 76 3248897 SRINIVASAN 1 0 4 2 10 8 1 P1 1 2 0 0 1 77 3252631 VELU 42 1 1 2 1 3 N 77 3252631 VELU 1 0 3 1 10 8 1 PC 6 2 1 8 1 78 3278553 UMARANI 21 2 1 1 3 3 2 N 78 3278553 UMARANI 1 0 4 3 8 2 1 PF 4 2 3 2 1 79 3168986 ANTHONY 70 1 1 2 2 1 N 79 3168986 ANTHONY 1 0 4 2 10 8 1 P2 2 2 2 8 1 80 3274937 SUGATHAN 50 1 1 3 2 1 N 80 3274937 SUGATHAN 1 0 4 2 2 1 1 P2 2 2 1 2 1 81 3139614 VALARMATHY 50 2 1 2 1 2 N 81 3139614 VALARMATHY 1 0 4 2 2 1 1 P2 2 2 1 1 1 82 3306204 KARUPASAMY 54 1 1 3 2 1 N 82 3306204 KARUPASAMY 1 0 4 2 2 1 1 P2 2 2 2 1 1 83 3309268 ANITHA 33 2 1 2 1 1 N 83 3309268 ANITHA 1 0 4 1 10 8 1 PF 4 1 1 8 1 84 3262414 RAJARAM 41 1 1 3 2 2 N 84 3262414 RAJARAM 1 0 4 3 8 2 1 P2 2 2 3 2 1 85 3329028 MOHAMMED FAROOK 41 1 1 2 2 1 N 85 3329028 MOHAMMED FAROOK 1 0 4 2 2 1 1 P2 2 2 2 1 1 86 3338258 JAHANGIR 45 1 1 2 1 1 N 86 3338258 JAHANGIR 1 0 4 2 10 1 1 P2 2 2 1 1 1 87 3340994 MALATHI 44 2 1 1 1 1 1 1 6 87 3340994 MALATHI 2 0 2 1 10 8 1 P3 3 2 1 1 1 88 3338442 MANIVANNAN 51 1 1 2 1 2 N 88 3338442 MANIVANNAN 1 0 4 2 2 1 1 P2 2 2 2 2 1 89 3348959 LAKSHMI 52 2 1 1 2 1 1 N 89 3348959 LAKSHMI 1 0 4 1 10 8 1 PF 4 1 1 1 1 90 3349079 CHENNAKESAVARULU 51 1 1 3 3 3 N 90 3349079 CHENNAKESAVARULU 1 0 4 3 8 2 1 P2 2 2 3 2 1 91 3349800 THANGAMMAL 45 2 1 3 3 1 N 91 3349800 THANGAMMAL 1 0 4 3 8 2 1 P2 2 2 0 0 1 92 3338550 VIDHYADHARAN PILLAI 63 1 1 3 1 2 N 92 3338550 VIDHYADHARAN PILLAI 1 0 4 2 2 1 1 P2 2 2 0 0 1 93 3352202 KALIAMMAL 55 2 1 3 3 2 N 93 3352202 KALIAMMAL 1 0 4 3 8 2 1 P2 2 2 3 2 1 94 3352461 SUMANGALA AMMA 55 2 1 3 3 2 N 94 3352461 SUMANGALA AMMA 1 0 4 2 2 1 1 P2 2 2 3 2 1 95 3354583 VELUMANI 34 2 1 3 1 2 N 95 3354583 VELUMANI 1 0 4 2 1 1 1 P2 2 2 1 2 1 96 3353008 RAMAKRISHNA REDDY 55 1 1 3 3 2 N 96 3353008 RAMAKRISHNA REDDY 1 0 4 2 1 1 1 P2 2 2 0 0 1 97 3074018 PALANISAMY 65 1 1 1 2 1 1 PT 97 3074018 PALANISAMY 3 0 1 2 10 1 1 PC 6 2 1 1 1 98 3405527 JERINA BEGAM 28 2 1 1 2 1 1 N 98 3405527 JERINA BEGAM 1 0 4 1 10 1 1 P2 2 2 0 0 1 99 3403679 SATHYA 29 2 1 1 2 1 1 3,6 99 3403679 SATHYA 2 0 3 2 10 1 1 P2 2 2 1 1 1 sno mrno name age gender dv h v t hoh g f dip fv tov pto o onset bcva pupil nerlayer sno mrno name antseg nystag nystagpre eom cv cf fundus cns diagnosis diag rx follbcva follfund tumour 100 3418815 NAMMALWAR 52 1 1 1 2 1 2 N 100 3418815 NAMMALWAR 1 0 4 2 2 1 1 P2 2 2 0 0 1 101 3424537 GANESH 34 1 1 2 2 2 N 101 3424537 GANESH 1 0 4 2 1 2 1 P2 2 2 2 2 1 102 3471099 ESHWARAN 22 1 1 2 1 1 N 102 3471099 ESHWARAN 1 0 4 2 10 1 1 P2 2 2 1 1 1 103 3451037 JAYARANI 40 2 1 1 1 3 1 1 N 103 3451037 JAYARANI 1 0 4 1 10 8 1 PF 4 1 1 8 1 104 3453375 NASERA KHATUN 17 2 1 1 2 3 2 N 104 3453375 NASERA KHATUN 1 0 4 3 8 1 1 P3 3 2 0 0 1 105 3456249 PANDIAMMAL 46 2 1 2 1 1 N 105 3456249 PANDIAMMAL 1 0 4 2 2 1 1 P2 2 2 1 1 1 106 3248656 REGI ABRAHAM 38 1 1 3 3 2 N 106 3248656 REGI ABRAHAM 1 0 4 3 8 2 1 P2 2 2 0 0 1 107 3457909 SAMSU NIHAR 40 2 1 3 1 2 N 107 3457909 SAMSU NIHAR 1 0 4 2 2 1 1 P2 2 2 1 1 1 108 3470690 JEYA MARY 58 2 1 1 2 1 2 6 108 3470690 JEYA MARY 2 0 1 2 10 1 1 PC 6 2 0 0 1 109 3430783 THANGAVEL 70 1 1 3 2 2 N 109 3430783 THANGAVEL 1 0 4 2 10 1 1 P2 2 2 2 1 1 110 3433575 ANANDHI 38 2 1 2 1 1 N 110 3433575 ANANDHI 1 0 4 2 2 1 1 PC 6 2 0 0 1 111 3403174 AMUTHALAKSHMI 39 2 1 3 2 1 N 111 3403174 AMUTHALAKSHMI 1 0 4 2 2 1 1 P2 2 2 0 0 1 112 3390824 GRAHADURAI 45 1 1 2 1 1 N 112 3390824 GRAHADURAI 1 0 4 2 2 1 1 P2 2 2 1 1 1 113 3375943 BABURAM 38 1 1 2 1 1 N 113 3375943 BABURAM 1 0 4 2 2 1 1 P2 2 2 0 0 1 114 3379695 KALIAMMAL 56 2 1 1 2 2 2 N 114 3379695 KALIAMMAL 1 0 4 2 2 1 1 P3 3 2 2 1 1 115 3290814 S.CHITRA 35 2 1 2 1 1 N 115 3290814 S.CHITRA 1 0 4 2 9 2 1 P2 2 2 2 2 1 116 3240630 ADAIKALAM 16 2 1 1 2 1 1 N 116 3240630 ADAIKALAM 1 0 4 1 10 1 1 P2 2 2 1 8 1 117 3317327 MURUGAN.V 33 1 1 3 3 2 N 117 3317327 MURUGAN.V 1 0 4 3 8 2 1 P2 2 2 3 2 1 118 3205715 KANDIAMMAL 47 2 1 2 1 2 N 118 3205715 KANDIAMMAL 1 0 4 2 2 2 1 P2 2 2 0 0 1 119 3344354 MURUGAN.T 40 1 1 2 2 2 N 119 3344354 MURUGAN.T 1 0 4 1 1 1 1 P2 2 2 1 1 1 120 3296291 NATRAJAN.R 55 1 1 2 2 1 N 120 3296291 NATRAJAN.R 1 0 4 2 10 8 1 P2 2 2 2 1 1 121 3606334 KAMBA RAMAN SHA 63 1 1 2 1 1 N 121 3606334 KAMBA RAMAN SHA 1 0 4 2 10 8 1 P2 2 2 1 1 1 122 3581017 PALANISAMY 58 1 1 2 3 3 3 122 3581017 PALANISAMY 2 0 3 3 8 1 1 PC 6 2 0 0 1 123 3593178 ALAGUTHAI 38 2 1 1 3 2 2 N 123 3593178 ALAGUTHAI 1 0 4 2 2 1 1 P2 2 2 2 1 1 124 3614320 SEETHALAKSHMI 54 2 1 3 2 2 N 124 3614320 SEETHALAKSHMI 1 0 4 2 2 2 1 P2 2 2 2 2 1 125 3547579 MANICKAM 57 1 1 2 2 2 N 125 3547579 MANICKAM 1 0 4 2 2 1 1 P2 2 2 2 1 1 126 3487776 RAJALAKSHMI 55 2 1 3 2 2 N 126 3487776 RAJALAKSHMI 1 0 4 2 2 2 1 P2 2 2 0 0 1 127 3488474 SUBBURAJ 23 1 1 2 1 1 N 127 3488474 SUBBURAJ 1 0 4 2 2 8 1 P2 2 2 1 8 1 128 3491152 RATHINAVELU 71 1 1 2 1 3 3 128 3491152 RATHINAVELU 2 0 3 2 10 1 1 PC 6 2 0 0 1 129 3501886 HAYATH KHAN 59 1 1 2 1 1 N 129 3501886 HAYATH KHAN 1 0 4 2 10 1 1 P2 2 2 1 1 1 130 3493740 MOTTAIYA SAMY 57 1 1 3 1 1 N 130 3493740 MOTTAIYA SAMY 1 0 4 2 10 1 1 P2 2 2 1 1 1 131 3517325 SAROJA 72 1 1 1 2 1 1 N 131 3517325 SAROJA 1 0 4 2 10 1 1 P2 2 2 1 1 1 132 3519549 SAKUNTHALA 57 2 1 2 1 3 3 132 3519549 SAKUNTHALA 2 0 3 2 10 1 1 PC 6 2 0 0 1 sno mrno name age gender dv h v t hoh g f dip fv tov pto o onset bcva pupil nerlayer sno mrno name antseg nystag nystagpre eom cv cf fundus cns diagnosis diag rx follbcva follfund tumour 133 3494200 VANJIYATHAL 59 2 1 3 1 2 N 133 3494200 VANJIYATHAL 1 0 4 2 10 1 1 P2 2 2 1 2 1 134 3497859 SHENBAGAM 37 2 1 1 2 1 1 N 134 3497859 SHENBAGAM 1 0 4 1 10 8 1 PF 4 1 1 8 1 135 3523867 KALIAMMAL 42 2 1 2 2 2 N 135 3523867 KALIAMMAL 1 0 4 2 10 1 1 P2 2 2 2 1 1 136 3540415 SOUNDARAM 55 2 1 1 2 3 2 N 136 3540415 SOUNDARAM 1 0 4 3 8 8 1 P2 2 2 3 1 1 137 3612307 ARAVIND KUMAR 25 1 1 1 2 1 1 N 137 3612307 ARAVIND KUMAR 1 0 4 2 10 8 1 P3 3 2 0 0 1 138 2988658 JOSPHINE 30 2 1 1 2 1 1 N 138 2988658 JOSPHINE 1 0 4 1 10 8 1 PF 4 1 1 8 1 139 2948857 KASTHURI THILAGAM 56 2 1 3 2 2 N 139 2948857 KASTHURI THILAGAM 1 0 4 2 2 1 1 P2 2 2 2 1 1 140 2062152 RATHINASAMY 65 1 1 2 1 1 N 140 2062152 RATHINASAMY 1 0 4 2 2 1 1 P2 2 2 1 1 1 141 2979349 BASHEER 33 1 1 2 1 2 N 141 2979349 BASHEER 1 0 4 2 2 2 1 P2 2 2 2 2 1 142 2274999 DEVAKI 40 2 1 2 2 2 N 142 2274999 DEVAKI 1 0 4 2 2 1 1 P2 2 2 2 1 1 143 2587634 VIJI DEVI 31 2 1 1 2 1 1 N 143 2587634 VIJI DEVI 1 0 4 1 10 8 1 PF 4 1 1 8 1 144 1785776 SETHU RAMAN 68 1 1 2 1 1 N 144 1785776 SETHU RAMAN 1 0 4 2 10 8 1 P2 2 2 1 8 1 145 2931981 VALLIMAYIL 45 2 1 2 1 1 N 145 2931981 VALLIMAYIL 1 0 4 2 2 1 1 P2 2 5 1 1 1 146 3128180 SAKUNTHALA 58 2 1 2 1 1 N 146 3128180 SAKUNTHALA 1 0 4 2 2 1 1 P2 2 2 1 1 1 147 3416577 RAMADEERGAN 40 1 1 3 3 2 N 147 3416577 RAMADEERGAN 1 0 4 3 8 2 1 P2 2 2 3 2 1 148 1256773 VALLIAMMAL 58 2 1 3 3 2 N 148 1256773 VALLIAMMAL 1 0 4 3 8 2 1 P2 2 2 3 2 1 149 1134851 LAKSHMI DEVI 55 2 1 3 2 2 N 149 1134851 LAKSHMI DEVI 1 0 4 2 2 2 1 P2 2 2 2 2 1 150 3514826 PERUMAL 75 1 1 3 3 2 N 150 3514826 PERUMAL 1 0 4 3 8 2 1 P2 2 2 3 2 1 151 1905919 BALIAH 58 1 1 3 3 2 N 151 1905919 BALIAH 1 0 4 3 8 2 1 P2 2 2 3 2 1 152 1213154 PENCHALAMMA 48 2 1 3 2 2 N 152 1213154 PENCHALAMMA 1 0 4 2 2 2 1 P2 2 2 2 2 1 153 3208014 VADIVEL 20 1 1 1 2 3 2 N 153 3208014 VADIVEL 1 0 4 3 8 2 1 C 25 2 0 0 4 154 3240555 MUNIYAPPAN 39 1 1 2 3 2 N 154 3240555 MUNIYAPPAN 1 0 4 3 8 2 1 C 25 2 1 2 4 155 3324255 KOUSHIK 24 1 1 2 1 1 N 155 3324255 KOUSHIK 1 0 4 2 10 1 1 C 25 2 1 1 4 156 3347665 KUMAR 15 1 1 3 3 2 N 156 3347665 KUMAR 1 1 6 4 3 8 2 1 C 25 6 3 2 4 157 3348580 JAI AKASH 9 1 1 3 1 1 N 157 3348580 JAI AKASH 1 1 6 4 2 10 1 1 C 25 6 1 1 4 158 3372746 ANBUMANI 13 1 1 3 3 2 N 158 3372746 ANBUMANI 1 0 4 3 8 2 1 C 25 6 3 2 4 159 3245466 RAMADEVI 45 2 1 1 2 1 2 N 159 3245466 RAMADEVI 1 0 4 2 10 1 1 C 25 2 1 1 4 160 3248520 MOHAMMED THOUSIF 5 1 1 2 1 1 N 160 3248520 MOHAMMED THOUSIF 1 1 6 4 3 8 2 1 C 25 2 1 2 4 161 3483366 SANTHOSH KUMAR 3 1 1 2 1 1 N 161 3483366 SANTHOSH KUMAR 1 0 4 1 10 1 1 C 25 2 1 1 4 162 3487094 ANUGRAHA 12 2 1 2 1 1 N 162 3487094 ANUGRAHA 1 1 6 4 2 2 2 1 C 25 2 1 2 4 163 3474608 ABIMANYU 11 1 1 1 2 3 2 N 163 3474608 ABIMANYU 1 0 4 3 8 2 1 C 25 2 3 2 4 164 3507297 MURUGESAN.A 42 1 1 2 1 1 N 164 3507297 MURUGESAN.A 1 0 4 2 1 1 1 C 25 6 1 1 4 165 3498737 PURUSHOTHAM REDDY 56 1 1 2 2 1 N 165 3498737 PURUSHOTHAM REDDY 1 0 4 2 2 2 1 C 25 6 2 2 4 sno mrno name age gender dv h v t hoh g f dip fv tov pto o onset bcva pupil nerlayer sno mrno name antseg nystag nystagpre eom cv cf fundus cns diagnosis diag rx follbcva follfund tumour 166 1184914 VALLIAPPAN 30 1 1 1 1 2 3 4 N 166 1184914 VALLIAPPAN 1 0 4 3 8 4 1 C 25 6 0 0 4 167 3201194 RANI 33 2 1 3 2 2 N 167 3201194 RANI 1 0 4 2 10 4 1 OG 30 2 0 0 5 168 3256225 THUVISHRAM 6 1 1 1 2 2 1 N 168 3256225 THUVISHRAM 1 1 2 4 1 10 1 1 OCHG 32 1 2 1 5 169 3259818 KALAIVANAN 16 1 1 1 3 1 1 N 169 3259818 KALAIVANAN 1 0 4 1 10 4 1 ONG 31 2 0 0 5 170 3259604 NATRAJAN 27 1 1 1 1 3 3 1 N 170 3259604 NATRAJAN 1 0 4 3 8 3 1 TG 27 2 0 0 5 171 3409473 VARUN 8 1 1 2 2 1 N 171 3409473 VARUN 1 1 2 4 3 8 2 1 OCHG 32 7 2 2 5 172 3415836 HARIHARAN 26 1 1 1 2 3 2 N 172 3415836 HARIHARAN 1 0 4 3 8 3 1 AG 33 2 3 3 5 173 3182743 KASTHURI 32 2 1 3 3 2 N 173 3182743 KASTHURI 1 0 4 3 8 2 1 ONG 31 2 3 2 5 174 3322500 POTHIYAN 32 1 1 1 3 2 1 N 174 3322500 POTHIYAN 1 0 4 3 8 4 1 BG 28 2 0 0 5 175 3610522 DINESH KANNAN 8 1 1 2 3 2 N 175 3610522 DINESH KANNAN 1 0 4 3 8 2 1 OCHG 32 7 3 2 5 176 3614616 RAJA 18 1 1 2 1 1 3 176 3614616 RAJA 2 1 7 3 2 10 1 1 TG 27 2 0 0 5 177 3132010 MARIA MERCHI 6 2 1 2 1 1 N 177 3132010 MARIA MERCHI 1 1 1 4 1 10 8 1 BG 28 3 1 8 5 178 3212438 THIRUMALAIAMMAL 45 2 1 1 2 3 1 N 178 3212438 THIRUMALAIAMMAL 1 0 4 3 8 4 2 GBM 34 4 0 0 6 179 3218181 MURUGAN 40 1 1 1 3 3 2 2,3,4,5,6,7,8 179 3218181 MURUGAN 2 0 3 3 8 1 1 SM 37 2 3 2 6 180 3237449 SIVANATH 47 1 1 3 1 2 N 180 3237449 SIVANATH 1 0 4 1 3 8 1 AS 38 3 0 0 6 181 3259818 KALAIVANAN 16 1 1 1 3 1 1 N 181 3259818 KALAIVANAN 1 0 4 1 10 4 1 AS 38 2 0 0 6 182 3480960 AJITH KUMAR 16 1 1 2 1 1 N 182 3480960 AJITH KUMAR 1 1 2 4 1 10 4 1 GS 39 3 0 0 6 183 3509678 SADANANDAN 68 1 1 2 1 2 N 183 3509678 SADANANDAN 1 0 4 1 3 8 1 GBM 34 3 0 0 6 184 3514086 RAJENDRAN 47 1 1 1 1 2 1 1 6 184 3514086 RAJENDRAN 2 0 1 1 10 4 1 GBM 34 7 0 0 6 185 3611950 AHAMMED MOHAMED BAAB 25 1 1 3 2 3 3 185 3611950 AHAMMED MOHAMED BAAB 2 1 7 3 1 10 1 1 GBM 34 1 2 1 6 186 2177985 SABURA AMMAL 69 2 1 1 2 2 1 6 186 2177985 SABURA AMMAL 2 0 1 1 10 8 1 CS 36 4 2 8 6 187 3335815 HEMAPRIYA 10 2 1 1 2 1 1 N 187 3335815 HEMAPRIYA 1 0 4 1 10 4 1 MB 40 2 0 0 6 188 1144582 KRISHNAN 13 1 1 1 2 2 1 3,4,5,6 188 1144582 KRISHNAN 2 0 3 3 8 4 5 MB 40 2 0 0 6 189 3260029 VENKIAH 65 1 1 3 3 2 3,6 189 3260029 VENKIAH 2 0 3 2 10 1 1 SL 42 3 0 0 7 190 3426432 SEBASTI AMMAL 60 2 1 1 2 2 3 3,6 190 3426432 SEBASTI AMMAL 2 0 3 1 10 1 1 SL 42 3 0 0 7 191 3561476 ARUMUGAM.V 50 1 1 2 1 1 6 191 3561476 ARUMUGAM.V 2 0 1 1 10 8 1 SN 44 3 1 1 7 192 3565918 SELVAMARY 33 2 1 2 3 1 N 192 3565918 SELVAMARY 1 0 4 1 10 4 1 SB 43 7 0 0 7