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Transcript
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE,
KARNATAKA
SYNOPSIS
OF
DISSERTATION
“CLINICAL STUDY, ETIOPATHOGENESIS AND MANAGEMENT OF
OCULOMOTOR NERVE PALSY”
Submitted by
Dr. PRANITHA PRABHU. M.B.B.S.
POST GRADUATE DEGREE STUDENT IN
OPHTHALMOLOGY (M.S.)
Under the guidance of
Prof .Dr. PADMINI, H.R, M.B.B.S., M.S.,D.O.M.S
DEPARTMENT OF OPHTHALMOLOGY
A.I.M.S, B.G.NAGARA-571448.
DEPARTMENT OF OPHTHALMOLOGY
ADICHUNCHANAGIRI INSTITUTE OF MEDICAL SCIENCES,
B.G.NAGARA-571448
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE, KARNATAKA
ANNEXURE II
PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION
Dr. PRANITHA PRABHU.
# 18, KALPATHARU BHAVANA,
P.G. HOSTEL, A.I.M.S.,
B.G.NAGARA. NAGAMANGALA TALUK,
MANDYA DISTRICT-571448
KARNATAKA.
1
NAME OF THE CANDIDATE
AND ADDRESS
(in block letters)
2.
NAME OF THE INSTITUTION
ADICHUNCHANAGIRI INSTITUTE OF
MEDICAL SCIENCES, B.G.NAGARA.
3.
COURSE OF STUDY AND SUBJECT
M.S. IN OPHTHALMOLOGY
4.
DATE OF ADMISSION TO COURSE
5.
TITLE OF THE TOPIC
08-07-2013
A CLINICAL STUDY,ETIOPATHOGENESIS AND
MANAGEMENT OF OCULOMOTOR NERVE PALSY”
.
BRIEF RESUME OF INTENDED WORK
6.
7
APPENDIX-I
6.1 NEED FOR THE STUDY
APPENDIX-IA
6.2 REVIEW OF LITERATURE
APPENDIX-IB
6.3 OBJECTIVES OF THE STUDY
APPENDIX-IC
MATERIALS AND METHODS
APPENDIX-II
7.1 SOURCE OF DATA
APPENDIX-IIA
7.2 METHOD OF COLLECTION OF DATA
: (INCLUDING SAMPLING PROCEDURE
IF ANY)
APPENDIX-IIB
7.3 DOES THE STUDY REQUIRE ANY
INVESTIGATION OR INTERVENTIONS
TO BE CONDUCTED ON PATIENTS OR
OTHER ANIMALS, IF SO PLEASE
DESCRIBE BRIEFLY.
APPENDIX-IIC
7.4 HAS ETHICAL CLEARENCE BEEN
OBTAINED FROM YOUR INSTITUTION
IN CASE OF 7.3
8.
YES
APPENDIX-IID
APPENDIX – III
LIST OF REFERENCES
1
9.
SIGNATURE OF THE CANDIDATE
10.
REMARKS OF THE GUIDE
11
NAME AND DESIGNATION
(in Block Letters)
Isolated oculomotor nerve palsy cases do come to
our department next in order to abducent nerve
palsy. Hence this study may be of clinical
significance since the modalities of diagnostic
techniques are available in this institution. Hence
I recommend this study for submission.
11.1 GUIDE
Dr. PADMINI,H.R., M.B.B.S., M.S., D.O.M.S.,
PROFESSOR AND HEAD
DEPARTMENT OF OPHTHALMOLOGY
AIMS, B.G. NAGARA-571448
11.2 SIGNATURE OF THE GUIDE
-
11.3 CO-GUIDE (IF ANY)
11.4 SIGNATURE
Dr. PADMINI,H.R., M.B.B.S., M.S., D.O.M.S.,
PROFESSOR AND HEAD
DEPARTMENT OF OPHTHALMOLOGY,
AIMS, B.G. NAGARA-571448
11.5 HEAD OF DEPARTMENT
11.6 SIGNATURE
2
12
12.1 REMARKS OF THE CHAIRMAN
AND PRINCIPAL
The facilities required for the investigation will
be made available by the college
Dr. M.G SHIVARAMU MBBS, MD
PRINCIPAL,
AIMS, B.G. NAGARA.
12.2 SIGNATURE
3
APPENDIX-I
6.
BRIEF RESUME OF THE INTENDED WORK:
APPENDIX-IA
6.1
NEED FOR THE STUDY:
A perfect alignment between the motor system of two eyes is responsible
for viewing an object as single. The extraocular muscles of both eyes work in coordination. When any one or more of these falter, it may manifest as double
vision , deviation of eyes or sometimes with pain. Patients may sometimes
present to the ophthalmologist for one of these complaints ,may be referred by
another physician or be seen accidentally while they just come for a routine
checkup. This may be one of the first manifestation of a serious emergency like a
posterior communicating artery aneurysm or a multisystem disease like diabetes.
So every case has to be evaluated and its probable etiology identified. Here lies
the role of an ophthalmologist to decide whether follow up and observation will
suffice or may require emergency intervention by a neurosurgeon.
The diagnosis and management of third nerve dysfunction vary according
to the age of the patient, the characteristics of the third nerve palsy, and the
presence of associated symptoms and signs. Third nerve palsies can result from
lesions located anywhere from the oculomotor nucleus to the termination of the
third nerve in the extraocular muscles within the orbit, and may be the herald
manifestation of underlying neurological emergencies such as intracranial
aneurysm, pituitary apoplexy, and giant cell arteritis. Recent advances in
noninvasive neuroimaging facilitate early diagnosis, but the management of a
patient presenting with isolated third nerve palsy remains a challenge.
4
APPENDIX-IB
6.2
REVIEW OF LITERATURE
Isolated third nerve palsies in patients over age 50 most commonly
result from microvascular ischemic demyelination in patients with vasculopathic
risk factors including diabetes, hypertension, hyperlipidemia and advanced age.
Cranial mononeuropathies have been recognized for centuries. Until the
early and middle part of the twentieth century, most palsies were thought to arise
as a result of tumors, trauma, infections or nutritional deficiencies. Syphilis,
tuberculosis and vitamin deficiencies were felt to be important causes. The first
important pathologic papers on this topic were written by Dreyfus et al 1, and
Asbury, et al2,3. The Asbury paper2, details the histopathology of an 88 year old
woman with diabetes that had a recovered third nerve palsy on one side and died
while about 1 month after developing a pupil sparing third nerve palsy on the
other. Their findings were highlighted by a non inflammatory, presumably
ischemic, demyelinating focus in the intracavernous portion of the third nerve on
the acutely involved side. No evidence of any axonal damage in either the acutely
involved or recovered nerve was found nor was any occlusion of any of the large
blood vessels off of the posterior cerebral, posterior communicating or
intracavernous carotid arteries. However, there was widespread thickening and
hyalinization of arteriolar and capillary walls with luminal narrowing of the
vasonervorum (50-80u diameter vessels). These changes were most extensive in
the intracavernous portion of both third nerves and to a lesser extent in the
subararchnoid sections and uncommon elsewhere in the body. They concluded
that ischemia was the mechanism of the dysfunction based on the focal nature of
the lesion, its bland non inflammatory character, the blood vessel changes
described above and the clinical pattern of recovery. However, they did not
5
discover what precipitated the ischemic event. In attempting to explain the
commonly associated pain, they did not find involvement of the intracavernous
trunks of the trigeminal nerve but they posited that perhaps there were pain
sensitive nerve endings within the sheath and endoneurium itself. They noted
relative sparing of the most peripheral parts of the nerve where the smaller
(presumably) pupillary fibers were located.
In adults, the most common cause of acute ocular motor mononeuropathies
is microvascular ischemia4,5. It is worth noting that the microvascular nature of
this ischemia remains a presumptive diagnosis based on very limited
histopathologic data and presumed because of the absence of other associated
neurologic symptoms or signs, no new findings in the follow up period, a chronic
stable course associated with spontaneous recovery and the setting in which these
palsies generally occur, namely older adults with vasculopathic risk factors, most
notably diabetes but also hypertension, hyperlipidemia and simply advancing
age6-8 . In all of the large series that have found “ischemia” as the most common
cause of the ocular motor nerve palsy, the diagnosis was presumptive and not
based on negative high quality imaging. In the past era when the pathogenesis
and benign nature of the ischemic cranial nerve palsies were first recognized,
only very primitive and invasive tests were available to diagnose vascular lesions
and brain tumors and in vivo demonstration of brainstem stroke was impossible.
The ischemic third nerve palsy can arise in the setting of diabetes,
hypertension, hyperlipidemia and advanced age.7,9 Pain is a common feature and
can be quite severe especially in the young vasculopathy making it an unreliable
method of distinguishing ischemic palsies from more ominous causes. However
isolated third nerve palsies10-20 can arise in many different circumstances.
Midbrain strokes and hemorrhages have been reported to cause isolated pupil
involving or pupil sparing third nerve palsies. Isolated and relative pupil sparing
third nerve palsies have also been described in patients with meningioma,
6
metastases, neurocysticercosis, and severe internal carotid artery stenosis. As well
even divisional palsies have been reported as manifestations of midbrain stroke
or mass lesions.16 The assumption that these alternative diagnoses must be very
rare may be faulty if neuroimaging has only been rarely ordered in these patients.
Other vascular lesions such as posteriorly draining dural fistulas , and cavernous
sinus aneurysms can cause isolated third nerve palsies. Third nerve palsy is also
the most common motility deficit in patients with pituitary apoplexy and it may
be isolated and present with a great degree of variability in the severity of pain
and headache. Lastly, third nerve palsies are well recognized to arise in the
setting of vasculitis, particularly temporal arteritis, and after minor trauma in
patients harboring a mass lesion.
In 1967, Zorilla and Kozak reported pupil sparing in 16 of 20 patients with
oculomotor palsy in association with diabetes mellitus. When the astute physician
could recognize the pupil sparing feature of a third nerve palsy and pronounce
that this was unlikely to be a compressive or vascular lesion, a patient could be
spared an invasive test such as an angiogram or pneumoencephelogram. More
recently, it is well recognized that vasculopathic palsies frequently involve the
pupil to some extent, and as well that, in some patients, diabetic changes affect
the iris sphincter and that pupillary efferent function maybe abnormal in patients
who have had pan retinal photocoagulation. These exam features can limit the
clinician’s ability to use the pupil exam to exclude aneurysms. With this in mind,
the most “high stakes” situations would include third nerve palsy presenting with
pupillary involvement, only relative pupil sparing or younger patients in whom
the pupil exam can not be relied upon in a patient that maybe harboring an
aneurysm. In addition, although rare, relative or complete pupil sparing has been
reported in patients with aneurysms especially early in the clinical course.
7
Causes of Oculomotor Palsy:
Oculomotor palsy can arise as a result of a number of different conditions.
A. Congenital Oculomotor Palsy
The origins of the vast majority of congenital oculomotor palsies are unknown, or
idiopathic to use the medical term. There is some evidence of a familial tendency
to the condition, particularly to a partial palsy involving the superior division of
the nerve with an autosomal recessive inheritance. The condition can also result
from aplasia or hypoplasia of one or more of the muscles supplied by the
oculomotor nerve. It can also occur as a consequence of severe birth trauma.
B. Acquired Oculomotor Palsy
1. Vascular disorders such as diabetes, heart disease, atherosclerosis and
aneurysm, particularly of the posterior communicating artery
2. Space occupying lesions or tumours, both malignant and non-malignant
3. Inflammation and Infection
4. Trauma
5. Demyelinating disease (Multiple sclerosis)
6. Autoimmune disorders such as Myasthenia gravis
7. Post operatively as a complication of neurosurgery
8. Cavernous sinus thrombosis
8
Pathophysiology:
The anatomical relationship of the various portions of the third cranial
nerve accounts for many of the clinical features of third cranial nerve palsy as
outlined below.
Nuclear portion: The cell bodies for axons that travel in the oculomotor
nerve reside in the column-shaped nuclear groups on either side of the midbrain
tegmentum. The axons destined for each extraocular and intraocular muscle
derive from a specific subnucleus.
Fascicular intraparenchymal midbrain portion: The fascicular portion of
the oculomotor nerve courses ventrally from the nucleus in the dorsal midbrain
tegmentum, passes through the red nucleus, and emerges from the medial aspect
of the cerebral peduncle.
Fascicular subarachnoid portion: The cisternal portion of the nerve is in the
subarachnoid space anterior to the midbrain and in close proximity to the
posterior communicating artery. Berry aneurysm at the junction between the
posterior communicating artery and the internal carotid artery is an important
cause of oculomotor nerve palsy.
Fascicular cavernous sinus portion: The next segment of the oculomotor
nerve runs through the lateral wall of the cavernous sinus superiorly. It enters the
cavernous sinus just above the petroclinoid ligament and inferior to the
interclinoid ligament. Masses invading the cavernous sinus from within the sella
are most likely to cause third cranial nerve dysfunction prior to involvement of
the other cranial nerves in the cavernous sinus. This is probably because of the
oculomotor nerve's close proximity to the unyielding interclinoid ligament above
and the petroclinoid ligament below.
9
Fascicular orbital portion: The oculomotor nerve enters the orbit through
the superior orbital fissure adjacent to the fourth cranial nerve. The nerve
branches into superior and inferior divisions, usually within the posterior orbit,
but, occasionally, the branching occurs as far back as the cavernous sinus
segment. The superior division innervates the levator palpebrae and the superior
rectus muscles; the inferior division innervates all the other muscles, including
the iris sphincter, which constricts the pupil.
The axons for most of the muscles are uncrossed from the nucleus to the
eye, but there are 2 exceptions: (1) Axons for the levator palpebrae come from
both sides of the central caudal subnucleus via crossed and uncrossed pathways.
(2) Those for the superior rectus muscle come from the superior rectus
subnucleus on the contralateral side.
The pupillomotor and ciliary muscle neurons derive from the EdingerWestphal subnucleus, which is in the midline in the most rostral and anterior part
of the oculomotor nerve nucleus. These autonomic pathways are all ipsilateral or
uncrossed.
The oculomotor nerve innervates the following extraocular muscles of
either eye: superior rectus, inferior rectus, medial rectus, inferior oblique, levator
palpebrae, ciliary muscle, and iris sphincter.
Third nerve palsy results from damage to the oculomotor nerve anywhere
in its course from the nucleus in the dorsal mesencephalon, its fascicles in the
brainstem parenchyma, the nerve root in subarachnoid space, or in the cavernous
sinus or posterior orbit. Damage to the third nerve nucleus results in an ipsilateral
third nerve palsy with contralateral superior rectus under action and bilateral
ptosis. Damage to the third nerve fascicles results in an ipsilateral third nerve
palsy with contralateral hemiparesis (Weber's syndrome), contralateral intention
10
tremor
(Benedikt's syndrome),
or
ipsilateral
cerebellar
ataxia
(Nothnagel's syndrome). Vascular infarct, metastatic disease and demyelinization
are the common causes of brainstem involvement.
Damage to the third nerve within the subarachnoid space produces an
isolated third nerve palsy. The main causes are compression of the nerve by an
expanding aneurysm of the posterior communicating artery or the basilar artery,
and ischemic vasculopathy. There will always be pain in aneurysmal
compression and pupillary involvement is typical, though there have been
infrequent cases of aneurysmal compression that did not initially affect pupillary
function. In ischemic vascular nerve third palsies, pain is frequent and the pupil is
typically normal and reactive.
Damage to the third nerve in the cavernous sinus, superior orbital fissure,
or posterior orbit is unlikely to present as third nerve palsy due to the confluence
of other structures in these areas. Cavernous sinus involvement may also include
pareses of cranial nerves IV, VI and V1, and an ipsilateral Horner's syndrome.
The most common causes of damage in these areas include metastatic disease,
inflammation, herpes zoster, carotid artery aneurysm, pituitary adenoma and
apoplexy, and sphenoid wing meningioma.
Features of Oculomotor Palsy:
The features of third nerve palsy are: It may be complete or incomplete and
it may be congenital or acquired.
1. Ptosis - due to paralysis of Levator Palprebrae Superioris
11
2. Deviation - eyeball is turned down , out and slightly intorted due to unopposed
action of the lateral rectus and the superior oblique
3. Ocular movements – restriction of the following movements:
i. adduction - due to paralysis of medial rectus,
ii. elevation - due to paralysis of superior rectus and inferior oblique,
iii. depression - due to paralysis of inferior rectus and
iv. extorsion - due to paralysis of inferior rectus and inferior oblique.
4. Pupil - is fixed and dilated due to paralysis of sphincter pupillae
5. Accomodation - completely lost due to paralysis of ciliary muscle
6. Crossed diplopia - appears on manually raising the eyelid, which occurs due to
paralytic divergent squint
7. Head posture - if the pupillary area is uncovered the head takes a posture
consistent with the directions of actions of paralysed muscle i.e head is turned to
the opposite side , tilted towards the same side and chin is slightly raised.
12
APPENDIX-IC
6.3
AIM OF THE STUDY
 To analyse the various etiologies and pathogenic factors leading to
oculomotor nerve paralysis.
 To analyse the common clinical patterns arising in the background of
acquired oculomotor nerve palsy .
6.4
OBJECTIVES OF THE STUDY
 To assess the visual outcome in patients with isolated third nerve palsy.
 To assess the binocular alignment in patients with isolated third nerve
palsy.
13
APPENDIX-II
7.0
MATERIALS AND METHODS
APPENDIX-II A
7.1
SOURCE OF DATA
The material for the present study is proposed to be collected from
the patients presenting themselves directly to Department of Ophthalmology
(Hospital: Adichunchanagiri Institute of Medical Sciences, B.G.Nagara, Mandya
district) or referred by Physician will be undertaken for the study.
A prospective cohort study of a sample size of a minimum of 20 patients
fulfilling the mentioned inclusion criteria will be a part of this study.
APPENDIX-II B
7.2
METHOD OF COLLECTION OF DATA
 Those patients on routine screening having isolated oculomotor nerve palsy
have been selected for this study.
Inclusion criteria:
 Both male and female patients.
 Isolated oculomotor nerve palsy.
Exclusion criteria:
 Congenital oculomotar nerve palsies have been excluded.
 Patients with incomitant squint due to myogenic, myasthenic and
restrictive causes have been excluded.
14
APPENDIX-II C
7.3
Does the study require any investigation or intervention to be conducted on the
patients, if so please describe briefly.
Yes it requires the following investigations to be conducted on patients
included in this study.
 Patients with paralytic squint were identified and details regarding their
name, age, sex, symptoms, and its duration and any change in the
symptoms between their presentation and their onset have been recorded.
Detailed history regarding the incidences that preceded the onset of
symptoms like trauma [trivial or severe], headache fainting attacks,
numbness, etc., was taken.
 Past history of any previous episodes of similar nature and the treatment
given for the same has been noted. History of systemic illnesses like
hypertension, diabetes-mellitus, thyroid abnormalities, and seizure disorder
and previous neurological involvement in any other disorders like
tuberculosis, syphilis, were noted.
 History specific to ocular complaints such as double vision, blurring of
vision, field defects, and vestibular complaints like vertigo, tinnitus, ear
discharge, and bleeding per year have been recorded.
 Personal history regarding smoking, alcohol intake and diet pattern were
asked and recorded.
 A complete haemogram, urine analysis for albumin, sugar, and deposits,
blood sugar VDRL, Mantoux test, X-ray of skull (both anteroposterior and
lateral)and paranasal sinuses and optic foramen has been done for all
patients. CT-scan was done in almost all trauma cases and in other cases
whenever possible. MRI-scan was done whenever it was possible. Certain
special tests like neostigmine test has been done in certain cases to
diagnose and to differentiate myasthenia gravis from nerve palsies.
15
 Follow up of these cases has been done at the end of 4 weeks, 8weeks,
12weeks, and 6 months in case of patients living nearby and at an interval
of 4weeks, 12weeks, and 6months in case of patients coming from far off
places.
OPTHALMOLOGICAL EXAMINATION:
 General:
 Systemic (CNS):
 Higher Function
 Cranial Nerves
 Sensory and Motor Reflex
 Cerebellar Systems
 Ocular:
 Head Posture
 Facial Asymmetry
 Lid Position
 Extra Ocular Movements
 Anterior Segment
 Pupil
 Visual acuity
 Fundus
 Investigations
General:
 Pulse
 BP
 Temperature
Ocular:
16
 Visual acuity
 Refraction
 Intra-ocular Pressure
 Hess charting
 Diplopia Charting
 Fields
Orthoptic evaluation:
 Cover Test
 Prism Bar Cover Test
 Worth’s Four Dot Test
 Binocular Single Vision
Lab Investigations:
 Haemogram
 RBS
 Urine Routine
 Mantoux, VDRL
 X-Ray, CT Scan and MRI Scan
Intervention:
 Medical management is watchful waiting, since nearly all patients
undergo spontaneous remission of the palsy, usually within 6-8 weeks.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the first-line
treatment of choice for the pain. When diplopia is from large-angle
divergence of the visual axes, patching one eye is the only short-term
solution. When the angle of deviation is smaller, fusion in primary
position often can be achieved using horizontal or vertical prism or
both.
17
 Surgical management includes clipping, gluing, coiling, or wrapping of
the berry aneurysm by a neurosurgeon in the acute stage. Patients who
do not recover from third cranial nerve palsy after 6-12 months may
become candidates for eye muscle resection or recession to treat
persistent and stable-angle diplopia. Some of these patients also may
require some form of lid-lift surgery for persistent ptosis that restricts
vision or is cosmetically unacceptable to the patient.
18
APPENDIX-II D
PROFORMA APPLICATION FOR ETHICS COMMITTEE
APPROVAL
SECTION-A
a) Title of the Study
“CLINICAL STUDY, ETIOPATHOGENESIS
AND MANAGEMENT OF OCULOMOTOR
NERVE PALSY”
b) Principal Investigator (Name and
Designation)
Dr.PRANITHA PRABHU
P.G.IN OPHTHALMOLOGY
ADICHUNCHANAGIRI INSTITUTE OF
MEDICAL SCIENCES, B.G.NAGARA
MANDYA DISTRICT-571448
c) Co-investigator (Name and
Designation)
d) Name of the Collaborating
Department/ Institutions
e) Whether permission has been
obtained from the Heads of the
collaborating departments &
Institution
SECTION-B
a) SUMMARY OF THE Project
Prof.Dr.PADMINI, H.R., M.B.B.S., M.S., D.O.M.S.
PROFESSOR & HEAD
DEPARTMENT OF OPHTHALMOLOGY
A.I.M.S., B.G.NAGARA-571448
DEPARTMENT OF MEDICAL EDUCATION
YES
APPENDIX-I
SECTION-C
a) Objectives of the Study
APPENDIX-I C
SECTION-D
a) Methodology
APPENDIX-II B
A
Where the proposed study will be
undertaken
ADICHUNCHANAGIRI INSTITUTE OF
MEDICAL SCIENCES, B.G.NAGARA
MANDYA DISTRICT-571448
B
Duration of the Project
18 Months
19
C
Nature of the subjects
Does the study involve adult patients?
YES
Does the study involve Children?
NO
Does the study involve normal volunteers?
NO
Does the study involve Psychiatric patients?
NO
Does the study involve pregnant women?
YES
D
If the study involves health volunteers
i.
Will they be institute students?
NO
ii.
Will they be institute employees?
NO
iii. Will they be paid
NO
iv. If they are to be paid, how much per session?
NA
E
Is the study a part of multi central trial?
NO
F
If yes, who is the coordinator (Name and Designation
NA
Has the trial been approved by the Ethics Committee of the other centers?
NA
If the study involves the use of drugs, please indicate whether:
NA
i.
The drug is marketed in India for the indication in which it will be used in the
study
ii. The drug is marketed in India but not for the indication in which it will be used in
the study
iii. The drug is only used for experimental use in human
iv. Clearance of the drugs controller of India has been obtained for.
G
NA
 Use of the drug in healthy volunteers
-
 Use of the drug in-patients for a new indication
-
 Phase one and two clinical trials
-
 Experimental use in-patients and healthy volunteers.
-
How do you propose to obtain the drug to be used in the study?
NA
 Gift from a drug company
-
 Hospital supplies
-
 Patients will be asked to purchase
-
 Other sources (explain)
-
20
H
Funding (If any) for the project please state
NA
 None
-
 Amount
-
 Source
-
 To whom payable
-
I
Does any agency have a vested interest in the outcome of the Project?
NO
J
Will data relating to subjects/controls be stored in a computer?
YES
K
Will the data analysis be done by:
L
 The researcher?
YES
 The funding agent
NO
Will technical/nursing help be required from the staff of hospital
NO
If yes, will it interfere with their duties?
-
Will you recruit other staff for the duration of the study?
-
If Yes, give details of:
-
i.
Designation
ii.
Qualification
iii. Number
iv. Duration of employment
M
N
Will informed consent be taken? If yes,
Will it be written informed consent
NO
Will it be oral consent?
YES
Will it be taken from the subject themselves?
YES
Will it be from the legal guardian? If no, give reason
YES
Describe design, Methodology and techniques
APPENDIX-II
Ethical clearance has been accorded
Chairman
PG Training-cum-Research Institute
AIMS, B.G.Nagara
21
APPENDIX-III
8.
LIST OF REFERENCES
1. Dreyfus PM, Hakim S, Adams RD. Diabetic ophthalmoplegia; report of case,
with postmortem study and comments on vascular supply of human oculomotor
nerve. AMA Arch Neurol Psychiatry 1957;77:337-349.
2. Asbury AK, Aldredge H, Hershberg R, et al. Oculomotor palsy in diabetes
mellitus: a clinico-pathological study. Brain 1970;93:555-566.
3. Asbury AK, Fisher CM, Aldredge H, et al. Diabetic ophthalmoplegia: a
clinico-pathologic investigation. Trans AmNeurol Assoc 1969;94:64-68.
4. Richards BW, Jones FR, Jr., Younge BR. Causes and prognosis in 4,278 cases
of paralysis of the oculomotor, trochlear, and abducens cranial nerves. Am J
Ophthalmol 1992;113:489-496.
5. Rush JA, Younge BR. Paralysis of cranial nerves III, IV, and VI. Cause and
prognosis in 1,000 cases. Arch Ophthalmol 1981;99:76-79.
6. Sanders SK, Kawasaki A, Purvin VA. Long-term prognosis in patients with
vasculopathic sixth nerve palsy. Am J Ophthalmol 2002;134:81-84.
7. Jacobson DM, McCanna TD, Layde PM. Risk factors for ischemic ocular
motor nerve palsies. Arch Ophthalmol 1994;112:961-966.
8. Capo H, Warren F, Kupersmith MJ. Evolution of oculomotor nerve palsies. J
Clin Neuroophthalmol 1992;12:21-25.
9. Teuscher AU, Meienberg O. Ischaemic oculomotor nerve palsy. Clinical
features and vascular risk factors in 23 patients. J Neurol 1985;232:144-149.
10. Shintani S, Tsuruoka S, Minato Y, et al. Radiologic-clinical correlation.
Isolated third nerve palsy caused by midbrain hemorrhage. AJNR Am J
Neuroradiol 1994;15:1508-1511.
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11. Rabadi MH, Beltmann MA. Midbrain infarction presenting isolated medial
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