study of ocular motor nerve palsies in diabetes...

Dissertation on

STUDY OF OCULAR MOTOR NERVE PALSIES IN DIABETES MELLITUS

Submitted in partial fulfilment of requirements of

M. S. OPHTHALMOLOGY

BRANCH III Of

REGIONAL INSTITUTE OF OPHTHALMOLOGY

MADRAS MEDICAL COLLEGE CHENNAI – 600 003

THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY

CHENNAI-600 003

MAY – 2019

CERTIFICATE

This is to certify that this dissertation titled “ Study of ocular motor

nerve palsies in diabetes mellitus” is a bonafide record of the research work

done by Dr.V.SARANYA., Post graduate in Regional Institute of

Ophthalmology, Madras Medical College and Research Institute, Government

General Hospital,Chennai-03, in partial fulfilment of the regulations laid down

by The Tamil Nadu Dr.M.G.R. Medical University for the award of

M.S.Ophthalmology Branch III, under my guidance and supervision during the

academic years 2016-2019.

Prof. Dr.M.V.S. PRAKASH MS.DO.,

Department of Orbit and

Oculoplasty services,

Regional Institute of Ophthalmology

Madras Medical College & Research Institute, Govt. General Hospital,

Chennai – 600 008

Prof. .M.ANAND BABU M.S. D.O.,

Director and Superintendent, Regional Institute of Ophthalmology

Madras Medical College & Research Institute,

Govt. General Hospital,

Chennai – 600 008

Prof. DR.R.JAYANTHI M.D.,FRCP(Glas)

DEAN

Madras Medical College,

Government General Hospital & Research Institute,

Chennai-600003

ACKNOWLEDGEMENT

I would like to thank Prof. DR.R.JAYANTHI., M.D.,FRCP (Glas),

Dean, Madras Medical College and Research Institute for giving me

permission to conduct the study in this Institution.

With due respect and gratitude, I thank Prof.Dr.M.ANAND BABU,

M.S., D.O., Director and superintendent, Regional Institute of Ophthalmology

and Govt. Ophthalmic Hospital, Chennai for permitting me to conduct this

study.

Prof.Dr.M.V.S.PRAKASH, M.S.,D.O., Unit Chief, Orbit and

Oculoplasty services, and my guide for assigning me this topic for study and

guiding me throughout my Post graduate course. I wish to express my sincere

thanks for the valuable help, encouragement and guidance at various stages of

the study.

My sincere thanks to my Assisstant Professors

Dr. T.G. Uma Maheswari, MS, Dr.P.Geetha, MS.DO, Dr.R.Sujatha,MS.,

for their timely help and guidance in conducting this study.

I wish to express my sincere thanks to my family, friends and all my

colleagues who helped me in bringing out this study. Last but not the least, my

heartful gratitude and sincere thanks to all my patients without whom this

endeavour would not have been possible.

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled, “STUDY OF OCULAR

MOTOR NERVE PALSIES IN DIABETES MELLITUS” is a bonafide and

genuine research work conducted by me under the guidance of

Prof. Dr.M.V.S.PRAKASH, M.S., D.O., Head of Department of Orbit and

Oculoplasty services, Regional institute of ophthalmology & Government

Ophthalmic hospital. Chennai-600008.

Dr. V.SARANYA

Place: Chennai

Date:

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This is to certify that this dissertation work titled “STUDY OF

OCULAR MOTOR NERVE PALSIES IN DIABETES MELLITUS” of the

candidate DR.V.SARANYA with registration number 221613012 for the

award of MS in the branch of OPHTHALMOLOGY.

I personally verified the urkund.com website for the purpose of

plagiarism Check. I found that the uploaded thesis file contains from

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in the dissertation.

Guide & Supervisor sign with Seal

CONTENTS

S.No. Title Page No.

PART 1

1 INTRODUCTION AND REVIEW OF

LITERATUREND REVIEW OF

LITERATURE

2 DEFINITION AND CLASSIFICATION

3 BIOCHEMICAL MECHANISM OF

DIABETIC TISSUE DAMAGE

4 OCULAR MANIFESTATIONS OF

DIABETES MELLITUS

5 OCULOMOTOR NERVE

6 TROCHLEAR NERVE

7 ABDUCENS NERVE

8 FEATURES OF OCULAR MOTOR NERVE

PALSY IN DM

9 TREATMENT OF OCULAR MOTOR

NERVE PALY

PART 2

10 AIM OF THE STUDY

11 MATERIALS AND METHODS

12 RESULTS AND ANALYSIS

13 DISCUSSION

14 CONCLUSION

PART 3

15 BIBLIOGRAPHY

16 PROFORMA

17 KEY TO MASTER CHART

18 MASTER CHART

ABBREVIATIONS

DM - Diabetes mellitus

SOF - Superior orbital fissure

AGEs - Advanced glycation end products

VEGF - Vascular endothelium growth factor

NPDR - Non proliferative diabetic retinopathy

PDR - Proliferative diabetic retinopathy

NAD - No abnormal deviations

EOM - Extra ocular movements

FBS - Fasting blood sugar

PPBS - Post prandial blood sugar

HbA1C - Glycated haemoglobin

1

INTRODUCTION

2

INTRODUCTION

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

co-ordination. When any one or more of these falter, it may manifest as double

vision, drooping of eyelids, deviation of eyes or sometimes with pain. Patients

may present to the ophthalmologist for one of these complaints, may be

referred by another physician or be seen accidentaly while they come for a

routine checkup. This may be one of the first manifestation of a multisystem

disease like diabetes mellitus.

3

REVIEW OF LITERATURE

4

REVIEW OF LITERATURE

The best early evidence of description of diabetes in worlds literature is

recorded in EbersPapyres dated 1550 BC. Arateus of Cappadocia coined the

term `diabetes’ meaning “siphon”, to explain the liquefaction of flesh and bone

into urine

In 400B.C. Susrata , an indian surgeon had described the diabetic

syndrome as characterised by a “honeyed urine”.

Diabetic retinopathy was first described in 1869 by Eduard von

Jauger,and specific lesions like –“Microaneurysms and new vessels”-were

described by Stephan Mackenzie and Edward Nettleship in 1880.

In 1964 ,Marchal de calvi associated neuropathy with diabetes and

symptoms were clearly reported by Frederide pavy in1885.Albuminuria was

noted as a common abnormality in diabetic patients by Joslin in 1916.

5

DEFINITION AND

CLASSIFICATION

6

DEFINITION

Diabetes mellitus is defined as a group of metabolic diseases

characterized by hyperglycaemia resulting from defects in insulin secretion,

insulin action or both. The chronic hyperglycaemia is associated with long-

term damage, dysfunction and failure of various organs, especially the eyes,

kidney, nerves, heart and blood vessels.

CLASSIFICATION OF DIABETES MELLITUS

Type 1 (β-cell destruction usually leading to absolute insulin deficiency )

Autoimmune

Idiopathic

Type 2

Ranges from predominantly insulin- resistant with relative insulin

deficiency to a predominantly insulin - secretory defect with or without insulin

resistance.

7

Other specific types

Genetic defects β – cell function

Genetic defects of insulin action

Diseases of exocrine pancreas

Endocrinopathies

Drug induced or chemical – induced

Infections

Uncommon form of immune mediated diabetes

Other genetic syndromes sometimes associated with diabetes

Gestational diabetes

8

BIOCHEMICAL MECHANISMS OF

DIABETES TISSUE DAMAGE

9

BIOCHEMICAL MECHANISMS OF DIABETES TISSUE DAMAGE

• Chronic tissue damage in diabetes is generally related to the severity and

duration of hyperglycaemia. Other determinants of specific complication

include genetic predisposition and hypertension. Tissue damage may

continue to evolve even after hyperglycaemia has been improved

(hyperglycaemic memory).

• Diabetes particularly affects tissue in which glucose uptake increases

during hyperglycaemia, leading to raised intracellular glucose

concentration. High glucose levels may cause cumulative and

progressive tissue damage through irreversible alteration of structural

protein and other long-lived molecules, or (e.g.in the retina) through the

summation of micro vascular occlusion.

• At cellular level, hyperglycaemia may damage tissues by enhanced

glucose flux through the polyol pathway; formation of advanced

glycation end-product (AGEs); activation of protein kinase (PKC); and

stimulation of the hexosamine pathway. All these mechanism may stem

ultimately from overproduction of superoxide by mitochondria, which

metabolize excess glucose.

10

• The polyol pathway, whose rate-limiting enzyme is aldose reductase,

reduce glucose and several other sugars (e.g. glucose to sorbitol). The

pathway operates in tissues that express aldose reductase (e.g. lens,

retina, endothelium), particularly during hyperglycaemia. Cellular

damage may result from enhanced production of glycating sugars (e.g.

methyglyoxal) and thus AGE formation, and/or depletion of reduced

glutathione (a scavenger of reactive oxygen species ,ROSs),resulting in

oxidative damage.

Normal glucose

↓

Normal intracellular glucose

↙ ↘

Glucokinase Aldose reductase

(low Km high affinity) (high Km low affinity)

↓ ↓

Glycolytic > polyol

Pathway pathway

Fig 1 a : The Polyol pathway

The pathway is normally inactive ,but becomes active when intracellular

glucose level rise.

11

Glucose Methylglyoxal

NADPH

NADP AGE formation

Sorbitol ₊ Aldone reductase ₊ Acetol

NADPH

₊ Sorbitol dehydrogenase

NADP

Fructose

1.↓NADPH causes

• Reduced glutathione depletion

• Oxidative damage

2.↑NADH/NAD⁺ causes

• Increase Triose Phosphates(AGE formation)

• PKC activation

Fig.1 b: Polyol Pathway

1

2

12

Consequences of increased glucose flux through polyol pathway

includes the generation of powerful glycating sugars (methyglyoxal, acetol and

triose phosphates), enhanced oxidative damage protein kinase C (PKC)

activation.

• AGEs are the irreversible products of proteins that react with glycating

sugars such as 3- deoxy glucosone, methyglyoxal and the relatively

weak glucose. Covalent cross-linking and other changes damage

structural proteins (e.g.collagen) and extracellular matrix components,

while circulating AGE-modified proteins bind to specific receptors for

advanced glycation endproducts (RAGEs) on macrophages and

endothelial cells. Macrophages release proinflammatory cytokines,

while endothelial cells express procoagulant and adhesion proteins that

favour thrombosis and ultimately atheroma formation; endothelial

expression of vascular endothelium-derived growth factor (VEGF) also

increases vascular permeability.

13

Glucose Early glycation

₊ products

Protein

↕ Advanced glycation

Schiff base end products

↕

Amadori product

↓ Electrophilic pyrolle

3 deoxy glucosone intermediates

Fig.2:

Formation of reversible, early, non-enzymatic glycation products and of

irreversible advanced glycation and products (AGEs). Through a complex

series of chemical reaction, amadori products can form families of imidazole

based and pyrrole – based glucose derived cross-link.

Reversible stage Poorly reversible Completely irreversible

14

PKC isoforms (especially β and δ) are activated by diacyl glycerol (DAG),

synthesized de-novo from increased intracellular glucose. This may decrease

tissue blood flow (by inhibiting production of the potent vasodilator, nitric

oxide) and enhance vascular permeability via increased VEGF expression,

induction of plasminogen activator inhabitor – 1 (PAI-1) expression may

favour thrombosis.

Fig.3

Glucose flux

Diacylglycerol

Protein kinase C activity

Hyperglycemia

Permeability vasoactive harmones basement membrane

VEGF Blood flow changes synthesis

Endothelin ‐ 1

15

Activation of protein kinase – C by de-novo synthesis of diacylglycerol,

following increased glucose utilization.

• High intracellular glucose levels result in increased production of

glucosamine,which by leading to glycation of transcription factors

(forming their O-Glc Nacylated derivatives) may enhance transcription

of specific genes including PAI – 1 and transforming growth factor β1

(TGF-β1).

16

Fig. 4 The Glucosamine pathway

Glucosamine-6phosphate,generated from fructose-6 phosphate and

glutamine(gln) ,is converted to UDP-N acetyl glucosamine, which can glycate

transcription factors and thus enhance transcription of genes including PAI-1

Extra cellular

Cystosol

Nucleus

UDP ‐ Glc NAc

Transcription PAI‐1 TGF‐ β₁

Glucosamine 6 phosphate

AZA Glu

Fructose 6 phosphate

Gln

Glucose 6 phosphate

Glucose

Glycation of transcription factors – o – Glc NAc

GFAT

Glycolytic pathway

Glucose

17

and TGF β₁ Glutamine:fructose-6 phosphate amidotransferase(GFAT),the rate -

limiting enzyme is inhibited by azaserine(AZA).

Excess mitochondrial production of the ROS, superoxide, may cause all

the above abnormalities. Superoxide production via the tricarboxylic acid(

TCA) cycle is increased by hyperglycaemia; consequences include

stimulation of aldose reductase activity, enhanced formation of methylglyoxal

and thus AGE, increased DAG synthesis and PKC activation, and hexosamine

pathway overactivity.

18

OCULAR MANIFESTATIONS OF DIABETES MELLITUS

S. No STRUCTURE MANIFESTATIONS

EXTRAOCULAR

1

LIDS Ptosis, xanthelasma, chronic blepharitis,

Recurrent stye & chalazion

2 EXTRAOCULAR

MUSCLES

Mononeuropathy

3 LACRIMAL

APPARATUS

Decreased tear secretion, increased tear

glucose levels

4 ORBIT Orbitorhinomucormycosis

OCULAR

1 CORNEA Corneal hypoesthesia, Recurrent erosions,

corneal abrasions, punctate keratopathy,

neurotrophic keratitis

2 IRIS AND PUPIL Rubeosis iridis, small pupil, neovascular

glaucoma

3 ANGLE

STRUCTURES

Open angle glaucoma, secondary

glaucoma

4 LENS Fluctuating myopia, snowflake cataract,

senile cataract

5 VITREOUS Posterior vitreous detachment, asteroid

bodies

6 RETINA Diabetic retinopathy, lipaemia retinalis,

decreased contrast sensitivity and colour

vision

7 OPTIC NERVE Anterior ischemic optic neuropathy, optic

atrophy

These are the associated findings in diabetes. We can look for them ,so that

they aid in clinical diagnosis of ocular motor nerve palsies.

19

EARLY TREATMENT DIABETIC RETINOPATHY STUDY (ETDRS)

CLASSIFICATION OF DIABETIC RETINOPATHY

NON PROLIFERATIVE DIABETIC RETINOPATHY(NPDR)

1.MILD NPDR Any or all of microaneurysms,

retinalhaemorrhages, exudates, cotton

wool spots, upto the level of moderate

NPDR

2.MODERATE NPDR Severe retinal haemorrhages: about 20

medium-large per quadrant in 1-3

quadrants or mild IRMA

Significant venous beading can be present

in no more than one quadrant

Cotton wool spots commonly present

3.SEVERE NPDR The4-2-1 rule;one or more of:

• Severe haemorrhages in all 4

quadrants

• Significant venous beading in 2 or

more quadrants

• Moderate IRMA in 1 or more

quadrants

PROLIFERATIVE DIABETIC RETINOPATHY (PDR)

1.EARLY PDR New vessels on the disc (NVD) or new

vessels elsewhere(NVE) but extent

insufficient to meet the high risk criteria

2.HIGH RISK PDR NVD about one 1/3 disc area

Any NVD with vitreous

haemorrhage,NVEgreater than1/2 disc

area with vitreous haemorrhage

20

OCULOMOTOR NERVE

21

OCULOMOTOR NERVE

ANATOMY

The third cranial nerve is entirely motor in function. It supplies all the

extraocular muscles of the eyeball except the lateral rectus and superior

oblique. It also supplies the intraocular muscles namely the sphincter pupillae

and the ciliary muscles.

FUNCTIONAL COMPONENTS

1.SOMATIC EFFERENT- concerned with movements of the eyeball.

2.GENERAL VISCERAL EFFERENT(parasympathetic)- for accommodation

and constriction of the pupil.

3.GENERAL SOMATIC AFFERENT- for carrying proprioceptive impulses

from the muscles supplied by the third nerve.

THE OCULOMOTOR NUCLEAR COMPLEX

LOCATION

It is situated in the midbrain at the level of the superior colliculus in the

ventromedial part of the central grey matter that surrounds the cerebral

aqueduct.

22

It is a longitudinal column, 10mm long extending above from the floor of the

third ventricle and below it is related to the nucleus of the fourth nerve. There

are two motor nuclei.

1.Main motor nucleus of the large multipolar neurons.

2.Accessory Edinger Westpal nucleus of small multipolar neurons.

The main motor nucleus has the following subnuclei:

1.DORSOLATERAL NUCLEUS-supplies ipsilateral inferior rectus

2.INTERMEDIATE NUCLEUS-supplies ipsilateral inferior oblique

3.VENTROMEDIAL NUCLEUS-supplies ipsilateral medial rectus

4.PARAMEDIAL NUCLEUS-supplies contralateral superior rectus

5.CAUDAL CENTRAL NUCLEUS-supplies bilateral levator palpebrae

superioris.

The Edinger Westphal nucleus lies posterior to the main occulomotor

nuclear mass.It consists of a median and two lateral parts.It gives rise to

preganglionic parasympathetic fibres.

23

CONNECTIONS OF THE NUCLEUS

1.Cerebral cortex

• Motor cortex of both sides through the corticonuclear tracts

• Visual cortex through the superior colliculus

• Frontal eye field

2.Nuclei of 4,6 and8 cranial nerves through the medial longitudinal fasciculus.

3.Pretectal nucleus of both sides

4. Vertical and torsional gaze centres.

5. Cerebellum through the vestibular nuclei.

COURSE AND DISTRIBUTION

It can be divided into four parts

1. The fascicular part

2. The basilar part

3. The intracavernous part

4. The intraorbital part

24

THE FASCICULAR PART

It consist of efferent fibres that pass from the third nerve nucleus

through the red nucleus and the medical and small lateral root, which unite to

from a flattered nerve, which then gets twisted bringing the inferior fibres

superiorly and vice versa. Thus the nerve becomes a rounded cord. The nerve

then passes between the posterior cerebral and superior cerebellar arteries.

Then it runs forward in the interpeduncular cistern (running lateral and parallel

to the posterior communicating artery) to reach the cavernous sinus.

THE INTRACAVERNOUS PART

The nerve enters the cavernous sinus by piercing the posterior part of its

roof on the lateral side of the posterior clinoid process. It then descends on the

lateral wall sinus, where it lies above the trochlear nerve. In the anterior part of

the cavernous sinus, the nerve divides into superior and inferior divisions

which enter the orbit through the middle part of the superior orbital fissure

within the annulus of Zinn.

THE INTRAORBITAL PART

In the orbit the smaller superior divisions ascends on the lateral side of

the optic nerve and supplies the superior rectus and levator palpebrae

superioris. The larger inferior division divides into three branches.

25

i. Nerve to medial rectus passes inferior to the optic nerve.

ii. Nerve to inferior olique (longest of the three branches) passes in

between the inferior rectus and lateral rectus and supplies the

oblique from its posterior border. It gives off the motor root to

the ciliary ganglion.

iii. Nerve to inferior rectus passes and enters the muscle on its upper

aspect.

LATERAL VIEW OF THE COURSE OF THIRD NERVE

26

THE FEATURES OF THIRD NERVE PALSY

It may be complete or incomplete and it may be congenital or acquired.

1. Ptosis-due to paralysis of LPS.

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.

• Adduction –due to paralysis of medial rectus

• Elevation –due to paralysis of superior rectus and inferior oblique

• Depression- due to paralysis of inferior rectus

• Extortion-due to paralysis of inferior rectus and inferior oblique

4. Pupil-is fixed and dilated due to paralysis of sphincter pupillae.

5. Accommodation – 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 papillary 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, titled towards the same side and chin

is slightly raised.

27

PUPIL SPARING ISOLATED III NERVE PARESIS

The pupillomotor fibres of the III nerve travel in the outer layers of the

nerve and are therefore closer to the nutrient blood supply enveloping the

nerve. The outer fibres are supplied by the pial plexus whereas the inner fibres

are supplied by the vasa nervosum.

So this explains why the diabetics (where the vasa nervonum are

affected) have pupillary sparing in 80% and similarly in any ischaemic vascular

etilogy. In contradiction when compressive lesions involve the III nerve the

superficial fibres are affected resulting in pupillary involvement in 90%.

Most patients with ischaemic III nerve paresis demonstrate improvement

in motility measurements within one month or may have complete recovery by

3 months (maximum : 6 months).

LOCATION OF PUPILLOMOTOR FIBRES WITHIN THE TRUNK OF

THE THIRD NERVE

28

RIGHT THIRD NERVE PALSY

29

LEFT III NERVE PALSY

30

Cranial imaging like MR scanning – MRI, MRA, Four vessel angiography and

Lumbar puncture are recommended if:

i. The pupil is involved i.e. dilates or becomes dilated in the initial

5 – 7 days after onset.

ii. No significant improvement in 3 months.

iii. The patient develops signs of aberrant regeneration of III nerve.

iv. Other neurologic findings develop.

ABERRANT REGENERATION OF III NERVE

This is seen after trauma and tumour compression of the III nerve, but

never after an ischaemic III nerve paresis. If the patient is followed with a

presumed diagnosis of ischaemic III nerve palsy and then develops signs of

aberrant regeneration, then MR scanning and cerebral angiography are

indicated.

31

TROCHLEAR NERVE

32

TROCHLEAR NERVE

The trochlear nerve is entirely motor in function and supplies only the superior

oblique muscle of the eyeball.

PECULIARITIES

• The only cranial nerve to arise from the dorsal aspect of the brain.

• The only cranial nerve to cross completely to the other side i.e.the

trochlear nerve arises from the contralateral nucleus.

• The longest and thinnest of all cranial nerves.


1. SOMATIC EFFERENT- concerned with the primary,secondary and

tertiary actions of superior oblique.

2. GENERAL SOMATIC AFFERENT-carries proprioceptive impulses

from the superior oblique. The impulses are relayed to the mesencephalic

nucleus of the trigeminal nerve

33

NUCLEUS

Situated in the ventromedial part of the central gray matter of the

midbrain at the level of inferior colliculus. It is continuous with the III

nerve nuclear complex. It belongs to the somatic efferent column of nuclei.


1. Cerebral cortex

i. Motor cortex-of both sides through the corticonuclear tracts.

ii. Visual cortex-through the superior colliculus

iii. Frontal eye fields.

2. Nuclei of 3, 6 and 8 cranial nerves through the medial longitudinal

bundle.

3. Superior colliculi through the descending predorsal bundle.

4. Vertical and torsional gaze centres.

5. Cerebellum through the vestibular nuclei.

COURSE AND DISTRIBUTION

It is divided into

i. The fascicular part

ii. The precavernous part

iii. The intracavernous part

iv. The intraorbital part

34

TROCHLEAR NERVE

DORSAL VIEW OF THE COURSE OF TROCHLEAR NERVE

35

THE FASCICULAR PART

It consists of efferent fibres which after leaving the nucleus ,pass

posteriorly around the aqueduct in the central grey matter and decussate

completely in the anterior medullary velum.

THE PRECAVERNOUS PART

The trochlear nerve trunk emerges from the superior medullary velum

just below the inferior colliculus on the dorsal aspect of midbrain. It then winds

round the superior cerebellar peduncle and the cerebral peduncle just above the

pons.

It runs beneath the free edge of the tentorium, and like the III nerve

passes between the posterior cerebral and superior cerebellar arteries to appear

ventrally lateral to cerebral peduncle. It then pierces the dura on the posterior

corner of the roof of the cavernous sinus to enter into it.


In the cavernous sinus, the nerve runs forwards in its lateral wall lying

below the III nerve and above the first division of the fifth cranial nerve. In the

anterior part of the cavernous sinus, it rises, crosses over the III nerve and

leaves the sinus to pass through the lateral part of the superior orbital fissure

36

(where it passes superolateral to the annulus of Zinn and medial to the frontal

nerve).


After entering through the lateral part of the superior orbital fissure, the

nerve passes medially above the origin of the LPS and ends by supplying the

superior oblique on its orbital surface.

The number of fibres in the intraorbital part of the trochlear nerve are

greater than its intracranial part. These extra fibres carrying the proprioceptive

impulses from the superior oblique leave the trochlear nerve to join the

ophthalmic division of fifth nerve in the cavernous sinus.

FEATURES OF IV NERVE PALSY

1. Hyperdeviation due to weakness of superior oblique. This becomes

more obvious when the head is titled towards ipsilateral shoulder (Park

Bielchowsky head tilt test).

2. Ocular movements – depression is limited in adduction. Intorsion is also

limited .

3. Diplopia – vertical diplopia occurs on looking down.

37

4. Abnormal head posture – To avoid diplopia head adopts a posture such

that the action of superior oblique is less needed i.e face is slightly

turned to opposite side, chin is depressed and head is titled towards the

opposite side.

PARK-BIELCHOWSKY’S THREE STEP TEST

The medial and lateral rectus muscles do not have a vertical

action. Therefore hypertropia of paretic etilogy is due to weakness of one or

more of the following vertically acting muscles. If the hypertropia is due to

weakness of only one of these eight muscles, answering the following three

questions identifies the paretic muscle.

1. First step - which is the higher eye?

a) If the patient has a right hypertropia then the weak muscle is

either a depressor of the right eye (right inferior rectus / right

superior oblique) or an elevator of the left eye (left superior

rectus / left inferior oblique).

b) If the patient has left hypertropia then the weak muscle is either

an elevator of the right eye (right superior rectus/right inferior

oblique) or depressor of the left eye (left inferior rectus are left

superior oblique).

38

2. Second step – hypertropia worse on right or left gaze?

The vertical rectus muscles (superior and inferior recti) have their

greatest vertical (and least torsional action) when the eye is abducted. The

oblique muscles (superior and inferior obliques) their greatest vertical action

(and least torsional action) when the eye is adducted.

So in each case.

i. Right hypertropia worse on right gaze (right inferior rectus/left inferior

oblique).

ii. Right hypertropia on left gaze (right superior oblique/left superior

rectus).

iii. Left hypertropia worse on right gaze (left superior oblique/right superior

rectus).

iv. Left hypertropia worse on left gaze (right inferior oblique/left inferior

rectus).

3. Third step - Is the hypertropia worse on head tilt to right or left?

a. The superior muscles (superior rectus and superior oblique) intort

the eye; the inferior muscles (inferior rectus and inferior oblique)

extort the eye.

39

b. When the head is titled to the right, right eye will be intorted by

the contraction of the right superior rectus and right superior

oblique; these two muscles work together in effecting the

intorsion and neutralize each other’s vertical action (right

superior rectus is an elevator and right superior oblique is a

depressor).

c. If one of these muscles is the paretic muscle responsible for the

hypertropia, then the vertical action will not be neutralized and

the hypertropia will be worse on tilting the head to the right

shoulder.

40

ABDUCENS NERVE

41

ABDUCENS NERVE

It is an entirely motor nerve that supplies lateral rectus muscles of the

eyeball.


i. SOMATIC EFFERENT – for lateral movement of the eye.

ii. GENERAL SOMATIC AFFERENT for proprioceptive impulses

from the lateral rectus muscle. These impulses ultimately reach

the mesencephalic nucleus of the trigeminal nerve.

NUCLEUS

Situated in the lower part of pons, close to the midline beneath the floor

of the IV ventricle. It is closely related to the fasciculus of the facial nerve. It

consists of two types of multipolar cells-large and small. The large multipolar

cells give rise to fibres of the abducens nerve, while the fibres of the small

multipolar cells relay in the oculomotor nucleus via the medial longitudinal

fasciculus. The small multipolar cells are believed to from the paraabducens

nucleus. Since the abducens nucleus belongs to the group of somatic efferent

nuclei, it lies in line with the nuclei of IV and III nerves above and the

hypoglossal nucleus below.

42


1. Cerebral cortex

i. Motor cortex (precentral gyrus) through the afferent

corticonuclear fibres from both cerebral hemispheres.

ii. Visual cortex, through the superior colliculus.

iii. Frontal eye fields.

2. Nuclei of III, IV and VIII cranial nerves through the medial

longitudinal bundle.

3. Pretectal nucleus of both sides.

4. Horizontal gaze centre through the medial longitudinal bundle.

5. Cerebellum through vestibular nuclei.

COURSES AND DISTRIBUTION

It is divided into

i. The fascicular part

ii. The basilar part

iii. The intracavernous part and

iv. The intraorbital part.

43

THE FASCICULAR PART

It consists of efferent fibres which start from the nucleus, pass forward

traversing the medial lemniscus and pyramidal tract. These then emerge by 7-8

rootless from the junction of pons and medulla just lateral to the pyramidal

prominence of medulla. The rootlets join to form one nerve, at varying

distances from the origin.

THE BASILAR PART

The nerve then runs forwards, upwards and slightly laterally through the

cisterna pontis between the pons and the clivus. The nerve then runs upwards

on the back of petrous temporal bone near its apex. At the sharp upper border

of the petrous bone, the nerve bends forward at right angles under the

petrosphenoidal ligament through the Dorello’s canal and enters the cavernous

sinus by piercing its posterior wall at a point lateral to the dorsum sellae and

superior to the apex of petrous temporal bone.


In the cavernous sinus, the nerve runs horizontally forward, occupying a

position below and lateral to the internal carotid artery. The internal carotid

artery is surrounded by the sympathetic plexus. The nerve then leaves the

cavernous sinus to enter the orbit through the middle part of the superior orbital

44

fissure through the annulus of Zinn. In the superior orbital fissure, the abducens

nerve lies inferolateral to the oculomotor and nasociliary nerves.


In the orbit the nerve runs forward and enters the ocular surface of the

lateral rectus muscle just behind its middle portion after dividing into three or

four branches.

CLINICAL FEATURES OF SIXTH NERVE PALSY

1. Deviation – In the primary position, the eyeball in convergent due to

unopposed action of the medial rectus muscle.

2. Ocular movements – Abduction is restricted.

3. Diplopia – Uncrossed horizontal diplopia occurs,

Worse towards the action of the paralysed muscle.

4. Head posture – The face is turned towards the action of the paralysed

muscle to minimize diplopia.

45

LATERAL VIEW OF THE COURSE OF SIXTH NERVE

LOCATION OF CRANIAL NERVES IN THE CAVERNOUS

SINUS

46

LEFT ABDUCENS NERVE PALSY

47

FEATURES OF OCULAR MOTOR NERVE

PALSIES IN DIABETES

• III nerve commonly affected

• More common in eldery

• Pupillary sparing

Because the peripherally situated papillary fibres supplied by the pial

plexus are spared whereas the centrally located fibres supplied by vasa

nervorum are affected.

• Usually recover spontaneously and completely in months.

• Can manifest as multiple episodes of transient ophthalmoplegia

affecting different muscles of either one or both eyes.

• Ocular motor nerve palsies in diabetes can be painless or painful

48

DIFFERENT DIAGNOSIS OF PAIN LESS OPHTHALMOPLEGIA

Diabetes

Hypertension

Atherosclerosis

Weber’s syndrome

Tumours of orbit

DIFFERENT DIAGNOSIS OF PAINFUL OPHTHALMOPLEGIA

Cavernous sinus thrombosis

Tolosa Hunt syndrome

Mucormyosis

Nasopharyngeal carcinoma

Herpes Zoster

Lymphoma

49

TREATMENT OF OCULAR MOTOR NERVE PALSIES

Management of Diabetes mellitus mainly consists of

1. Life style modification

2. Tight glycemic control with insulin

Follow up of cases of ocular motor nerve palsy that do not need urgent

management, like the posterior communicating artery aneurysm must be at 6

weekly intervals till 6 months or till two consecutive 6 weeks follow-ups reveal

no change in motility. Every time diplopia charting, Hess charting, recording

of deviations in nine gazes is done. During the meantime, patient is greatly

disturbed by diplopia. So some nonsurgical modalities are practiced for

symptomatic relief. It no resolution occurs after about 8-12 months then

surgery is considered.

1. Prisms – are helpful in providing binocular vision as well as reducing

the changes of development of contracture, but are useful only in small

angle squints. Fresnel prisms are also used.

2. Botulinum toxin – the ipsilateral antagonist is paralysed by

chemodenervation. The effect lasts for about 2-3 months. If necessary

the injection can be repeated.

50

3. Occlusive prisms or opaque contact lens.

4. Surgery – mainly to weaken the antagonist, usually ipsilateral and

sometimes also the contralateral antagonist, in addition to

strengthening the paralysed muscle. The amount of recession

resection varies depending upon which eye habitually fixates

(secondary deviation or primary deviation needs to be corrected).

Another principle is to restrain the contralateral antagonist by

performing retroequatorial myopexy.

In the case of III nerve, the aim is to achieve diplopia free ocular

position in primary position and downgaze. The latter should never be

compromised for the upgaze. Anyway it is difficult because the III nerve

supplies most of the extraocular muscles except two. Moreover aberrant

regenerations alter the clinical picture. Each case has to be considered on an

individual basis.

In the case of IV nerve, either strengthening of superior oblique or

weakening of ipsilateral inferior oblique or contralateral inferior rectus is done.

The results of surgery for both congenital and acquired IV nerve palsy is

excellent.

51

AIM OF THE STUDY

52

AIM OF THE STUDY

1. To study the ocular motor nerve palsy pattern in diabetes mellitus

2. To study the correlation of glycemic status in ocular motor nerve palsies

3. To study the association of diabetic retinopathy in case of ocular motor

nerve palsies.

4. To study the recovery pattern

53

MATERIALS AND

METHODS

54

MATERIALS AND METHODS

The cases studied, included those patients with neurogenic ocular motor

nerve palsies who presented to the regional institute of ophthalmology and

Govt. ophthalmic hospital. All age groups and both sexes were included.

A complete ophthalmological workup was done.

INCLUSION CRITERIA

All infranuclear ocular motor nerve palsies with DM

EXCLUSION CRITERIA

All supranuclear, nuclear nerve palsies, myogenic and restrictive

neuropathies. Associated combined condition like heart disease, were excluded.

55

REGISTRATION

Name

Age

Sex

Occupation

Address

HISTORY OF PRESENT ILLNESS

The common complaints were:

a. Double vision-whether uniocular /binocular, constant/intermittent,

fluctuating or not, more for near or distance, whether images were

horizontally or vertically separated, whether it is increased on any

particular direction, onset and progress.

b. Pain – headache / periorbital pain, location, nature, any radiation,

aggravating and relieving factors, any association with

nausea/vomiting.

c. Drooping of lids- unilateral/bilateral, total/partial

d. Defective vision- apart from double vision, any blurring or inability

to see due to drooping of lid.

e. Deviation of eyeball-right/left, eye, duration

f. Abnormal head posture

56

g. Vertigo (sensation of rotation of self/surroundings)

Details of the progress from onset, the treatment undergone to the

present state is noted. Any other significant medical/surgical history is also

recorded.

PAST HISTORY

H/o diabetes, hypertension, tuberculosis, syphilis, AIDS, malignancy in

the present or past.

H/o migraine or neurologic disease

H/o xanthems and vaccination

PERSONAL HISTORY

Diabetes, smoking, alcoholism etc.

GENERAL EXAMINATION

General vital data like pulse, blood pressure, peripheral pulses are noted.

Also gives an idea of the health status of the patients.

57

OCULAR EXAMINATION

• Head posture, facial symmetry are noted.

• Any deviation of eyeball is recorded. Under slit lamp, details of the

anterior segment from the lids to the lens are noted.

• Extraocular movements are noted down-both ductions and versions.

While looking for EOM, the aberrant innervation patterns are also

looked for.

• Pupil size, reaction, any anisocoria is noted.

• A dialted fundus examination and refraction is done. Ptosis and

proptosis if present are evaluated.

• Diplopia charting- is done in a dark room. Patient is asked to wear

goggles with red in front of the right eye and green before the left eye. A

torch light with a stenopaeic slit is used. The patient is asked to look at

the torch held 120cm away and then the torch is moved to various

positions. The false image is usually the fainter and farther one. Any tilt

of the image and variation in the distance between images at various

position is asked for.

• If a superior oblique palsy is suspected, Parks Bielchowsky’s 3 step

head tilt test is done.

• A forced duction test is performed in doubtful cases to rule out

restrictive etiology.

• Tensilon test is performed in some cases to rule out myasthenia gravis,

58

NEUROLOGIC EXAMINATION

Examination of other cranial nerves, Motor, sensory, cerebellar

symptoms and signs.

EXAMINATION OF THYROID

Any neck swelling is looked for

EXAMINATION OF SPINE & BACK

To look for congenital anomalies and neurocutaneous markers.

EXAMINATION OF ENT STRUCTURE

59

INVESTIGATIONS

Both right and left eyes (for all cases)

1. Vision a. uncorrected ( using Snellen’s charts at 6 metres)

b. best corrected.

2. Intra ocular pressure-with applanation tonometer after topical

anaesthesia.

3. Detailed slit lamp examination

o Lid

o Conjunctiva

o Cornea

o Iris

o Pupil

o Anterior chamber

o Lens/Pseudophakia/Aphakia

4. Fundus examination-any abnormalities, diabetic retinopathy etc.

5. Diplopia charting

6. Park 3 step test

7. Measurement of deviation-primary & secondary deviation, cover

uncover test in various gaze positions, for near and distance as well.

8. Hess charting

9. Exophthalmometry

10. Visual field examination

60

BLOOD TEST: (For all cases)

Total count

Differential count

Erythrocyte sedimentation rate

Blood sugar – Fasting, Post prandial

In doubtful cases, Glucose tolerance test/Hb A1c

Mantoux intradermal test

Serum cholesterol

Blood VDRL

Rheumatoid factor

RADIOLOGY (in indicated cases)

X ray orbit – fractures/erosions

X ray skull

X ray chest – tuberculosis

X ray PNS – (paranasal sinuses) – mucocoele, antral growth, sinusitis,

orbit floor fractures.

ORBITAL USG – (in indicated cases)

NEURO IMAGING – (in indicated cases)

• CT

• MRI

• MRA

• Cerebral angiography

61

SPECIALIST OPINION (IN INDICATED CASES)

o Diabetologist

o Otorhinolaryngologist

o Neurophysician/Neurosurgeon

o Radiologist

FOLLOW UP

Recording of patient’s complaints-whether stable/improving/worsening.

‐ Vision

‐ Pupil assessment

‐ Extraocular movements

‐ Diplopia charting

‐ Fundus

‐ Examining for signs of papillary involvement or aberrant

regeneration in case of third nerve palsy

‐ Investigations

Blood sugar FBS and PPBS

Hb A1c

BP

Imaging studies, if necessary

62

RESULTS

63

RESULTS AND ANALYSIS

Table1:Mean of age distribution and glycemic status

The mean age of the study population was 55.34 with a standard

deviation of 8.92. The mean fasting blood sugar value of the study population

was 145.84 mg% with a mean HbA₁C of 7.73.

Variable Obs Mean Std. Dev. Min Max

Age 50 55.34 8.92 24 70

FBS 50 145.84 47.01 60 322

PPBS 50 219.20 72.49 110 486

HbA1C 50 7.73 1.32 5.5 11

58%

with nerve

% of the m

e palsy .In t

58

Wome

Men

Total

SE

Tab

male patien

this study ,

SEX

en

64

EX DISTR

ble2:sex di

Chart1

nts and 4

, males we

Gend

F

RIBUTION

istribution

1:sex distr

42% of fem

ere more af

der

Freq.

21

29

50

N

n

ribution

male patie

ffected tha

42

Percen

42

58

100

ents were a

an females.

Women

Men

nt

affected

62%

in right ey

1

2

3

4

5

6

7

Tabl

Char

% of the pa

ye. In this s

0

10

20

30

40

50

60

70

LAT

LE

RE

Total

le3:lateral

rt2: lateral

atients had

tudy most

LE

TERALIT

65

LATE

lity of ocul

lity of ocu

nerve pals

patients ha

Latera

TY

ERALITY

lar motor

ular motor

sy in left ey

ad left eye

RE

ality

Freq.

31

19

50

nerve pals

nerve pal

ye and 38%

preponder

Percen

62

38

100

sy

lsy

% had nerv

rance.

LE

RE

nt

ve palsy

E

In

patients pr

patients pr

D

Dr

PRES

COM

Diplopia

Droopin

Total

Chart3

this study

resented w

resented wi

0

Diplopia

ooping

SENTING

MPLAINT

a

ng

Table4 :

3: Distribu

64% of th

with droopin

ith diplopia

20

66

COMPLA

TS

Distributi

ution of p

he patients

ng of the u

a.

40

Compla

AINTS OF

Freq.

32

18

50

ion of pre

resenting

s presented

upper eyel

60

aints

F NERVE

Percen

64

36

100

esenting co

complaint

d with dipl

id. In this

80

E PALSY

nt

omplaints

ts

lopia. 36%

study maj

Diplopia

Drooping

% of the

ority of

g

In t

and 16%

post PRP s

F

FUN

NAD

MILD NP

MOD NPD

POST PRP

HTR

Total

Table5

Chart

this study 5

have mod

status.4% p

0

10

20

30

40

50

60

NAD

FUNDUS I

NDUS

PDR

DR

P

5:Fundus

t4: Fundus

52% patien

erate NPD

patients ha

D MILD NPDR

67

IN DIABE

F

findings i

s findings

nts does no

DR and mi

d hyperten

MOD NPDR

P

FUN

ETES MEL

Freq.

26

13

8

1

2

50

in nerve pa

in nerve p

t have asso

ild NPDR

nsive retino

OST PRP H

NDUS

LLITUS

Perce

52

26

16

2

4

100

alsy patien

palsy patie

ociated ret

respective

opathy.

HTR

ent

2

6

6

0

nts

ents

tinopathy.

ely.2% pati

NAD

MILD NP

MOD NP

POST PR

HTR

26 %

ients in

PDR

PDR

P

III

VI

III

To

In o

by VI ner

palsies. No

1

2

3

4

5

6

DI

Nerve P

NERVE

I NERVE

& VI NER

otal

C

our study 4

rve palsy

one of the p

0

10

20

30

40

50

60

III NER

ISTRIBUT

Palsies

RVES

Tab

Chart5: D

40% of pa

and two p

patient is a

RVE VI N

68

TION OF

ble6: Distr

Distribution

atients affec

percent aff

affected by

NERVE III &

Nerve P

NERVE P

Freq.

20

29

1

50

ribution of

n of nerve

cted by III

fected by

y IV nerve p

& VI NERVES

Palsies

PALSIES

Pe

1

f nerve pal

e palsies

I Nerve pa

both third

palsy in ou

V

ercent

40

58

2

100

lsies

alsy, 58% a

d and sixth

ur study.

III NERVE

VI NERVE

III & VI NERVE

affected

h nerve

ES

It h

complete r

showed no

ful

No

pa

To

has been f

recovery o

o signs of r

0

10

20

30

40

50

60

DISTRIB

RECOV

ll

o recovery

artial

otal

Table7:

Chart 6:

found out,

of the third

recovery.

full

69

BUTION O

VERY

Distribut

: Distribut

, on follow

nerve pals

par

OF RECO

Freq

30

5

15

50

ion of reco

tion of rec

w up, tha

sy, 30% ha

rtial No

Recove

VERY

q.

overy

covery

at 60% of

ad partial r

o recovery

ery

Percent

60

10

30

100

the patien

recovery an

f

p

N

nts had

nd 10%

full

partial

No recovery

H

<7

7.1

>9

To

I

HbA1C F

1 - 9.0

.1

otal 2

In o

than 7%,

than 9.1%

7%, 48.28

than 9.1%

with both

9.0%.

0

20

40

60

80

100

H

III NERVE

Freq P

7

8

5

20

Table8:

Chart7:

our study,

40% had H

%. 44.83%

8% had Hb

%. One amo

third and

III NERVE P

HbA1C LE

E PALSY

Percent

35

40

25

100

Distributi

Distributi

35% of pa

HbA₁c bet

of patients

bA₁c betwe

ong the stu

sixth nerv

PALSY V

HbA1

70

EVEL IN N

VI NERV

Freq

13

14

2

29

ion of HbA

ion of HbA

atients with

tween 7.1%

s with sixth

een 7.1% a

udy popula

ve palsies h

VI NERVE PALS

1C in Ne

NERVE P

VE PALSY

Percent

44.83

48.28

6.90

100

A1C level i

A1C level

h third ner

% and 9%

h nerve pa

and 9% an

ation , 2%

had a HbA

SY III & VI N

erve Pal

ALSIES

Y III &

Freq

0

1

0

1

in nerve p

in nerve p

rve palsy h

and 25%

alsy had H

nd 6.9% ha

% of patient

A₁c value b

NERVE PALSY

lsies

VI NERVE

Per

0

10

0

10

palsies

palsies

had HbA₁c

had HbA₁

HbA₁c of le

ad HbA₁c o

ts, who pr

between 7.

E PALSY

cent

0

00

0

00

of less

₁c more

ess than

of more

resented

1% and

<7

7.1 ‐ 9.0

>9.1

71

GLYCEMIC STATUS Vs RECOVERY

Full Recovery Partial Recovery No Recovery

Variable Mean Std. Dev. Mean Std. Dev. Mean Std. Dev.

N 30 15 5

Fbs 135.30 36.55 145.33 43.56 210.60 68.37

Ppbs 202.87 56.95 221.07 66.58 311.60 112.51

Hbac 7.44 1.21 8.03 1.29 8.60 1.71

Table8:Glycemic status Vs recovery

Chart7: Glycemic status Vs recovery

0.00

50.00

100.00

150.00

200.00

250.00

300.00

350.00


Recovery Vs Blood Sugar Levels

fbs

ppbs

72

Chart8:Distribution of mean HbA1C according to recovery

The patients in this study who did not show any signs of recovery

following ocular motor nerve palsies, around 10 %, had a high HbA₁C levels of

8.6%

6.50

7.00

7.50

8.00

8.50

9.00


Mean HbA1C according to Recovery

hbac

73

DISTRIBUTION OF MEAN BLOOD SUGARS AND HbA1C LEVELS

IN DIABET DIABETIC RETINOPATHY

Fundus NAD Mild NPDR MOD NPDR POST PRP HTR

Variable Mean

Std.

Dev. Mean

Std.

Dev. Mean

Std.

Dev. Mean

Std.

Dev Mean Std. Dev.

N 26 13 8 1 2

Fbs 140.08 43.22 132.85 26.50 162.38 49.04 322.00 0.00 151.00 1.41

Ppbs 212.88 61.33 199.23 48.73 239.63 87.98 486.00 0.00 216.00 5.66

Hbac 7.20 1.15 7.95 1.13 8.69 1.25 11.00 0.00 7.75 0.35

Table9: DISTRIBUTION OF MEAN BLOOD SUGARS AND HbA1C

LEVELS IN DIABET DIABETIC RETINOPATHY

Chart9: DISTRIBUTION OF MEAN BLOOD SUGARS IN DIABETIC

RETINOPATHY

0.00

100.00

200.00

300.00

400.00

500.00

600.00

NAD Mild NPDRMOD NPDR POST PRP HTR

Mean Blood Sugars in Diabetic Retinopathy

fbs

ppbs

74

Chart10: DISTRIBUTION OF MEAN HbA1C LEVELS IN DIABETIC

RETINOPATHY

In this study the mean FBS, PPBS and HbA₁C were estimated and their

correlation with the changes in the retina has been assessed. It has been found

that the patients with elevated glycated haemoglobin had more severe diabetic

retinopathic changes.

0.00

2.00

4.00

6.00

8.00

10.00

12.00

NAD Mild NPDRMOD NPDR POST PRP HTR

Mean HbA1C in Diabetic Retinopathy

hbac

75

DISCUSSION

76

DISCUSSION

1. AGE DISTRIBUTION AND GLYCEMIC STATUS

In our study, 50 cases of diabetes mellitus with ocular motor nerve

palsies were examined. Most patients with either third or sixth nerve palsies

were found to belong to 51 to 60 year age group. In a study of 22 cases of third

nerve palsy by Jack. E. Goldstein and David G. Cogan the average age was 62

years. The mean FBS of patients was 145.84mg%, mean PPBS was

219.20mg% and mean HbA₁C was 7.73 in this study. In a study conducted by

Vidhya chandran et al., on 61 diabetic patients with ocular motor nerve palsies,

the mean FBS was 116.61mg%, the mean PPBS was 179.62mg% and the mean

HbA₁C was 7.80.

2. SEX DISTRIBUTION

In our study,males were more affected as compared to female which is also

noted in a study conducted by kaushik U Dhume et al.

77

3. LATERALITY

The most common affected eye in our study was left eye. Bilaterality was

not found in our study. However the laterality has got no statistical significance

with the degree of nerve palsy or recovery from it in our study.

4. PRESENTING COMPLAINT

In our study 64% of the patients presented with complaints of diplopia

and the remaining with drooping of eyelids. Majority of patients had diplopia

in the study conducted by Saber et al on diabetes mellitus associated ocular

motor nerve palsies.

5. GLYCEMIC STATUS AND DIABETIC RETINOPATHIC CHANGES

Glycosylated haemoglobin was taken to assess the glycemic control of

the patient who presented with ocular motor nerve palsies. The American

diabetes association recommends the goal of diabetes therapy should be an

HbA₁c of less than 7%. In our study we analysed the retinal findings of all the

patients and their association with HbA₁c levels. It has been found that patients

who had normal retina had a mean HbA₁c of 7.2%. Those patients who

presented with mild NPDR and moderate NPDR had a mean HbA₁c of 7.95

and 8.69 percent respectively. One patient among the group who presented

78

with proliferative diabetic retinopathy had a HbA₁c of 11%. Thus there seems

to be a positive correlation between the HbA₁c levels and the degree of

retinopathic changes in diabetic patients who primarily presented to us with

ocular motor nerve palsies. These findings have also been observed by study

conducted by Vidhya chandran et al., on significance of HbA₁c in diabetic

ocular motor cranial nerve palsies.

6. OCULAR MOTOR CRANIAL NERVE INVOLVEMENT AND

GLYCEMIC STATUS

In our study involving 50 patients, 20 patients(40%) had third nerve

palsy where as 29patients(58%) presented with sixth nerve palsy. One patient

(2%) among 50 with both the nerve palsies. No one presented with fourth

cranial nerve palsy in our study. The most common nerve involved in a study

conducted on diabetic patients by Saber et al was the third nerve. 35% of

patients with third nerve palsy had HbA₁c of less than 7%, 40% had HbA₁c

between 7.1% and 9% and 25% had HbA₁c more than 9.1%. 44.83% of

patients with sixth nerve palsy had HbA₁c of less than 7%, 48.28% had HbA₁c

between 7.1% and 9% and 6.9% had HbA₁c of more than 9.1%. One among the

study population , 2% of patients, who presented with both third and sixth

nerve palsies had a HbA₁c value between 7.1% and 9.0%

79

7. RECOVERY OF NERVE PALSIES

Upon follow up of patients included in this study, 60% of the population

had complete recovery of nerve palsies who had a mean HbA₁c value of

7.44%. 30% of the population had partial recovery from ocular motor nerve

palsies who had a mean HbA₁c value of 8.03%. 10 % of the population showed

no signs of recovery who had a mean HbA₁c value of 8.60%

80

CONCLUSION

81

CONCLUSION

• The diabetic ocular motor nerve palsies occur in a wide range of age but

are more common in the age group of 51 to 60 yrs with mean age of

55.34 years.

• The males were more affected than females in our study

• Our study has shown more of left eye involvement

• The patient population presented more frequently with diplopia in our

study which was due to a slightly more common involvement of sixth

cranial nerve.

• Fourth nerve palsy associated with diabetes mellitus is less frequent than

third and sixth nerve involvements and no patient in our study presented

with fourth cranial nerve palsy.

• It has been found that the involvement of ocular motor cranial nerves in

diabetic patients has been associated with the glycemic status.

• There was a positive correlation between HbA₁c values and degree of

retinopathic changes in diabetes mellitus.

• Ninety percent of patients in our group had either a complete or partial

recovery from the ocular motor nerve palsies due to diabetes mellitus.

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KEY TO MASTER CHART

M-Male

F-Female

RE- Right eye

LE-left eye

FBS- Fasting blood sugar

PPBS-Post prandial blood sugar

NAD- No abnormal diagnosis

MILD NPDR- Mild non proliferative diabetic retinopathy

MOD NPDR-Moderate non proliferative diabetic retinopathy

HTR-hypertensive retinopathy

Post PRP-Post pan retinal photocoagulation

N –Negative

P-Paralysis

HbA1C- Glycated haemoglobin

PROFORMA

Name :

Age :

Sex :

Hospital No :

Occupation :

Date :

Complaints :

History:

1.Visual complaints

2.Diplopia

3.Nausea

4.Vomiting

5.Consciousness

6.Gait

7.Sphincter control

8.Weakness

9.Injury

10.Personality disturbances

EXAMINATION

Visual acuity :

RIGHT EYE LEFT EYE

VA

UA

Sph Cyl axis VA VA

UA

Sph cyl axis VA

DV

NV

Head position : Head tilt/face turn/chin/other skull Abnormalities

Eyelids : Ptosis, retraction, lid lag, macusgunn Phenomenon

Eye position : Deviation / proptosis

Movements : Uniocular & binocular, conjugate or disconjugate

Nystagmus : Present/absent

Right eye Left eye

Pupils:

Fundus:

Tension:

Fields:

Central Nervous system

Higher Functions:

Right Left

Cranial nerves:

(1,2,5,7,8,9,10,11,12&3,4,6)

Motor system: tone, power,

wasting, involuntary movements

Sensory system: touch, pain,

temperature, position & vibration

Cerebellar system: co ordination,

tandem walking

Reflexes

Hess Screening, Diplopia charting (Separate Charts Attached)

Lab investigations

Blood routine

TC

DC

ESR

Blood sugar fasting and postprandial

Urine routine

Mantoux

VDRL

Special investigations: (CT,MRI)

Treatment:

Follow up:

study of ocular motor nerve palsies in diabetes...

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