HISTORY

450 BC: HIPPOCRATES describe HEMIANOPIA

150 BC: Ptolemy estimating the outer limits of the Visual field

1568: EDME MARIOTTE discover blind spot.

1856: Clinically campimetry first started by Graefe.

1851-1920: Prof.J.P.Bejerrum of Copenhagen devised Tangent screen. He drew his first screen on the back of his door. He also first described Arcuate scotoma, Bjerrum/Tangent screen was popular in USA for 100 years.

1869: Forster and Aubert developed an arc perimeter. It was very popular and became known as Forster perimeter.

1945: First Cupola perimetry was designed by Professor. Hans Goldman, Bern.

First Automated Static perimetry also came out from Switzerland, Bern.

First Automated Octopus 201 in late 1970 room size costing excess of US $ 100000 for unknown technology. And high cost kept perimetry in "IVORY TOWER".

1982: First Humphrey field analyzer was displayed at "AAO"

1983: Production unit delivery began. Because of small size & low cost the machine became very popular

Key Issue

Understanding the Principles

STATIC vs KINETIC

WHAT IS PERIMETRY

Is the measurement of the differential light Sensitivity of the retina at a defined number ofLocations.

HOW TO INTERPRET THE HUMPHREY FIELD FOR GLAUCOMA & NEUROLOGICAL CASES

WHEN WILL YOU SEND A PATIENT FOR FIELD?

ELEVATED IOP

SUSPECTED OPTIC NERVE

ASYMMETRIC CUP:DISC > 0 .3

IOP DIFFERS 3mmHg FROM OTHER EYE

UNEXPLAINED LOW VISUAL ACUITY

UNEXPLAINED HEADACHE

GLAUCOMA IN OTHER EYE

PREVIOUS RETINAL DETACHMENT

H/O OCULAR TRAUMA

SUSPECTED OR ESTABLISHED GLAUCOMA

1. OPTIC NERVE HEAD CHANGE OR NERVE FIBER LAYER DEFECT
2. VISUAL FIELD DEFECT
3. RAISED INTRAOCULAR PRESSURE

NORMAL GROUP

INTRA OCULAR PRESSURE <21 mmHg

NO VISUAL FIELD CHANGE

NO OPTIC NERVE HEAD OR RETINAL NERVE FIBER LAYER CHANGES SUGGESTIVE OF GLAUCOMA

NO INTRA- OCULAR DISEASE OR INTRA OCULAR SURGERY

NO H/O HYPERTENSION, DIABETES.

NO FAMILY HISTROY OF GLAUCOMA.

AAO VOLUME 109,NUMBER 3,MARCH 2002

The Eye Care America Glaucoma Project

Is your patient or their family at Risk forGlaucoma? Score below to see.

1.Family History (Chose one)	No F/H	0
	Parent & Child has glaucoma	2
	Siblings	4
	Parents & Siblings	4
2.Race(Chose one)	Caucasian	0
	Hispanic	1
	Black	3
3.Age(Chose one)	<40	0
	39-49	1
	49-59	2
	59+	4

To Score: Add one score in each of the above categories. If you have atotal score 4 or higher, you have a high risk for having Glaucoma.

GREATER RISK OF GLAUCOMA

OLDER THAN 45 YEARS

A FAMILY HISTROY OF GLAUCOMA

HIGH INTRAOCULAR PRESSURE

DIABETES

MYOPIA

USED STEROIDS FOR LONG TIME

HAD A PREVIOUS EYE INJURY

Risk Factors

Now CCT

Family History

Older Age

Race

The Threshold of Sensitivity

The threshold is the crucial concept in perimetry. The threshold is the dimmestLight seen by a subject, 50% of the time.

The threshold is not a distinct borderline. It is a transition region from seeing to not seeing like the transition from daylight to darkness.

NORMAL THRESHOLD VALUES

First four paracentral points are 3 ºfrom vertical & horizontal lines,12.7 º from the fixation point & next all stimulus points are 6 degree apart.

Maximum threshold is at the fovea say,35dB dimmest light,with each degree to periphery threshold decreases by .03 dB.

STRATEGY/METHOD/TECHNIQUE HUMPHREY HAS MANY OPTIONS

FULL THRESHOLD	1983	Normal 12-20 Min
FASTPAC	1991	Normal 10-15 Min
SITA	1997

SITA

SWEDISH INTERACTIVE THRESHOLD ALGORITHM

From MALMO UNIVERSITY OF SWEDEN 1997

Developed by Anders Heijl & Boel Bengtsson and group over 10yrs period.

New test Algorithm (a set of rules or procedures that must be followed in solving a particular problem)

Beginning of test estimates based on normative data.

Testing based on a model of "estimates" of normal and glaucomatous fields.

SITA knows when to quit, it computes when to stop at each test location. SITA compares with a Senior Professor. Spends more time when unsure of the result and spends less time when with consistent result.

SITA is time saving but results are equivalent to FULL THRESHOLD(SS) or FASTPAC(SF). Calculations are done after the test, so there is less fatigue for the patient.

There are two types of SITA STANDATD(SS) or SITA FAST(SF) like, TOP (Tendency oriented perimetry of OCTOPUS)

SITA STANDARD 24-2

IS

SIMPLE

SHORT

SUPER

SOUND

SOLID

SCIENTIFIC

SINGLE FIELD ANALYSIS

SMART

SENIOR PROFESSOR

BOTH FOR GLAUCOMA & NEUROLOGY

USED ALL MOST ALL OVER THE WORLD

SO USING FASTER STRATEGIES

SHORT TEST PROCEDURES :-

Reduce the fatigue effect caused by both

1. Retinal fatigue
2. Physical fatigue

Therefore a quicker test can be morereliable and accurate compare to testing with longer elaborate test strategies.

Types of Glaucomatous field loss

First field loss was described by Albrecht von Graefe in 1856

A decade later, he demonstrated preservation of the temporal and central regions in advanced glaucoma.

Later,Bjerrum(1889) & Ronne(1909) demonstrated the presence of arcuate field defects, and nasal steps.

The very large study by Aulhorn and Harms in 1967 demonstrated the importance of paracentral defects as an early sign of glaucoma.

Aulhorn's & Harms' classification of glaucomatous field loss

Isolated paracentral scotomas

Bjerrum's scotoma

Bjerrum's scotoma breaking through to the periphery

Central or temporal island

Blindness

THE KEY PATTERN DEVIATION PLOT CHART

LOOK ONLY LOWER RIGHT DEVIATION PLOT CHART

SINGLE FIELD ANALYSIS

SINGLE FIELD ANALYSIS

EVALUTING OF A SINGLE FIEL

KEY POINTS

Combined evaluation of Optic disc & Visual field

The defect should be reproducible, in particular peripheral defects in the first visual field should be confirmed before accepted.

The shape of the field defect should correspond to retinal nerve fiber anatomy.

The defect should correspond to changes at the optic disc.

Diffuse loss is more likely to be due to cataract or more miotic therapy in glaucoma.

PATTERN DEVIATION PLOT CHART

IF YOU CAN ONLY READ THE PATTERN DEVIATION PROBABILITY PLOT CHART 6B THATS ALL.
OF COURSE IT MUST CORRELATES WITH THE DISC

INSIDE HUMPHREY PERIMETER

A GLANCE GUESS FROM GRAY SCALE

GRAY SCALE

TYPES OF SCOTOMAS

CREENING TEST

A screening test of the same RP case. Two zones with central and peripheral ref. were 34dB.Outof 120 points pt. sees only 59 points R/E & 40 points in L/E.It's a suprathreshold type of test.A threshold test should be performed when a pt. cannot see 10 points out of 120 points or atany area 2 or 3 adjacent points of non seen points are detected.

SCREENING PROGRAMS HFA II

TEST PROG	AREA & POINTS	APPLICATION
CENTRAL 76	30 °	GLAUCOMA
	76 Points	Neurological
Full Field 120	60 º	General
	120 Points	Glaucoma
		Neurological

SCREENING FOR GLAUCOMA MAJOR POINTS

No single good screening tool for Glaucoma exist.

Tonometry suffers from a poor balance between sensitivity and specificity.

Optic nerve head examination requires skilled observers and does not have a defined end point.

Perimetry is expensive, and has a learning curve.

NAME DOB ID

By mistake her DOB was given 1969, instead of 1959.Gray scale shows slightDeep GHT GRS. But when her exact DOB is given 1959,GHT is WNL. So,always give Correct DOB as well as last corrected distance vision.

BUT THIS IS A HIGHLY SUSPECTED FIELD.

PUPIL SIZE 3 TO 7 mm

All fields should be done with normal reacting pupil within 3-7 mm in size. Dilated pupilgives less false result than the small pupil. So, please check pupil size before seeing a Visual field (VF) Humprey's latest version 12.3 will give you the pupil size on the screen before starting the field.

PUPIL SIZE

AREA OF CIRCLE = x r²

2mm Pupil Area=3.14 x 1 mm²=1 mm²

8mm Pupil Area=3.14 x 4 mm²=15 mm²

SO,IF YOU SHIFT PUPIL FROM 2mm TO 8mm, YOU WILL GET AN INCREASE OF 15 FOLD AREA OF THE PUPIL SIZE

SO,WIDE VARIATION OF THE PUPIL SIZE WILL GIVE YOU A FALSE VISUAL FIELD DEFECT, SO PUPIL SIZE SHOULD BE BETWEEN 3 mm TO 7 mm AND IT SHOULD REACT TO LIGHT ON PUPIL .

GHT & PROBABILITY

GHT- This test assumes that glaucoma does not cause a generalized Global depression of the field of vision. It takes advantage of the asymmetric field loss pattern generally seen in glaucoma. The testanalyses defects in the superior hemi field and makes comparisonwith mirror image locations in the inferior hemi field.

1. GHT may be OUT SIDE NORMAL LIMIT (ONL)
2. BORDER LINE (BL)
3. GENERAL REDUCTION OF SENSITIVITY (GRS)
4. ABNORMALLY HIGH SENSITIVITY
5. WITH IN NORMAL LIMIT (w.N.L)

GHT

The GHT has been evaluated by both Peter Åsman and Heijl(1992) and by Katz(1996). IT WILL GIVE YOU FIVE RESULTS.

1. Abnormally high sensitivity. The general height of the field is beyond the 99.5% limit for normal.
2. Out side normal limits (ONL) - The asymmetry is beyond the 99% limit for normal in any of sector pairs. If seen twice in two consecutive fields early glaucomatous defect criteria by "Anderson".
3. Borderline (BL) - The asymmetry is beyond the 97% limit for normal in sector pairs. It's not a pathological field.
4. General reduction in sensitivity (GRS) - The general height is below the 0.5% limit for normal. Seen in Cataract, High Myopia, Media opacity, Dilated pupil.
5. Within normal limits (WNL) - When none of the above four criteria are seen.

 

GAZE TRACKER

By seeing this tracing at lower end of the field you can judge whether the fixation is OK or not.

INTERPRETATION CRITERIA INTERPRETATION CRITERIA

THE REASON FOR DOING FIELD.

CORRECT DATA AND RELIABLE FIELD.

PUPIL SIZEn PATIENT'S PERFORMANCE

READ CHART WITH OTHER FINDINGS

DIAGNOSE THE CASE, IF IN DOUBT REPEAT THE SAME TEST BUT NOT THE SAME DAY

INTERPRETATION OF A FIELD IS NOT A CHILD'S PLAY

AN EARLY FIELD DEFECT ACCORDING TO "ANDERSON "

Cluster of 3 or more adjacent points in an expected, suspected location (Typical for glaucoma) of central 24 degree field. ON AT LEAST

LEARNING CURVE

First field is not always areliable field (of course notall the time). She is a youngschool teacher. First VF done after seeing her IOP R30 &17 L. healthy NRR .6 & .5 are the cup : disc ratio R/L respectively. Since 5 th June '00 she was on anti- Glaucoma drug. We stopped her drops after Seeing the 2 nd field .On the3 rd field on 29 th Oct '01 herVF is within Normal limit & IOP too. It's a long term fluctuation.

FOLLOW UP

First field is not always reliable

This young girl of 10 yrs.has been dig. in Marfan Sy with NTG.It can not occur before 45yrs.Diag.Out side BD.In Dhaka It has been dig. Marfan Without Glaucoma her first field is not reliable. Second field done at Dhaka is OK GHT ONL is due to high myopic cylinder.Doing field is like a Baby sitter. Glaucomamay be associated with sub laxation of the lens.Here her IOP is normal Her both NRR are healthy.

I LOVE MY COUNTRY

BEFORE SENDING THE PATIENT

1. GIVE LAST CORRECTED DISTANCE VISION
2. DETAIL OF OPTIC NERVE EXAMINATION IF POSSIBLE WITH DIAGRAM
3. INTRA OCULAR PRESSURE (IOP)FLEXIBILITY IS THE ENEMY OF STANDARDIZATION

COMMON PROBLEMS WITH PERIMETRY

LEARNING / FATIGUE EFFECTS

PUPIL SIZE

REFRACTIVE ERROR

ARTIFACTS

PATIENT COOPERATION

REPORT

PHYSIOLOGICAL FUNDUS

This young man of 34yrs a typist came for red eyes. V.A. 6/6 B/E and IOP !7 mmhg. Both Funds showed ISNT rule are OK.Fields are normal too. It's nothing but a normal physiological cup.still than he should be on follow up.

ALWAYS CORRELATES WITH THE FUNDUS

NORMAL TENSION GLAUCOMA

A CONDITION IN WHICH GLAUCOMATOUS CUPPING OF OPTIC NERVE HEAD, LOSS OF NERVE FIBER LAYER AND VISUAL FIELD LOSS OCCURS AT AN IOP BELOW <21mmHg MEASURED AT DIFFERENT TIMES, WITH OPEN AND NORMAL APPEARING ANGLE .

VARIENTS OF NTG

NON-PROGRESSIVE FORM

PROGRESSIVEFORM

OPTIC NERVE HEAD CHANGES IN NTG

Large cupping disproportionate to field loss

Sloping edges

Thinning of NRR especially inferiorly & Inf.temp

Hourglass pattern of lamina cribrosa

High incidence of acquired pit of the Optic head

Greater frequency & extent of Peripaillary atrophy

Higher incidence of splinter hemorrhage of OND

More localized nerve fiber layer defect

VISUAL FIELD DEFECT

Localized, deep, steep defects

Close to fixation

OTHER ASSOCIATES OF NTG

NTG usually seen in elderly F>M 6:1

More common in ASIANS

F/H ,Myopia, Systemic hypotension, hypertension, Postural hypotension, Nocturnal hypotension, Cardiovascular disease, Migraine, Raynaud's , Acute blood loss, Hypovolemia following severe vomiting & diarrhea

Differential Diagnosis of NTG

POAG with a wide diurnal fluctuations

Pigmentary glaucoma

Intermittent IOP elevation as in, glaucomatocyclitic crisis and intermittent angle closure

Previous episode of IOP elevation: Steroid induced Glaucoma

Non-Glaucomatous optic nerve disease like ischemic optic neuropathy, Congenital optic disc pit, compressive lesions of optic nerve etc.

DIAGNOSIS of NTG

OCULAR EVALUTION :

Apart from routine ocular & FUNDUS examination.
LOOK FOR

1. Central corneal thickness(520 µM) , thin cornea may give false low IOP reading,POAG might appear as NTG
2. Record of a diurnal curve
3. Perimetry
4. HRT
5. Record of ocular blood flow

MEDICAL EVALUTION

1. Cardiovascular examination including 24 hrs. BP monitoring to rule out nocturnal hypotension, Carotid artery Doppler imaging to assess blood flow, capillary filling time on exposure to cold.
2. Complete blood picture, ESR, Blood profile, Lipid profile to ruled out Hypercholesterolemia
3. MRI to ruled out Diffuse cerebral ischemia

MANAGEMENT OF NTG

Goal of treatment is to preserve the visualFUNCTION

Non-Progressive form does not require anytreatment, as it rarely progresses. Monitoring& follow up is required every 6-12 months.

Progressive form needs treatment. Targetshould be to reduce 30% IOP from the initial, maydelay the progression.

NTG

A GARDEN VARIETY OF POAG (30% out of 66%)

MOST LIKELY GENETIC (OPTINEUON GENE)

A BENIGN VARIETY OF POAG

BUT DIFFICULT TO TREAT IOP TO BE REDUCED BY 30%

BLINDNESS IS UNUSUAL IN NTG

F>M 6:1

PATIENTS ARE HYPOTENSIVE

LOCALIZED VFD & FIXATION THREATENING

Age must be above 45years & F/H

IT IS EASY TO MAKE IOP 4OmmHG TO 20mmHG BUT TOUGH TO BRING IOP 15mmHG TO14 mmHG

TREATMENT

Avoid beta blockers; non selective Beta-blockers may decrease the perfusion pressure. But selective blockers like Betaxolol may increase OBF but at the same time it has less IOP lowering.

Brimonidine (Alphagan)

Calcium channel blocker of systemic use Nifedipine is benificial

Prostaglandin

ALT

Surgery

PROGRESSION OF NTG

Deepening of existing field defect

Expansion of existing field defect

Appearance of new defect

Threat to fixation

PLAN OF TREATING LTG

HIGHER RISK OF PROGRESSION NTG

IOP near the upper limit of normal

Wider diurnal variation

Deep localized notch of the disc

New optic disc hemorrhage

Systemic hypotension

Young age

Black race

Myopia

Vasopasam

No history of hemodynamic crisis (Hemodynamic episode is associated with non-progressive form)

COMMON IN NTG

NTG PATIENT'S VF AND FUNDUS

LAST PT'S 24 MONITORING OF BP

24 hrs. Monitoring of a LTG pt. done with mild hypertension. She is on Atenolol 50mg in the morning Amlodipine 5mg at bed time. After shehas been diagnosed as NTG on Jan 02 and on Azopt thrice daily. During Night her diastole drops below 60.She has been advised to consult her cardiologist about her low diastole tendency at late Night.

COLOR DOPPLER SONOGRAPHY

OVER VIEW

DUANE'S CD-ROM 2003 EDITION

WHY 21 CONSIDERED "NORMAL"

TARGET PRESSURE RANGES; Goal for lowering IOP

Intraocular Pressure
Damage Pressure(mmHg)	Decrease Desired(%)	Absolute level desired (mmHg)
Above 35	About 50%	18-25
25-35	About 40-50%	13-18
21-25	About 40%	14-15
17-20	About 40%-30%	12-15
13-15	About 20%	10-12
10-12	About 10%-20%	8-9

A target pressure will not damage the optic nerve any further.

TARGET IOP

Slight damaged mean a change in the optic nerve ± small VFD

Dr. Rick Wilson

Establishing Initial Target IOP (CIGTS Study)

Target IOP = (1 - Reference IOP + Visual Field Score ) x Reference IOP 100

Example

MODE OF ACTION

	IOP Decrease	Decreases Aqueous Production	Increases Uveoscleral Outflow	Increases Trabecular Outflow
Brimonidine	20%-30%			.
ß-Blockers	20%-30%		.	.
Pilocarpine	10%-20%	.	.
Dorzolamide	15%-20%		.	.
Prostaglandin	25%-30%	.		.

DISEASE CAPSULE ; POAG

1. EPIDEMIOLOGY

Major Risk Factors

Advanced age

Black race

Positive F/H

Elevated intraocular pressure

2. MINOR RISK FACTORS

Diabetes mellitus

Myopia

3. SYMPTOMS

Early; none

Late; loss of peripheral vision

Very late; loss of central vision

4.SIGNS

Cornea.............................Normal

Anterior Chamber............ Normal

Iris................................... Normal

TREATMENT

Topical medication

Laser trabeculoplasty

Trabeculectomy

TILTED DISC/HIGH MYOPIA

CT Scan of Tilted Disc

TILTED DISC HAS

1. TILTED DISC SYNDROME OCCURS TO1%-2% OF THE WHOLE POPULATION
2. THE LONG AXIS OF THE OVAL DISC ISOBLIQUELY DIRECTED,UPPER & TEMPORALREGIONS OF THE DISC ARE ANTERIORTO THE INFERONASAL AREA.
3. THE RETINAL VESSELS EMERGE FROM THE DISC IN THE SUP.TEMP AREA, RATHERTHAN NASALLY(SITUS INVERSUS)
4. HYPOPIGMENTATION INEFRONASALLYTO DISC
5. IN CONTRAST WITH THE GLAUCOMATOUSDISC,TEMPORAL DISC USUALLY IS NOT EXCAVATED BUT IS EVEVATED SUPERIORLY
6. AN OBLIQUE DIRECTION OF RETINALVESSEL
7. A CRESCENT ON THE SIDE OF THE DISCDEPRESSION
8. HIGH MYOPIA OR MODERATE OBLIQUEMYOPIC ASTIGMATISM PRESENT
9. OBLIQE INSERTION OF THE OPTIC NERVE IN THE GLOBE
10. IN TITLES DISC RETINAL ECTASIA WILL BE FOUND IN CT SCAN

ISNT NOT OK BUT NORMAL VF

THUMB NAIL OF FUNDUS

CONGENITAL ANOMALIES OF DISC

OPTIC DISC COLOBOMA

MORNING GLORY SYNDROME

OPTIC NERVE HYPOPLASIA

TILTED DISC

OPTIC DISC DRUSEN

OPTIC DISC PIT

HORIZONTAL C:D 0.4, CUP OCCUPIES 4/10 WIDTH OF DISC

Measuring Disc Diameter

1. Normal optic nerve's head size is 1.5mm in diameter.
2. But the disc diameter vary from 0.96mm to 2.91mm
3. As a result, physiological cup can be as small as 0.1:1 or as large as 0.8:1.
4. Clinical estimation of optic nerve can be done by WELSCH ALEENOR
5. Slit lamp with +78D or +90D

By WELSCH ALEEN Ophthalmoscope

The smallest white round spot of the Welsch Aleen ophthalmoscope casts alight of 1.5mm in diameter on the retina.This retinal spot size remains constant in phakic eyes with refractive errorsbetween -5.00 & +4 dioptres. When this size coincides with the disc, thenthe disc diameter will be 1.5 mm.In eyes with large physiological cups due to large discs the area illuminated isless than the area occupied by the cup.

BY SLIT LAMP

Vertical Slit beam to create rectangle of light

Beam 1/4 to 1/3 of size of disc diameter wide

Adjust length of beam to match vertical "height" of the disc

Example

Measuring Disc Diameter

Read length of light column from the continuous scale on the slit lamp

Multiply this length by a conversion factor

Example;
1.6mm(Vertical length)x1.11(Volk 78)=1.78mm, will be the disc diameter.

Optic Nerve head change in Glaucoma

Large cup-disc-ratio

Progressive Optic Nerve head Cupping

CUP V>H

Asymmetric optic nerve head Cupping

Disc Hemorrhage

Baring of circumlinear vessels overpass vessels

Bayonetting of vessels

Baring of Circumlinear Vessel

Dr.Jeff Henderer

Murshed.  Good case.  I'm here at the Academy meeting in Orlando.  Greetings from Disney World!  I think this guy looks normal.  The nerve OD looks a bit odd with the superior rim thickness, but I'm thinking that's a normal variant.  I don't see the NFL defect. I'm not bothered by the vasculature in this monoscopic view.  The PPA I never pay much attention to, but if it gets larger (the beta zone) then that can be glaucoma.  I'd watch him.  Great video by the way!  I'm seriously impressed!  Good to hear from you and I hope you are well too.  Take care!

Jeff

Baring of Circumlinear Vessel

This vessel was originally at the rim but is now hanging out in space. A sign of GLAUCOMA and indication of Progressive cupping.

Evaluation of OPTIC NERVE HEAD & NFLD

QUALITATIVE	QUANTITATIVE
Contour of NRR Disc hemorrhage Parapapillary atrophy Bared CCL Vessels Appearance of RNFL	Optic disc V>H Cup H>V Rim / disc ratio RNFL Height

OLD IS GOLD

NRR

NRR COLOR IS FROM PINK RED TOO RANGE

RIM PALLOR>CUPPING=NEURO DISEASE

RIM PALLOR &CUPPING=GLAUCOMA

IF ANY ONE CAN DIAGNOSE THE NRR/NFLD IS THE KEY TO DIAGNOSE OF THE CASE

NORMAL NERVE-NRR SHAPE

DIFFUSE & LOCALIZED FIELD DAMAGE

Diffuse visual damage is highly co-related with IOP(HTG) with Concentric ONH excavation.

Focal or local visual damage is weakly related to IOP.

Patients

With normal pressure (NTG) tend to have localized nerve fiber defects with ONH notching.

PATHOGENITIC CONCEPT

IOP and Glaucoma

Normal "IOP" is debatable value between 18-24 More 60%> population have IOP below 21 mmHg

WHY CENTRAL 30/24 DEGREE

The central 30 ° field represents 66% of the ganglion cells and 83% of the visual cortex

Nearly all pathology are within this area of 30 °

If in doubt, it is recommended to repeat the central field rather than test the periphery

More than 99% of the static perimetry examination for diagnostic purposes are done in the central 30 ° area both for Glaucomatous & as well as Neurological cases.

WHY 24 ° -2

THE VISUAL FIELD

Periphery is five times the central 30 °area. A static perimetry examination would take almost one hour to do the whole field. For the periphery, Goldman Kinetic perimetry is more accurate and faster. Kinetic type of perimetry can also be done in the HUMPHREY

Manual Goldmann Perimetry

STEROID

Risk factors for Steroid Induced GLAUCOMA

PATIENT WITH POAG

FIRST DEGREE RELATIVES OF POAGPATIENTS

HIGH MYOPIA

DIABETES MELLITUS

CONNECTIVE TISSUE DISORDERS

EYES WITH TRAUMATIC ANGLE RECESSION

FELLOW EYES OF ANGLE RECESSION GLAUCOMA

PIGMENT DISPERSION SYNDROME

ENDOGENOUS HYPERCORTISOLISM

MECHANISM FOR IOP ELEVATION

CORTICOSTEROIDS CAUSE ELEVATION OF IOPBY DECREASING THE FACILITY OFAQUEOUS OUTFLOW.
According to BECKER & ARMALY 5%-6% of normal populationresponder to steroid given over a 4-6 weeks period.

MOST POTENT	S T E R O I D	LESS POTENT
BETAMETHASONE FLUOROMETHOLONE DEXAMETHASONE		LOTEPREDNOL PREDNISOLONE MEDRYSONE RIMOXOLONE

COMPARE

CORRELATION WITH OPTIC DISC

Always correlate changes in visual field with the optic disc.

When correlation is lacking, other causes of visual loss should be considered, such asOPTIC NEUROPATHY,DEMYELINATING OR NEUROLOGICAL DISEASE, PITUITARY TUMOUR

In the next cases look for the following situations;

Disc seems less cupped than it is expected for the degree of field loss.

Pallor of the disc is more impressive than the cupping.

The progression of the visual field loss seems excessive.

Non classical for Glaucoma, respecting the vertical midline.

PALE DISC

Neuro 5

ALTITUDINAL FIELD DEFECT

POOR FOVEAL THRESHOLD

WHEN POOR FOVEAL THRESHOLD MACULAR 10-2 ISMANDATORY

UPPER TEMPORAL BRANCH VEIN OCCLUSSION

ALTITUDINAL FIELD DEFECTS MAY BE UNILATERAL OR BILATERAL CAUSESE ARE

RETINAL CAUSES

Branch Retinal Artery Occlusion

Branch Retinal Vein Occlusion

Retinal Coloboma

OPTIC NERVE LESION

Ischaemic optic neuropathy (both arteritic and non-arteritic types)

Papilloedema

Optic disc Coloboma

LESION IN CEREBRAL CORTEX

Superior or Inferior calcarine cortex lesion

Temporal lobe lesion

Parietal lobe lesion

Neuro 6

CHIASMAL COMPRESSION

High Myopic cylinder. First reported to an ophthalmologist.His main complain was loss of bilateral temporal vision.

BINASAL HEMIANOPIA

Brief History

58 yrs. Old a retired engineer

Main complain difficulty in near reading, not so much.

R/E -2.5D,+1Dcyl 95 ° 6/9,L/E -7.5D, 6/9

H/O Vaso vagal attack, anginal pain, Hypertension, High lipid profile, Non diabetic

No lental opacity

On much ocular complain

C:D .6 B/E WNL

IOP WNL B/E

WHAT'S YOUR DIAGNOSIS

First ruled out common cause of Binasal inf.nasal quadrantonopia

Glaucoma

Sector retinitis pigmentosa

Retinoschisis

RARE CAUSE

Bilateral Occipital Disease

Optochiasmatic arachnoditis

Dilation of the third ventricle

INTERNAL CAROTID ARTERY ANEURYSM

Here for final diagnostic investigation depends on available resource to diagnose Internal Carotid artery aneurysm we advice for MRA & MRI (NORMAL STUDY)

JEFF HENDERER REPLIES

Murshed,
Great to hear from you again!  I look forward to seeing you in California!  I have never seen a case like this, but I think that you are correct in everything you are doing and thinking.  In fact I was thinking the aneurysm as I read through your workup and then when you said it "bingo" I thought!  Well, its a rare condition and a very rare field, but the consequences of missing this diagnosis are so great that I think it is an appropriate use of resources.  Rupture would almost certainly be horrible, if not fatal.  By the way, I agree with you on the reliability of the fields.  Take care!  
Jeff

BINASAL

A lady came for field for uncomfortable in near reading.C:D .3 R/E,.5 L/E 6/6 O.U N 5 B/E IOP WNL Disc normal

FD OCCIPITAL RADIATION OR THE STRIATE CORTEX

Congruous quadrantanopia

Homonymous hemianopia

Altitudinal hemianopia

Checkboard quadrantanopia

TO DETECT TEPORO OCCIPITAL FD NEEDS

MRA/MRI

COLOUR FLOW DOPPLER

BITEMPORAL HEMIANOPIA

CHIASMAL LESION

PITUTIARY ADENOMA

MENINGIOMA,CHRANIPHARYNGIOMA,A NEURYSM,GLIOMA

CAUSES OF CENTRAL SCOTOMAS

MACULAR DISEASES

OPTIC NEURITIS

ISCHEMIC OPTIC NEUROPATHY

OPTIC ATROPHY

OCCIPITAL CORTEX LESION

EASTABLISHED POAG

Right disc has no inferior NRR at all as well as nasal shifting of the vessels are seen with deep cupping and lamellar dot signs are seen which well corresponds with the right field. Dense arcuate scotomas emanating from the blind spot to join the superior arcuate scotoma later joins the upper nasal step to form half dense arcute ring scotoma. His IOP was 24mmHg R/E when first diagnosed. Now he is on anti Glaucoma drops B/E and IOP 14mmHg.Left field & fundus are normal.Lt.fundus shows inf.temp. PPA in an emmatrop is suspicious.

DENSE SUP ARCUATE SCOTOMA

D/D OF ARCUATE SCOTOMA

1. CHORIORETNIAL LESIONSJUXTAPAPILLARY CHOROIDITIS &RETINOCHORODITIS MYOPIA WITH PPA
2. OPTIC HEAD LESIONDRUSEN, PAPILLITIS, COLOBOMAS,CHRONIC PAPILLOEDMA
3. ANTERIOR OPTIC NERVE LESIONRETROBULBAR NEURITIS,ELECTRIC SHOCK
4. POSTERIOR LESION TO VISUAL PATHWAYPITUTIARY ADENOMA,PSEUDOTUMOUR CERIBRI

ADVANCE POAG

This middle aged woman diagnosed POAG 5yrs.back.V.A R/E 6/9Tubular.L/E 6/6.C;D R/E .99/1,L/E .5.Rt. VF shows only a small central field withan island of small temporal field. Lt.shows cluster of scotomas in the mostSuspected & expected zone Sup & infra nasal quadrant.L/E an early POAG.Rt. Eye an advanced POAG. She was very irregular in putting drops.

Temp. zone. Here out of 120 points, he can see 109 & cannot See 11 points. When not seen crosses 10>in screening test than full Threshold test to be done. This is an advance case of POAG R>L.

BRIEF HISTROY

One eyed R/E vitreous hemorrhage due to uncontrolled blood pressure 47yrs. old. No H/O Diabetes

H/o road traffic accident with macular hemorrhage L/E 5/6 yrs back vision 6/6 with +2D small hypermetropic eye.

L/E healthy NRR slight thinning of inferior NRR/ Superior NRR thinning C:D .5 IOP L/E 20 R/E 18 mmHg.

Three consecutive fields in one year shows inferior arcuate scotmas, does not so much well correlated with the disc findings.

Last of all phasing done. Diurnal variation R/E 4mmHg L/E 6mmhg very much suspected.

So, here we should not wait to treat him.

Here increased variability of the fields is an early sign of glaucomatous field defect, in spite of healthy NRR L/E

It takes about 3.5yrs to become a normal field to be an abnormal field (Haejil)

PHASING

SCOTOMAS

ISOLATED PARACENTRAL DEFECTS OCCUR AS THE INITIAL GLAUCOMA DEFECT IN ABOUT
40% OF PATIENTS. OTHEREARLY MANIFESTATIONS OF GLAUCOMA

ARCUATE DEFECTS

NASAL STEPS

TEMPORAL WEDGE DEFECT

NEIL T.CHOPLIN RUSSEL P.EDWARDS ............................................................................Page 119 2ed.

NTG

First detected when he comes for near reading glass.NTG Fixation threatening, localised VFD,
30% of all POAG,30% IOP to be reduced

GLAUCOMA AT A GLANCE

Glaucoma is the second leading cause of preventable blindness in the world.

Glaucoma has no early S/S(POAG), often called the "Sneak thief of Sight" Early detection
and treatment can save your sight. Testing for Glaucoma is simple, quick and painless.

70 million people are suffering from Glaucoma in the world, half of them do not known even
they have it. Of them 7 million are totally blind. Highest number of blind due to Glaucoma are
in NIGERIA. Half of this patient are from ASIA.

Some 120,000 Americans are blind due to Glaucoma. The tragedy is that 90% of those are
blind didn't have to be. Then what about BANGLADESH.

PLEASE THINK!!!
PREVENTION IS BETTER THAN CURE

EARLY DETECTION

Early Detection of Glaucoma

There are several methods claiming to detect glaucomatous damage in the very early stage.
Such As:

Analusis of the disk

Nerve fiver analysis

Multifocal ERG

Blue-on-Yellow Perimetry (Konio>Magno cells?)

Testing the retina using temporal and/or special modulated stimuli (Parvo, Magno cells?)

REFERRED

PLEASE DO NOT HESITATE TO REFER THE EARLY CASES OF GLAUCOMA FOR SECOND OR THIRD
OPINION . IT IS VERY TOUGH TO DIAGNOSE AN EARLY POAG GLAUCOMA.BECAUSE OF
INDIVIDUAL & INTEROBSERVER SUSPECTED DISC EVALUATION

FIELD DEFECT COMES AFTER 20% OF NERVE DAMAGE,SO VERY TUFF TO DIAGNOSE EARLY
POAG

REFERENCE WILL RELIEF

GLAUCOMA AWARENESS

Most people are not aware of Glaucoma, although not to be taken lightly glaucoma is very
treatable if caught in its early stage.

RISK FACTORS ARE THE ODDS

Family history increases risk 4 to 9 times

African Americans race increases risk 4 times

Diabetes increases risk 2 times

Glaucoma in one eye,29% chance of getting in other eye within 5 years

People over age of 60 yrs are 6 times more likely than under age of 60 yrs .

SO YOU'RE A GLAUCOMA SUSPECT, NOW WHAT ?

Get your eyes checked regularly

Take it seriously

Educate yourself about Glaucoma

Talk to your Doctor, ask questions, get answers

Don't hesitate to get a second, third opinion, or as many as you need it.

Lead a healthy life

Get Glaucoma support if you feel you need it.

ARE YOU A PARENT WITH GLAUCOMA ?

CHECK IOP PRIOR TO STARTING KINDERGARTEN PLEASE CONTACT DR.MOHIBUL ISLAM
OF "NURUL ISLAM CLINIC" OR DR.MD.FAZLUL HAQUE(SUBECHA PLAZA) FOR NON
CONTACT PUFF TONOMETRY"

EVERY 2 OR 3 YEARS IN CHILDHOOD

EVERY 2 YEARS IN THEIR TEENS

EVERY YEAR AFTER THAT

HOW DOES ONE COPE WITH GLAUCOMA

GET SUPPORT FROM FRIENDS,FAMILY AND OTHER PATIENTS

THINK POSITIVE ABOUT LIFE,GLAUCOMA IS NOT A DEATH SENTENCE

STOP TO SEE THE ROSES

SEE THE WORLD ...GO SOME PLACE YOU'VE NEVER BEEN

EDUCATE YOURSELF ABOUT YOUR CONDITION

PLAY AN ACTIVE ROLE IN YOUR TREATMENT PLAN

WHAT CAN YOU DO TO RAISE GLAUCOMA AWARENESS ?

TALK WITH YOUR FAMILY ABOUT GLAUCOMA AND THE RISK FACTORS

TALK WITH YOUR FRIENDS ABOUT GLAUCOMA AND RISK FACTORS

TALK WITH YOUR CO-WORKERS ABOUT GLAUCOMA AND THE RISK FACTORS

ENCOURAGE FAMILY,FRIENDS AND CO- WORKERS TO GET REGULAR CHECK-UPS EVEN IF NOT
AT RISK

ADVICE

IF OVER WEIGH, CONTROL IT

HYOPO, HYPERTENSION,DIABETES TO BE CORRECTED. SPECIALLY B.P DURING SLEEP SHOULD
BE RECORDED WHEN YOU SEE FLUCTUATION OF B.P.CONSULT YOUR CARDIOLOGIST ABOUT
B.P/IOP

ASPRIN IN LOW DOSE,VITAMIN E, ANTI OXIDANT

20 MIN AEROBIC EXERCISE FOUR TIMES A WEEK

DON'T TAKE LARGE AMOUNT OF WATER WHILE HAVING EMPTY STOMACH. TAKE WATER
IN DIVIDED AMOUNT THROUGHOUT THE DAY

COLOUR INDICES

Gentle Request

Please let me know what you think about this topics.

I would appreciate all forms of comments and suggestions.

Any query, HEALTHY criticism, questions are most welcome at any time without any hesitation.

Please let me know your comments on this topics.

Total deviation	Octopus

MD		B/Y

PROVIEW TONOMETER