Diagnosis and Therapy Audrey KaplanMessas Head of glaucoma service Assaf Harofe Medical center NTG think about it How common is NTG Population studies 3040 Sommer 1991 Dielemans 1994 Bonomi 1998 ID: 472167
Download Presentation The PPT/PDF document "Normal Tension Glaucoma" is the property of its rightful owner. Permission is granted to download and print the materials on this web site for personal, non-commercial use only, and to display it on your personal computer provided you do not modify the materials and that you retain all copyright notices contained in the materials. By downloading content from our website, you accept the terms of this agreement.
Slide1
Normal Tension GlaucomaDiagnosis and Therapy
Audrey Kaplan-MessasHead of glaucoma serviceAssaf Harofe Medical centerSlide2
NTG:think about it !
How common is NTG?Population studies30-40% (
Sommer 1991, Dielemans 1994, Bonomi 1998)
Clinical presentation and screening
5% (Grodum, Heijl 2002)Slide3
NTGDiagnosis and therapy
DiagnosisDifferential diagnosisNatural History
Investigation
TreatmentSlide4
NTG: Description
Glaucomatous optic neuropathyCharacteristic pattern of visual field lossIOP within the normal range
Progressive diseaseSlide5
NTG: Description
Normal-tension glaucoma (NTG) is an optic neuropathy of unknown etiology characterized by cupping of the disc, typical visual field loss, and normal IOP. The diagnosis of NTG is made by exclusion, and an extensive differential must be considered in evaluating patients with suspected NTG. Slide6
Vascular patophysiology
Vascular and cardio-vascular risk factors associated (Broadway 1998, Hayreh 1999)Nocturnal Hypotension (Hayreh 1999, Meyer 1996 )
Exacerbated when topical beta- used
( Hayreh 1999)
Relationship with migraine (up to 62% VF def when both) , vasospasm (Gasser 1999)Slide7
Auto-immune patophysiology?
30 % of NTG have an AI disease (8% OHT) (Cartwright 1992)Monoclonal paraproteinemia, IgG, Ig A in RGC layer
(Wax 1999)
Antiphospholipid Ab
( Kremmer 1999), Rhodopsine Ab in NTG (Romano 1999)
Ab to Heat Shock Protein NTG> POAG> control (Wax, Tezel 1998)Slide8
NTG: Differences with POAG
Thinner NR rim, inf-temporally, focal rim defect (Caprioli
1985,Jonas 2000
)
Shallower cupping, saucerization (Fazio 1990)
Focal RNFL defects (Jonas 2000
)Visual field loss deeper and steeper paracentral, dense scotoma close to fixation (up to 50% of NTG)
(Caprioli 1985, Hitchings 1984),
Prevalence of Disc Hemorrhages (up to 25%)
( Kitazawa 1988, Jonas 2000)
CCT thinner in NTG
(Morad 1998,Copt 1999, Whitacre 2000)Slide9
DiagnosisSlide10
NTG: discsSlide11
NTG: discsSlide12
Disc hemorrhage at 5 o'clock and peripapillary atrophy in a left eye with high cup to disc ratio and thinned neuroretinal rim from NTG
NTG: discsSlide13
Severe visual field loss near fixation
NTG:VF defectSlide14
Normal Pressure Glaucoma
DiagnosisDifferential diagnosisNatural History
Phenotype and genotype
Investigation
TreatmentSlide15
NTGDifferential Diagnosis
Differential diagnosisGlaucoma?Optic Neuropathy?
Visual pathway disease?
Acquired or developmental optic nerve disease?
Does the diagnosis fit?
YES-evaluateNO-look for other disease
Remember Co-morbidity: vascular, auto-immuneSlide16
NTGWhen is neuro-imaging indicated
Rapidly progressingPatient less than 50 yoUnilateral condition
Disc palor> cupping+++
Dyschromatopsia or VA reduction
Discrepancy between disc and VF defectSlide17
DD: Physiological cuppingSlide18
DD: Physiological cuppingSlide19
Diagnosis
NTG suspect
Gl cupping + specificVF defect
No
Acquired
Developmental
Neurologist
Yes
HPG
NPG
DischargeSlide20
Normal Pressure Glaucoma
DiagnosisDifferential diagnosis3-Natural History
Investigation
TreatmentSlide21
How do we detect progression
Visual Field
Before progression identify baseline
Refraction
reliability
effect of pupil size
effect of lens opacities
fatigue effects
test/ retest variationSlide22
‘92
‘99
OS
OD
Binocular
Progression with visual perception of it
Slide23
1989
2001
Progression without visual perceptionSlide24
1/ Ophthalmoscopy
Dilated, indirect or direct
2/ SDP
3/ Imaging of disc and NRFL:
HRT, OCT, GDX
How do we detect progression
S
tructureSlide25
Focal or diffuse narrowing of Neuroretinal rim
Increase of CDR
Narrowing of vessels
Increase f PPA
How do we detect progression
S
tructureSlide26
Natural history: CNTG StudySlide27
CNTG study: purpose
Is IOP part of the pathophy in NTG?Does aggressive IOP lowering halt damage (ON and VF) in NTG at high risk of progression?What are the risk and side effects of aggressive Rx?Slide28
CNTGS methods
230 eyes NTG defined as:Glaucomatous cupping of discCharacteristic VF defectMedian IOP 20mmHg or less in 10 baseline measurementsSlide29
CNTGS results
One eye randomized tono Rx Meds, LTP or filter
30% IOP –
IOP from mean 16 to 11 mmHg
Progression is reduced from 60 to 20% in treated
(after correction for cataract)Slide30
CNTG study: results
IOP is part of the pathogenic processLowering IOP by 30% slows VF loss
Hidden by cataract
Achieved in 50% of medical Rx
Rate of VF progression in NTG very variable Risk factors for progression: DH, migraine, femaleSlide31
0
12
24
36
48
60
72
84
0
0.2
0.4
0.6
0.8
1.0
Months
Proportion not showing visual field progression
ONLY 1/3 at 5 years
NO progression
Time to progression
No RX
Hitchings
Rx CNTG and HitchingsSlide32
Normal Pressure GlaucomaDiagnosis and therapy
DiagnosisDifferential diagnosis
Natural History
Investigation
TreatmentSlide33
NTG: Investigation
Baseline dataIOP -Mean/Max/posturalOptic disc area, RNFL
Visual function
Additional studies
Blood flow if available?
Genetics if familial?Slide34
NTG: Investigation
CausationIOPPerfusion pressure
Other Neurological
Investigations
CCT,
Diurnal, postural IOP
Vascular, vasospasmVisual pathways-MRISlide35
Normal Pressure GlaucomaDiagnosis and therapy
DiagnosisDifferential diagnosis
Natural History
Investigation
TreatmentSlide36
NTG: Treatment
NilIOP reductionMedical LaserSurgery
Non IOP reducing
Ca channel blockers
NeuroprotectionSlide37
NTG: Treatment ?
38% of the treated group developed cataract: NNT=17 (needing Rx to prevent VF progression in 1 patient)7/ 17 will develop visual loss from cataractIs Rx justified? for a condition where:
1/3 will show no progression in 5 years
Age at presentation c. 66 yrs Slide38
Treated- No
lens ops
No Rx:Controls
P=0.0018
1
2
3
4
5
6
0
0.2
0.4
0.6
0.8
1.0
Proportion
surviving
Time in years
Treated-inc
lens ops
NTG: Treatment
P=0.21
Collaborative. NTG studySlide39
NTG: TreatmentMedical
Avoid the Beta –blockers and Alpha-adrenergic agonists: they may affect perfusion pressure
PG can give 15-30% IOP reduction
PG good in the NTG range,
PG increase pulsatile OBF
Brimonidine reduce 20% and may be neuroprotective
If necessary consider SLTSlide40
NTG: TreatmentSurgery
CNGTS 30% IOP on meds in 50% casesEMGT 25% IOP on Betaxolol and ALTP
Surgery
+ 25 %
Traby + 5 FU (Membrey et al)
Traby in CNGTS 50% casesSlide41
Normal Pressure GlaucomaTrabeculectomy? YES
Bhandari et alSlide42
NTG-diagnosis and therapy
Is the diagnosis correct? GON + VF What investigations do I need? Risk factorsWhat type of follow-up tests? VF, Imaging
Do I treat? YES! -30%Slide43
Thank you