WHAT IS NEW IN GLAUCOMA MANAGEMENT? FROM DRUGS TO STEM THERAPY TO YOGA AND MEDITATION, IT'S ALL THERE. GOOD FOR EVERY OPHTHALMOLOGIST AND POST - GRADUATES. INNOVATION IS THE NEW NORMAL.

1. NEWER DRUGS &
SOMETHING DIFFERENT IN
MANAGEMENT OF
GLAUCOMA
ARVIND KUMAR MORYA
ASSOCIATE PROFESSOR & UNIT-II HEAD
MS(GOLD – MEDALIST),MNAMS
GLAUCOMA,CATARACT,SQUINT,REFRACTIVE,PAEDIATRIC
OPHTHALMOLOGY
& MEDICAL RETINA SERVICES
DEPT. OF OPHTHALMOLOGY
AIIMS,JODHPUR

2. WHAT IS THE NEED ?
• SINGLE CLASS OF DRUG – NOT ENOUGH - COLLABORATIVE INITIAL GLAUCOMA
TREATMENT STUDY AND THE OCULAR HYPERTENSION TREATMENT STUDY
• ADHERENCE & COMPLIANCE – DRUGS WHICH ARE FREQUENT DOSES . SIMPLY
NOT WELL ACCEPTED . MORE ADDITION OF GROUP OF AGM – AGAIN NOT WELL
ACCEPTED

3. SO WE NEEDS TO LOOK FOR A PERFECT
SOLUTION
• DRUGS WITH GREAT MILEAGE (LONGER ½ LIFE)
• ADHERENCE
• HIGH IOP LOWERING CAPACITY
• LESSER SIDE EFFECTS
• ECONOMICAL
• MODIFICATIONS AT GENETIC LEVEL
• IMPROVES OBF
• NEUROPROTECTIVE WITH MORE ACCEPTABILITY

4. IOP – ONLY MODIFIABLE FACTOR
• PILOCARPINE – FIRST AGD – YR 1877
• LATANOPROST – IN YR 1996
• SO AFTER >2 DECADES – A NEW GROUP OF AGD NOW AVAILABLE
• DEVELOPED IN JAPAN

5. NEWER CLASS & MOA AGD
• RHO KINASE INHIBITORS
• A1 RECEPTORS AGONISTS
• BKCA IONIC CHANNEL MODULATORS
• CANNABINOIDS
• LOCAL CALCIUM CHANNEL BLOCKERS - LATRUNCULINIC DERIVATES

6. RHO KINASE INHIBITORS
RHO DEPNDANCE MOA ATTACHES TO TRANSMEMBRANE RECEPTORS
RHO GTP ASE
ROCK
MLC PHOSPHORYLATION
SMOOTH MS CONTRACTION,CELL MOT
&CYTOSKELETON ALTERATIONS
TM – SMOOTH MS CELL PROPERTY ACTIV
ENHANCED AQ OUTFLOW ACTIVITY

7. RIPASUDIL(0.4%HCL HYDRATE/K-115)
• S CONFIGURATION AT THE 2-POSITION ON THE 1,4-DIAZEPANE RING OF RIPASUDIL - GIVES
THIS DRUG ITS CHARACTERISTIC EFFECT ON SMMOTH MS CONTRACTILITY
• DERIVATIVE / FASUDIL, BOTH SHARE THE SAME CORE STRUCTURE OF 5-(1,4-DIAZEPAN-1-
YLSULFONYL)ISOQUINOLINE.
• FASUDIL WAS A POTENT RHO-KINASE INHIBITOR, BUT ON INCORPORATION OF A FLUORINE
ATOM AT THE C4 POSITION OF ISOQUINOLINE MOIETY AND THE CHIRAL ATTACHMENT OF A
METHYL GROUP TO THE C2’ POSITION OF 1,4-DIAZEPANE MOIETY
• IOP LOWER ACTION INCREASED CONSIDERABLY
• SO "RIPASUDIL PROVED TO BE MUCH MORE POTENT AND SELECTIVE RHO-KINASE INHIBITOR >
FASUDIL"

8. PHARMACOKINETICS
• NO EFFECT ON RESPIRATORY OR NEUROLOGICAL FUNCTION.
• NO CARCINOGENICITY STUDIES EVER PERFORMED, IT SEEMS TO BE NON-
CARCINOGENIC BY ITS RAPID ELIMINATION & LACK OF ACCUMULATION IN TISSUE
• LACK OF INFLAMMATORY RESPONSE IN THE EYE POST-ADMINISTRATION
• RIPASUDIL ACHIEVES A HALF-LIFE OF 0.49 TO 0.73 HOURS IN HUMANS AND IS
PREDOMINANTLY EXCRETED IN THE URINE.
• A REPORT SUBMITTED TO JAPANESE PHARMACEUTICALS AND MEDICAL DEVICES
AGENCY - IT SHOWED NO BINDING AFFINITY FOR RECEPTORS OF
THE ADRENERGIC, ANGIOTENSIN
II, ENDOTHELIN, GLUTAMATE, HISTAMINE, MUSCARINIC, OR PROSTANOID VARIETY.
THIS LACK OF AFFINITY ALSO APPLIES TO CA2+ AND K+ CHANNELS, CARBONIC
ANHYDRASE, AND HMG-COA REDUCTASE
• BD DOSE

9. OTHER MOA
• MARCH 2016 IT PROVES TO PROMOTE CORNEAL ENDOTHELIAL CELL (CEC)
PROLIFERATION IN CULTURED HUMAN CELLS AS WELL AS WOUND HEALING AND
ENDOTHELIUM REGENERATION IN A RABBIT WOUND MODEL
• SCIENTISTS BELIEVED THESE PROPERTIES COULD PREVENT OR IMPROVE THE CEC
DENSITY DROP ASSOCIATED WITH CATARACT SURGERY OR CORNEAL TRAUMA-
MECH INDUCED OR NATURAL.
• SO GENERAL HAZINESS, EDEMA OF THE CORNEA, OR KERATOPATHY CAN BE
PREVENTED
• GENERAL IMPROVEMENT IN THE RECOVERY OF A POST-OPERATIVE PATIENT.
• IN 2016, IT SEEMS TO PREVENT EXCESSIVE SCARRING AFTER GLAUCOMA
FILTRATION SURGERY BY ATTENUATING THE ACTIVATION OF
CONJUNCTIVAL FIBROBLASTS
• THE DRUG WAS ALSO UNDER CLINICAL REVIEW FOR ITS ABILITY TO ALLEVIATE

10. SIDE EFFECTS
• CONJUCTIVAL HYPEREMIA
• CONJUNCTIVAL HAEMORRHAGE(5.7%)
• TRANSIENT CORNEAL GUTTAE FORMATION
• OCULAR IRRITATION (3.8%)
RIPATEC IS AVAILABLE IN INDIA NOW

11. ADRENERGIC RECEPTOR AGONIST-
TRABODENOSON(INO-8875)
M O ACTION
MATRIX METALLOPROTEINASES –II ACTIVATED
SCAVENGING OF TYPE-IV COLLAGEN IN TM REMOVAL
OUTFLOW RESISTANCE DECREASED – IOP LOWERS
PHASE-III TRIAL- IOP LOWERS UPTO
4.1 MM/HG

12. BKCA IONIC CHANNEL MODULATORS
LATANOPROSTENE BUNOD
(LBN,BOL-303259-X)
ENHANCES NO LEVEL IN TM
IONIC CHANNEL ACTIVATION – SMOOTH MS
RELAXATION
AQ.OUTFLOW INCREASES – TM &
UVEOSCLERAL PATHWAY
MODIFIED PG ANALOGUE & NO DONOR PHASE-III , 8.4 MM/HG

13. SI RNA’S - BAMOSIRAN(SYL040012)
SPECIFIC GENE SILENCING ACTION
INHIBIT B2 ADR. RECEPTOR
CB AQ. PRODUCTION IS REDUCED
PHASE-I ACTUAL IOP CHANGING ABILITY NOT KNOW

14. CANNABINOIDS/MARIJUANA
FEW STUDIES PROVED CANNABINOID R1(CB1) IN TM & CB EPI
ACTIVATES
AGONIST
IOP DECREASES
VERY EARLY STAGES

15. LOCAL CCB
VERAPAMIL
INCREASES OBF IN ANIMAL&HUMAN MODELS
LIMITATIONS DUE TO SIDE EFFECTS
BRADYCARDIA SYST. HYPOTENSION

16. ANECORTAVE ACETATE
STEROID AGONIST
INHIBITS
PLASMINOGEN ACTIVATOR 1 INHIBITOR
EARLY STAGES & ACTUAL IOP LOWERING MECH. UNKNOWN

17. DRUGS MODULATING OXIDATIVE
STRESS,MITOCHON.DYSFUNCTION &
NEUROPROTECTION
GLAUCOMATOUS DEGENERATION DIRECTLY PROPORTIONAL TO OXIDATIVE STRESS&MITOCHOND. DYSFUN
RAISED IOP ISCHAEMIA INCREASED LEVEL OF FREE OXYGEN RADICALS&CELL DEATH MEDIAT
ANTI-APOPTOTIC DRUGS RGC PROTECTION
ALPHA – LIPOIC A.
ALPHA- LUMINOL
GINKGO BILOBA EXTRACTS
RESVERATROL
NEUROPROTECTIVE DRUGS
MEMENTINE-R ANTAGONIST NMDA
GLUTAMETERGIC
BRIMONIDINE-ALPHA-2ADR. AGONIST

18. EXOGENOUS NEUROTROPHIC FACTORS
ADMINISTRATION
INTRAVIT. 5UG BDNF & 2UG CNTF- SHOWED 10-25% FALL IN CELL DEATH RATE
TOPICAL NGF QID X 7WEEKS – INCREASED CELL DENSITY BY 37%
MORE CLINICAL TRIALS WITH CONTROL GROUP ARM IS REQUIRED
EFFECTS SHORT LIVED , TEMPORARY & RAPIDLY WANES- SO APOPTOSIS IS INEVITABLE
SUSTAINED RELEASE PREPARATIONS MIGHT HELP IN FUTURE TRIALS

19. GENE THERAPY – REPLACEMENT/SILENCING
• IDEAL THERAPY – EXPRESSION SPECIFICALLY IN TARGET CELLS IN DESIRED AMOUNT IN A TIME
DEPENDANT MANNER
• NON-PATHOGENIC,NON-IMMUNOGENIC & NON-TOXIC
• LONG TERM GENE EXPRESSION WITH SINGLE DOSE
• EYE – SUITABLE TARGET ORGAN – COMPARTMENTALIZED –ACCURATE DELIVERY OF VECTOR TO
SPECIFIC TISSUE UNDER DIRECT MICROSCOPIC VISUALIZATION
- MIN. SYSTEMIC DISSEMINATION & S/E
- SMALL SIZE/OCULAR TISSUE – STABLE POPULATION CELLS TRANSDUCED EFFICIENTLY BY SMALL
VOL/VECTOR DOSES
- NON INVASIVE & PRECISE OPTICAL IMAGING AVAILABLE
- VISUAL FUNCTION – BOTH PHYSIOL & ELECTROPHYS EASILY MEASURABLE
- CONTRA LATR EYE – NATURAL CONTROL GROUP

20. GENE THERAPY – 1.RECESSIVE DS.-LESS
FUNC/GENE:REPLACEMENT
2.DOMINANT DS. –REMOVAL/GENE MUTANT
TRANSCRIPT: SILENCING & REPLACEMENT
REQD
GLAUCOMA GENES
GENE DS. MOA THERAPY
MYOC-MENDELIAN JUV&AD POAG PROTEIN AGGREGATION CRISPR GENE EDITING
TEK,ANGPTI. CONG,JU&AD POAG. SCHL. CANAL DEVELOP. ENHANCED TEK SIGNALING
ABCA1,CAV1,DGKG, POAG LIPID METABOLISM & TM
ARHGEF12. DYSFUNCTION STATINS?
TXNRD2&4 OTHER
MITOCHOND. GENE. POAG. MITOCHOND. DYSFUNCTION RESTORE MITOCHOND
FUNCTION

21. GENE THERAPY IN GLAUCOMA – RGC
SURVIVAL
• WORK OF KEITH MARTIN – MODULATION/BDNF SIGNALLING - RGC PROTECTION – STRONG
NEUROPROTECTION IN ANIMAL MODEL -38.3% RESCUE/RGC
• AAV TRKB BDNF > AAV BDNF AFTER O.N. CRUSH – 67% INCREASE IN RGC SURVIVAL RATE
• GT – PROVIDES PROTECTION AGAINST LOSS OF EEG AS O.N. CONNECTIVITY TO BRAIN
MAINTAINED IN ANIMAL MODELS IN PRESENCE OF RAISED IOP
• WORK OF PAUL KAUFMAN & SHAMIRA PERERA – MODULATION OF X – GENE TO UPREGULATE
TM OUTFLOW
• CUSTOMIZED 125 MICROMETER CATHETER AVAILABLE FOR SCHLEMM’S CANAL DELIVERY(S-
PERERA)
• EXPERIMENTS UNDERGOING IN PRIMATES
• BY AAV VECTOR

22. GENE THERAPY
VIRAL VECTORS ADMINISTRATION INTEGRATION WITHIN TARGET RETINAL CELLS
INCREASED PRODUCTION/NEUROTROPHIC FACTORS IN RETINAVIRAL VECTOR GENE EXPRESSION -
SHORTLIVED
NON VIRAL VECTORS MAY BE TRIED
POLY ETHYLENE OXIDE –POLY PROPYLENE OXIDE-POLY ETHYLENE OXIDE(PEOPPO-PEO)EYE DROPS-NON INVA
TRKA R-AGONIST-PEPTIDOMIMETIC LIGAND SURVIVAL RATE OF RGC INCREASES IN GLAUCOMA

23. GENE THERAPY IN BRIARD CANINES WITH LCA
• DELIVERY OF RPE65 USING VIRAL GENE THERAPY IN 2000 TO THESE AFFLICTED
DOGS GAVE ENCOURAGING RESULTS: THE DOGS HAD IMPROVED VISION AS
SHOWN BY THEIR ELECTRORETINOGRAMS AND THEIR ABILITY TO NAVIGATE
OBSTACLE COURSES IN DIM LIGHT (ACLAND ET AL., 2001).

24. STEM CELL THERAPY
HUMAN BONE MARROW AUTOLOGOUS MESENCHYMAL STEM CELLS(MSC’S)
INTRAVIT. INJECTIONREGENERATION OF RGC AT RETINA & ONH BY
STEM CELLS
RETINAL PRECURSSOR CELLS FROM EMBRYONIC RETINA SUB RETINAL SPACE OF MICE
REAL FUNCTIONAL RECOVERY ON LOWER SIDE WITH ONLY SOME VISUAL
RESTORATION ONLY

25. IMMUNOMODULATION
• IT’S BEEN POSTULATED THAT IMMUNE SYSTEM PLAYS KEY ROLE IN
ABILITY/O.N.& RETINA TO WITHSTAND GLAUCOMA
• INNATE & ADAPTIVE IMMUNE CELLS – PROTECTIVE NISHE TO HALT GLAUCO.
PROGRESSION
• GLATIRAMER ACETATE (COP1) THERAPEUTIC VACCINATION

26. OTHER NEWER AGENTS- FOR FUTURE
CLINICAL TRIALS
• TETRAHYDRO CORTISOL – LOWER STEROID(DEXA) INDUCED OHT
• MIFEPRISTONE- ASPECIFIC GLUCOCOTICOID RECEPTOR ANTAGONIST – DEC. IOP
• SPIRONOLACTONE A- STEROID ALDOSTERONE ANTAGONIST WITH POT. SPARING
DIURETIC MOA- SIGNIFICANT LOWERING/IOP
• ANTAZOLINE- ANTIHISTAMINE TOPICALLY BY LOWERING AQ. PRODUCTION

27. PRESERVATIVE FREE/SELF PRESERVED
• PURITE – SOC
• SOFZIA
• POLYQUAD

28. NEWER DRUG DELIVERY SYSTEM
• NANO PARTICLES BASED EYE DROPS
• CONTACT LENS BASED DELIVERY SYSTEM

29. TAFLUPROST
• FIRST PPF PG ANALOGUE
• US FDA APPROVAL IN 2012
• LESSER SIDE EFFECTS
• .0015%
• OD EVENING DOSE
• BETTER ADHERENCE AND COMPLIANCE

30. SOMETHING NEW AND LITTLE DIFFERENT
A COMBI – WONDER PILL : MOST ECONOMICAL , WELL ADHERE
BEST COMPLIANCE

31. MEDITATION
• YOGA – UNION OF MIND BODY & SOUL
• 3RD CENTURY BC – MAHIRSHI PATANJALI
• FOCUSSED ATTENTION BY BREATH,MANTRA & SOUND
• RELAXATION INDUCTION & INTROSPECTION
• DETACHMENT FROM OUR OWN THOUGHTS – SO A CALM STATE & MENTAL
EQUANIMITY

32. RELAXATION RESPONSE – HERBERT
BENSEN(MD)
CO-ORDINATED PHYSIOLOGICAL RESPONSE
CONTROLLED BY PS N. SYSTEM
• AROUSAL WITH ALPHA-FRONTAL EEG ACTIVITY
• VOLUMETRIC O2 CONSUMPTION & CO2 ELIMINATION
• HT. RATE , RESP. RATE & BP
• UNIQUE STATE TO NEGOTIATE STRESS IN OUR LIFE

33. STRESS -
• RISE IN IOP
• POAG PT. ARE HIGH STEROID RESPONDERS
• HIGH PLASMA CORTISOL LEVELS IN OHT AS COMPARED TO NORMAL
POPULATION WITHOUT GLAUCOMA
CORTISOL LEVELS WITHOUT ANY
SYST/TOPICAL INTAKE

34. GLAUCOMA > NEURODEGEN < EYE DS.
RGC APOPTOSIS INITIATION
• MECH. STRESS (IOP)
• ISCHAEMIA/HYPOXIA
• GLUTAMATE EXCITOTOXICITY
• LOW LEVELS OF BDNF NEUROTROPHINS
• GLIAL CELL INFLAMMATION(TNF)
• DECREASED NO – CGMP DYSFUNCTION

35. MRI – BRAIN CHANGES IN GLAUCOMA
PATIENT
• TRANS – SYNAPTIC NEURODEGENERATION IN LATR GENICULATE BODY &
OCCIPITAL CORTEX
• RAISED IOP & INJURY TO RGC TRIGGERS NEURODEGENERATION IN DISTANT
CONNECTED NEURONS IN MAJOR VISUAL CENTRES / BRAIN
• BRAIN IS A POTENTIAL TARGET TO BE TREATED IN GLAUCOMA

36. STRESS – HIPPOCAMPAL NEURONAL
DEGENERATION
HYPOTHALAMUS PITUITARY
RELEASE OF ACTH – STIMULATION/ADRENAL GLANDS – RELEASE/GLUCO CORTICOIDS
HIPPOCAMPUS CORTICOSTEROIDS
MODULATION/SYNAPTIC PLASTICITY DENDRITIC STRUCTRAL ALTERATION NEURO
CAUSES MEMORY LOSS & NEURODEGEN :- MAIN CAUSE OF POOR COMPLIANCE/ADHERENCE IN GLAUCOMA

37. MAC ARTHUR STUDY OF AGING POPULATION
• COGNITIVE DECLINE IS DIRECTLY PROPORTIONAL TO RAISED CORTISOL LEVELS
• REVERSIBLE WITH LOWERING / CORTISOL LEVELS
• MOST GLAUCOMA PT. – DEMENTIA , ANXIETY, DEPRESSION, POOR
PSYCHOSOCIAL BEHAVIOUR, DEC. LIBIDO & POOR QUALITY OF LIFE THAT
FURTHER DETIORATES WITH INITIATION OF AGM

38. MEDITATION & GREY MATTER
• FOREVER YOUNG:POTENTIAL AGE DEFYING EFFECT/LONG TERM
MEDITATION/GREY MATTER ATROPHY E.LUDERS ET.AL. PROVES REVERSAL OF
NEURO COGNITIVE DECLINE BY NEUROGENESIS IN ADULT BRAIN
• SARA W.LAZER STUDY. MEDITATION STOPS/ SLOWS DOWN AGE RELATED
CORTICAL THINNING
• META ANALYSIS BASED ON 21 NEURO IMAGING STUDIES BY KIERAN C R FOX ET
AL. PROVES THAT ENHANCED GREY MATTER SYNTHESIS IN LONG TERM
MEDITATING GROUP.
• SHORT TERM (8 WEEKS) MEDITATION MRI STUDY BY BRITTA K HALZEL ET AL.
HAD SHOWN INCREASED GREY MATTER CONC. IN HIPPOCAMPUS, POSTR
CINGULATE CORTEX, TEMPORO-PARIETAL JUNCTION & CEREBELLUM WITH
IMPROVED HIGHER ORDER BRAIN FUNCTION LIKE – LEARNING, MEMORIZING &
BETTER EMOTIONAL REGULATION

39. MEDITATION AND WHITE MATTER
• D.LANERI ET AL. STUDY SHOWED INCREASED WHITE MATTER
DENSITY(THALAMUS&INSULA) & NO OR SLOWED DOWN DECLINE IN AGE
RELATED WHITE MATTER ATROPHY BY FOLLOWING MOA - INCREASED :-
MYELINATION, AXON DENSITY, AXON DIAMETER , AXON MEMB. INTEGRITY &
FIBRE GEOMETRY
• E.LUDERS STUDY. AI BASED BRAIN AGE INDEX IN MEDITATORS VS NON
MEDITATORS. AVG 7.5 YR YOUNGER THAN NORMAL CONTROL GROUP.
• HENCE, MEDITATION PROTECTS AGAINST AGE RELLATED WHITE MATTER
ATROPHY.

40. MEDITATION & CEREBRAL BLOOD FLOW
GLAUCOMA PT. WITH DEC. CBF&OBF AFFECTS
VISUAL
CORTEX
• 3T ARTERIAL SPIN LABELLING MRI STUDY BY QUIAN WANG ET AL. PROVES THAT
REDUCED BLD FLOW IN VISUAL CORTEX(V1,2 & VP) IS DIRECTLY PROPORTIONAL
TO THE CD RATIO & GCC THICKNESS
• SHORT TERM MEDITATION(30 MINS X 5 DAYS) INCREASES BLD FLOW IN ANTR
CINGULATE CORTEX & INSULA
• MEGHAL ET AL. AIIMS,DELHI,AN RCT ON 6 WEEKS MEDITAION SHOWED
INCREASED BRAIN OXYGENATION,UPREGULATION/BDNF, IMPROVED QOL/POAG
PT., SIGNIFICANT RISE IN OXYGENATED HB. IN PRE FRONTAL CORTEX

41. MEDITATION & GLUTAMATE EXCITOTOXICITY
• N.FAYED STUDY. LONG TERM ZEN MEDITATION SHOWED REDUCTION IN
CEREBRAL GLUTAMATE LEVEL (THALAMUS)
• NEGATIVE CO-RELATION BETWEEN GLU EXCITOTOXICITY & YEARS / ZEN
MEDITATION

42. MEDITATION & AUTONOMIC DYSFUNCTION &
NTG
• NTG PT. - SYMP. ACTIVITY & DEC. P.SYMP. ACTIVITY > CHANCES OF
ARTERIOSCLEROSIS, HYPO/HYPERTENSION, VASOSPASM, DM, POOR IMMUNE
STATUS, THYROID DS., NEURODEGEN. DS., SLEEP DISTURBANCES, POOR PSYCHO
SOCIAL ABILITIES
• H. Y L PARK ET AL. STUDY SHOWED THAT INC. STRESS LEVELS LEADS TO
AUTONOMIC DYSFUNCTION THAT IS IN PROPORTIONATE TO VISUAL FIELD
CHANGES IN VISUAL FIELD
• Y Y TANG ET AL STUDY PROVES THAT SHORT TERM MEDITATION(20MINS X 5 D)
INC. P.SYMP. ACTIVITY WITH DEC. IN SYMP. ACTIVITY THROUGH BETTER
REGULATION OF ANS BY FRONTAL CORTEX.

43. MEDITATION & CHRONIC SYSTEMIC DS.
• A DAVE ET AL. STUDY SHOWS THAT GLAUCOMA PT. HAD MORE CO-
MORBODITIES LIKE DM/HTN.
• G N LEVINE ET AL STUDY PROVED THAT MEDITATING POPULATION HAD DEC.
RISK OF CARDIOVAS. ATTACKS
• R H SCHNEIDER ET AL STUDY PROVES 48% REDUCTION IN MORTALITY IN
CARDIAC PT. & AVG FALLIN BP BY 5 MM/HG

44. MEDITATION – SLOW NASAL BREATHING ?
SLOW BREATHING HIGHLY SENSITIVE NASAL
RECEPTORS
MODULATION OF OLFACTORY BULB ACTI
MODULATION/CORTICAL&BRAINSTEM FSPIKE IN EEG ACTIVITY & IMPROVED AUTONOM P.SYMP. ACTIVITY

45. MINDFUL MEDITATION EFFECT ON GLAUCOMA
T.DADA ET AL.STUDY 21 D X 1HR
• DEC. CORTISOL LEVELS
• DEC. INFLAMMATORY MARKERS LIKE IL-6&TNF- ALPHA
• 54 GENES UPREGULATION & 56 GENES DOWNREGULATION
• LOWERS IOP BY P.SYMP ACTIVATION, INC.TM OUTFLOW, DEC. CORTISOL LEVELS,
CENTRAL REGULATION
• INC. NIGHT TIME PLASMA MELATONIN LEVEL

46. ORAL AGOMELATINE 25 MG/D – 30% DEC. /
IOP
• N. PESCOSOLIDO STUDY PROVES THIS BY MOA:- UPREGULATION OF ALPHA-2 R
– AGONIST , DOWNREGULATION OF BETA 2 R – ANTAGONIST ,
MODULATION/DOPAMINERGIC PATHWAYS, DOWNREGULATION OF CARBONIC
ANHYDRASE ACTIVITY & MODULATION/GAG BIOSYNTHESIS TO INC. TM
OUTFLOW
• JI JIN ET AL. STUDY SHOWS THAT OPIOD PEPTIDE DEC. IOP BY ACTIVATING
ARCUATE NUCLEUS/HYPOTHALAMUS MEDIATED BY BETA-ENDORPHINS

47. MEDITATION – BEST ADJUNCT COMBO-PILL
EFFECTS
• DEC. IOP - INC. OBF & CBF - BETTER AUTONOMIC
FUNCTION
• DEC. OXIDATIVE STRESS. - DEC. MITOCHOND. DYSFUNCTION
• DEC. IL-6 & TNF LEVELS. - DEC. GLU IN BRAIN.
• UPREGULATION OF NEUROTROPHIC GENE EXPRESSION LEADS TO
NEUROPROTECTION
• DEC. AGE RELATED CNS ATROPHY & BRAIN AGING
• REDUCED STRESS & HAPPY MOOD LEADS TO IMPROVED QOL
• DOWNREGULATION OF TGF-BETA IN TM & BLOOD
• DEC. RISKS DUE TO CHR. SYST. DS BY DEC. BP & PSYCHO SOCIAL STRESS
• USEFUL ADJUNCT “NO COST THERAPY “ IN PSYCHIATRIC CONDITIONS &

48. OUR STUDY – 107 REGULAR YOGA DOING
SUBJECTS(12 WEEKS)
• 10 COMMONLY PRACTISED ASANA’S WERE INCLUDED
• KAPALBHATI , ANULOMVILOM SIGNIFICANTLY DECREASES MEAN IOP
• SHIRSASANA , BHARSTIKA & PRANAYAMA INCREASES IOP

49. TAKE HOME MESSAGE
MANAGEMENT OF EYE ALONE IS SIMPLY NOT ENOUGH – MANAGE A PERSON
HIDING BEHIND
DISEASE OF GLAUCOMA
DECREASING STRESS AND QUALITY OF LIFE IMPROVEMENT MUST BE THE TARGET
THERAPY FOR GLAUCOMA PATIENTS

50. THANK YOU