Homoeopathy and glaucoma

Dr Amrutha Manoharan  

ABSTRACT
Glaucoma is one of the chronic progressive disorder of eye characterized  by visual loss, mainly occurring due to rise in intraocular pressure. One of the major cause of blindness, homoeopathy have a good role in  managing this disease.

INTRODUCTION
Glaucoma is a chronic, progressive optic neuropathy caused by a group of ocular conditions which lead to damage of optic nerve with loss of function. Glaucoma is not a single disease process but a group of disorders characterized by a progressive optic neuropathy resulting in a characteristic appearance of the optic disc and a specific pattern of irreversible visual field defects that are associated frequently but not invariably with raised intraocular pressure (IOP).^[3]

ETIOLOGY
The most important factor which causes rise in intraocular pressure is obstruction of the drainage of the aqueous humor through the angle of anterior chamber and at the pupil.

PATHOGENESIS

There are a combination of factors affecting the axon the main influence are 

1. Mechanical changes  –  a raised in the intraocular pressure  caused mechanical pressure on lamina cribrosa altering capillary blood flow and decreasing axoplasamic  flow in the initial stages, later significant backward displacement and compaction of the lamina plates narrows the opening through which the axon passes and directly damage the nerve bundles.
2. Vascular perfusion  – the perfusion of optic nerve head is affected  due to lack of an adequate auto regulatory  mechanism. A substantial rise in the intraocular pressure can also decrease the capillary blood flow. ^[1] 

INTRAOCULAR PREASSURE
The intraocular pressure (IOP) refers to the pressure exerted by intraocular fluids on the coats of the eyeball. The normal IOP varies between 10 and 21 mm of Hg (mean 16 ± 2.5 mm of Hg).

Rate of aqueous formation influences IOP levels. The aqueous formation in turn depends upon many factors such as

1. Ppermeability of ciliary capillaries and osmotic pressure of the blood.
2. Resistance to aqueous outflow (drainage). 
3. Increased episcleral venous pressure may result in rise of IOP. 
4. General factors  Heredity and age. The mean IOP increases after the age of 40 years, possibly due to reduced facility of aqueous outflow.
5.  Sex. IOP is equal between the sexes in ages 20 – 40 years. In older age groups increase in mean IOP with age is greater in females.
6.  Diurnal variation of IOP. Usually, there is a tendency of higher IOP in the morning and lower in the evening.
7.  Postural variations. IOP increases when changing from the sitting to the supine position.

PRIMARY DEVELOPMENTAL/CONGENITAL GLAUCOMA 

It refers to abnormally high IOP which results due to developmental anomaly of the angle of the anterior chamber, not associated with any other ocular or systemic anomaly. Depending upon the age of onset the developmental glaucomas are termed as follows: 

1. True congenital glaucoma is labelled when IOP is raised during intrauterine life and child is born with ocular enlargement. 

2. Infantile glaucoma is labelled when the disease manifests prior to the child’s third birthday. 3. Juvenile glaucoma is labelled in the rest 10 percent of cases who develop pressure rise between 3-16 years of life.

Clinical features  –  Photophobia, blepharospasm, lacrimation and eye rubbing often occur together. These are thought to be caused by irritation of corneal nerves, which occurs as a result of the elevated IOP. Photophobia is usually the initial sign, but is not enough by itself to arouse suspicion in most cases. Corneal signs include its oedema, enlargement and Descemet’s breaks and Corneal oedema. 

PRIMARY OPEN ANGLE GLAUCOMA
As the name implies, it is a type of primary glaucoma, where there is no obvious systemic or ocular cause of rise in the intraocular pressure. It occurs in eyes with open angle of the anterior chamber. Primary open angle glaucoma (POAG) also known as chronic simple glaucoma of adult onset and  is typically characterised by slowly progressive raised intraocular pressure (>21 mmHg recorded on at least a few occasions) associated with characteristic optic disc cupping and specific visual field defects.

CLINICAL FEATURES

Symptoms

1. The disease is insidious and usually asymptomatic, until it has caused a significant loss of visual field. Therefore, periodic eye examination is required after middle age.
2.  Patients may experience mild headache and eyeache.
3.  Occasionally, an observant patient may notice a defect in the visual field. 
4. Reading and close work often present increasing difficulties owing to accommodative failure due to constant pressure on the ciliary muscle and its nerve supply. 
5. Patients develop delayed dark adaptation, a disability which becomes increasingly disturbing in the later stages.

INVESTIGATIONS

1. Tonometry. 
2. Diurnal variation test is especially useful in detection of early cases 
3. Gonioscopy. It reveals a wide open angle of anterior chamber. Its primary importance in POAG is to rule out other forms of glaucoma. 

PRIMARY ANGLE-CLOSURE GLAUCOMA
It is a type of primary glaucoma (wherein there is no obvious systemic or ocular cause) in which rise in intraocular pressure occurs due to blockage of the aqueous humour outflow by closure of a narrower angle of  the anterior chamber.

ETIOLOGY
Predisposing risk factors. These can be divided into anatomical and general factors: Anatomical factors and General factors.

CLINICAL FEATURES
Symptoms are absent in this stage. In suspected eyes following signs may be elicited: 

Eclipse sign – which indicates decreased axial anterior chamber depth, can be elicited by shining a penlight across the anterior chamber from the temporal side and noting a shadow on the nasal side.

DIAGNOSIS
Diagnosis is made by: Clinical signs described above, and positive provocative tests Provocative tests. 

SECONDARY GLAUCOMAS
Secondary glaucoma per se is not a disease entity, but a group of disorders in which rise of intraocular pressure is associated with some primary ocular or systemic disease. Therefore, clinical features comprise that of primary disease and that due to effects of raised intraocular pressure.

PIGMENTARY GLAUCOMA
It is a type of secondary open-angle glaucoma wherein clogging up of the trabecular meshwork occurs by the pigment particles. Exact mechanism of pigment shedding is not known. It is believed that, perhaps, pigment release is caused by mechanical rubbing of the posterior pigment layer of iris with the zonular fibrils.

NEOVASCULAR GLAUCOMA (NVG)
It is an intractable glaucoma which results due to formation of neovascular membrane involving the angle of anterior chamber. It is usually associated with neovascularization of iris (rubeosis iridis). Neovascularization develops following retinal ischaemia, which is a common feature of Diabetic retinopathy,  Central retinal vein occlusion,  Sickle-cell retinopathy and Eales’ disease. 

HOMOEOPATHY AND GLAUCOMA

GLAUCOMA eyes
com, phos, ceder, cocc, coloch, kali.i, lac-c, osm, phys, spigelia.

Caust, euphr, nitric ac, sil, sulph.

afternoon and evening – belladonna

injury after – physostigma

pain with –  acon, phos, mez, 

preassure amel – coloch

vision iridescent  – osmium^[4]

MEDICINES FOR GLAUCOMA

1. COMOCLADIA DENTATA – Glaucoma, sense of fullness; eyeball feels too large. Motion of eyes aggravates. Ciliary neuralgia with eyes feeling large and protruded, especially right. Worse, near warm stove; feels as if pressed outward. Sees only glimmer of light with left eye.^[5]
2. PHOSPHROUS –  Glaucoma. Thrombosis of retinal vessels and degenerative changes in retinal cells. Degenerative changes where soreness and curved lines are seen in old people. Retinal trouble with lights and hallucination of vision. Black points seem to float before the eyes. Patient sees better by shading eyes with hand. Fatigue of eyes and head even without much use of eyes.
3. CEDRON – Shooting over left eye. Severe pain in eyeball, with radiating pains around eye, shooting into nose. Scalding lachrymation. Supra-orbital neuralgia periodic. Iritis, choroiditis.
4. PHYSOSTIGMA  – Vision dim; from blur or film; objects mixed. Pain after using eyes; floating black spots, flashes of light, twitching of lids and muscles of eyes Nystagmus. ^[6]
5. OSMIUM  – Glaucoma; with iridescent vision. Violent supra and infra-orbital neuralgia; violent pains and lachrymation. Green colors surround candle-light. Conjunctivitis. Increase in intra-ocular tension, dim sight, photophobia.
6. BELLADONNA  – Throbbing deep in eyes on lying down. Pupils dilated . Eyes feel swollen and protruding, staring, brilliant; conjunctiva red; dry, burn; photophobia; shooting in eyes. Exophthalmus. Ocular illusions; fiery appearance. Diplopia, squinting, spasms of lids. Sensation as if eyes were half closed. Eyelids swollen. Fundus congested.
7. SPIGELIA ANTHELMIA  – Feel too large; pressive pain on turning them. Pupils dilated; photophobia; rheumatic ophthalmia. Severe pain in and around eyes, extending deep into socket. Ciliary neuralgia, a true neuritis.

BIBILIOGRAPHY

1. Parson’s diseases of eye .Ramanit Sihota. Radhika Tandon.21^st edition.Elsevierpublication. Page 280.
2. Basic ophthalmology. Dr.Renu Jogi. The health sciences publisher. Page 2587.
3. Comprehensive ophthalmology 4^th edition.A.K.Khurana.
4. Homoeopathic medical repertory .Robin murphy.B.Jain publishers(P) Ltd. Page 426.
5. Boerick  William.Boerick’s new  manual of homoeopathic materia medica and repertory.
6. Allen.H.C.keynotes rearranged and classified with leading remedies of materia medica and bowel nososdes.

Dr. Amrutha Manoharan B.H.M.S, Dip.Yoga . M.D(Hom.)                                                                                  
PG SCHOLAR DEPARTMENT OF ORGANON OF MEDICINE
SARADA KRISHNA HOMOEOPATHIC MEDICAL COLLEGE,
KULASEKARAM , TAMIL NADU.