What Causes Chronic Glaucoma

Glaucoma is a group of eye diseases often associated with elevated intraocular pressure and the loss of retinal nerve cells and nerve fibers. Resulting in a defective visual field and ultimately, loss of all vision in those with severe conditions.

The process of seeing transpires in several steps:
  1. When light enters the eye, it is absorbed by the retinal photoreceptors (rods and cones) 
  2. The photoreceptors transform this light into nerve impulses before transmitting to retinal ganglion cells and its axons for processing in the brain
  3. All retinal ganglion cell axons converge at the optic disc (sometimes called optic nerve head, papilla) and emerge as optic nerve
  4. The brain receives visual information from nerve impulses through the optic nerve
The axons or the optic nerve fibers in Glaucoma patients, particularly at the optic disc, progressively die. The morphological aspect appears as "Cupping or excavation."  Consequently, the connection between the eye and brain is gradually severed, interrupting the visual information transmitted to the brain - this is called, "Glaucomatous damage."

In the early stage of glaucoma, the visual function may seem to remain intact. This phenomenon is due to the ability of the brain to compensate for some visual field defects. When the patient begins to notice visual field loss, the condition is already in an advanced stage. When sufficient amount of ganglion cells die, the affected region appears as "cupping", seen in the Fundus exam.

There are three types of glaucoma:

1. Primary Open-Angle Glaucoma (POAG or Chronic Glaucoma)
2. Closed-Angle Glaucoma (Acute Angle-Closure Glaucoma)
3. Congenital Glaucoma

Further discussion about treatment on this page focuses on POAG or Chronic Glaucoma - the most common form of Glaucoma. 

While some experts regard POAG as solely a problem of increased intraocular pressure and focus their treatment modalities on lowering the intraocular pressure. This treatment may temporarily stabilize the condition, but rarely improve patient's vision, said Dr. Athikhomkulchai. 

Dr. Somkiat Athikhomkulchai, M.D. was trained to treat chronic glaucoma with the same theory of lowering the intraocular pressure. But he became dissatisfied with the result.

In an attempt to find a better way of treating POAG, through observations of his patients, he found three contradictions to the standard treatments in which he was trained.  For instance:

1. Many POAG patients he treated have normal or even low intraocular pressure (IOP).

2. POAG patient's condition failed to improve clinically after lowering the IOP with either pill, eye drop or laser surgery.

3. In some POAG patients, no cupping of the optic nerve occurs even in high IOP patient.

Risk factors for POAG
Through Dr. Athikhomkulchai's observations, he found the following two factors to be significant risk factors leading retinal ganglion cells to die. In each patient,  either factor may be dominant:

1. Inadequate intraocular blood flow to retinal ganglion cells caused them to die. 

If inadequate blood flow is a dominant factor; the optic disc will appear pale and less change in the cupping.
2. Interruption of the flow of proteins, enzymes, hormones, and neurotransmitters along the nerve fibers (axoplasmic flow), results in degeneration of axons and programmed cell death (apoptosis). If this is a dominant factor, the optic disc will have a distinct and deep "cupping" appearance.

From these two major risk factors, POAG can be further classified as:
  1. High-tension POAG
    Cause: the stiffness and dysfunction of Lamina Cribrosa and Trabecular Meshwork cause higher intraocular pressure and impede intraocular perfusion (passage of fluid through the lymphatic system or blood vessels), results in ganglion cell death.

    Treatment: Practice "Palm Pressure Therapy (PPT) " to stretch the Lamina Cribrosa and Trabecular Meshwork, allowing more ocular vessels passage. Lower the intraocular pressure to enhance intraocular perfusion

  2. The normal-tension or low-tension POAG
    Cause: the degenerative change or stiffness of Lamina Cribrosa
    Treatment: Practice "Palm Pressure Therapy (PPT) "

  3. The ocular hypertension
    Cause: the degenerative change of Trabecular Meshwork leads to increasing intraocular pressure.  The Lamina Cribrosa still allows adequate blood supply to Ganglion cells; therefore, no Glaucomatous damage occur.
    : no treatment is necessary, but Dr. Athikhomkulchaithe recommends a periodic assessment.
Aggravating factors for POAG 

In addition to inadequate blood flow and impeding axoplasmic flow, there are four aggravating factors in Glaucoma patients:
  1. High Intraocular pressure creates a wedge-like force between the Lamina cribrosa, the blood vessels, and the optic nerve fibers, resulting in restriction of blood flow and axoplasmic flow. The fluctuation of intraocular pressure (IOP) causes more damage than the stable IOP.  Sharp increases in IOP creates an even greater effect.

  2. Diabetes Mellitus and anemia. The high glucose level in diabetic patients produces "sticky blood" that is too difficult to transport, resulting in inadequate intraocular blood flow. Patients with severe anemia have the same ischemic outcome.

  3. High myopia
    In high myopia (a severe form of nearsightedness), the eyeball stretches too long in the anteroposterior direction, causing more prominent of S-shape in the optic nerve.  These changes decrease the temporal angle between the optic nerve and the eyeball, results in narrowing or contraction of the optic nerve fiber and blood vessels, causing the restriction of blood flow and axoplasmic flow.
  4. Heat collection on the retina found in computer users especially in far-east and Southeast Asian people may result in retinal cell damage.
Dr. Athikhomkulchai discovered that a morphological change in the Lamina Cribrosa can increase its strength, causing a restriction of the intraocular blood circulation and interferes with the axoplasmic flow. With the loss of blood supply and nourishment, the axons gradually die.  To resolve this morphological change of Lamina Cribrosa, Dr. Athikhomkulchai developed "Palm Pressure Therapy" in 2004.

Functions of the Lamina Cribrosa that may have an effect in Glaucoma include:
  1. Regulates the passage of the central retinal vessels (arteries and veins) and axoplasmic flow

  2. Preserves a pressure gradient between the retrobulbar (behind the eyeball) space, which has lower pressure and intraocular space, which has higher pressure. This function as a pressure barrier may have a significant role in ocular diseases in which the pressure on either side becomes abnormally high and low

  3. Prevents a significant leakage of aqueous humor from the intravitreal space into the retrobulbar cerebrospinal fluid space surrounding the retrobulbar part of the optic nerve

Some other eye conditions that Dr. Athikhomkulchai treated using a combination of prescription drugs, laser and "Palm Pressure Therapy" are:

  • Dry Age-related Macular Degeneration (AMD)
  • Optic atrophy
  • Central Retinal Vein Occlusion (CRVO)
  • Retinitis Pigmentosa
  • Epiretinal membrane
  • Central Serous Retinopathy (CSR)
Dr. Athikhomkulchai believes further research will help improve the treatment to end blindness from retinal diseases.  Lack of funds is a major drawback in performing scientific research to collect further evidence relating to "Palm Pressure Therapy or PPT."  In any case,  we should not ignore the 90% success rate with POAG in Dr. Athikhomkulchai's practice.