However, this activation is unlikely to be the dominant mechanism of gabapentins therapeutic effects.Despite the fact that gabapentin is a structural GABA analogue, and in spite of its name, it does not bind to the GABA receptors, does not convert into GABA or another GABA receptor agonist in vivo, and does not modulate GABA transport or metabolism. Pharmacokinetics
Gabapentin is absorbed from the intestines by an active transport process mediated via an amino acid transporter, presumably, LAT2. As a result, the pharmacokinetics of gabapentin is dose-dependent, with diminished bioavailability and delayed peak levels at higher doses.The oral bioavailability of gabapentin is approximately 80% at 100 mg administered three times daily once every 8 hours, but decreases to 60% at 300 mg, 47% at 400 mg, 34% at 800 mg, 33% at 1,200 mg, and 27% at 1,600 mg, all with the same dosing schedule. Drugs that increase the transit time of gabapentin in the small intestine can increase its oral bioavailability; when gabapentin was co-administered with oral morphine, the oral bioavailability of a 600 mg dose of gabapentin increased by 50%.Gabapentin at a low dose of 100 mg has a Tmax (time to peak levels) of approximately 1.7 hours, while the Tmax increases to 3 to 4 hours at higher doses. Food does not significantly affect the Tmax of gabapentin and increases the Cmax and area-under-curve levels of gabapentin by approximately 10%.Gabapentin can cross the blood–brain barrier and enter the central nervous system. Gabapentin concentration in cerebrospinal fluid is approximately 9–14% of its blood plasma concentration.
As a rough guide, a non-infected ulcer can be expected to heal at approximately 0.6mm/day. Complications
In cases where the ulcer is not healing:

Is there a persistent source of irritation? Foreign body
Self traumatisation
Iatrogenic. Is it infected? Review antibiotic therapy
C+S if not already performed. Immunosuppression? Cushings
Steroid therapy. Compliance? Is what youve prescribed getting onto the eye? None of the above? Abnormal epithelium may have formed, keratectomy may be appropriate.Melting ulcers reflect inappropriate collagenolysis of the corneal stroma, by matrix-metalloproteinases (MMPs). Bacterial pathogens (especially Pseudomonas and β-haemolytic Streptococcus) induce the corneal epithelial cells and resident leucocytes to upregulate pro-inflammatory, and MMP-activating cytokines (IL-1,-6 and -8). These bacteria can also produce their own proteinases. The combination of exogenous, and upregulated endogenous, proteinases leads to a rapid breakdown of collagen, with the characteristic melting appearance. Untreated this can lead to perforation within 12 hours (so act hard and fast!). There are several therapeutic options for inhibiting MMPs:

Autogenous serum – administer topically as often as possible. Keep refrigerated and change every 8 days. EDTA  - 0.05% q1h
Acetylcysteine – 5-10% q1h
Tetracyclines – Doxycycline especially has been shown to have anti-MMP effects
Tetanus antitoxin – can be delivered sub-conjunctivally. Contains macroglobulins with anti-collagenase effects.A combination of the above may be necessary early in the disease course. Effective antibiosis is also paramount, and gentamicin is a good empirical choice (although there are some reports of gentamicin-resistant Pseudomonas species). Obviously, treating an eye this frequently in practice will be difficult, so referral is probably the best option. See also
Corneal abrasion
Keratitis


== References ==