Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Light application
Reexamination Certificate
1998-06-22
2001-11-20
Shay, David M. (Department: 3739)
Surgery: light, thermal, and electrical application
Light, thermal, and electrical application
Light application
C607S088000, C607S090000, C606S003000, C606S013000
Reexamination Certificate
active
06319274
ABSTRACT:
BACKGROUND OF THE INVENTION
1. Field of the Invention
The present invention relates to the field of medical therapeutics and more specifically relates to the field of glaucoma and ocular hypertension therapy utilizing novel instruments and techniques for opto-thermal mediation of a patient's trabecular meshwork for enhancing the mitotic rate of endothelial meshwork cells and for reduction of biostructural laxity within the meshwork, which meshwork biocharacteristics may be subject to cell-division inhibitions and/or other degradations.
2. Description of the Related Art
Glaucomas comprise a group of debilitating eye diseases that are the leading cause of blindness in the United States and around the world. The pathophysiological mechanisms of glaucomas are not fully understood. The principal sign of the disease is elevated intraocular pressure (IOP). Such elevations of IOP ultimately can cause damage to the optic nerve head and result in impairment to, or loss of, normal visual function. It is known that elevated IOP is caused by an excess of fluid or aqueous AQ within the eye, which is continually produced by the ciliary body CB and drained through the trabecular meshwork M to leave the eye or globe
5
(see FIGS.
1
A-
1
D). The excess intraocular fluid generally results from blockage or impairment of the normal drainage from the anterior chamber AC via the trabecular meshwork M. The meshwork consists of about 10 to 25 layers of perforated trabecular plates (TP
1
. . . TP
r
) or sheets around the filtration angle FA of the anterior chamber AC, having a width of about 1,000 &mgr;m to 1,500 &mgr;m (1.0 mm. to 1.5 mm.) in a circumference ranging from 35,000 to 40,000 &mgr;m.
FIGS. 1A-1B
show electron micrographs of trabecular plates TP with
FIG. 1B
including a representation of an endothelial cell layer EC of trabecular beam B with the beam core BC believed to be predominantly collagen and GAGs (glucosaminoglycans) or ground substance.
FIG. 1C
illustrates that each successively deeper plate (more anterior plate) of the meshwork M has smaller perforations PF or openings between the beams B than more exposed (posterior) trabecular plates. Further, the intraplate spacing IPS diminishes with the successively deeper plates (FIG.
1
C). The meshwork M thus serves as a filtration mechanism wherein cellular detritus, etc. in the aqueous outflow is captured before it passes into Schlemm's canal SCH where the aqueous is transported away form the eye (FIG.
1
D). The meshwork M lies about 750 &mgr;m to 950 &mgr;m beneath the anterior surface of the sclera SC.
A number of ophthalmic disease conditions are related to the trabecular meshwork and can be linked to distinct processes or pathological conditions within a patient's eye. Any disease of the trabecular meshwork shares the characteristic of elevating IOP. Chandler et al. described many forms of glaucoma, the principal ones being: primary open-angle glaucoma (POAG); progressive low-tension glaucoma; pigment dispersion and pigmentary glaucoma; angle-closure glaucoma; combined open-angle and angle-closure glaucoma, exfoliation and open-angle glaucoma; angle-closure glaucoma due to multiple system cysts of iris and ciliary body; angle-closure glaucoma secondary to occlusion of the central retina vein; angle-closure glaucoma secondary to bilateral transitory myopia; ghost-cell glaucoma; lens-induced glaucoma; glaucoma due to intraocular inflammation; neovascular glaucoma; glaucoma associated with extraocular venous congestion; essential atrophy of the iris with glaucoma. among others. (Chandler, et. al.,
Glaucoma,
3rd Ed., Lea & Febliger; Phila. (1986)) In all of the above-listed glaucoma syndromes, elevated IOP results from an increase in resistance to aqueous humor outflows through the trabecular meshwork.
In terms of incidence, primary open-angle glaucoma (POAG) is the most prevalent form of the disease affecting up to 0.5% of the population between ages of 35 to 75. The incidence of glaucoma rises with age to over 6% of the population 75 years are older. One identifiable component of the POAG syndrome is the loss of endothelial cells within the meshwork which is associated with a degeneration of the normal trabecular biostructure. It is known that the human aging process itself leads to a progressive loss of trabecular endothelial cells EC which compromises normal aqueous outflows therethrough. When examined in tissue cultures, degraded endothelial tissue from POAG patients appears similar to that of “aging” individuals.
Other characteristics believed common to POAG (as well as many other glaucomas listed above) relate to a biostructural obstructive syndrome of the trabecular plates TP, for example, resulting from compression of the plates into a matt-like form that reduces intraplate spacing IPS (FIG.
1
C). This factor reduces the capacity of the meshwork to act as a filtering mechanism and may develop after the meshwork is clogged with cellular detritus, pigments, etc. Such an obstructive syndrome, it is believed, also is characterized by increased laxity of the trabecular beams B allowing their collapse which thus reduces intraplate spacing. The most likely causes of the meshwork degradations described above may be cumulative stresses from various factors (e.g., oxidative, phagocytic, glucocorticoidal stresses). The fact that increased outflow resistance appears in the non-glaucoma “aging” population further suggests that both trabecular endothelial cellular processes and an obstructive meshwork syndrome play significant roles in decreasing aqueous outflows.
The normal IOP for humans usually ranges from about 10 to 22 mm. Hg. (1.3-2.7 kilopascals) and is maintained by a balance in the aqueous production by the ciliary body CB, inflows to the anterior chamber AC and outflows therefrom. As described above, in a normal eye, the aqueous drains from the anterior chamber through the meshwork into Schlemm's canal SCH, through which it leaves the eye. In patients in a glaucomous state, besides passing through Schlemm's canal, the aqueous may also pass through the ciliary muscle CM into the suprachoroidal space and finally leave the eye through the sclera SC (FIG.
1
D).
For purposes of description, the intraocular pressure (IOP) in a human can be defined by a formula of the following type:
IOP=P
e
+(
F
t
−F
uv
)×
R
:(
TM
cep
, TM
sp
, TM
br
)
where P
e
is the episcleral venous pressure (generally regarded as being around 9 mm. Hg.); F
t
is the total outflow of the aqueous humor from the anterior chamber, F
uv
is the fraction of aqueous passing by the uveoscleral route; R is the resistance to outflow of aqueous through the trabecular meshwork into Schlemm's canal, which can be considered to be functionally related to (i) the vitality of trabecular endothelial cellular cellular and enzymatic processes (TM
cep
), (ii) the dimensions of intraplate spacing between (TM
ips
) relative to a norm, and (iii) the trabecular beam resiliency (T
br
) or biostructural tension within the meshwork under the pressure of aqueous outflow therethrough. Such a formula is useful for understanding the targets of various prior art therapies, if not for use as an actual mathematical model.
Among several therapies targeted at various elements of the above equation, two forms of treatment are common: (i) medical or drug therapies, and (ii) trans-corneal laser irradiation of the trabecular meshwork via a goniolens (see FIG.
2
A). In medication therapies, the objective may be to lower IOP by either of several routes: reducing the aqueous flow total (F
t
in the above equation); increasing uveoscieral flow (F
uv
in above equation); or altering resistance to outflow (R), by stimulating endothelial cellular processes (TM
cep
) which is believed to act on outflow resistance. Drug therapies have the disadvantages of requiring a lifelong treatment; causing significant side effects; being very costly (between $1,000-$2,000/yr.); and being unavailable or unaffordable in lesser developed countries of the world w
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