TREATMENT OF GLAUCOMA USING LAQUINIMOD This application claims priority of U.S. Provisional Application No. 61/904,962, filed November 15, 2013, the entire content of which is hereby incorporated by reference herein. Throughout this application, various publications are referred to by first author and year of publication. Full citations for these publications are presented in a References section immediately before the claims. Disclosures of the documents and publications referred to herein are hereby incorporated in their entireties by reference into this application. Background Glaucoma is a group of ocular diseases characterized by progressive damage to the eye at least partly due to elevated intraocular pressure (IOP) (Merck Manual of Diagnosis and Therapy (1999)) . Additionally, glaucoma is characterized by retinal ganglion cell (RGC) death, axon loss and an excavated appearance of the optic nerve head (Alward 1998) . Glaucoma can be diagnosed before vision loss occurs by visual field testing and by ophthalmoscopic examination of the optic nerve to detect "cupping." The mean IOP in normal adults is 15 to 16 mm Hg; the normal range is 10 to 2 1 mm Hg . One form of management of glaucoma is based on lowering the IOP using topically applied medications (Coleman 1999) . Currently there are five major classes of medications that are used to lower the IOP: b-adrenergic antagonists, adrenergic agonists, parasympathomimetics, prostaglandin-like analogues and carbonic anhydrase inhibitors (Medeiros et al . 2002) . Although most medications are applied topically to the eye, they can cause severe systemic side effects and adversely affect the quality of the patient's life. If additional lowering of IOP is indicated or if medication fails to sufficiently lower the IOP, laser trabeculoplasty is usually the next step. If IOP is still not adequately controlled, incisional glaucoma surgery is indicated (Id) . The lowering of IOP, despite significantly reducing the extent of neuronal loss, does not ensure cessation of the disease process, because the loss of RGCs may continue. Recent studies of the association between IOP regulation and visual field loss after medical or surgical intervention showed that ongoing neuronal loss reflected in visual field tests can be diminished if the IOP is low. However, neuronal loss may continue to occur after reduction of IOP (Bakalash et al . 2002) . Glaucomatous optic neuropathy appears to result from specific pathophysiological changes and subsequent death of RGCs and their axons. The process of RGC death is thought to be biphasic: a primary injury responsible for initiation of damage followed by a slower, secondary degeneration attributable to the hostile environment surrounding the degenerating cells (Kipnis et al . 2000) . The molecular mechanism triggering RGC death has not been identified. Deprivation of neurotrophic factors, ischemia, chronic elevation of glutamate and disorganized nitric oxide metabolism are suspected to be possible mechanisms (Farkas et al . 2001) . In addition, it is possible that the mechanisms leading to RGC death share common features with other types of neuronal injury, such as signaling by reactive oxygen species, depolarization of mitochondria, or induction of transcriptionally regulated cell death (Weinreb et al . 1999) . Laquinimod Laquinimod (LAQ) is a novel synthetic compound with high oral bioavailability which has been suggested as an oral formulation for the treatment of Multiple Sclerosis (MS) (Polman, 2005; Sandberg-Wollheim, 2005) . Laquinimod and its sodium salt form are described, for example, in U.S. Patent No. 6,077,851. The mechanism of action of laquinimod is not fully understood. Animal studies show it causes a Thl (T helper 1 cell, which produces pro-inflammatory cytokines) to Th2 (T helper 2 cell, which produces anti-inflammatory cytokines) shift with an anti inflammatory profile (Yang, 2004; Bruck, 2011) . Another study demonstrated (mainly via the NFkB pathway) that laquinimod induced suppression of genes related to antigen presentation and corresponding inflammatory pathways (Gurevich, 2010) . Other suggested potential mechanisms of action include inhibition of leukocyte migration into the CNS, increase of axonal integrity, modulation of cytokine production, and increase in levels of brain-derived neurotrophic factor (BDNF) (Runstrom, 2006; Bruck, 2011) . The effects of laquinimod on glaucoma have not previously been studied . Summary of the Invention The subject invention provides a method of treating a subject afflicted with glaucoma comprising administering to the subject an amount of laquinimod effective to treat the subject. The subject invention also provides a method of treating a subject suffering from retinal ganglion cell loss or retinal ganglion cell damage, or of reducing retinal ganglion cell loss or damage in a subject, comprising administering to the subject an amount of laquinimod effective to reduce retinal ganglion cell loss or retinal ganglion cell damage in the subject. The subject invention also provides a method of treating a subject suffering from elevated intraocular pressure, or of reducing intraocular pressure in a subject, comprising administering to the subject an amount of laquinimod effective to reduce intraocular pressure in the subject. The subject invention also provides a package comprising a ) a pharmaceutical composition comprising an amount of laquinimod; and b ) instruction for use of the pharmaceutical composition to treat a subject afflicted with glaucoma. The subject invention also provides a therapeutic package for dispensing to, or for use in dispensing to, a subject afflicted with glaucoma, which comprises a ) one or more unit doses, each such unit dose comprising an amount of laquinimod thereof, wherein the amount of said laquinimod in said unit dose is effective, upon administration to said subject, to treat the subject, and b ) a finished pharmaceutical container therefor, said container containing said unit dose or unit doses, said container further containing or comprising labeling directing the use of said package in the treatment of said subject. The subject invention also provides a pharmaceutical composition and a package as described herein for use in treating a subject afflicted with glaucoma. The subject invention also provides a pharmaceutical composition in unit dosage form, useful in treating a subject afflicted with glaucoma, which comprises an amount of laquinimod; which amount of said laquinimod in said composition is effective, upon administration to said subject of one or more of said unit dosage forms of said composition, to treat the subject. The subject invention also provides a package comprising a ) a pharmaceutical composition as described herein; and b ) instruction for use of the pharmaceutical composition to treat a subject afflicted with glaucoma. The subject invention also provides laquinimod for the manufacture of a medicament for use in treating a subject afflicted glaucoma. Brief Description of the Figures Figure 1 : Example 1 : Mean DIOR (OHT minus Non-OHT) (mmHg) . Figure 2 : Example 1 : % Fluoro-gold Labeled RGC Loss. Figure 3 : Example 1 : Mean Fluoro-gold Labeled RGC count per mm2 . Figure : Optic Nerve Injury Grade (1-5) . Figure 5A : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 48, Group 1 , Left Eye. Figure 5B : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 48, Group 1 , Right Eye. Figure 5C : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 59, Group 2 , Left Eye. Figure 5D : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 59, Group 2 , Right Eye. Figure 5E : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 22, Group 3 , Left Eye. Figure 5F : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 22, Group 3 , Right Eye. Figure 5G : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 31, Group 4 , Left Eye. Figure 5H : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 31, Group 4 , Right Eye. Figure 5 : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 35, Group 5 , Left Eye. Figure 5 : Example 1 : Representative images of the retinas with FG-labeled RGC - Animal Number 35, Group 5 , Right Eye. Detailed Description of the Invention The subject invention provides a method of treating a subject afflicted with glaucoma comprising administering to the subject an amount of laquinimod effective to treat the subject. In one embodiment, the administration of laquinimod is effective to reduce or inhibit a symptom of the glaucoma in the subject. In another embodiment, the symptom is retinal ganglion cell damage, retinal ganglion cell loss, or elevated intraocular pressure. In another embodiment, laquinimod is laquinimod sodium. In one embodiment, the route of administration of laquinimod is intraocular, periocular, systemic or topical. In another embodiment, laquinimod is administered via oral administration. In another embodiment, laquinimod is administered via ocular administration. In another embodiment, laquinimod is administered in the form of an aerosol, an inhalable powder, an injectable, a liquid, a gel, a solid, a capsule or a tablet. In an embodiment, the concentration of laquinimod in the liquid or gel is 5-100 mg/ml solution, 20-100 mg/ml solution, 10-15 mg/ml solution, or 20-50 mg/ml solution. In another embodiment, laquinimod is administered periodically. In another embodiment, laquinimod is administered daily. In another embodiment, laquinimod is administered more often than once daily. In yet another embodiment, laquinimod is administered less often than once daily. In one embodiment, the amount laquinimod administered is at least 0.2 mg/day and/or less than 0.6 mg/day. In another embodiment, the amount laquinimod administered is 0.03-600 mg/day, 0.1-40.0 mg/day, 0.1-2.5 mg/day, 0.25-2.0 mg/day or 0.5-1.2 mg/day. In another embodiment, the amount laquinimod administered is 0.25 mg/day, 0.3 mg/day, 0.5 mg/day, 0.6 mg/day, 1.0 mg/day, 1.2 mg/day, 1.5 mg/day or 2.0 mg/day. In yet another embodiment, the amount of laquinimod administered is 0.05-4.0 mg per administration, 0.05-2.0 mg per administration, 0.2-4.0 mg per administration, 0.2-2.0 g per administration, about 0.1 mg per administration, or about 0.5 mg per administration. In one embodiment of the present invention, the method further comprises administration of a second agent for the treatment of glaucoma. In another embodiment, the second agent is a b- adrenergic antagonist, adrenergic agonist, parasympathomimetic, prostaglandin-like analog, or carbonic anhydrase inhibitor. In one embodiment, the periodic administration of laquinimod continues for at least 3 days, more than 30 days, more than 42 days, 8 weeks or more, at least 12 weeks, at least 24 weeks, more than 24 weeks, or 6 months or more. In another embodiment, the subject is a human patient. The subject invention also provides a method of treating a subject suffering from retinal ganglion cell loss or retinal ganglion cell damage, or of reducing retinal ganglion cell loss or damage in a subject, comprising administering to the subject an amount of laquinimod effective to reduce retinal ganglion cell loss or retinal ganglion cell damage in the subject. The subject invention also provides a method of treating a subject suffering from elevated intraocular pressure, or of reducing intraocular pressure in a subject, comprising administering to the subject an amount of laquinimod effective to reduce intraocular pressure in the subject. The subject invention also provides a package comprising a ) a pharmaceutical composition comprising an amount of laquinimod; and b ) instruction for use of the pharmaceutical composition to treat a subject afflicted with glaucoma. In one embodiment of the present invention, the package comprises a second pharmaceutical composition comprising an amount of a second agent for the treatment of glaucoma. In another embodiment, the second agent is a b-adrenergic antagonist, adrenergic agonist, parasympathomimetic, prostaglandin-like analog, or carbonic anhydrase inhibitor. n one embodiment, the pharmaceutical composition is the form of an aerosol, an inhalable powder, an injectable, a liquid, a gel, a solid, a capsule or a tablet. In another embodiment, the pharmaceutical composition is in a liquid or a gel form. In one embodiment, the concentration of laquinimod in the liquid or gel is 5-100 mg/ml solution, 20-100 mg/ml solution, 10-15 mg/ml solution or 20-50 mg/ml solution. In another embodiment, the pharmaceutical composition is in capsule form or in tablet form. In another embodiment, the tablets are coated with a coating which inhibits oxygen from contacting the core. In another embodiment, the coating comprises a cellulosic polymer, a detackif ier, a gloss enhancer, or pigment . In one embodiment, the pharmaceutical composition further comprises mannitol . In another embodiment, the pharmaceutical composition further comprises an alkalinizing agent. In another embodiment, the alkalinizing agent is meglumine. In another embodiment, the pharmaceutical composition further comprises an oxidation reducing agent. In one embodiment, the pharmaceutical composition is stable and free of an alkalinizing agent or an oxidation reducing agent. In another embodiment, the pharmaceutical composition is free of an alkalinizing agent and free of an oxidation reducing agent. In one embodiment, the pharmaceutical composition is stable and free of disintegrant . In another embodiment, the pharmaceutical composition further comprises a lubricant. In another embodiment, the lubricant is present in the pharmaceutical composition as solid particles. In another embodiment, the lubricant is sodium stearyl fumarate or magnesium stearate. In one embodiment, the pharmaceutical composition further comprises a filler. In another embodiment, the filler is present in the pharmaceutical composition as solid particles. In another embodiment, the filler is lactose, lactose monohydrate, starch, isomalt, mannitol, sodium starch glycolate, sorbitol, lactose spray dried, lactose anhydrouse, or a combination thereof. In another embodiment, the filler is mannitol or lactose monohydrate . In one embodiment, the package further comprises a desiccant. In another embodiment, the desiccant is silica gel. In one embodiment, the pharmaceutical composition is stable and has a moisture content of no more than 4%. In another embodiment, laquinimod is present in the pharmaceutical composition as solid particles. In another embodiment, the package is a sealed packaging having a moisture permeability of not more than 15 mg/day per liter. In another embodiment, the sealed package is a blister pack in which the maximum moisture permeability is no more than 0.005 mg/day. In another embodiment, the sealed package is a bottle. In another embodiment, the bottle is closed with a heat induction liner. In another embodiment, the sealed package comprises an HDPE bottle. In another embodiment, the sealed package comprises an oxygen absorbing agent. In another embodiment, the oxygen absorbing agent is iron. In one embodiment, the amount of laquinimod in the pharmaceutical composition is at least 0.2 mg or less than 0.6 mg . In another embodiment, the amount of laquinimod in the pharmaceutical composition is 0.1-40.0 mg, 0.03-600 mg, 0.1-2.5 mg, 0.25-2.0 mg, 0.5-1.2 mg, 0.25 mg, 0.3 mg, 0.5 mg, 0.6 mg, 1.0 mg, 1.2 mg, 1.5 mg, or 2.0 mg . In another embodiment, the pharmaceutical composition comprises unit doses of laquinimod of 0.05-4.0 mg, 0.05-2.0 mg, 0.2-4.0 mg, 0.2-2.0 mg, about 0.1 mg, or about 0.5 mg . In one embodiment, the pharmaceutical composition is formulated for intraocular, periocular, systemic or topical administration. In another embodiment, the pharmaceutical composition is formulated for oral or ocular administration. The subject invention also provides packages as described herein for use in treating a subject afflicted with glaucoma. The subject invention also provides a therapeutic package for dispensing to, or for use in dispensing to, a subject afflicted with glaucoma, which comprises a ) one or more unit doses, each such unit dose comprising an amount of laquinimod thereof, wherein the amount of said laquinimod in said unit dose is effective, upon administration to said subject, to treat the subject, and b ) a finished pharmaceutical container therefor, said container containing said unit dose or unit doses, said container further containing or comprising labeling directing the use of said package in the treatment of said subject. In one embodiment, the therapeutic package comprises a second pharmaceutical composition comprising an amount of a second agent for the treatment of glaucoma. In another embodiment, the second agent is a b-adrenergic antagonist, adrenergic agonist, parasympathomimetic, prostaglandin-like analog, or carbonic anhydrase inhibitor. The subject invention also provides a pharmaceutical composition comprising an amount of laquinimod for use in treating a subject afflicted glaucoma. In one embodiment, the pharmaceutical composition comprises an amount of a second agent for the treatment of glaucoma. In another embodiment, the second agent is a b-adrenergic antagonist, adrenergic agonist, parasympathomimetic, prostaglandin-like analog, or carbonic anhydrase inhibitor. In an embodiment, the pharmaceutical composition is in the form of an aerosol, an inhalable powder, an injectable, a liquid, a gel, a solid, a capsule or a tablet. In another embodiment, the pharmaceutical composition is in a liquid or a gel form. In an embodiment, the concentration of laquinimod in the liquid or gel is 5-100 mg/ml solution, 20-100 mg/ml solution, 10-15 mg/ml solution or 20-50 mg/ml solution. In another embodiment, the pharmaceutical composition comprises a unit dose of 10 of an aqueous pharmaceutical solution which contains in solution at least 0.2 g laquinimod. In another embodiment, laquinimod is laquinimod sodium. In one embodiment, the pharmaceutical composition is in capsule form or in tablet form. In another embodiment, the tablets are coated with a coating which inhibits oxygen from contacting the core. In another embodiment, the coating comprises a cellulosic polymer, a detackif ier , a gloss enhancer, or pigment. In another embodiment, the pharmaceutical composition further comprises mannitol . In one embodiment, the pharmaceutical composition further comprises an alkalinizing agent. In another embodiment, the alkalinizing agent is meglumine. In another embodiment, the pharmaceutical composition further comprises an oxidation reducing agent. In one embodiment, the pharmaceutical composition is free of an alkalinizing agent or an oxidation reducing agent. In another embodiment, the pharmaceutical composition is free of an alkalinizing agent and free of an oxidation reducing agent. In one embodiment, the pharmaceutical composition is stable and free of disintegrant . In another embodiment, the pharmaceutical composition further comprises a lubricant. In another embodiment, the lubricant is present in the pharmaceutical composition as solid particles. In another embodiment, the lubricant is sodium stearyl fumarate or magnesium stearate. In one embodiment, the pharmaceutical composition further comprises a filler. In another embodiment, the filler is present in the pharmaceutical composition as solid particles. In another embodiment, the filler is lactose, lactose monohydrate, starch, isomalt, mannitol, sodium starch glycolate, sorbitol, lactose spray dried, lactose anhydrouse, or a combination thereof. In another embodiment, the filler is mannitol or lactose monohydrate . n one embodiment, the amount of laquinimod in the pharmaceutical composition is at least 0.2 mg or less than 0.6 mg . In another embodiment, the amount of laquinimod in is 0.1-40.0 mg, 0.03-600 mg, 0.1-2.5 mg, 0.25-2.0 mg, 0.5-1.2 mg, 0.25 mg, 0.3 mg, 0.5 mg, 0.6 mg, 1.0 mg, 1.2 mg, 1.5 mg, or 2.0 mg . In another embodiment, the pharmaceutical composition comprises unit doses of laquinimod of 0.05-4.0 mg, 0.05-2.0 mg, 0.2-4.0 mg, 0.2-2.0 mg, about 0.1 mg, or about 0.5 mg . In one embodiment, the pharmaceutical composition is formulated for intraocular, periocular, systemic or topical administration. In another embodiment, the pharmaceutical composition is formulated for oral or ocular administration. The subject invention also provides a pharmaceutical composition as described herein for use in treating a subject afflicted with glaucoma. The subject invention also provides a pharmaceutical composition in unit dosage form, useful in treating a subject afflicted with glaucoma, which comprises an amount of laquinimod; which amount of said laquinimod in said composition is effective, upon administration to said subject of one or more of said unit dosage forms of said composition, to treat the subject. The subject invention also provides a package comprising a ) a pharmaceutical composition as described herein; and b ) instruction for use of the pharmaceutical composition to treat a subject afflicted with glaucoma. The subject invention also provides laquinimod for the manufacture of a medicament for use in treating a subject afflicted glaucoma. For the foregoing embodiments, each embodiment disclosed herein is contemplated as being applicable to each of the other disclosed embodiments. For instance, the elements recited in the method embodiments can be used in the pharmaceutical composition, package, and use embodiments described herein and vice versa. Terms As used herein, and unless stated otherwise, each of the following terms shall have the definition set forth below. As used herein, "laquinimod" means laquinimod acid or a pharmaceutically acceptable salt thereof. A "salt thereof" is a salt of the instant compounds which have been modified by making acid or base salts of the compounds. The term "pharmaceutically acceptable salt" in this respect, refers to the relatively non-toxic, inorganic and organic acid or base addition salts of compounds of the present invention. For example, one means of preparing such a salt is by treating a compound of the present invention with an inorganic base. As used herein, an "amount" or "dose" of laquinimod as measured in milligrams refers to the milligrams of laquinimod acid present in a preparation, regardless of the form of the preparation. A "dose of 0.6 mg laquinimod" means the amount of laquinimod acid in a preparation is 0.6 mg, regardless of the form of the preparation. Thus, when in the form of a salt, e.g. a laquinimod sodium salt, the weight of the salt form necessary to provide a dose of 0.6 mg laquinimod would be greater than 0.6 mg (e.g., 0.64 mg) due to the presence of the additional salt ion. As used herein, a "unit dose", "unit doses" and "unit dosage forra (s )" mean a single drug administration entity/entities . As used herein, "about" in the context of a numerical value or range means ±10% of the numerical value or range recited or claimed . As used herein, a composition that is "free" of a chemical entity means that the composition contains, if at all, an amount of the chemical entity which cannot be avoided although the chemical entity is not part of the formulation and was not affirmatively added during any part of the manufacturing process. For example, a composition which is "free" of an alkalizing agent means that the alkalizing agent, if present at all, is a minority component of the composition by weight. Preferably, when a composition is "free" of a component, the composition comprises less than 0.1 wt%, 0.05 wt%, 0.02 wt%, or 0.01 wt% of the component. A s used herein, "alkalizing agent" is used interchangeably with the term "alkaline-reacting component" or "alkaline agent" and refers to any pharmaceutically acceptable excipient which neutralizes protons in, and raises the pH of, the pharmaceutical composition in which it is used. A s used herein, "oxidation reducing agent" refers to a group of chemicals which includes an "antioxidant", a "reduction agent" and a "chelating agent" . A s used herein, "antioxidant" refers to a compound selected from the group consisting of tocopherol, methionine, glutathione, tocotrienol, dimethyl glycine, betaine, butylated hydroxyanisole, butylated hydroxytoluene, turmerin, vitamin E , ascorbyl palmitate, tocopherol, deteroxime mesylate, methyl paraben, ethyl paraben, butylated hydroxyanisole, butylated hydroxytoluene, propyl gallate, sodium or potassium metabisulf ite, sodium or potassium sulfite, alpha tocopherol or derivatives thereof, sodium ascorbate, disodium edentate, BHA (butylated hydroxyanisole), a pharmaceutically acceptable salt or ester of the mentioned compounds, and mixtures thereof . The term "antioxidant" as used herein also refers to Flavonoids such as those selected from the group of quercetin, morin, naringenin and hesperetin, taxifolin, afzelin, quercitrin, myricitrin, genistein, apigenin and biochanin A , flavone, flavopiridol , isof lavonoids such as the soy isof lavonoid, genistein, catechins such as the tea catechin epigallocatechin gallate, flavonol, epicatechin, hesperetin, chrysin, diosmin, hesperidin, luteolin, and rutin. A s used herein, "reduction agent" refers to a compound selected from the group consisting of thiol-containing compound, thioglycerol , mercaptoethanol , thioglycol, thiodiglycol , cysteine, thioglucose, dithiothreitol (DTT) , dithio-bis-maleimidoethane (DTME) , 2 ,6-di-tert-butyl-4-methylphenol (BHT) , sodium dithionite, sodium bisulphite, formamidine sodium metabisulphite, and ammonium bisulphite ." A s used herein, "chelating agent" refers to a compound selected from the group consisting of penicillamine, trientine, N,N '- diethyldithiocarbamate (DDC) , 2,3,2 '-tetraamine (2, 3 ,2 '-tet) , neocuproine, N , , ', '-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN) , 1,1O-phenanthroline (PHE), tetraethylenepentamine , triethylenetetraamine and tris (2-carboxyethyl) phosphine (TCEP) , ferrioxamine, CP94, EDTA, def eroxainine B (DFO) as the methanesulf onate salt (also known as desf errioxanilne B mesylate (DFOM) ), desferal from Novartis (previously Ciba-Giegy) , and apof erritin . A s used herein, a pharmaceutical composition is "stable" when the composition preserves the physical stability/integrity and/or chemical stability/integrity of the active pharmaceutical ingredient during storage. Furthermore, "stable pharmaceutical composition" is characterized by its level of degradation products not exceeding 5% at 40°C/75%RH after 6 months or 3% at 55°C/75% RH after two weeks, compared to their level in time zero. A s used herein, "effective" when referring to an amount of laquinimod refers to the quantity of laquinimod that is sufficient to yield a desired therapeutic response. Efficacy can be measured by e.g., a reduced intraocular pressure (IOP) . Administering to the subject" or "administering to the (human) patient" means the giving of, dispensing of, or application of medicines, drugs, or remedies to a subject/patient to relieve, cure, or reduce the symptoms associated with a condition, e.g., a pathological condition. The administration can be periodic administration. A s used herein, "periodic administration" means repeated/recurrent administration separated by a period of time. The period of time between administrations is preferably consistent from time to time. Periodic administration can include administration, e.g., once daily, twice daily, three times daily, four times daily, weekly, twice weekly, three times weekly, four times weekly and so on, etc. The route of administration can be, e.g., topical. Routes of administration can also be classified by whether the effect is local (e.g., in topical administration) or systemic (e.g., in enteral or parenteral administration) . "Local administration" as used herein shall mean administration of a compound or composition directly to where its action is desired, and specifically excludes systemic administration. "Topical administration" of a compound or composition as used herein shall mean application of the compound or composition to body surfaces such as the skin or mucous membranes such as eyes. "Ocular administration" as used herein shall mean application of a compound or composition to the eye of a subject or to the skin around the eye (periocular skin) of a subject, i.e., local administration. Examples of ocular administration include topical administration directly to the eye, topical application to the eye lid or injection into a portion of the eye or eye socket. In addition, an "ocular pharmaceutical composition" as used herein means a pharmaceutical composition formulated for ocular administration . "Treating" as used herein encompasses, e.g., inducing inhibition, regression, or stasis of a disease or disorder, e.g., glaucoma, or alleviating, lessening, suppressing, inhibiting, reducing the severity of, eliminating or substantially eliminating, or ameliorating a symptom of the disease or disorder. "Inhibition" of disease progression or disease complication in a subject means preventing or reducing the disease progression and/or disease complication in the subject. A "symptom" associated with glaucoma includes any clinical or laboratory manifestation associated with glaucoma and is not limited to what the subject can feel or observe. As used herein, a subject "afflicted" with glaucoma means the subject has been diagnosed with glaucoma. A s used herein, a subject at "baseline" is as subject prior to administration of laquinimod in a therapy as described herein. A "pharmaceutically acceptable carrier" refers to a carrier or excipient that is suitable for use with humans and/or animals without undue adverse side effects (such as toxicity, irritation, and allergic response) commensurate with a reasonable benefit/risk ratio. It can be a pharmaceutically acceptable solvent, suspending agent or vehicle, for delivering the instant compounds to the subject. It is understood that where a parameter range is provided, all integers within that range, and tenths thereof, are also provided by the invention. For example, "0 .1-2 .5mg/day" includes 0.1 mg/day, 0.2 mg/day, 0.3 mg/day, etc. up to 2.5 mg/day. This invention will be better understood by reference to the Experimental Details which follow, but those skilled in the art will readily appreciate that the specific experiments detailed are only illustrative of the invention as described more fully in the claims which follow thereafter. Experimental Details Example 1 : Assessment Of The Neuroprotective Efficacy of Laquinimod For The Retinal Ganglion Cell (RGC) Survival In A Rat Glaucoma Model The purpose of this study was to assess the efficacy of laquinimod in protecting against chronic ocular hypertension (OHT) and RGC degeneration in a rat model of glaucoma, created by injecting hypertonic saline into the episcleral veins in one eye of the Brown Norway rat. In this model, RGC degeneration occurs in response to increased IOP and OHT similar to that in human patients with glaucoma. SUMMARY The study included 5 groups (n=8 each) : Group 1 (1% Laquinimod for topical administration) , Group 2 (Vehicle for topical administration) , Group 3 (4% Laquinimod for topical administration), Group 4 (0.25% Laquinimod for topical administration) and Group 5 (0.1% Laquinimod for oral administration) . Prior to any experimental procedure, clinical observations were performed daily, body weights were obtained, intraocular pressure (IOP) was measured and detailed ocular examinations were performed on both eyes. Animals that were found to be clinically normal with no baseline ocular abnormalities were selected for use in the study. The rat model of chronic ocular hypertension (OHT) /glaucoma was created in the left eye of each animal via two hypertonic saline injections (HSI) each one week apart. The un-injected right eye served as the control. Throughout the study, the vehicle control and the test articles were prepared weekly. Rats were dosed once daily for oral administration (Group 5 ) and twice daily for topical administration groups (Groups 1-4) , starting on the day of the first HSI until euthanasia. Detailed ocular examinations were performed one week after the 2nd HSI and on the day of euthanasia. Approximately one week prior to euthanasia, RGCs were retrogradely-labeled by bilateral injections of Fluoro-Gold (FG) into the superior colliculus in the brain. Post-dose IOP was measured weekly for 5 weeks starting one week after the 2nd HSI until euthanasia. For each IOP measurement time-point following the 2nd HSI, the IOP elevation was calculated as the difference between the IOP in the left eye with OHT and that in the non-OHT right eye (DIOR ) . The DIOR for the 5 weekly post-HSI IOP measurements were averaged and constituted the Mean DIOR for each animal. Rats which did not have individual IOP measurements of ³ 50 mmHg in the OHT eyes were selected from a larger pool and groups (n=8 each) were matched for the Mean DIOR . Other animals were removed from the study . Animals were euthanized 5 weeks after the 2nd HSI. The retinas were flat-mounted, slide IDs were masked and 8 regions per retina were imaged using a confocal microscope. RGC at these regions were counted using the Image J software. After the optic nerves were extracted, they were plastic-embedded, sectioned and stained with Toluidine Blue at Schepens Eye Research Institute, Boston, MA. The injury in the optic nerves was evaluated and graded by microscopic examination in a masked fashion. There were no abnormal clinical signs or ocular abnormalities noted in any of the 40 animals in the beginning of the study. There were no treatment-related findings in the clinical observations or ocular examinations during the study in any of the animals . A One-Way ANOVA indicated that the group body weights were not statistically different on the day of dosing among groups (P = 0.957) . Groups also did not differ in the amount of weight gained between the day of dosing and the day of euthanasia (One-Way ANOVA; P = 0.559) . For five weeks post-dose, the mean DIOR values (OHT - Non-OHT) (Mean ± SD) were 9.1 ± 2.2 mmHg, 9.1 ± 2.6 mmHg, 9.3 ± 2.7 mmHg, 9.2 ± 1.5 mmHg, and 9.1 ± 2.9 mmHg for Groups 1 , 2 , 3 , 4 and 5 , respectively. A One-Way ANOVA analysis indicated that the groups were well-matched for Mean DIOR (P > 0.9) . Compared to the non-OHT retinas, % Fluoro-gold labeled-RGC Loss (Mean ± SD) in the OHT retinas was 17.6 ± 33.8, 34.8 ± 42.7, 26.8 ± 36.4, 21.6 ± 21.7, and 22.9 ± 33.1 for Groups 1 , 2 , 3 , 4 and 5 , respectively. FG-Labeled RGC counts per mm2 were compared between the Non-OHT and the OHT retinas for each group using two-tailed paired-t tests. Group 2 (vehicle topical; P = 0.047) and Group 4 (0.25% Laquinimod topical; P = 0.033) had fewer RGCs in the OHT eye compared to the Non-OHT eyes. The number of RGCs in Group 3 (4% Laquinimod topical; P = 0.071) and Group 5 (0.1% Laquinimod oral; P = 0.075) were statistically different between the OHT and Non-OHT eyes. However, in Group 1 (1% Laquinimod topical), there was no statistically significant difference in the RGC counts between the OHT and Non-OHT eyes (P = 0.189) . This suggests that the daily topical application of 1% Laquinimod may be neuroprotective for the RGC . For the optic nerves in the Non-OHT (control) eyes, the Mean Injury Grades (Mean ± SD) were 1.1 ± 0.1, 1.2 ± 0.2, 1.2 ± 0.2, 1.2 ± 0.3 and 1.2 ± 0.2 for Groups 1 , 2 , 3 , 4 and 5 , respectively. For the optic nerves in the OHT eyes, the Mean Injury Grades (Mean ± SD) for the OHT optic nerves were 2.5 ± 1.3, 3.0 ± 1.6, 3.0 ± 1.5, 2.8 ± 1.3 and 2.7 ± 1.5 for Groups 1 , 2 , 3 , 4 , and 5 respectively. As a secondary analysis, Mean ON Injury Grades were compared between the Non-OHT and the OHT optic nerves for each group using two-tailed paired-t tests. The Mean ON injury grades were significantly greater in the OHT eyes compared to the Non-OHT control eyes in all groups (P < 0.05) . MATERIALS Test Article: laquinimod sodium stored at room temperature protected from light. Control Article: 0% laquinimod sodium stored under refrigeration. ANIMALS Number and Species: The study quote and outline-specified data were collected on 40 Brown Norway rats (Rattus norvegicus) . Rats have been used historically as OHT models and there are no other approved alternative (non-animal methods) . The study started with 90 animals to ensure that sufficient data were available at the end of the study. Sex: male Weight/Age Range: approximately 271.2-366.4 grams/at least 12 weeks old (adult) weighed to nearest 0.1 g . PROCEDURE Ocular and oral exposure corresponds to the route of human exposure. For the four topical administration groups, the test and control articles were applied topically to the surface of one eye of the test system. The test article was administered orally for the fifth group of animals. Preparation of Test and Control Articles All test and control articles were prepared as described below. The final volume for the formulations described below is 200 mL but the formulations were proportionally changed to the required volume for each preparation. Three different concentrations (0.25%, 1%, and 4%) of the test article for topical application and the test article for oral gavage (0.1%) were prepared weekly. The control article for topical application was also prepared weekly. The identification of the test and control articles for the topical administration was masked after preparation of the topical formulations. Table 1 : LAQ 4.0% Topical Formulation (40 mg/mL of LAQ) Table 1 Process: The entire process is performed under yellow light or at dark conditions . Weigh 175 g (175 mL) of water for injection in a glass container containing a stirrer. Weigh and add the Sodium Phosphate Monobasic Monohydrate and Sodium Phosphate Dibasic 7 Hydrate and stir for approximately 5 minutes. Verify complete dissolution by visual inspection of a clear transparent solution. Measure the pH (Approximately 7.7-8.3) 5 . Weigh and add Laquinimod Sodium to the solution. Rinse the weighing boat from the Laquinimod Sodium remaining with ~5 mL of water and to the solution. Stir for approximately 5 minutes and verify complete dissolution by visual inspection of a clear transparent solution. Weigh and add the Hydroxy Ethyl Cellulose H . Stir for approximately 2 hours. Remove the stirrer and add the solution to a 200 mL volumetric flask. Add water for injection up to 200 mL . Shake manually for approximately two minutes. Transfer into an appropriate container. Wrap with aluminum foil and keep the solution refrigerated. Table 2 : LAQ 1.0% Topical Formulation (10 mg/mL of LAQ) Table 2 Process : 1 . The entire process is performed under yellow light or at dark conditions . 2 . Weigh 175 g (175 mL) of water for injection in a glass container containing a stirrer. 3 . Weigh and add the Sodium Phosphate Monobasic Monohydrate and Sodium Phosphate Dibasic 7 Hydrate and stir for approximately 5 minutes. Verify complete dissolution by visual inspection of a clear transparent solution. Measure the pH (Approximately 7.7 to 8.3) . Weigh and add Laquinimod Sodium to the solution. Rinse weighing boat from the Laquinimod Sodium remaining with mL of water and to the solution. Stir for approximately 5 minutes and verify complete dissolution by visual inspection of a clear transparent solution. 6 . Weigh and add the Sodium Chloride to the solution. Stir for approximately 2 minutes. Verify complete dissolution by visual inspection of a clear transparent solution. 7 . Weigh and add the Hydroxy Ethyl Cellulose H . 8 . Stir for approximately 2 hours. 9 . Remove the stirrer and add the solution to a 200mL volumetric flask. 10. Add water for injection up to 200 mL . 11. Shake manually for approximately two minutes. Transfer into an appropriate container. Wrap with aluminum foil and keep the solution refrigerated. Table 3 : LAQ 0.25% Topical Formulation (2.5 mg/mL of LAQ) Table 3 Process : 1 . The entire process is performed under yellow light dark conditions . Weigh 175 g (175 mL) of water for injection in a glass container containing a stirrer. Weigh and add the Sodium Phosphate Monobasic Monohydrate and Sodium Phosphate Dibasic 7 Hydrate and stir for approximately 5 minutes. Verify complete dissolution by visual inspection of a clear transparent solution. Measure the pH (Approximately 7.7-8.3) . Weigh and add Laquinimod Sodium to the solution. Rinse the weighing boat from the Laquinimod Sodium remaining with ~5 mL of water and to the solution. Stir for approximately 5 minutes and verify complete dissolution by visual inspection of a clear transparent solution. Weigh and add the Sodium Chloride to the solution. Stir for approximately 2 minutes. Verify complete dissolution by visual inspection of a clear transparent solution. Weigh and add the Hydroxy Ethyl Cellulose H . Stir for approximately 2 hours. Remove the stirrer and add the solution to a 200 mL volumetric flask. Add water for injection up to 200 mL . Shake manually for approximately two minutes. Transfer into an appropriate container. Wrap with aluminum foil and keep the solution refrigerated. Table 4 : LAQ 0% Topical Formulation (Control Article) Table 4 Process : 1 . The entire process is performed under yellow light or at dark conditions . 2 . Weigh 175 g (175 mL) of water for injection in a glass container containing a stirrer. Weigh and add the Sodium Phosphate Monobasic Monohydrate and Sodium Phosphate Dibasic 7 Hydrate and stir for approximately 5 minutes. Verify complete dissolution by visual inspection of a clear transparent solution. Measure the pH (Approximately 7.7 to 8.3) . Weigh and add the Sodium Chloride to the solution. Stir for approximately 2 minutes. Verify complete dissolution by visual inspection of a clear transparent solution. Weigh and add the Hydroxy Ethyl Cellulose H . Stir for approximately 2 hours. Remove the stirrer and add the solution to a 200 mL volumetric flask. Add water for injection up to 200 mL . Shake manually for approximately two minutes. Transfer into an appropriate container. Table 5 : LAQ 0.1% Oral Formulation (1.0 mg/mL of LAQ) Table 5 Process : 1 . The entire process is performed under yellow light or at dark conditions . 2 . Weigh 150 g (150 mL) of autoclaved tap water in a glass container containing a stirrer. 3 . Weigh and add Laquinimod Sodium to the solution. Rinse the remaining Laquinimod Sodium in the weighing boat with ~5 mL of water and add to the solution. Stir for approximately 5 minutes and verify complete dissolution by visual inspection of a clear transparent solution. 4. Add autoclaved tap water up t o 200 mL . 5. Sti r for 5 minutes . 6. Trans fer into an appropriate amber Pre-Dose Administration and Selection of Animals: Cl inical observat ions were performed dai l y according t o Table 6 bel ow: Table 6: Cl inical Signs and Obs ervations Animal s were we ighed wee kly prior t o initiation of dos ing . The f i rst day the rats are weighed was des ignated as Study Day 1, and the beginning of Study Week 1. Ophthalmi c Examinations : Animal s selected for the study were examined prior t o the initial admini stration of the test or the control arti cles t o ensure that both eyes we r e free of abnormal ity, damage , and di sease . Both eyes were examined, scored and recorded prior t o the initial dose admini stration u s ing a hand held s l it- lamp and a d i rect ophthalmo scope o r the surgical microscope according t o the Cl a s s i fication System for Grading Ocular Les ions a s described i n Table 7 , and the Ocular Poste rior Segment Scoring Scale o f Tabl e 8 . Po sterio r segment examinati on was perfo rmed after topical appl icati on o f Tropicamide i n the conscious s tate , o r after the rats are anestheti zed with i s o florane inhalation . Onl y rat s showing n o s igns o f eye i rritat ion , ocular d e fects , o r preexi sting corneal inj ury were used i n the study . CONJUNCTIVA A. REDNESS / CONGESTION 0 Vessels normal. May appear blanched to reddish pink without perilimbal injection (except at 12:00 and 6:00 o'clock positions) with vessels of the palpebral and bulbar conjunctivae easily observed. 1 Vessels definitely injected above normal. A flushed, reddish color predominately confined to the palpebral conjunctivae with some perilimbal injection but primarily confined to the lower and upper parts of the eye from, the 4:00 and 7:00 and 11:00 to 1:00 o'clock positions. 2*† More diffuse, deeper crimson red, individual vessels not easily discernible. Bright red color of the palpebral conjunctiva with accompanying perilimbar injection covering at least 75% of the circumference of the perilimbal region. 3*† Diffuse beefy red. Dark beefy red color with congestion of both the bulbar and palpebral conjunctiva along with pronounced perilimbal injection and the presence of petechia on the conjunctiva. The B. CHEMOSIS: 0 Normal. No swelling of the conjunctival tissue. 1 Any swelling above normal (includes nictitating membrane). Swelling above normal without eversion of the lids (can be easily ascertained by noting that the upper and lower eyelids are positioned as in the normal eye); swelling generally starts in the lower cul-de-sac near the inner canthus which needs slit-lamp examination. 2*† Obvious swelling with partial eversion of lids. Swelling with misalignment of the normal approximation of the lower and upper eyelids; primarily confined to the upper eyelid so that in the initial stages the misapproximation of the eyelids begins by partial eversion of the upper eyelid. In this stage, swelling is confined generally to the upper eyelid, although it exists in the lower cul-de-sac. Swelling with lids about half closed. 3*† Swelling definite with partial eversion of the upper and lower eyelids essentially equivalent. This can be easily ascertained by looking at the animal straight head on and noticing the positioning of the eyelids; if the eye margins do not meet, eversion has occurred. *† Swelling with lids about half closed to completely closed. Eversion of the upper eyelid is pronounced with less pronounced eversion of the lower eyelid. It is difficult to retract the lids and observe the perilimbal region. C. DISCHARGE: 0 Normal or no discharge. 1 Any amount different from normal (does not include small amounts observed in inner canthus of normal animals). Discharge above normal and present on the inner portion of the eye but not on the lids or hairs of the eyelids. One can ignore the small amount that is in the inner and outer canthus if it has not been removed prior to starting the study. 2 Discharge with moistening of lids and hairs just adjacent to lids. Discharge is abundant, easily observed, and has collected on the lids around the hairs of the eyelids. 3 Discharge with moistening of the lids and hairs, and considerable area around the eye. CORNEA D. OPACITY-degree of density (areas most dense taken for reading): 0 No ulceration or opacity. Normal cornea. Appears with the slit lamp as having a bright gray line on the endothelial surface and a bright gray line on the endothelial surface with a marble-like gray appearance of the stroma. 1* Scattered or diffuse areas of opacity (other than slight dulling of normal luster), details of iris clearly visible. Some loss of transparency. Only the anterior one-half of the stroma is involved as observed with an optical section of the slit lamp. The underlying structures are clearly visible with diffuse illumination, although some cloudiness can be readily apparent with diffuse illumination. 2*† Easily discernible translucent areas, details of iris slightly obscured. Moderate loss of transparency. In addition to involving the anterior stroma, the cloudiness extends all the way to the endothelium. The stroma has lost its marble-like appearance and is homogeneously white. With diffuse illumination, underlying structures are clearly visible. 3*† Opalescent/nacreous areas, no details of iris visible, size of pupil barely discernible. Involvement of the entire thickness of the stroma. With optical section, the endothelial surface is still visible. However, with diffuse illumination the underlying structures are just barely visible (to the extent that the observer is still able to grade flare, iritis, observe for pupillary response, and note lenticular changes. *† Opaque cornea, iris not discernible through opacity. Involvement of the entire thickness of the stroma. With the optical section, cannot clearly visualize the endothelium. With diffuse illumination, the underlying structures cannot be seen. Cloudiness removes the capability of judging and grading aqueous flare, iritis, lenticular changes, and pupillary response. E. AREAS OF CORNEA INVOLVED: 0 Normal cornea with no area of cloudiness. 1 One-quarter (or less), but not zero. 2 Greater than one-quarter, but less than one-half. * Greater than one-half, but less than three-quarters. * Greater than three-quarters, up to whole area. F. FLUORESCEIN STAINING: 0 Absence of fluorescein staining. 1 Slight fluorescein staining confined to a small focus. With diffuse illumination the underlying structures are easily visible. The outline of the papillary margin is as if there were no fluorescein staining. 2 Moderate fluorescein staining confined to a small focus. With diffuse illumination the underlying structures are clearly visible, although there is some loss of detail. 3 Marked fluorescein staining. Staining may involve a larger portion of the cornea. With diffuse illumination the underlying structures are barely visible but are not completely obliterated. 4 Extreme fluorescein staining. With diffuse illumination the underlying structures cannot be observed. G. CORNEA PANNUS: 0 No pannus 1 Vascularization is present but vessels have not invaded the entire corneal circumference. Where localized vessel invasion has occurred, they have not penetrated beyond 2 mm. 2 Vessels have invaded 2 mm or more around the entire corneal circumference. IRIS 0 Normal iris without any hyperemia of the iris vessels. Occasionally around the 12:00 to 1:00 position near the pupillary border and the 6:00 and 7:00 position near the pupillary border there is a small area around 1-3 mm in diameter in which both the secondary and tertiary vessels are slightly hyperemia 1*† Folds above normal, congestion, swelling, circumcorneal injection (any or all of these or combination of any thereof), iris still reacting to light (sluggish reaction is positive). Minimal injection of secondary vessels but not tertiary. Generally, it is uniform, but may be of greater intensity at the 1:00 or 6:00 position, the tertiary vessels must be substantially hyperemia 2*† No reaction to light, hemorrhage, gross destruction (any or all of these). Minimal injection of tertiary vessels and minimal to moderate injection of the secondary vessels. 3*† Moderate injection of the secondary and tertiary vessels with slight swelling of the iris stroma (this gives the iris surface a slightly rupose appearance which is usually most prominent near the 3:00 and 9:00 positions). *† Marked injection of the secondary and tertiary vessels with marked swelling of the iris stroma. The iris appears rugose; may be accompanied by hemorrhage (hyperemia) in the anterior chamber. AQUEOUS FLARE 0 Absence of visible light beam in the anterior chamber (no Tyndall effect). 1 Tyndall effect is barely discernible. The intensity of the light beam in the anterior chamber is less than the density of the slit beam as it passes through the lens. 2 The Tyndall effect in the anterior chamber is easily discernible and is of equal intensity as the density of the slit beam as it passes through the lens. 3 The Tyndall effect in the anterior chamber is easily discernible; its intensity is greater than the intensity of the slit beam as it passes through the lens. PUPILLARY LIGHT REFLEX: 0 Normal pupillary light reflex 1 Sluggish pupillary light reflex 2 No pupillary light reflex LENS 0 Normal 1 The presence of lenticular opacities should be described and the location noted as defined below: • Anterior capsule • Anterior subcapsule • Anterior cortical • Nuclear • Posterior cortical • Posterior subcapsule • Posterior capsule Table 7 : Combined Draize and McDonald-Shadduck Scoring System Positive Reaction (ISO) Positive Reaction (OECD) VITREOUS BODY 0 Normal, the vitreous body is clear or transparent. 1 Abnormal, the vitreous body is not clear or not transparent and homogenous gel that fills the space between the posterior axial lens capsule, posterior chamber, and ocular fundus. OPTIC DISC/OPTIC NERVE 0 Normal, the optic disc and optic nerve are with light red color, cupping size normal (cup-to-disc ratio < 0.2), and normal sharpness of edge, without swelling, hemorrhages, notching in the optic disc and any other unusual anomalies. 1 Abnormal, the optic disc and optic nerve are not with light red color or cupping size normal (cup-to-disc ratio > 0.2), and no normal sharpness of edge or with swelling, hemorrhages, notching in the optic disc and any other unusual anomalies. RETINAL BLOOD VASCULATURE 0 Normal, the retinal arteries and veins fill in blood and normalize sharpness without hemorrhage and exudation. 1 Abnormal, the retinal arteries and veins don't fill in blood and don't have normalize sharpness or with hemorrhage and exudation. RETINAL HEMORHAGE, EXUDATION, AND DETACHMENT 0 Normal retina with no area of hemorrhage or/and exudation or/and detachment 1 Retinal hemorrhage or/and exudation or/and detachment < 1 quadrant area 2 1 quadrant area < retinal hemorrhage or/and exudation or/and detachment < 2 quadrant areas 3 2 quadrant areas < hemorrhage or/and exudation or/and detachment < 3 quadrant areas 4 3quadrant areas 0.9) (Figure 1 ) . Representative images of the retinas with FG-labeled RGC are shown in Figures 5A-5J. % FG-Labeled RGC loss in the OHT retinas compared with the corresponding non-OHT retinas is shown in Table 10. Compared to the non-OHT retinas, % RGC Loss (Mean ± SD) in the OHT retinas was 17.6 ± 33.8, 34.8 ± 42.7, 26.8 ± 36.4, 21.6 ± 21.7, and 22.9 ± 33.1 for Groups 1 , 2 , 3 , 4 and 5 , respectively (Figure 2 ) . FG-labeled RGC counts: A Two-Way ANOVA on the RGC counts in the OHT and Non-OHT (control) eyes versus groups did not show a significant eye versus group interaction (P = 0.919), indicating that groups did not differ for the RGC counts in the OHT and Non-OHT eyes (Figure 3 ) . As a secondary analysis, FG-Labeled RGC counts per mm2 were compared between the Non- OHT and the OHT retinas for each group using a paired-t test (two-tailed) . Group 2 (vehicle topical; P = 0.047) and Group 4 (0.25% Laquinimod topical; P =0.033) had fewer RGCs in the OHT eye compared to the Non-OHT eyes. The number of RGCs in Group 3 (4% Laquinimod topical; P = 0.071) and Group 5 (0.1% Laquinimod oral; P = 0.075) were statistically marginally different between the OHT and Non-OHT eyes. However, in Group 1 (1% Laquinimod topical), there was no statistically significant difference in the RGC counts between the OHT and Non-OHT eyes (P = 0.189) . This suggests that the daily topical application of 1% Laquinimod may be neuroprotective for the RGC . 6 . Optic Nerve (ON) Injury Grades: Mean ON Injury Grades (Mean ± SD) for the Non-OHT eyes were 1.1 ± 0.1, 1.2 ± 0.2, 1.2 ± 0.2, 1.2 ± 0.3 and 1.2 ± 0.2 for Groups 1 , 2 , 3 , 4 and 5 , respectively. Mean Injury Grades (Mean ± SD) for the OHT optic nerves were 2.5 ± 1.3, 3.0 ± 1.6, 3.0 ± 1.5, 2.8 ± 1.3 and 2.7 ± 1.5 for Groups 1 , 2 , 3 , 4 , and 5 , respectively. A Two-Way ANOVA on the Mean ON injury grades in the OHT and Non-OHT (control) eyes versus groups did not show a significant eye versus group interaction (P = 0.98) , indicating that groups did not differ for the injury in the OHT and Non-OHT optic nerves (Figure 4 ) . As a secondary analysis, Mean ON Injury Grades were compared between the Non-OHT and the OHT optic nerves for each group using two-tailed paired-t tests. The Mean ON injury grades were significantly greater in the OHT eyes compared to the Non-OHT control eyes in all groups (P < 0.05) . Ophthalmic Examinations (OEs) : At baseline ocular examinations prior to initial dose, there were no ocular abnormalities observed in either eye in any of the animals included in the study. During the post-dose OEs, there were no ocular problems observed in any of the animals in the Non-OHT eyes. However, , there were some ocular abnormalities observed in the OHT eyes due to the glaucoma-model creation procedures (hypertonic saline injection surgeries into the episcleral veins) in all groups. These abnormalities included minor congestion and chemosis (swelling) in the conjunctiva, minor corneal opacities, lack of sufficient dilation of the pupil after application of the pupil-dilating agent Tropicamide, slight opacities in the lens and presence of free-floating iris pigments in front of the lens in the OHT eyes. The post-HSI ocular findings in the OHT eyes were observed in all groups with a similar occurrence and were not test articlerelated . CONCLUSION The study involved daily dosing of five groups for approximately six weeks: Group 1 (1% Laquinimod topical), Group 2 (Vehicle topical), Group 3 (4% Laquinimod topical), Group 4 (0.25% Laquinimod topical) and Group 5 (0.1% Laquinimod oral) . The analyses for the RGC counts in Group 1 animals suggested a trend towards neuroprotection following daily topical application of 1% Laquinimod . EXAMPLE 2 : Assessment of Efficacy of laquinimod for treating patients afflicted with glaucoma Periodic (e.g., daily or twice daily) administration of laquinimod (oral or topical) is effective in treating glaucoma human patients Periodic (e.g., daily or twice daily) administration of laquinimod (oral or topical) is effective to reduce a glaucoma-associated symptom in the subject. A laquinimod composition as described herein is administered systematically or locally to the eye of a subject suffering from glaucoma. The administration of the composition is effective to treat the subject suffering from glaucoma. The administration of the composition is also effective to reduce a glaucoma-associated symptom of glaucoma in the subject. The administration of the composition is also effective to reduce intraocular pressure in the subject. The administration of the composition is effective to reduce RGC damage and/or RGC loss, and improve RGC viability in the subject. "Glaucoma", Merck Manual of Diagnosis and Therapy (1999), Merck Research Laboratories, (Whitehouse Station, NJ) , 733- 738 . Alward, "Medical Management of Glaucoma", N Eng J Med, 1998; 339:1298-1307) . Bakalash et al ., "Resistance of Retinal Ganglion Cells to an Increase in Intraocular Pressure is Immune-dependent", Invest Ophthalmol Vis Sci 2002; 43:2 64 8-2 653. Brod et al . 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What is claimed is : 1 . A method of treating a subject afflicted with glaucoma comprising administering to the subject an amount of laquinimod effective to treat the subject. 2 . The method of claim 1 , wherein the administration of laquinimod is effective to reduce or inhibit a symptom of the glaucoma in the subject. 3 . The method of claim 2 , wherein the symptom is retinal ganglion cell damage, retinal ganglion cell loss, or elevated intraocular pressure. 4 . The method of any one of claims 1-3, wherein laquinimod is laquinimod sodium. 5 . The method of any one of claims 1-4, wherein the route of administration of laquinimod is intraocular, periocular, ocular, oral, systemic or topical. 6 . The method of any one of claims 1-5, wherein laquinimod is administered in the form of an aerosol, an inhalable powder, an injectable, a liquid, a gel, a solid, a capsule or a tablet . 7 . The method of claim 6 , wherein the concentration of laquinimod in the liquid or gel is 5-100 mg/ml solution, 20- 100 mg/ml solution, 10-15 mg/ml solution, or 20-50 mg/ml solution . 8 . The method of any one of claims 1-7, wherein laquinimod is administered periodically. 9 . The method of claim 8 , wherein laquinimod is administered daily . 10. The method of claim 8 , wherein laquinimod is administered more often than once daily or less often than once daily. The method of any one of claims 1-10, wherein the amount laquinimod administered is at least 0.2 mg/day and/or less than 0.6 mg/day. The method of any one of claims 1-10, wherein the amount laquinimod administered is 0.03-600 mg/day, 0.1-40.0 mg/day, 0.1-2.5 mg/day, 0.25-2.0 mg/day, 0.5-1.2 mg/day, 0.25 mg/day, 0.3 mg/day, 0.5 mg/day, 0.6 mg/day, 1.0 mg/day, 1.2 mg/day, 1.5 mg/day or 2.0 mg/day. The method of any one of claims 1-12, wherein the amount of laquinimod administered is 0.05-4.0 mg per administration, 0.05-2.0 mg per administration, 0.2-4.0 mg per administration, 0.2-2.0 mg per administration, about 0.1 mg per administration, or about 0.5 mg per administration. The method of any one of claims 1-13, further comprising administration of a second agent for the treatment of glaucoma . The method of claim 14, wherein the second agent is a b- adrenergic antagonist, adrenergic agonist, parasympathomimetic, prostaglandin-like analog, or carbonic anhydrase inhibitor. The method of any one of claims 8-15, wherein the periodic administration of laquinimod continues for at least 3 days, more than 30 days, more than 42 days, 8 weeks or more, at least 12 weeks, at least 24 weeks, more than 24 weeks, or 6 months or more. The method of any one of claims 1-16, wherein the subject is a human patient. A method of treating a subject suffering from retinal ganglion cell loss or retinal ganglion cell damage, or of reducing retinal ganglion cell loss or damage in a subject, comprising administering to the subject an amount of laquinimod effective to reduce retinal ganglion cell loss or retinal ganglion cell damage in the subject. 19. A method of treating a subject suffering from elevated intraocular pressure, or of reducing intraocular pressure in a subject, comprising administering to the subject an amount of laquinimod effective to reduce intraocular pressure in the subject. 20. A package comprising: a ) a pharmaceutical composition comprising an amount of laquinimod; and b ) instruction for use of the pharmaceutical composition to treat a subject afflicted with glaucoma. 21. The package of claim 20, wherein the package comprises a second pharmaceutical composition comprising an amount of a second agent for the treatment of glaucoma. 22. The package of claim 21, wherein the second agent is a b- adrenergic antagonist, adrenergic agonist, parasympathomimetic, prostaglandin-like analog, or carbonic anhydrase inhibitor. 23. The package of any one of claims 20-22, wherein the pharmaceutical composition is the form of an aerosol, an inhalable powder, an injectable, a liquid, a gel, a solid, a capsule or a tablet. 24. The package of claim 23, wherein the concentration of laquinimod in the liquid or gel is 5-100 mg/ml solution, 20- 100 mg/ml solution, 10-15 mg/ml solution or 20-50 mg/ml solution . 25. The package of claim 23, wherein the tablets are coated with a coating which inhibits oxygen from contacting the core . 26. The package of claim 25, wherein the coating comprises a cellulosic polymer, a detackifier, a gloss enhancer, or pigment . 27. The package of any one of claims 20-26, wherein the pharmaceutical composition further comprises mannitol, an alkalinizing agent, an oxidation reducing agent, a lubricant, a filler, and/or a desiccant. 28. The package of claim 27, wherein the alkalinizing agent is meglumine . 29. The package of any one of claims 20-27, wherein the pharmaceutical composition is stable and free of an alkalinizing agent or an oxidation reducing agent, preferably the pharmaceutical composition is free of an alkalinizing agent and free of an oxidation reducing agent. 30. The package of any one of claims 20-29, wherein the pharmaceutical composition is stable and free of disintegrant . 31. The package of claim 27, wherein the lubricant is present in the pharmaceutical composition as solid particles. 32. The package of claims 27 or 31, wherein the lubricant is sodium stearyl fumarate or magnesium stearate. 33. The package of claim 27, wherein the filler is present in the pharmaceutical composition as solid particles . 34. The package of claims 27 or 33, wherein the filler is lactose, lactose monohydrate, starch, isomalt, mannitol, sodium starch glycolate, sorbitol, lactose spray dried, lactose anhydrouse, or a combination thereof. 35. The package of claim 27, wherein the desiccant is silica gel . 36. The package of any one of claims 20-35, wherein the pharmaceutical composition is stable and has a moisture content of no more than 4%. 37. The package of any one of claims 20-36, wherein laquinimod is present in the pharmaceutical composition as solid particles . 38. The package of any one of claims 20-37, wherein the package is a sealed packaging having a moisture permeability of not more than 15 mg/day per liter or a blister pack having a maximum moisture permeability of not more than 0.005 mg/day . 39. The package of claim 38, wherein the sealed package is a bottle or comprises an HDPE bottle, preferably the bottle is closed with a heat induction liner. 40. The package of claims 38 or 39, wherein the sealed package comprises an oxygen absorbing agent, which oxygen absorbing agent is preferably iron. 41. The package of any one of claims 20-40, wherein the amount of laquinimod in the pharmaceutical composition is at least 0.2 mg, less than 0.6 mg, 0.1-40.0 mg, 0.03-600 mg, 0.1-2.5 mg, 0.25-2.0 mg, 0.5-1.2 mg, 0.25 mg, 0.3 mg, 0.5 mg, 0.6 mg, 1.0 mg, 1.2 mg, 1.5 mg, or 2.0 mg . 42. The package of any one of claims 20-41, wherein the pharmaceutical composition comprises unit doses of laquinimod of 0.05-4.0 mg, 0.05-2.0 mg, 0.2-4.0 mg, 0.2-2.0 mg, about 0.1 mg, or about 0.5 mg . 43. The package of any one of claims 20-42, wherein the pharmaceutical composition is formulated for intraocular, periocular, ocular, oral, systemic or topical administration . 44. The package of any one of claims 20-43, for use in treating a subject afflicted with glaucoma. 45. A therapeutic package for dispensing to, or for use in dispensing to, a subject afflicted with glaucoma, which comprises : a ) one or more unit doses, each such unit dose comprising an amount of laquinimod thereof, wherein the amount of said laquinimod in said unit dose is effective, upon administration to said subject, to treat the subject, and b ) a finished pharmaceutical container therefor, said container containing said unit dose or unit doses, said container further containing or comprising labeling directing the use of said package in the treatment of said subject. The therapeutic package of claim 45, wherein the package comprises a second pharmaceutical composition comprising an amount of a second agent for the treatment of glaucoma. The therapeutic package of claim 46, wherein the second agent is a b-adrenergic antagonist, adrenergic agonist, parasympathomimetic, prostaglandin-like analog, or carbonic anhydrase inhibitor. A pharmaceutical composition comprising an amount of laquinimod for use in treating a subject afflicted glaucoma The pharmaceutical composition of claim 48, comprising an amount of a second agent for the treatment of glaucoma. The pharmaceutical composition of claim 49, wherein the second agent is a b-adrenergic antagonist, adrenergic agonist, parasympathomimetic, prostaglandin-like analog, or carbonic anhydrase inhibitor. The pharmaceutical composition of any one of claims 48-50, in the form of an aerosol, an inhalable powder, an injectable, a liquid, a gel, a solid, a capsule or a tablet . The pharmaceutical composition of claim 51, wherein the concentration of laquinimod in the liquid or gel is 5-100 mg/ml solution, 20-100 mg/ml solution, 10-15 mg/ml solution or 20-50 mg/ml solution. 53. The pharmaceutical composition of claim 51, comprising a unit dose of 10 of an aqueous pharmaceutical solution which contains in solution at least 0.2 mg laquinimod. 54. The pharmaceutical composition of any one of claims 48-53, wherein laquinimod is laquinimod sodium. 55. The pharmaceutical composition of claim 51, wherein the tablets are coated with a coating which inhibits oxygen from contacting the core. 56. The pharmaceutical composition of claim 55, wherein the coating comprises a cellulosic polymer, a detackif ier, a gloss enhancer, or pigment. 57. The pharmaceutical composition of any one of claims 48-56, further comprising mannitol, an alkalinizing agent, an oxidation reducing agent, a lubricant and/or a filler. 58. The pharmaceutical composition of claim 57, wherein the alkalinizing agent is meglumine. 59. The pharmaceutical composition of any one of claims 48-57, which is free of an alkalinizing agent or an oxidation reducing agent, preferably the pharmaceutical composition is free of an alkalinizing agent and free of an oxidation reducing agent . 60. The pharmaceutical composition of any one of claims 48-59, which is stable and free of disintegrant . 61. The pharmaceutical composition of claim 57, wherein the lubricant is present in the pharmaceutical composition as solid particles. 62. The pharmaceutical composition of claims 57 or 61, wherein the lubricant is sodium stearyl fumarate or magnesium stearate . 63. The pharmaceutical composition of claim 57, wherein the filler is present in the pharmaceutical composition as solid particles. 64. The pharmaceutical composition of claims 57 or 63, wherein the filler is lactose, lactose monohydrate, starch, isomalt, mannitol, sodium starch glycolate, sorbitol, lactose spray dried, lactose anhydrouse, or a combination thereof . 65. The pharmaceutical composition of any one of claims 48-64, wherein the amount of laquinimod is at least 0.2 mg, less than 0.6 mg, 0.1-40.0 mg, 0.03-600 mg, 0.1-2.5 mg, 0.25-2.0 mg, 0.5-1.2 mg, 0.25 mg, 0.3 mg, 0.5 mg, 0.6 mg, 1.0 mg, 1.2 mg, 1.5 mg, or 2 .0 mg . 66. The pharmaceutical composition of any one of claims 48-65, comprising unit doses of laquinimod of 0.05-4.0 mg, 0.05-2.0 mg, 0.2-4.0 mg, 0.2-2.0 mg, about 0.1 mg, or about 0.5 mg . 67. The pharmaceutical composition of any one of claims 48-66, formulated for intraocular, periocular, ocular, oral, systemic or topical administration. 68. The pharmaceutical composition of any one of claims 48-67, for use in treating a subject afflicted with glaucoma. 69. A pharmaceutical composition in unit dosage form, useful in treating a subject afflicted with glaucoma, which comprises an amount of laquinimod; which amount of said laquinimod in said composition is effective, upon administration to said subject of one or more of said unit dosage forms of said composition, to treat the subject. 70. A package comprising: a ) a pharmaceutical composition of any one of claims 48- 9 and b ) instruction for use of the pharmaceutical composition to treat a subject afflicted with glaucoma. 71. Laquinimod for the manufacture of a medicament for use in treating a subject afflicted glaucoma.