Treatment optic nerve

A 65-year-old male complains of losing his vision Retinal examination reveals optic nerve cupping. Peripheral vision loss is observed on visual field tests, and his intraocular pressure is increased. Following treatment with a drug, he has improved visual acuity and decreased intraocular pressure. 

Genetic evidence supports the importance of coordinated expression and distributions of a2 or a3 Na+/K+ pump isoforms with the Na+/Ca2+ exchanger (NCX) and Ca2+ pumps to function in excitable and contractile cells deletion of one copy of the a2 Na+/K+ pump gene in mice leads to increased contractile force in cardiac and skeletal muscle while deletion of one copy of the al gene leads to reduction of contractile force [25]. In rat optic nerve astrocytes, deletion of the a2 gene or ouabain treatment of cells expressing a2 leads to increased capacitative calcium entrance responses, which reflect a decreased ability to rapidly remove cytosolic Ca2+ [26]. 

Ocular Effects. Histopathological examination of the eye and optic nerve after intermediate-duration inhalation exposure revealed no treatment-related lesions in male Sprague-Dawley rats exposed to 500 ppm M-hexanc 22 hours a day for 6 months (IRDC 1981) or in Fischer 344 rats of both sexes exposed to up to 10,000 ppm for 6 hours a day, 5 days a week for 13 weeks (Cavender et al. 1984). Effects caused by direct contact of -hexane vapor with the eye are discussed in Section 2.2.3 (Dermal Exposure). 

Strychnine, a very poisonous alkaloid to animals, binds to glycine receptors. Applications of strychnine can be considered only in clinical doses. Their purpose is to activate neurotransmitters in the spinal cord, which is generally suppressed by glycine. Strychnine competes only with glycine in the receptor. This alkaloid may be used to stimulate respiration and circulation in cases of physical weakness. Moreover, strychnine products are used in the treatment of eye and optic nerve disorders. Larger doses are lethal. 

Methanol is metabolized to formaldehyde and formic acid, which injure the retinal cells and optic nerves, and lead to severe acidosis. Treatment delay increases morbidity. Thus, early recognition and management are crucial. Clinical features emerge up to 36 hours after ingestion. Nausea, vomiting, abdominal pain, headache, dizziness, paraesthesia, blurred vision, and diminished visual activity may occur, and coma supervenes. Dilated, unreactive, pupils predict permanent blindness. 

A 64-year-old woman was included in a randomized, double-blind trial of drugs used in the treatment of ocular hypertension. After 3 months, examination of the optic nerve showed bilateral edema. She had been using latanoprost 0.0005% eye-drops at night to both eyes. Latanoprost was withdrawn and the disc edema resolved at 1 week. 

This hypothesis is further supported by studies reporting that intravitreous administration of IGF-I or BDNF prevents RGCs death in axotomized eye by activating Akt (Klocker et al., 2000 Nakazawa et al., 2002) and treatment with PI3-K inhibitors increases the loss of RGCs after optic nerve clamping (Nakazawa et al., 2003) and IOP elevation (Huang et al., 2008). 

In two experimental models of ischaemia, it has been shown that HU-211 significantly increases cell survival. It was seen that after forebrain ischaemia produced by 20 min of carotid occlusion, the number of viable neurons in the hippocampal CA1 region of HU-211-treated rats was significantly higher than in controls. The same effect was seen in gerbils after 10 min of bilateral carotid occlusion on treatment with HU-211 [197, 198]. A related effect has been noted after rat optic nerve crush injury. Administration of HU-211 improved recovery of the nerve, with the visual evoked response amplitude increasing significantly [199],... 

Deficiency of cyanocobalamin, or vitamin B12, can result in reduced visual acuity secondary to optic nerve dysfunction. Causes range from malabsorption to alcohol abuse.Treatment is with oral (1,000 to 2,000 meg daily)... 

The treatment of choice for leukemia is chemotherapy, but because of the blood-brain barrier cytotoxic drugs are ineffective in treating leukemic optic neuropathy. Radiotherapy is the preferred treatment for the optic neittopathy because the optic nerve is relatively insensitive to radiotherapy but the leukemic cells are very radiosensitive. Chemotherapy and local irradiation have not shown promise in the treatment of lymphomatous optic neittopathy Meningiomas, likewise, are insensitive to chemotherapy and irradiation and require surgical excision. 

No medical or snrgical treatment is effective for NAION. Optic nerve sheath decompression surgery has been shown to be ineffective and may be harmful in the treatment of NAION. Up to 43% of NAION patients experience spontaneons recovery of vision by three or more lines of Snellen acnity at 6 months. 

Posterior segment disease is unaffected by topical therapy and minimally requires periorbital administration of corticosteroids systemic therapy is needed if the condition is bilateral or sight threatening. Indications for posterior segment treatment include significant vision loss from macular edema or severe vitreitis, choroidal granulomas, optic nerve involvement, or retinal neovascularization. Conversely, if vision remains at 20/40 or better and there are no complicating factors, systemic... 

Direct interstitial infusion has been applied to the treatment of patients with advanced Parkinson s disease, and the design of the protocol is instructive (29). Motor control is severely compromised in these patients because degradation of the substantia nigra ultimately results in massive overinhibition of the motor cortex by the globus pallidus interna (Gpi). One therapeutic approach is to thermally ablate a portion of the Gpi to reduce this inhibition and restore freedom of movement. However, thermal ablation also risks destroying the optic nerve that forms the floor of the Gpi structure. Hence, a chemical means of destroying the Gpi has been evaluated as a potentially more selective alternative. 

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