lamotrigine has been researched along with Optic Nerve Diseases in 2 studies
Optic Nerve Diseases: Conditions which produce injury or dysfunction of the second cranial or optic nerve, which is generally considered a component of the central nervous system. Damage to optic nerve fibers may occur at or near their origin in the retina, at the optic disk, or in the nerve, optic chiasm, optic tract, or lateral geniculate nuclei. Clinical manifestations may include decreased visual acuity and contrast sensitivity, impaired color vision, and an afferent pupillary defect.
| Excerpt | Relevance | Reference |
|---|---|---|
| " We evaluated the neuroprotective effects of lamotrigine, a Nav blocker, in the acute and chronic rat ocular hypertension models." | 7.79 | Functional and structural evaluation of lamotrigine treatment in rat models of acute and chronic ocular hypertension. ( Bähr, M; Hein, K; Könnecke, B; Levkovitch-Verbin, H; Ofri, R; Sandalon, S; Sättler, MB; Simons, M, 2013) |
| "In other animals with ocular hypertension, the optic nerves were examined by immunohistochemistry for the expression of the inducible form of nitric oxide synthase (iNOS) at 7 and 28 days." | 5.38 | Lamotrigine monotherapy does not provide protection against the loss of optic nerve axons in a rat model of ocular hypertension. ( Berry, D; Bull, ND; Hyatt, AJ; Marina, N; Martin, KR; Sajic, M; Smith, KJ, 2012) |
| " We evaluated the neuroprotective effects of lamotrigine, a Nav blocker, in the acute and chronic rat ocular hypertension models." | 3.79 | Functional and structural evaluation of lamotrigine treatment in rat models of acute and chronic ocular hypertension. ( Bähr, M; Hein, K; Könnecke, B; Levkovitch-Verbin, H; Ofri, R; Sandalon, S; Sättler, MB; Simons, M, 2013) |
| "In other animals with ocular hypertension, the optic nerves were examined by immunohistochemistry for the expression of the inducible form of nitric oxide synthase (iNOS) at 7 and 28 days." | 1.38 | Lamotrigine monotherapy does not provide protection against the loss of optic nerve axons in a rat model of ocular hypertension. ( Berry, D; Bull, ND; Hyatt, AJ; Marina, N; Martin, KR; Sajic, M; Smith, KJ, 2012) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 2 (100.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Sandalon, S | 1 |
| Könnecke, B | 1 |
| Levkovitch-Verbin, H | 1 |
| Simons, M | 1 |
| Hein, K | 1 |
| Sättler, MB | 1 |
| Bähr, M | 1 |
| Ofri, R | 1 |
| Marina, N | 1 |
| Sajic, M | 1 |
| Bull, ND | 1 |
| Hyatt, AJ | 1 |
| Berry, D | 1 |
| Smith, KJ | 1 |
| Martin, KR | 1 |
2 other studies available for lamotrigine and Optic Nerve Diseases
| Article | Year |
|---|---|
Functional and structural evaluation of lamotrigine treatment in rat models of acute and chronic ocular hypertension.
Topics: Acute Disease; Administration, Topical; Animals; Axons; Chronic Disease; Disease Models, Animal; Ele | 2013 |
Lamotrigine monotherapy does not provide protection against the loss of optic nerve axons in a rat model of ocular hypertension.
Topics: Animals; Axons; Calcium Channel Blockers; Cell Count; Chromatography, High Pressure Liquid; Disease | 2012 |