Tiagabine may induce seizures in those without epilepsy, particularly if they are taking another drug which lowers the seizure threshold. There may be an increased risk of psychosis with tiagabine treatment, although data is mixed and inconclusive. Tiagabine can also reportedly interfere with visual color perception. Warning
CNS depression
Dermatologic reactions
Generalized weakness
Ophthalmic effects
Suicidal ideation

Overdose
Tiagabine overdose can produce neurological symptoms such as lethargy, single or multiple seizures, status epilepticus, coma, confusion, agitation, tremors, dizziness, dystonias/abnormal posturing, and hallucinations, as well as respiratory depression, tachycardia, hypertension, and hypotension. Overdose may be fatal especially if the victim presents with severe respiratory depression and/or unresponsiveness. Pharmacology
Tiagabine increases the level of γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system, by blocking the GABA transporter 1 (GAT-1), and hence is classified as a GABA reuptake inhibitor (GRI). Pharmacodynamics
Tiagabine is primarily used as an anticonvulsant in the treatment of epilepsy as a supplement. Although the exact mechanism by which Tiagabine exerts its antiseizure effect is unknown, it is thought to be related to its ability to increase the activity of gamma aminobutyric acid (GABA), the central nervous systems major inhibitory neurotransmitter. Tiagabine attaches to the GABA uptake carriers recognition sites. Tiagabine is thought to block GABA uptake into presynaptic neurons as a result of this action, allowing more GABA to be available for receptor binding on the surfaces of post-synaptic cells.
In humans, mebendazole (200–400 mg three times a day for three days) or albendazole (400 mg twice a day for 8–14 days) is given to treat trichinosis. These drugs prevent newly hatched larvae from developing, but should not be given to pregnant women or children under two years of age.Medical references from the 1940s described no specific treatment for trichinosis at the time, but intravenous injection of calcium salts was found to be useful in managing symptoms related to severe toxemia from the infection.. Secondary treatment
After infection, steroids, such as prednisone, may be used to relieve muscle pain associated with larval migration. Vaccine research
Researchers trying to develop a vaccine for Trichinella have tried using either "larval extracts, excretory–secretory antigen, DNA, or recombinant antigen protein." Currently, no marketable vaccine is available for trichinosis, but experimental mouse studies have suggested possibilities. In one study, microwaved Trichinella larvae were used to immunize mice (orally or intraperitoneally), which were subsequently infected. Depending on the dosage and frequency of immunization, results ranged from a decreased larval count to complete protection from trichinosis. Another study used extracts and excretory–secretory products from first-stage larvae to produce an oral vaccine. To prevent gastric acids from dissolving the antigens before reaching the small intestine, scientists encapsulated the antigens in microcapsules. This vaccine significantly increased CD4+ cell levels, and increased antigen-specific serum IgGq and IgA, resulting in a statistically significant reduction in the average number of adult worms in the small intestines of mice.