This research has been performed on mice with the gene for producing cystatin B removed, to provide a similar set of symptoms to individuals with ULD. The mechanism currently supported by research is very similar to another theory of epilepsy progression known as kindling. Onset
Current research links cystatin B to production of inhibitory neurons known as GABAergic neurons. It has shown that a lack of cystatin B due to a mutation of the CSTB gene leads to a decrease in the number of inhibitory neurons, and this lack of inhibition makes the cells in the brain, particularly the hippocampus, more excitable. It is hypothesized that this increase in excitability is what causes the myoclonic jerks and tonic-clonic seizures in patients with ULD. Progression
Research also gives evidence to support the idea that cystatin B may be a type of "protecting" molecule in the brain. Normally, after a seizure, the presence of cystatin B prevents the neurons from dying due to toxic levels of neurotransmitters. Studies suggest that the absence of cystatin B leads to the death of affected neurons, leading to a damaged portion of the brain. This damage coupled with the increased excitability of the cells then leads to more damage, which is what makes Unverricht–Lundborg disease progressive. Diagnosis
The only currently available method to diagnose Unverricht–Lundborg disease is a genetic test to check for the presence of the mutated cystatin B gene. If this gene is present in an individual suspected of having the disease, it can be confirmed.
Due to the abundance of readily-bound erythrocytes and minimal known metabolism, Brinzolamides whole blood half-life is very long (111 days). Metabolism
While definitive sites of metabolism have not been firmly established, there are several metabolites worthy of note. N-Desethylbrinzolamide is an active metabolite of the parent compound, and thus exhibits carbonic anhydrase inhibitory activity (largely carbonic anhydrase-I, when in the presence of Brinzolamide) and also accumulates in the erythrocytes. However, Brinzolamides other known metabolites (N-Desmethoxypropylbrinzolamide and O-Desmethylbrinzolamide) either have no activity or their activity is currently unknown. Excretion
Brinzolamide is excreted primarily unchanged (60%) in the urine, although the renal clearance rate has not been definitively determined. N-Desethylbrinzolamide is also found in the urine along with lower concentrations of the inactive metabolites, N-Desmethoxypropylbrinzolamide and O-Desmethylbrinzolamide; exact levels have not been definitively determined. Cautions
Side effects
Common, but mild: blurred vision; bitter, sour, or unusual taste; itching, pain, watering, or dryness of the eyes; feeling that something is in the eye; headache; runny nose
Rare, but serious: fast or irregular heartbeat; fainting; skin rash, hives, or itching; severe eye irritation, redness, or swelling; swelling in the face, lips, or throat; wheezing or trouble breathing

Precautions
Hypersensitivity to other sulfonamides
Acute angle-closure glaucoma
Concomitant administration of oral carbonic anhydrase inhibitors
Moderate-to-severe chronic kidney disease or liver disease

Combinations
With timolol
The combination of brinzolamide with timolol is marketed under the trade name Azarga. This combination may be more effective than either medication alone. With brimonidine
The combination of brinzolamide with brimonidine is marketed under the trade name Simbrinza. This combination may be more effective than either medication alone. References
Further reading
External links
"Brinzolamide".