The Chemical Structure Of Pregabalin

Treatment for epilepsy is often focused on controlling the seizures with the least amount of medication as possible. Antiepileptic drugs (AEDs) are the class used to accomplish this. Some of the AEDs that are used most often are Clonazepam, Diazepam, Divalproex, Gabapentin, and Phenytoin. The most common side effects of these medications include nausea, vomiting, sedation, fatigue, and lethargy. (Kwan,1; Benbadis, 3-5; Huethers,637)

Action: It action is widespread. It’s same as that of phenytoin, although effects on GABA and calcium channels also makes this drug similar to benzodiazepines and succinimides.

Gabapentinoids are analogues of gamma-aminobutyric acid (GABA). They bind to the α2δ subunit of the calcium channels on neurons. Both of them have a relatively benign side effect profile, lack significant drug interactions, are not liver metabolized, and are renally excreted. Pregabalin has quicker absorption and higher absolute bioavailability compared to gabapentin.1

These medications have evolved and changed due to availability in the past few years. Cost has also had an impact on what medications are available to a dying patient. A patient self-administers an oral liquid suspension or a powdered mixed with a soft food such as applesauce. The mix of medications include barbiturates, chloral hydrate, and morphine which are compounded into a single dose prescription to facilitate death. Premedication is required prior to taking this final dose. The most common barbiturates are phenobarbital, pentobarbital or secobarbital. Phenobarbital is the longest acting and is typically used for seizures. Pentobarbital and secobarbital are used to sedate prior to surgery and are not as long acting as phenobarbital. Barbiturates effect the central nervous system. They are classified by their how long they take to effect and their duration of action. Barbiturates increase GABA (gaba amino-butyric acid) neurotransmissions in the brain. The increase in GABA causes drowsiness. They are highly addictive, and patients may become tolerant. The addiction is not an issue when a patient has reached this stage and does not need to be a concern. More importantly, if they have used them during the disease process as a sleep aid the patient may have built a tolerance and would require a higher dosage to be effective. Barbiturates do not provide pain relief, to provide pain relief a patient would need to reach a dose high enough to cause a comatose state. Chloral hydrate is a sleep aid or tranquilizer prior to surgery. This medication is quick

2. What would be the expected outcome when a patient is given gamma-aminobutyric acid? What is this medication prescribed for? What side effects would we teach about? GABA Is a neurotransmitter that helps send messages between the brain and the nervous system. GABA is a mediator of anxiety level therefore it reduces anxiety by suppressing the circuitry in the brain that causes anxiety.

It is hypothesized that dysregulation at the presynaptic terminals can impact functionality at post-synaptic terminals and alter dopamine and glutamate levels (Egbujo et al., 2016). This impact on dopamine and glutamate could be the precursor to the altered functional connectivity seen in schizophrenia (Egbujo et al., 2016). The molecular processes that underlie this process include presynaptic SNARE proteins, synaptic membrane proteins, synapsins, syntaxin-1, synaptobrevin, and complexins (Egbujo et al., 2016). In many cases, these proteins are under or over expressed in certain areas of the brain crucial to schizophrenia (Egbujo et al., 2016). The overall mechanism operating efficiently would involve neurotransmitter recruitment and concentration within vesicles, targeting the pooled vesicles to the presynaptic terminal, and vesicle exocytosis, endocytosis, and recycling (Egbujo et al., 2016). The previously mentioned proteins play a significant role in this process. In my novel medication, I would include a unique chemical property that increased or decreased synaptic efficiency based on under or overexpression of these crucial pre-synaptic proteins. This would allow dopamine and glutamate levels to return to appropriate levels and hopefully allay symptoms of schizophrenia.

Gamma-Aminobutyric acid commonly referred to as GABA, and glutamate make up around 80 percent of the neurotransmitters found in brain. GABA dampens the activity in the brain while

Anticonvulsants main domains consist of treating seizures and bipolar disorder. Many researchers believe that anticonvulsants increase concentration of the neurotransmitter GABBA. Valproate, Carbamazepine, Lamotrigine, and Gabapentin are the main anticonvulsants used to treat the disorder.

Pregabalin is an antiepileptic agent, which acts by reducing calcium inpouring in neuronal cells. As a results, this decrease the release of some neurotransmitters involved in pain processing (Mease, 2011). Pregabalin is one of the most effective drugs to treat fibromyalgia. However, there are many side effects associated with it. These side effects are drowsiness, dizziness, dry mouth, constipation, difficulty concentrating, swollen arms, and legs (Mease, 2011). Duloxotine is also used to treat fibromyalgia. It is SNRI, serotonin- norepinephrine reuptake inhibitor. This medication acts by inhibiting the reuptake of serotonin and norepinephrine, which modulates the sesation of pain (Mease, 2011). Milnacipran a SNRI, acts in the same way. Some side effects of Duloxotine and Milnacipran are nausea vomiting, dizziness, drowsiness, headaches, hot flashes, and weight changes (Mease, 2011). Nevertheless, the side effects of these drugs. These drugs have had documented success in the treatment of fibromyalgia. As a matter of fact, a 12-month study conducted by researchers, showed the responses of a research group to Pregabalin, Duloxotine, and Milnacipran. Overall, Pregabalin was the most successful in the treatment of fibromyalgia. Overall, the study revealed that over a 12-month period 50% of the research group have had a significant reduction in pain, while

GABA is one of the oldest-known neurotransmitters, is an inhibitory brain chemical. Ambien allows more of the calming chemical to flood brain synapses — and the brain is littered with GABA receptors. It inhibits the reward pathway.

The second neurotransmitter family includes amino acids, compounds that contain both an amino group (NH2) and a carboxylic acid group (COOH) and which are also the building blocks of peptides and proteins. The amino acids known to serve as neurotransmitters are glycine, glutamic and aspartic acids, all present in all proteins, and gamma-amino butyric acid (GABA), produced only in brain neurons. Glutamic acid and GABA are the most abundant neurotransmitters within the central nervous system, particularly in the cerebral cortex; glutamic acid tends to be excitatory and GABA inhibitory. Aspartic acid and glycine subserve these functions in the spinal cord (Cooper, Bloom, and Roth 1996).

There have been studies conducted that show that targeting melatonin receptors may be a novel way of reducing the threshold of seizure propensity. Currently, progabide is an established drug that is used to control epileptic seizures. However, there are no studies conducted that combine both melatonin agonists and GABA agonists together to treat epileptic seizures. Our results showed that there was a decrease in seizure propensity when treating the mice with melatonin and GABA agonists, however, there was an even significant decrease in seizure propensity when these two treatments were combined together. The two-way ANOVA test also revealed that treatment and seizure propensity had a significant difference that was

Benzodiazepine receptors are linked mainly to γ amino butyric acid (GABA) receptors, which sensitize benzodiazepine receptors to the neurotransmitter GABA, the most prominent inhibitory neurotransmitter in the central nervous system.

Lorazepam binds to an allosteric site on GABA-A receptors, which are pentameric ionotropic receptors in the CNS. Binding potentiates the effects of the inhibitory neurotransmitter GABA, which upon binding opens the chloride channel in the receptor, allowing chloride influx and causing hyperpolerization of the neuron.

Anticonvulsants have an edge with rapid-cycling and mixed mood states (e.g. depression with racing thoughts). Except for gabapentin (Neurontin) and lamotrigine (Lamictal), they require blood tests. Carbamazepine (Tegretol) is monitored with blood levels; also CBC, platelets and liver function tests. Valproate (Depakote) requires CBC, platelet count and liver function tests; blood levels may be helpful. Lamotrigine (Lamictal) requires caution because of its association with a rare but dangerous skin rash (exfoliative dermatitis); risk can be minimized by starting with low doses and increasing gradually. Use lower doses with medications that slow lamotrigine metabolism (e.g. valproate). Gabapentin is generally safe and does not require blood tests.