Paxil CR Drug Uses

Paxil is an agent in a newer class of antidepressant medication known as selective serotonin reuptake inhibitors (SSRIs). Depression and anxiety disorders might be caused by a chemical imbalance in the brain. One of these chemicals is serotonin, which helps send electrical signals from one nerve cell to another. In the process, serotonin is released from one nerve cell (the sender) and travels to the next (the receiver), where it is either absorbed or returns back to the original sender cell.

How Taken

Paxil comes as a tablet to take it orally. It is usually taken once daily and may be taken with or without food. Do not take more or less of it or take it more often than prescribed by your doctor. Continue to take Paxil even if you feel well. Do not stop taking Paxil without talking to your doctor, especially if you have taken large doses for a long time. Your doctor probably will want to decrease your dose gradually. This drug must be taken regularly for a few weeks before its full effect is felt.

Paxil CR Warnings/Precautions

Before taking Paxil, tell your doctor if you have liver disease, kidney disease, seizures or epilepsy, or a manic disorder or suicidal thoughts. You may not be able to take Paxil, or you may need a dosage adjustment or special monitoring during treatment if you have any of the conditions listed above. Paxil is in the FDA pregnancy category C. This means that it is not known whether it will be harmful to an unborn baby. Do not take Paxil without first talking to your doctor if you are pregnant or could become pregnant during treatment. Paxil passes into breast milk and may affect a nursing baby. Do not take Paxil without first talking to your doctor if you are breast-feeding a baby.

Paxil CR Missed Dose

Take the missed dose as soon as you remember it. However, if it is almost time for the next dose, skip the missed dose and continue your regular dosing schedule. Do not take a double dose to make up for a missed one.

Paxil CR Possible Side Effects

If you experience any of the following serious side effects, stop taking Paxil and contact your doctor immediately or seek emergency medical treatment: an allergic reaction (difficulty breathing; closing of the throat; swelling of the lips, tongue, or face; or hives); an irregular heartbeat or pulse; low blood pressure (dizziness, weakness); high blood pressure (severe headache, blurred vision); unusual bleeding or bruising; or fever or chills. Less serious side effects may be more likely to occur. Continue to take Paxil and talk to your doctor if you experience headache; tremor, nervousness, or anxiety; nausea, diarrhea, dry mouth, or changes in appetite or weight; sleepiness or insomnia; or decreased sex drive, impotence, or difficulty having an orgasm. Side effects other than those listed here may also occur. Talk to your doctor about any side effect that seems unusual or that is especially bothersome.

Paxil CR Storage

Store at controlled room temperature between 20-25°C (68-77°F).

Paxil CR Overdose

Seek emergency medical attention if an overdose is suspected. Symptoms of a Paxil overdose include nausea, vomiting, tremor, seizures, agitation, drowsiness, hyperactivity, and enlarged pupils.

More Information

Use caution when driving, operating machinery, or performing other hazardous activities. Paxil may cause dizziness or drowsiness. If you experience dizziness or drowsiness, avoid these activities. Use alcohol cautiously. Alcohol may increase drowsiness or dizziness while taking Paxil.

Disclaimer

This drug information is for your information purposes only, it is not intended that this information covers all uses, directions, drug interactions, precautions, or adverse effects of your medication. This is only general information, and should not be relied on for any purpose. It should not be construed as containing specific instructions for any particular patient. We disclaim all responsibility for the accuracy and reliability of this information, and/or any consequences arising from the use of this information, including damage or adverse consequences to persons or property, however such damages or consequences arise. No warranty, either expressed or implied, is made in regards to this information.

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A new study has revealed more about how the medication ketamine, when used experimentally for depression, relieves symptoms of the disorder in hours instead of the weeks or months it takes for current antidepressants to work. While ketamine itself probably won’t come into use as an antidepressant because of its side effects, the new finding moves scientists considerably closer to understanding how to develop faster-acting antidepressant medications — among the priorities of the National Institute of Mental Health (NIMH), part of the National Institutes of Health.
Ketamine blocks a receptor called NMDA on brain cells, an earlier NIMH study in humans had shown, but the new study in mice shows that this is an intermediate step. It turns out that blocking NMDA increases the activity of another receptor, AMPA, and that this boost in AMPA is crucial for ketamine’s rapid antidepressant actions. The study was reported online in Biological Psychiatry on July 23, by NIMH researchers Husseini K. Manji, MD, Guang Chen, MD, PhD, Carlos Zarate, MD, and colleagues.
“Our research is showing us how to develop medications that get at the biological roots of depression. This new finding is a major step toward learning how to improve treatment for the millions of Americans with this debilitating disorder; toward eliminating the weeks of suffering and uncertainty they have to endure while they wait for their medications to work,” said NIH Director Elias Zerhouni, M.D.
Almost 15 million American adults have a depressive disorder. During the long wait to begin feeling the effects of conventional medications, patients may worsen, raising the risk of suicide for some. Depressive disorders also affect children and adolescents.
By aiming new medications at more direct molecular targets, such as NMDA or AMPA, scientists may be able to bypass some of the steps through which current antidepressants indirectly exert their effects — a roundabout route that accounts for the long time it takes for patients to begin feeling better with the conventional medications.
While ketamine appears to achieve this, it is an unlikely candidate to become a new treatment for depression, because of the side effects it can cause in humans, including hallucinations. It is approved as an anesthetic by the Food and Drug Administration at much higher doses than those given in the study, but its use is limited because it may cause hallucinations during recovery from anesthesia.
Both NMDA and AMPA are receptors for the neurotransmitter glutamate, one of the chemical messengers that enable brain cells to communicate with each other. The glutamate system has been implicated in depression recently, leading to efforts to unravel its molecular machinery in search of abnormalities and of better targets for antidepressant medications.
This focus on the glutamate system is a departure from the thinking that led to currently available antidepressants, which are thought to relieve depression through a lengthy trickle-down process of biochemical reactions that affect the circuitry underlying depression.
The fact that NMDA and AMPA receptors are part of the glutamate system and that targeting them directly led to such rapid, sustained relief of depression-like behaviors in this study — and that a single dose of ketamine did the same in humans in the earlier study — suggests that they are probably the key targets for antidepressant medications.
“In any other illness of depression’s magnitude, patients aren’t expected to just accept that their treatments won’t start helping them for weeks or months. The value of our research on compounds like ketamine is that it tells us where to look for more precise targets for new kinds of medications that can close the gap,” said NIMH Director Thomas R. Insel, MD. “We’re making tremendous progress.”
To conduct the new study, researchers induced depression-like behaviors in mice; for example, the mice gave up after being forced to engage in hopeless tasks, such as prolonged swimming. A dose of ketamine reversed the depression-like behaviors for at least two weeks.
When the researchers gave the mice a substance that blocks the AMPA receptor beforehand, ketamine was not able to reverse the depression-like behaviors. The boost in AMPA thus appears to be a necessary ingredient for ketamine’s antidepressant effects.
In a related experiment, the scientists used two different compounds instead of ketamine to try to block just one part of the NMDA receptor, an even more precise target. These other compounds also reduced depressive behaviors, suggesting that it may be feasible to develop other fast-acting antidepressants without ketamine’s side effects.
“Today’s antidepressant medications eventually end up doing the same thing, but they go about it the long way around, with a lot of biochemical steps that take time. Now we’ve shown what the key targets are and that we can get at them rapidly,” said Zarate. “Ketamine probably can’t become the medication of choice, but this research is leading to some very real possibilities for a whole new generation of antidepressant medications.”

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