The search for a new anti-migraine drug was started by Glaxo in 1972. In the 1960s, studies showed that vasoconstriction from 5-HT, ergotamine and nor-adrenaline could reduce migraine attacks. Research also showed that platelet 5-HT level reduces during migraine attacks. Many side-effects were associated with the use of 5-HT as a drug and then scientists started research on the receptors of 5-HT in order to discover and develop a more specific agonist for 5-HT receptors. Research on the 5-HT receptors and their effect led to discovery of several types and subtypes of 5-HT. AH24167 showed a vasodilatory effect instead of vasoconstrictory due to the agonist effect on another type of 5-HT receptors later assigned the name 5-HT7. AH25086 was the second compound developed and showed a vasoconstrictory effect but was not released as a drug due to low per oral bioavailability. …show more content…
Clinical trials with subcutaneous sumatriptan showed that 70–80 per cent of patients had reduced pain by one hour after treatment. Sumatriptan was launched in the subcutaneous formulation in 1991. In subsequent studies of oral sumatriptan 100mg–300mg, around 70 % of patients responded to treatment within two hours of administration and this led to the launch of 100mg sumatriptan tablets. Sumatriptan was first launched in the Netherlands in 1991 and became available in the USA during 1993. In year 2008, Treximet, a combination of sumatriptan and naproxen was approved by US-FDA for the treatment of migraine attacks. This combination has shown better efficacy in treating migraine attacks over other anti-migraine
Patient was in the ER room when first seen. PT was with her family members and family states that she speaks little English and that she has had abdominal pain for the past day along with bloody stools. Family states that she is on calcium supplements and no other medications. Last oral intake is 24 hours ago. Family states no known past medical history. Pt is in the hospital bed in the fetal position and towards the right side. Patient's airway is clear and breathing is normal. Skin is warm and dry. Patent is AAOx4. Assessment of head, neck, and chest show no signs of deformities. Abdominal area not assessed due to severe pain. Back is without deformity. The upper extremity shows no sign of deformities or trauma. The lower extremity shows
In the movie, Whale Rider, there are great examples of Joseph Campbell’s article, Four Functions of Myth, which are: mystical myth, cosmological myth, social myth, and psychological myth. In the film, Whale Rider, Pai discovers her sense of self as she reinvents the Maori tribe’s creation myth to save the dying culture.
Escitalopram was discovered in 1997 and submitted to the Food and Drug Administration for approval in the United States of America in 2001. It was approved for the treatment of major depressive disorder in 2002 and for the treatment of generalized anxiety disorder in
Hofmann worked for Bayer, which then named acetylsalicylic acid compound aspirin. Aspirin became commercially available in 1899 and today it is estimated that over a trillion aspirin tablets have been consumed by those in need of its curative effects.
“The first television war” is a common term given to the Vietnam War - the first war where American families were able to see the horrors their sons were sent into. Consequently, the draft taking place was met with much resistance, and upon the boys’ return, the question of mental health was quickly raised. The families had seen for themselves, the carnage and bloodshed. If simply witnessing the horrors through a screen left people scarred, what would the effects of actually participating in the war do to a person? Once Vietnam soldiers returned home from war, the carnage witnessed led many to experience PTSD (both in the immediate and long term , which led to a broad range studies on PTSD specifically in these veterans immediately after
The new drug blocks the sodium channel 1.7 according to the channel's level of activity - the more active the channel is the stronger will be the drugs hampering effect. Current drugs, in comparison, block the sodium channels without accounting for the activity level, which results in unecessary side effects. Sodium channels are located in nerve cell membranes. Their activation triggers the sensation of pain, the severity of which is proportional to the channels' activity level. According to the Zurich researchers, trigeminal neuralgia is believed to stem from a nerve deficiency or damage at the base of the skull. Given that local injections cannot reach this region, drugs are the first line of defense against the
This was the simplest way to obtain all the drug information needed from the package insert. The approved indication for this drug is PAH for patients in WHO functional classes II-III. Treprostinil is classified as a prostanoid drug meaning that its mechanism of action causes vasodilation of arterioles, which halts proliferation of smooth muscle cells and platelet aggregation. For patients without hepatic impairment, treprostanil is started at a dose of 0.25 mg BID or 0.125 mg TID. Every 3-4 days the dose is increased by 0.25-0.5 mg BID or 0.125 mg TID. The goal is to titrate up to the maximal tolerated dose. The use of treprostinil is contraindicated in patients with moderate to severe hepatic impairment (Child Pugh Class B and C), but can be used for those with mild impairment (Child Pugh Class A). In this case, the initial dose would be 0.125 mg BID and is increased by 0.125 mg BID every 3-4 days as the patient can tolerate. Oral treprostinil has a 17% bioavailability, with maximum concentration occurring approximately 4 to 6 hours after administration. The absorption of this drug is increased with the administration of food. The AUC increased by 49% and the Cmax by 13% following a meal in healthy participants. Also, treprostinil is highly protein bound. The drug is mainly hepatically metabolized by enzyme CYP2C8 and is excreted mostly as metabolites and very little as the parent drug. Treprostinil has drug interactions with anti-hypertensive medications due to risk of hypotension and CYP2C8 inhibitors. Common adverse effects include: headache, diarrhea, nausea and flushing. Rare adverse drug reactions include: hypokalemia, pain in jaw and abdominal discomfort. Precautions and warnings are an increased risk of bleeding, rebound PAH symptoms after sudden discontinuation, increased drug release when taken with alcohol, and aggravation of
After the successful synthesis, studies on Piracetam were done from all around the world to focus on specific aspects such as to improve memories and the neuroprotection on patients with the Alzheimer’s disease. These studies expanded to other racetams such as Aniracetam and Oxiracetam. Aniracetam was developed by Hoffman-La Roche in 1970’s which contributes to the neurotransmission by activating the Acetylcholine receptors. Oxiracetam was developed in 1993. Its main goal is to improve the capacity to process information. Racetams were revolutionary because there are no side effects and they combine both physiological and medical
Eicosapentaenoyl serotonin is a hybrid molecule patterned after arachidonoyl serotonin. Arachidonoyl serotonin is an inhibitor of fatty acid amide hydrolase (FAAH) and also acts as an antagonist of transient receptor potential vanilloid-type 1 (TRPV1) channels. Arachidonoyl serotonin is analgesic, reducing both acute and chronic peripheral pain in rodents [1, 2]. The effects of replacement the arachidonoyl portion with eicosapentaenoic acid have not been investigated. Replacement of arachidonate with saturated 11- or 12-carbon fatty acids generated compounds that potently inhibited capsaicin-induced TRPV1 channel activation with an IC50 of 0.76 μM. This compound showed no effects on wblocking FAAH-mediated hydrolysis of arachidonoyl ethanolamide
Using rat models of neuropathic pain, Nav 1.7 selective blockers have been seen to be successful in inhibiting Nav 1.7 activity (4).
Classification can be difficult, however, due to overlapping effects. Sicilian Gambit, can more accurately show receptor blocking properties, but is very complex and hard to memorize. Due to those factors the Vaughan-Williams classification is used (Homound, 2008). The Vaughan-Williams classification has five levels. Class I slow electrical conductions in the heart by sodium channel blockers. Class II are beta-blockers, which reduce the transmission of impulses within conduction by blocking sympathetic nervous system stimulation. Class III agents prolong the repolarization of the cell membrane by blocking the potassium channels. Class IV is calcium-channel blockers. They reduce the movement of ions during the calls action potentials. And lastly class V are variable mechanisms, an example of this would magnesium sulfate. (Levine) (www.drugs.com). They can also be classified clinically by agents that work on ventricular arrhythmias and supraventricular arrhythmias. Ventricular arrhythmias tend to be more serious and are treated with medications like lidocaine and moricizine. Supraventricular arrhythmias are less serious and may not even require treatment
Many genetic factors are also clearly an indicative of the susceptibility to migraine headaches. While the exact mechanism remains uncertain, it is thought that migraines are caused by genetic abnormalities that cause hyper-excitability of the nervous system. The nerve terminals release neurotransmitters such as substance P, neurokinin A (NKA), and calcitonin gene-related peptide (CGRP), which then binds to the receptors on intracranial blood vessels, causing vasodilation, mast cell degranulation, increased vascular permeability and blood vessel edema, plasma protein extravasation, and sterile inflammation. The cranial nerves are then reactivated causing the pain experienced during a migraine.
Jae Y. Choe, PhD., Drug action and interactions: antihistaminic drugs. Unites States: McGriw Hill Medical; 1937, p. 93-94.
Additionally, there is no specific cure for migraine headaches. In addition, the goal in treating migraines is to treat migraines symptoms. Also, migraines can be treated with amitriptyline or venlafaxine. Furthermore, a migraine can be treated with blood pressure medicines such as propanolol. Researchers have also proven that migraines can be treated with seizure medicines such as valproic acid. (http://www.sciencedaily.com/news). In addition, when I read that you can treat a migraine with seizure medications, I thought that research finding was interesting to be aware of. Also, researchers stated that you could treat a
Throazine, other major tranquilizers developed 1952 - The French psychiatrists Jean Delay and Pierre Deniker report that Thorazine ® calms hospitalized chronic schizophrenic patients without causing clinically significant depression. The drug is called 'hibernotherapie' because patients became quiet, like