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Medications

Mild pain medications can reduce inflammation and pain when taken properly. Medications will not stop degeneration, but they will help with pain control.

Aspirin
Aspirin compounds are over-the-counter pain relievers that can help relieve minor pain and back ache. The main potential side effect of aspirin is the development of stomach problems, particularly ulcers with or without bleeding. You should not take aspirin if you are pregnant. In fact, you should not take any medication unless you have discussed it with your obstetrician.

NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)
NSAIDs include over-the-counter pain relievers such as ibuprofen or naproxen. These medications were once only available by prescription. NSAIDs are very effective in relieving the pain associated with muscle strain and inflammation. They block the inflammatory response in joints. However, be aware that NSAIDs can decrease renal function if you are an older patient. Excessive use can lead to kidney problems. Again, do not take them if you are pregnant.

Non-narcotic Prescription Pain Medication
Non-narcotic analgesics (the term analgesics means "pain relievers") address pain at the point of injury. Analgesics are ideal in the treatment of mild to moderate chronic pain. Tylenol and aspirin are the most widely used over-the-counter analgesics. Analgesics that require a prescription from the doctor include NSAIDs such as: carprofen, fenoprofen, ketoprofen, and sulindac. To reduce any side effects: do not lie down for 15 to 30 minutes after taking medication, avoid direct sunlight, wear protective clothing, and use sun block. Avoid using these medications if you are pregnant, have recurrent ulcers, or liver problems.

Pills

Narcotic Pain Medications
If you experience severe pain, your health provider might prescribe a narcotic pain medication such as codeine or morphine. Narcotics relieve pain by acting as a numbing anesthetic to the central nervous system. The strength and length of pain relief differs for each drug. Narcotics can cause related side effects such as nausea, vomiting, constipation, and sedation or drowsiness. These side effects are predictable and can often be prevented. Common preventative measures include: not taking sleeping aids or antidepressants in conjunction with narcotics, avoiding alcohol, increasing fluid intake, eating a high fiber diet, and using a fiber laxative or stool softener to treat constipation. Remember that narcotics can be addictive if used excessively or improperly.

Muscle Relaxants
If you are having muscle spasms, muscle relaxants can help relieve pain, but they are only shown to be marginally effective. They also have a significant risk of drowsiness and depression. Long-term use is not suggested; only three to four days is typically recommended.

Antidepressants
Back pain is actually a common symptom of depression and could be an indicator of its presence. Antidepressants can relieve emotional stress that leads to symptoms of back pain. An important fact to note - it seems that the same chemical reactions in the nerve cells that trigger depression also control the pain pathways in the brain. Some antidepressant medications seem to reduce pain, probably because they affect this chemical reaction in the nerve cells. Some types of antidepressants also make rather good sleeping medications. If you are having trouble sleeping due to your back pain, your doctor may prescribe an antidepressant to help you get back to a normal sleep routine. Antidepressants can have several side effects such as: drowsiness, loss of appetite, constipation, dry mouth, and fatigue.

Epidural Steroid Injections
An ESI can be used to relieve the pain of stenosis and irritated nerve roots, as well as to decrease inflammation. Injections can also help reduce swelling from a bulging or herniated disc. The steroid injections are a combination of cortisone (a powerful anti-inflammatory steroid) and a local anesthetic that are given through the back into the epidural space. Epidural steroid injections are not always successful in relieving symptoms of inflammation. They are used only when conservative treatments have failed.

Non-steroidal anti-inflammatory drugs (NSAIDs) have been used for 150 years in Europe, and probably for a great deal longer in the East, in the form of willow bark extract.

Nsaids
Traditional NSAIDS inhibit both COX-1 and COX-2, but two agents that selectively inhibit COX-2 thereby minimising GI toxicity have recently been introduced. The theory behind the COX-2 inhibitors is that if COX-2 can be selectively inhibited, while sparing COX-1, it may be possible to decrease acute inflammation and pain while sparing the complications in the GI tract, platelets and other tissues. Because COX-2 is also expressed constitutively in the brain, kidney, and uterus, these agents do not appear to be renally sparing, and like traditional NSAIDs, are associated with renal toxicity when used chronically.

Useful when given appropriately, examination of the chronic pain population indicates that a very high number of patients are intolerant to these drugs because of gastrointestinal or other side-effects. There are two possible hypotheses for this. Firstly, chronic pain sufferers tend to be somewhat hypochondriacal and intolerant of body symptoms in general and thus less tolerant of real or perceived side-effects when taking medication. The second is that there may be a sub-group of patients whose pain is not managed well early on. NSAIDs may produce side-effects, limiting their use. With no pain relief, the patient fails to exercise. This hampering of their rehabilitation because of inadequate analgesia may contribute significantly towards the chronicity.

Recently COX2 antagonists have come on the scene, but the first wave of these have been disappointing in the UK, in that the side-effect profile does not appear to be particularly better than the present drugs (Meloxicam, Etodolac). The newer drugs, Vioxx and Celebrex, are now available in the USA and Europe and will soon become available in the UK. Their arrival is awaited with eager anticipation, but the results may prove to be disappointing. The products may not be as side-effect free as they first seem.

The use of opioid drugs for the management of chronic non-malignant pain is fraught with difficulties, some real and some perceived. Morphine itself has tended not to be prescribed for chronic pain, because of a fear or stigma concerning Morphine. Physicians may fear dependence, tolerance and side-effects. There is a wide difference of opinion, which is still to be resolved; however, some patients can have their pain adequately controlled with opioids, without an unacceptable level of addiction problems. The potential risk of addiction remains a very real problem for a minority. Also, a significant number of patients with chronic pain complain of bothersome side-effects from medication. Mobility and distress must be monitored and benefits must accrue in both these parameters, as well as in reduction of pain.

In the UK and in the USA, traditionally most patients with chronic pain receive an opioid derivative such as Codeine, Dihydrocodeine or Dextropropoxyphene. In the past Pentazocine and Buprenorphine enjoyed a passing vogue but are now little used. Pentazocine proved to have unacceptable side-effects, and Buprenorphine, originally thought to be non-addictive, was shown to have addictive potential and since being classified as a controlled drug has enjoyed little popularity. Nefopam has limited efficacy and popularity, and Meptazinol is short-acting, and often associated with an unacceptable level of side-effects.

Recent work suggests that Codeine and Dihydrocodeine are merely pro drugs for Morphine, and exert their action through metabolism to this compound. Given that a significant number of the population do not have the metabolic pathway to facilitate this, it is not surprising that there is a significant failure rate to produce any analgesia at all and that patients getting analgesia seem to get limited relief-hence possibly the popularity of these preparations being compounded with Paracetamol.

There is good evidence that in some patients, much of the analgesic effect in these combined preparations lies with the Paracetamol itself, whilst many of the side-effects lie with the opioid.

Tramadol hydrochloride is an orally active, clinically effective, centrally-acting analgesic. It can produce analgesia that has been compared to Codeine or Dextropropoxyphene. It has been used in post-surgical pain, obstetric pain, cancer pain and chronic pain of mechanical and neurogenic origin. Analgesic tolerance is not a significant problem, and psychological dependence and euphoric effects are minimal. There are a significant number of patients in the chronic group who develop side-effects, but many of those who tolerate the drug get useful benefit in pain reduction. This slow-release formulation is an appropriate vehicle for chronic pain management.

Tramadol has an affinity, albeit relatively weak, for mu opioid receptors. It is also a neuronal uptake inhibitor. The monoamine neurotransmitters 5HT (Serotonin) and Noradrenaline (NA) are involved in the inhibition of spinal cord dorsal horn neurone responses to painful stimulation (i.e. closing the gate). Analgesia can result from activating the pain inhibitory pathways originating from higher CNS levels, and containing these neurotransmitters. Tramadol inhibits the uptake of 5HT and Noradrenaline but not Adenosine, Cyclic AMP, Dopamine, or Gaba.

Metanalysis by Moore and McQuay indicates an appropriate dose response curve for Tramadol, and suggests a reduced number needed to treat to show therapeutic efficacy as compared with Codeine, in doses of 75 to 150 mg. Nausea, vomiting and dizziness are greater than with Codeine, somnolence about the same and constipation much less. In the chronic pain situation nausea and vomiting are attenuated with usage, as is somnolence for both drugs, but constipation remains a particular problem with Codeine and Dihydrocodeine, and less of a problem with Tramadol.

Side-effects from Tramadol can be minimised by starting with a low dose and increasing gradually. There is evidence that this reduces the side-effects and improves tolerance. According to need, it can be started in a low dose of 50 mg daily or twice a day, and gradually titrated to reach 50 mg three times a day by day 3. Once a patient is established on a therapeutic dose, they can be put on the slow-release formulation to provide round-the-clock analgesia.