Gabapentin is better Analgesic than Tramadol

gabapentin

traditional calcium channel blockers . Gabapentin is the firs pharmacological agent described to act at this site . Inhibition of the calcium channel would allow the reducticn of transmitter . release essential to the action of Crabapentin .

Gabapentin is eliminated almost exclusively via the kidneys with no metabolism. Dosing therefore must be adjusted in renal failure . It does not bind to plasma proteins, does not induce hepatic enzymes and therefore , unlike standard anticonvulsants, it has little interaction with other drugs such as oral contraceptives or H-2 blockers.

The uptake of gabapentin from the gut is dose dependent not dose related which suggests the involvement of a saturable transport site. Bioavailability therefore varies with dose from 74% at 100 mg dose to 36% at 1600 mg.

The reported side effect profile is considerable with somnolence, ataxia, dizziness and nystagmus as the most common adverse effects. When gabapentin was studied as an add-on therapy in seizure prone patients had a 75% adverse effect profile compared to placebo but one must keep in mind that the patients were concurrently taking other high side effect medications such as carbamazepine.

Most side effects are transient and do not require cessation of drug in most patients. Gabapentin has been reported to cause pancreatic acinar tumors in rats fed a large dose for a prolonged period . On analysis of all the animal data it has been concluded that gabapentin at therapeutic doses has low carcinogenic risk in humans.

The suggested dosing scheme is to start with 100mg at night and advance to 100 mg BID then TID over 2 – 3day intervals. From this point on one can increase by 100 mg in each dosing interval, as doses increase one can increase to 300 mg capsules. The serum half life is relatively short at 6-8 hours therefore it must be dosed on at least a Q8H schedule .

Gabapentin is available in 100, 300 and 400mg capsules. Doses can be increased ua to 3000 to even 6000 mg per day with minimal side effects. After the initial dosing regimen. One must consider increasing the number of doses to avoid the reduced bioavailability found with large single doses .

At this time gabapentin has no proven efficacy as an analgesic but many anecdotal reports of erncacy in neuropathic pain states and the relatively high safety profile make it attractive for

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can also occur 7 – 10 % of European and African derived populations can be deficient in CYP2D6 whereas Oriental and Middle Eastern populations have less than i % deficiency.

Tramadol has several advantages as an analgesic including the lack of gastric irritation or organ toxicity, good safety profile in elderly patients (at a reduced total dose). The non scheduled status of trmadol is important for consultants in pain management to provide an analgesic to the patient that the referring physician will be comfortable prescribing.

Tramadol has been shown to be effective for pain associated with osteoarthritis in two U .S . studies. Tramadol is as effective as ibuprofen for stable pain and more effective than placebo for breakthrough pain when added to stable NSAID. Tramadol is also effective in moderate and severe cancer pain with less sedation and constipation compared to morphine and no signs of respiratory depression.

In consideration that up to 10% of cancer patients may have an enzyme deficiency preventing the activation of codeine t amadol would seem to be a better choice for step two of the analgesic ladder.

Tramadol fills a niche for an analgesic between NSAIDs and opioids for aching musculoskeletal pain. This is especially important as an alternative for patients with a sensitivityto the NSAID gastric and renal adverse effects. Tramadol can also play a role as first line therapy for moderate neuropathic pain associated with diabetic neuropathy or postherpetic neuralgia to avoid the side effects of tricyclic agents. Current clinical protocols include a placebo controlled trial of Tramadol in painful diabetic neuropathy, a NSAiD sparing effect in osteoarthritis pain, analgesic effect in chronic low back pain, and a placebo controlled trial in fibromyalgia.

Several concerns have been raised regarding trmadol including seizure potential and abuse potential. The seizure potential appears to be real but low in patients treated with tramadol. To date Qut of approximately 8 million prescriptions there have been less than 200 cases of seizure noted. This is lower than the predicted spontaneous seizure rate but underreporting must considered. When the seizures have been examined over half can be attributed to excess dose (> seizure disorder or susceptibility (i .e . head 100mg per dose or > 400 mg per day), preexisting injury) or concomitant use of other seizure threshold lowering drugs (i.e. tricyclic agents, SSRIs and certain opiates). Many cases however are not readily attributable to a known risk factor. Some of these may represent deficiencies in the cytochrome P450 enzyme responsible for metabolizing tramadoI to the M1 metabolite .

 

When all available data is examined Lramadol used in the recommended dose range does not appear to increase seizure potential in humans.
The abuse potential of tramadol as been a concern from the beginning since it is a muopiate receptor OR3 acting agent. When tramadol was approved for use in the U .S it was given a nonscheduled status. This designation was contingent upon the action of a drug abuse advisory panel.  This panel has a network informants to seek information on possible tramadol abuse reports. When cases are reported a representative visits the site and institutes a corrective or educational program to deal with any possible misinformation or misdirection of tramadol .

 

Thus far the cases have been minimal and the decision not to schedule the drug has been supported .  The most important considerations are that tramadol has LOW potential for addiction or abuse rather
than NO potential. One should be careful in considering use of tramadol in patients with a history of drug misuse or abuse . The typical profile of an individual at risk for tramadol abuse is a person with along history of opiate abuse in drug-free treatment program. Experience to date confirms the FDA decision not to schedule tramadol. The rate of abuse is consistent with the rate observed in Europe (1 .5 cases / 100,000 patient exposures) . Many of the cases of abuse have arisen when a physician views tramadol as a “safe” alternative to opioids for a former addict or drug abusing patient.

The usual staring dose is 25 – 50 mg po QID up to 400 mg per day . The major side effects appear early and tend to fade over a week with chronic dosing and include : nausea, dizziness and agitation. Tramadol provides analgesia equivalent to oral meperidine or acetaminophen codeine preparations but with minimal respiratory depression, constipation or sedation, low tolerance development and low abuse liability or euphoric effects. Tramadol does not have the potency to substitute for oxycodcne or morphine preparations .

2 thoughts on “Gabapentin is better Analgesic than Tramadol”

  1. Baking soda works far better than drugs for neuropathic pain without side effects. Unless you are sodium sensitive.
    I know many people who have chronic pain and neuropathy that uses the baking soda in moderation and have found relief.
    No brain fog. No dizziness.
    No expensive drugs.

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