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Gabapentin is better Analgesic than Tramadol and It is Illegal to Buy Tramadol Online

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.

Gabapentin Tramadol
Gabapentin Tramadol

What’s the Difference Between Gabapentin and Tramadol?

  • Gabapentin and tramadol are used to treat different types of pain.
  • Gabapentin is an anti-seizure (anticonvulsant) medication used to prevent seizures and to treat post-herpetic neuralgia, the pain that follows an episode of shingles.
  • Tramadol is an opioid pain reliever (analgesic) used to manage moderate to moderately severe pain.
  • Brand names for gabapentin include Neurontin, Horizant, and Gralise.
  • Brand names for tramadol include Ultram and ConZip.
  • Side effects of gabapentin and tramadol that are similar include nausea, vomiting, dizziness, or drowsiness.
  • Side effects of gabapentin that are different from tramadol include sleepiness, loss of control of bodily movements, fatigue, fluid retention (edema), hostility, difficulty speaking, jerky movements, unusual eye movements, double vision, tremors, memory loss, unsteadiness, weight gain, joint pain, motion sickness, blurred vision, or viral infection.
  • Side effects of tramadol that are different from gabapentin include constipation, headache, euphoria, indigestion, spasticity, and weakness.
  • As with other narcotics, withdrawal symptoms may occur if you suddenly stop taking tramadol.

What Are Gabapentin and Tramadol?

Gabapentin is an anti-seizure (anticonvulsant) drug that is used for preventing seizures and for treating post-herpetic neuralgia, the pain that follows an episode of shingles. Other off-label uses for gabapentin include anxiety, alcohol withdrawal, cocaine withdrawal, hiccups, restless leg syndrome, hyperhidrosis, headaches, diabetic neuropathy, hot flashes, and fibromyalgia.
Tramadol is an opioid pain reliever (analgesic) used to manage moderate to moderately severe pain. The exact mechanism of action of tramadol is unknown, but it is similar to morphine. Like other narcotics used to treat pain, patients taking tramadol may abuse the drug and become addicted to it. Tramadol is not a nonsteroidal anti-inflammatory drug (NSAID) and it does not have the increased risk of stomach ulcers and internal bleeding that can occur with NSAIDs.

What is the advantages of Gabapentin Over Trmadol ?

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, and 600mg, 800mg tablets. Doses can be  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 efficacy in neuropathic pain states and the relatively high safety profile make it attractive for nerve pain especial for diabet patients.
gabapentin2
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 Tramadol 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 .
 
Mechanism of Action of Gabapentin
The mechanism by which gabapentin exerts its analgesic action is unknown, but in animal models of analgesia, gabapentin prevents allodynia (pain-related behavior in response to a normally innocuous stimulus) and hyperalgesia (exaggerated response to painful stimuli). In particular, gabapentin prevents pain-related responses in several models of neuropathic pain in rats or mice (e.g., spinal nerve ligation models, streptozocin-induced diabetes model, spinal cord injury model, acute herpes zoster infection model). Gabapentin also decreases pain-related responses after peripheral inflammation (carrageenan footpad test, late phase of formalin test). Gabapentin did not alter immediate pain-related behaviors (rat tail flick test, formalin footpad acute phase, acetic acid abdominal constriction test, footpad heat irradiation test). The relevance of these models to human pain is not known.
gabapentinnociceptivetransmission
The mechanism by which gabapentin exerts its anticonvulsant action is unknown, but in animal test systems designed to detect anticonvulsant activity, gabapentin prevents seizures as do other marketed anticonvulsants. Gabapentin exhibits antiseizure activity in mice and rats in both the maximal electroshock and pentylenetetrazole seizure models and other preclinical models (e.g., strains with genetic epilepsy, etc.). The relevance of these models to human epilepsy is not known.
Gabapentin is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but it does not modify GABAA or GABAB radioligand binding, it is not converted metabolically into GABA or a GABA agonist, and it is not an inhibitor of GABA uptake or degradation. Gabapentin was tested in radioligand binding assays at concentrations up to 100 μM and did not exhibit affinity for a number of other common receptor sites, including benzodiazepine, glutamate, N-methyl-D-aspartate (NMDA), quisqualate, kainate, strychnine-insensitive or strychnine-sensitive glycine, alpha 1, alpha 2, or beta adrenergic, adenosine A1 or A2, cholinergic muscarinic or nicotinic, dopamine D1 or D2, histamine H1, serotonin S1 or S2, opiate mu, delta or kappa, cannabinoid 1, voltage-sensitive calcium channel sites labeled with nitrendipine or diltiazem, or at voltage-sensitive sodium channel sites labeled with batrachotoxinin A 20-alpha-benzoate. Furthermore, gabapentin did not alter the cellular uptake of dopamine, noradrenaline, or serotonin.
In vitro studies with radiolabeled gabapentin have revealed a gabapentin binding site in areas of rat brain including neocortex and hippocampus. A high-affinity binding protein in animal brain tissue has been identified as an auxiliary subunit of voltage-activated calcium channels. However, functional correlates of gabapentin binding, if any, remain to be elucidated.
gabapentinanalgesicmechanism Pharmacokinetics and Drug Metabolism
All pharmacological actions following gabapentin administration are due to the activity of the parent compound; gabapentin is not appreciably metabolized in humans.
Oral Bioavailability
Gabapentin bioavailability is not dose proportional; i.e., as dose is increased, bioavailability decreases. Bioavailability of gabapentin is approximately 60%, 47%, 34%, 33%, and 27% following 900, 1200, 2400, 3600, and 4800 mg/day given in 3 divided doses, respectively. Food has only a slight effect on the rate and extent of absorption of gabapentin (14% increase in AUC and Cmax).
Distribution
Less than 3% of gabapentin circulates bound to plasma protein. The apparent volume of distribution of gabapentin after 150 mg intravenous administration is 58±6 L (mean ±SD). In patients with epilepsy, steady-state predose (Cmin) concentrations of gabapentin in cerebrospinal fluid were approximately 20% of the corresponding plasma concentrations.
Elimination
Gabapentin is eliminated from the systemic circulation by renal excretion as unchanged drug. Gabapentin is not appreciably metabolized in humans.
Gabapentin elimination half-life is 5 to 7 hours and is unaltered by dose or following multiple dosing. Gabapentin elimination rate constant, plasma clearance, and renal clearance are directly proportional to creatinine clearance (see CLINICAL PHARMACOLOGY, Special Populations: Adult Patients With Renal Insufficiency, below). In elderly patients, and in patients with impaired renal function, gabapentin plasma clearance is reduced. Gabapentin can be removed from plasma by hemodialysis.
Dosage adjustment in patients with compromised renal function or undergoing hemodialysis is recommended.
 
Pharmacokinetics and Drug Metabolism
All pharmacological actions following gabapentin administration are due to the activity of the parent compound; gabapentin is not appreciably metabolized in humans.
Oral Bioavailability
Gabapentin bioavailability is not dose proportional; i.e., as dose is increased, bioavailability decreases. Bioavailability of gabapentin is approximately 60%, 47%, 34%, 33%, and 27% following 900, 1200, 2400, 3600, and 4800 mg/day given in 3 divided doses, respectively. Food has only a slight effect on the rate and extent of absorption of gabapentin (14% increase in AUC and Cmax).
Distribution
Less than 3% of gabapentin circulates bound to plasma protein. The apparent volume of distribution of gabapentin after 150 mg intravenous administration is 58±6 L (mean ±SD). In patients with epilepsy, steady-state predose (Cmin) concentrations of gabapentin in cerebrospinal fluid were approximately 20% of the corresponding plasma concentrations.
Elimination
Gabapentin is eliminated from the systemic circulation by renal excretion as unchanged drug. Gabapentin is not appreciably metabolized in humans.
Gabapentin elimination half-life is 5 to 7 hours and is unaltered by dose or following multiple dosing. Gabapentin elimination rate constant, plasma clearance, and renal clearance are directly proportional to creatinine clearance (see CLINICAL PHARMACOLOGY, Special Populations: Adult Patients With Renal Insufficiency, below). In elderly patients, and in patients with impaired renal function, gabapentin plasma clearance is reduced. Gabapentin can be removed from plasma by hemodialysis.
Dosage adjustment in patients with compromised renal function or undergoing hemodialysis is recommended (see DOSAGE AND ADMINISTRATION, Table 6).
Special Populations
Adult Patients With Renal Insufficiency: Subjects (N=60) with renal insufficiency (mean creatinine clearance ranging from 13-114 mL/min) were administered single 400 mg oral doses of gabapentin. The mean gabapentin half-life ranged from about 6.5 hours (patients with creatinine clearance > 60 mL/min) to 52 hours (creatinine clearance < 30 mL/min) and gabapentin renal clearance from about 90 mL/min ( > 60 mL/min group) to about 10 mL/min ( < 30 mL/min). Mean plasma clearance (CL/F) decreased from approximately 190 mL/min to 20 mL/min.
Dosage adjustment in adult patients with compromised renal function is necessary (see DOSAGE AND ADMINISTRATION). Pediatric patients with renal insufficiency have not been studied.
Hemodialysis: In a study in anuric adult subjects (N=11), the apparent elimination half-life of gabapentin on nondialysis days was about 132 hours; during dialysis the apparent half-life of gabapentin was reduced to 3.8 hours. Hemodialysis thus has a significant effect on gabapentin elimination in anuric subjects.
Dosage adjustment in patients undergoing hemodialysis is necessary (see DOSAGE AND ADMINISTRATION).
Hepatic Disease: Because gabapentin is not metabolized, no study was performed in patients with hepatic impairment.
Age: The effect of age was studied in subjects 20-80 years of age. Apparent oral clearance (CL/F) of gabapentin decreased as age increased, from about 225 mL/min in those under 30 years of age to about 125 mL/min in those over 70 years of age. Renal clearance (CLr) and CLr adjusted for body surface area also declined with age; however, the decline in the renal clearance of gabapentin with age can largely be explained by the decline in renal function. Reduction of gabapentin dose may be required in patients who have age related compromised renal function. (See PRECAUTIONS, Geriatric Use, and DOSAGE AND ADMINISTRATION.)
Pediatric: Gabapentin pharmacokinetics were determined in 48 pediatric subjects between the ages of 1 month and 12 years following a dose of approximately 10 mg/kg. Peak plasma concentrations were similar across the entire age group and occurred 2 to 3 hours postdose. In general, pediatric subjects between 1 month and < 5 years of age achieved approximately 30% lower exposure (AUC) than that observed in those 5 years of age and older. Accordingly, oral clearance normalized per body weight was higher in the younger children. Apparent oral clearance of gabapentin was directly proportional to creatinine clearance. Gabapentin elimination half-life averaged 4.7 hours and was similar across the age groups studied.
gabapentinpharmacokinetics
A population pharmacokinetic analysis was performed in 253 pediatric subjects between 1 month and 13 years of age. Patients received 10 to 65 mg/kg/day given TID. Apparent oral clearance (CL/F) was directly proportional to creatinine clearance and this relationship was similar following a single dose and at steady state. Higher oral clearance values were observed in children < 5 years of age compared to those observed in children 5 years of age and older, when normalized per body weight. The clearance was highly variable in infants < 1 year of age. The normalized CL/F values observed in pediatric patients 5 years of age and older were consistent with values observed in adults after a single dose. The oral volume of distribution normalized per body weight was constant across the age range.
These pharmacokinetic data indicate that the effective daily dose in pediatric patients with epilepsy ages 3 and 4 years should be 40 mg/kg/day to achieve average plasma concentrations similar to those achieved in patients 5 years of age and older receiving gabapentin at 30 mg/kg/day (see DOSAGE AND ADMINISTRATION).
Gender: Although no formal study has been conducted to compare the pharmacokinetics of gabapentin in men and women, it appears that the pharmacokinetic parameters for males and females are similar and there are no significant gender differences.
Race: Pharmacokinetic differences due to race have not been studied. Because gabapentin is primarily renally excreted and there are no important racial differences in creatinine clearance, pharmacokinetic differences due to race are not expected.
 

Gabapentin Adverse Events

Postherpetic Neuralgia

The most commonly observed adverse events associated with the use of Neurontin in adults, not seen at an equivalent frequency among placebo-treated patients, were dizziness, somnolence, and peripheral edema.

In the 2 controlled studies in postherpetic neuralgia, 16% of the 336 patients who received Neurontin and 9% of the 227 patients who received placebo discontinued treatment because of an adverse event. The adverse events that most frequently led to withdrawal in Neurontin®-treated patients were dizziness, somnolence, and nausea.

Incidence in Controlled Clinical Trials

Table 3 lists treatment-emergent signs and symptoms that occurred in at least 1% of Neurontintreated patients with postherpetic neuralgia participating in placebo-controlled trials and that were numerically more frequent in the Neurontin group than in the placebo group. Adverse events were usually mild to moderate in intensity.

TABLE 3: Treatment-Emergent Adverse Event Incidence in Controlled Trials in Postherpetic Neuralgia (Events in at least 1% of Neurontin®-Treated Patients and Numerically More Frequent Than in the Placebo Group)

 

BODY SYSTEM/ PREFERRED TERM NEURONTIN®
N=336 %
PLACEBO
N=227 %
Body as a Whole
  Asthenia 5.7 4.8
  Infection 5.1 3.5
  Headache 3.3 3.1
  Accidental injury 3.3 1.3
  Abdominal pain 2.7 2.6
Digestive System
  Diarrhea 5.7 3.1
  Dry mouth 4.8 1.3
  Constipation 3.9 1.8
  Nausea 3.9 3.1
  Vomiting 3.3 1.8
  Flatulence 2.1 1.8
Metabolic and Nutritional Disorders
  Peripheral edema 8.3 2.2
  Weight gain 1.8 0.0
  Hyperglycemia 1.2 0.4
Nervous System
  Dizziness 28.0 7.5
  Somnolence 21.4 5.3
  Ataxia 3.3 0.0
  Thinking abnormal 2.7 0.0
  Abnormal gait 1.5 0.0
  Incoordination 1.5 0.0
  Amnesia 1.2 0.9
  Hypesthesia 1.2 0.9
Respiratory System
  Pharyngitis 1.2 0.4
Skin and Appendages
  Rash 1.2 0.9
Special Senses
  Amblyopiaa 2.7 0.9
  Conjunctivitis 1.2 0.0
  Diplopia 1.2 0.0
  Otitis media 1.2 0.0
aReported as blurred vision

 

Other events in more than 1% of patients but equally or more frequent in the placebo group included pain, tremor, neuralgia, back pain, dyspepsia,dyspnea, and flu syndrome.

There were no clinically important differences between men and women in the types and incidence of adverse events. Because there were few patients whose race was reported as other than white, there are insufficient data to support a statement regarding the distribution of adverse events by race.

Epilepsy

The most commonly observed adverse events associated with the use of Neurontin in combination with other antiepileptic drugs in patients > 12 years of age, not seen at an equivalent frequency among placebo-treated patients, were somnolence, dizziness, ataxia, fatigue, and nystagmus. The most commonly observed adverse events reported with the use of Neurontin in combination with other antiepileptic drugs in pediatric patients 3 to 12 years of age, not seen at an equal frequency among placebo-treated patients, were viral infection, fever, nausea and/or vomiting, somnolence, and hostility (see WARNINGSNeuropsychiatric Adverse Events-Pediatric Patients 3-12 years of age).

GabapentinAdvertiseEvents

Approximately 7% of the 2074 patients > 12 years of age and approximately 7% of the 449 pediatric patients 3 to 12 years of age who received Neurontin in premarketing clinical trials discontinued treatment because of an adverse event. The adverse events most commonly associated with withdrawal in patients > 12 years of age were somnolence (1.2%), ataxia (0.8%), fatigue (0.6%), nausea and/or vomiting (0.6%), and dizziness (0.6%). The adverse events most commonly associated with withdrawal in pediatric patients were emotional lability (1.6%), hostility (1.3%), and hyperkinesia (1.1%).

Incidence in Controlled Clinical Trials

Table 4 lists treatment-emergent signs and symptoms that occurred in at least 1% of Neurontintreated patients > 12 years of age with epilepsyparticipating in placebo-controlled trials and were numerically more common in the Neurontin group. In these studies, either Neurontin or placebo was added to the patient’s current antiepileptic drug therapy. Adverse events were usually mild to moderate in intensity.

The prescriber should be aware that these figures, obtained when Neurontin was added to concurrent antiepileptic drug therapy, cannot be used to predict the frequency of adverse events in the course of usual medical practice where patient characteristics and other factors may differ from those prevailing during clinical studies. Similarly, the cited frequencies cannot be directly compared with figures obtained from other clinical investigations involving different treatments, uses, or investigators. An inspection of these frequencies, however, does provide the prescribing physician with one basis to estimate the relative contribution of drug and nondrug factors to the adverse event incidences in the population studied.

 

Other Adverse Events Observed During All Clinical Trials

Clinical Trials in Adults and Adolescents (Except Clinical Trials in Neuropathic Pain)
Neurontin has been administered to 4717 patients > 12 years of age during all adjunctive therapy clinical trials (except clinical trials in patients with neuropathic pain), only some of which were placebo-controlled. During these trials, all adverse events were recorded by the clinical investigators using terminology of their own choosing. To provide a meaningful estimate of the proportion of individuals having adverse events, similar types of events were grouped into a smaller number of standardized categories using modified COSTART dictionary terminology. These categories are used in the listing below. The frequencies presented represent the proportion of the 4717 patients > 12 years of age exposed to Neurontin who experienced an event of the type cited on at least one occasion while receiving Neurontin. All reported events are included except those already listed in Table 4, those too general to be informative, and those not reasonably associated with the use of the drug.
Events are further classified within body system categories and enumerated in order of decreasing frequency using the following definitions: frequent adverse events are defined as those occurring in at least 1/100 patients; infrequent adverse events are those occurring in 1/100 to 1/1000 patients; rare events are those occurring in fewer than 1/1000 patients.
Body As A Whole: Frequent: asthenia, malaise, face edema; Infrequent: allergy, generalized edema, weight decrease, chill; Rare: strange feelings, lassitude, alcohol intolerance, hangover effect.
Cardiovascular System: Frequent: hypertension; Infrequent: hypotension, angina pectoris, peripheral vascular disorder, palpitation, tachycardia, migraine, murmur; Rare: atrial fibrillation, heart failure, thrombophlebitis, deep thrombophlebitis, myocardial infarction, cerebrovascular accident, pulmonary thrombosis, ventricular extrasystoles, bradycardia, premature atrial contraction, pericardial rub, heart block, pulmonary embolus, hyperlipidemia, hypercholesterolemia, pericardial effusion, pericarditis.
Digestive System: Frequent: anorexia, flatulence, gingivitis; Infrequent: glossitis, gum hemorrhage, thirst, stomatitis, increased salivation, gastroenteritis, hemorrhoids, bloody stools, fecal incontinence, hepatomegaly; Rare: dysphagia, eructation, pancreatitis, peptic ulcer, colitis, blisters in mouth, tooth discolor, perlèche, salivary gland enlarged, lip hemorrhage, esophagitis, hiatal hernia, hematemesis, proctitis, irritable bowel syndrome, rectal hemorrhage, esophageal spasm.
Endocrine System: Rare: hyperthyroid, hypothyroid, goiter, hypoestrogen, ovarian failure, epididymitis, swollen testicle, cushingoid appearance.
Hematologic and Lymphatic Systems: Frequent: purpura most often described as bruises resulting from physical trauma; Infrequent: anemia, thrombocytopenia, lymphadenopathy; Rare: WBC count increased, lymphocytosis, non-Hodgkin’s lymphoma, bleeding time increased.
Musculoskeletal System: Frequent: arthralgia; Infrequent: tendinitis, arthritis, joint stiffness, joint swelling, positive Romberg test; Rare: costochondritis, osteoporosis, bursitis, contracture.
Nervous System: Frequent: vertigo, hyperkinesia, paresthesia, decreased or absent reflexes, increased reflexes, anxiety, hostility; Infrequent: CNS tumors, syncope, dreaming abnormal, aphasia, hypesthesia, intracranial hemorrhage, hypotonia, dysesthesia, paresis, dystonia, hemiplegia, facial paralysis, stupor, cerebellar dysfunction, positive Babinski sign, decreased position sense, subdural hematoma, apathy, hallucination, decrease or loss of libido, agitation, paranoia, depersonalization, euphoria, feeling high, doped-up sensation, psychosis; Rare: choreoathetosis, orofacial dyskinesia, encephalopathy, nerve palsy, personality disorder, increased libido, subdued temperament, apraxia, fine motor control disorder, meningismus, local myoclonus, hyperesthesia, hypokinesia, mania, neurosis, hysteria, antisocial reaction.
Respiratory System: Frequent: pneumonia; Infrequent: epistaxis, dyspnea, apnea; Rare: mucositis, aspiration pneumonia, hyperventilation, hiccup, laryngitis, nasal obstruction, snoring, bronchospasm, hypoventilation, lung edema.
Dermatological: Infrequent: alopecia, eczema, dry skin, increased sweating, urticaria, hirsutism, seborrhea, cyst, herpes simplex; Rare: herpes zoster, skin discolor, skin papules, photosensitive reaction, leg ulcer, scalp seborrhea, psoriasis, desquamation, maceration, skin nodules, subcutaneous nodule, melanosis, skin necrosis, local swelling.
Urogenital System: Infrequent: hematuria, dysuria, urination frequency, cystitis, urinary retention, urinary incontinence, vaginal hemorrhage, amenorrhea, dysmenorrhea, menorrhagia, breast cancer, unable to climax, ejaculation abnormal; Rare: kidney pain, leukorrhea, pruritus genital, renal stone, acute renal failure, anuria, glycosuria, nephrosis, nocturia, pyuria, urination urgency, vaginal pain, breast pain, testicle pain.
Special Senses: Frequent: abnormal vision; Infrequent: cataract, conjunctivitis, eyes dry, eye pain, visual field defect, photophobia, bilateral or unilateral ptosis, eye hemorrhage, hordeolum, hearing loss, earache, tinnitus, inner ear infection, otitis, taste loss, unusual taste, eye twitching, ear fullness; Rare: eye itching, abnormal accommodation, perforated ear drum, sensitivity to noise, eye focusing problem, watery eyes, retinopathy, glaucoma, iritis, corneal disorders, lacrimal dysfunction, degenerative eye changes, blindness, retinal degeneration, miosis, chorioretinitis, strabismus, eustachian tube dysfunction, labyrinthitis, otitis externa, odd smell.
Clinical Trials in Pediatric Patients With Epilepsy
Adverse events occurring during epilepsy clinical trials in 449 pediatric patients 3 to 12 years of age treated with gabapentin that were not reported in adjunctive trials in adults are:
Body as a Whole: dehydration, infectious mononucleosis
Digestive System: hepatitis
Hematologic and Lymphatic Systems: coagulation defect
Nervous System: aura disappeared, occipital neuralgia
Psychobiologic Function: sleepwalking
Respiratory System: pseudocroup, hoarseness
Clinical Trials in Adults with Neuropathic Pain of Various Etiologies
Safety information was obtained in 1173 patients during double-blind and open-label clinical trials including neuropathic pain conditions for which efficacy has not been demonstrated. Adverse events reported by investigators were grouped into standardized categories using modified COSTART IV terminology. Listed below are all reported events except those already listed in Table 3 and those not reasonably associated with the use of the drug.
Events are further classified within body system categories and enumerated in order of decreasing frequency using the following definitions: frequent adverse events are defined as those occurring in at least 1/100 patients; infrequent adverse events are those occurring in 1/100 to 1/1000 patients; rare events are those occurring in fewer than 1/1000 patients.
Body as a Whole: Infrequent: chest pain, cellulitis, malaise, neck pain, face edema, allergic reaction, abscess, chills, chills and fever, mucous membrane disorder; Rare: body odor, cyst, fever, hernia, abnormal BUN value, lump in neck, pelvic pain, sepsis, viral infection.
Cardiovascular System: Infrequent: hypertension, syncope, palpitation, migraine, hypotension, peripheral vascular disorder, cardiovascular disorder, cerebrovascular accident, congestive heart failure, myocardial infarction, vasodilatation; Rare: angina pectoris, heart failure, increased capillary fragility, phlebitis, thrombophlebitis, varicose vein.
Digestive System: Infrequent: gastroenteritis, increased appetite, gastrointestinal disorder, oral moniliasis, gastritis, tongue disorder, thirst, tooth disorder, abnormal stools, anorexia, liver function tests abnormal, periodontal abscess; Rare: cholecystitis, cholelithiasis, duodenal ulcer, fecal incontinence, gamma glutamyl transpeptidase increased, gingivitis, intestinal obstruction, intestinal ulcer, melena, mouth ulceration, rectal disorder, rectal hemorrhage, stomatitis.
Endocrine System: Infrequent: diabetes mellitus.
Hematologic and Lymphatic Systems: Infrequent: ecchymosis, anemia; Rare: lymphadenopathy, lymphoma-like reaction, prothrombin decreased.
Metabolic and Nutritional: Infrequent: edema, gout, hypoglycemia, weight loss; Rare: alkaline phosphatase increased, diabetic ketoacidosis, lactic dehydrogenase increased.
Musculoskeletal: Infrequent: arthritis, arthralgia, myalgia, arthrosis, leg cramps, myasthenia; Rare: shin bone pain, joint disorder, tendon disorder.
Nervous System: Frequent: confusion, depression; Infrequent: vertigo, nervousness, paresthesia, insomnia, neuropathy, libido decreased, anxiety, depersonalization, reflexes decreased, speech disorder, abnormal dreams, dysarthria, emotional lability, nystagmus, stupor, circumoral paresthesia, euphoria, hyperesthesia, hypokinesia; Rare: agitation, hypertonia, libido increased, movement disorder, myoclonus, vestibular disorder.
Respiratory System: Infrequent: cough increased, bronchitis, rhinitis, sinusitis, pneumonia, asthma, lung disorder, epistaxis; Rare: hemoptysis, voice alteration.
Skin and Appendages: Infrequent: pruritus, skin ulcer, dry skin, herpes zoster, skin disorder, fungal dermatitis, furunculosis, herpes simplex, psoriasis, sweating, urticaria, vesiculobullous rash; Rare: acne, hair disorder, maculopapular rash, nail disorder, skin carcinoma, skin discoloration, skin hypertrophy.
Special Senses: Infrequent: abnormal vision, ear pain, eye disorder, taste perversion, deafness; Rare: conjunctival hyperemia, diabetic retinopathy, eye pain, fundi with microhemorrhage, retinal vein thrombosis, taste loss.
Urogenital System: Infrequent: urinary tract infection, dysuria, impotence, urinary incontinence, vaginal moniliasis, breast pain, menstrual disorder, polyuria, urinary retention; Rare: cystitis, ejaculation abnormal, swollen penis, gynecomastia, nocturia, pyelonephritis, swollen scrotum, urinary frequency, urinary urgency, urine abnormality.
Postmarketing and Other Experience
In addition to the adverse experiences reported during clinical testing of Neurontin, the following adverse experiences have been reported in patients receiving marketed Neurontin. These adverse experiences have not been listed above and data are insufficient to support an estimate of their incidence or to establish causation. The listing is alphabetized: angioedema, blood glucose fluctuation, breast enlargement, elevated creatine kinase, elevated liver function tests, erythema multiforme, fever, hyponatremia, jaundice, movement disorder, rhabdomyolysis, Stevens-Johnson syndrome.
Adverse events following the abrupt discontinuation of gabapentin have also been reported. The most frequently reported events were anxiety, insomnia, nausea, pain, and sweating.

3 Comments

  1. PhyAnnie

    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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