Gabapentin is widely used for Diabetic neuropathy

A double‐blind, placebo‐controlled, parallel group multicentre study of 165 diabetic patients with a 1–5‐year history of painful peripheral diabetic neuropathy reported a beneficial effect with gabapentin .

A post-marketing surveillance study of gabapentin usage in Filipino patients with neuropathic pain wasconducted. Safety, tolerability and analgesic efficacy were assessed after a minimum of two weeks ofgabapentin treatment, with starting and final doses determined by the prescribing physician.

Of the1,214 patients who entered the study, 95.7% completed the minimum two weeks duration of therapy.The mean age was 54 years, and the most common neuropathic pain diagnoses were painful diabeticneuropathy (30.4%), nonspecific neuropathies (20.2%), trigeminal neuralgia (12.8%), central pain afterstroke (8.8%), and post-herpetic neuralgia (8.4%). Ninety-two percent of patients were maintainedwithin a dose range of 300mg/day to 1200mg/day.

The incidence of adverse events was 6%, andconsisted mostly of somnolence and dizziness, with 76% of patients reporting “very good” to“excellent” tolerability. There were 34 documented dropouts (2.9%), of which only seven (0.6%) werethought to be related to an adverse event from gabapentin.

Visual analog scale pain scores declinedsignificantly from a mean of mm at baseline, to mm after treatment (p< 0.05). Inconclusion, gabapentin at 300mg/d to 1200mg/d is well tolerated and efficacious among Filipinopatients with various neuropathic pain syndromes.Gabapentin showed significant reduction in pain and other related symptoms in all types of neuropathic painNeurol J Southeast Asia 2002; 7 : 25 – 34

Eighty‐four patients were allocated to the␣gabapentin group and 81 to the placebo group.

Gabapentin was titrated to a maximum of 3600 mg daily.

Gabapentin was generally well tolerated and 67% of the gabapentin group reached 3600 mg.day⁻¹. A statistically significant (p < 0.0001) reduction in mean daily pain score (using an 11‐point Likert scale) in the gabapentin group (baseline 6.4, endpoint 3.9), compared with placebo (baseline 6.5, endpoint 5.1), was achieved.

The number‐needed‐to‐treat (NNT, defined as the number of patients needed to be treated for one patient to receive at least 50% pain relief) for the analgesic effects in neuropathic pain with gabapentin in this study was 3.8 . This compares with a NNT of 2.3 for carbemazepine and 2.1 for phenytoin in other randomised controlled trials . Another double‐blind, placebo‐controlled trial of gabapentin in 32 diabetic patients with neuropathic pain showed a statistically significant analgesic effect during the first month of treatment.

Morello et al. conducted a randomised, double‐blind cross‐over study comparing the efficacy of gabapentin with that of amitriptyline in diabetic peripheral neuropathy and found both drugs provided equal pain relief.

Gabapentin in neuropathic pain syndromes: a randomised, double-blind, placebo-controlled trial.

In an open‐label pilot study over 12 weeks involving 25 randomised patients (13 received gabapentin, 12 received amitriptyline), gabapentin significantly reduced pain scores (p = 0.026) and paraesthesia (p = 0.004) compared with amitriptyline . Adverse effects were also less frequent in the gabapentin group (p = 0.003). Further trials are required to confirm these preliminary results indicating that gabapentin is more efficacious than amitriptyline in diabetic peripheral neuropathy.

A double-blind, randomised, placebo-controlled 8-week study was conducted to evaluate the efficacy and safety of gabapentin in the treatment of neuropathic pain, using doses up to 2400 mg/day.

The study used a novel design that was symptom- rather than syndrome-based; an approach that aimed to reflect the realities of clinical practice. Participants had a wide range of neuropathic pain syndromes, with at least two of the following symptoms: allodynia, burning pain, shooting pain, or hyperalgesia.

Patients were randomised to gabapentin (n=153) or placebo (n=152). Gabapentin was given in three divided doses, initially titrated to 900 mg/day over 3 days, followed by two further increases, to a maximum of 2400 mg/day if required by the end of week 5.

The primary outcome measure was changed in average daily pain diary score (baseline versus final week). Over the 8 week study, this score decreased (i.e. improved) by 1.5 (21%) in gabapentin treated patients and by 1.0 (14%) in placebo treated patients (P=0.048, rank-based analysis of covariance).

Significant differences were shown in favour of gabapentin (P<0.05) for the Clinician and Patient Global Impression of Change, and some domains of the Short Form-McGill Pain Questionnaire. Improvements were also shown in patient-reported outcomes in quality of life, as seen by significant differences in favour of gabapentin in several domains of the Short-Form-36 Health Survey.

Gabapentin was well tolerated and the majority of patients completed the study (79 versus 73% for placebo). The most common adverse events were mild to moderate dizziness and somnolence, most of which were transient and occurred during the titration phase.

This study shows that gabapentin reduces pain and improves some quality-of-life measures in patients with a wide range of neuropathic pain syndromes.

Buy Gabapentin (Neurontin) without Prescription

What is gabapentin?

Gabapentin is an anti-epileptic drug, also called an anticonvulsant. It affects chemicals and nerves in the body that are involved in the cause of seizures and some types of pain.

Buy COD Fioricet and COD Gabapentin Online

All brands of gabapentin are used in adults to treat neuropathic pain (nerve pain) caused by herpes virus or shingles (herpes zoster).

The Gralise brand of gabapentin is indicated for the management of neuropathic pain only. It is not used for epilepsy.

The Horizant brand of gabapentin, in addition to treating neuropathic pain, is also used to treat restless legs syndrome (RLS).

The Neurontin brand of gabapentin is also used to treat seizures in adults and children who are at least 3 years old, in addition to neuropathic pain.

Use only the brand and form of gabapentin your doctor has prescribed. Check your medicine each time you get a refill to make sure you receive the correct form.

Gabapentin Description

Generic Gabapentin target is the treatment of seizures. Generic Gabapentin can also be used to relieve the pain of diabetic neuropathy and postherpetic neuralgia. It is taken to prevent and treat hot flashes in women with menopause or breast cancer. Generic Gabapentin can be used together with other seizures medicines.

Generic Gabapentin is acting by affecting certain nerves and chemicals which cause seizures and pain. It is anticonvulsant.

Generic name of Generic Gabapentin is Gabapentin.

Brand names of Generic Gabapentin are Gabapentin, Gabarone.

Gabapentin Dosage

Generic Gabapentin is available in:

300mg Low Dosage400mg Standard Dosage

Generic Gabapentin is available in tablets, liquid form and capsules(300 mg, 400 mg).

The dosage of Generic Gabapentin depends on the type of your disease and health state.

Take Generic Gabapentin tablets, liquid form and capsules orally at the same time every day with water.

Generic Gabapentin can be used together with other seizures medicines.

Take Generic Gabapentin 3 times a day with or without food.

If you want to achieve most effective results do not stop taking Generic Gabapentin suddenly.

Gabapentin Missing of dose

Do not take double dose. If you miss a dose you should take it as soon as you remember about your missing. If it is the time for the next dose you should continue your regular dosing schedule.

Gabapentin Overdose

If you overdose Generic Gabapentin and you don’t feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Gabapentin overdosage: feeling drowsy, double vision, slurred speech, diarrhea, difficulties with breathing, problems with coordination.

Gabapentin Side Effects

Applies to gabapentin: oral capsule, oral solution, oral suspension, oral tablet

Along with its needed effects, gabapentin may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.

Check with your doctor immediately if any of the following side effects occur while taking gabapentin:

More common

Clumsiness or unsteadiness
continuous, uncontrolled, back-and-forth, or rolling eye movements

More common in children

Aggressive behavior or other behavior problems
anxiety
concentration problems and change in school performance
crying
depression
false sense of well-being
hyperactivity or increase in body movements
rapidly changing moods
reacting too quickly, too emotional, or overreacting
restlessness
suspiciousness or distrust

Less common

Black, tarry stools
chest pain
chills
cough
depression, irritability, or other mood or mental changes
fever
loss of memory
pain or swelling in the arms or legs
painful or difficult urination
shortness of breath
sore throat
sores, ulcers, or white spots on the lips or in the mouth
swollen glands
unusual bleeding or bruising
unusual tiredness or weakness

Incidence not known

Abdominal or stomach pain
blistering, peeling, or loosening of the skin
clay-colored stools
coma
confusion
convulsions
dark urine
decreased urine output
diarrhea
dizziness
fast or irregular heartbeat
headache
increased thirst
itching or skin rash
joint pain
large, hive-like swelling on the face, eyelids, lips, tongue, throat, hands, legs, feet, or sex organs
loss of appetite
muscle ache or pain
nausea
red skin lesions, often with a purple center
red, irritated eyes
unpleasant breath odor
vomiting of blood
yellow eyes or skin

Some side effects of gabapentin may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. Also, your health care professional may be able to tell you about ways to prevent or reduce some of these side effects. Check with your health care professional if any of the following side effects continue or are bothersome or if you have any questions about them:

More common

Blurred vision
cold or flu-like symptoms
delusions
dementia
hoarseness
lack or loss of strength
lower back or side pain
swelling of the hands, feet, or lower legs
trembling or shaking

Less common or rare

Accidental injury
appetite increased
back pain
bloated or full feeling
body aches or pain
burning, dry, or itching eyes
change in vision
change in walking and balance
clumsiness or unsteadiness
congestion
constipation
cough producing mucus
decrease in sexual desire or ability
difficulty with breathing
dryness of the mouth or throat
earache
excess air or gas in the stomach or intestines
excessive tearing
eye discharge
feeling faint, dizzy, or lightheadedness
feeling of warmth or heat
flushed, dry skin
flushing or redness of the skin, especially on the face and neck
frequent urination
fruit-like breath odor
impaired vision
incoordination
increased hunger
increased sensitivity to pain
increased sensitivity to touch
increased thirst
indigestion
noise in the ears
pain, redness, rash, swelling, or bleeding where the skin is rubbed off
passing gas
redness or swelling in the ear
redness, pain, swelling of the eye, eyelid, or inner lining of the eyelid
runny nose
sneezing
sweating
tender, swollen glands in the neck
tightness in the chest
tingling in the hands and feet
trouble sleeping
trouble swallowing
trouble thinking
twitching
unexplained weight loss
voice changes
vomiting
weakness or loss of strength
weight gain

Gabapentin Contra-indications

Do not take Generic Gabapentin if you are allergic to Generic Gabapentin components.

Do not take Generic Gabapentin if you are pregnant, planning to become pregnant. Avoid breast-feeding.

Be careful with Generic Gabapentin if you are taking morphine (such as MSIR, Avinza, Kadian), hydrocodone (in Vicodin, in Hydrocet), naproxen (such as Anaprox, Aleve, Naprosyn).

Generic Gabapentin can be used together with other seizures medicines.

Be very careful with Generic Gabapentin if you suffer from or have a history of heart, kidney or liver disease.

Be careful with Generic Gabapentin if you are going to have a surgery.

Children should be very careful with Generic Gabapentin because it can cause changes in behavior.

If you experience drowsiness and dizziness while taking Generic Gabapentin you should avoid any activities such as driving or operating machinery.

Avoid alcohol.

It can be dangerous to stop Generic Gabapentin taking suddenly.

Gabapentin Frequently asked questions

Q: What does Generic Gabapentin mean?

A: Generic Gabapentin is the medication of high quality, which is taken in treatment of seizures. Generic Gabapentin can also be used to relieve the pain of diabetic neuropathy and postherpetic neuralgia. It is taken to prevent and treat hot flashes in women with menopause or breast cancer. Generic Gabapentin can be used together with other seizures medicines.

Q: What is the target?

A: The target of this perfect remedy is the treatment of seizures. Generic Gabapentin can also be used to relieve the pain of diabetic neuropathy and postherpetic neuralgia. It is taken to prevent and treat hot flashes in women with menopause or breast cancer.

Q: What are Generic Gabapentin side effects?

A: Generic Gabapentin has its common side effects such as: lightheadedness, feeling drowsy, vomiting, weakness, tremor, fatigue, nausea, anxiety, migraine, uncontrolled body shaking, problems with memory, dry mouth, unwanted eye movements, heartburn, constipation, diarrhea, gain of weight, back pain, itchy or red eyes, arthralgia, high temperature, symptoms of the flu, pain of ear, problems with coordination, double or blurred vision. But in case of rejection of Generic Gabapentin ingredients you can experience more serious side effects: amnesia, hyperactivity, emotional instability, thought disorders, aggressiveness, pruritus, convulsions, difficulties with swallowing, huskiness, symptoms of allergy reaction (hives, difficulties with breathing, rash, swelling, closing ), restlessness.

Q: What are generic and brand names of Generic Gabapentin?

A: The brand names of Generic Gabapentin are Gabapentin, Gabarone. The generic name of Generic Gabapentin is Gabapentin.

Q: In what way does Generic Gabapentin operate?

A: Generic Gabapentin is acting by affecting certain nerves and chemicals which cause seizures and pain. It is anticonvulsant.

How does Gabapentin Work ?

Gabapentin works by changing the way that nerves send messages to your brain. If the messages are reduced, then the pain will be reduced.

Gabapentin has no direct GABAergic action and does not block GABA uptake or metabolism. Gabapentin blocks the tonic phase of nociception induced by formalin and carrageenan, and exerts a potent inhibitory effect in neuropathic pain models of mechanical hyperalgesia and mechanical/thermal allodynia.

Gabapentin binds preferentially to neurons in the outer layer of the rat cortex at sites that are distinct from other anticonvulsants [20]. It is likely that gabapentin acts at an intracellular site as the maximal anticonvulsant effect is achieved 2 h after an intravenous injection of gabapentin in rats. This occurs after the plasma and interstitial fluid concentrations have peaked and reflects the additional time required for intraneural transport [21].

Several theories have been proposed to explain the cellular mechanism of its anticonvulsant effect. The most favoured theory involves an interaction with an as yet undescribed receptor linked with the l‐system amino acid transporter protein. Suman Chauhan et al. [22] demonstrated that l‐amino acids potently inhibited binding of an␣active enantiomer of gabapentin ([3H]gabapentin). This was further supported by Taylor et al. [23] who showed that the potent anticonvulsant, 3‐isobutyl GABA (an analogue of gabapentin) potently and stereoselectively bound to the same receptor. These findings renewed interest in the isolation of the receptor protein that may responsible for this anticonvulsant effect.

Other proposed biochemical events in the central nervous system (CNS) that may explain its anti‐epileptic effect include the increased extracellular GABA concentrations in some regions of the brain caused by an increase in activity of glutamic acid decarboxylase that produces GABA, and a decreased breakdown by GABA decarboxylase [3, 24]. Although a study [25], using magnetic resonance imaging (MRI) spectroscopy showed a global increase in GABA in the brain after the administration of gabapentin, there is no evidence that gabapentin increases intraneuronal GABA concentrations, binds GABAA or GABAB receptors, or exerts any GABA‐mimetic action [3, 23].

Other effects of gabapentin have been described but are not considered to play a significant pharmacodynamic role. These include small decreases in the release of monoamine neurotransmitters (dopamine, noradrenaline and serotonin) [26, 27] and the attenuation of sodium‐dependent action potentials (suggesting sodium channel blockade) after prolonged exposure to gabapentin [28].

The mode of action of gabapentin in the treatment of neuropathic pain has not been fully elucidated. Although early studies [29] indicated that gabapentin had only a central anti‐allodynic effect, gabapentin has been shown to inhibit ectopic discharge activity from injured peripheral nerves [30]. The mechanisms of the anti‐allodynic effects of gabapentin proposed include: CNS effects (potentially at spinal cord or brain level) due to either enhanced inhibitory input of GABA‐mediated pathways (and thus reducing excitatory input levels); antagonism of NMDA receptors; and antagonism of calcium channels in the CNS and inhibition of peripheral nerves [29-46]. Of these, antagonism of the NMDA receptor and calcium channel blockade have the most supporting evidence. Field et al. [31] discounted an antihyperalgesic action via opioid receptor binding after demonstrating that morphine tolerance does not alter the efficacy of gabapentin and naloxone does not reduce its antihyperalgesic effect.

Research into a peripheral site of action for gabapentin has produced contradictory results [29, 30]. Intrathecal administration of gabapentin blocks thermal and mechanical hyperalgesia without affecting sympathetic outflow or acute nociception, and this suggests a spinal site of action [32-34]. Patel et al. [35] demonstrated a presynaptic site of action for gabapentin in the rat spinal cord.

Although gabapentin does not bind to GABAA or GABAB receptors, increased synthesis and reduced breakdown of GABA have been described [3, 24]. Potentiation of inhibitory GABA‐ergic pathways seems unlikely to be responsible for its anti‐allodynic effect because GABA receptor antagonists do not reduce this effect [8, 36].

The NMDA receptor complex is a ligand‐gated ion channel that mediates an influx of calcium ions when activated. The NMDA receptor complex has a number of binding sites for various ligands that regulate its activity, including the strychnine‐insensitive glycine binding site, phencyclidine binding site, polyamine binding site, redox modulatory site and a proton‐sensitive site. Partial depolarisation of the neuron after glutamine activation will release a magnesium plug and allow calcium influx into the neuron. These receptors are known to be found in high concentrations in the hippocampus and have been attributed a key role in the process of central sensitisation of painful stimuli, commonly known as the ‘wind‐up’ phenomenon, leading to hyperalgesia. Evidence linking gabapentin to the NMDA receptor follows research demonstrating the reversal of the antihyperalgesic effect of gabapentin by d‐serine, an agonist at the NMDA‐glycine binding site [33, 34, 36, 37]. However, receptor binding studies have failed to demonstrate a direct binding site for gabapentin at the NMDA receptor [38-40].

The α2δ subunit of the voltage‐dependent calcium channel is a binding site for gabapentin and the S‐isomer of pregabolin (S‐(+)‐3‐isobutylgaba) [4, 33, 37, 41]. Because only gabapentin and the S‐isomer of pregabolin produce antihyperalgesic effects, it is postulated that the antihyperalgesic action for gabapentin is mediated by its binding to this site on the voltage‐dependent calcium channel. Fink et al. [45] showed that, in the rat neocortex, gabapentin inhibits neuronal calcium influx in a concentration‐dependent manner by inhibiting P/Q‐type calcium channels. The decreased calcium influx reduces excitatory amino acid (e.g. glutamate) release leading to decreased AMPA receptor activation, and noradrenaline release in the brain. These findings support the hypothesis that calcium channel inhibition mediates the analgesic effects of gabapentin in chronic neuropathic pain. A decrease in potassium ion‐evoked glutamate release from rat neocortical and hipppocampal slices by gabapentin has been demonstrated [46].

Gabapentin is a medicine that may be used for the treatment of certain seizure disorders or nerve pain.

Experts aren’t sure exactly how gabapentin works, but research has shown that gabapentin binds strongly to a specific site (called the alpha2-delta site) on voltage-gated calcium channels. This action is thought to be the mechanism for its nerve-pain relieving and anti-seizure properties.

Gabapentin enacarbil (brand name Horizant) is a prodrug of gabapentin which has been designed to overcome the limitations of gabapentin, such as poor absorption and a short duration of action. Gabapentin enacarbil is effective for restless legs syndrome (RLS) and postherpetic neuralgia (nerve pain that occurs following Shingles).

Gabapentin belongs to the group of medicines known as anticonvulsants.

Gabapentin, impotence and other problems?

I was just hoping that you might have the answer I am hoping for? I started taking gabapentin 300mg twice a day, then 3 times a day, then 600mg twice a day then 3 times a day, now after 2 to 3 years later 800mg 3 times a day.

My doctor says it won’t cause erectile dysfunction but it started very soon after the 300mg 3 times a day.

I tried Viagra and Cialis very little help. My wife is very displeased and sometimes thinks it is something to do with her. I know it has nothing to do with her as she is my bride of 24 years and my soul mate spirit. I have very bad pain that the gabapentin used to help with but it now seems it helps no more.

I would rather have my manhood back and my bride be happy and me than be in pain that just won’t go away. To get to the real question, how slowly should I get off the gabapentin and will I ever be able to get back to normal?

I will have to just have to tolerate the pain now that I have my diabetes under control. I rarely have to take my diabetes medicine but a few times a week because it makes my numbers to low and I black out when they get to low.

Usually 82 morning, 92 lunch, and 98 dinner. Any help will be greatly appreciated.

Answers:

Unfortunately gabapentin can cause impotence.

Side effects of the 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.

Talk to your doctor about coming off gabapentin and he/she could put you on some other medicine to help the pain. You don’t have to ween off gabapentin but please get your doctor to monitor you once you are off.

Gabapentin Drug Interaction

Alcohol (Ethyl): CNS Depressants may enhance the CNS depressant effect of Alcohol (Ethyl). Monitor therapy

Alizapride: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Aluminum Hydroxide: May decrease the serum concentration of Gabapentin. Management: Administer gabapentin at least 2 hours after administration of antacids containing aluminum hydroxide or magnesium hydroxide. Consider therapy modification

Azelastine (Nasal): CNS Depressants may enhance the CNS depressant effect of Azelastine (Nasal). Avoid combination

Blonanserin: CNS Depressants may enhance the CNS depressant effect of Blonanserin. Consider therapy modification

Brexanolone: CNS Depressants may enhance the CNS depressant effect of Brexanolone. Monitor therapy

Brimonidine (Topical): May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Bromopride: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Bromperidol: May enhance the CNS depressant effect of CNS Depressants. Avoid combination

Buprenorphine: CNS Depressants may enhance the CNS depressant effect of Buprenorphine. Management: Consider reduced doses of other CNS depressants, and avoiding such drugs in patients at high risk of buprenorphine overuse/self-injection. Initiate buprenorphine at lower doses in patients already receiving CNS depressants. Consider therapy modification

Cannabidiol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Cannabis: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Chlormethiazole: May enhance the CNS depressant effect of CNS Depressants. Management: Monitor closely for evidence of excessive CNS depression. The chlormethiazole labeling states that an appropriately reduced dose should be used if such a combination must be used. Consider therapy modification

Chlorphenesin Carbamate: May enhance the adverse/toxic effect of CNS Depressants. Monitor therapy

CNS Depressants: May enhance the adverse/toxic effect of other CNS Depressants. Monitor therapy

Dimethindene (Topical): May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Doxylamine: May enhance the CNS depressant effect of CNS Depressants. Management: The manufacturer of Diclegis (doxylamine/pyridoxine), intended for use in pregnancy, specifically states that use with other CNS depressants is not recommended. Monitor therapy

Dronabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Droperidol: May enhance the CNS depressant effect of CNS Depressants. Management: Consider dose reductions of droperidol or of other CNS agents (eg, opioids, barbiturates) with concomitant use. Exceptions to this monograph are discussed in further detail in separate drug interaction monographs. Consider therapy modification

Esketamine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Flunitrazepam: CNS Depressants may enhance the CNS depressant effect of Flunitrazepam. Consider therapy modification

HYDROcodone: CNS Depressants may enhance the CNS depressant effect of HYDROcodone. Management: Avoid concomitant use of hydrocodone and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Consider therapy modification

HydrOXYzine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Kava Kava: May enhance the adverse/toxic effect of CNS Depressants. Monitor therapy

Lofexidine: May enhance the CNS depressant effect of CNS Depressants. Management: Drugs listed as exceptions to this monograph are discussed in further detail in separate drug interaction monographs. Monitor therapy

Magnesium Salts: May enhance the CNS depressant effect of Gabapentin. Specifically, high dose intravenous/epidural magnesium sulfate may enhance the CNS depressant effects of gabapentin. Magnesium Salts may decrease the serum concentration of Gabapentin. Management: Administer gabapentin at least 2 hours after use of a magnesium-containing antacid. Monitor patients closely for evidence of reduced response to gabapentin therapy. Monitor for CNS depression if high dose IV/epidural magnesium sulfate is used. Consider therapy modification

Mefloquine: May diminish the therapeutic effect of Anticonvulsants. Mefloquine may decrease the serum concentration of Anticonvulsants. Management: Mefloquine is contraindicated for malaria prophylaxis in persons with a history of convulsions. Monitor anticonvulsant concentrations and treatment response closely with concurrent use. Consider therapy modification

Methotrimeprazine: CNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Methotrimeprazine may enhance the CNS depressant effect of CNS Depressants. Management: Reduce adult dose of CNS depressant agents by 50% with initiation of concomitant methotrimeprazine therapy. Further CNS depressant dosage adjustments should be initiated only after clinically effective methotrimeprazine dose is established. Consider therapy modification

MetyroSINE: CNS Depressants may enhance the sedative effect of MetyroSINE. Monitor therapy

Mianserin: May diminish the therapeutic effect of Anticonvulsants. Monitor therapy

Minocycline: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Minocycline (Systemic): May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Morphine (Systemic): Gabapentin may enhance the CNS depressant effect of Morphine (Systemic). Morphine (Systemic) may increase the serum concentration of Gabapentin. Monitor therapy

Nabilone: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Opioid Agonists: CNS Depressants may enhance the CNS depressant effect of Opioid Agonists. Management: Avoid concomitant use of opioid agonists and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Consider therapy modification

Orlistat: May decrease the serum concentration of Anticonvulsants. Monitor therapy

Orphenadrine: CNS Depressants may enhance the CNS depressant effect of Orphenadrine. Avoid combination

Oxomemazine: May enhance the CNS depressant effect of CNS Depressants. Avoid combination

OxyCODONE: CNS Depressants may enhance the CNS depressant effect of OxyCODONE. Management: Avoid concomitant use of oxycodone and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Consider therapy modification

Paraldehyde: CNS Depressants may enhance the CNS depressant effect of Paraldehyde. Avoid combination

Perampanel: May enhance the CNS depressant effect of CNS Depressants. Management: Patients taking perampanel with any other drug that has CNS depressant activities should avoid complex and high-risk activities, particularly those such as driving that require alertness and coordination, until they have experience using the combination. Consider therapy modification

Piribedil: CNS Depressants may enhance the CNS depressant effect of Piribedil. Monitor therapy

Pramipexole: CNS Depressants may enhance the sedative effect of Pramipexole. Monitor therapy

ROPINIRole: CNS Depressants may enhance the sedative effect of ROPINIRole. Monitor therapy

Rotigotine: CNS Depressants may enhance the sedative effect of Rotigotine. Monitor therapy

Rufinamide: May enhance the adverse/toxic effect of CNS Depressants. Specifically, sleepiness and dizziness may be enhanced. Monitor therapy

Selective Serotonin Reuptake Inhibitors: CNS Depressants may enhance the adverse/toxic effect of Selective Serotonin Reuptake Inhibitors. Specifically, the risk of psychomotor impairment may be enhanced. Monitor therapy

Sodium Oxybate: May enhance the CNS depressant effect of CNS Depressants. Management: Consider alternatives to combined use. When combined use is needed, consider minimizing doses of one or more drugs. Use of sodium oxybate with alcohol or sedative hypnotics is contraindicated. Consider therapy modification

Suvorexant: CNS Depressants may enhance the CNS depressant effect of Suvorexant. Management: Dose reduction of suvorexant and/or any other CNS depressant may be necessary. Use of suvorexant with alcohol is not recommended, and the use of suvorexant with any other drug to treat insomnia is not recommended. Consider therapy modification

Tapentadol: May enhance the CNS depressant effect of CNS Depressants. Management: Avoid concomitant use of tapentadol and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Consider therapy modification

Tetrahydrocannabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Tetrahydrocannabinol and Cannabidiol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Thalidomide: CNS Depressants may enhance the CNS depressant effect of Thalidomide. Avoid combination

Trimeprazine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Zolpidem: CNS Depressants may enhance the CNS depressant effect of Zolpidem. Management: Reduce the Intermezzo brand sublingual zolpidem adult dose to 1.75 mg for men who are also receiving other CNS depressants. No such dose change is recommended for women. Avoid use with other CNS depressants at bedtime; avoid use with alcohol. Consider therapy modification

Gabapentin is used for Restless legs syndrome

Gabapentin in the management of restless legs syndrome (RLS) has been evaluated in small controlled trials, demonstrating benefits compared with placebo. Gabapentin enacarbil is FDA-approved for the treatment of RLS .

The American Academy of Sleep Medicine (AASM) guidelines regarding RLS management consider gabapentin effective based on low-level evidence and note that patients with pain symptoms appeared to benefit most.

The benefit-risk ratio is unclear. The European Federation of Neurological Societies/European Neurological Society/European Sleep Research Society (EFNS/ENS/ESRS) Task Force guidelines consider gabapentin effective for short-term management and possibly effective for long-term management of RLS.

Additional study is needed to establish optimal dosing. Based on the International Restless Legs Syndrome Study Group, European Restless Legs Syndrome Study Group, and RLS Foundation (IRLSSG/EURLSSG/RLS-F) guidelines for the prevention and treatment of dopaminergic augmentation in restless legs syndrome, α2δ ligands (eg, gabapentin) are effective and should be considered for the initial treatment of patients with RLS due to their minimal risk of augmentation.

Please do spend some time researching more information on Restless Legs Syndrome for when you do you will find that the very best course of action will be first to get that condition diagnosed by a Doctor and then the best treatment available will be by you then taking Gabapentin regularly to control that condition.

One of the additional ways that you are going to be able to learn more about Restless Legs Syndrome is by watching some of the many videos that are available on sites such as You Tube and also on some of the forums and message boards that people who do suffer from Restless Legs Syndrome visit and engage in.

Below you will find a very informative video presentation that does cover the topic and subject of Restless Legs Syndrome in great detail, so if you do have some additional spare time to watch that video presentation then please do so.

If not then bookmark our website and pay it another visit when you next have some spare time, as you will also find that we do update this site with lots of additional information on topics and subjects such as Restless Legs Syndrome.

If you do want to take Gabapentin to treat restless legs syndrome then please do be aware there can be some side effects, and before you make a purchase of Gabapentin you will be best advised to find out what the side effect of Gabapentin when taking it to treat restless legs syndrome, and if at any time you start to experience any of those side effects then please seek the advice of a Doctor or a medical professional.

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Additionally, patients who experience augmentation on dopaminergic agents may benefit from a switch to α2δ ligands (eg, gabapentin). However, the guidelines note that long-term studies are needed.

Gabapentin is used for Neuropathic pain (other than postherpetic neuralgia)

In a meta-analysis of trials evaluating the treatment of neuropathic pain, including painful polyneuropathy and spinal cord injury pain, gabapentin was shown to be safe and effective .

Data from meta-analyses support the use of immediate-release gabapentin for reducing pain by more than 50% in diabetic neuropathy.

Data from a limited number of clinical trials support the use of extended-release gabapentin in reducing pain by more than 50% and improving sleep in diabetic neuropathy.

Not many people are aware of the medical condition that is known as Diabetic Neuropathy however more and more people are being diagnosed with having it, and if you have been recently diagnosed with Diabetic Neuropathy then you will need to start to take drug to help manage and control that condition.

The best drug you can take is the fast acting Gabapentin and one of the main reasons why many people who do have Diabetic Neuropathy will take that drug is that it is not only fast acting as mentioned but it is also a very low cost drug to purchase too.

Please do spend some time researching more information on Diabetic Neuropathy for when you do you will find that the very best course of action will be first to get that condition diagnosed by a Doctor and then the best treatment available will be by you then taking Gabapentin regularly to control that condition.

You will also be best advised to also spend a few minutes watching the following video that is going to explain to you more about Diabetic Neuropathy including the Types, Symptoms, Prevention and Treatment of Diabetic Neuropathy which you will certainly find very informative and educational too.

Also please do be aware that we do have a range of other articles and guides dotted around this website that will also give you additional information on a range of similar medical conditions that you may be suffering from or experiencing, so please do spend as much time as you like looking around our website as all of that information is free to access.

We also update our website continually with other related news stories and articles so do consider bookmarking this website and checking back regularly too.

If you do want to take Gabapentin to treat diabetic neuropathy then please do be aware there can be some side effects, and before you make a purchase of Gabapentin you will be best advised to find out what the side effect of Gabapentin when taking it to treat diabetic neuropathy, and if at any time you start to experience any of those side effects then please seek the advice of a Doctor or a medical professional.

There are going to be plenty of places online that you can buy Gabapentin, however when you make the very wise decision of using us as your official suppler of Gabapentin you are guaranteed of having the very lowest prices available to you and also as an approved stockiest you will of course always be guaranteed of receiving genuine Gabapentin too. To place an order right away simply click onto any of the order now links displayed on this site.

Based on guidelines from the International Association for the Study of Pain (IASP), European Federation of Neurological Societies (EFNS), and Society of Critical Care Medicine (SCCM), gabapentin is effective and recommended for the management of peripheral neuropathy .

Based on guidelines from the EFNS, IASP, and National Institute for Health and Care Excellence (NICE), gabapentin is effective and recommended as first-line therapy, supported by strong evidence, in the management of diabetic neuropathy.

The IASP guidelines recommend both immediate- and extended-release gabapentin . In contrast, a guideline from the American Academy of Neurology (AAN), American Association of Neuromuscular and Electrodiagnostic Medicine, and American Academy of Physical Medicine and Rehabilitation states that gabapentin is probably effective and should be considered an alternative treatment for painful diabetic neuropathy based on limited benefit in 2 controlled trials.

Similarly, a position statement from the American Diabetes Association (ADA) recommends gabapentin as a second-line option .

Gabapentin has been shown to be beneficial in treating several types of neuropathic pain; however, the mechanism of action by which gabapentin exerts its analgesic effect is still unknown.¹ It is suggested that gabapentin may block the calcium channel alpha(2)delta (a2d)-1 receptor in the brain. This protein-modulated receptor is involved in excitatory synapse formation. Therefore, the therapeutic effects of gabapentin may be attributed to prevention of new synapse formations.

Gabapentin for neuropathic pain — neuropathic pain

Gabapentin was shown to offer substantial improvement in neuropathic pain with side effects that were similar to those on placebo.

Even with sufficient data supporting the use of gabapentin in the treatment of various neuropathic pain conditions, gabapentin only has Food and Drug Administration (FDA) approval for PHN. Dosing recommendations for off-label use of gabapentin can be somewhat ambiguous, if a recommendation exists at all. Therefore, several studies further investigate dosing regimens specific to other neuropathic pain syndromes.

Gabapentin Dosing Considerations

Three gabapentin products are FDA approved to treat PHN. The different formulations cannot be interchanged and each has its own dosing schedule.

For immediate-release gabapentin (Neurontin), dosing may be initiated with 300 mg on day 1, doubled on day 2 (300 mg twice a day), and tripled on day 3 (300 mg 3 times a day). The dose can then be titrated up as needed for pain relief to a maximum dose of 1,800 mg daily (divided into 3 daily doses). Clinical studies referenced in the package insert state that efficacy for a range of doses from 1,800 mg/day to 3,600 mg/day were observed; however, there was no additional benefit seen with doses greater than 1,800 mg/d.
Gralise is an extended-release gabapentin formulation that also is FDA approved for PHN with a titration schedule that begins with 300 mg on day 1; 600 mg on day 2; 900 mg on days 3 to 6; 1,200 mg on days 7 to 10; 1,500 mg on days 11 to 14; and 1,800 mg on day 15 and thereafter.
The third gabapentin formulation for PHN treatment is another extended-release product, Horizant. The starting dose is 600 mg in the morning for 3 days, increased to 600 mg twice daily on day 4 and thereafter. A daily dose of Horizant greater than 1,200 mg provided no additional benefit at the expense of side effects.³

Several studies have evaluated off-label use of gabapentin in the treatment of other neuropathic pain conditions. A randomized, double-blind trial compared gabapentin to placebo in 135 patients with DPN over 8 weeks. The results showed a statistical benefit of gabapentin compared to placebo, at all end points, for pain improvement.⁴ The gabapentin dosing regimen used in this study was 900 mg/d for week 1; 1,800 mg/d for week 2; 2,400 mg/d for week 3; and 3,600 mg/d for week 4. All the patients were titrated up to a dose of 3,600 mg/d, regardless of efficacy at lower doses. Patients who could not tolerate this dose were titrated down to the greatest tolerable dose.

Of the 84 patients randomized to the gabapentin group, 56 (67%) were able to tolerate 3,600 mg/d.⁴During the first week, gabapentin resulted in improvement in sleep interference compared to placebo. By the second week, gabapentin resulted in improvement in all pain rating scales compared to placebo. Of the 84 patients in the gabapentin group, 70 completed the study, and 7 patients withdrew due to adverse drug events (ADEs). Most ADEs reported in the gabapentin group were of mild or moderate intensity, and the most frequently reported effects were dizziness (23.8%), somnolence (22.6%), headache (10.7%), diarrhea (10.7%), confusion (8.3%), and nausea (8.3%).

A double-blind crossover study (n=40) assessed gabapentin for the treatment of DPN. The dose of gabapentin used in this trial was much lower, with patients titrated up every

3 days to a maximum dose of 900 mg/d. The end points evaluated in this study included level of pain on a visual analog pain scale (VAS), and scores on the present pain intensity scale, the McGill pain questionnaire (MPQ), and the global assessment of pain relief. Statistical improvement between gabapentin and placebo was noted in only 1 end point, the MPQ score, with a mean reduction of 8.9 points for gabapentin compared to 2.2 points with placebo (P=0.03).

No serious ADEs were noted, and the most common ADEs of gabapentin were drowsiness, fatigue, and imbalance. The results of this study suggest that gabapentin is not effective or is only minimally effective in treating painful DPN at a dose of 900 mg/d.

A search in the Cochrane Database of Systematic Reviews was conducted to further examine dosing regimens for neuropathic pain. In a review analyzing 37 studies for gabapentin treatment in chronic neuropathic pain, the main outcome was Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (IMMPACT) definitions for moderate and substantial benefit in chronic pain studies.⁶ These were defined as follows:

30% reduction in pain over baseline (moderate)
50% reduction in pain over baseline (substantial)
Much or very much improved on Patient Global Impression of Change (PGIC) (moderate)
Very much improved on PGIC (substantial)
Gabapentin was shown to be better than placebo across all studies for IMMPACT outcomes. The review concentrated on gabapentin doses of 1,200 mg/d or greater and reported that doses at or above this threshold were reasonably effective for treatment of various neuropathic pain types. The upper threshold for maximum effective gabapentin doses ranged from 2,400 mg/d to 3,600 mg/d in the majority of studies reviewed.⁶ Table 1, on page 16, provides a more detailed description of the maximum gabapentin doses evaluated for different neuropathic pain types.

ADEs and withdrawal rates for patients taking gabapentin doses of 1,200 mg/d or greater were compared to those for patients taking placebo in 20 studies with 4,125 participants. Common ADEs seen were somnolence, drowsiness, and sedation. These occurred in 14% of participants in the gabapentin group versus 5% of those taking placebo. Data also showed gabapentin was associated with a higher incidence of dizziness (19% vs 5%), peripheral edema (7% vs 2.2%), and ataxia or gait disturbances (8.8% vs 1.1%). The rate of serious events was similar between gabapentin and placebo groups. Twenty-two studies involving 4,448 patients reported on participant withdrawals due to ADEs, which occurred in 11% of patients taking gabapentin compared to 7.9% of those taking placebo.⁶

Postmarketing Abuse

Postmarketing reports have described symptoms of agitation, confusion, and disorientation upon abrupt withdrawal of gabapentin. Cases usually involve other potentiating factors, such as the use of higher than recommended doses for unapproved indications, a history of poly-substance abuse, or the use of gabapentin to relieve symptoms of withdrawal from other substances.

In a study of postmortem toxicology, cases that tested positive for gabapentin or pregabalin were included to determine if abuse of these drugs contributed to the fatalities. Of the 13,766 cases investigated, 0.31% were positive for gabapentin. Of the gabapentin cases, 18.6% were considered abuse, and 4.7% were poisonings.

An overwhelming majority of abuse cases (87.5%) also involved opioid intoxication, and 100% involved alcohol and/or opioids. In addition, a greater number of pregabalin cases were designated as abuse cases than gabapentin cases (48.1% vs 18.6%, respectively).

Conclusion

Gabapentin has sufficient evidence showing its efficacy and safety in treating neuropathic pain. Effective treatment doses of gabapentin for neuropathic pain tend to be higher compared to effective treatment doses for other conditions. Gabapentin is a relatively safe medication. The most prevalent effects seen are drowsiness, somnolence, and sedation. It is necessary to start at lower doses of gabapentin and titrate up to a therapeutic dose. Ataxia and somnolence appear to exhibit a positive dose-response relationship; therefore, titrating the dose of gabapentin may help manage possible ADEs.

Gabapentin Usage for Alcohol disorder and Alcohol withdrawal

Alcohol use disorder, moderate to severe (alternative agent)

Data from randomized, double-blind, placebo-controlled studies support the use of gabapentin in the maintenance of abstinence in patients with alcohol use disorder.

Based on the American Psychiatric Association (APA) guidelines for the pharmacological treatment of patients with alcohol use disorder, gabapentin is suggested for patients with alcohol use disorder (moderate to severe) who want to decrease or abstain from use of alcohol and either prefer gabapentin or are unable to tolerate or are unresponsive to naltrexone and acamprosate .

Based on the VA/DoD clinical practice guideline for the management of substance use disorders, gabapentin given for moderate to severe alcohol use disorder is effective and suggested when first-line pharmacotherapy is contraindicated or ineffective.

Alcohol withdrawal, mild (alternative agent)

Data from a randomized, double-blind, active-controlled study support the use of gabapentin in the treatment of alcohol withdrawal.

Based on the VA/DoD clinical practice guideline for the management of substance use disorders, gabapentin given for mild alcohol withdrawal is effective and suggested when the risk of benzodiazepines outweigh the benefits (eg, inadequate monitoring available, abuse liability, contraindication, adverse reaction).

Gabapentin Pharmacology

Gabapentin is structurally related to GABA. However, it does not bind to GABA_A or GABA_B receptors, and it does not appear to influence synthesis or uptake of GABA.

High affinity gabapentin binding sites have been located throughout the brain; these sites correspond to the presence of voltage-gated calcium channels specifically possessing the alpha-2-delta-1 subunit.

This channel appears to be located presynaptically, and may modulate the release of excitatory neurotransmitters which participate in epileptogenesis and nociception.

Although its exact mode of action is not known, gabapentin appears to have a unique effect on voltage-dependent calcium ion channels at the postsynaptic dorsal horns and may, therefore, interrupt the series of events that possibly leads to the experience of a neuropathic pain sensation.

Gabapentin is especially effective at relieving allodynia and hyperalgesia in animal models. It has been shown to be efficacious in numerous small clinical studies and case reports in a wide variety of pain syndromes. Gabapentin has been clearly demonstrated to be effective for the treatment of neuropathic pain in diabetic neuropathy and postherpetic neuralgia.

This evidence, combined with its favourable side-effect profile in various patient groups (including the elderly) and lack of drug interactions, makes it an attractive agent. Therefore, gabapentin should be considered an important drug in the management of neuropathic pain syndromes.

Absorption

Variable, from proximal small bowel by L-amino transport system; saturable process; dose-dependent

Distribution

V_d: 58 ± 6 L; CSF concentrations are ~20% of plasma concentrations

Metabolism

Not metabolized

Excretion

Proportional to renal function; urine (as unchanged drug)

Clearance: Apparent oral clearance is directly proportional to CrCl: Clearance in infants is highly variable; oral clearance (per kg) in children <5 years of age is higher than in children ≥5 years of age

Time to Peak

Immediate release: Infants 1 month to Children 12 years: 2 to 3 hours; Adults: 2 to 4 hours; Extended release: 8 hours

Half-Life Elimination

Infants 1 month to Children 12 years: 4.7 hours

Adults, normal: 5 to 7 hours; increased half-life with decreased renal function; anuric adult patients: 132 hours; adults during hemodialysis: 3.8 hours

Protein Binding

<3%

Gabapentin Side Effects For Healthcare Professionals

Applies to gabapentin: compounding powder, oral capsule, oral solution, oral tablet, oral tablet extended release

Cardiovascular

Common (1% to 10%): Peripheral edema, vasodilation, hypertension

Rare (less than 0.1%): Atrial fibrillation, heart failure, myocardial infarction, cerebrovascular accident, ventricular extrasystoles, bradycardia, premature atrial contraction, pericardial rub, heart block, pericardial effusion, pericarditis

Postmarketing reports: Cardiac arrest, chest pain, palpitation, tachycardia^[Ref]

Dermatologic

Common (1% to 10%): Abrasion, facial edema, purpura, rash, pruritus, acne

Uncommon (0.1% to 1%): Alopecia, eczema, dry skin, increased sweating, urticaria, hirsutism, seborrhea, cyst, herpes simplex

Rare (less than 0.1%): Stevens-Johnson syndrome, angioedema, erythema multiforme, drug rash (with eosinophilia and systemic symptoms), herpes zoster, skin discolor, skin papules, photosensitive reaction, psoriasis, desquamation, maceration, skin nodules, subcutaneous nodule, melanosis, skin necrosis, local swelling

Frequency not reported: DRESS/multiorgan hypersensitivity^[Ref]

Endocrine

Rare (less than 0.1%): Hyperthyroid, hypothyroid, goiter, hypoestrogenism, ovarian failure, epididymitis, cushingoid appearance^[Ref]

Gastrointestinal

Common (1% to 10%): Diarrhea, dry mouth or throat, constipation, nausea, vomiting, dyspepsia, dental abnormalities, gingivitis, abdominal pain, flatulence

Uncommon (0.1% to 1%): Glossitis, gum hemorrhage, thirst, stomatitis, increased salivation, gastroenteritis, hemorrhoids, bloody stools, fecal incontinence

Rare (less than 0.1%): Pancreatitis, dysphagia, eructation, pancreatitis, peptic ulcer, colitis, blisters in mouth, tooth discoloration, perlèche, salivary gland enlarged, lip hemorrhage, esophagitis, hiatal hernia, hematemesis, proctitis, irritable bowel syndrome, rectal hemorrhage, esophageal spasm

Frequency not reported: Dehydration^[Ref]

General

The most common adverse reactions associated with the use of this drug were dizziness, somnolence, and peripheral edema.^[Ref]

Genitourinary

Common (1% to 10%): Incontinence, impotence

Uncommon (0.1% to 1%): Hematuria, dysuria, urinary frequency, cystitis, urinary retention, vaginal hemorrhage, amenorrhea, dysmenorrhea, menorrhagia

Frequency not reported: Breast hypertrophy, gynecomastia, sexual dysfunction (including changes in libido, ejaculation disorders, and anorgasmia)^[Ref]

Hematologic

Common (1% to 10%): Leucopenia, purpura

Uncommon (0.1% to 1%): Anemia, lymphadenopathy

Rare (less than 0.1%): Thrombocytopenia, thrombophlebitis, leukocytosis, lymphocytosis, increased bleeding time

Frequency not reported: Blood creatine phosphokinase increased, coagulation defect^[Ref]

Hepatic

Rare (less than 0.1%): Hepatitis, jaundice, elevated liver function tests SGOT (AST), SGPT (ALT), and bilirubin, hepatomegaly, hepatotoxicity^[Ref]

Hypersensitivity

Very rare (less than 0.01%): Hypersensitivity syndrome, a systemic reaction with a variable presentation that can include fever, rash, hepatitis, lymphadenopathy, eosinophilia, and sometimes other signs and symptoms^[Ref]

Metabolic

Common (1% to 10%): Weight gain, hyperglycemia

Postmarketing reports: Hyponatremia^[Ref]

Musculoskeletal

Common (1% to 10%): Back pain, arthralgia, myalgia, twitching

Uncommon (0.1% to 1%): Tendonitis, arthritis, joint stiffness, joint swelling

Frequency not reported: Rhabdomyolysis, myoclonus

Postmarketing reports: Elevated creatine kinase, rhabdomyolysis^[Ref]

Nervous system

Very common (10% or more): Somnolence (21%), dizziness (17%), ataxia (13%)

Common (1% to 10%): Abnormal gait, incoordination, neuralgia, tremor, dysarthria, hyperkinesia, seizures, dysarthria, paresthesia, hypesthesia, coordination abnormal, increased/decreased/absent reflexes, vertigo

Uncommon (less than 1%): Hypokinesia

Rare (less than 0.1%): Movement disorders (e.g., choreoathetosis, dyskinesia, dystonia), loss of consciousness

Frequency not reported: Withdrawal precipitated seizure/status epilepticus

Postmarketing reports: Movement disorder^[Ref]

Ocular

Common (1% to 10%): Amblyopia, conjunctivitis, diplopia, nystagmus

Uncommon (0.1% to 1%): Cataract, dry eyes, eye pain, visual field defect, photophobia, bilateral or unilateral ptosis, eye hemorrhage, hordeolum, eye twitching

Rare (less than 0.1%): Eye itching, abnormal accommodation, eye focusing problem, watery eyes, retinopathy, glaucoma, iritis, corneal disorders, lacrimal dysfunction, degenerative eye changes, blindness, retinal degeneration, miosis, chorioretinitis, strabismus^[Ref]

Oncologic

Uncommon (0.1% to 1%): Breast cancer

Rare (less than 0.1%): Non-Hodgkin’s lymphoma^[Ref]

Other

Very common (10% or more): Fatigue (11%), fever (11%)

Common (1% to 10%): Asthenia, accidental injury, otitis media, tremor, pain

Rare (0.01% to 0.1%): Tinnitus

Very rare (less than 0.01%): Sudden unexplained death in patients with epilepsy

Frequency not reported: Sleepwalking, withdrawal symptoms, hearing loss, earache, tinnitus, inner ear infection, otitis, taste loss, unusual taste, ear fullness, perforated ear drum, sensitivity to noise, eustachian tube dysfunction, otitis externa, odd smell, labyrinthitis^[Ref]

Psychiatric

Common (1% to 10%): Abnormal thinking, amnesia, depression, hostility, confusion, emotional liability, anxiety, nervousness, insomnia

Uncommon (0.1% to 1%): Mental impairment

Rare (less than 0.1%): Hallucinations

Frequency not reported: Suicidal behavior and ideation, hypomania^[Ref]

Renal

Rare (less than 0.1%): Acute renal failure^[Ref]

Respiratory

Common (1% to 10%): Pharyngitis, dyspnea, cough, bronchitis, respiratory infection, rhinitis

Rare (less than 0.1%): Pulmonary thrombosis, pulmonary embolism

Frequency not reported: Pseudo-croup, hoarseness