Buy Neurontin Online UK

Gabapentin, the active substance of Neurontin, is able to prevent seizures.

Gabapentin by structure is similar to GABA, but does not affect its metabolism. Once in the body, it connects with alpha-2-beta-ribosomal-dependent calcium channels, which leads to a decrease in the flow of calcium ions and reduce the likelihood of neuropathic pain.

Gabapentin reduces the level of glutamate-dependent nerve cells, increases the formation of GABA, reduces the release of Neuroneurotransmitters Monoaminova group.

£0.46Per pill

Neurontin is used for treating seizures associated with epilepsy.

Pharmacotherapy and pharmacokinetics

NEURONTIN® (Gabapentin):

The tablet includes 600 mg or 800 mg gabapentin, and auxiliary substances: corn starch, talc, magnesium Stearat, Kopovidon, Gipolazu, Poloxamer 407, wax polishing, white "opadrai" (Opadry White).

Capsules contain on 100, 300 or 400 mg gabapentin.

Release form

The drug Neurontin is produced in the following forms:

  • Capsules for 100 mg, 300 mg and 400 mg; Outside capsules White (100 mg), light yellow (300 mg) or gray-orange (400 mg), with the inscription of blue or gray (the name of the drug, the number of active substance and "PD"), inside white or almost white powdered substance;
  • Tablets covered with white shell, 600 mg and 800 mg, elliptical, with the inscription black (600 mg) or orange (800 mg) color.

and capsules, and tablets of 10 pieces packed in blister. In packages can be 2, 5 or 10 pieces.

Pharmacological action

The drug Neurontin refers to anticonvulsant, antiepileptic drugs.


The maximum level of bioavailability is 60%, but it is reduced by increasing the dose. The maximum concentration in blood plasma is reached in 2-3 hours after taking the medicine. Gabapentin is almost not associated with plasma proteins (no more than 3%).

The half-life period is approximately 5-7 hours, regardless of the dose accepted. Excreted from the body unchanged due to the work of the kidneys.


Gabapentin (Neurontin) for epilepsy - effectiveness

Gabapentin for epilepsy - the effectiveness of Gabapentin is proven by the research of neurologists. Now there is evidence that it inhibits glutamate synthesis and increases the level of GABA in brain tissue.

The drug is also used to treat neuropathic pain. Gabapentin is absorbed in the intestines and absorbed. This leads to 60% digestibility, 300 mg doses, but only 40% digestibility at a dose of 900 mg. Absorbency can be reduced when taking fatty foods.

It is also known that antacids bind to gabapentin and reduce its bioavailability by 20%. Gabapentin does not bind to plasma proteins and does not cause the production of hepatic enzymes. In case of renal failure it is necessary to reduce the dose.

Side effects - drowsiness, dizziness and ataxia.

This article describes the instructions for use of the drug Gabapentin. There are reviews of consumers of this drug, as well as the views of British medical scientists on the use of Gabapentin. Gabapentin should be used to treat epilepsy and partial seizures, neuralgia pain in adults, children, as well as during pregnancy and breastfeeding.

Composition and interaction of the drug with alcohol.

Studies of the drug have shown that Gabapentin binds to the alpha2-omega-subunit of voltage-dependent calcium channels and reduces the flow of calcium ions, which play an important role in causing neuropathic pain. Other mechanisms of action of Gabapentin in neuropathic pain are the reduction of glutamate-dependent neuronal death, an increase in GABA synthesis, the suppression, and release of the neurotransmitters of the monoamine group. At clinically relevant concentrations, gabapentin does not bind to receptors for other common drugs or neurotransmitters, including the GABAA, GABAH, benzodiazepine, glutamate, glycine or N-methyl-D-aspartate receptors.

Unlike phenytoin and carbamazepine, Gabapentin does not interact with sodium channels. Gabapentin partially attenuated the effects of the N-methyl-D-aspartate glutamate receptor agonist in some in vitro tests, but only at a concentration of more than 100 μmol, which is not achieved in vivo. Gabapentin partially reduces the release of monoamine neurotransmitters.

Medical properties of the drug, pharmacological action.

  • Gabapentin is a nootropic agent. It facilitates the transmission of nerve impulses in the central nervous system, also has tranquilizing, psychostimulating and antioxidant effects.
  • Improves the functional state of the brain and affects the cerebral circulation. It helps to reduce or completely eliminate feelings of anxiety, tension, anxiety, fear, normalizes sleep, has an anticonvulsant effect.
  • Reduces the manifestations of asthenia (including headache, feeling of heaviness in the head, sleep disturbances, irritability), increases mental performance.
  • Improves psychological indicators (attention, memory).
  • When taking exchange rate, it increases physical and mental performance, improves memory, normalizes sleep;
  • improves the condition of patients with motor and speech disorders. Patients with asthenia from the first days of treatment improves health. When applied after severe TBI improves the course of bioenergetic processes in the brain.
  • Elderly people do not cause congestion and excessive lethargy, a relaxing after-effect is not observed. It improves microcirculation in the tissues of the eye, reduces the effect on the central nervous system. Nontoxic.


How to treat epilepsy
Depression, mania, anxiety
Anticonvulsant, Anti-Seizure Medication
How to overcome neuropathic pain

The withdrawal of the drug from the body

Gabapentin is excreted exclusively by the kidneys in unchanged form, is not subjected to metabolism.

Instructions for use and dosage

Capsules 100 mg, 300 mg and 400 mg

Swallowing whole, regardless of the meal, with plenty of water. If there is a need to reduce the dose, discontinue the drug or replace it with an alternative means, this should be done gradually over one week.

The initial daily dose is 300 mg (1 dose), if necessary, gradually increase the dose to the maximum. Treatment can begin immediately with a dose of 300 mg per day, gradually increase to 900 mg per day according to the following scheme:

  • 1st day: 300 mg 1 time per day;
  • 2nd day: 300 mg 2 times a day;
  • 3rd day: 300 mg 3 times a day.

Adults and children from 12 years old: effective dose - from 300 to 900 mg per day (divided into 3 equal doses). The maximum interval between taking the drug should not exceed 12 hours in order to avoid the resumption of seizures.

Adults and children from 12 years old: effective dose - from 300 to 900 mg per day (divided into 3 equal doses). The maximum interval between taking the drug should not exceed 12 hours in order to avoid the resumption of seizures.

Dosage should be under the supervision of a physician. Uncontrolled reception will lead to unpleasant consequences.

For the treatment of neuropathic pain and partial seizures, physicians first use the minimum daily dose, divide the drug in three parts. If necessary, to achieve a clinical effect, the dosage of gabapentin is increased to the maximum.

If you abruptly stop treatment with anticonvulsants, then the patient with epilepsy may develop convulsive status. If it is necessary to start treatment with other medicines, then they do it gradually, within a week, they begin to reduce the dosage of gabapentin, and only then begin treatment with another drug.

If kidney pathologies are identified, patients need to adjust the dosage of the drug to prevent the development of complications.

Use during pregnancy and lactation

There are no data on the use of the drug in pregnant women, so gabapentin should be used during pregnancy only if the intended benefit to the mother justifies the possible risk to the fetus.

The effect of Gabapentin on the infant is unknown, so during treatment, breastfeeding should be abandoned.

Contraindicated in the age of 12 years with convulsions. For the treatment of neuropathic pain, do not prescribe to children and adolescents under 18 years of age.

Influence on ability to drive motor transport and control mechanisms

Patients while taking Gabapentin should not drive a car, nor do work that requires psychomotor speed, because gabapentin affects consciousness and concentration.

Neurontin, pharmacology.

Neurontin is a drug intended to treat epileptic seizures. The main active ingredient of the drug is gabapentin, a white powder that dissolves easily in water.

Mechanism of action

Once in the body Neurontin begins to act. This leads to the fact that the flow of calcium ions is significantly reduced, and therefore the risk of neuropathic pain is reduced.

In the body, Neurontin promotes an increase in GABA synthesis. Bioavailability decreases with increasing dose. Its maximum concentration in the body is reached some time after taking the capsule.

Analogues of the drug.

Gabagamma (manufacturer Germany - Artesan Pharma)

Tebantin (Gideon-Richter)

These drugs contain gabapentin in their composition. The difference between these drugs is in appearance and price, which is formed depending on the manufacturer, the technology used to manufacture the drug, and the quality of the raw materials used.


Prescribe the drug to people who suffer from the following diseases:

  • Epilepsy, accompanied by partial convulsions. Children over 12 years old are prescribed only this drug. Adults in the treatment of epilepsy prescribed in combination, Neurontin and other anticonvulsant drugs.
  • Neuropathic pain (over 18 years).


Neurontin should not be used if a person is hypersensitive to the active component, has a tendency to psychotic reactions, and also is under 12 years old. The prescription of this drug in patients with renal insufficiency requires caution.

Side effects

Gabapentin is a potent drug that affects the entire body.

Drowsiness, dizziness, fatigue, increased nervous irritability.

Indications for use

Assign gabapentin, with:

  • Localized epilepsy.
  • Symptomatic epilepsy and epileptic syndromes with convulsive seizures.
  • Neuralgic pains.

Clinical characteristics of neuropathic pain.


From the standpoint of pathophysiology, it is now customary to distinguish between nociceptive and neuropathic pain. Nociceptive is the pain caused by the action of a factor (mechanical trauma, burn, inflammation, etc.) on peripheral pain receptors, with intactness of all parts of the nervous system. By neuropathic is meant the pain that occurs when an organic lesion or dysfunction of various parts of the nervous system. The causes of NB can be damage to the nervous system at any level, ranging from peripheral nerves to the cortex of the cerebral hemispheres. In neurology, the term neuropathic or neuropathic usually refers to peripheral nerve damage. In this regard, there may be a misconception that neuropathic pain is pain arising exclusively from peripheral neuropathy or polyneuropathy. Here it should be emphasized once again that the term neuropathic pain refers to pain syndrome that occurs with the defeat or dysfunction of both the peripheral and central nervous system at any level (Table 1).

In the NB population, it occurs in 1-1.5% of cases. Today NB unites a whole group of chronic pain syndromes that were previously considered independently. This group includes pain in various mono- and polyneuropathies. Among them, the most frequent pain occurs in diabetic and alcoholic polyneuropathy (25-45%). Postherpetic neuralgia (in old age, this complication occurs in 70% of cases of herpes zoster) is also a variant of NB. The complex regional pain syndrome (local pains with swelling, trophic disorders and osteoporosis), previously referred to as reflex sympathetic dystrophy, is a neuropathic form of pain. Neuralgia of the trigeminal nerve, phantom pain, post-stroke central pain, pain in multiple sclerosis, syringomyelia, spinal cord lesions are typical examples of neuropathic pain. According to various authors, NB occurs: in diabetic polyneuropathy - up to 45%, multiple sclerosis - 28%, syringomyelia - 75%, cerebral stroke - 8%, nerve injury - 5%. Among all patients with NB, the majority (about 50%) are in patients with diabetic polyneuropathy. Unfortunately, the pain in these patients is often interpreted as vascular or vertebral. This leads to inadequate therapeutic interventions.

Nociceptive pains are often acute in their development, while neuropathic pains are predominantly chronic. In certain cases there is a combination of nociceptive and neuropathic components of pain (with compression radiculopathy).

Pathophysiological aspects of NB

The pathophysiological mechanisms of neuropathic pain syndrome are complex. Neuropathic pain is the result of impaired interaction between nociceptive and antinociceptive systems as a result of their defeat or dysfunction at various levels of the nervous system. The most studied are the mechanisms of pathogenesis concerning the functions of peripheral nerves, roots, the posterior horn of the spinal cord, pain neurotransmitters, glutamate receptors, sodium and calcium channels. These include spontaneous ectopic activity of damaged axons, sensitization of pain receptors, pathological interactions of peripheral sensory fibers, and hypersensitivity to catechol amines. Much attention is paid to the study of the mechanisms of central sensitization, the phenomenon of "inflation", the lack of antinociceptive descending effects on the posterior horn of the spinal cord.

The central sensitization of a group of spinal cord neurons is the result of neuronal plasticity activated by primary afferent stimulation. This process is considered crucial in the formation of neuropathic pain syndrome, leading to the development of allodynia and Hyperpathies.

Voltage-dependent calcium N-channels are located in the surface plate of the posterior horn of the spinal cord and are involved in the formation of neuropathic pain. There is evidence of an increase in the release of neurotransmitters with the activation of N and P types of voltage-dependent calcium channels. The a2d subunit, which is part of all voltage-dependent calcium channels, is thought to be the target of the anti-allodynic action of Neurontin.

Treatment of neuropathic pain

NB therapy is often very difficult, which is reflected in the wide variety of treatments used.

In the treatment of neuropathic pain, non-drug and drug approaches are used. Among non-pharmacological approaches are used that enhance the activity of antinociceptive systems: acupuncture, transcutaneous electro stimulation, spinal cord stimulation, physiotherapy, biofeedback, psychotherapy. Less commonly used are blockades and neurosurgical treatment methods (destruction of the posterior root occurrence zone) that block the flow of afferent nociceptive afforestation. In NB pharmacotherapy, the following groups of drugs are used: local anesthetics, opioid drugs, central muscle relaxants, antiarrhythmic drugs, antidepressants and anticonvulsants. It should be noted that simple analgesics (paracetamol, aspirin) and nonsteroidal anti-inflammatory drugs (diclofenac, indomethacin, etc.) are ineffective in NB and are not used to treat it. This is due to the fact that in NB the main path genetic mechanisms are not inflammation processes, but neuronal and receptor disorders, peripheral and central sensitization.

Local anesthetics (lidocaine 5% cream or patch) are used to block peripheral nociceptors; Perineal injections of corticosteroids or a combination of corticosteroids and local anesthetics can be used to treat pain with mono neuropathy and neuroma. Other drugs used in patients with neuropathic pain include central muscle relaxants (baclofen, tizanidine) and opioid analgesics (morphine, codeine, oxycodone, tramadol, dextromethorphan, metodon). Some membrane stabilizing drugs, which include lidocaine and meksiletin, are sometimes used to treat NB in diabetic and alcoholic polyneuropathy. However, frequent side effects limit the use of these agents.

Most often, antidepressants are prescribed for NB. However, the use of these drugs is often limited by their side effects (especially in tricyclic antidepressants), associated with anticholinergic effects, the likelihood of orthostatic hypotension and arrhythmias.

Anti-consultants have been used in the treatment of chronic pain since 1942 (defining). Carbamazepine was recognized as the drug of first choice in the treatment of trigeminal neuralgia. Information on the effectiveness of Valproic acid in neuropathic pain is contradictory and is mainly based on the results of uncontrolled studies and individual clinical cases.

Even the earliest reports indicated the limited use of anticonvulsants in the treatment of pain syndromes. Thus, their higher efficacy was shown for pain associated with peripheral lesions than for central pain. Despite the available data on the positive response of persistent pain to anticonvulsants, the higher efficacy of antiepileptic drugs in acute and paroxysmal pain has been shown. In addition, the effectiveness of anticonvulsants can be achieved at the cost of quite serious side effects (anemia, hepatotoxicity, endocrinopathy, etc.).

Given the above limitations, anti-epileptic drugs can be effective when other drugs are unsuccessful or contraindicated, and research on the role of anticonvulsants of the new generation in pain therapy is quite justified.

The emergence of a new drug gabapentin (Neurontin, firm Pfizer, USA) has opened up new perspectives in the treatment of NB and many other chronic pain syndromes.

Application of Neurontin in Neuropathic Pain

Mechanism of action and properties

Neurontin was originally synthesized as a structural analogue of gamma-aminobutyric acid (GABA) and belongs to the widely used antiepileptic drugs. According to the results obtained in experimental animal models, it has been shown that the drug enhances GABA synthesis, has a modulating effect on NMDA receptors, blocks the a2d subunit of calcium channels, reduces the release of monoamines, reduces the synthesis and transport of glutamate, and reduces the frequency of action potentials of peripheral nerves. Probably a combination of the above mechanisms of action provides a high therapeutic efficacy of Neurontin in various forms of neuropathic pain syndrome.

The drug is well tolerated, side effects are extremely rare. The most common may be light dizziness or drowsiness. The drug has no serious interactions with other drugs. However, one should refrain from combining Neurontin with alcohol, tranquilizers, antihistamines, barbiturates, anticonvulsants, hypnotics, muscle relaxants, drugs. The combination of Neurontin with other anti-pain drugs (lidocaine, antidepressants) enhances the therapeutic effect.

The concentration of drugs in the plasma reaches a peak after 2-3 hours after administration. The interval between doses of the drug should not exceed 12 hours. Bioavailability is 60%. Eating does not affect the pharmacokinetics. Due to the fact that antacids (Maalox) reduce the concentration of Neurontin in the blood, it is recommended to take it no earlier than 2 hours after taking antacids. The drug is excreted mainly by the kidneys, without being metabolized in the liver. In case of kidney pathology, to avoid an increase in the concentration of Neurontin in the blood, the dose is adjusted in accordance with creatinine clearance.

In children, side effects are more common than in adults. In elderly Neurontin is slowly excreted from the body, and therefore the dose of the drug should be reduced. It is known that tabs is excreted in breast milk, but the effect of the drug on a child has not been studied. The possible teratogenic effect of the drug is also unknown.

The appointment in all forms of NB is carried out according to the scheme indicated in Table 2. The most common daily therapeutic dose of Neurontin is 1800-3600 mg / day.

Effectiveness of Neurontin in neuropathic pain

Clinical studies of Neurontin in the treatment of neuropathic pain differ in a systematic approach using a sufficient number of patients and a large number of positive results of therapy.

Neurontin in peripheral polyneuropathy.

In the work of Backonja et al (1999) on the example of 165 patients according to the results of a double-blind, placebo-controlled study, the high efficacy of Neurontin in reducing neuropathic pain in diabetic polyneuropathy was shown.

In the study Merren (1998), among 59 patients with various nosologies who received Neurontin, 26 had peripheral NB, six had a central, and 14 had a migraine. In the remaining 13 patients, essential tremor or restless legs syndrome was observed. Treatment was most effective among patients with peripheral neuropathies and trigeminal neuralgia.

According to the results of the aforementioned and a number of other double-blind, placebo-controlled studies of Neurontin studies, it is currently one of the most effective drugs in the treatment of NB in diabetic polyneuropathy.

The recommended dose of Neurontin for the treatment of neuropathic pain in diabetic polyneuropathy is 1800-2400 mg / day. Treatment begins with 300 mg / day, then during the first week increase to 1800 or 2400 mg / day. The course of treatment should be carried out continuously for 2-4 months.

Neurontin in the treatment of pain with Postherpetic neuralgia.

The effectiveness of Neurontin in Postherpetic neuralgia was shown in a large randomized study using 229 patients as an example. At the same time, there was not only a marked reduction in pain, but also an improvement in the sleep, mood and quality of life of the patients. These data are confirmed by a number of other works.

The dose of Neurontin for the treatment of Postherpetic neuralgia is 1800-3600 mg / day for 2-4 months with an initial dose of 300 mg.

This drugs in the treatment of pain in multiple sclerosis.

Cutter et al (2000) showed a pronounced clinical improvement in pain and spasticity when conducting a prospective, double-blind, placebo-controlled study of the effectiveness of Neurontin in 21 patients with multiple sclerosis. Solaro et al. (1998, 2000) Neurontin was prescribed in several studies for the treatment of various paroxysmal pain symptoms in 21 patients with multiple sclerosis, already treated with carbamazepine and phenytoin, which were canceled due to inefficiency or undesirable side effects; and for the treatment of paroxysmal night painful spasms in 24 patients with multiple sclerosis. Significant improvement or complete disappearance of the pain syndrome was obtained with the use of Neurontin in both cases.

A significant decrease in spasticity, muscle cramps and pain in the treatment of patients with multiple sclerosis with Neurontin was also observed in the works of other authors. In this case, the initial dose of the drug standard is 300 mg / day, then rises to 900 mg and higher within 3 weeks. The average dose reaches 900 mg (range from 600 to 2400 mg / day).

Neurontin in the treatment of trigeminal neuralgia.

In a study of Khan (1998), Neurontin was administered to seven patients with multiple sclerosis for treating trigeminal neuralgia, recognized as being refractory to other drugs (carbamazepine, phenytoin, valproate, amitriptyline, intravenous methylprednisolone, various types of NSAIDs). In 6 cases out of seven, complete relief of pain was observed. In the seventh patient, a significant reduction in pain was observed with recurring pain attacks of light intensity.

In addition, there are studies on the effectiveness of Neurontin in trigeminal neuralgia, not path genetically associated with multiple sclerosis.

This medicaments in complex regional pain syndrome (CRPS).

Stevens et al (1999), when conducting a double-blind, placebo-controlled study of the action of Neurontin in reducing pain in 18 patients with upper limb CRPS, concluded that the drug was not effective in this case. However, a number of other studies have shown a significant improvement in health in patients with CRPS in the treatment of Neurontin, which is accompanied by a decrease in Hyperpathies, allodynia, hyperalgesia and the return of the normal color of the limb skin.

Gabapentin in the treatment of lower back pain.

In an open study on the role of Neurontin in the treatment of back pain, 62 patients were included. Therapy lasted at least 4 weeks. The pain sensation decreased by an average of 46%, with the majority of patients being able to stop taking one or more drugs that they received before the study.

It's with muscle cramps of various etiologies

Serrao et al (2000) conducted a study on the effectiveness in 30 patients with muscular cramps of various etiologies, which included neuropathies, radiculopathies, familial hereditary crumps, as well as cramps in the framework of Parkinson's disease, multiple sclerosis and vascular diseases. The average dose of gabapentin was 850 mg / day (600-1200 mg / day), the course of treatment lasted 3-6 months. The drug was effective in reducing the intensity or disappearance of crump in more than 80% of patients.


  • By Angela, 31 years’ old

    My epilepsy "protected" me from everything: from egoism of relatives, nervous overloads, not for years of big responsibility and many other things. It began I have convulsive seizures in 4 years. The doctor relieved the seizures. He's still having seizures. After more than 10 years without seizures, with the appearance of powerful, long-term provoking factors in my life, convulsive ones returned, although by that time I had already experienced seizures. I was helped by Neurontin, which the doctor recommended to me, I buy Neurontin online. Now the time for remission has increased significantly, and I feel like a full member of society. I tried not to talk about their illness, others is much frightened they looked at me like I was a leper. And this fact also caused the attacks. After taking Neurontin, I feel confident.

  • By Paul, 30 years’ old

    I have spasms. The cause is a cyst in the right temporal lobe of my poor skull. Seizures were very frequent - forgot to take pills - Wake up with the consciousness that the proportion of the brain is burned, the flesh is aching, as if beaten in the mouth and blood from bitten cheeks and tongue. But there was no forgetting, in my case the fuse of consciousness did not turn on, and I felt the whole palette of information by convulsions of limbs and joints. Disgusting, but it's my way of life. I just couldn't rule out all the triggers. My mother treated my illness as if I'd invented it to get her attention. I have my own territory: a bed, a table, a shelf in the closet, maybe a room or an apartment. Everything that happens on this site, there is only so when I want to. I decide whether to make the bed or not. And even a loving mother cannot tell her epileptic child when to make my bed (every morning and always like this). Such an indication, it deprives me of control over my territory, and in fact deprives me of the opportunity to have a place where I can rest from attacks, to regain strength after them. Without this territory I found myself in constant stress. We can say that life without personal space is a continuous provoking factor. The consequence of this – life in the system of a constant attack, in this case-finding its territory. Hence the endless hysterics. I try to exclude the provoking factors from my life, and I take medicines in time. Now everything began to come back to normal. I take Neurontin in time, my seizures have decreased significantly, I'm no longer afraid to take a bath, I used to constantly think that I would drown. Now that I understand epilepsy is not a sentence. I can move on.

  • By Sam, 20 years’ old

    My mom had a head injury and she became an epileptic. I remember all my childhood several times a night had to Wake up to her screaming, poke wrapped the spoon in his mouth. Sometimes, they did not manage and then a week she couldn't speak - the language was severely bitten. The worst thing is when the seizure is over, and breathing, sharp, wheezing, with abundant salivation. It happened that her medication "is not delivered to the pharmacy", and then the attacks were every day. Then at school I pecked my nose, did not learn the material, because at night I almost did not sleep. I was small, but so grown-up and very tired. At the age of 42, his endless suffering without proper medical treatment, my mother planted the heart, resulting in his dilation and at one point it stopped. I want to wish everyone that they can afford to save their lives and the lives of their loved ones.


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