The study of chronic pain syndromes lumbosacral localization (low back pain) has traditionally received much attention. According to epidemiological studies conducted in the United States and Western Europe, the prevalence of pain in the lower back reaches 40-80%, and the annual incidence is 5%. Between the ages of 20 and 64, 24% of men and 32% of women suffer from back pain. It is known that in 10–20% of working-age patients, acute back pain transforms into chronic. This group of patients is characterized by an unfavorable prognosis for recovery, and it accounts for about 80% of all health care costs for the treatment of back pain.
One of the causes of chronic pain in the lumbosacral region is compression radiculopathy.
The currently accepted pathophysiological approach to the analysis of pain syndromes in terms of their nociceptive or neuropathic nature allows us to consider radiculopathy as a mixed pain syndrome, where both nociceptive and neuropathic components are present. In this case, in the treatment of these patients, the use of drugs specifically used for the treatment of neuropathic pain, as well as their combination with NSAIDs, can be fully justified. In the pharmacotherapy of neuropathic pain, anticonvulsants, antidepressants and opioid analgesics are most commonly used. One of the most recognized and approved drugs for the treatment of neuropathic pain in the world is buy neurontin online (gabapentin). The mechanism of its action is associated with the effect on the central mechanisms of pain – reducing central sensitization, improving neurotransmitter balance in the direction of enhancing the anti-pain GABA-ergic effects and reducing the effects of glutamate, the main neurotransmitter of pain.
The purpose of this work was to assess the clinical efficacy of the neurontin drug in patients with chronic pain of lumbosacral localization.
The study material consisted of 18 people (10 men and 8 women, average age of 36.4 years). The selection criteria were: chronic pain syndrome on the background of unilateral radiculopathy of lumbosacral localization and refusal to take all drugs 2 weeks before the start of treatment. In 13 patients, radiculopathy of the S1 root was detected, in 5 patients, L5. All had some type of sensitive disorder (hypesthesia – in 10 people, paresthesia – in 5, hyperesthesia – in 3).
Research methods: clinical and neurological examination, psychometric testing, which included a subjective assessment of pain on a visual analogue scale (from 0 to 100mm), a comprehensive pain questionnaire (CCD), a Spilberger questionnaire for assessing personal and reactive anxiety, Beck’s questionnaire for identify the level of depression. We also used a new scale of clinical evaluation of the typicality of neuropathic pain – the scale DN4. This questionnaire consists of ten points concerning the characteristic clinical characteristics of neuropathic pain. As a result of questioning and neurological analysis, a total score is determined (from 0 to 10). The higher the score, the more reliable the diagnosis of neuropathic pain. To evaluate pain as neuropathic, you need to get at least 4 points.
To confirm the diagnosis of radiculopathy, electroneuromyographic research methods were used: F-wave and H-reflex.
Neurontin was administered at a dose of 1800 mg per day (600 mg 3 times a day) for 3 months with a preliminary titration: on the first day – 300 mg / day; in the 2nd – 600, on the 3rd – 900, on the 4-6th – 1200, on the 7-10th – 1500 and from 11h – 1800 mg / day. After 3 months, re-examination was conducted.
Results. Tolerability of the drug in most patients was satisfactory, only three people during the first two weeks of treatment were disturbed by mild drowsiness and slight dizziness. At the end of the course of treatment, 6 people rated the effect of the reception as good, 8 – satisfactory, 4 – unsatisfactory (without effect). The intensity of the pain syndrome on the visual analogue scale significantly decreased from 69 ± 16 mm to 29 ± 12 mm. Reception of neurontin promoted decrease in intensity of pain, influence of pain on life and negative emotional influence according to the BWC.
3 months after the start of treatment, the level of depression (from 14.2 ± 2.9 to 7.6 ± 1.9), as well as reactive (from 38.4 ± 3.6 to 31.2 ± 2.7) and personal (from 36.6 ± 2.8 to 29.5 ± 2.6) alarm. According to the DN4 scale, the overall score decreased from 5.6 ± 0.8 to 3.2 ± 1.2. No reliable results were obtained before and after treatment with neurophysiological indicators.
Ideas about the mechanisms of pain in the defeat of the nerve root in recent years have changed significantly. Today it is obvious that the severity of the pain syndrome does not always correlate with the size of the disc herniation and the degree of compression of the nerve root. Clinicians are well aware of the situation when a patient with an intense pain during MRI shows minor changes, and, conversely, a large disc herniation can be detected in a patient with moderate pain. Currently, several mechanisms of pain formation in compression radiculopathy are being considered. In addition to the direct mechanical compression of the root, the source of pain can be damage to the nociceptors of the intervertebral disk itself. In addition, inflammation plays a certain role, when inflammatory mediators, locally acting on the nerve endings in the tissues, also participate in the generation of pain.
A relatively new hypothesis is the early structural changes in chronic pain syndromes. It has been shown that intense nociceptive impulses entering the spinal cord result in the death of spinal inhibitory interneurons, which are normally in constant tonic activity and suppress nociceptive afferentation. By reducing the number of these inhibitory neurons, a situation is created where peripheral nociceptive neurons are chronically disinfected, which leads to the generation of pain, even in the absence of painful stimuli. Another mechanism of chronic pain is central sensitization – hypersensitivity and activity of the sensory neurons of the horn. As a result of lowering the threshold for the excitation of these neurons, any non-painful peripheral stimulation can lead to the generation of pain impulses. Of course, one should not forget about the essential role of psychogenic factors in the development and chronification of pain syndrome. All these mechanisms can partly explain the discrepancy between the intensity of pain and the severity of structural changes in the spine with chronic back pain.
Thus, both nociceptive (activation of nociceptors, inflammation) and neuropathic mechanisms (root damage, central sensitization, dying inhibition) are involved in the formation of chronic pain in radiculopathy. Structural damage most likely plays the role of trigerra, or the triggering factor, and further chronic pain persists with the dominant role of the neuropathic mechanisms of pathogenesis (neuroplasticity) and psycho-social factors, and not of the morphological changes in the structures of the spine.
The study showed the overall effectiveness of neurontin in the treatment of chronic back pain. However, the clinical effect was noted in varying degrees in different patients. Since monotherapy was performed only with neurontin, it can be assumed that the greatest analgesic effect was observed in patients with the leading neuropathic pain mechanisms that are affected by the drug. A less pronounced improvement and lack of therapeutic effect in some patients can probably be associated with nociceptive and / or psychogenic mechanisms dominant in these patients.
It is clinically very difficult to assess the exact ratio of nociceptive, neuropathic and psychogenic components in chronic radiculopathic pain syndrome. Unfortunately, the existing additional diagnostic methods also do not always allow to specify the participation and role of a particular mechanism in the pathogenesis of pain. Nevertheless, such an analysis is very important primarily in terms of the selection of adequate therapy. Traditionally, pharmacotherapy of chronic back pain in most cases comes down to the use of nonsteroidal anti-inflammatory drugs (NSAIDs). However, the effectiveness of these drugs is not in all cases satisfactory. From our point of view, pharmacotherapy of such patients should be combined, taking into account the contribution of nociceptive, neuropathic and psychogenic components, since they all occur in patients with the studied form of chronic pain. In the presence of the neuropathic component of pain, neurontin should be recommended, with the nociceptive component of pain dominating, it is probably better to use safe selective NSAIDs. The purpose of psychotropic drugs (antidepressants) is aimed at correcting both neuropathic and psychogenically caused changes.
Thus, the results obtained indicate the effectiveness of neurontin in the treatment of chronic pain of lumbosacral localization. Given the good tolerability of the drug, suitability for oral administration on an outpatient basis, it can be recommended for use both as monotherapy and in combination with other drugs (NSAIDs and antidepressants).
Gabapentin in chronic neuropathic pain in adults
There is evidence of moderate quality that oral gabapentin in doses of 1200 mg per day and more has a significant effect on pain in some people with moderate or severe neuropathic pain that occurs after shingles or due to diabetes.
Neuropathic pain results from damage to the nerves. It differs from pain, which is transmitted through healthy nerves from damaged tissue (for example, as a result of a fall, a cut, or arthritis of the knee joint). In neuropathic pain, other medications are often used other than those used in pain associated with tissue damage, such as painkillers. Medications sometimes used for depression or epilepsy can be effective in some patients with neuropathic pain. One of them is gabapentin. We determine the result obtained as good if a patient with a high level of pain as a result of taking the drug gets rid of the pain without side effects, forcing the patient to stop taking the drug.
Characteristics of research
In January 2017, we searched for clinical trials that used gabapentin to treat neuropathic pain in adults. We found 37 trials that met the inclusion criteria, with 5914 participants randomly assigned to receive gabapentin, placebo or other drugs. Studies lasted from 4 to 12 weeks. Most studies reported positive outcomes, which patients with neuropathic pain noted were important. The results were obtained mainly with the participation of patients after shingles or with diabetic nerve damage.
In the case of patients with shingles, gabapentin administration reduced pain by half in 3 out of 10 people; and in 2 out of 10 patients on placebo. The pain decreased by a third or more in 5 of 10 patients taking gabapentin and 3 of 10 people taking a placebo. In the case of patients with shingles, the pain was reduced by half in 4 out of 10 people taking gabapentin; and in 2 out of 10 patients taking placebo. Pain decreased by a third or more in 5 of 10 patients taking gabapentin, and in 4 of 10 people taking a placebo. There was no reliable evidence for other types of neuropathic pain.
Side effects were more common with gabapentin (6 out of 10) compared with placebo (5 out of 10). Dizziness, drowsiness, water retention and walking problems were observed in 1 out of 10 people taking gabapentin. Serious side effects were rare and there was no difference between the groups taking gabapentin and placebo. Somewhat more people stopped taking gabapentin due to side effects.
Taking gabapentin helps some people with chronic neuropathic pain. It is impossible to know in advance who will help gabapentin, and who will not. The available data suggest that short-term testing is the best way to determine effectiveness in a particular case.
Quality of evidence
The evidence was mostly of average quality. This means that this study gives a good idea of the likely effect. The probability that the effect will be significantly different, moderate.
Gabapentin is an antiepileptic drug, also known as an anticonvulsant. It has an impact on the chemical and nervous mechanisms of seizures and certain types of pain. Gabapentin is also used to treat other nerve lesions (for example, diabetic neuropathy, peripheral neuropathy, trigeminal neuralgia) and restless legs syndrome.
Antiepileptic and anticonvulsant drug
Indications for use
- Postoperative pain relief
- Migraine Prevention
- Pain on the background of diabetic neuropathy
- Essential tremor
- Generalized tonic and clonic convulsions
- Post-traumatic stress disorder (PTSD)
- Irritable Bowel Syndrome (IBS)
- Neuralgia of the trigeminal nerve
- Alcohol addiction
- Persistent Chronic Cough
Gabapentin interacts with the neurons of the cerebral cortex in auxiliary subunits of potential-dependent calcium channels. The drug increases the synaptic concentration of gamma-aminobutyric acid (GABA), enhances GABA reactions in non-synaptic sites in tissues, including neurons, and reduces the release of monoamine neurotransmitters. It was found that the antihyperalgesic and antiallodynic effects of gabapentin are mediated by the descending noradrenergic system, which leads to the activation of spinal alpha 2-adrenergic receptors. Gabapentin also binds to adenosine A1 receptors and activates them.
Epilepsy: 300 mg orally, 3 times a day
Postherpetic neuralgia: 300 mg orally, once daily (evening)
Restless legs syndrome: 600 mg orally, once a day
Diabetic neuropathy: 900 mg orally, once a day
Pain: 10-15 mg / kg / day by mouth, in three doses in equal doses
Gabapentin is rapidly absorbed by the L-amino acid transport system, a carrier-mediated saturable transport system. The volume of distribution is 58 ± 6 l, binding to plasma proteins <3%. The half-life of plasma is 5-7 hours.
- Kidney disease
- Heart disease
- Liver disease
- The effect of the drug Neurontin is weakened when used with antacids.
- Frequent consumption of alcohol can significantly reduce the effectiveness of the drug Neurontin
- Concentration in the blood may increase when used with the drug Tagamet (Zimetidin)
- May cause phenytoin toxicity when used with Dilantin
Often (> 1/10, <1/100)
- Changes in vision, including double vision
- Runny nose
- Weight gain
- Indigestion or nausea
- Muscle pain
- Dry mouth or sore throat
- Unusual thoughts
- Memory loss
- Diarrhea or constipation
- Swelling of the hands or feet
- Itchy eyes
Infrequently (> 1/100, <1/1000)
- Chest pain
- Sore throat
Very rare (<1/10000)
- Skin peeling
- Swelling of limbs
- Care should be taken when using the drug in patients with depression, suicidal thinking, impaired kidney function, allergies in children, especially those under 3 years of age, during pregnancy and breastfeeding.
- You should avoid driving and working with machinery, because the drug causes drowsiness, dizziness and blurred vision.
- The drug can change the level of sugar in the blood, so you need to regularly monitor this indicator.
- Patients are at high risk of suicidal thinking, therefore it is necessary to ensure close monitoring of them.
- Data obtained from 5 randomized, placebo-controlled studies were included in the review. One of them has not yet been published. Gabapentin is more effective in treating pain with diabetic neuropathy, postherpetic neuralgia, and other neuropathic pain syndromes. Based on the available data, a dose of 1800 mg / day is recommended to increase effectiveness. When used in doses of 1800-3600 mg / day, gabapetin was effective and well tolerated in the treatment of neuropathic pain in adult patients.
- Seven patients with neuropathic pain completed the study more than 30 days after spinal cord injury (FCM). Two groups received a 4-week course of gabapentin and placebo in a randomized, crossover study with a 2-week washout period. The data was analyzed using Wilcoxon’s signed rank test. Gabapentin has a beneficial effect on certain types of neuropathic pain. There was a slight relief from the “unpleasant feeling” and the “intensity of pain” and the “burning sensation” at week 4 of gabapentin, but not placebo.
- A study involving 122 patients with chronic pain [97 with neuropathic pain (postherpetic neuralgia, diabetic neuropathy, sympathetically supported pain and phantom pain)] who received gabapentin treatment for at least 30 days showed statistically significant (p <0.0001) reduction in pain with an average dose of 1200 mg / day in patients with neuropathic pain. The average on a visual analog scale decreased from 7.3 to 5.4.