Neuropathic pain is a pain caused by damage or disease affecting the somatosensory nervous system. Neuropathic pain may be associated with an abnormal sensation called disesthesia or pain from a painless stimulus (allodynia). It may have a continuous and/or episodic (paroxysmal) component. The latter resembles a stabbing or electric shock. Common qualities include burning or cold, the sensation of "pinch and needle", numbness and itching.
Up to 7% to 8% of Europe's population is affected, and in 5% people may be severe. Neuropathic pain may result from peripheral nervous system disorders or the central nervous system (brain and spinal cord). Thus, neuropathic pain can be divided into peripheral neuropathic pain, central neuropathic pain, or mixed neuropathic pain (peripheral and central).
Video Neuropathic pain
Cause
Central neuropathic pain is found in spinal cord injury, multiple sclerosis, and multiple strokes. In addition to diabetes (see diabetic neuropathy) and other metabolic conditions, a common cause of painful peripheral neuropathy is herpes zoster infection, HIV-associated neuropathy, nutritional deficiencies, toxins, remote manifestations of malignancy, immune mediation disorders and physical trauma to the neural stem.. Neuropathic pain often occurs in cancer as a direct result of cancer in peripheral nerves (eg compression by tumors), or as a side effect of chemotherapy (chemotherapy-induced peripheral neuropathy), radiation injury or surgery.
Maps Neuropathic pain
Mechanism
Peripherals
After peripheral nerve lesions, aberrant regeneration may occur. Neurons become very sensitive and develop spontaneous pathological activity, abnormal stimulation, and increased sensitivity to chemical, thermal and mechanical stimuli. This phenomenon is called "peripheral sensitization".
Middle
Dorsal horn neurons (spinal cord) give rise to the spinotalamic tract (STT), which is the main nociceptive pathway. As a result of peripheral spontaneous activity occurring in the periphery, STT neurons develop increased background activity, enlarged receptive fields and increased response to afferent impulses, including harmless tactile stimulation. This phenomenon is called central sensitization. Central sensitization is an important mechanism of persistent neuropathic pain.
Other mechanisms may occur at the central level after peripheral nerve damage. Loss of afferent signals induces functional changes in dorsal horn neurons. Decreasing large fiber inputs reduces the activity of interneurons inhibiting nociceptive neurons ie loss of afferent inhibition. Hypoactivity of a declining antinociceptive system or loss of descending inhibition may be another factor. With the loss of neuronal input (deafferentation) STT neurons begin to shoot spontaneously, a phenomenon called "deafferentation hypersensitivity."
Neuroglia ("glial cell") may play a role in central sensitization. Peripheral nerve injury induces glia to release proinflammatory cytokines and glutamate - which in turn affects neurons.
Mobile
The phenomenon described above depends on changes in cellular and molecular levels. Changes in ion channel expression, changes in neurotransmitters and their receptors and changes in gene expression in response to nerve input are being played.
Treatment
Neuropathic pain can be very difficult to treat only with about 40-60% of people who achieve partial relief.
Preferred treatments are specific antidepressants (tricyclic antidepressants and serotonin-norepinephrine reuptake inhibitors), anticonvulsants (pregabalin and gabapentin), and topical lidocaine. Opioid analgesics are recognized as useful agents but are not recommended as first-line treatment.
Antikonvulsan
Pregabalin and gabapentin can alleviate the pain associated with diabetic neuropathy. Anticonvulsant carbamazepine and oxcarbazepine are very effective in trigeminal neuralgia. Gabapentin can reduce symptoms associated with neuropathic pain or fibromyalgia in some people. There is no predictor test to determine if it will be effective for a particular person. A short trial period of gabapentin therapy is required, to determine the effectiveness of the person. 62% of people taking gabapentin may have at least one side effect, but serious incidence of adverse events is found to be low.
Lamotrigine appears to be ineffective for neuropathic pain.
Antidepressants
Multiple serotonin-norepinephrine reuptake inhibitors such as duloxetine, venlafaxine, and milnacipran, as well as tricyclic antidepressants such as amitriptyline, nortriptyline, and desipramine are considered first-line drugs for this condition. While amitriptyline and desipramine have been used as first-line treatment, the quality of evidence to support their use is poor.
Bupropion has been found to have efficacy in the treatment of neuropathic pain.
botulinum toxin type A
Local intradermal injections of botulinum toxin are helpful in chronic chronic pain neuropathy.
Cannabinoids
Cannabis and a number of cannabinoid receptor agonists seem to be effective for neuropathic pain.
The dominant side effects are CNS depression and cardiovascular effects - which are mild and well-tolerated, but psychoactive side effects limit their use.
Long-term studies are needed to assess the likelihood of weight gain and possible harmful psychological effects.
Dietary supplements
A 2007 study review found that administration of alpha lipoic acid (ALA) injection (parenteral) was found to reduce the range of symptoms of peripheral diabetic neuropathy. While some studies on ALA given orally demonstrated a decrease in both positive symptoms of diabetic neuropathy (disestesia including stabbing and burning pain) and neuropathic deficits (paresthesia), meta-analysis showed "more conflicting data whether it improves sensory symptoms, or only a deficit of neuropathy alone ". There is some limited evidence that ALA also helps in some other non-diabetic neuropathy.
Benfotiamine is an oral prodrug of Vitamin B1 that has multiple placebo-controlled double-blind trials that demonstrate efficacy in treating neuropathy and other diabetes comorbidities.
Neuromodulator
Neuromodulation is a field of science, medicine and biotechnology that includes implantable and non-implantable technologies (electricity and chemistry) for maintenance purposes.
The plant is expensive and carries the risk of complications. The available studies have focused on conditions that have a different prevalence than patients with neuropathic pain in general. More research is needed to determine the range of conditions they may be exploiting.
Brain stimulation in
The best long-term results with deep brain stimulation have been reported with targeted periventricular/periaqueductal gray matter (79%), or periventricular/periaqueductal gray matter plus thalamus and/or internal capsule (87%). There are significant levels of complications, which increase over time.
Motor cortex stimulation
Primary motor cortex stimulation through electrodes placed inside the skull but outside the thick meningeal membrane (dura) has been used to treat pain. The level of stimulation below that for motor stimulation. Compared with spinal stimulation, which is associated with real tingling (paresthesia) at the treatment level, the only palpable effect is pain relief.
Spinal bone marrow and spinal pump implanted
The spinal cord stimulator uses electrodes placed adjacent but outside the spinal cord. The overall rate of complications is one-third, most often caused by migration or lead damage but advances in the last decade have pushed the rates of complications much lower. Lack of pain sometimes asks for removal of the device.
The intrathecal pump provides the drug directly into a fluid-filled space (subarachnoid) around the spinal cord. Opioids alone or opioids with adjuvant drugs (either local anesthetics or clonidine) or newer zikonotida infused. Complications such as serious infections (meningitis), urinary retention, hormonal disorders and intrathecal granuloma formation have been noted with intrathecal infusions.
There was no randomized study of intravenous pumps. For the selected patient, 50% or greater pain relief was achieved in 38% to 56% at six months but decreased over time. These results should be viewed skeptically because the placebo effect can not be evaluated.
NMDA antagonism
The N -methyl-D-aspartate (NMDA) receptor appears to play a major role in neuropathic pain and in the development of opioid tolerance. Dextromethorphan is a NMDA antagonist at high doses. Experiments on animals and humans have determined that NMDA antagonists such as ketamine and dextromethorphan can alleviate neuropathic pain and reverse opioid tolerance. Unfortunately, only a few clinically available NMDA antagonists and their use are limited by very short half-life (ketamine), weak activity (memantine) or unacceptable side effects (dextromethorpan).
Opioid
Opioids, although commonly used in chronic neuropathic pain, are not recommended for first or second line treatment. In the short and long term they have no clear benefits. In the medium term, low quality evidence supports utilities.
Some opioids, especially levorphanol, methadone and ketobemidone, have NMDA antagonism in addition to their Â--opioid agonist properties. Methadone does it because it is a mixture of racemates; only l-isomers are potent opioid agonists. D-isomers have no action of opioid agonists and act as NMDA antagonists; d-methadone is an analgesic in the experimental model of chronic pain.
There is little evidence to suggest that a strong opioid is more effective than others. Expert opinion rests on the use of methadone for neuropathic pain, in part because of its NMDA antagonism. It is reasonable to base opioid choices on other factors. It is unclear whether fentanyl provides pain relief to people with neuropathic pain.
Topical agents
In some forms of neuropathy, especially post herpes neuralgia, topical applications of local anesthesia such as lidocaine are reported to provide relief. Transdermal patches containing lidocaine are commercially available in some countries.
Repeated application of capsaicin, followed by a prolonged period of skin sensitivity called desensitization, or inactivation of a nociceptor. Capsaicin not only depletes P substances but also produces reversible degeneration of the epidermal nerve fibers. Nevertheless, the benefits seem simple with the preparation of standard (low) strength, and topical capsaicin can induce pain.
Surgical Interventions
In some cases, neural blocks can be used to treat.
Carbamazepine works by inhibiting the voltage-gated sodium channel, thereby reducing nerve membrane stimulation. Carbamazepine has also been shown to potentiate gamma aminobutyric acid (GABA) receptors consisting of alpha1, beta2, and gamma2 subunits. This may be relevant to its efficacy in neuropathic pain. Carbamazepine is commonly used to help with nighttime pain attacks.
Direction of research
Other topical agents such as amitriptyline, gabapentin, Citrullus colocynthis extract, nifedipine, and pentoxifylline are also under investigation.
History
The history of pain management can be traced back to ancient times. Galen also suggests neural networks as a route of pain transfer to the brain through invisible psychic pneuma. The idea of ​​the origin of pain from the nerves itself, without the exciting pathology of other organs presented by medieval medical experts such as Rhazes, Haly Abbas and Avicenna. They call this type of pain specifically as " vaja al asab ", describing the numbness, tingling and quality of the needle, discussing its etiology and distinguishing characteristics. Description of neuralgia made by John Fothergill (1712-1780). In a medical article entitled "Clinical Lecture on Lead Neuropathy" published in 1924, the word "Neuropathy" was used for the first time by Gordon.
References
External links
- Clinical Practice Center at NICE (UK). Pharmacology Management of Neuropathic Pain in Adults in Non-Specialist Settings. NICE Clinical Guidelines . March 2010.
Source of the article : Wikipedia
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