Reducing your risk of developing neuralgia and nerve damage due to diabetes. Neuralgia in adults

For quotation: Strokov I.A., Akhmedzhanova L.T. Treatment neuropathic pain for diabetic polyneuropathy // Breast cancer. 2008. No. 28. S. 1892

In 2007, pain experts formulated a new definition of neuropathic pain, according to which it is caused by a primary injury or disease of the somatosensory system. Neuropathic pain is based on pathological activation of pain pathways, which may be associated with damage to the nervous system at the level of peripheral nerves, plexuses and dorsal roots (peripheral neuropathic pain) or the spinal cord and brain (central neuropathic pain). Research conducted in various countries, showed that neuropathic pain is observed in 6-8% of the population and is associated with chronic pain syndromes, female gender, elderly patients and low levels of social status, which can be considered as risk factors. Neuropathic pain caused by wide range injuries and diseases is associated with greater pain intensity and frequent visits to medical care. In the presence of neuropathic pain, the quality of life of patients decreases, their social adaptation and disability, and in many cases, neuropathic pain is difficult to treat. This indicates the high social and medical-economic significance of the problem of diagnosing and treating neuropathic pain.

Patients with diabetes may develop various forms of painful diabetic neuropathy, which differ in the localization of pain, severity of occurrence and nature of pain, although in all cases the pain is neuropathic (Table 1). The classic variant of peripheral neuropathic pain is pain syndrome in diabetic distal symmetrical sensory-motor polyneuropathy. Epidemiological studies conducted in the USA have shown that neuropathic pain occurs with diabetic polyneuropathy more often than with all polyneuropathies of other etiologies combined. According to the Russian EPIC study, neuropathic pain in diabetic polyneuropathy is second only to back pain in prevalence.
Diabetic polyneuropathy (DPN) is observed in approximately 50% of patients with diabetes, while neuropathic pain is observed in 11-24% of patients with polyneuropathy, which depends on the duration of diabetes and polyneuropathy, as well as the type of diabetes. Already with the first description of a patient with DPN in 1798. English doctor J. Rollo identified pain and paresthesia as the main symptoms. Clinical manifestations, frequency, severity and duration of pain syndrome in DPN are very diverse, they are united by a common feature - the neuropathic nature of pain. Among patients suffering from diabetes, chronic pain occurs in 25% of cases, while in the population the prevalence of chronic pain syndromes is about 15%, and the difference is formed to a greater extent due to neuropathic pain.
Neuropathic pain in DPN is represented by two main components: spontaneous (stimulus-independent) and evoked (stimulus-dependent) pain. Spontaneous pain can be a constant concern ( burning pain) or occur paroxysmally with pain lasting from seconds to hours (shooting pain). Spontaneous pain is caused by the ectopic activity of nociceptive C-fibers as a result of the appearance on them under pathological conditions large number sodium channels and changes in the excitability of pain receptors, leading to their activation under low-threshold stimuli, which is not observed under normal conditions. It is also possible that excitation is transferred from one fiber to another - the phenomenon of ephaptic excitation. Thus, pain afferentation increases, further leading to changes in the excitability of nociceptive neurons of the dorsal root ganglion and dorsal horn. Violation processes functional state dorsal horn neurons associated with the mechanisms of ambient pre- and postsynaptic inhibition, deafferentation, as well as the mechanisms of central sensitization in case of damage to peripheral nerves are described in detail in reviews of foreign and domestic authors. Nociceptive signals from the neurons of the dorsal horn enter the visual thalamus and then to the somatosensory cortex, where the sensation of pain is realized. It has been shown that, unlike patients with diabetes mellitus without pain, patients with painful DPN undergo a change in metabolism in the thalamus. Neurons of central sensory structures can also change their excitability with the formation of the phenomenon of sensitization. All central structures for the conduction and perception of pain have close connections with descending inhibitory and activating pathways. The main inhibitory (antinociceptive) influences are associated with descending ways from the periaqueductal gray matter and rostroventral regions medulla oblongata to the posterior horn. These descending inhibitory influences are realized through the norepinephrine and serotonin neurotransmitter systems.
In clinical practice, diagnosing the neuropathic nature of pain is often difficult. The sensation of pain is always subjective, it cannot be accurately measured, and there are no absolute criteria to distinguish neuropathic pain. It is possible to judge the pathophysiological mechanisms underlying the pain syndrome only tentatively, based on the characteristics pain, data from a neurological examination and the results of a neurophysiological study. Moreover, the identification of clinical signs and changes in electrophysiological parameters showing a pathological change in the state of the nociceptive system does not reliably prove the presence of neuropathic pain. Neuropathic pain can occur immediately after damage to the nociceptive system (for example, with acute small fiber neuropathy in diabetes mellitus), or it can develop years or even decades after damage (for example, with DPN). It is possible to diagnose the non-uropathic nature of pain if a dysfunction of the nociceptive system is confirmed in the presence of: 1) spontaneous sensory symptoms; 2) the results of a clinical examination identifying symptoms of damage to the nervous system: positive neuropathic symptoms (stimulus-dependent pain) and negative neuropathic symptoms (neurological deficit); 3) data from neurophysiological studies (EMG, quantitative sensory testing, caused by somatosensory potentials). In this case, the choice of research methods is determined by the results of a neurological examination. Neurological symptoms make it possible to determine the presence, degree and localization of damage to the nervous system. To diagnose the phenomenon of neuropathic pain, the doctor is primarily interested in the state of the sensory system. It is clear that, depending on the peripheral or central localization of the pathological process, a study of the general neurological status, including motor and autonomic system. In this case, negative symptoms will include, for example, decreased reflexes, muscle strength, the presence of muscle atrophy, dryness and discoloration of the skin. When identifying damage to the sensory system, to diagnose neuropathic pain, they focus on the state of sensitivity associated with the activation of thin, weakly myelinated A- (cold stimuli and blunt prick) and thin, unmyelinated C-fibers (painful and thermal stimuli). It should be remembered that neuropathic pain usually occurs in the area of decreased or lack of sensitivity, that is, the area of pain and sensitivity disorders in these cases coincides. IN last years Conducting epidemiological studies to study the prevalence of pain is based on the use of special questionnaires that make it possible to determine the nature of pain with a high degree of accuracy.
Treatment of neuropathic pain is based on modern ideas about the pathophysiological mechanisms of its development. Are used pharmacological effects, aimed at reducing peripheral afferentation, which supports changes in the excitability of nociceptive structures of the spinal cord and brain, drugs that reduce the excitability of nociceptive neurons, and drugs that enhance supraspinal descending inhibitory antinociceptive effects. In severe cases, administration of pharmacological drugs close to the central receptors (intradural) is used. It is possible to use electrical stimulation of peripheral nerves, primarily proprioceptive fibers, to enhance the inhibitory effects on the excitability of nociceptive neurons of the spinal cord, and acupuncture. Surgical treatment for cases refractory to pharmacotherapy may include the use of implanted electrodes in the brain or spinal cord, nerve release or decompression, chemical destruction, or nerve transection. Table 2 presents recently published Russian recommendations for the diagnosis and treatment of neuropathic pain, prepared by a group of leading experts in the field of pain treatment and published under the editorship of Academician of the Russian Academy of Medical Sciences, Professor N.N. Yakhno.
As can be seen from Table 2, from the point of view of evidence-based medicine, the use of 4 classes of drugs for the treatment of NB is most justified: anticonvulsants, antidepressants, opioid analgesics and local anesthetics.
The use of local anesthetics leads to a reduction in neuropathic pain, especially in cases where its development is primarily due to pathological changes in the peripheral nerves. However, local anesthetics in the form of patches are not recommended for long-term use or if the affected area is large enough.
Antidepressants are widely used in the treatment of neuropathic pain of various etiologies. Tricyclic antidepressants (TCAs), which have been used since the 1950s, most notably amitriptyline, are highly effective for neuropathic pain. In diabetic painful polyneuropathy, in more than 80% of cases, their administration reduces pain or leads to its disappearance. The main mechanism of action of TCAs is to block the reuptake of norepinephrine and serotonin into the presynaptic terminal through their action on sodium and calcium channels, which leads to increased activity of central antinociceptive structures.
Selective serotonin reuptake blockers (paroxetine, fluoxetine) do not act on postsynaptic receptors and therefore have fewer side effects, but their ability to reduce neuropathic pain is significantly inferior to TCAs. Amitriptyline has been studied in a few controlled studies for painful diabetic polyneuropathy. Standard dose amitriptyline, with which treatment begins at 25 mg, the usual therapeutic range of the drug is 75-150 mg. TCAs are limited in use for neuropathic pain, especially in older patients, due to numerous and sometimes severe side effects. Orthostatic hypotension, urinary retention, constipation, tachycardia, “dry syndrome” can occur not only in older people. Presence of glaucoma and adenoma prostate gland are a contraindication for the use of TCAs. In addition, long-term use of TCAs has been shown to increase the risk of myocardial infarction by 2.2 times. Additional disadvantages of amitriptyline include nonlinearity of pharmacokinetics, that is, when taking small doses, the concentration of the substance in plasma may be higher than when taking large doses.
Anticonvulsants have been used to treat pain syndromes since the 40s of the 20th century, when the effectiveness of phenytoin in the treatment of trigeminal neuralgia was shown. In 1962, the anticonvulsant carbamazepine, similar in structure to TCAs, was first used to treat trigeminal neuralgia, which remains the first-line drug in the treatment of trigeminal neuralgia to this day. Gabapentin, an anticonvulsant that appeared in the 90s of the 20th century, has proven itself to be an effective drug for the treatment of neuropathic pain of various etiologies. Gabapentin is close in structure to g-aminobutyric acid(GABA). The effectiveness of the original gabapentin (Neurontin) was shown in double-blind, placebo-controlled studies in cases of neuropathic pain in patients with diabetic polyneuropathy. However, it should be remembered that the optimal therapeutic dose of gabapentin for the treatment of NB is 1800-2400 mg, the drug must be titrated over 2 weeks, which makes it very inconvenient to take.
From anticonvulsants latest generation, which have been studied in recent years in the treatment of neuropathic pain, pregabalin (Lyrica) attracts attention. pharmaceutical company Pfizer), which is currently in first place among drugs used to treat neuropathic pain syndrome in DPN. Pregabalin (Lyrica), according to Russian recommendations for the treatment of NB, is the first-line drug for the treatment of NB in DPN. 10 randomized, double-blind, placebo-controlled studies were conducted, mainly in painful diabetic polyneuropathy and postherpetic neuralgia, which involved almost 10,000 patients. Pregabalin has been shown to be highly effective for all neuropathic pain. Suffice it to say that pregabalin is registered in the USA and Russia as a drug for the treatment of all types of neuropathic pain. Pregabalin has a unique mechanism of action - it modulates neuronal activity. Pregabalin binds to voltage-dependent protein a2-delta calcium channels on the presynaptic membrane and reduces the entry of calcium into the cytoplasm. This leads to a decrease in the release of neurotransmitters, primarily the excitatory transmitter glutamate, which leads to a decrease in the excitability of dorsal horn neurons. Moreover, pregabalin has this effect predominantly on hyperexcited neurons.
An important advantage of pregabalin is its pharmacokinetics. It is very quickly absorbed from the intestine, reaching a maximum concentration in the blood within one hour and remains in the blood for a long time in high concentration, which allows the drug to be prescribed 2 times a day in equal doses. Over the entire range of therapeutic doses (from 150 to 600 mg), pregabalin has linear pharmacokinetics, which is not observed with other drugs, including gabapentin. Pregabalin has a very high bioavailability (90%), superior to gabapentin (60%) in this regard. Food intake does not affect the bioavailability of the drug. Treatment usually begins with a dose of 75 mg 2 times a day, then after 3 days, the dose must be increased to 300 mg per day. Studies have shown that pregabalin significantly reduces the intensity of neuropathic pain during the first three days of taking the drug. Such a high effectiveness of pregabalin in relieving NB sets it apart from the previous generation of anticonvulsants, such as gabapentin. Long-term studies (15 months) of the use of pregabalin for neuropathic pain showed that it retains its analgesic effect throughout the entire period of use without developing tolerance to the drug. The excellent analgesic effect of pregabalin is confirmed by improvements in sleep, mood and quality of life in patients. Pregabalin is well tolerated in patients with neuropathic pain. The most common side effects are increased drowsiness and dizziness, which usually disappear fairly quickly (2-4 weeks), even if the patient continues to take the drug or increases its dose. Due to the fact that the drug is not metabolized in the liver, does not interact with the cytochrome P450 system and is excreted by the kidneys as an unchanged molecule, it does not have hepatotoxicity. The drug does not act on renal tissue and does not cause kidney pathology, so it can be used in patients with renal pathology, however, the dose of the drug in this case should be selected according to the instructions. Pregabalin does not interact with other drugs and can be used in various combinations, for example with antidiabetic drugs. In clinical studies, pregabalin has shown its high efficiency for neuropathic pain caused by diabetic damage to peripheral nerves. Thus, in a randomized, double-blind, placebo-controlled study in 146 patients with painful DPN, a significant reduction in the intensity of neuropathic pain was obtained already during the first week of the study, which was maintained over the next 8 weeks of taking the drug. The study used a graded visual analogue Likert scale as the main criterion. There was also a significant improvement in the sleep and social abilities of patients. Another study on 81 patients showed that when other pharmacological drugs were ineffective for painful diabetic polyneuropathy, pregabalin at a dose of 150-600 mg was significantly effective.
Thus, modern pharmacological preparations, primarily pregabalin, used in the treatment of neuropathic pain in patients with DPN allows, using them as monotherapy or in combination, to reduce pain in most patients and significantly improve their quality of life.

Literature
1. Pain syndromes in neurological practice. Edited by A.M. Vein - M. - 2001
2. Bone M, Critchley P, Buggy D.J. Gabapentin in postamputation limb pain: a randomized, double-blind, placebo-controlled, cross-over study // Reg Anesth Pain Med - 2002 - Vol.27 - P. 481-486.
3. Kukushkin M., L., Khitrov N.K. General pathology of pain // M. - 2004 - 144 pp.
4. Cohen H.W., Gibson G., Alderman M.H. Excess risk of myocardial infarction in patients treated with antidepressant medication. Association with use of tricyclic agents // Am J Med - 2000 - Vol.108 - P.2-8.
5. Backonja M. Anticonvulsants and antiarrhythmics in the treatment of neuropathic pain syndromes // In Neuropathic Pain: Pathophysiology and Treatment. Ed. Hansson P.T. - Seattle, IASP Press - 2001 - P.185-201.
6. Rose M.A., Kam P.C.A. Gabapentin: pharmacology and ist use in pain management // Anaesthesia - 2002 - Vol.57 - P.451-462.
7. McLean M.J., Morell M.J., Willmore L.J. et al. Safety and tolerability of gabapentin as adjunctive therapy in a large, multicenter study // Epilepsia - 1999 - Vol.40 - P. 965-972.
8. Bakonja M. Gabapentin monotherapy for the symptomatic treatment of painfuk neuropathy: a multicenter, double-blind, placebo-controlled trial in patients with diabetes mellitus // Epilepsia - 1999 - Vol.40 (Suppl.6) - P.57- 59.
9. Singh D., Kennedy D. The use of gabapentin for the treatment of postherpetic neuralgia // Clin Ther - 2003 - Vol.25 - P.852-889.
10. Cheshire W. Defining the role for gabapentin in the treatment of trigeminal neuralgia: a retrospective study // J.Pain - 2002 - Vol.3 - P.137-142.
11. Solaro C., Ucelli A., Inglese M. et al. Gabapentin is effective in treating paroxysmal symptoms in multiple sclerosis // Neurology - 1998 - Vol.50 (Suppl.4) - P.A147.
12. Attal N., Cruccu G., Haanpaa M. et al. EFNS guidelines on pharmacological treatment of neuropathic pain // European Journal of Neurology - 2006 - Vol.13 - P.1153-1169.
13. Rosenstock J., Tuchman M., LaMoreaux L. et al. Pregabalin for the treatment of painful diabetic peripheral neuropathy/ A double-blind placebo-controlled trial // Pain - 2004 - Vol.110 - P.628-638.
14. Sabatowski R., Galevz R., Cherry D.A. et al. Pregabalin reduced pain and improves sleep and mood disturbances in patients with post-herpetic neuralgia. Results of a randomized, placebo-controlled clinical trial // Pain - 2004 - Vol.109 - P. 26-35.
15. Yakhno N.N., Kukushkin M.L., Davydov O.S. and others. Results of a Russian epidemiological study of the prevalence of neuropathic pain, its causes and characteristics in a population of outpatients who consulted a neurologist // Pain - 2008 - No. 3 - pp. 24-32.
16. Danilov A.B., Davydov O.S. Neuropathic pain // From Borges, Moscow - 2007 - pp. 32-55.
17. Chan A.W., MacFarlane I.A., Bowsher D.R. et al. Chronic pain in patients with diabetes mellitus: comparison with non-diabetic population // Pain Clinic - 1990 - No. 3 - P.147-159.
18. Novikov A.V., Solokha O.A. Neuropathic pain: Review based on materials from the journal “The Lancet” (May-June 1999) // Neurological Journal - 2000- No. 1 - P.56-61.
19. Besson J. The neurobiology of pain // Lancet - 1999 - Vol.353 - P.1610-1615.
20. Sorensen L., Siddall P.J., Trenell M.I. et al. Differences in metabolites in pain-processing brain regions in patients with diabetes and painful neuropathy // Diabetes Care - 2008 - Vol.31 - P.980-981.
21. Stacey B. R., Dworkin R. H., Murphy K. et al. Pregabalin in the treatment of refractory neuropathic pain: results of a 15-month open-label trial // Pain Med - 2008 Mar 11.
22. Jann M.W., Slade J.H. Antidepressant agents for the treatment of chronic pain and depression // Pharmacotherapy - 2007 - Vol.27 -P.1571-1587.
23. Guidelines for the diagnosis and treatment of neuropathic pain. Edited by Academician of the Russian Academy of Medical Sciences N.N. Yakhno //Moscow, Publishing House of the Russian Academy of Medical Sciences - 2008 - 32 pages.

A disease associated with damage to the peripheral nerve is called neuralgia. Physically manifests itself through pain of a paroxysmal nature on the left or right, which appears in the area of the irritated nerve. How to treat neuralgia will depend on its correct diagnosis.

Causes of neuralgia

Microtraumas occur during prolonged physical activity. nerve trunk. These disorders can occur due to damage by toxins of various etiologies, which are either infectious nature, or occur due to alcohol intoxication, taking medications or interaction with heavy metals. Causes, symptoms and treatment depend on the type of disease: knee joint, lower extremities, facial nerve, solar plexus, pelvic, intervertebral, vagus nerve, etc. Other causes of neuralgia:

osteochondrosis;
hypothermia;
diseases associated with musculoskeletal system And hip joint(congenital anomalies of joints and bones, spinal injuries);
tumors;
diabetes;
peripheral vascular diseases that impair blood supply nerve tissue;
atherosclerosis.

Intercostal neuralgia

Symptoms of intercostal neuralgia (ICD-10 code: M79.2) are pain in the left-sided or right-sided intercostal space, which is encircling in nature in the left or right side of the body. Common cause occurrence is osteochondrosis in the thoracic spine area. Symptoms of the disease appear if a person turns sharply (from left to right and vice versa). The pain appears unexpectedly and is accompanied by an increase in blood pressure. The disease does not occur in adolescents and children. Treatment for intercostal neuralgia is prescribed only by a doctor.

Trigeminal neuralgia

Doctors have found that out of 10 thousand people, 50 exhibit trigeminal neuralgia (trigeminal). Women over 40 years of age are at risk of the disease. The causes of development are colds, infections, injuries and hypothermia. Painful attacks occur suddenly when loud sounds, bright light, in response to eating very cold or too hot food. Treatment and elimination of symptoms of this type of disease occurs through the use of Trileptal and Finlepsin. The method of radiofrequency destruction of the root is used.

Neuralgia of the glossopharyngeal nerve

In medicine neuralgia glossopharyngeal nerve(glossopharyngeal) is not often diagnosed. You can learn about the disease by the first signs: paroxysms of pain in the pharynx, throat, root of the tongue, soft palate, tonsils. The pain spreads to lower jaw and ear. The reason may be chronic infections. The disease is accompanied by symptoms such as inhibition of reflexes in the throat and palate, impaired salivation and taste perception of the back of the tongue in the affected area. In medicine, there are 2 forms of this type of disease: idiopathic and symptomatic.

Occipital neuralgia

The disease manifests itself as pain from the back of the head to the temporal region, which can extend to the eye area. Painful sensations are caused by irritation of the nerve roots in the occipital area. In some cases, the small and large spinal nerves in the area of the second and third cervical vertebrae are affected. The most important symptom of neuralgia occipital nerve Doctors call the pain a throbbing nature that is difficult to endure. It occurs when moving the head and coughing. During an attack, movement can cause nausea and vomiting in the patient.

Neuralgia of the femoral nerve

The pathological process is characterized by excruciating painful sensations along the nerve. The pain is paroxysmal, “shooting” in nature. Middle-aged people are at risk; men are more susceptible to femoral neuralgia than women. When walking, changing body position to vertical, on the back with outstretched legs, the painful sensations worsen, numbness and burning appear on the skin.

Light compression in the area where the nerve exits causes an unbearable feeling of pain. The disease may manifest as intermittent claudication. Paresthesia (impaired sensitivity) occurs only when walking. The main cause is compression of the external lateral cutaneous nerve of the thigh under the inguinal fold. Infringement nerve root may occur as a result of trauma to surrounding tissues, with the appearance of scars, proliferation of adipose or fibrous tissue, during pregnancy (venous congestion in the pelvic organs), and with uterine fibroids.

Herpetic neuralgia

The consequence of a herpetic infection is herpetic neuralgia. This dangerous disease often occurs in patients with reduced immunity and in elderly people. This pathological process differs from others in its skin manifestations in the form of a herpetic rash. The postherpetic type of the disease manifests itself after suffering from herpes zoster in the form of pain from a drying rash.

Neuralgia of the pterygopalatine ganglion

Ganglioneuritis (ganglionitis) is also called “neuralgia of the pterygopalatine ganglion”, Slader’s syndrome. Refers to neurodental syndromes (diseases in the oral cavity and facial area). The disease is expressed through vegetative symptoms. Half of the face may turn red, swelling of the tissues, lacrimation may occur, and secretion may be released from one half of the nose. Attacks of painful paroxysms can develop at night, last and not go away for more than 2 days.

The symptom complex includes sharp painful sensations and can spread in the following places:

eyes;
upper jaw;
temporal zone;
ear area;
back of the head;
scapula and scapular area;
shoulder region;
forearms;
brushes.

Symptoms of neuralgia

Exist general signs neuralgia, which will help to recognize it even at home. The neuralgic process of damage to the peripheral nerve is accompanied by severe painful sensations, which can be acute, aching in nature. The painful area may turn red. The location of pain depends on the area of irritation of the nerve trunk. The following places of pain are identified depending on the type of disease and lesion:

Defeat	Localization	Special symptoms
trigeminal nerve	neck, teeth, eyeball, half face	salivation and lacrimation, pain occurs when touching the “trigger” zones (the skin area of the chin), spasms of the jaw muscles.
lumbar nerve	small of the back	the pain manifests itself in attacks, “shoots”
intercostal nerve	chest, rib	lumbago (lumbago) of a paroxysmal nature, which intensifies when turning the body (from left to right or vice versa) and taking a deep breath
sciatic nerve	posterior thigh	aching pain, debilitating, burning due to damage to many branches of small nerve branches

Treatment of neuralgia

You should go to the clinic to see a neurologist, dentist, or otolaryngologist. Specialists will make a diagnosis, conduct an examination, CT scan of the brain or MRI, give you a sick leave certificate and tell you what neuralgia is – symptoms and treatment.

Treatment for neuralgia consists of conservative therapy, which consists of taking:

vitamins;
antibiotics;
tablets or injections of analgesics;
general strengthening medications;
anticonvulsants;
sedatives.

Painkillers for neuralgia

To relieve pain symptoms, the doctor prescribes painkillers for neuralgia. Among the analgesics medications Nise (Nimesil), Analgin, Movalis, Baralgin are prescribed. Mydocalm is used to relieve muscle spasms. Moderate pain ceases to bother you for several hours. For a long-lasting effect, you must follow the dosage regimen: at least 3 times daily after meals. A long course of use leads to dysfunction of the liver and gastrointestinal tract. Treatment with analgesics is not carried out.

Nonsteroidal anti-inflammatory drugs for neuralgia

Complex therapy includes nonsteroidal anti-inflammatory drugs for neuralgia (NSAIDs), which have a versatile effect on the disease, relieve pain, and have an anti-inflammatory effect. Forms of release of such drugs: injections, ointments, rectal suppositories, tablets for neuralgia. Injections of Ketorol, Analgin or Ketonal instantly eliminate painful symptoms for 3 hours. Medicines for neuralgia of the NSAID group:

Ketoprofen;
Ibuprofen;
Indomethacin;
Naproxen;
Piroxicam;
Diclofenac.

Warming ointments for neuralgia

The effect of warming ointments for neuralgia is achieved by increasing blood circulation. In the area where the nerve is pinched, tissue nutrition improves and oxygen saturation occurs, which is especially effective after hypothermia, stress, and decompression. The vasodilating effect is exerted by natural ( essential oils, camphor, turpentine, pepper tincture, snake or bee poisons) or synthetic irritants (nonivamide, dimethyl sulfoxide, nicoboxyl, benzyl nicotinate). Menovazin is one of these ointments.

Pepper patch for neuralgia

At home, for treatment and to create an irritating effect, a pepper patch is used for neuralgia, which warms the area and can relieve pain. Before applying the patch, you need to degrease the painful area with cologne or alcohol. Wipe dry with a clean cloth. When you feel warmth spreading throughout your body, then you should remove the patch. Treatment with this remedy manifests itself through improved blood circulation and muscle relaxation.

Treatment of neuralgia with folk remedies

If for some reason you cannot see a doctor for professional help, then you can use folk remedies to treat neuralgia. Effective treatment A decoction of willow is considered, which should be taken 1 tbsp. l. 4 times before meals. To prepare the product you need:

pour chopped willow bark (10 g) with boiling water (200 ml);
simmer over low heat for 20 minutes;
strain through cheesecloth, drink when cool.

You can treat yourself with an effective mixture at home, which should be used every other day. whole month:

Mix iodine and glycerin in equal proportions in a dark glass bottle.
Shake the bottle and moisten a clean swab with the solution.
Lubricate sore areas except the spine area.

Video: what is neuralgia

A predisposition to degenerative processes and infections is essential in diabetes. Diabetic retinitis and optic nerve atrophy are sometimes observed.

Diabetic amblyopia is close in pathogenesis to alcohol-nicotine amblyopia. Vitamin B complex deficiency apparently plays a significant role in its pathogenesis.

IN cerebrospinal fluid The sugar content corresponds to its concentration in the blood (normal ratios). Acetone in the fluid can be detected before coma; acetoacetic acid in the fluid is detected only in severe cases of coma. With prolonged ketonuria, ketone bodies pass into liquid.

The most dangerous complication of diabetes is hyperglycemic coma. The cause of coma is the accumulation of metabolic products of fatty acids and acetone in the body. Disorders of carbohydrate metabolism make it impossible to oxidize fats, as well as proteins, to their normal final breakdown products. To cover the necessary energy needs, the body is forced to use a large number of proteins and fat. In this case, the ability to further burn ketone bodies is lost, which leads to their accumulation in the body and the development of acidosis. Beta-hydroxybutyric acid, which accumulates in the body, has a toxic effect on the central nervous system. According to S.S. Genes, B-hydroxybutyric acid inhibits enzymatic processes in the central nervous system and deprives its cells of normal nutrition. Severe biochemical disturbances can cause the breakdown of cellular protein.

In this regard, a significant amount of potassium and phosphates are released, which are excreted in the urine.

The appearance of a coma can be caused by stopping the usual dose of insulin, an error in diet, an infectious disease, mental trauma. Most often, a diabetic coma develops gradually over several days. Initially, gastrointestinal disorders appear in the form of lack of appetite, abdominal pain, nausea, vomiting, constipation or diarrhea. Very soon a feeling of general exhaustion, apathy, and headache arise. Then difficulty breathing occurs, which becomes deep and slow (Kussmaul breathing). The smell of acetone is felt in the air exhaled by the patient. The patient lies in prostration, then stupor appears, turning into a deep coma. The pulse becomes frequent and very small, the temperature is normal or low, arterial pressure falls. The pupils are dilated. Tendon reflexes are reduced or absent, muscle tone is reduced. General intoxication of the body occurs, in which the leading role is played by poisoning of the central nervous system, which causes breathing problems, vascular collapse, decreased muscle tone and disorders of higher nervous activity.

Pathohistological changes found in the brain, similar to those observed in general asphyxia. The vessels are dilated and stasis is visible in them. Impaired capillary permeability leads to cerebral edema and death nerve cells due to metabolic disorders and their great sensitivity to lack of oxygen.

Three types of spinal cord lesions have been described:

1. Changes in the motor cells of the anterior horns of the spinal cord and in the brain stem. In the clinic, in some cases, a picture of chronic poliomyelitis was observed. For the most part, it remained unclear whether these changes were primary or secondary, due to changes in the roots and peripheral nerves.

2. Degeneration of the dorsal roots and dorsal columns, similar to changes in tabes dorsalis. It has long been known that diabetes can cause a syndrome resembling tabes of the spinal cord (pseudotabes diabetica). Modern authors believe that this syndrome in diabetes is caused by damage to the peripheral nerves.

3. Degenerative changes in the posterior columns and, to a lesser extent, in the lateral columns, similar to the picture of funicular myelosis in Biermer's anemia. Griege and Olsen, who described this kind of case, believe that the narrowing of the lumen of the vessels and the thickening of their walls caused long-term deficiency blood supply to the spinal cord, which was the cause of pathological changes in it. We observed a 57-year-old patient who had suffered from diabetes for 30 years. The disease was aggravated by the symptoms of polyneuritis. Then a trophic ulcer of the foot developed, and a picture of transverse myelitis of the thoracic spinal cord developed subacutely. An autopsy revealed necrosis of the thoracic segments of the spinal cord. Histological examination revealed arteriosclerotic changes without any indication of syphilis.

Spinal cord lesions in diabetes are rare. Waltman and Wilder collected 42 cases of diabetes in the literature in which pathohistological examination of the spinal cord was performed. In 20 of them, changes were found in the spinal cord. The authors emphasize that most of these cases were described before the introduction of the Wassermann reaction, and the anatomical picture does not provide grounds to completely exclude syphilis.

Polyneuritis in diabetes affects almost exclusively the lower extremities. Some authors believe that polyneuritis occurs in more than half of all cases of diabetes, while others find it in less than 1% of cases. This sharp discrepancy is explained by the different approaches of the authors to the definition of diabetic polyneuritis. Some believe that polyneuritis should include all cases in which, even in the absence of objective phenomena, patients complain of pain. Others classify as polyneuritis only those cases in which objective symptoms are detected. Based on this more stringent selection, Randles found polyneuritis in 4% of 400 diabetic patients. Martin observed objective symptoms of polyneuritis in 5% of diabetic patients, another 12% of patients complained of paresthesia and pain, but no objective symptoms were found in them. Typically, the appearance of signs of polyneuritis is preceded by long-term illness diabetes, poorly treated or not treated at all.

More often than the fully developed form, abortive forms of polyneuritis occur, often in the form of isolated symptoms: muscle pain, paresthesia, loss of tendon reflexes, trophic disorders. Leg pain that appears as an isolated symptom is localized in calf muscles, an objective examination often does not reveal any violations. There are often complaints of burning paresthesia in the fingers and feet that worsens at night. Patients experience relief when the legs are cooled (“diabetic causalgia”). Finally, isolated loss of knee and Achilles reflexes is very common. According to Goldflam, various disorders reflexes occur in 13% of diabetic patients.

Diabetic polyneuritis develops gradually, rarely subacutely. Slowly progressing, it can begin with neuralgia of individual nerves: sciatic, femoral, brachial plexus nerves. With the development of diabetic neuralgia, attention is drawn to the tendency towards symmetrical lesions, for example, bilateral neuralgia of the sciatic nerve. Neuralgia of the femoral nerve is quite common, so this kind of unilateral and especially bilateral neuralgia should raise suspicion of diabetes.

At the end of the last century, Leiden identified three main forms of diabetic polyneuritis: sensitive, motor and atactic. Further research has shown that diabetes is characterized by a sensitive form, in which dull persistent pain comes to the fore, rarely taking on the character of shooting pains. Most often, pain is localized in the legs, mainly the calf muscles. They usually get much worse at night. The pain can be continuous, but is sometimes intensified by paroxysms.

More than half of the patients, along with pain, experience paresthesia in the form of tingling, burning, numbness, and goosebumps. Objectively, sensitivity disorders are expressed primarily in a disorder of the vibration sense. Less common are disturbances of all types of sensitivity in the distal parts of the lower extremities. Among other symptoms in the sensitive form of diabetic polyneuritis, loss of tendon reflexes, mainly Achilles, is common. Cases of a combination of this type of polyneuritis with signs of retrobulbar optic neuritis have been described.

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Neuralgia – pathological condition, which progresses due to damage to certain parts of the peripheral nerves. This disease is characterized by acute and intense pain throughout its entire length. nerve fiber, as well as in the zone of its innervation. Neuralgia can begin to develop in people from different age categories, but representatives of the fair sex are more susceptible to it after 40 years.

Peripheral nerves have certain receptors that take over all information about the state of organs and systems, and then transmit it to the spinal cord and brain. If a certain area of the nerve is compressed or irritated, this information is distorted, which leads to pain. Usually the pathology progresses against the background of a pathological process already existing in the body.

Muscular neuralgia most often occurs in those parts of the human body where the nerve fiber passes through narrow channels. It is there that there is a high probability of it being compressed or pinched. It is worth noting that this disease can affect any nerve. More often diagnosed are neuralgia of the back, neuralgia of the sciatic nerve, neuralgia of the glossopharyngeal nerve, as well as trigeminal. The diagnosis, as well as the treatment of the disease, is carried out by a neurologist.

Many people confuse neuralgia and. But these are two completely different diseases. With neuritis, inflammation of the nerve fiber is observed, manifested not only by the occurrence of pain, but also by a decrease in sensitivity in the area of the skin that innervates the affected nerve. It is important to immediately consult a doctor if signs of neuralgia of the heart, trigeminal nerve, back or other organs and tissues appear for diagnosis and to draw up a correct treatment plan.

Varieties

Neuralgia can “attack” any nerve, but still more often clinicians diagnose the following types of illness:

neuralgia of the facial or trigeminal nerve;
back neuralgia;
sciatic nerve neuralgia;
neuralgia of the glossopharyngeal nerve;
neuralgia of the occipital nerve.

Etiology

The reasons for the progression of the disease may differ depending on which nerve fiber was affected.

Causes of damage to the occipital nerve:

a tumor of a benign or malignant nature, localized in the area of the cervical vertebrae;
trauma to the cervical spine varying degrees heaviness;
hypothermia of the back of the head.

Etiology of facial neuralgia:

aneurysm of the arteries supplying the brain;
a benign or malignant tumor localized in the brain;
hypothermia of the face;
infectious processes with chronic course in the facial area. In this case we are talking about, and so on.

Etiology of sciatic nerve neuralgia:

lower back trauma;
fracture of the pelvis or femur;
a tumor of a benign or malignant nature, localized at the site of passage of the nerve;
hypothermia of the lower back, hips and buttocks;
overweight bodies;
pregnancy;
the presence of infectious or inflammatory diseases in the pelvic organs.

Etiology of neuralgia of the glossopharyngeal nerve:

the presence of infectious diseases, such as, etc.;
allergic reaction;
metabolic disorder;
intoxication of the body;
excessive consumption of alcoholic beverages;

Symptoms

The symptoms of neuralgia, as well as the reasons for its progression, directly depend on which nerve fiber was compressed or injured.

Trigeminal nerve compression

Neuralgia of the facial nerve occurs quite often. The reason is simple - this nerve exits the skull through a very narrow opening, and therefore nearby tissues can compress it. This nerve is responsible for innervation of the face.

Usually the disease begins to progress acutely - intense pain appears in the facial area. It is paroxysmal in nature. Patients note that it feels like an electric current is passing through. They often freeze and try not to make any movements during such an attack. Its duration varies for each person - for some it is only a few seconds, for others it is several minutes. It is worth noting that attacks can be repeated up to 300 times per day, which is very exhausting for a person. The pain syndrome is most often localized on the right side of the face. It is rare that neuralgia is bilateral.

A trigeminal attack can begin to progress with physical impact on some special points on the face (the wings of the nose, the corners of the eyes, etc.). This often occurs when chewing food, brushing teeth, applying makeup, or shaving.

Sciatic nerve compression

Neuralgia of the sciatic nerve is manifested by the following symptoms:

“shooting” pain along the nerve;
There may be a burning sensation in the lower back, buttocks;
predominantly one branch of the nerve is affected;
The patient notes that on the affected side he has a feeling of “crawling goosebumps.”

Occipital nerve compression

pain attack comes upon a person suddenly. Sometimes it may be preceded by slight irritation of the nerves, for example, a person may simply scratch his head or turn it sharply;
severe pain in the form of a “lumbago” occurs in the back of the neck, back of the head or behind the ears;
the pain syndrome is often localized only on one half of the head and neck, but bilateral damage is possible.

girdle pain;
a painful attack occurs spontaneously. But still, more often it is preceded by a sharp change in body position, deep breath, coughing;
the duration of pain varies - from a couple of hours to several days;
At the location of the affected nerve fiber, a decrease in the sensitivity of the skin may be observed.

Glossopharyngeal nerve damage

Symptoms of glossopharyngeal neuralgia can be triggered by yawning, eating, or coughing. As a result, the patient experiences severe pain at the root of the tongue, at the location of the tonsils, and pharynx. During an attack, dry mouth is noted, and after it stops, increased salivation occurs. It is noteworthy that all the food that a person eats at this time will seem bitter to him.

Diagnostics

If you experience the symptoms listed above, you must contact a medical facility as soon as possible for treatment. complex diagnostics and prescribing the correct treatment plan. The doctor can assume the presence of such an ailment when conducting initial examination and evaluation of patient complaints. To confirm the preliminary diagnosis, the patient is referred for additional examinations.

Diagnostic methods:

X-ray;

Therapeutic measures

You need to start treating neuralgia as soon as the diagnosis has been confirmed. Many believe that this condition is not dangerous to the human body. This is not an entirely correct assumption. As mentioned above, neuralgia progresses secondarily, which means that before its manifestation, some dangerous pathological process had already progressed in the body. So it can pose a serious threat to human health and life, and first of all it needs to be treated. Neuralgia is especially dangerous during pregnancy, as it can aggravate its course and even provoke a miscarriage.

All methods of treating neuralgia are divided into conservative and surgical. Doctors usually first do conservative therapy, and only because of its ineffectiveness they resort to surgical techniques treatment.

Conservative treatment methods:

prescription of anti-inflammatory and analgesic pharmaceuticals. It is imperative to treat neuralgia with such remedies, as they will help relieve pain and relieve inflammation in the affected nerve fiber. The treatment plan may include baclofen, ibuprofen, etc.;
taking vitamins from group B. More often for the treatment of illness they are prescribed in the form of injections;
acupuncture gives very good results in the treatment of illness;
physiotherapeutic treatment. They use ultraviolet, laser, magnetic fields And so on.

Therapy can be supplemented with certain means, depending on what type of illness was diagnosed:

at intercostal neuralgia traction of the spinal column, swimming and wearing special corsets are indicated. The treatment plan also includes sedatives. pharmaceuticals;
Compression of the trigeminal nerve is treated with anticonvulsants. Sometimes doctors resort to surgical destruction of part of the affected nerve fiber;
for pathology of the sciatic nerve, bed rest, taking anti-inflammatory drugs, nerve blockades and electrical stimulation are indicated.

Neuralgia during pregnancy should be treated with special care. Pregnant women should be treated only in hospital settings so that doctors can constantly monitor the woman’s condition.

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