Treatment of intercostal neuralgia using UVT

Causes of intercostal neuralgia

There are several causes of chest pain, which are caused by compression (compression) of nerve fibers, their damage or irritation.
Most often, intercostal neuralgia is caused by :

• Degenerative-dystrophic diseases of the spine (osteochondrosis, hernia and protrusion of intervertebral discs, scoliosis and kyphosis, spondylosis)
• Systemic infectious and metabolic diseases (diabetes mellitus, rheumatism, gout, tuberculosis, ankylosing spondylitis, brucellosis, herpes zoster, hepatitis, herpes and influenza virus)
• Mechanical causes (chest and spine injuries, physical overload, hypothermia)
• Chronic deficiency of vitamins, mainly group B, with hepatitis, alcoholism, diseases of the gastrointestinal tract
• Intoxication with heavy metals, drugs, alcohol, acute infectious diseases
• Psychogenic diseases (stress, depression, fatigue, psychogenic “cardialgia”, myofascial pain syndrome)
• Diseases of the nervous system (multiple sclerosis, polyradiculoneuritis)
• Diseases of the thoracic organs (angina pectoris due to ischemic heart disease, myocardial infarction, myocarditis, pericarditis, heart disease, mitral valve prolapse, dissecting aortic aneurysm, pulmonary embolism, pleurisy, pneumonia, pulmonary oncology, gastrointestinal diseases, diaphragmatic abscess)

As can be seen from the list above, chest pain can be caused by a variety of diseases, which is why it is imperative to undergo examination by a specialist and not self-medicate. One of the effective ways to treat intercostal neuralgia is shock wave therapy.

Chest pain can be caused by cardiovascular diseases, but in the vast majority of cases it is a consequence of non-physiological stress or osteochondrosis, and not a manifestation of angina pectoris. It can be difficult to distinguish these two pain symptoms on your own, but in general their difference lies in the nature of the pain: with angina pectoris, the pain with deep inhalations and exhalations does not change its intensity, whereas with, say, osteochondrosis, it can change paroxysmally. Also, you can get rid of angina by taking appropriate medications (for example, nitroglycerin), but in cases with intercostal neuralgia, of course, this will not help.

Trigeminal neuralgia

Trigeminal neuralgia (TN) - (synonyms: tic douloureux, or Fothergill's disease) is one of the most common facial pain (prosopalgia - (Greek prosopon (face) + algos (pain)) and is one of the most persistent pain syndromes in clinical neurology TN is a typical example of neuropathic pain and is considered the most painful type of prosopalgia. TN most often has a chronic or recurrent course, much more difficult to treat than many other types of chronic pain. High intensity and persistence of trigeminal neuralgia, its special, often painful nature, resistance traditional methods of pain relief give this problem exceptional relevance. According to WHO, the prevalence of TN is up to 30–50 patients per 100,000 population, and the incidence is 2–4 people per 100,000 population. TN is more common in women than in men, debuts in fifth decade of life and in 60% of cases has a right-sided localization.Causes of TN The most common cause of TN is compression of the proximal part of the trigeminal root within a few millimeters from the entrance of the root to the pons (i.e. n. "entry zone of the spine"). In approximately 80% of cases, compression occurs by an arterial vessel (most often a pathologically tortuous loop of the superior cerebellar artery). In other cases, such compression is caused by an aneurysm of the basilar artery, space-occupying processes in the posterior cranial fossa, tumors of the cerebellopontine angle and multiple sclerosis plaques. At the extracranial level, the main factors leading to the occurrence of TN are: tunnel syndrome - compression in the bone canal through which the nerve passes ( often in the infraorbital foramen and lower jaw), associated with its congenital narrowness, the addition of vascular diseases in old age, as well as as a result of a chronic inflammatory process in adjacent areas (caries, sinusitis); local odontogenic or rhinogenic inflammatory processes. The development of TN can be provoked by infectious processes, neuroendocrine and allergic diseases, demyelination of the trigeminal nerve root in multiple sclerosis.

Clinical manifestations of TN

The disease, in most cases, develops on one side; a bilateral process is extremely rare. First, pain occurs at the site of innervation of any of the three branches; later, as the disease progresses, pain can gradually cover areas of the face innervated by neighboring branches. The localization of pain depends on which branches are involved in the process:

• when the first branch is affected, pain is localized in the area of ​​the superciliary arch, forehead, temple, sometimes pain occurs in the eyelids and eyeball;
• when a pathological process occurs in the second branch, pain occurs in the upper lip, wing of the nose, in the projection of the zygomatic bone, upper cheek, upper jaw and palate;
• when the third branch is affected, the pain zone is localized in the lower lip, chin, cheek, lower jaw, half of the tongue and soft palate.

Taxonomy of trigeminal prosopalgia

From the point of view of topical diagnosis, the development of any form of trigeminal prosopalgia is associated with damage to the peripheral trigeminal neuron - the peripheral trigeminal branches, the sensory trigeminal ganglion (located at the base of the skull), the sensory root of the trigeminal nerve that follows it in the direction of the brain stem, as well as those entering the brain stem sensory trigeminal fibers and sensory nuclei of the trigeminal nerve. Depending on the impact of the pathological process on the corresponding part of the trigeminal system, TN is divided into predominantly central and peripheral genesis. In the occurrence of TN of central origin, neuroendocrine, immunological and vascular factors play an important role, which lead to impaired reactivity of cortical-subcortical structures and the formation of a focus of pathological activity in the central nervous system. In the pathogenesis of peripheral TN, the compression factor, infections, injuries, allergic reactions, and odontogenic processes play an important role. Despite the difference in the symptomatology of the clinical forms of trigeminal prosopalgia, the features of facial pain are of primary importance for their differentiation, in some cases manifested by prolonged (constant) pain, and in others in the form of paroxysms of pain. Paroxysmal forms of trigeminal pain are traditionally referred to as neuralgia, and non-paroxysmal forms - trigeminal neuropathy. These forms of facial pain—neuralgia and trigeminal neuropathy—fundamentally differ in their approaches to treatment. Deafferentation trigeminal neuropathy (prosopalgia)

Deafferentation facial pain (prosopalgia) is the most severe form of trigeminal lesion, manifested by highly intense facial pain, often resistant to conservative therapy, and severe sensory impairment. Develops as a result of significant damage (destruction) of the peripheral or central structures of the trigeminal system. The concept of “deafferentation trigeminal prosopalgia”, as a general syndromological definition, was proposed by Yu. V. Grachev and Yu. A. Grigoryan (1995) to designate a special form of facial pain that develops as a result of deafferentation in the sensory system of the trigeminal nerve. The pathophysiological term “deafferentation” (de- + lat. afferentis bringing), literally means the separation of the receptor zones of peripheral nerves from the central sensory structures, due to a violation of the integrity or conductivity of nerve fibers. Typical peripheral forms of deafferentation trigeminal prosopalgia are postherpetic, tumor and iatrogenically caused facial pain (caused by destruction of the ganglion and trigeminal nerve root), and central are two quite rare forms caused by syringobulbia and medulla oblongata infarction.

Diagnostics of TN

Clinical interview plan for the evaluation of patients with facial pain. Description of pain:

1. Localization of pain
2. Temporary characteristics of pain (paroxysmal/non-paroxysmal, prolonged)
3. Frequency of pain attacks
4. Pain intensity
5. Sensory nature of pain
6. Other sensations accompanying facial pain (associated signs)
7. Conditions and time of pain occurrence
8. Medicines (other factors) that reduce or eliminate pain

Anamnestic data:

1. Duration of the disease
2. Conditions for the development of the first exacerbation
3. The nature of the course of prosopalgia (acute, recurrent, continuous)
4. Frequency of exacerbations of prosopalgia
5. Previous treatment
6. Disorders (neurological, somatic) accompanying the development of the disease.

When conducting palpation examination of the facial area, it is necessary to distinguish between “neuralgic” and “myofascial trigger” (English trigger). Neuralgic trigger points or zones (in patients with trigeminal neuralgia) are hyperexcitable areas of the skin and mucous membrane, with mechanical irritation, including light touch, causing a painful attack. At the same time, strong pressure, usually applied by the patient himself, not only does not cause pain, but in some cases leads to a decrease or disappearance of pain. Myofascial trigger points (essentially pain points) are located in the soft tissues of the face in the projection of the masticatory muscles. “Pressing” on them is accompanied by localized or radiating pain.

Treatment of TN The main directions of drug therapy are:

• elimination of the cause of TN, if it is known (treatment of diseased teeth, inflammatory processes in adjacent areas, etc.),
• carrying out symptomatic treatment (pain relief).
• Anticonvulsants are the drugs of choice for the treatment of TN, and carbamazepine was one of the first drugs officially approved for the treatment of this condition.

In the early 90s of the last century, a new generation of antiepileptic drugs appeared, and now anticonvulsants are usually divided into first and second generation drugs. First-generation drugs are practically not considered as the first line of treatment for NB (with the exception of carbamazepine for TN). Second generation anticonvulsants include pregabalin (Lyrica), gabapentin (Neurontin, Gabagamma, Tebantin), lamotrigine (Lamictal), oxcarbazepine (Trileptal), topiramate (Topamax), levetiracetam (Keppra), tiagabine (Gabitril), zonisamide (Zonegran), vigabatrin (Sabril), felbamate (Taloxa). These drugs have more favorable pharmacokinetic characteristics and safety profiles, as well as a lower risk of drug interactions compared to first-generation anticonvulsants. According to the recommendations of the European Federation of Neurological Societies (2009), pharmacotherapy for TN is based primarily on the use of carbamazepine (Finlepsin, Tegretol) proposed by S. Blum in 1962 (200–1200 mg/day), which is the drug of first choice (level of evidence A) . The analgesic effect of this drug is mainly due to its ability to reduce the permeability to sodium of the membranes of neurons involved in nociceptive reactions. The following treatment regimen with carbamazepine is usually prescribed: in the first two days the daily dose is 200 mg (1/2 tablet in the morning and evening), then within two days the daily dose is increased to 400 mg (morning and evening), and after that - to 600 mg (1 tablet in the morning, lunch and evening). Gabapentin (Neurontin) is the first drug in the world to be registered for the treatment of all types of neuropathic pain. Many studies have shown the effectiveness of gabapentin in patients with TN who do not respond to treatment with other drugs (carbamazepine, phenytoin, valproate, amitriptyline); in most cases, complete relief of pain was observed. The therapeutic dose ranges from 1800 to 3600 mg/day. The drug is taken 3 times a day according to the following regimen: 1st week - 900 mg/day, 2nd week - 1800 mg/day, 3rd week - 2400 mg/day, 4th week - 3600 mg/day. The results of an open-label, prospective, 12-month study of 53 patients with TN were recently published, evaluating the effectiveness of pregabalin (Lyrica) at a dose of 150–600 mg/day. Treatment with pregabalin resulted in pain relief or at least a 50% reduction in pain intensity in 25% and 49% of patients, respectively. The use of levetiracetam (Keppra) in the treatment of TN was first reported in 2004 by KR Edwards et al. The properties of this drug are particularly suitable for the treatment of TN patients with severe pain who require a rapid response to therapy. Unlike other anticonvulsants, especially carbamazepine, the hepatic cytochrome P450 system is not involved in the metabolism of levetiracetam and the drug is excreted through the kidneys. In addition, this drug has a favorable therapeutic index and has few adverse side effects (which is the main problem when using drugs to treat TN). A 10-week, prospective, open-label study showed that higher doses of levetiracetam, ranging from 3000–5000 mg/day (50–60 mg/kg/day), were required for the treatment of TN compared with the treatment of epilepsy, but did not caused significant side effects. This circumstance indicates the prospect of using this drug for the treatment of TN. Since the 1970s, antidepressants have been used to treat TN. Currently, the effectiveness of the use of tricyclic antidepressants (TCAs) in the treatment of TN has been proven. Pathogenetic treatment of patients with TN includes the use of drugs with neurometabolic, neurotrophic, antioxidant, and antihypoxic effects. In recent years, high efficiency of the use of metabolic drugs has been discovered. In the treatment of patients with TN, the high effectiveness of the metabolic drug Actovegin, a deproteinized derivative from the blood of young calves, has been shown. The main effect of this drug is to stabilize the energy potential of cells. Actovegin also has an antihypoxic effect, being an indirect antioxidant. In addition, the effect of Actovegin is manifested by indirect vasoactive and rheological effects by increasing capillary blood flow, reducing peripheral vascular resistance and improving the perfusion of organs and tissues. During an attack, it is advisable to use Actovegin intravenously in a slow stream or drip for 10 days at a dose of 400–600 mg/day. In the interictal period, the drug is prescribed orally at a dose of 200 mg 3 times a day for 1–3 months. The pathogenetic treatment of patients with TN includes the use of high doses of B vitamins as part of multicomponent preparations, which is due to their multimodal neurotropic effect (impact on metabolism, metabolism of mediators, transmission of excitation in the nervous system), as well as the ability to significantly improve nerve regeneration. In addition, B vitamins have analgesic activity. Such drugs, in particular, include Milgamma, Neuromultivit, Neurobion. Until now, the selection of analgesic therapy for NB is more an art than a science, since the choice of drugs is carried out mainly empirically. There are often situations when the use of one drug is not effective enough and there is a need for a combination of drugs. Prescribing “rational polypharmacotherapy” (simultaneous use of drugs with neurotropic, neurometabolic and analgesic mechanisms of action) allows increasing the effectiveness of treatment with lower dosages of drugs and fewer side effects.

Differentiated therapeutic approaches for paroxysmal and non-paroxysmal trigeminal prosopalgia.
Differentiated therapeutic approaches for paroxysmal and non-paroxysmal trigeminal prosopalgia

For patients suffering from unbearable pain for a long time, and if conservative therapy is ineffective in the case of classical TN, surgical treatment is recommended. The following approaches are currently used:

1. surgical microvascular decompression;
2. stereotactic radiation therapy, gamma knife;
3. percutaneous balloon microcompression;
4. transdermal glycerol rhizolysis;
5. Percutaneous radiofrequency treatment of the Gasserian node.

In conclusion, we note that the treatment of TN should be multidisciplinary in nature, and the choice of various treatment methods and the risks of possible complications should be discussed with the patient.

Treatment of intercostal neuralgia

Typically, treatment of intercostal neuralgia includes the following::

• Treatment of degenerative-dystrophic diseases of the spine, if they are the causes of intercostal neuralgia, using shock wave therapy
• Relieving the load on the thoracic spine: correction of movements, short-term bed rest on a hard surface, wearing a corset
• Local anesthesia with anesthetics (blockade of trigger points), and in the presence of intense pain - together with glucocorticosteroids
• Intramuscular injections of nonsteroidal anti-inflammatory drugs (NSAIDs) for 5–10 days to prevent inflammatory processes, often with simultaneous administration of omeprazole, a proton pump inhibitor
• Taking muscle relaxants - drugs that prevent muscle spasms and increase pain
• Local warming ointments and patches
• For chronic chest pain - take tricyclic antidepressants, which reduce anxiety, seizure activity and improve sleep quality
• Therapeutic exercises - during remission
• Massage and manual therapy
• Various types of physical therapy

Treatment of intercostal neuralgia using the UVT device is effective and has a minimum of contraindications, and due to the mechanism of action on the cells of damaged tissues, it performs pronounced analgesic, decongestant, anti-inflammatory, resolving, warming and restorative functions.