Neurological pathology, which is called radicular syndrome, can develop in any part of the spine. The second name is radiculopathy. Most often, the disease spreads in the lumbar region due to compression of the spinal roots. They become inflamed and the pathological process begins.
Lumbar radicular syndrome: symptoms, treatment
Why do the roots become inflamed?
Another disease is known as radiculitis, and this is the most common name among people, meaning the phenomenon is not dangerous and does not require special treatment. Just think, my back is hurt. The classic image of bent old men and women of the Soviet era, who, groaning, hold their lower back, illustrating sciatica, has today been replaced by younger patients. And the disease, from the category of not dangerous, becomes a serious pathology, as public awareness is growing, and many already know that radiculopathy should not be treated with turpentine or grated radish.
Radicular syndrome is a serious disease, and therefore it needs to be treated by a specialist, and not with folk remedies
By the way. Recipes for radiculitis are a huge section of traditional medicine, which includes numerous homemade preparations of varying degrees of adequacy. Doctors recognize this method of treatment and do not prohibit it, but only as an auxiliary one to help medications relieve swelling, inflammation and pain. Folk remedies cannot eliminate the causes of radicular syndrome.
Prices for orthopedic corsets and posture correctors
A syndrome in which the nerve roots become inflamed is a complication, and the most common of all complications of spinal diseases. For example, osteochondrosis complicated by radicular syndrome is a classic consequence of the fact that timely treatment of this disease was not undertaken. Osteophytes form and grow, intervertebral spaces decrease, orifices become deformed and narrowed, and nerve endings are pinched. That is why pain with radiculopathy is not a symptom, but a syndrome.
The most common cause of radicular syndrome is advanced osteochondrosis
Protrusions and hernias can equally cause pinching. The same list includes injuries, tumors and spinal instability. And, of course, age, with which the supply of nutrients necessary for vertebral cartilage is depleted. The vertebrae “sag” and put pressure on the nerve endings.
Protrusions and herniations of discs also provoke radicular syndrome
Important! Almost any problem with the spine that causes disruption of its functioning can cause radicular syndrome.
Spinal pathology, age, excess weight or injury, especially if provoking factors are added to them, become the cause of vertebral subsidence. The spinal nerve leaves its canal as the entire spinal structure is deformed. The openings through which the nerves pass narrow. Inflammation of the roots begins, swelling and pain, which the swelling intensifies.
When the nerve is compressed, the nerve becomes inflamed, swelling and pain occur at the pinched site.
Most often, despite the fact that radiculitis can be both cervical and thoracic, the name of the disease is associated specifically with the lumbar region, and here's why. This zone bears the heaviest load, both from work, heavy physical activities, and from human existence itself, marked by the ability to walk on two legs. The lower back is the most mobile part of the spine (except for the neck, but the load on them is incomparable). It is in this area that various pathologies most often occur.
The lumbar spine is subject to the greatest loads, as a result of which this is where the risk of pinched nerve fibers is highest
Causes of radicular syndrome:
- osteochondrosis, if not treated;
- tumors in the spine;
The cause of radicular syndrome may be a tumor in the spine - intervertebral hernia - when the cartilage ruptures and the nucleus comes out, deformation and compression of the nerves occurs;
- violation of the spinal structure;
- injury directly and incorrectly fused vertebrae after injury;
Radicular syndrome often occurs due to spinal injury - weakening of bones and cartilage, which may be genetic, caused by age, or infection.
By the way. The pathology may develop more intensely if there are provoking factors. These include obesity and low mobility, age and physical overload, hypothermia and taking certain medications (in this case we are talking about pseudoradicular syndrome).
Pain due to spinal hernia
So, the sources that cause pain during a herniated disc can be:
Nerve root.
This is a nerve formation emerging from the spinal cord in the form of two separate roots - the anterior (motor) one, which innervates the muscles and is responsible for the preservation of their characteristics such as strength and tone, and the posterior (sensitive) one, which is responsible for the superficial (sensations of pain, touch, heat, cold) and deep (sensations of position, movement of a body part in space, its weight, feelings of pressure, vibration) sensitivity. These (intradural) sections of the root are extremely rarely affected by a disc herniation. Much more often, the hernia compresses the extradural part of the root, located outside the dura mater, namely the Nageotte radicular nerve (the area from the dura mater to the dorsal ganglion) or the ganglioradicular segment (the spinal ganglion and the corresponding length of the anterior root).
Radicular pain with a spinal hernia can be caused by the following mechanisms of its damage:
1) compression (squeezing) of the root. It can be carried out:
- directly by the hernia itself or by bone growths (osteophytes), thickened (hypertrophied) ligaments and capsules of the intervertebral joints, which often accompany a herniated disc;
- enlarged due to impaired blood outflow by the epidural venous plexuses located in close proximity to the disc herniation;
- edema that develops around the hernia as a result of venous stagnation, leading to increased permeability of the vein walls, or as a result of contact of the part of the nucleus pulposus that has fallen into the epidural space with vascular structures and cells of the immune system.
2) traction (stretching) of the root. Sometimes the location or side of the hernia may not coincide with the area of radicular damage. For example, damage to the L5 root can occur with a LI-II hernia, which cannot be explained by a compression mechanism, since the L1 and L2 roots can be compressed at the level of the LI-II disc, but the L5 root cannot be compressed, since this can only happen at the level LIV-V or LV-SI disks. The mechanism of such a lesion is explained precisely by the stretching of the L5 root due to compression of the dural sac by a hernia, at a higher level LI-II, with its displacement and, as a consequence, stretching of the root. Similarly, due to stretching, damage to the roots on the right side is sometimes observed with a left-sided hernia and vice versa.
3) intraradicular edema of the root. Swelling can be localized not only around the root at the point of its contact with the hernia, but also inside the root itself, leading to mechanical irritation of its fibers and the appearance of pain impulses due to this.
4) chemical irritation of the root. At the point of contact of the root with the disc herniation, as well as inside the root itself, an inflammatory reaction is usually present in the acute phase. It represents not only swelling, but also the presence of cells of the immune system, as well as chemicals involved in starting and maintaining inflammation. Some of them function as algogens, that is, substances capable of stimulating the appearance of pain impulses in them when in direct contact with the fibers of the root.
Radicular pain is not the only type of pain that occurs in patients with disc herniation, however, as can be seen from the previous description, it has many triggering mechanisms. Moreover, in different clinical cases one or another mechanism may predominate.
So, for example, with subligamentous (subglottic) hernias, the nucleus pulposus does not come into contact with the vessels of the epidural tissue. It is closed from it by the posterior longitudinal ligament in subligamentous extrusions and by the posterior longitudinal ligament along with the unruptured part of the fibrous ring in protrusions. As a result of the absence of such contact, a massive autoimmune inflammatory reaction usually does not develop. At the same time, at the first deep ruptures of the fibrous ring, an autoimmune inflammatory reaction is still possible, since the outer third of the fibrous ring contains vessels that are injured during tears. As a result, cells of the immune system can come into contact with the tissue of the nucleus pulposus, which is embedded in the site of the rupture, which triggers an inflammatory reaction. The nucleus pulposus itself, protruding into the site of rupture, edema, which forms in parallel with the accumulation of pro-inflammatory cytokines, irritate the pain receptors of the outer third of the fibrous ring (with protrusions) and the outer third of the fibrous ring and the posterior longitudinal ligament (with subligamentary extrusions) mechanically, and algogens (substances which, upon contact with nerve endings, lead to the occurrence of a pain impulse) cause chemical stimulation of these receptors. However, this inflammatory reaction cannot lead to radicular pain, since it occurs subglottically and does not affect the root. After relief of inflammation, chemical irritation is leveled out, mechanical irritation is reduced due to regression of edema and, as a result, a decrease in pressure on nerve receptors. Gradually, the receptor apparatus of the outer third of the fibrous ring and the posterior longitudinal ligament adapt to the mechanical pressure exerted by the nucleus pulposus embedded in the rupture site and the pain regresses.
Moreover, the development of radicular pain during an exacerbation due to swelling, inflammation and venous stagnation at the site of contact of the hernia with the root and inside the root itself with subglottic hernias, especially extrusions, is not uncommon. In this case, another mechanism for the development of these disorders is triggered. So, if the tear in the annulus fibrosus is deep enough or there is a complete rupture, then the hernia zone becomes a source of stimulation from the receptors of the outer third of the annulus fibrosus and the posterior longitudinal ligament. If the irritation is only mechanical due to the tissue of the nucleus pulposus and there is no additional mechanical (edema) and chemical (inflammatory substances) stimulation, then there may be no pain manifestations at all. This usually happens in the initial stages of development of a disc herniation, when after stopping the exacerbation, usually through medication, the pain usually regresses completely. However, regular mechanical stimulation by the nucleus pulposus of the receptor apparatus of the fibrous ring and the posterior longitudinal ligament leads to the emergence of a chronic muscular-tonic reaction at the level of the hernia and nearby segments, which gradually changes the muscles structurally, leading them not only to spasm, but also to dystrophy and fibrosis. As a result, despite the absence of acute spasm, the muscles become shortened and tightened. This changes the relative position of their fixation points on the vertebrae, which creates an asymmetrical installation of the herniated spinal motion segment. The muscles thus become more prone to developing acute spastic reactions as a result of exposure to various provoking factors. They can be heavy lifting, unsuccessful, uncoordinated movement, stress, hypothermia, draft, infectious disease and many other, sometimes seemingly unimportant, factors. They essentially represent the last straw, which further shortens the muscles, leading to the development of more pronounced asymmetry of the vertebrae at the level of the hernia. This leads to a change in the position of the hernia in the spinal canal. It begins to compress the epidural venous plexuses, blocking the blood outflow pathways from the canal at this level. As a result, the veins increase in volume, their walls stretch and become more permeable, swelling develops and blood cells leave the vascular bed, with the development of an inflammatory reaction. The root begins to be compressed by a conglomerate consisting of a hernia, enlarged veins and edematous fluid, which leads to mechanical compression of its fibers and vessels with the development of edema, inflammation and cellular infiltration of the root itself.
The change in the position of the vertebrae described above and, as a consequence, the hernia in the spinal canal, can lead not only to compression of the veins with a subsequent cascade of the described reactions, but also to the movement of the hernia closer to the root, leading to its mechanical compression by the hernia itself. Along with a change in the spatial location of the hernia, the localization can also be changed by other structures - osteophytes, thickened ligaments and joint capsules, which can also lead to a compressive effect on the roots.
The described mechanism for the development of radicular pain is predominant, since it is characteristic of subligamentary (subglottic) hernias, and they are found in practice much more often than transligamentous (transligamentous) hernias. Subglottic hernias, as a rule, form slowly, increasing gradually, so most of them are quite dense. As the nucleus pulposus moves beyond the fibrous ring into the subglottic space, its ability to receive nutrients and moisture from somewhere is gradually lost, it turns into a fairly dense cartilaginous mass, which, as the hernia grows, is filled with more and more dehydrated cartilaginous masses. In this case, exacerbations of subglottic hernias, however, occur in most cases quite acutely, which is explained by the muscle reactions described above with the development of vertebral asymmetry with subsequent relocation of the hernia towards the radicular nerve.
With transligamentous hernias, the mechanism of radicular pain is somewhat different. These hernias usually form against the background of subligamentous hernias. Initially, a subligamentous hernia gradually develops, which then simultaneously, as a result of rupture of the posterior longitudinal ligament, enlarges and becomes transligamentous. A fragment of the nucleus pulposus suddenly appears in the epidural space, coming into contact with a large abundance of vessels located here. It is regarded by the immune system as foreign because it has not previously come into contact with it, which triggers a powerful autoimmune inflammatory response. Also, a fallen fragment of the nucleus pulposus can mechanically compress the root itself. At the same time, by compressing the veins, it can cause stagnation of venous blood in the epidural space, exacerbating swelling and inflammation around and inside the root. The muscular-tonic reaction here, as a rule, is secondary and develops as a result of intense irritation of the root, although it can further enhance the asymmetry of the vertebrae and the narrowing of the canal, bringing the hernia even closer to the root, thereby aggravating its compression.
Having described in detail the radicular version of pain, we can move on to other sources of pain that cause pain during a spinal hernia. The next, and most common, source of pain during a hernia is:
Muscles and fascia.
Pain from a herniated spine, the source of which is these structures, is called myofascial. The source of pain manifestations in myofascial disorders are muscle pain receptors (nociceptors). The main mechanism of their activation is mechanical irritation by spasmed and compacted muscle fibers and fascia (connective tissue membranes surrounding muscle fibers and muscles). This irritation can occur due to diffuse shortening of the muscles or the formation of local compactions in them, called trigger points (trigger points). The peculiarity of muscle disorders in patients with hernias is that due to the presence of a persistent source of mechanical irritation in the structures of the fibrous ring and the posterior longitudinal ligament, regular impulses are maintained, causing chronic spasm of the muscles of the hernial and nearby segments. It leads to disruption of the blood supply to muscle fibers and, as a consequence, to their dystrophy, and subsequently atrophy and fibrosis. Dystrophic-atrophic reactions are aggravated by a decrease in the size of the intervertebral foramen, which traditionally accompanies disc herniation. In the narrowed foramen, regular trauma to the radicular nerve occurs, the fibers of which, outside the intervertebral foramen, become part of the spinal nerve, and its posterior branch provides innervation to the paravertebral muscles. As a result, not only a deficiency in the supply of nutrients to the muscles develops, but also a disruption in the processes of their absorption, since it is the nerves that are responsible for trophism, that is, the consumption of nutrients in accordance with needs. When innervation disorders develop as a result of trauma to the nerve root, the ability of muscles to absorb the required amount of nutrients is reduced. As a result, the muscle fibers fall into a state of contracture, their atrophy develops, and the layers of connective tissue between the muscle fibers thicken. All this gradually increases the irritation of muscle pain receptors, creating impulses from them, and when its severity exceeds the pain threshold, that is, the ability of spinal cord cells to resist the entry of pain impulses, myofascial pain occurs. Increased impulses from the muscles can occur smoothly as their compaction increases, or acutely due to the additional layering of spasm. It can be triggered by various factors, from heavy lifting, awkward movements and uncomfortable positions, to hypothermia, drafts, stress, infectious diseases and other factors that can cause weakening of the body.
The described sequence of processes in the muscles is valid not only for the paravertebral muscles of the spinal motion segment affected by a hernia, but also for distant muscles included in the zone of innervation of the root, which is subject to periodic trauma due to the narrowing of the canal at the level of the hernia localization. The fact is that each root innervates not only the skin and muscles along the spine, but also remote areas: cervical roots - the shoulder girdle and arm, pectoral roots - the torso, lumbar roots - the pelvis and legs. As a result, myofascial disorders can develop in these areas, gradually leading to the development of pain in them. Thus, a person without signs of gross compression of the root may experience pain associated with tightening and spasm of muscles in the arm, shoulder girdle, shoulder blade with a cervical hernia, in the buttock, groin, lower limb - with a lumbar hernia.
Myofascial pain during a spinal hernia cannot always be explained by the localization of the hernia, since to a certain extent they are always present even before the hernia appears, both at the level of the part of the spine in which the hernia subsequently formed, and at the level of other areas of the spine. Myofascial disorders are an important component of biomechanical disorders that develop for various reasons before the appearance of a hernia, often from childhood, accumulating over the years and gradually leading to overload of the most vulnerable regions of the spine with the subsequent development of osteochondrosis and hernias. These disorders, against the background of the addition of myofascial disorders caused by the hernia itself, can be aggravated, leading to the appearance of pain in other regions of the spine not associated with the hernia.
In addition to the nerve root, muscle and fascial structures, pain from a spinal hernia can also be caused by:
Ligaments.
Most often, the posterior longitudinal ligament is involved in the pathological process. Pain with a spinal hernia that occurs when it is involved in the process may be associated with mechanical irritation due to compression by the nucleus pulposus. In the acute phase, mechanical compression can be aggravated due to the addition of edema; also, as a result of the development of the inflammatory reaction, chemical irritation of the receptors appears.
When a hernia appears, a violation of the stability of the spinal motion segment often develops due to the deterioration of the fixation of the vertebral bodies by the weakened disc. This may involve other ligaments of the spinal motion segment in the pathological process, leading to irritation of their receptors due to overstretching as a result of increased mobility of the vertebrae. Irritation of the receptor apparatus of the ligaments usually produces fairly local pain, at the level of the location of the ligament involved in the pathological process, but so-called sclerotomal pain can also occur, the source of which is the spinal ligaments, and the pain is localized at a distance in the extremities.
Disks.
Pain receptors of the discs, as mentioned above, are localized in the outer third of the fibrous ring, therefore discogenic pain occurs during a spinal hernia, this is associated with a complete or almost complete rupture of the ring, reaching the indicated sections of the disc. The mechanism of irritation of receptors in the acute stage is associated with their mechanical compression by the nucleus pulposus and edema, as well as with the influence of proinflammatory cytokines that irritate them chemically. As the exacerbation subsides, the role of edematous and chemical factors is significantly reduced or disappears. The factor of compression of receptors by the nucleus pulposus persists, which can lead to chronic pain in the affected part of the spine. Adaptation of receptors to mechanical stress may develop with gradual relief of pain. A significant role is played by therapeutic effects that reduce the load on the hernial disc, which leads to a more uniform distribution of intradiscal pressure and a decrease in the degree of compression of the receptors in the zone of rupture of the fibrous ring.
Joints.
The asymmetrical position of the intervertebral joints is a frequent companion to herniated intervertebral discs, which is caused by the development of changes in the paravertebral muscle structures. Densified and spasmed muscles, attaching to the vertebrae, create asymmetrical traction, removing the vertebrae and their joints from a state of stable equilibrium into asymmetrical positions. This can cause mechanical pressure on the cartilaginous structures of the joints with irritation of their receptors, as well as stretching or compression of the joint capsules, leading to joint pain in a spinal hernia.
All the mechanisms described above can lead to two types of pain when a disc herniation occurs - nociceptive and neuropathic. Nociceptive pain is associated with irritation of nociceptors (pain receptors), and neuropathic pain is associated with nerve trunks, that is, roots. Nociceptive pain includes myofascial, ligamentous, discogenic and arthrogenic (articular) pain, and neuropathic pain includes radicular pain. Wherever pain impulses arise, in pain receptors or a root, they then enter the spinal cord, and then along pathways into the subcortical structures and cerebral cortex, where awareness of the presence of pain and all its characteristics occurs. When pain impulses reach brain structures, certain areas of the brain are also activated, which are involved in the fight against pain due to a number of chemicals - serotonin and norepinephrine. The nerve fibers of the analgesic system are directed in the opposite direction to the paths of the pain system, that is, from top to bottom, from the brain to the spinal cord and end on the pain cells of the posterior horn, inhibiting them by increasing the pain threshold. The higher the level of serotonin and norepinephrine acting on the neurons of the dorsal horn, the higher their pain threshold and the fewer pain impulses enter the brain.
At the initial stages, in most patients, the activity of the analgesic system is quite high and the success of pain relief is determined by the speed of elimination of all the sources of pain impulses described above, which directly depends on the correctness and timeliness of therapeutic measures. If treatment measures are carried out correctly and as quickly as possible, increasing the activity of the analgesic system allows for faster recovery. If the timing of correct therapeutic measures aimed at eliminating all sources of pain is delayed, then the anti-pain system begins to gradually deplete due to a decrease in the reserves of serotonin and norepinephrine in the central nervous system. This lowers the pain threshold of dorsal horn cells that transmit pain impulses to the brain, making them easier to pass. The lack of adequate therapeutic measures over time makes these cells so excitable that they not only cease to prevent pain impulses from entering the brain, but also begin to generate them themselves. Plus, the number of cells conducting pain impulses increases. All this leads to a gradual chronicization of pain, as well as the development of depressive states, since a decrease in the level of serotonin and norepinephrine in the structures of the central nervous system is also responsible for the development of emotional and affective disorders, in particular depression.
Having considered the importance of timely and correct pain relief for spinal hernia, we should indicate the main areas in which pain manifestations in this disease can be localized.
Pain due to a spinal hernia may have a deep, unclear localization or, conversely, a superficial pain, occurring in one or more of the following areas:
For cervical hernias:
- cervical spine;
- head;
- lateral, anterolateral surface of the neck;
- shoulder girdle, interscapular region;
- areas of the scapula, shoulder, elbow, wrist joints;
- arm (shoulder, forearm, hand);
- supra- or subclavian region;
- anterior surface of the chest.
For hernias of the thoracic spine:
- thoracic spine;
- posterior, lateral, anterior surface of the chest;
- epigastric region.
For hernias of the lumbar spine:
- lumbar spine;
- sacrum;
- coccyx;
- buttocks;
- areas of the hip, knee, ankle joints;
- leg (thigh, lower leg, foot);
- groin area;
- area of the anterior abdominal wall.
The nature of the pain can be:
- pulling;
- aching;
- aching;
- twisting;
- piercing;
- shooting.
Symptoms of the disease
Before listing the symptoms, it is worth referring to the classification. For this disease it is not too complicated. The pathology is not divided into congenital and acquired, since most doctors consider it an acquired syndrome. It also does not have pronounced degrees of development (complexity) that would affect diagnostic and therapeutic measures. The only classification is by zones of the spine, and even here there is an exception.
Radicular syndrome can occur in any part of the spine
Radicular syndrome can manifest itself in the cervical area, in the thoracic area and (most often) in the lumbar area. In the sacrum and coccyx, radiculitis is observed so rarely that it is considered an exception and is not included in the classification.
There are only three main symptoms of this disease:
Symptoms of radiculitis
The first manifestations and main permanent symptoms of radiculitis of the lumbosacral spine are pain, impaired sensitivity and muscle weakness.
The affected area corresponds to the innervation zone. Depending on the affected area, pain can be observed in the lumbar and gluteal regions, the posterolateral and anterior part of the thigh, along the anterior outer surface of the lower leg, on the dorsum of the foot, big toe, in the calf muscle, in the area of the outer ankle and heel.
Lumbosacral radiculitis is often chronic, with acute relapses. Lumbosacral radiculitis is characterized by increased pain when the body suddenly changes from a horizontal to a vertical position or vice versa, as well as when engaging in an active lifestyle (sports, walks, fitness classes).
Exacerbation of pain syndrome in radiculopathy of the lumbosacral region is observed when the interradicular nerve is compressed by an intervertebral hernia.
According to the types of radiculopathy of the lumbosacral spine, there are:
- Lumbago (lumbodynia) is acute pain in the lower back during sudden physical exertion, and also provoked by overheating or hypothermia of the body. The painful attack itself can last in different ways: from several minutes to several hours and even days. The main cause of this type of radiculopathy is muscle strain in the lumbar region, intervertebral hernia or displacement of the vertebrae relative to each other.
- Sciatica (sciatica) - with this type of radiculitis, pain is localized in the buttock, on the back of the thigh and lower leg and can reach the foot. Sometimes, in addition to pain, muscle weakness is noted. This is due to damage or irritation to the sciatic nerve, the largest nerve in the body. The pain with sciatica is shooting, like an electric shock; burning, tingling, “pins and needles” and numbness are also possible at the same time. Pain of varying degrees of intensity is possible: from mild to very intense, such that the patient cannot sleep, sit, stand, walk, bend or turn.
- Lumboischialgia is lower back pain radiating to the leg or legs. With this type of radiculitis, the pain spreads mainly along the buttock and along the posterior surface of the leg, without reaching the toes; most often it is an aching, burning, growing pain.
Diagnosis of lumbar radicular syndrome
To make a diagnosis, the doctor will need to conduct an examination and instrumental studies. You should contact a neurologist with this syndrome. It is advisable to voice specific complaints, paying attention to the most accurate description of symptoms. The doctor will conduct a neurological examination, during which areas of decreased sensitivity, muscle atrophy, and pain points will be identified. Thanks to a physical examination, it will be determined in the area of which vertebra the nerve pinching occurred.
During the initial examination, the doctor determines the most likely cause of the disease and the area where the nerve is pinched.
When diagnosing, it is imperative to palpate the painful area, where muscle tension should be detected.
By the way. During palpation, when the doctor passes the most painful areas, the patient will involuntarily lean to the side to reduce the pain.
Next, the patient will receive a referral for an x-ray or computed tomography. If the diagnosis remains unspecified, an MRI or electroneuromyography may be performed (this study will show pathologies in the transmission of nerve impulses to the muscles).
If you want to learn in more detail how the MRI procedure of the spine is performed, as well as get acquainted with the preparation and implementation, you can read an article about it on our portal.
MRI will allow you to accurately determine the location and extent of damage to nerve fibers
By the way. The most accurate diagnostic test for detecting radicular syndrome is magnetic resonance imaging. But the procedure is not always possible, not only due to the patient’s contraindications (for example, fixed metal prostheses), but also due to the high cost of the study.
Treatment
As with other diseases of the spine, the specifics of treatment may depend on the cause of the radicular syndrome and the degree of its severity. But the differences are not fundamental, and consist mainly in the fact that before applying surgical treatment, the doctor will try all conservative therapeutic methods.
Treatment of radicular syndrome in most cases is carried out using conservative methods.
Important! Surgical intervention for radiculopathy is resorted to only when conservative treatment for a long period does not bring effect, or the patient’s condition begins to rapidly deteriorate.
The most important thing to remember is that treatment of radiculitis is not carried out at home, in any case, without consulting a doctor, and limiting yourself to self-diagnosis. Perhaps, if the symptoms do not manifest themselves to an extreme degree and do not affect the rhythm and quality of life, the doctor will advise you to limit physical activity, balance your diet and make an appointment with a massage therapist. But if the pain is severe, you should never try to cope with it without the help of a doctor.