Sciatica and back pain

Sciatica is pain that spreads along the sciatic nerve. Sciatica is usually caused by compression of the nerve roots of the lumbar spine. The most common causes are disc pathology, osteophytes, narrowing of the spinal canal (stenosis of the spinal canal). Symptoms of sciatica include pain radiating from the buttock to the foot. Diagnosis involves the conduct of an MRI or CT scan. Electromyography and determination of nerve conduction velocity help to clarify the level of lesion. Treatment includes symptomatic therapy and sometimes surgery, particularly in the presence of neurological deficits.

[1], [2], [3]

Causes of sciatica

Sciatica is usually caused by compression of the nerve roots, usually due to protrusion of the intervertebral disc, bone deformities (osteoarthritic osteophytes, spondylolisthesis). Tumor or abscess in the vertebral canal. Compression can occur in the vertebral canal or intervertebral foramen. Nerves can also be compressed beyond the spine, in the pelvic cavity or in the buttock area. The most commonly affected L5-S1, L4-L5, L3-1.4 roots.

[4], [5], [6], [7]

Symptoms of sciatica

The pain radiates along the sciatic nerve, most often in the lower part of the buttock and the posterior surface of the foot below the knee joint. Usually the pain is burning, shooting, dagger. It can be combined with lumbar pain or be without it. The Valsalva test can increase pain. Compression of roots can cause sensory, motor, or more objective findings - reflex deficiency. A herniated L5-S1 disc may cause a decrease in the Achilles reflex, a herniated L3-L4 disc - a decrease in the knee reflex. Raising a straightened leg more than 60 ° (sometimes less) can cause pain radiating to the foot. This is typical of sciatica, but the pain radiating downward in the lifted limb in combination with pain arising in the contralateral leg (cross syndrome) is more specific for sciatica.

Diagnosis of sciatica

Sciatica can be suspected on the basis of a characteristic algic pattern, while the study of sensitivity, muscle strength and reflexes is necessary. If the neurologic deficit or symptoms persist for more than 6 weeks, it is necessary to perform neuroimaging (MRI) and electroneuromyography (if necessary). Structural abnormalities that cause sciatica, including stenosis of the spinal canal, are well diagnosed by MRI (preferably) or CT. Electromyographic examination can be performed with a persisting or growing pattern of radicular compression to exclude states that mimic sciatica, such as polyneuropathy and tunneling neuropathies. This study can help in determining whether there is one level of nerve damage or more, whether there are clinical correlations with the results of MRI (especially before surgery).

[8], [9], [10]

Treatment of sciatica

In the treatment of acute pain, bed rest is possible for 24-48 hours with the head of the bed raised at 30 ° (Fowler's half-position). In the treatment, it is possible to prescribe NSAIDs (for example, diclofenac, lornoxicam) and acetaminophen, adjuvants (tizanidine). Improvement may also occur with the administration of drugs for the treatment of neuropathic pain, such as gabapentin or other anticonvulsants or low doses of tricyclic antidepressants. Caution should be exercised when prescribing sedatives to elderly patients, as they increase the risk of falls and arrhythmias. Muscle spasm can be reduced by prescribing tizanidine, as well as heat or cooling, physiotherapy. The use of corticosteroids for acute radicular pain is discreet. Epidural administration of corticosteroids can accelerate the regress of pain, but probably should be used in severe or persistent pain. The epidural route of administration of glucocorticosteroids allows local creation of a high concentration of the pharmaceutical preparation, and accordingly, minimization of side effects associated with their systemic action. However, the literature data on the effectiveness of glucocorticosteroids with epidural administration are still insufficient and in some cases are contradictory.

The presence of pain with subsequent changes in the habitual motor stereotype may lead to a more or less rapid formation of MTW, which will contribute to the overall algic picture. The presence of radial compression accelerates the formation of MTZ. MTZ treatment is carried out according to the principles described above, with the exception of kinesitherapy, which, with discogenic pain, can cause an increase in the discogenic conflict in the vertebral canal.

Indications for surgical treatment may be a sheer disc hernia with muscle weakness or progressive neurologic deficit, as well as pain-resistant therapy that prevents professional and social adaptation of an emotionally stable patient, which is not cured for 6 weeks by conservative methods. An alternative for some patients may be epidural corticosteroids.