What makes an extraspinal adjustment of chiropractic

Guideline Category: Neurotraumatology and diseases of the spine and nerve root

What's new?

  • Lumbar disc herniations are found in healthy individuals in 20–30% of people under 60 years of age and in> 60% of those over 60 years of age [1].
  • Degenerative changes do not correlate with the clinical picture [2]. The image morphological pathology has no predictive value for the occurrence of clinical symptoms [3]. Correct assignment of clinical symptoms to morphological changes is therefore of crucial importance, with segmentation disorders (four-membered or six-membered lumbar spine) also being observed, as this can change the neuroanatomical relationships [4, 5].
  • In patients operated on at an early stage, pain and neurological deficits recede more quickly than in patients who have not been operated on or who have operated late. After one year there is no significant difference between the two groups [6, 7].
  • In the case of high lumbar disc herniations, especially if they are located extraspinally, back pain may largely be absent. With L3 compression, knee pain can be the main focus and simulate a primary knee joint disease [8].
  • Degenerative muscle diseases with an axial focus (e.g. myotonic dystrophy type 2, facioscapulohumeral muscular dystrophy) can cause treatment-refractory lumbar pain and simulate a disc disease and lead to unnecessary surgical interventions that can be avoided with careful neurological evaluation [9, 10].
  • Chronic back pain without radicular radiation cannot usually be improved by surgical measures [11, 12].
  • The best surgical therapy for lumbar spinal stenosis with and without grade 1 spondylolisthesis has not yet been clarified, despite extensive studies. The results are contradictory with regard to the additional benefit of simultaneous spinal fusion to decompression surgery [13, 14]. Whether surgical or conservative therapy is superior for lumbar spinal stenosis cannot be assessed on the basis of the available studies [15, 16]. What is noticeable, however, is the significantly increasing frequency of operations in Europe and the USA [17].
  • Limitation of somatic diagnostics in chronic back pain.
  • Consideration of psychosocial and psychosomatic aspects [18, 19].

The most important recommendations at a glance

  • Bed rest should only be prescribed in the acute phase, as long as mobilization is not possible because of the pain.
  • Early mobilization and light to moderate exercise should be aimed for.
  • Early and adequate analgesic therapy with non-steroidal anti-inflammatory drugs (NSAIDs) and, if necessary, muscle relaxants should be given.
  • In the case of severe pain, short-term retarded opioids may be indicated.
  • In the case of pain-related immobility that cannot be treated on an outpatient basis and “red flag” symptoms, acute inpatient hospitalization is necessary.
  • An early operation must be indicated in the case of progressive paresis or bladder-rectal disorder.
  • Elective surgery should be performed in the event of unsuccessful conservative outpatient and / or inpatient therapy if the morphological cause of the pain symptoms is confirmed.
  • If chronic pain develops, a combination with physiotherapy and psychotherapeutic methods (behavioral therapy, pain management programs) is indicated.
  • In the transition from acute to chronic pain, pain-relieving drugs (antidepressants) and membrane-stabilizing drugs (antiepileptic drugs) can be used in analogy to other pain syndromes and neuralgia [20–24].

Introduction: scope and purpose of the guideline

To give key recommendations for the diagnosis and treatment of diseases associated with specific lower back pain and leg pain as a result of lumbar nerve root damage. Coordination and coordination of the care of the medical disciplines involved. To define key points of the treatment and to show the respective approach of the choice. Identify special features of the German health care system and justify the recommendations deviating from the international literature

Justification of the need for a guideline

Improvement of the old guideline under the impression of newly gained knowledge as well as improvement and standardization of care beyond the specialist boundaries (when operational, when conservative?)

Objectives of the guideline

To update the recommendations in accordance with the best available medical knowledge, taking into account the criteria of evidence-based medicine. Standardization of the diagnostic and therapeutic procedure for lumbar radiculopathies

Patient target group

Adult patients with acute back pain / leg pain or lumbar sciatica due to irritation / damage to lumbar nerves

Supply area

Acute outpatient, partial inpatient and inpatient care, diagnostics, therapy, aftercare, rehabilitation

Addressees of the guideline

Neurologists, neurosurgeons, surgical and conservative orthopedists, rehabilitation doctors, physiotherapists


Back pain, lumbago, herniated disc, lumbar sciatica, lumbofemoralgia, spinal stenosis, lumbar pain, radiculopathy, L5 syndrome, S1 syndrome

Definition and classification

After headache, back pain is the most common pain syndrome with a point prevalence of 37%, a 1-year prevalence of 76% and a lifetime prevalence of 87% [25]. In Germany, according to different calculations, back pain causes 15–30% of the days of incapacity for work and 18% of all early retirement. The direct and indirect costs amounted to approx. 49 billion euros in 2005, or up to 2.2% of the gross national product [26, 27]. The vast majority of patients suffer from so-called non-specific back pain. These are comprehensively presented in the S3 guideline "NVL Kreuzschmerz" (AWMF register no. Nvl / 007) and are not the subject of this guideline, which deals with the specific back pain as a result of lumbar nerve root damage. The guideline “Specific Low Back Pain” (AWMF Register No. 033-051) covers a wide range of different forms of back pain and is surgically oriented.

Regardless of whether acute back pain is classified as specific or non-specific, 90% of patients with acute back pain are able to go back to work after about six weeks, whereas freedom from pain is achieved in only 40–60% [28]. Relapses occur in 44–78% of patients after a first episode of pain. In addition to acute processes, which are self-limiting in the absence of structural defects, there are also chronic complaints that are more difficult to treat therapeutically. If pain does not subside within twelve weeks, there is a risk of chronification. Estimates of the prevalence of chronic back pain are 23%. They are responsible for around 30–35 billion euros in social spending and are the most common cause of premature disability.


Pathogenesis and differential diagnosis

Most often, lumbar radiculopathies are the result of a herniated disc. When diagnosing, however, careful attention must be paid to the correspondence of a proven morphological change in the CT / MRI with the clinic and the symptoms, as more than half of all detected disc hernias do not cause any symptoms [1, 29] and other differential diagnoses are otherwise easily overlooked. With age, the gelatinous nucleus pulposus turns into a fibrous nucleus, and the annulus fibrosus loses its firm texture. Histologically detectable changes are already pronounced in early adulthood, increase in mid-adulthood, and then lead to cell-poor fibrosis of the nucleus nucleus between 50 and 80 years of age [30]. It has been shown experimentally that mechanical compression of the nerve root does not necessarily have to cause pain [31]. Thus, in addition to the mechanical component, there are other pathomechanisms in the development of pain. Direct evidence of an inflammatory component was provided by an experiment which showed that, even without mechanical compression, in animal experiments, nerve root damage can only be caused by the loose application of intervertebral disc tissue on the nerve root; a cellular infiltration of the nerve root could be demonstrated [32]. In addition, oxidative processes cause the accumulation of metabolic products that influence the induction of proteases and cytokines [33,34].

In the case of a median disc herniation, local low back pain is triggered by stretching the anulus fibrosus and releasing inflammatory substances and / or pressure on the posterior longitudinal ligament and can be isolated without leg pain. Leg pain is caused by the compression and inflammatory response of the nerve root.

The differential diagnoses most often incorrectly attributed to the intervertebral disc and thus missed are inflammatory radiculopathies, neuralgic amyotrophy and diabetic radiculopathy.

Specific lower back pain are triggered by clearly defined causes and require specific, sometimes interdisciplinary therapy. The most common causes in the lumbar spine are, in addition to herniated discs, bony degenerative changes (spondylarthrosis, spondylolisthesis, hypertrophy of the vertebral arch joints) and hypertrophy of the ligamenta flava. More rarely, radiculopathies can also be caused by local masses (tumors, bone metastases), intraspinal processes (e.g. ependymomas, epidural bleeding, epidural lipomatosis) or inflammatory changes (spondylodiscitis, Lyme radiculitis, zoster, AIDP, epidural abscess). Meningiosis carcinomatosa sive lymphomatosa can also lead to radiculopathy.

This is a special case Caudae equinae claudication in the case of a primarily or secondarily narrow spinal canal with walking distance-dependent unilateral or bilateral pain and possibly additional sensorimotor deficits. Typically, there are no complaints when resting or sitting. Any posture associated with hyperlordosis leads to an increase in lumbar canal stenosis and thus to an intensification of pain, whereas lumbar spine kyphosis leads to pain relief. While in vascular intermittent claudication simply standing still leads to pain relief, in spinal claudication it is therefore also necessary to change the position of the spine - typically sitting down or bending over.

A strict differentiation between lumbar radiculopathy and lower back pain, which appear radicular and can radiate into the legs, but have a different origin, is necessary [35]. These are so-called. pseudoradicular syndromes. However, the neurological examination findings are mostly normal. The causes are usually orthopedic diseases (coxarthrosis, gonarthrosis, facet syndrome, sacroiliac joint syndrome, coccygodynia, piriformis syndrome, osteoporotic vertebral body fractures, tendomyopathies in the event of excessive strain or muscle strains), and occasionally also primary muscular diseases with axial stress, e.g. which can often be associated with low back pain and referred pain. A facet joint blockade with infiltration of the ramus medialis of the corresponding facet joints with a local anesthetic (medial branch block = MBB) can be helpful for the differential diagnostic differentiation between radicular and pseudoradicular.

As a non-radicular disease, meralgia paraesthetica can also show a sensitive deficit and appear clinically radicular.

Finally, in terms of differential diagnosis, metabolic plexopathies and radiculopathies, especially in the context of diabetes mellitus, should also be considered. In principle, any nerve structure can be affected in diabetes mellitus, but the lower extremities are the most common femoral nerve-accentuated deficits. This must be distinguished from lumbosacral plexus affections of other origins, especially idiopathic plexus neuritis, which occurs less often here than in the area of ​​the arm plexus, and postradiogenic plexus affection, which is also rare. This can manifest itself with a latency of five to 20 years after irradiation. Radicular sensorimotor disorders also occur with and without pain in spinal dural arteriovenous fistulas (dAVF). In the MRI, congested venous convolutions are particularly evident. Digital spinal subtraction angiography is then indicated.

Symptoms and course

In principle, a differentiation is made between low back pain and leg pain, since leg pain or provoked leg pain is a good clinical indicator of a herniated disc [36]. Acute or subacute shooting pains or tingling sensations in the area of ​​spread of a nerve root are rarely absent. Sensitivity disorders in the corresponding dermatome, motor failures of the key muscles and possibly reflex failures can also occur depending on the severity. In the majority of cases, there is a sometimes unilateral paravertebral hard tension, knocking or pressure pain over the spine, coughing, pressing and sneezing pain and positive signs of nerve stretching (Lasègue and reversed Lasègue sign, Bragard sign). A ventral radiation of pain (femoralgia) is the result of an affection of L4 or nerve roots extending further cranially, so that the cause must be a foraminal, lateral process in LWK4 / 5 or a further cranial damage. A dorsal radiation of pain (sciatica) is the result of compression of the L5 and / or S1 roots, with the damage usually being found in the area of ​​the intervertebral disc compartments LWK4 / 5 and LWK5 / SWK1. In the case of polyradicular processes, e.g. medial herniated discs with compression of the cauda equina, a polyradicular failure occurs, under certain circumstances with riding breeches sensitivity disorders and bladder emptying disorders.

The L3 radiculopathy is characterized by quadriceps, hip flexor and adduction palsy of the affected leg as well as a weakening of the PSR and a radiation of pain up to the knee joint. Occasionally, knee pain can be in the foreground, giving the impression of primary knee joint damage.

At the L4 syndrome In addition to the leading quadriceps palsy, there is almost always a significant weakness in the hip flexor (must be specifically examined), but only rarely is a palsy of the foot and practically never an adductor weakness. The PSR has weakened or has failed. The pain radiation typically goes to the front edge of the tibia or, more rarely, to the inner side of the lower leg.

The most common L5 syndrome is characterized by a palsy of the big toe, the foot of the foot, the foot version, the foot inversion and the gluteus medius palsy with a positive Trendelenburg sign of the affected leg as well as the radiation of pain to the outside of the lower leg and the back of the foot up to the big toe. The tibialis posterior reflex, if it can be used, is weakened or has failed. L5 syndromes resulting from lumbosacral foraminal compression (LWK5 / SWK1) are often overlooked. Some of the patients with an isolated L5 root compression may have a weakened PSR. This is explained by the changed proprioception and not by supplying the knee extensor with the L5 root [37].

The S1 radiculopathy can lead to paresis of the lower foot and gluteus maximus. The gluteus medius muscle can also be affected in S1 syndrome (Trendelenburg's sign). The pain typically radiates into the dorsal calf to the lateral edge of the foot and the little toe. The Achilles tendon reflex is usually weakened or has failed.

If there are no signs of stretching of the nerves and if there is pain that occurs particularly at night and is resistant to therapy, which cannot be influenced by movement of the lumbar spine, you should always contact a Radiculitis (Borrelia, herpes zoster) or a tumor.

The transition into a chronic pain syndrome, in which the extent of the pain is usually inadequately explained by the morphological findings, depends on other factors such as psychological disposition, accompanying social circumstances, but also on iatrogenic factors such as lack of information about the benign nature of the disorder, overestimation of radiological findings, prolonged sick leave , uncritically long use of analgesics or local infiltration as well as failure to take into account psychiatric comorbidities such as depression, anxiety disorders or personality disorders.

Persistent radicular complaints after surgical interventions in the sense of a Post nucleotomy syndrome are due to recurrences, incomplete removal of the intervertebral disc prolapse, segment instabilities or the formation of scar tissue.


The aim of a correct diagnosis by neurologists, orthopedists and neurosurgeons in an increasingly commercialized medical environment is to avoid unnecessary, costly surgical interventions on the spine due to changes in the intervertebral discs that are wrongly accused of the symptoms, as can be demonstrated in almost all people over the age of 30 .

Here come the capture of the "Red flag" symptomsthat make an immediate interdisciplinary therapy concept necessary, as well as the consideration of the risk factors for chronification (yellow flags, see "NVL Kreuzschmerz", AWMF register no. nvl / 007) are of particular importance.

Clinical examination

History taking

  • What, when, how, where, by what means?
  • Indications of trauma, fractures, infections
  • Differentiation: back pain and / or leg pain and pain at rest / movement-induced pain
  • Ask about bladder and rectal function
  • Collection of psychological and social anamnesis (risk of chronification)
  • Medication history (what works, what doesn't?)

Clinical-neurological examination

  • Inspection (zoster efflorescences), observance of the shape, painful knocking and restricted movement of the spine
  • Signs of nerve stretching
  • Tenderness of the Valleix points
  • Examination of the strength of the identification muscles, including the gluteal muscles, which are often affected in isolation with L5 and S1 damage (gluteus medius weakness with positive Trendelenburg sign, usually with L5 affection, gluteus maximus muscle -Weakness mostly with S1 affection). Mild pareses of the lower feet are best tested using a one-legged toe stand, as these cannot be tested manually while lying down. The same applies to a slight paresis of the quadriceps muscles, which can only be recognized by climbing steps of different heights. The adductors and hip flexors can be reliably checked while sitting or lying down with the legs bent.
  • Examination of surface sensitivity (usually much less productive than motor testing)
  • Examination of the muscular reflexes on the legs. When the nerve root is affected, they are usually weakened or extinguished, but occasionally they can also be triggered normally despite clear radicular symptoms.

Neuro-orthopedic examination

  • Finger-floor distance, Schober sign
  • Side bending pain (often positive for lateral and extraspinal disc hernias)
  • Reclination pain (often positive in spinal canal stenosis and / or facet syndrome)
  • Knocking pain over the lumbar spine (spondylodiscitis, tumor, osteoporotic fracture)

Laboratory tests

  • Basic laboratory with ESR, CRP, blood count, platelets, liver and kidney values, creatine kinase (caution: possibly increased by previous paravertebral infiltration), Hb1Ac
  • Extended blood serology if there is sufficient suspicion: Lyme disease, herpes zoster
  • CSF diagnostics, possibly with cytology: polyradiculitis, neuroborreliosis, meningeosis carcinomatosa sive lymphomatosa, subacute subarachnoid hemorrhage


Due to the self-limiting course, no routine imaging is initially required in patients with low back pain without “red flag” symptoms [38, 39]. The correlation between the imaging findings and the clinical symptoms is not good [2]. Findings in the MRI scan are often overestimated, contribute to patient uncertainty and thus to chronification, and have little prognostic relevance [40].

A plain x-ray of the lumbar spine in two planes is indicated for patients with newly developed symptoms and radiculopathy, for whom no further sectional image diagnosis is required, for the detection of osteodestructions, osseous malformations, step formation and osteoporotic fractures. If instability is suspected, additional functional recordings may be required.

Native images showing the 12th rib are also used to detect transitional disorders in order to understand any discrepancies between the detected herniated disc and the clinically affected nerve root. Other cross-sectional imaging methods are only indicated if there are “red flag” symptoms [41] and if there are unclear or therapy-resistant findings, i.e. insufficient response to therapy measures over six to eight weeks. Then an MRI examination should also be carried out without a native examination [42].

in the MRI Soft tissue changes and the dislocation of intervertebral disc sequesters are usually better captured than with CT. The sensitivity of MRI for detecting nerve root compression is high, but the specificity is low, so that the clinical findings must always be correlated with the imaging [43]. CT is sometimes superior in assessing bony changes as well as foraminal and extraspinal herniated discs. A repeated CT examination should only be carried out in the case of a new or progressive neurological deficit or severe comorbidities [44].

The Functional and stress myelography with subsequent Myelo CT is indicated for polysegmental spinal stenoses, if instability is suspected and for stress-dependent complaints, e.g. from a mobile disc herniation that only compresses under stress. However, it can also be useful in previously operated patients to differentiate a scar from a recurrent hernia.

The diagnostic benefit of upright MRI (MRI while standing) is still unclear [45].

When interpreting MRI images after an intervertebral disc surgery, it must be taken into account that over the course of approximately one year, 23% of patients develop a relapse incident that can be detected on MRI (immediately postoperative MRI with no evidence of residual disc herniation). However, this was clinically silent in 56% of the patients, and these patients did not develop any corresponding symptoms in the further observation interval of two years [46].

Neurophysiological examinations

Basically, a monoradicular syndrome with appropriate imaging and evidence of compression does not require electrophysiological confirmation. In special cases, however, this can make it easier to assess the course and prognosis.