Back pain

Fifty percent to 80% of the population will experience one episode of low back pain during adult life that temporarily interferes with performance of normal activities. The typical age of onset is in the 3rd decade of life; low back pain reaches its peak in persons 55-64 years old and then decreases in those older than 65 years. Of all patients with low back pain, only ten to twelve percent have concomitant sciatica. Fifty percent of patients with low back pain recover by two weeks and 90% have no pain by three months. Persistent symptoms are present in 7% at six months; by one year only two percent still have pain.

Lumbar disc herniation can cause low back pain as well as symptoms of sciatica, or pain in the distribution of the sciatic nerve. Disc herniation can occur without known injury or can be the result of a lifting injury, fall, or motor vehicle accident. The majority of patients can be treated with brief bed rest, use of NSAIDS, and physical therapy. The use of epidural steroid injections may reduce inflammation of the nerve root and may provide short-term pain relief. Only five to ten percent of patients with persistent sciatica will ultimately require surgical intervention. The ideal diagnostic procedure for evaluation of a suspected disc herniation is magnetic resonance imaging.




Acute low back (lumbar/sacroiliac muscular) strain or myofascial strain: This is a common cause of LBP and is usually self-limited.  It is often caused by lifting heavy objects in an uncomfortable posture. Pain caused by low back strain is exacerbated during bending forward, standing and twisting motions in the absence of radicular signs, whereas pain caused by central disc herniation is worse in positions (such as sitting) that produce increased pressure on the annular fibers. There is often severe paravertebral spasm. In sacroiliac strain there is tenderness over the sacroiliac joint and pain irradiating to the buttock and posterior thigh. Abduction of the thigh against resistance is painful. Physical therapy and use of non-steroidal anti-inflammatory drugs (NSAIDS) are commonly used for the treatment of acute lumbar strain. Two days of bed rest is as effective as 7 days. Increased endurance and overall physical fitness have been shown as positively influencing the recurrence rate and natural history of LBP.

Tumor of vertebral column or epidural space: Focal tenderness of the spine and signs of myelopathy strongly indicate acute cord compression caused by epidural metastatic process or epidural tumor (plasmocytoma or multiple myeloma). Benign tumors include eosinophilic granulomas, aneurysmal bone cyst, giant-cell tumor, hemangioma, osteochondroma, osteoid osteoma, osteoblastoma. Malignant tumors consist of primary bone tumors (osteogenic sarcoma, Ewing sarcoma and non-Hodgkin lymphoma). The most common neoplasms causing epidural metastases include carcinomas of the lung, breast, prostate (elevated prostate-specific antigen), kidney, lymphoma (Hodgkin and non-Hodgkin), acute leukemia, neuroblastoma, rhabdomyosarcoma, primitive neuroectodermal tumor, germ-cell tumor, medulloblastoma, Wilms tumor and sarcoma. Most metastases occur in the thoracic spine and nocturnal pain is quite common. Spinal MRI is the most useful diagnostic procedure.

Primary tumor: Primary intradural tumor of spinal cord, conus or cauda equina e.g. myxopapillary ependymoma of the conus or cauda equina.

Carcinomatous meningitis: Spinal cord compression or polyradiculopathy can both be caused by carcinomatous meningitis. Lymphoma, leukemia, adenocarcinoma and melanoma often result in carcinomatous meningitis. CSF shows mild pleocytosis, reduced glucose and raised protein. Oligoclonal bands are found and cytology is positive.

Herniated intervertebral disc: The most common lumbar levels (90%) for a herniated disc are L4-5 and L5-S1, which causes pain in the L5 nerve or S1 nerve, respectively. The onset of symptoms is characterized by a sharp, burning, stabbing pain radiating down the posterior or lateral aspect of the leg, to below the knee. Pain is generally superficial and localized, and is often associated with numbness or tingling. L5 nerve impingement can cause weakness in extension of the big toe and potentially in the ankle (foot drop), while S1 nerve impingement may cause loss of the ankle reflex and/or weakness in ankle push off (e.g. patients cannot do toe rises). Numbness and pain can radiate down to the sole or outside of the foot. Numbness and pain can be felt on top of the foot, and the pain may also radiate into the buttock. In more advanced cases, motor deficit, diminished reflexes or weakness may occur. Generally, only the relatively uncommon central disc herniation provokes low back pain and saddle pain in the S1 and S2 distributions. A central herniated disc may also compress nerve roots of the cauda equina, resulting in difficult urination, incontinence or impotence. The medical history and physical examination may disclose bowel or bladder dysfunction. The lateral disc herniation distinguishes itself from the postero-lateral herniation in that the disc ruptures outside the spinal canal, lateral to the root foramen. The disc, instead of tethering the traversing nerve root compresses the more rostral nerve root which has already exited its more rostral nerve root foramen. The neurologic symptoms therefore, correspond to a lesion at the upper disc level. In most cases, if low back and/or leg pain is going to resolve it will do so within about six weeks. Physical therapy, osteopathic/chiropractic manipulations, NSAIDs or an epidural (cortisone) injection may help. MRI of the spine and EMG or other nerve conduction studies are generally used to diagnose disc herniations.  If the pain continues after six weeks, it is reasonable to consider microdiscectomy surgery as an option to alleviate the pain. Often the most difficult aspect of evaluating patients with symptoms of a central herniated disc is differentiation between low back strain and herniated disc. The pressure on the intervertebral disc is increased during sitting and bending postures, as opposed to standing or recumbent positions. This explains the exacerbation of herniated disc symptoms when the patient is in the sitting position.

At the cervical level, herniations at C5-C6 and C6-C7 are most common.

Intervertebral discitis or osteomyelitis: The inflammation of intervertebral disc is most often a consequence of a disseminated endogenous foci or an infection during surgical procedures on intervertebral disc such as disc removal or chemonucleolysis (injection of chymopapain into intervertebral disc). Post-operative or post-chemonucleolysis infection usually develops within 3 - 30 days after surgical procedure and it is of exogenous nature. The infectious agents most frequently responsible for discitis are Staphylococci, Streptococci and E. coli, as well as pathogenic fungi e.g. Candida albicans or Aspergillus. Discitis may develop in low immunity patients in the course of AIDS or as a result of therapy with immunosuppressants. Discitis may be suspected when the following symptoms are observed: intensive pain, located usually at the point of some intervertebral space restricting spinal mobility at that level as well as increased paraspinal hypertonus. The symptoms of general infection are also observed, e.g. fever, increased ESR and leucocytosis. The first radiological symptoms of the disease may be observed in a plain film of the spine around 3-6 weeks from the onset of the disease and they may take the form of intervertebral space narrowing. Blood cultures, MRI and CT scan of the spine are important in the diagnosis.Adjacent osteomyelitis may be found. TB should be ruled out. The treatment of discitis typically lasts for a long time, and it involves iv antibiotic therapy, administration of anti-inflammatory and analgesic drugs, keeping patient immobile and even surgical intervention if necessary.


Epidural hematoma:This is more likely to be seen in patients with anticoagulant therapy.

Epidural abscess: Similarly to brain abscesses, the triad of fever, back pain and neurological deficit is very suggestive for an epidural abscess.

Transverse myelitis: Acute transverse myelitis occurs in association with various viral and bacterial infectious, MS, ADEM, Devic disease as well as systemic autoimmune diseases such as SLE, MCTD, scleroderma, Sjögren syndrome, Behçet disease, RA, atopic dermatitis, primary urticarial vasculitis, immune-complex allergic vasculitis, and APLS. ATM of parainfectious origin is most common and accounts for 38% of cases, followed by 36% 'idiopathic forms' and MS-related ATM (22%).

AVM of the spinal cord or spinal dural arteriovenous fistula

Acute myelopathy from spinal cord infarction: This is usually not associated with severe back pain.

Spinal fractures

Noncompressive radiculopathies: GBS, CMV-associated radiculitis, vasculitis and diabetes mellitus.

Nonspinal conditions: Abdominal or thoracic aortic aneurysms, kidney infections, nephrolithiasis, pancreatitis, peptic or duodenal ulcer, endometriosis, other abdominal and pelvic processes.

Rheumatoid arthritis: The ages of onset ranges from the 5th to 8th decades with the majority being in their 60s. Criteria for the classification includes four of the seven which have been present for at least six weeks: morning stiffness, arthritis of three or more joints, symmetric arthritis, rheumatoid nodules, arthritis of hand joints, serum rheumatoid factor (>1/40) and radiologic changes. The vasculitis is most frequently evidenced as skin infarctions/ulcerations and a mononeuritis multiplex. CNS manifestations include myelopathies associated with cervical spine instability and entrapment neuropathies. Neck pain and headache are universal in patients with RA and cervical spine disease. Complications may be: atlantoaxial subluxation (atlantodental interval < 14 mm, flexion cord diameter < 6mm or  canal diameter < 13 mm) with or without invagination, isolated basilar invagination and subaxial subluxation. There is a loose correlation with severity of disease and RA titer.



Degenerative osteoarthritic disease: This includes central lumbar canal stenosis and lateral recess stenosis. Osteoarthritis is characterized by the slow, steady progression of articular pain. The pain worsens with use, is relieved with rest, and has little associated morning stiffness. Radiculopathy either from encroachment of the neural foramina by osteophytes and bony spurs is the most common cause of radiculopathy. Excessive mobility of the neck or back will exacerbate the symptoms. Spurling maneuver (extension and rotation of neck towards affected sign worsens radicular signs) confirms the diagnosis of cervical radiculopathy. Compression test of the neck exacerbates the pain while abduction of the affected arm relieves the radiculopathy in cervical radiculopathy. The straight leg raising sign is positive if the patient reports pain radiating down the posterior aspect of the leg into the calf or foot when the hip is flexed greater than 20 degrees while knee is maintained in extension. A positive crossed straight leg raising maneuver (pain is elicited in the opposite leg from the one raised) is more specific. EMG studies are positive while sensory NCVs are normal. Spinal MRI should be performed. Pain is not a common feature of spinal stenosis. Symptoms vary and include UMN weakness, spasticity hyperreflexia, Hoffman sign, Lhermitte sign, clumsiness, anesthesia, gait difficulties and incontinence. Pseudoclaudication or neurogenic claudication occurs in 94% of patients with lumbar spinal stenosis. Mild or early symptoms can be treated with physical therapy, NSAIDS, or epidural steroid injections. Lumbar surgery in the form of a decompression can be of great benefit in restoring the ability to stand and ambulate in patients with refractory symptoms.

Lumbar disc degeneration: This can be the cause of chronic, disabling low back pain. Treatment has ranges from physical therapy, electrical stimulation, acupuncture, trigger point injections, epidural steroid injections, as well as surgical intervention with lumbar fusion. Unfortunately, no one treatment has been found to be uniformly successful, and therefore, conservative treatment is most commonly used.

Congenital: tethered cord and intraspinal lipoma.

Facet syndrome: In one form, the hypertrophic facet joint may induce lumbar monoradiculopathy, indistinguishable from disc herniation. In the other form it gives rise to lumbar back pain, often parasagittal. The symptoms can be reproduction by injection of hypertonic saline into the facet joints. These symptoms may often be relieved by an injection of a local anaesthetic into the facet joint.

Spinal canal stenosis: The most common form of spinal stenosis is acquired degenerative stenosis. The spinal canal becomes narrow as a result of thickening of the ligamentum flavum, bulging of the intervertebral disc, and degeneration with hypertrophy of the facet joint. Once the canal narrows, the cross-sectional area decreases and nerve root compression w/ or w/o neurogenic claudication can develop. Nerves within the cauda equina do not have a myelin sheath and are therefore more susceptible to compression than are the peripheral nerves.

Failed back syndrome: One fourth of patients who underwent a surgical intervention have persistent back pain. In those patients MRI and EMG are essential to rule out causes such as: reruptured disc, lateral recess stenosis, incomplete removal of disc, or rupture of another disc. If all this excluded the remaining explaination may be: radiculitis, lumbar arachnoiditis, lateral recess syndrome, facet syndrome or unstable spine.