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Radiculopathy or radicular syndrome (Commonly known as Sciatica pain) is the presence of pain or other symptoms that radiate down a person’s arms or legs. Symptoms may include one or all of the following: pain, burning, numbness, tingling, pins and needles, weakness and muscle cramps. Radiculopathy is usually caused by a pinched nerve or pathology in the spinal column. When the nerve affected is in the lower back area of the spine, symptoms go down the legs into the thighs, calves and sometimes into the feet.  If nerve affected in the neck area, the shoulders, shoulder blades, arms and hands are affected. Similarly, if the affected spinal nerves are in the upper to mid area, symptoms usually manifest in the chest or abdomen.


  • Sharp shooting pains down extremity
  • Numbness
  • Tingling
  • Weakness
  • Muscle cramp
  • Aching
  • Burning

Seek immediate care if you experience:

– New bowel or bladder problems

– Progressive extremity weakness

– Is associated with pain or throbbing (pulsation) in the abdomen, or fever

– Follows a fall, blow to your back or other injury


It is often caused by direct pressure on the nerve, causing nerve root irritation and inflammation. This can be caused by:

  • Herniated discs
  • Central canal stenosis, direct pressure on the spinal cord
  • Foraminal stenosis
  • Degenerative Disc degeneration
  • Degenerative Joint Degeneration (Spondylosis)
  • Slippage of a vertebra from its proper alignment (Spondylolisthesis)

Screening and Diagnosis of Radicular pain:

Complete physical examination, especially flexibility, muscle strength, sensation and reflexes. X-rays and CT scan may be indicated to show the bony anatomy of the spine. An MRI scan may also be ordered, as they are of a higher diagnostic value, because useful of its usefulness in showing compression of nerve roots by giving a detailed picture of soft tissue structures. A nerve conduction study / electomyography can also help further test the condition of the nerve-muscle connection, and determine which nerve is affected.


Non surgical:

  • Physical therapy
  • Non-steroidal anti- inflammatory medications (NSAIDS), muscle relaxants, anti-seizure medications and in some instances pain medication.
  • Epidural steroid injection, to decrease nerve inflammation, thus decreasing symptoms.

Surgical intervention:

  • When conventional and conservative treatments fail to give acceptable relief, surgical intervention is at times necessary to relieve the pressure off of the spinal cord and/or the affected nerves. This can range from minimally invasive approaches, to disc replacement and fusion.

Peer-Reviewed Scientific Reseach:

Crosby, N. D., et al. (2015). “Burst and Tonic Spinal Cord Stimulation Differentially Activate GABAergic Mechanisms to Attenuate Pain in a Rat Model of Cervical Radiculopathy.” IEEE Trans Biomed Eng 62(6): 1604-1613.

OBJECTIVE: Spinal cord stimulation (SCS) is widely used to treat neuropathic pain. Burst SCS, an alternative mode of stimulation, reduces neuropathic pain without paresthesia. However, the effects and mechanisms of burst SCS have not been compared to conventional tonic SCS in controlled investigations. This study compares the attenuation of spinal neuronal activity and tactile allodynia, and the role of gamma-aminobutyric acid (GABA) signaling during burst or tonic SCS in a rat model of cervical radiculopathy. METHODS: The effects of burst and tonic SCS were compared by recording neuronal firing before and after each mode of stimulation at day 7 following a painful cervical nerve root compression. Neuronal firing was also recorded before and after burst and tonic SCS in the presence of the GABAB receptor antagonist, CGP35348. RESULTS: Burst and tonic SCS both reduce neuronal firing. The effect of tonic SCS, but not burst SCS, is blocked by CGP35348. In a separate study, spinal cord stimulators were implanted to deliver burst or tonic SCS beginning on day 4 after painful nerve root compression; allodynia and serum GABA concentration were measured through day 14. Burst and tonic SCS both reduce allodynia. Tonic SCS attenuates injury-induced decreases in serum GABA, but GABA remains decreased from baseline during burst SCS. CONCLUSION AND SIGNIFICANCE: Together, these studies suggest that burst SCS does not act via spinal GABAergic mechanisms, despite its attenuation of spinal hyperexcitability and allodynia similar to that of tonic SCS; understanding other potential spinal inhibitory mechanisms may lead to enhanced analgesia during burst stimulation.

Atallah, J., et al. (2008). “Use of spinal cord stimulator for treatment of lumbar radiculopathy in a patient with severe kyphoscoliosis.Pain Physician 11(4): 555-559.

Spinal cord stimulation (SCS) has been a therapeutic option for chronic pain for over 40 years with a common indication being failed back surgery syndrome (FBSS). This case reports the successful implantation of a spinal cord stimulator in a patient with FBSS and kyphoscoliosis for treatment of radicular pain. Technical considerations and anatomical difficulties that may be encountered during placement with kyphoscoliosis will be discussed. This patient had failed other therapies including oral medications, epidural steroid injections, spinal surgeries, and physical and aquatic therapies. On physical examination the patient had a severely deformed lumbar spine. Careful review of the spine radiographs and CT scan revealed lead placement might be possible at the level of T12-L1 or L1-2. A Medline search did not reveal a case of kyphoscoliosis with radicular pain treated with SCS. After a successful percutaneous trial, a SCS was implanted. Fourteen weeks later, the patient reported being pain free with an increased physical activity level and opioid discontinuation. Technical considerations with kyphoscoliosis may discourage pain physicians from attempting SCS. This case illustrates that with careful selection, some of these patients may be candidates for SCS with good results.