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Review Question - QID 214057

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QID 214057 (Type "214057" in App Search)
A 53-year-old woman with a history of multiple spinal lumbar decompressions and an L4-sacrum spinal fusion presents with chronic back pain 3 years after undergoing her last procedure, which is depicted in Figure A. She denies any symptoms of radiculopathy or stenosis. Her infection workup is negative. The difference between her pelvic incidence and lumbar lordosis is 9 degrees. A CT is obtained and demonstrates a solid fusion. Which of the following most likely explains her continued pain?
  • A

Residual coronal plane deformity in her lumbar spine

3%

39/1505

Amplification of neural signaling within the central nervous system that elicits pain hypersensitivity

43%

646/1505

She is experiencing proximal junctional kyphosis at the level above her instrumentation

8%

115/1505

She is experiencing adjacent disk degeneration at the level above her instrumentation

28%

418/1505

She has a significant pelvic incidence-lumbar lordosis mismatch

18%

277/1505

  • A

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The patient in the stem has continued low back pain after undergoing multiple spine surgeries, with the most recent being a spinal cord stimulator implantation. As she has no pathology on her imaging studies and infection has been ruled out, the most likely explanation of her pain is central sensitization, which is the amplification of neural signaling within the central nervous system (CNS) that elicits pain hypersensitivity.

The awareness of central sensitization is increasing in the field of spine surgery and becoming a treatment target for unexplained chronic back pain. This phenomena is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. With central sensitization, changes in the properties of neurons in the CNS causes the pain to be no longer coupled, as with acute nociceptive pain, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, pain hypersensitivity is produced by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations.

Nijs et al. reviewed guidelines for the clinical classification and differentiation of neuropathic, nociceptive, and central sensitization pain. They reported that the first step involves excluding the presence of neuropathic low back pain. After, the differential diagnosis between predominant nociceptive and central sensitization pain may be undertaken using a clinical algorithm.

Corrêa et al. investigated changes in local and segmental hypersensitivity and endogenous pain inhibition in people with chronic nonspecific low back pain. They reported that people with chronic low back pain have significantly lower pressure pain thresholds than controls at the lumbar region, which was again demonstrated during conditioned pain modulation. They concluded that the understanding of the underlying mechanisms of chronic pain may help to target therapies designed to normalize pain physiology.

Figure A depicts AP and lateral radiographs of a lumbar spine status post lumbar decompression, fusion, and implantation of spinal cord stimulator.

Incorrect Answers:
Answer 1: The radiographs do not demonstrate any significant coronal plane deformity which would be responsible for her pain.
Answer 3 and 4: There is no evidence of proximal junctional kyphosis or adjacent disk degeneration at the level of above the construct.
Answer 5: The pelvic incidence-lumbar lordosis mismatch is 9, which is normal.

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