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Low Back Pain.pdf

  1. 1. NOVEMBER 2022 BAGHDAD - IRAQ Lumbago General Term for LBP By: Dr. Muhannad M. Hadi Almukhtar Supervised by: Prof. Dr. Iyad Abbas Salman
  2. 2. LBP DEFINITION • Global Burden of Disease studies have de fi ned low back pain (LBP) as: • “pain in the area on the posterior aspect of the body from the lower margin of the twelfth ribs to the lower gluteal folds with or without pain referred into one or both lower limbs that lasts for at least one day”
  3. 3. INTRODUCTION • Low back pain is a common global problem. • The point prevalence of low back pain (LBP) in 2017 was estimated to be about 7.5% of the global population, or around 577.0 million people. • LBP has been the leading cause of years lived with disability (YLDs) since 1990 and remains a signi fi cant global public health concern. • 85-95% of people presenting to primary care providers do not have a speci fi c identi fi able pathoanatomical origin for their pain
  4. 4. INTRODUCTION • Low back pain is extremely common. Most is ‘mechanical’, and caused by degenerative changes in discs and facet joints (spondylosis). • More than 90% of these patients are mostly pain free within 8 weeks, although recurrences are common. • Analyse the symptoms using ‘SOCRATES’. • For back pain, ask speci fi cally about: • occupational or recreational activity that may strain the back • Red fl ag features suggesting signi fi cant spinal pathology..
  5. 5. Red Flags • Serious spinal pathology is rare. However, the fi rst step in the assessment of back pain is to eliminate ‘red fl ags’ secondary to serious spinal pathology. A mnemonic to identify the red fl ags is TUNA FISH: • Trauma, history of a fall. • Unexplained weight loss/history of malignancy. • Neurological fi ndings: cauda equina syndrome (unsteady gait, perineal numbness and sphincter disturbance). • Age >55 years. • Fever/systemic illness. • Immunocompromised. • Steroid use. • History of HIV, tuberculosis, cancer.
  6. 6. Yellow flags are psychosocial patient factors that although not associated with serious organic pathology nonetheless indicate an increased likelihood of chronic back pain and resultant long term disability and potential loss of work
  7. 7. Classification • Low back pain can be classi fi ed depending on the duration into: • 1. Acute low back pain: • Low back pain persisting for less than 6 weeks. • 2. Sub-acute low back pain: • Low back pain persisting between 6 and 12 weeks • 3. Chronic low back pain: • Low back pain persisting for 12 weeks or more.
  8. 8. Causes What is the cause of lumbago? Below are 15 medical conditions that may cause lumbago and low back pain: • Muscle strain • Ligament injury • Sciatica • Osteoporosis • Osteoarthritis • Spinal stenosis (compression of the spinal nerves) • Herniated disc • Degenerative disc disease • Scoliosis (or the related conditions lordosis and kyphosis) • Tumors near the spine • Fibromyalgia • Spondylitis • Spondylosis • Osteomyelitis • Broken bone near the spinal region Sprain
  9. 9. Causes
  10. 10. Causes
  11. 11. Causes
  12. 12. Pathophysiology • In a large number of mechanical spinal pain cases, it may not be possible to identify the precise pain generator as many spinal structures are involved in nociception. • Nociceptors are primary sensory neurons specialized to detect intense stimuli and represent, therefore, the first line of defence against any potentially threatening or damaging environmental inputs • the distribution of lumbosacral nociceptive receptor systems, known at that time to be sensitive to mechanical and chemical tissue dysfunction, as being present in:
  13. 13. • 1. Fibrous capsules of zygapophysial (facet) joints and in sacroiliac joints. • 2. Longitudinal spinal (anterior and posterior), interspinous, flaval, and sacroiliac ligaments. • 3. Periosteum on vertebral bodies and arches (and attached fasciae, tendons and aponeuroses). • 4. Dura mater and epidural fibro-adipose tissue. • 5. Walls of blood vessels supplying the spinal and sacroiliac joints, and in vertebral cancellous bone.
  14. 14. • 6. Walls of epidural and paravertebral veins. • 7. Walls of intramuscular arteries within lumbosacral muscles. • 8. Skin, subcutaneous and adipose tissue.
  15. 15. • Pain in any structure requires the release of inflammatory agents, including bradykinin, prostaglandins, and leukotrienes, which stimulate pain receptors and generate a nociceptive response in the tissue and it is known that the spine is unique in that it has multiple structures that are innervated by pain fibres (Haldeman et al 2002). • For example, stretching and distorting the articular capsule of a facet joint may result in traumatic synovitis with release of noxious neuropeptides, kinins, or other inflammatory agents.
  16. 16. Mechanical Back Pain • The term ‘mechanical’ refers to ‘movement’ and is generally due to a musculoskeletal cause. • Not all pain radiating to the leg is ‘sciatica’. • In most patients with back and leg pain, this is due to a musculoskeletal cause with referred pain to the lower limbs. • Mechanical back pain can originate from the bone, joints, discs or the adjacent soft tissues such as muscles and ligaments.
  17. 17. • about 3% of patients presenting with back pain have non-MSK causes. • a signi fi cant proportion of women have pelvic conditions such as ovarian cysts or endometriosis. Pain may be cyclical. • Alway ask the Women of reproductive age (15-49 years) population
  18. 18. Anatomy Any structure in the spine (bone, joint, intervertebral disc, nerve root, ligament) or the surrounding structure (muscles, viscera) can become the source of pain (pain generator) causing LBP. Hence treating physician should be aware of the anatomy and the pain patterns caused by these structures.
  19. 19. The Lumbar Vertebra • There are 5 lumbar vertebrae, articulated with each other by: • intervertebral discs anteriorly • and facet joints posteriorly with forward lordotic curve. • Each vertebra has two pedicles projecting posteriorly, two transverse processes, a pair of superior and inferior articular processes, a pair of lamina and one spinous process.
  20. 20. • Each vertebra is divided into three functional components namely: • The vertebral body(anterior element), • The pedicle with intervertebral foramen (middle element). • lamina and its processes (posterior element)
  21. 21. • It is supported by various ligaments like anterior and posterior longitudinal ligaments which are present on the anterior and posterior surface of the vertebral body and the disc, • Interspinous ligament which is present between the two consecutive spinous processes, • Supraspinous ligament which connects tip of two spinous processes. • Ligamentum fl avum which connects the laminae of consecutive vertebrae
  22. 22. • The lumbar spine is strengthened by numerous paraspinal muscles which include: • The spinalis, longissimus, • Quadratus lumborum, • Iliopsoas, iliocostalis. • These muscles stability as well as mobility to the spine. • In between the anterior and posterior elements is spinal canal which contains spinal cord surrounded by vertebral body intervertebral disc anteriorly, • Pedicle and vertebral foramen laterally • Lamina with ligamentum fl avum posteriorly.
  23. 23. • Anterior element is supplied by: • Sympathetic chain and Sinuvertebral nerve which again is a part of grey rami communicants. • Posterior element is supplied by: • posterior rami of spinal nerve which again has three branches namely medial, intermediate and lateral. • All anterior and posterior elements have nerve supply except inner 2/3rd of annulus fi brosus and nucleus pulposus of intervertebral which are the potential pain generators.
  24. 24. Sacrum and Coccyx • Sacrum is a single triangular or wedge shaped bone formed by the fusion of 5 sacral vertebrae. • It articulates with the L5 vertebra above. • It also articulates with the right and left iliac bones to form right and left sacroiliac joints. • The sacrum has 4 anterior and 4 posterior sacral foramina through which the anterior and posterior rami of the upper four sacral spinal nerves exits.
  25. 25. Sacroiliac Joints • The sacroiliac joint is a diarthrodal joint but only anteroinferior part of the joint is synovial. • The sacroiliac joints are designed primarily for stability. • Their functions include the transmission of the truncal load to the lower limbs. • The sacroiliac joint is largely immobile and is maximally loaded while sitting.
  26. 26. Coccyx Tail Bone • is formed by fused 3–5 coccygeal vertebrae. • It is articulated to the sacrum by sacrococcygeal joint and sometimes can be mobile. • The spinal cord ends at the level of lower border of L1 but the dural sac continues till the level of S2.
  27. 27. • The spinal nerve roots exit the spine via the intervertebral foramen. • Each nerve root exits below the corresponding vertebra.
  28. 28. How to diagnose LBP Vertebral Column
  29. 29. SOCRATS Aggravating and Relieving Factors • Discogenic pain again increases on axial loading (sitting, lumbar fl exion) and reduced by recumbancy. • Similarly the pain due to vertebral compression fracture also increases when the patient is sitting. • Pain due to ligament sprain and myofascial pain syndrome is aggravated by movements which stretches the a ff ected ligament and muscle. • In case of myofascial pain syndrome a ff ecting quadratus lumborum, • the pain is worsened in sitting position as the muscle stretched in this position and relieved by standing.
  30. 30. SOCRATS Aggravating and Relieving Factors • Whereas pain of iliopsoas is least in sitting position and aggravated during change of posture from sitting to standing. • Pain due to piriformis syndrome is aggravated during squatting which again stretches the piriformis muscle. • Similarly, interspinous ligament pain is more while the patient is sitting or bending forwards. • Radicular pain is aggravated by bending forwards which stretches the a ff ected nerve, coughing and straining (which increases the intradiscal pressure momentarily) and partial relief is obtain when patient is at rest. • Patients with lumbar canal stenosis give a typical history of back pain, numbness and heaviness in the lower limbs while walking which are completely relieved by rest and forward bending.
  31. 31. History • Radicular pain caused by sciatic nerve root compression radiates down the posterior aspect of the leg to the lower leg or ankle (sciatica). • Groin and thigh pain in the absence of hip abnormality suggests referred pain from L1– 2. • Consider abdominal and retroperitoneal pathology, such as abdominal aortic aneurysm. • Mechanical low back pain: • is common after standing for too long or sitting in a poor position. • Symptoms worsen as the day progresses and improve after resting or on rising in the morning.
  32. 32. History You should Exclude Axial Spondyloarthritis • Insidious onset of back or buttock ache and sti ff ness in an adolescent or young adult suggests in fl ammatory disease of the sacroiliac joints and lumbar spine (Axial Spondyloarthritis, Box 13.13). • Symptoms are worse in the morning or after inactivity, and ease with movement. • Morning sti ff ness is more marked than in osteoarthritis, lasting at least 30 minutes. • Other clues to the diagnosis are peripheral joint involvement, extra-articular features or a positive family history.
  33. 33. History • Acute onset of low back pain in a young adult, often associated with bending or lifting, is typical of acute disc protrusion (slipped disc). • Coughing or straining to open the bowels exacerbates the pain. • There may be symptoms of lumbar or sacral nerve root compression. • Cauda equina syndrome occurs when a central disc prolapse, or other space- occupying lesion, compresses the cauda equina. There are features of sensory and motor disturbance, including diminished perianal sensation and bladder function disturbance. The motor disturbance may be profound, as in paraplegia. Cauda equina syndrome and spinal cord compression are neurosurgical emergencies.
  34. 34. DN4 Questionnaire for Neuropathic Pain
  35. 35. ‫الحمداني‬ ‫فراس‬ ‫ابو‬ ِ‫يه‬ّ‫ق‬َ‫و‬َ‫ت‬ِ‫ل‬ ‫ن‬ِ‫ك‬َ‫ل‬ ِ‫ر‬ َ ‫لش‬ِ‫ل‬ ‫ال‬ َّ‫ر‬ َ ‫الش‬ ُ‫فت‬َ‫ر‬َ‫ع‬ ِ‫فيه‬ ‫ع‬َ‫ق‬َ‫ي‬ ِ‫ر‬‫ي‬َ‫خ‬‫ال‬ َ‫ن‬ِ‫م‬ َّ‫ر‬ َ ‫الش‬ ِ‫ف‬ِ‫ر‬‫ع‬َ‫ي‬ ‫م‬َ‫ل‬ ‫ن‬َ‫م‬َ‫و‬ 3 Messages Should you know
  36. 36. History and Examination A normal measurement is greater than or equal to 2 cm.
  37. 37. • Look for obvious deformity (decreased/increased lordosis, scoliosis) and soft-tissue abnormalities such as a hairy patch or lipoma that might overlie a congenital abnormality: for example, spina bi fi da. Palpate the spinous processes and paraspinal tissues. Note overall alignment and focal tenderness. • After warning the patient, lightly percuss the spine with your closed fi st and note any tenderness. - Flexion. - Extension. - Lateral Flexion. Examination
  38. 38. Examination Look (Inspection) • Look for asymmetry or deformity; skin lesion, muscle wasting, muscle hypertrophy, muscle fasciculation, gait, posture, range of motion. • Muscle wasting may be sign of motor neuron disease. • Gait may be antalgic (painful) gait, steppage gait (due to foot drop) or a gait abnormality due to sti ff back as a result of paraspinal muscle spasm. • Posture is again a cause for chronic strain on di ff erent ligaments.
  39. 39. Feel (Palpation) • 1. Tenderness • 2. Swelling • 3. Local rise of temperature. • Tenderness over particular part indicates pathology which can extend from super fi cial skin to underlying organ.
  40. 40. Examination Move (ROM) • Flexion: (40°) ask the patient to try to touch their toes with their legs straight. Record how far down the legs they can reach. Some of this movement depends on hip fl exion. Usually, the upper segments fl ex before the lower ones, and this progression should be smooth. • Extension: ask the patient to straighten up and lean back as far as possible (normal 10−20 degrees from a neutral erect posture). • Lateral fl exion: ask them to reach down to each side, touching the outside of their leg as far down as possible while keeping their legs straight.
  41. 41. Neurological Examination Motor Testing
  42. 42. Neurological Examination Motor Testing
  43. 43. Neurological Examination Muscle Power
  44. 44. Neurological Examination Deep Re fl exes
  45. 45. Neurological Examination Sensory •
  46. 46. You should always remember to do … Neurological Examination Why ?? —>
  47. 47. Neurological Examination I see the following… • It will precisely locate the level of lesions. • The radiculopathic symptoms are not always mentioned by the patients. So you should look for the signs by the Neurological examination. • In order to know the extent of the damage caused to the patient, by di ff erentiating between radiculopathy and radicular pain.
  48. 48. Radiculopathy vs Radicular Pain • Chemical Irritation of the nerve root causes severe radicular pain which is generally worse distally than proximally. • Caused by damage of disc which causes release of local in fl ammatory chemicals. • Chemicals damage and irritate the nerve root at that level. • Radicular pain is generally caused by chemical irritation, not mechanical compression. • Sharp, burning pain is greater distally.
  49. 49. Radiculopathy vs Radicular Pain Radiculopathy: • Mechanical compression of the nerve root causes parethesias in a dermatomal pattern and other neurological symptoms. • Numbness • Tingling • Eventually, muscle atrophy • LMN signs
  50. 50. Radiculopathy = Mechanical Compression Radicular Pain = Chemical irritation
  51. 51. Do not miss … The Sensory Examination Light Touch Pin Prick
  52. 52. Neurological Examination Sensory - Pin Prick Test Wartenberg wheel, also called a Wartenberg pinwheel or Wartenberg neurowheel
  53. 53. Neurological Examination Dermatome
  54. 54. Special Tests The Lasegue straight leg raising test (SLR) • The basis for the SLR is the belief that the stretching of the lumbar nerve trunks that form the sciatic nerve is non-painful in healthy but is painful when in fl amed, irritated or entrapped. • This test also has good correlation with positive fi ndings on (MRI) of the lumbar spine and lumbar plexus as well as (EMG). • Normally an individual can tolerate 90° fl exion of hip joint with full knee extended without any pain except if any sti ff ness in hamstrings is there.
  55. 55. Special Tests The Lasegue straight leg raising test (SLR) • At 30° of hip fl exion the nerve roots begins to replace in its foramen and in presence of any compression reproduction of the same pain which patient is experiencing is felt in the distribution of sciatic nerve. It has high sensitivity but low speci fi city. However, if it is positive it is a very useful test in 85-90% of the cases • 2- to 7-mm distal migration of the spinal nerve roots during performance this test. • The classic SLR test is considered positive when the supine leg is elevated to between 30 and 70 degrees and pain is reproduced down to the posterior thigh below the knee.
  56. 56. Special Tests The Lasegue straight leg raising test (SLR) • Pain below 30 degrees is not considered to be related to nerve root irritation. • SLRs with pain induced beyond 70 degrees of leg elevation is not believed to be due to nerve root tension. {{Mostly Joints Pain}} • In patients with herniations from L4 to S1, positive SLR was noted in 96% to 98% of cases, while in those with herniations from L1–L2 to L3–L4, it was positive in only 73%. Of note, 88% of those patients with negative exploration had a positive SLR on examination.
  57. 57. Special Tests SLR + Ankle dorsi fl exion = Bragard’s Sign • Bragard’s sign If the Lasegue test does not cause pain on the examined side, the examination should be appended by performing dorsiflexion of the ankle (Bragard’s sign). • If pain is provoked by this manoeuvre, a radicular irritation is suspected. • Neri’s test, fl exing the neck to bring the head on to the chest, indicating dural irritation.
  58. 58. • The pain is assumed to be caused by stretching of an irritable femoral nerve when there is compression of the L2, L3, or L4 nerve roots. • It has been observed that these traction forces result in a 2-mm movement of the L4 root. • It is probably the single best screening test to evaluate lumbar radiculopathy secondary to an upper lumbar disc herniation. • It has been shown to be positive in 84% to 95% of patients with a high lumbar disc. FEMORAL NERVE STRETCH TEST
  59. 59. • 94.2% of patients with frank disc herniation had pain reproduction with slump testing compared with 78% of those with bulging discs and 75% with no positive imaging fi ndings on CT or MRI. THE SLUMP TEST
  60. 60. After History and Examination • Patients presenting with back pain can be categorised into three groups: • Simple mechanical back pain +/- referred pain to the lower limbs. • Back pain + radicular pain (due to nerve root irritation — ‘sciatica’). • Serious spinal pathology.
  61. 61. Blood Tests • Complete hemogram with in fl ammatory markers like ESR, CRP, platelets, RA factor, HLA B 27, uric acid levels is must when infective or in fl ammatory back pain is suspected.
  62. 62. When will you refer the Patient to Surgeon ?? ?
  63. 63. Recommendations and levels of evidence for treatment of CLBP By the clinical guidelines committee of the ACP. • The initial approach to chronic CLB should focus on: • nonpharmacologic treatment, including exercise, multidisciplinary rehab, acupuncture, mindfulness-based stress reduction (moderate evidence). • Tai chi, yoga, motor control exercise, progressive relaxation, EMG biofeedback, low level laser therapy, operant therapy, cognitive behavior therapy, or spinal manipulation (low quality evidence).
  64. 64. Recommendations and levels of evidence for treatment of CLBP By the clinical guidelines committee of the ACP. • 2. If there is an inadequate response to nonpharmacologic therapy, • consider pharmacologic treatment: • NSAIDs as fi rst line or tramadol or duloxetine as second line; • Opioids only if failed other treatments and only if the bene fi ts outweigh the risks (weak recommendation).
  65. 65. Recommendations and levels of evidence for treatment of CLBP The ACP clinical guidelines committee has rated the evidence for nonpharmacologic treatment of CLBP and concluded that: • super fi cial heat moderately improved pain relief (at fi ve days) and disability (at four days) and, combined with exercise, improved Roland disability questionnaire (RDQ) scores at seven days, with better outcomes than acetaminophen/ibuprofen treatment; • Acupuncture was found to have con fl icting evidence for e ffi cacy but did show a moderate improvement in pain intensity; • Massage therapy gave some relief to some patients and is considered safe.
  66. 66. Recommendations and levels of evidence for treatment of CLBP The ACP clinical guidelines committee has rated the evidence for nonpharmacologic treatment of CLBP and concluded that: • Spinal manipulation therapy improved pain and function if used for four weeks or less, but there was no long term bene fi t observed; • Exercise, including stretching, strengthening, or fl exion/ extension, are not recommended by either the United States or European guidelines. However, exercise is known to confer other bene fi ts; • Optimal time to start exercise after the onset of LBP symptoms is unclear; for patients in the: • Subacute phase (less than four to eight weeks), rehabilitation (physician, physical therapy, psychological or vocational interventions) are moderately e ff ective (yoga and tai chi have had some promising outcomes for CLBP).
  67. 67. Pharmacologic Therapy for LBP 2017 ACP clinical practice guideline: • Acetaminophen (APAP): appears to be no di ff erent from a placebo for acute or subacute LBP regarding pain intensity or function through four weeks; no indication for chronic LBP (moderate quality evidence); NSAIDs showed no di ff erence than acetaminophen at three weeks or less; although estimates favored NSAIDs for pain relief, acetaminophen had a lower risk for side e ff ects. • NSAIDs: were associated with greater mean improvements in pain intensity than placebo for acute back pain; for chronic LBP, NSAIDs were associated with greater mean pain relief than placebo after 12 weeks; no clear di ff erences between NSAIDs for acute or chronic LBP; for radiculopathy, small and inconsistent e ff ects were found. NSAIDs were associated with more adverse e ff ects than placebo, but COX-2 inhibitors had a lower risk for adverse events (AEs). • Opioids, tramadol, and tapentadol: no di ff erence for acute LBP between oxycodone or acetaminophen plus naproxen or placebo plus naproxen; for chronic LBP, strong opioids were associated with greater short term relief than placebo; tramadol also resulted in greater short term relief than placebo. Opioids had a higher risk for nausea, dizziness, constipation, vomiting, somnolence, and dry mouth than placebo.
  68. 68. Pharmacologic Therapy for LBP 2017 ACP clinical practice guideline: • Skeletal muscle relaxants: superior to placebo for short term pain relief; evidence insu ffi cient to determine e ff ects on function or for CLBP; no signi fi cant di ff erences among various skeletal muscle relaxants on any outcome. • Benzodiazepines: no clinically signi fi cant bene fi t compared with placebo were associated with CNS AEs (somnolence, fatigue, and lightheadedness). • Anti-depressants: no di ff erence in pain between tricyclic anti-depressants or selective serotonin reuptake inhibitors for CLBP; can be e ff ective, but their mechanisms of action are not clearly understood; serotonin norepinephrine reuptake inhibitor (SNRI) duloxetine was associated with lower pain intensity at 12 to 13 weeks, although e ff ects were small; duloxetine associated with greater improvement in function on the BPI. Anti-convulsant medications: gabapentin provides small short term bene fi ts for radiculopathy; evidence insu ffi cient to determine e ff ects of pregabalin versus other medication or pregabalin plus another medication versus the other medication alone. • Systemic corticosteroids: no di ff erences were found for nonradicular and radicular LBP compared with placebo when
  69. 69. Internal Disc Disruption Vertebral Column
  70. 70. Internal Disc Disruption a painful disc: IDD, Discogenic Pain, and painful DDD • Discogenic back pain is the most common cause a ff ecting nearly half of the patients with low back pain. • is thought to account for up to 42% of chronic low back pain • This produces the discogenic pain syndrome caused by disc degeneration not related to sciatica or nerve root referred pain • is a condition characterized by a set of chemical, morphological, and biophysical features.
  71. 71. Pathological Mechanisms of LBP • It is precipitated by a small fracture of the vertebral endplate, as a result of severe compression injury or fatigue failure under compression. • This results in progressive degradation of the nuclear matrix, and the development of radial fi ssures into the annulus fi brosus • In the healthy back, only the outer third of the annulus fi brosus of the intervertebral disk is innervated. • Pathomechanism for LBP is thought to be sensory nerve ingrowth into the inner layer of the degenerated intervertebral disk. • Extensive innervation of intervertebral disks has been found in patients with diskogenic pain
  72. 72. • These chemical and morphological changes a ff ect the biophysical properties of the disc. • Various proin fl ammatory molecules such as: • Tumor necrosis factor-α, interleukin-1, interleukin-6, interleukin-8, inducible nitric oxide synthase, prostaglandin E 2 , and nerve growth factor have been found in intervertebral disks.
  73. 73. Quality of Pain • Discogenic pain is very vague, and not well localized. • Radicular pain and pain due to entrapment neuropathy is sharp, shooting, lancinating or electric in nature. • There are no specific characteristics in the patients’ history that confirm or disprove the diagnosis of discogenic low back pain. • More typical features include persistent, nociceptive low back, groin and/or leg pain that worsens with axial loading and improves with recumbence. • Patients may have experienced a prior episode of acute, intense pain caused by an acute tear in the innermost part of the AF
  74. 74. Physical Examination • There are no typical characteristics of discogenic pain in the physical examination. • Biphasic straightening from flexion is considered by some to be an indication of a disk complaint. Pain as a result of pressure on the processus spinosus is considered characteristic of discogenic low back pain (“Federung”). • Vanharanta has described pain radiating from the disk due to provocation with a tuning fork pressed on the processus spinosus of the a ff ected segment. Although suggestive, these physical examination characteristics have not been validated, and the current criterion standard for confirming a clinical diagnosis of discogenic pain is a positive discogram and the demonstration of a Grade 3 AF tear
  75. 75. • Lumbar X-rays of IDD patients do not have any characteristic signs.
  76. 76. Can MRI accurately predict Discogenic LBP?
  77. 77. Normal or bulging disc in the presence of an HIZ
  78. 78. Disc protrusion in the presence of an HIZ
  79. 79. Lumbar Discography In Brief • Definitions Stimulation of a discus intervertebralis is a procedure that was developed for the purpose of confirming or refuting a clinical hypothesis of discogenic low back pain. • The procedure is performed by inserting a needle in the NP of the target disk and injecting contrast agent (or another suitable medium) in order to test the sensitivity of the disk to gradually increasing distending pressures. • Disk stimulation is the more accurate name for a procedure that until now has often been described as (provocative) discography.
  80. 80. Treatment Options Core muscle Exercise • MADI Clinic - Jeunju - South Korea
  81. 81. • Pharmacologic treatment typically includes (NSAIDs) and muscle relaxants, but the literature support for e ffi cacy of treatment is not strong with only minimal improvements in pain and function. • Chronic opioid therapy is only marginally e ff ective and is associated with signi fi cant side e ff ects and risk of addiction and overdose. • Physical therapy with core muscle strengthening along with manipulation has some temporary bene fi t and long-term e ff ects
  82. 82. 4 Important Exercise Pelvic Tilt Purpose: To strengthen your lower abdominal muscles and add fl exibility to your low back How to perform a pelvic tilt: •Lie on your back with your feet fl at on the fl oor. •As you exhale, squeeze your abdominal muscles, push your belly button toward the fl oor, and fl atten your low back. •Hold for 5 seconds. Relax. •Repeat 10 times, holding for 5 seconds each time.
  83. 83. 4 Important Exercise Knee to Chest Purpose: To reduce pressure on your lumbar spinal nerves and alleviate back pain. How to perform a knee to chest: •Lie on your back with feet fl at on the fl oor. •Bring your right knee toward your chest, using your hands to hold your leg in the stretched position. Hold for 10 seconds. •Lower your right leg and repeat the exercise with the left knee. Hold for 10 seconds. •Repeat with each leg 3 to 5 times. •After stretching each leg individually, perform the exercise by holding both knees in the stretched position. Hold for 10 seconds and repeat 3 to 5 times.
  84. 84. 4 Important Exercise Lower Trunk Rotation Purpose: To increase your spine’s mobility and fl exibility. How to perform a lower trunk rotation: •Lie on your back in the hook lying position (knees bent and feet fl at on the fl oor). •Rotate your knees to 1 side, holding them for 3 to 5 seconds. •While contracting your abdominal muscles, slowly rotate your knees to the other side and hold for 3 to 5 seconds. •Repeat up to 10 times on both sides.
  85. 85. 4 Important Exercise All Fours Opposite Arm and Leg Extension Purpose: To strengthen and stabilize your abdominal and low back muscles. How to perform an all fours opposite arm and leg extension: •Start in an all fours, or tabletop, position, contracting your abdominals throughout the entire exercise. Engaging your abdominals will keep your back in a straight position. •Gently raise your left leg behind you and hold for 3 to 5 seconds. •Repeat with your right leg and hold for 3 to 5 seconds.
  86. 86. How Do These Exercises Reduce Lumbar Degenerative Disc Disease Pain? These low-impact exercises focus on strengthening and conditioning your spine’s support system—your core (abdominal muscles) and spinal muscles. What’s the link between a strong core and back health? Your core and spinal muscles act as an internal brace to support your spine. Keeping these structures strong puts less pressure on your spine, so you’ll feel less pain. That’s why exercises designed to strengthen your spine and increase fl exibility are so important—stronger spines resist pain. Staying active also helps keep your discs healthy, as spinal discs need movement for nutrients.
  87. 87. Other Treatment Options • Epidural injections are performed for patients with discogenic low back pain and have been shown to produce fair results. • Intradiscal electrothermal annuloplasty (IDET) was used to treat discogenic low back pain starting in 1996, and a more recent meta-analysis of its e ff ectiveness has shown that this also produces fair results. • There are therapies that are focused on: • either treating the in fl ammatory pathways (i.e., steroid injections)disrupting the nerve conduction from the painful disc (i.e., methylene blue, ozone, biaculoplasty, etc.). • These types of therapies may be successful in reducing pain but do not have the ability to heal the disc or reverse the degenerative changes suspected to be responsible for the pain.
  88. 88. • Research e ff orts have been focusing more on the development of treatments that will repair or regenerate damaged intervertebral discs. • Treatments have been focused on restoring the cellular health of the intervertebral disc and on reducing the pain associated with IDD. • The bene fi ts of biologic treatments likely originate from tissue repair and changes in cytokine expression following injection of biologic material. • Some of the biologic materials that have been injected into the intervertebral disc include fi brin sealant, isolated growth factors, juvenile chondrocytes, platelet-rich plasma, and mesenchymal stem cells (MSCs)
  89. 89. Intradiscal Biologic Treatments Understudy • I. Fibrin Adhesives: Injection into the disc with fi brin adhesives involves fi brinogen combined with thrombin just prior to injection into the nucleus pulposis with enough volume to fi ll the potential space of the nucleus and extend into and seal the annular defects from inside • II. Bone Morphogenic Protein : GDF-5 with saline. • III. Alpha-2-Macroglobulin • IV. Platelet-Rich Plasma
  90. 90. Interventional Procedures • I. Intradiscal electrothermal therapy (IDET): • The procedure consists of percutaneous insertion of a thermocoil into the disk under radiographic examination. • The catheter must be placed along the internal aspect of the posterior AF. • The distal portion of the catheter (5 cm) is heated for 16 min to 90°C.
  91. 91. Interventional Procedures Intradiscal corticosteroid injections • The goal of intradiscal corticosteroid injections is the suppression of the inflammation that is considered to be responsible for discogenic pain. • The group with Modic Type-1 changes had significantly better results after intradiscal steroid injection compared with the group without Modic Type-1 changes.
  92. 92. Interventional Procedures Biacuplasty • is the latest in a series of minimally invasive posterior AF heating techniques. This technology works specifically by concentrating RF current between the ends of two straight probes. • Two TransDiscal 18 G electrodes via introducers are placed bilaterally in the posterior AF of the discus intervertebralis. • The generator controls the delivery of RF energy by monitoring the temperature measured by a thermocouple at the tip of the probe. The temperature increases gradually over a period of 7–8 min to 50°C, with final heating at 50°C for another 7 min. • It should be noted that although the temperature is set to 50°C on the RF generator, tissue temperature reaches 65°C due to ionic heating.
  93. 93. • The incidence of disc related pain was greatest in patients younger than 40 years of age. • The pain was located primarily in the low back and buttock regions. • The onset of pain was precipitated by a torsion injury of the low back and was exacerbated by axial loading such as with prolonged sitting and standing. • Although the pain experienced from disc pathology is characteristically axial in nature, it may also refer to the lower extremities in a non-dermatomal distribution.
  94. 94. The Grading or Degree of IDD • In grade I disruption, fi ssures reach the inner third of the annulus. • In grade II disruption fi ssures reach the middle third of the annulus. • Grade III disruption arises when the fi ssure reaches the outer third, and becomes grade IV if the fi ssure then extends circumferentially.
  95. 95. There are six possible categories that describe the severity of the radial annular tear. • The grade 0 is a normal disc; where no contract material leaks from the nucleus. • The grade 1 tear will leak contrast material only into the inner 1/3 of the annulus. • The grade 2 tear will leak contrast through the inner 1/3 and into the middle 1/3 of the disc. • The grade 3 tear will leak contrast through the inner and middle annulus. The contrast spills into the outer 1/3 of the annulus. • The grade 4 tear further describes a grade 3 tear. Not only does the contrast extend into the outer 1/3 of the annulus, but it is seen spreading concentrically around the disc. To qualify as a grade 4 tear the concentric spread must be greater than 30 degrees. Pathologically, this represents the merging of a full thickness radial tear with a concentric annular tear. • The ‘evil’ grade 5 tear describes either a grade 3 or grade 4 radial tear that has completely ruptured that outer layers of the disc and is leaking contract material out of the disc. This type of tear, which I most likely su ff ered from, can cause a chemical radiculopathy in one or both of the extremities and result in the dreaded
  96. 96. I. Lumbar Radicular Syndrome ALWAYS EXCLUDE HIP PATHOLOGY
  97. 97. Introduction • A lumbosacral radicular syndrome (LRS) is characterized by a radiating pain in one or more lumbar or sacral dermatomes; it may or may not be accompanied by other radicular irritation symptoms and/or symptoms of decreased function. • The terms radicular pain and radiculopathy are also sometimes used interchangeably, although they certainly are not synonyms. • Pain completely or partially resolves in 60% of the patients within 12 weeks of onset. 6 However, about 30% of the patients still have pain after 3 months to 1 year. • In patients under 50 years of age, a herniated disk is the most frequent cause of an LSR. • After the age of 50, radicular pain is often caused by degenerative changes in the spine
  98. 98. Symptoms • The patient may experience the radiating pain as sharp, dull, piercing, throbbing, or burning. Pain caused by a herniated disk classically increases by bending forward, sitting, coughing, or (excessive) stress on the lumbar disks and can be avoided by lying down or sometimes by walking. 5 Inversely, pain from a lumbar spinal canal stenosis can typically increase when walking and improve immediately upon bending forward. 8 In addition to the pain, the patients also often report paresthesia in the a ff ected dermatome. The distribution of pain along a dermatome can be indicative in the determination of the level involved; however, there is a large variation in radiation pattern. The S1 dermatome seems the most reliable. 9 If present, the dermatomal distribution of paresthesia is more specific.8
  99. 99. Symptoms • Pain, paresthesia, and numbness in a dermatomal distribution • a positive straight-leg raise (SLR) test, • with or without accompanying signs of sensory loss, weakness, and diminished re fl exes, are mediated by sensory spinal NRs (SSNRs) or dorsal root ganglia (DRG). • These symptoms of lumbar radicular syndrome (LRS) can be present in isolation.
  100. 100. • The incidence of LRS in patients with LBP is reported to range from 12% to 40%. • The term sciatica is also often used synonymously with LRS. • It is usually extended below the knee (radicular pain), can result from mechanical nerve root compression and chemical irritation from various in fl ammatory mediators that leak out of degenerated discs. • Unlike referred pain from joints, muscles, and discs, the pain typically radiates in a dermatomal distribution.
  101. 101. • Herniated nucleus pulposus is the most common cause of radicular pain. • From a radiological perspective: • Absolute central lumbar stenosis refers to anteroposterior spinal canal diameter smaller than 10 mm, • Whereas foraminal stenosis relates to a neuroforaminal diameter smaller than 3 mm. • A herniated disc is diagnosed when the nucleus pulposus extends beyond the normal con fi nes of the annulus fi brosis, but involves less than 25% of the circumference.
  102. 102. Examination Neurodynamic Test • SLR • SLUMP • FNST
  103. 103. Motor Examination
  104. 104. Interventional management • Epidural administration of corticosteroids is generally indicated in cases of subacute radicular pain. • In patients with chronic radicular complaints, corticosteroids will not provide any improvement in the outcome in comparison with local anesthetics alone. • This indicates that epidural corticosteroids are more e ff ective for (sub)acute radicular pain where a significant inflammatory pain component is present. • PRF treatment is a treatment option for chronic radicular pain.
  105. 105. • I. Interlaminar corticosteroids • II. Transforaminal corticosteroids • III. Caudal corticosteroids Interventional management 1. Epidural corticosteroid administration
  106. 106. Interventional management 2. Adhesiolysis and epiduroscopy • The goal of lysis of epidural adhesions is to remove barriers in the epidural space that may contribute to pain generation and prevent delivery of pain relieving drugs to target sites. • 1. Chemical Adhesiolysis: include • (1) Hyaluronidase1500 - 3000 iu • (2) hypertonic saline solution; • 2. Mechanical adhesiolysis
  107. 107. Interventional management 3. Spinal cord stimulation in FBSS • I. Interlaminar corticosteroids • II. Transforaminal corticosteroids • III. Caudal corticosteroids
  108. 108. Lumbar Spinal Stenosis Lumbar Neurogenic Intermittent Claudication NIC
  109. 109. Definition IASP • “lumbar spinal pain of unknown origin either persisting despite surgical intervention or appearing after surgical intervention for spinal pain originally in the same topographic location.” • Comprehensive history should include evaluation of: • Preoperative risk factors (psychosocial factors, smoking, obesity), • Intraoperative risk factors (operating at a single level, operating at the wrong level), • Postoperative risk factors.
  110. 110. Lumbar Spinal Stenosis • LSS is de fi ned as the clinical syndrome of neurogenic claudication or • radicular symptoms from narrowing of the spinal canal, neuroforaminae, and/ or lateral recess generally assumed to be from compression of the neural elements. • NIC is the most common reason for spine surgery in patients over 65 years of age. • The hallmark is the induction of gluteal and lower extremity pain with upright exercise or speci fi c postural positions and relieved by forward fl exion, sitting, or recumbency.
  111. 111. • The most common, the acquired degenerative variety, of LSS is characteristically because of disc degeneration and its sequelae. The typical lesions include • 1) loss of disc height, • 2) AF bulging, • 3) facet joint hypertrophy, • 4) thickening and redundancy of the ligamentum fl avum, • 5) local osteophyte formation
  112. 112. • Central stenosis can cause compression of the NRs of the cauda equina, • whereas lateral stenosis typically results in compression of the exiting spinal NRs. • The L5 NR is most commonly involved (75%), • followed by the L4 (15%), • L3 (5.3%), • L2 (4%) NRs
  113. 113. • compression and/or ischemia of the neural structures is generally thought to be responsible for the clinical manifestations, and in contrast to HD, the role played by the in fl ammatory changes is less clear. • In contrast to vascular claudication, the pain of neurogenic claudication continues to be present with standing and is eased by walking in a fl exed position, such as pushing a walker or shopping cart.
  114. 114. Treatment • Non-operative Treatments • including medications, activity modi fi cation, bracing, and physical therapy, • ESIs, particularly IL-ESIs, are e ff ective in the short term treatment of acute pain exacerbations and can provide symptomatic control of episodically worsening symptoms of neurogenic claudication. • Fluoroscopically guided TF-ESIs appears to be a treatment better suited for radicular symptoms secondary to LSS and have been shown to have both short term and long-term e ffi cacy. • Percutaneous image-based lumbar decompression (PILD) is a minimally invasive procedure indicated for lumbar spinal stenosis with neurogenic claudication primarily caused by hypertrophy of the ligamentum fl avum.
  115. 115. Lumbar Facet Syndrome ALWAYS EXCLUDE HIP PATHOLOGY
  116. 116. • The lumbar facet or zygapophyseal joints (LFJs) are synovial joints composed of an articular surface, synovial membrane, fi broadipose meniscoid, and fi brous capsule. • Each joint is composed of two articular processes, the superior and the inferior. • The orientation of facet joints is distinct at the lumbar, thoracic, and cervical levels, with the LFJs having a curved and oblique pro fi le. • The medial branch (MB) of the posterior primary ramus traverses the base of the superior articular process (SAP) at its junction with the transverse process to innervate both the facet joint at the same level and the vertebral level below.
  117. 117. • Each facet joint receives innervation from its corresponding vertebral level and the vertebral level above. • The course of the MB is relatively fi xed as it originates from the dorsal ramus, proximally at the base of the SAP. • The L5 dorsal ramus passes over the sacral ala at the base of the sacral SAP. • The fi brous capsule and the synovium of the LFJs are richly innervated by nociceptive fi bers
  118. 118. Diagnosis
  119. 119. Radiation • Non-dermatomal radiation • The upper lumbar facet joint pain may be referred to fl anks, hips and lateral thigh, • The lower lumbar facet joints pain are referred to posterior thigh. • Facet joint pain is rarely referred below knees
  120. 120. Diagnostic Injections for Lumbar Facet Syndrome • Local anesthetics of di ff erent duration, used on two separate occasions (double comparative blocks), with the patient reporting corresponding duration of pain relief, can enhance diagnostic speci fi city. • double comparative blocks are generally recommended for appropriate diagnosis of LFS to avoid the unacceptably high false-positive response rate of the single diagnostic procedure. • a definitive treatment is carried out if a patient experiences 50% or greater pain reduction lasting for the duration of action of the local anesthetic (e.g., >30 minutes with lidocaine and 3 hours with bupivacaine).
  121. 121. Facet Denervation • Denervation of a painful facet joint, referred to as facet rhizotomy, neurotomy, or ablation, is accomplished by lesioning of the MB at the painful vertebral level and one level above. • Optimal electrode p ing is con fi rmed both radiologically and by appropriate sensory and motor testing prior to the lesion creation. • The size of RF electrodes used varies between 18 and 22 gauge, the temperatures range between 80°C and 90°C, and the duration of RF lesioning can last from 60 to 90 s. • three RCTs of RFA for LFS e ffi cacy are available; while two demonstrated improved chronic LBP following the procedure, the third showed no bene f
  122. 122. • Currently, the gold standard for treating facetogenic pain is RF treatment. The major advantage of temperature-controlled TRF
  123. 123. Lumbar Spondylolisthesis
  124. 124. Key Points • Lumbar spondylolisthesis may result from: • congenital, • isthmic, • trauma-related, • degenarative, • iatrogenic causes. • A variety of radiographic studies may be necessary to comprehensively evaluate spondylolisthesis. • Di ff erentiating between stable and unstable spondylolisthesis may assist in selecting the appropriate treatment. • Treatment is variable and must be customized based on the presenting complaints and the underlying structural abnormalities.
  125. 125. Key Points • Lumbar spondylolisthesis is de fi ned as an acquired anterior displacement of one vertebra over the subjacent vertebra, associated with degenerative changes, without an associated disruption or defect in the vertebral ring. • The term spondylolisthesis is derived from the Greek for spondylos (vertebra) and olisthesis (to slip or slide down). • The direction of the spondylolisthesis is de fi ned based on the displacement of the upper vertebra as anterolisthesis or retrolisthesis. The intervertebral discs, the superior and inferior articular processes, the ligaments, and the paravertebral muscles work together to provide segmental stability.
  126. 126. • Disc dysfunction and horizontalization of the lamina and the articular process have been implicated as factors responsible for the development of spondylolisthesis. • During the aging process, the intervertebral discs undergo degenerative changes characterized by loss of hydration and delamination, ultimately resulting in segmental instability. • The L4–5 segment is particularly vulnerable to this issue because the almost completely sagittal orientation of the superior and inferior articular processes of the facet joint render it vulnerable to anteroposterior sheer forces.
  127. 127. Classification • 1. Congenital or dysplastic: caused by congenital defects of L5 and/or the upper sacrum • 2. Isthmic: caused by pars interarticularis defects • 3. Degenerative: due to articular process degeneration or abnormal orientation • 4. Traumatic: caused by fracture or dislocation of the lumbar spine, not involving the pars • 5. Pathologic: due to infection, malignancy (either primary or metastatic), or other types of abnormal bone • 6. Iatrogenic/postsurgical. • Isthmic spondylolisthesis, the most common subtype, is caused by pars interarticularis defects. Congenital or dysplastic spondylolisthesis is due to failure of normal genesis of the superior articular process.
  128. 128. • Isthmic
  129. 129. Grade
  130. 130. Diagnostic Imaging • Most commonly standing lateral radiographs, typically including fl exion– extension views, are the appropriate fi rst step in detecting DLS. • One speci fi c element of radiographic assessment is the need to understand whether there is fi xed or dynamic deformity at the a ff ected level. Typically standing lateral fl exion–extension radiographs are used to make this determination. Typically, the standard for DLS has been 5 mm of vertebral slippage. Dynamic deformity is suspected when there is incongruity between fl exion–extension radiographs as noted by attenuation or reduction of slippage between these views.
  131. 131. Lateral upright radiographs of patient with grade II spondylolisthesis at L5–S1.
  132. 132. Treatment • There are typically at least three general goals: • (1) reduce in fl ammation, • (2) reduce mechanical stressors, • (3) improve strength and stability. • All of these theoretically result in improved pain control.
  133. 133. Treatment • In fl ammation can be reduced in several ways. • Oral or injected medications may be a way to modulate in fl ammation. • There is good evidence supporting the use of NSAID and acetaminophen in the treatment of acute low back pain, and empirically their use has been common in DLS. • There is fair evidence supporting the use of muscle relaxants in acute LBP, and these agents are commonly prescribed in patients with chronic LBP, including that resulting from DLS. • We believe that traditional muscle relaxants such as cyclobenzaprine, methacarbamol, and metaxalone have very little role in the treatment of spasm associated with DLS; • instead, medications such as baclofen and tizanidine, which block spinal mono- and polysynaptic re fl exes should be considered. • These agents may also provide bene fi t in patients with primarily myofascial complaints.
  134. 134. Treatment • Bracing may be particularly bene fi cial in those with DLS complicated by other spinal alignment issues such as scoliosis, lateral listhesis, or hyperlordosis. • Typically bracing is used in a time-limited fashion, as overdependence on bracing may result in weakening of the core musculature, further exacerbating structural issues. • Braces are typically used only during daytime hours or whenever the patient expects to be active or in a pain-provoking position.
  135. 135. • It has been postulated that interlaminar and transforaminal steroid injections as well as intra-articular facet injections and medial branch neurotomy may provide pain relief and targeted delivery of potent anti-in fl ammatory agents to the site of the pathology in DLS. •
  136. 136. Sacroiliac Joint Complex (SIJC) Pain Vertebral Column
  137. 137. Intro • is a true diarthrodial joint with the articular surfaces of the sacrum and ilium separated by a joint space enclosed in a fi brous capsule. • It bears the characteristics of a synovial joint, especially in the superoanterior and inferior aspects. • The superoposterior joint surface lacks a joint capsule and contains the interosseous ligament. • The posterior aspect also contains the posterior sacroiliac, sacrotuberous, and sacrospinous ligaments that stabilize the joint.
  138. 138. Innervation • The anterior joint is suggested to be innervated by the ventral rami of L4 and L5 of the lumbosacral trunk . • The posterior innervation is presumed to be from lateral branches of the posterior rami of L5–S4. • The superior gluteal nerve (ventral rami of L4–S1) contributes to the innervation of the joint according to some study .
  139. 139. • back pain (LBP), with a reported prevalence rate ranging between 10% and 33% in individuals with a suspected mechanical etiology predominantly below L5. • Although sacroiliac joint pain most frequently presents in the buttocks, over two-thirds of individuals will have lumbar pain; in approximately 50% of cases, the pain radiates to the leg, sometimes below the knee.
  140. 140. • Intra-articular pathology is more common in older people, • whereas younger individuals with prominent tenderness and a traumatic cause are more likely to have extra-articular pathology.
  141. 141. I. Sacroiliac Joint Complex (SIJC) Pain
  142. 142. Diagnosis History • Constant pain and Localized around the SIJ and upper leg. • Radiated into the posterior buttocks and backs of the thigh and the groin. • Usually doesn't cross below the knee. • Aggravated by Sitting, from sitting to standing, and Stepping up and down. • Interfere with sleep. • Fortin Finger Test
  143. 143. Please don’t depend on: - Local Tenderness. - Faber test. ONLY USE Cluster of Laslett for Diagnosis SN: 0.77 SP: 0.28 SN: 0.94 SP: 0.78
  144. 144. Special Provocative Tests
  145. 145. SIJ radiofrequency
  146. 146. Bertolotti syndrome Unusual pain syndromes
  147. 147. In Brief • low-back pain due to a lumbosacral transitional vertebra (LSTV). • LSTV is an anatomical variation of the most caudal lumbar vertebra in which an enlarged transverse process can articulate or fuse with the sacrum or ilium. • is a congenital abnormality, it is often clinically manifested only after the second decade of life. • It is estimated this syndrome accounts for 4.6% - 7% of cases of LBP in adults, and for more than 11% of patients with LBP who are under 30 years old.
  148. 148. Castellvi’s classification • Type I – dysplastic transverse process with height> 19 mm • Type II – incomplete lumbarization/sacralization (diarthrosis) • Type III – complete lumbarization/sacralization with complete fusion with the neighboring sacral basis • Type IV – mixed • The type II transitional vertebra has been associated with an increased number of disc prolapses, and related to discogenic and/or contralateral facetogenic low back pain.
  149. 149. Symptoms • chronic, progressive midline, or paramedian LBP that is deep, sharp, or dull in nature or a sensation of pulled muscle or unilateral upper buttock pain. • The severity of pain is moderate to severe, • worse with physical exertion, and better with rest. • The provocative factors of pain include heavy lifting, forward fl exion, excessive extension or lateralization of the back to the same side of the megaapophysis. • It may be accompanied with sciatica, medial thigh cramping, leg radicular pain, weakness, or numbness. • Patients may have signi fi cant ambulatory and functional limitations.
  150. 150. Examination • Physical examination demonstrates • focal tenderness along the base of the LSS and near the PSIS, provoked by super fi cial and deep palpation. • Patients may have normal and symmetric muscle bulk and tone in their paraspinal muscles and in all extremities. • SLR test, may be positive; • range of motion may be impaired. • Pronator drift, Romberg signs, patellar and Achilles deep tendon re fl exes, and sensation test usually are intact.
  151. 151. Diagnosis • The correct diagnosis is made based on imaging studies which included • LS CT scans, • plain x-rays, • and MRI scans • in the context of typical history of low back pain and physical exam.
  152. 152. Treatment • Course of conservative management including: • activity modi fi cation, • medication management with NSAIDs, muscle relaxants, opioids, • rehabilitative physical therapy • should be o ff ered initially, with the recognition that these therapies are less likely to result in satisfactory pain control.
  153. 153. Treatment • If the primary origin of the pain is at the pseudoarticulation between the transverse process and ilium due to the arthritic changes, a local anesthetic and corticosteroid can be injected into this pseudoarticulation. • These blocks should be performed with a minimal amount of anesthetic delivered precisely to the point of interest to achieve temporary pain relief. • If rapid pain relief doesn’t occur almost instantaneously, alternative pain generators should be sought. • The anesthetic block can be repeated if in doubt. • If the patient experiences temporary pain relief and the pain is truly localized in the transitional joint without evidence of disc pathology, a minimally invasive approach may be taken to resect the anomalous transverse process with the accompanying pseudoarticulation.
  154. 154. Iliac Crest Pain Syndrome Iliolumbar ligament syndrome
  155. 155. In Brief • The iliolumbar ligament has not explicitly been shown to have an innervation but presumably it is innervated by the dorsal rami or ventral rami of the L4 and L5 spinal nerves. • Biomechanically, the iliolumbar ligament serves to resist fl exion, rotation and lateral bending of the L5 vertebra and could therefore be liable to strain during such movements. • The evidence implicating the iliolumbar ligament as a source of back pain is inconclusive. • Tenderness over the PSIS is a sign of iliolumbar ligament sprain, but this is hard to credit, for the ligament lies anterior to the ilium and is buried by the mass of the erector spinae and multi fi dus.
  156. 156. In Brief • Some Investigators have claimed to have relieved back pain by in fi ltrating the iliolumbar ligament. • all investigators have overlooked is that the site of tenderness in iliac crest syndrome happens to overlie the site of attachment of the lumbar intermuscular aponeurosis (LIA), which constitutes a common tendon for the lumbar fi bres of longissimus thoracis. • The LIA attaches to the iliac crest rostromedial to the posterior superior iliac spine and exhibits a morphology not unlike that of the common extensor origin of the elbow. • Thus, a basis for pain and tenderness in this region could be a tendonopathy of the LIA. On the other hand, it could be no more speci fi c than tenderness in the posterior back muscles, which has been recognised for many years under di ff erent rubrics.
  157. 157. In Brief • Iliac crest syndrome is de fi ned simply as tenderness over the medial part of the iliac crest, the kappa score for its diagnosis is 0.57. • If the criteria are extended to include reproduction of typical pain, the kappa score rises to 0.66. • These scores indicate that the syndrome can be identi fi ed. Its prevalence seems to be about 30–50%. • However, as long as the syndrome amounts to no more than tenderness, it is not evident whether it is a unique disorder or a feature that could occur in association with other sources and causes of back pain.
  158. 158. Treatment • Recognising the syndrome, however, has little impact on treatment. • Injecting the area with local anaesthetic is signi fi cantly more e ff ective than injecting it with normal saline, but only some 50% of patients bene fi t and only 30% obtain more than 80% improvement
  159. 159. Iliolumbar ligament • Originates from the L-5 transverse and is made up of an anterior and posterior band • Clinical Features: • Unilateral or bilateral low back pain • Exquisite tender point at the posterior iliac crest (Figure 56-8) • Positive hip fl exion test and Patrick maneuver • Constant ache aggravated by prolonged sitting and standing—referral pain to the greater trochanter and into the groin (“my testicles are in a vice”)
  160. 160. Iliolumbar ligament
  161. 161. Deep Gluteal Syndrome DGS
  162. 162. Introduction • Deep gluteal syndrome is characterized by pain and dysesthesias in the buttock area, hip, or posterior thigh due to a non-discogenic sciatic nerve entrapment in the subgluteal space. • It is caused by multiple pathologies: • “piriformis syndrome,” • the presence of fi brous bands, • obturator internus/gemellus syndrome, • quadratus femoris/ischiofemoral pathology, • hamstring pathology, • gluteal disorders.
  163. 163. Introduction • The subgluteal space is delimitated: • Posteriorly by: the gluteus maximus muscle, • Anteriorly by the posterior surface of the femoral neck, • Laterally by the linea aspera and the iliotibial tract (the union of middle and deep gluteal aponeurosis and the tensor fasciae latae muscle), • Medially by the sacrotuberous and falciform fascia, • Superiorly by the inferior margin of the sciatic notch, • Inferiorly by the hamstring tendons.
  164. 164. Introduction The subgluteal space contains: • Superior and Inferior gluteal nerves and vessels, • Sacrotuberous and Sacrospinous ligaments, • Internal pudendal vessels, • Sciatic nerve. • Piriformis, • Obturator internus and externus, • Gemelli, • Quadratus femoris • Hamstrings.
  165. 165. Ischiofemoral Impingement IFI & Hamstring Syndrome Quadratus femoris (QF) impingement Extra-articular hip impingement Distal Causes of Deep Gluteal Syndrome
  166. 166. • patients with IFI are more comfortable sitting, and walking during terminal hip extension when the space between ischium and the lesser trochanter is diminished, exacerbating the pain.
  167. 167. Internal and External Rotation of the Thigh
  168. 168. Internal and External Rotation of the Thigh Internal Rotator muscles of the hip … • Muscles that Internally Rotate the Hip: • Gluteus Medius (anterior fi bers) • Gluteus Minimus. • Piriformis (when fl exed past 90 degrees) • Tensor Fascia Latae. • Adductor Longus. • Adductor Brevis. Gracilis.
  169. 169. Internal and External Rotation of the Thigh External Rotator muscles of the hip … • Piriformis. • Superior and Inferior gemelli. • Obturator Internus. • Quadratus femoris.
  170. 170. • The present study shows normal and speci fi c sciatic nerve behavior during isometric contraction of the external and internal rotator muscles of the hip. • External rotators increase their volume by contracting (speci fi cally the gemelli, the internal obturator, and the quadratus femoris), causing the sciatic nerve dorsal to them to bulge to a posterior direction to adapt to the muscle dynamics. • In contrast, the obturator internus tendon, owing to its anatomical arrangement, is tensioned in the opposite (anterior) direction. This combination of increased volume of the gluteal muscles in the posterior direction with the tension of the internal obturator tendon in the anterior direction increases the sciatic nerve curvature signi fi cantly and repeatedly deforms it during isometric contraction movements. Conversely, during isometric contraction of the hip internal rotator muscles, the nerve tends to stretch (Figure 9).
  171. 171. PIRIFORMIS (Deep Gluteal Pain Syndrome) ALWAYS EXCLUDE HIP PATHOLOGY
  172. 172. • Piriformis syndrome, an etiology related to prolonged or excessive contraction of the piriformis muscle and its close relationship to the sciatic nerve and the inferior gluteal artery, is associated with pain in the buttocks, hip, and lower limb. • Pain aggravated on sitting, external tenderness near the greater sciatic notch, pain on any maneuver that increases piriformis muscle tension, and limitation of straight leg raising are features commonly observed in this syndrome. Injections of local anesthetics, steroids, and botulinum toxin into this muscle using ultrasound for guidance are often performed for diagnostic and therapeutic purposes.
  173. 173. Introduction • The piriformis muscle originates from the anterior surface of the sacrum and inserts on the upper surface of the greater trochanter, leaving the pelvis through the greater sciatic foramen.
  174. 174. Introduction • The piriformis syndrome is characterized by a clinical presentation with sciatica-like symptoms. • The etiology is not clearly known, but the entrapment and irritation of the sciatic nerve in the hip region could be in fl uenced by the piriformis muscle (contracture of the piriformis muscle, anatomical abnormalities of the piriformis muscle, problem after spinal surgery, overuse of the piriformis muscle, trauma, or sports injury).
  175. 175. Diagnosis Special Test • After central spinal cause of the Pain.
  176. 176. Ischiogluteal Bursitis • is also referred to as weaver’s bottom because traditionally weavers would sit in a position that aggravates the ischiogluteal bursa. • the ischiogluteal bursa lies between the hamstring tendon and the pelvic bone (ischial tuberosity). • Patients typically experience pain in the lower buttock, • it is estimated to account for less than 1% of cases. • Risk factors for ischial bursitis include obesity, autoimmune diseases, excessive or inappropriate exercise, and a sedentary lifestyle characterized by long periods of sitting;
  177. 177. Ischiogluteal Bursitis • On physical examination, tenderness to palpation was a prominent objective sign. MRI can be helpful in the diagnosis and may show low or intermediate signal intensity on T1 and T2 hyperintensity in the region of the ischial bursa. • The treatment of ischial bursitis is symptom-oriented and may include ergonomic modi fi cation, PT, NSAIDs, and steroid injections.
  178. 178. Maigne Syndrome Robert Maingne (1923-2012) Underdiagnosed Cause of Low Back Pain
  179. 179. Pathomechanic • I. The TLJ may be more susceptible to biomechanical disturbances due to lower stability compare to the thoracic spine as the last two ribs are not attached to the sternum. • II. The alignment of the facet joints from frontal plane in the thoracic facets to the sagittal plane in the lumbar facets, this transitional plane make the TLJ more susceptible
  180. 180. • Irritation of facets joint and / or articular capsule and / or excessive paraspinal muscle tone cause irritation of the neural structures (dorsal rami, ventral rami of the T11 - L2 NRs) produce clinical symptoms
  181. 181. Diagnosis • Tenderness upon palpation and pressure of TLJ • irritation of dorsal rami refer pain to the unilateral iliac crest upper gluteal region. • Irritation of the ventral rami can lead to unilateral • Pain is triggered by extension and or rotation but it doesn’t cross the half of the body. • Sharp pain on Tenderness upon iliac crest 7 cm laterally (rub the crest in an up and down motion) due to irritation of cutaneous branches of T11 - L1.
  182. 182. Cellulalgia (skin and subcutaneous tissues hypersensitivity to pinch and roll test) • Cellulagia located on iliac crest, inguinal canal and or greater trochanter of both side. • Kipler Fold Test
  184. 184. CLINICAL ANATOMY The posterior hip and buttocks receive sensory innervation from a variety of sources, including the: - T12 nerve, - the superior cluneal nerves. - the middle cluneal nerves. - The superior cluneal nerves provide sensory innervation of the upper, more lateral portion of the buttocks . The superior cluneal nerves are the terminal branches of the dorsal rami of the L1, L2, and L3 nerve roots.
  185. 185. Myofascial Pain Syndrome
  186. 186. • Myofascial pain is probably the most common reason for isolated low back pain. • The highest percentage of axial weight is carried in the lower back. With increased tension patients may develop muscle spasm or strain. • Muscle changes include the formation of taut muscle bands, painful taut muscle bands are known as trigger points
  187. 187. • Muscles, fascia, and ligaments can also be pain generators. • Muscles that can potentially contribute to low back pain include: • deep intrinsic (eg, multi fi dus or rotatores) • The more super fi cial longissimus, spinalis, and iliocostalis muscles, collectively referred to as erector spinae muscles. • Back muscles are integral to normal spine sti ff ness and function, and chronic low back pain could be paradoxically associated with both atrophy and increased myoelectric activity, which is consistent with studies showing both increased and decreased activation depending on context. • Muscle pathology represents an underappreciated source of low back pain, often misdiagnosed as non- speci fi c, and frequently arises consequent to other primary pathology. • Myofascial pain might result from overuse, acute stretch injuries or tears, and di ff use or localised (eg, trigger points) muscle spasm.
  188. 188. • At the lumbar levels, the lateral branches of the dorsal rami of the lumbar spinal nerves innervate the iliocostalis muscle • While the intermediate branches innervate the longissimus. • The spinotransverse muscle group is innervated by the medial branches of the dorsal rami of the appropriate spinal nerves.
  189. 189. Iliocostalis Lumborum • Iliocostalis lumborum TrPs at the upper lumbar level refer pain strongly downward, concentrating on the mid- buttock, and is a frequent source of unilateral posterior hip pain.
  190. 190. • When a patient has iliocostalis lumborum TrPs, the patient commonly draws an up-and-down pattern to represent the pain referred from iliocostalis TrPs but a crosswise pattern in the same region of the back to demonstrate the pain referred from TrPs in the lower rectus abdominus muscle.
  191. 191. longissimus Thoracis • Trigger points in the lower thoracic level of the longissimus thoracis muscle refer pain strongly low in the buttock. • This remote source of buttock pain is easily and often overlooked. • Longissimus thoracis TrPs in the most caudal portion of the muscle fibers, which are located in the upper lumbar area, usually refer pain several segments caudally but still within the lumbar region
  192. 192. • When the longissimus muscles are involved bilaterally, often at the L1 level, the patient has difficulty rising from a chair and climbing stairs if he or she faces forward in the usual manner.
  193. 193. Multifidi Muscles • Refers pain primarily to the region around the spinous process of the vertebra adjacent to the TrP. • Multifidus TrPs located from L1 to L5 may also refer pain anteriorly to the abdomen, which is easily mistaken as visceral in origin (Figure 48-4B on the right). • The multifidus muscle at L5 can also refer to the posterior thigh and/or leg and, less frequently, to the anterior thigh. • Multifidus TrPs at the S1 level project pain downward to the coccyx and render the coccyx hypersensitive to pressure (referred tenderness). • The condition is often identified as coccydynia.
  194. 194. Quadratus Lumborum Syndrome • Origin: Posterior half of iliac crest and iliolumbar ligament. • Insertion: Inferior border of twelfth rib, transverse processes of fi rst to fourth lumbar vertebrae. • Action: Extends and laterally fl exes trunk; stabilizes twelfth rib during inspiration. • Innervation: Anterior rami of twelfth thoracic and fi rst to fourth lumbar nerves.
  195. 195. Quadratus Lumborum Syndrome • is one of the most common causes of low back pain. • The quadratus lumborum muscle connects at the 12th rib, iliac crest, and lumbar vertebrae. • It is responsible for lateral bending of the lumbar spine. • Patients with QLS often have unilateral hip elevation because of muscle shortening. • Active quadratus lumborum trigger points refer pain to the hip and buttock
  196. 196. Quadratus Lumborum Syndrome • QLS lacks the characteristic features of radicular pain (such as radiating extremity pain, numbness, or weakness). • What causes quadratus lumborum pain? • Pain in the quadratus lumborum can be due to overuse, stress, and strain. Sometimes muscles cause pain and sti ff ness when they’re weak or too tight. • Activities such as sitting for long periods of time can reduce blood fl ow to an area, especially in the QL and surrounding areas. • Pain can also result from repetitive motions and weak back muscles, which lead to poor posture.