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Low Back Pain

Chapter 18 | Part 2: Cardinal Manifestations and Presentation of Diseases · Part 2 – Cardinal Manifestations & Presentation · Chapter 18


Key Clinical Points

  1. Pain categorization into Nociceptive, Neuropathic, and Nociplastic is critical for determining treatment pathways.
  2. Red flags (e.g., saddle anesthesia, rapid progression) indicate serious spinal or nonspinal pathology requiring urgent intervention.
  3. Imaging lacks specificity for acute LBP; many findings are common in asymptomatic populations.
  4. The Straight Leg Raise (SLR) has ~80% sensitivity for L5/S1 involvement; Crossed SLR has >85% specificity.
  5. Spinal stenosis is characterized by neurogenic claudication, often improved by sitting or forward flexion.
  6. Herniated disks typically resorb within 2 years but have a risk of reherniation.
  7. Waddell signs (e.g., nonanatomic tenderness, overreaction) are associated with higher risks of treatment failure.
  8. MRI is the gold standard for soft tissue (herniations), while CT has >90% sensitivity for most lumbar pathology.
  9. Risk factors for chronic LBP include female sex, older age, obesity, and sedentary lifestyle.
  10. Acute (<3 months) vs. Chronic (≥3 months) distinction is a primary determinant of prognosis.

DEFINITION & CLASSIFICATION

Definition (Harrison's 22e): Low back pain (LBP) is among the leading causes of years lived with disability worldwide and the principal cause of work-related disability in nearly all industrialized countries.Prevalence: 28–34% of Americans experienced LBP in the past 3 months; >57 million unique patient visits annually. • Economic Impact: Estimated to exceed $300 billion per year in the United States.

Pain Categorization

Importance: Categorization predicts treatment decisions at all levels of care. • Prevalence: >1/3 (range <10–55%) of chronic LBP patients report neuropathic qualities; 10–20% of the total population have nociplastic pain. • Simultaneity: Different pain categories may occur simultaneously. • Table 18-1: Distinguishing Characteristics of Nociceptive, Neuropathic, and Nociplastic Low Back PainNociceptive: → Etiology: Cumulative stress; degenerative spondylosis, myofascial pain → Description: Aching, deep, throbbing; rarely has sensory deficits → Distribution: May be referred into leg (usually proximally) in non-dermatomal distribution → Diagnosis: Imaging correlated with history/physical exam and diagnostic blocks ◦ Neuropathic: → Etiology: Usually preceded by spine degeneration; herniated disk may occur after inciting event → Description: Sharp, shooting, lancinating; common sensory deficits → Distribution: Reflects dermatomal pattern → Diagnosis: History/neurologic exam; instruments like s-LANSS and painDETECT ◦ Nociplastic: → Etiology: Usually insidious; sometimes follows physical/psychological trauma → Description: Similar to neuropathic, but may include nociceptive descriptors → Sensory deficits: Occur sometimes, often outside dermatomal distribution → Diagnosis: History, physical exam (diffuse tenderness), central sensitization inventory, and psychophysical tests.


EPIDEMIOLOGY

Risk Factors: ◦ Female sex ◦ African-American race ◦ Older age ◦ Unemployment ◦ Obesity ◦ Sedentary lifestyle • Phenotypes: Over half of individuals may have mixed pain phenotypes.


ETIOLOGY & PATHOPHYSIOLOGY

Nociceptive LBP: → Typically worsens with activities stressing the structure → Usually secondary to degenerative changes over time → Progression: Generally progressive (except myofascial pain) → Radiation: Mechanical pain may radiate based on magnitude of stimulus; however, referral is typically more proximal and non-dermatomal compared to radicular pain. • Myofascial Pain: ◦ Sources: Muscles, ligaments, and fascia ◦ Histology: Higher levels of neuropeptides (substance P, bradykinin), neurotransmitters (norepinephrine, 5-hydroxytryptamine), and inflammatory cytokines (TNF-α, interleukins) in active trigger points. ◦ EMG: Higher myoelectric tone in patients with back pain compared to controls. • Discogenic Pain: ◦ Prevalence: Reported in 26–42% of patients with axial LBP ◦ Pathophysiology: Degeneration leads to nerve fibers populating the inner annulus and nucleus pulposus; upregulation of inflammatory cytokines sensitizes intradiscal nerve endings. ◦ Mechanism: Tearing/degeneration of annular fibers increases stress on intact rings, exceeding mechanical pain thresholds.


CLINICAL FEATURES

Physical Examination: Used to identify patients requiring advanced therapies (e.g., surgery), but rarely pathognomonic. • Inspection/Gait: ◦ Birthmarks/doughy lipomas → potential spina bifida ◦ Unusual hair patch → underlying bony pathology ◦ Propulsive gait → Parkinson's or antipsychotic use ◦ Spastic gait → central lesion ◦ Waddling gait → muscular dystrophy, scoliosis, or hip pathology ◦ Steppage gait/foot drop → peroneal neuropathy, large herniated disk, GBS, or MS. • Palpation: → Paraspinal tenderness over 'fullness' → muscle spasm or tear (distinguishable via ultrasound) → Midline tenderness → potential ligamentous injury.

Red Flags

Definition: Signs/symptoms suggesting serious spinal (e.g., cauda equina) or nonspinal pathology (infectious, visceral, traumatic, vascular, neoplastic, inflammatory, endocrine). ◦ Prevalence: 92.6% of patients with LBP reported at least one red flag; most common is night pain (58.1%). ◦ Table 18-4: "Red Flag" Symptoms and Corresponding Pathology → Age ≤18 years → Congenital defect, tumor, spondylolysis, or spondylolisthesis → IV drug use → Infection → Recent procedure → Hematoma (complication) or infection → Trauma → Fracture, hematoma → Fever, night sweats, chills → Infection, tumor → Saddle anesthesia / Rapidly progressive symptoms → Cauda equina syndrome


DIAGNOSTIC APPROACH

  1. Initial Clinical Assessment: Perform thorough history and physical exam to establish the foundation for context; treatment decisions should rarely be based on imaging alone.
  2. Identify Red Flags/Urgency: → Presence of red flags or severe/progressive neurologic deficits → immediate investigation/intervention.
  3. Imaging Selection (Based on Duration): → Acute LBP: Image only if red flags or progressive deficits are present. → Chronic LBP: MRI considered case-by-case, especially for surgical planning; MRI does not change management of lumbar epidural steroid injections (ESIs).
  4. Imaging Modality Selection: → MRI: Gold standard for soft tissue (herniation); shows active inflammation. → CT: Better spatial contrast; more sensitive for bone abnormalities; sensitivity >90% for most lumbar pathology including disk herniations. → Plain Films: Used for scoliosis, spondylolisthesis, and fractures (e.g., pars interarticularis).
  5. Physical Examination Maneuvers (Table 18-2):Straight leg raising (SLR): → Sensitivity ≈80% for L5/S1; sensitivity decreases for roots ≤L4. → Note: Unreliable for symptoms from spinal stenosis. • Crossed SLR: → Specificity >85%; low sensitivity. • Femoral stretch: → Sensitivity 50% for L2–L4 nerve root impingement. • SI Joint Provocation (Compression/Distraction): → Distraction (gapping) → combination of ≥3 tests has sensitivity ≥90% and specificity ≥80%. • Standing hip flexion test (SHFT): → Identifies SI joint mobility dysfunction if motions are paradoxical or asymmetrical. • Freiberg's sign: → Assesses sciatic nerve impingement by nonspine structures (e.g., piriformis). • Schober test: → Positive result if distance between lines increases <5 cm; indicates decreased range of motion (not specific for inflammatory arthritis). • Hoover's sign: → Discordant response suggests malingering or functional neurologic disorder. • Tripod sign: → Failure to reduce pain by leaning back/resting hands → may suggest nonorganic pathology. • Waddell signs: → 5 categories: (1) nonanatomic tenderness, (2) sham stimulation pain, (3) distraction, (4) regional disturbances, (5) overreaction. → More positive signs = higher risk of treatment failure.

MANAGEMENT & TREATMENT

  1. Determine Clinical Status: Distinguish between acute (<3 months) and chronic (≥3 months) LBP to determine prognosis.
  2. Initial Management: → Provide optimal nonpharmacologic and pharmacologic treatments.
  3. Imaging-Guided Intervention: → If pain persists/worsens despite treatment or if red flags are present, use imaging (X-ray, CT, MRI) to clarify diagnosis. → Target focal lesions that are physiologically/anatomically plausible for interventional procedures or surgery.
  4. Address Nonorganic Signs: → Identify signs like overreaction or sham stimulation; these indicate psychopathology and correlate with treatment failure.
  5. Consultation: → Seek neurologic or psychiatric consultations prior to interventional procedures if indicated by nonorganic signs or neurological deficits.

PROGNOSIS & COMPLICATIONS

Acute Nonradicular Pain: 80% (1 mo), 67% (3 mo), 57% (6 mo), and 65% (12 mo) of patients experience pain. • Chronic LBP: Stagnant rates of improvement; few improve after 6 months; small percentage worsen. • Radicular Pain: 15–40% experience persistent symptoms at 6 months to 1 year. • Herniated Disks: Typically resorb within 2 years but often reherniate. • Spinal Stenosis: Generally stable; underlying pathology does not recede. • Risk Factors for Poor Outcome: Greater disease burden, older age, psychopathology, poor job satisfaction, and secondary gain. • Red Flag Complications: → Cauda Equina Syndrome (Saddle anesthesia, rapid progression). → Infection/Tumor (Fever, night sweats, chills). → Fracture/Hematoma (Trauma or post-procedure complications).


SPECIAL POPULATIONS

Cauda Equina Syndrome: → Suspected if saddle anesthesia or rapid progression of symptoms occurs. → Action: Assess perianal sensation and rectal exam (sphincter tone); urgent MRI confirmation may be needed. • Nonorganic Signs: → Includes overreaction, pain from sham stimulation, and distraction. → Associated with psychopathology and higher risk of treatment failure.


KEY PEARLS & HIGH-YIELD POINTS

Imaging Rule: Treatment decisions should rarely be predicted on imaging findings alone; history and physical exam are the foundation. • Symptom Correlation: High percentage of abnormalities found on MRI/CT in patients without back pain. • Clinical Distinction: Nociceptive (aching, deep) vs. Neuropathic (sharp, shooting) vs. Nociplastic (high distress, sleep issues). • Radicular Diagnosis: Cross SLR is highly specific (>85%) for radiculopathy; Straight Leg Raise is more sensitive (~80%) for L5/S1.\ • Herniation Dynamics: Most herniated disks resorb within 2 years but are prone to reherniation.


Reference Tables

TABLE 18-1 Distinguishing Characteristics of Nociceptive, Neuropathic, and Nociplastic Low Back Pain

Harrison's 22e, p.118

CLINICAL
CHARACTERISTIC
NOCICEPTIVE PAIN NEUROPATHIC PAIN NOCIPLASTIC PAIN
Etiology Cumulative stress Usually preceded by spine
degeneration; herniated disk may
sometimes occur after inciting
event
Usually insidious, but sometimes occurs after physically or
psychologically traumatic event
Insidious Usually insidious
Examples/causes Degenerative spondylosis, myofascial
pain
Herniated disk, spinal stenosis Nonspecific back pain; may present as mechanical or
radicular pain
Aching, deep, throbbing Sharp, shooting, lancinating
Sensory deficits Uncommon Common Occur sometimes, but often outside of any dermatomal
distribution
May be pain-induced Frequent
Hypersensitivity Occasionally, with myofascial pain Common Extremely common
May be referred into leg (usually
proximally) in nondermatomal
distribution
Reflects dermatomal pattern
Precipitating/relieving
factors
Worse with activities that stress
structure
More unpredictable; spinal
stenosis may be alleviated by
forward flexion
Unpredictable, typically worse with stress
Uncommon Present in up to 25% of patients
Accompanying
symptoms
Co-existing psychopathology common,
and increased rate of neck pain
Higher levels of psychological
stress and quality of life
decrements than in nociceptive
pain
Very high levels of psychological distress and sleep
abnormalities; generally co-prevalent with other nociplastic
conditions
Imaging correlated with history and
physical exam and diagnostic blocks
History and neurologic exam,
instruments such as s-LANSS and
painDETECTa

TABLE 18-2 Summary of Common Physical Exam Maneuvers for the Low Back TEST Lumbar Radiculopathy Straight leg raising…

Harrison's 22e, p.121

TEST DESCRIPTION COMMENTS
Lumbar Radiculopathy
Straight leg raising (SLR) The patient is in a supine position. The examiner passively flexes the leg of
the affected side at the hip, reproducing radicular pain.
SLR has greatest sensitivity (80%) for impingement of the L5 or
S1 nerve roots; sensitivity markedly decreases for nerve roots
cephalad to L4. Unreliable for eliciting radicular symptoms
from spinal stenosis.
Crossed SLR The patient is in a supine position. The examiner passively flexes the leg of
the nonaffected (contralateral) side at the hip, reproducing radicular pain in
the affected leg.
High specificity (>85%) but low sensitivity.
Femoral stretch The patient is in a prone position. The examiner passively extends the leg of
the affected side at the hip, reproducing radicular pain in the thigh.
Modest sensitivity (50%) for L2–L4 nerve root impingement.
Sacroiliac (SI) Joint Provocation
The patient is in a lateral decubitus position with the affected side up, with
hips and knees flexed; the examiner exerts downward pressure on the
superior border of the iliac crest.
The patient extends their unaffected leg while in a supine position.
On the affected side, the examiner flexes the patient’s hip to 90° and
simultaneously flexes the ipsilateral knee while applying downward
pressure along the longitudinal axis of the femur.
The patient is in a supine position. On the affected side, the examiner
applies downward (dorsolateral) pressure on the ipsilateral anterior
superior iliac spine (ASIS).
The patient is in a supine position. On the affected side, the examiner flexes
the patient’s hip and knee and positions the foot under the contralateral
knee (abduction). While stabilizing the contralateral ASIS with one hand,
the examiner uses their other hand to apply downward pressure on the
knee of the affected side (external rotation).
The patient is in a supine position, usually on the edge of an examining
table. The examiner hyperextends the leg of the affected side while
maximally flexing the hip and knee of the unaffected side against the
patient’s abdomen.
SI Joint Mobility/Alignment
Standing hip flexion test
(SHFT; Gillet’s test; Stork
test)
The patient stands upright with both feet on level ground. The patient is
instructed to lift one leg by flexing their hip and knee toward the chest. The
examiner stands behind the patient and observes the spine and pelvis. The
test is repeated in the other leg for comparison.
During hip flexion, the ipsilateral ASIS should rise slightly
while the posterior superior iliac spine (PSIS) drops slightly. If
these motions are paradoxical (i.e., PSIS rises with hip flexion)
or asymmetrical, this suggests SI joint mobility dysfunction.
Deep Gluteal Syndrome/Piriformis Syndrome
The patient is in a supine position. The examiner passively extends, adducts,
and internally rotates the thigh and calf (“log roll”) on the affected side.
The patient is in a supine position. On the affected side, the examiner
flexes the patient’s hip and knee, and while maximally adducting the thigh,
internally rotates the hip.
In a sitting position, the patient is asked to abduct and externally rotate
their hip, eliciting pain.
The patient is positioned in a lateral decubitus position with the affected
side up. Elevating the affected leg elicits pain in the buttocks.
Spondyloarthropathy/Ankylosing Spondylitis
Schober test The patient stands upright, and horizontal lines are drawn across L5 and
10 cm superior to L5. The patient is asked to bend forward and touch
their toes. If the distance between the drawn lines increases <5 cm, this
indicates decreased range of motion and is a positive result.
Numerous modifications exist regarding the location of the
drawn lines. Nonspecific for inflammatory spinal arthritis (i.e.,
other conditions such as discogenic pain associated with
decreased forward flexion can lead to a positive result).
Nonorganic Signs/Functional Disorders
The patient is in a supine position. The examiner asks the patient to flex the
leg of the affected side at the hip, against resistance. If an organic source
of neuropathy or paresis is present, with normal effort, the unaffected leg
will involuntarily push downward on the examination table.
With the patient in a seated position, elevating the affected leg may result
in pain in the leg and back.
Five categories of signs: (1) nonanatomic distribution of tenderness; (2)
pain from sham stimulation (i.e., lumbar pain from gentle downward force
on the shoulders); (3) distraction (i.e., positive SLR test in supine position
but not while sitting, or while preoccupied); (4) regional disturbances (i.e.,
motor or sensory findings that do not correlate with areas of pathology);
and (5) overreaction (i.e., disproportionate physical or emotional responses
on exam).

TABLE 18-4 “Red Flag” Symptoms and Corresponding Pathology Demographics Age ≤18 years Age >50 years Social and…

Harrison's 22e, p.126

Demographics
Age ≤18 years Congenital defect, tumor, spondylolysis, or
spondylolisthesis
Social and Treatment Related
Intravenous drug use Infection
Recent procedure Hematoma (complication after spine
procedure) or infection
Trauma Fracture, hematoma
Symptoms
Fever, night sweats, chills Infection, tumor
Saddle anesthesia Cauda equina syndrome
Rapidly progressive or severe
neurologic symptoms
Cauda equina syndrome
Physical Exam Signs
Saddle anesthesia Cauda equina syndrome