Clinical Evaluation of the Patient with a PDLS

Keywords: radicular pain, pyriformis syndrome, entrapment neuropathy, vascular claudication, axial low back pain, sacro-iliac joint pain, behavioral assessment

5.1 Predominant Neurogenic Pain in Hip and Leg

The surgery of the PDLS is primarily pain surgery. The vast majority of patients who undergo operative therapy do so for radicular pain. It is imperative, therefore, that the surgeon clearly establish that the presenting complaint is radicular and that there is radiographic confirmation of root compromise consistent with the clinical presentation. Frequently, in cases of stenosis, hip/leg pain symptomatology will present in a multidermatomal distribution. In central stenosis, for instance, the patient may present with a nonlocalizing diffuse unilateral or bilateral claudication. Similarly, in patients with unilateral claudication secondary to lateral recess stenosis, the radicular symptomatology may be clear but without definitive localization to a single root.

As radicular pain is the primary operative symptom in PDLS surgery, it is of great importance that the surgeon recognize and document other hip/leg pain syndromes, which may often present quite similarly to that of root compression—and thus avoid surgery on nonsymptomatic radiographic pathology. And patients commonly have coexistent pathologies to that of root pain, and the surgeon must determine the pertinent therapy and priority thereof.

5.1.1 Radicular Pain Evaluation

Historical Points

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  Discern as true radicular symptomatology: note symptoms suggestive of nonradicular pain, or of the absence of dermatomal pattern or sensory symptoms, or of origination from lumbar region; if radiation only into buttocks, then establish para-axial lumbar origination.

  
  
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  Onset: discogenic etiology most likely starting acutely.

  
  
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  Course: length and severity—stable, worsening, improving.

  
  
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  Discogenic or stenotic presentation: discogenic pain usually worse in sitting position; stenosis presenting with pain worse in upright position. If pain is worse in upright position, confirm neurogenic claudication: pain often severe in arising from chair; pain worse in walking up slight grades or stairs (occasionally worse walking down grades); pain relieved by sitting or bending forward. Mechanistically sitting stabilizes the pelvis, allowing the patient to reduce lumbar lordosis in a “slumping” posture. In the upright position, the patient can accomplish similar reduction in lumbar lordosis by anterior thrust of pelvis (hip extension/retroversion) and flexion of knees/ankles (▶ Fig. 5.1).

  
  
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  Motor symptoms consistent with suspected root involvement: weakness of foot dorsiflexion or slap-foot ambulation (L5); or weakness in leg/knee going up stairs (L3/L4); weakness in hip flexion getting into car (L1, L2, L3).

  
  
  
  

  Fig. 5.1 Postural compensation for lumbar stenosis: pelvis retroversion and knee flexion to provide support and balance for forced reduction of lumbar lordosis.

  
  

  

Minimal Examination with Radicular Pain—Focused on Suspected Root(s) Involvement

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  Lasègue (straight leg raise [SLR]): note degree bilaterally.

  
  
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  Dorsiflexion weakness: extensor hallucis longus/foot.

  
  
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  Deep tendon reflex (DTR) asymmetry in unilateral radicular pain syndrome: to confirm suspected root involvement (decreased patellar reflex [L4] and Achilles reflex [S1]).

  
  
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  DTR in claudication syndrome: patellar–Achilles disparity supporting stenosis at L4–L5.

  
  
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  Important: active Achilles reflexes in symptomatic lumbar stenosis mandate focused myelopathic history/examination for symptoms and signs in upper extremities to rule out concurrent cervical stenosis.

  
  
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  Atrophy: calf (S1) and quadriceps (L3/L4).

  
  
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  Ambulation: normal (for evidence of limp or hip waddle); toe-walking and heel-walking for evidence of nonphysiologic component, when suspected.

  
  
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  Additional exam with suspected nonradicular or concurrent etiology: degenerative hip signs; sacroiliac joint (SIJ) or piriformis tenderness; pedal pulses (note: presence of one palpable pedal pulse does not exclude vascular pain).

Radiographic Studies

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  Magnetic resonance imaging (MRI) is mainstay of radiographic confirmation of root compression—consistent with root(s) involved as determined clinically.

  
  
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  Plain lumbar spine films:

  
  
  
  
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    Standard anteroposterior/lateral to assess for any unusual bony pathology or any anatomic variant.

    
    
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    Standing flexion/extension to assess for abnormal translational movement. Mandatory in patients with listhesis and/or stenosis. ¹ And comparison of standing films with supine alignment (MRI or computed tomography [CT]).

5.2 Radicular Pain Presenting Predominantly in the Lower Back

Radicular pain can present with pain in para-axial lumbar region. This pain is not dermatomal but rather is dorsal rami pain via medial and intermediate branches (to facet and musculature). Thus, the common discogenic radicular pain from herniated nucleus within the spinal canal commonly radiates from this region. In contrast, spinal nerve pain from a lateral herniated nucleus pulposus will not present with para-axial lumbar pain.

Similarly, the radicular pain of lumbar stenosis often involves the para-axial lumbar spine and can be predominantly such. Hence, occasionally, patients with symptomatic lumbar stenosis will present with ambulatory/standing pain, unilateral or bilateral, in the para-axial lumbar area, sometimes radiating into the hips, but without overt leg pain (claudication).

5.3 Syndromes of Nonradicular Neurogenic Leg Pain

5.3.1 Piriformis Syndrome

Introduction

The piriformis syndrome remains a controversial diagnosis without consensus as to pathophysiology and diagnostic criteria. However, therapeutic results suggest that it is a bona fide clinical entity. ² Injection therapy can result in a good response, sometimes with lasting benefit. And in refractory cases, surgical exploration/decompression also has been reported, in several studies, to have a success rate of about 80%.

History

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  Pain emanating from buttocks without lumbosacral involvement.

  
  
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  Pain worse with sitting.

  
  
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  Possible dyspareunia in females.

  
  
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  Possible history of trauma to buttocks—recent or remote.

  
  
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  Pain predominantly of peroneal division of the sciatic nerve.

Examination

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  Unequivocal tenderness at sciatic notch (most sensitive/specific).

  
  
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  Straight leg raising—if positive, pain referred to buttocks (and not to lumbosacral spine).

  
  
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  Provocative contraction of piriformis: resisted abduction of legs in seated position ³; resisted abduction of flexed leg when in lateral decubitus position with asymptomatic side down. ⁴

  
  
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  Provocative stretching of piriformis: forceful internal rotation of extended leg ⁵; forceful internal rotation with hip flexed and leg adducted.

Image Pathology

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  Piriformis hypertrophy or abnormality (relative to asymptomatic side) on MRI or CT.

  
  
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  Piriformis asymmetry/sciatic nerve hyperintensity on MR neurography.

Electrodiagnostic Pathology

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  Delayed F waves and H reflex on nerve conduction studies (with external rotators tightened).

  
  
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  Delayed somatosensory evoked potentials (at entry to buttocks) on nerve conduction studies.

  
  
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  Electromyography (EMG) showing extrapelvic (nonradicular) compression.

Treatment

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  Physical therapy: stretching, massage, and ultrasound, osteopathic manipulation.

  
  
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  Guided injections: local anesthetic/steroids; botulinum type B.

  
  
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  Surgical exploration.

5.3.2 Other Entrapment Neuropathies

Essentially, any peripheral nerve in the leg can be either entrapped or injured and thus become symptomatic. There are three relatively common symptomatic presentations which are referred to the PDLS surgeon, as they may resemble a sciatic symptomatic distribution. It is not difficult to differentiate these entities from more common radicular syndromes, but only when a dedicated symptom-focused evaluation is performed. A perfunctory history/exam in such a patient with an “abnormal” MRI will result in missed diagnosis and unnecessary and unsuccessful surgery.

Neuropathy of the Lateral Femoral Cutaneous Nerve ⁶

Anatomy/pathophysiology: The lateral femoral cutaneous nerve is derived from posterior division of L2 and L3. Pathologic involvement occurs as it passes through the inguinal ligament just medial to the anterior superior iliac spine.

Symptomatology: Meralgia paresthetica is a common condition represented as hypesthesia/painful paresthesias of the cutaneous distribution of this afferent nerve. It does not have origin at the lumbar or buttocks region, and no symptoms should exist distal to the knee. In males, it is characteristically symptomatic by irritation from items in the over-lying trouser pocket and is often associated with a pendulous abdomen. In females, obesity also may precipitate it, or it may develop during pregnancy and persist after labor. Diabetes is the main comorbid factor as with any entrapment neuropathy.

Examination: Examination reveals hypesthesia in the characteristic distribution of the anterior/lateral thigh. There is usually asymmetric tenderness to deep pressure medial to the anterior superior iliac spine.

Therapy: Meralgia paresthetica is usually medically manageable (e.g., gabapentin) and is self-limiting. Rarely is surgery required. Its recognition by the PDLS surgeon will often save considerable diagnostic expense.

Neuropathy of the Common Peroneal Nerve ⁶

Anatomy/pathophysiology: The common peroneal nerve (L4–S1) divides just distal to the fibular head into the deep and superficial branches. These, respectively, supply the dorsiflexors and evertors of the foot. Sensory distribution is to the dorsum of foot, usually sparing the fifth digit. The common pathologic compression at the fibular head usually spares the lateral cutaneous branch to the lateral calf.

Symptomatology: This neuropathy is usually associated with some history of compression: cast, legs crossed, occupational position, etc., and/or with some form of peripheral neuropathy. However, it rarely can occur de novo in an elderly patient. Here, it is usually more symptomatic with walking and can be misinterpreted as an L5 radicular claudication, especially with concomitant lumbar degenerative symptoms. However, the motor dysfunction (slap-foot, steppage gate) is out of proportion to pain symptomatology.

Examination: Dorsiflexion weakness may or may not be demonstrable, as symptoms often are intermittently related to walking or other activities. Asymmetric tenderness at the fibular neck is usually present. Palpation of popliteal fossa is important in presence of symptoms suggestive of involvement of lateral cutaneous branch at lateral calf.

Evaluation: Definitive diagnosis by electrophysiologic testing. With sensory symptoms representing lateral cutaneous branch, MRI evaluation of popliteal fossa region indicated. Toxin screen (especially lead) may be indicated.

Therapy: Surgical exploration/decompression may be indicated when there is no acute compressive history and/or generalized peripheral neuropathy.

Neuropathy of Superior Cluneal Nerve ^{7,​ 8,​ 9}

Anatomy/pathophysiology: The superior cluneal nerve is a cutaneous afferent nerve deriving from the posterior rami of LI–L3. It perforates the thoracolumbar fascia just proximal to the ilium 7 to 8 cm from the midline supplying the skin of the lateral buttocks.

Symptomatology: Primary point of pain (PPP) described as radiating distinctly from ilium lateral to erector spinae at point of fascial perforation, radiating to lateral hip/thigh; without lumbar para-axial origin; usually worse with lumbar extension; often worse with walking and characteristically relieved by rest.

Examination: Tenderness at PPP with or without Tinel’s sign.

Evaluation: Clinical diagnosis without specific diagnostics.

Therapy: Injection with local anesthetic/steroids reported to be successful. ¹⁰ Refractory cases may require surgical decompression. ¹¹

5.4 Nonneurogenic Leg Pain

5.4.1 Vascular Claudication

Introduction

Vascular leg pain/claudication is underdiagnosed by the spinal surgeon. It can present in a localized distribution suggestive of a dermatomal representation. It exists concomitantly in 25% of cases with neurogenic claudication. The surgeon should consider vascular evaluation in any patient with equivocal clinical–radiographic correlation for neurogenic claudication or with abnormal pedal pulse exam.

History (Suggestive of Vascular Etiology)

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  Usually positive for other atherosclerotic arterial pathology and other risk factors (diabetes, hypertension, hyperlipidemia, smoking).

  
  
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  Rarely involves lumbosacral or iliac areas.

  
  
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  Claudication localized and nonradiating.

  
  
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  Claudication usually distal to knee but can involve buttocks/thigh.

  
  
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  No pain with standing or arising from chair.

  
  
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  Without dermatomal sensory symptoms.

  
  
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  Without subjective motor symptoms.

Examination

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  Clinical evaluation has limited reliability in distinguishing vasculogenic claudication. ^{2,​ 12,​ 13}

  
  
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  Attenuation or absence of pedal pulses (either dorsalis pedis or posterior tibialis) in only 60 to 70% of patients.

  
  
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  Poor sensitivities of palpable attenuation of popliteal and femoral pulses preclude their value in examination.

  
  
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  Noticeable palpable difference in temperature (cooler) of symptomatic side versus asymptomatic is significant.

Investigation

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  Ankle-brachial index (ABI ≤ 0.9) sensitive screening test for presence of peripheral arterial disease (PAD).

  
  
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  Exercise ABI for definitive diagnosis in patients with normal ABI.

  
  
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  Toe-brachial index (TBI ≤ 0.6) has stronger association with severity of PAD symptoms than ABI.

  
  
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  TBI recommended in patients with foot symptoms or severe diabetics, or as definitive study in elderly patients who cannot tolerate exercise ABI.

  
  
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  Only about 50% of patients with abnormal ABI have vascular claudication; hence, abnormal ABI does not prove vascular etiology of claudication symptoms.

  
  
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  However, a normal ABI essentially precludes vascular claudication (with symptoms above ankle).

  
  
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  EMG protocol of paraspinous mapping may be definitive to establish neurogenic claudication in cases of questionable diagnosis.

Treatment

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  All patients with abnormal ABI need vascular surgery referral (if ABI ≤ 0.5, then referral needs to be urgent) before lumbar surgery.

  
  
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  In patients with lumbar stenosis with clinically consistent claudication, a normal ABI rules out concomitant vascular claudication.

  
  
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  When neurogenic etiology for leg pain is not well defined in patients with normal ABI, more definitive studies for a vascular etiology (above) may be indicated.

5.4.2 Degenerative Hip Disease

Introduction

The pain of hip joint osteoarthritis may be difficult to distinguish from that from lumbar stenosis. And, not uncommonly, the two pathologic degenerative conditions coexist within the same patient, thus requiring prioritization of therapy. ¹⁴

Anatomy

Innervation of the hip joint stems from L2 to S1 via ventral rami and their contributions to the femoral, obturator, sciatic, and superior gluteal nerves. This broad multilevel source of innervation would account for the manifold presentation of hip joint pain via pain-referral mechanism.

History

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  Pain in the leg usually with hip pain in ambulating.

  
  
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  Pain in groin and/or buttocks most prevalent but pain can exist in anterior and/or posterior thigh and anterior knee.

  
  
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  Pain distribution is not restricted to above knee and may involve shin/calf.

  
  
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  It can present with a lateral leg distribution, closely mimicking a stenotic L5 monoradicular claudication.

  
  
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  Pain in bed with lateral recumbency and with the symptomatic side down is characteristic.

  
  
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  Of note, there are rarely sensory symptoms reported (the existence of which would mitigate strongly in favor of a neurogenic etiology).

Examination

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  Pain and restriction of motion with hip manipulation, especially with bent-knee thigh rotation (FABER test).

  
  
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  Definite tenderness at posterior greater trochanter and/or groin.

  
  
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  Observation of ambulation often reveals a distinctive waddle (when the patient elevates the diseased hip in order to rotate it forward).

  
  
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  Testing for hip contracture: forced supine extension; the Thomas test.

Investigation

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  Plain X-rays and CT scan will usually be appropriately positive.

  
  
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  An MRI scan may be required when there is incongruency between the bony radiography and symptoms. (Note: avascular necrosis may be diagnosed only via MRI.)

  
  
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  Diagnostic block of the hip joint is meaningful only if it yields an unequivocally positive response.

  
  
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  A diagnostic block of L5 may resolve the hip pain (because of the dominant contribution of this nerve to joint innervation) and thus is not useful to distinguish hip joint pain from radicular claudication.

Treatment

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  Referral to an orthopaedic surgeon.

  
  
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  With evidence of concomitant symptomatic stenotic radiculopathy, initial root decompression will allow appropriate rehabilitation after hip surgery.

5.5 Chronic Pain Predominant in the Lower Back

5.5.1 Nonspecificity of the Term “Chronic Low Back Pain”

The NIH Task Force defined “chronic low back pain” (CLBP) as pain involving the area between the lower posterior margin of the rib cage and the horizontal gluteal fold (i.e., lumbar/sacral-coccyx/buttocks) which has been an ongoing problem for at least 3 months to the extent that it has been problematic for at least half the days over the past 6 months. ¹⁵ This definition has no anatomic specificity that is relevant to pathophysiologic processes. And yet hundreds of investigational articles have been published, and continue to be, concerning therapeutic intervention on this amorphous entity; all such publications are corrupted by the lack of clinical specificity.

Presently, the subclassification of CLBP is one the greatest imperatives in the science of spine care. There has been no substantial progress in this endeavor since the seminal paper of Bernard and Kirkaldy-Willis 30 years ago. ¹⁶

The “problem” in chronic lower back pain classification has been well defined. ¹⁷ The legitimization of pain by diagnostic labeling has far-reaching ethical consequences. Such labels as “annular tear,” “bulging disc,” “facet pain,” “discogenic,” etc., are theories of pain etiology that are not subject to falsifiability testing and thus cannot be considered “scientific theory.” In fact, diagnostic labels and etiologies are regularly falsified. Therapy (result) is not considered to have diagnostic value, and untestable hypotheses are used by practitioners to account for treatment failures: “poor technique,” ”poor patient selection,” “psychosocial profile,” etc. And, thus, the patient must bear this failure as a “difficult,” “challenging,” or “problem” patient. And, although the label has been falsified, the diagnosis is recirculated and used on the next willing and able patient. ¹⁷

A recent study has subgrouped “nonspecific” lower back pain according to clinical course patterns (trajectories). ¹⁸ The documentation of such patterns would have more clinical relevance if they could be related to a greater specificity of symptom presentation. This could be provided by a subclassification system based on precise clinical description. This is the fundamental step in eliminating the “nonspecificity” of lower back pain, and would establish a foundation for developing etiological and therapeutic investigation.

5.5.2 Precise Clinical Description of Pain in the Lower Back

Precision of terms: the term “chronic low back pain” (and its acronym “CLBP”) should be abandoned as it is not a clinical entity. It needs to be subclassified anatomically relevant to a specific area within the lower back. The acronymic “L” should refer to the “lumbar” area (and it will be done so in this book when used outside the use of the common non-specific term “CLBP”).

Localization of the Primary Point of Pain (PPP) is defined as area of “worse pain” or where “pain starts” or “trigger point of pain” and localized by patient’s hand and confirmed with the examiner’s hand.

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  Area: upper lumbar, midlumbar, lower lumbar; sacrum; coccyx; hip.

  
  
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  Laterality: axial (midline); para-axial; flank (if lumbar area); medial hip (ilial); central hip; lateral hip (femoral); inferior hip (gluteal fold).

  
  
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  Side/symmetry: right; left; predominant side if bilateral.

  
  
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  Radiation (precise description).

5.5.3 Specific Activity Causing Exacerbation of Pain

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  Lumbar flexion/compression: sitting; bending forward (grossly or slightly as in standing at the sink).

  
  
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  Lumbar extension: standing erect; walking, going up stairs; recumbency; reaching overhead.

  
  
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  Antigravity: elevating from bent-over position; getting things off floor; getting out of chair.

  
  
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  Nocturnal recumbency (note any specific position).

  
  
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  No specific exacerbating physical activity determined.

5.5.4 Evaluation of Chronic Pain Predominant in the Lower Back

Historical Points

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  Definition (see above).

  
  
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  Precise localization of pain (see above).

  
  
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  Mechanisms of exacerbation (see above).

  
  
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  Onset and course (of progression or remittance).

  
  
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  Secondary symptoms in hips/legs.

Examination

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  Observe if patient has difficulty arising from chair to examining table.

  
  
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  Extend/tilt patient to right/left to reproduce unilateral pain.

  
  
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  Grading scale for mechanical (antigravity) axial pain: Flexion/re-erection: ask patient to touch toes with knees unflexed—note if any pain on flexion and grade antigravity pain (on re-erection):

  
  
  
  
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    Grade 0—patient re-erects without noticeable difficulty and denies any pain.

    
    
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    Grade 1—patient re-erects without noticeable difficulty but admits some pain (subjective pain).

    
    
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    Grade 2—patient re-erects with noticeable difficulty (slowly = objective pain).

    
    
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    Grade 3—patient re-erects with assistance (pushes on knees or furniture, etc.) (▶ Fig. 5.2).

    
    
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    Grade 4—patient has pain/muscle spasm in standing, will not attempt flexion, may have crutch or cane.

  
  
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  Palpate PPP area (lumbar or buttocks) in prone position: in patients with antigravity pain, note any area/level of exquisite tenderness with fasciculations in midline to thumb pressure; in patients with focal unilateral pain, note focal area of tenderness to thumb pressure (vs contralateral asymptomatic side); in patients with primary buttocks pain, palpate primary pain site.

  
  
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  Observation of normal ambulation.

  
  
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  Provocative tests (hip, SIJ, piriformis) when pain not clearly from lumbar generator (see above for detail).

  
  
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  Examination for leg-length discrepancy.

  
  
  
  

  Fig. 5.2 Axial antigravity pain, grade 3: patient requiring assistance in elevating from seated or flexed position.

  
  

  

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