Diskogenic pain from the lumbar spine, unlike the facet and sacroiliac joint, is highly variable and depends on whether the disk itself has intimate contact with neighboring tissues. Diskogenic pain is predominantly reported in the lower back, focal to the site of involvement. Evidence suggests that central disk disorders would produce central LBP, with right-sided disk disease producing focal right LBP.5,8 Sources of referred pain from diskogenic disorders seem interdependent on the affected tissue, whereas disk protrusion compressing a nerve root would be expected to cause back and buttock pain, as well as symptoms in the leg and foot, representative of the particular nerve root pattern of innervation. Unique to diskogenic disorders is the concept of variable pain patterns often referred to as centralization and peripheralization.7,8 Centralization occurs when symptoms move from distal to a more proximal location,16 and it tends to be a positive prognostic indicator because it implies a clinical presentation amenable to treatment.17 Peripheralization, conversely, occurs when symptoms extend or move in a distal manner16 and is generally a poor prognostic indicator.17 More serious disk disease, such as extrusions or large protrusions compressing a nerve root, are more likely to peripheralize in response to interventions. From a clinical perspective, it would seem logical that right-sided diskogenically induced LBP pain that peripheralizes into the foot with movement or over time is suggestive of a morphologic change (e.g., progression from a bulge to a protrusion or extrusion) suggestive of nerve root irritation. Conversely, centralization may imply resolution of intimate contact between the disk and neighboring tissue or a more anatomic relocation of a displaced nucleus.11,18,19
Although nerve root or dorsal root ganglia irritation from a chemical or mechanical means is indeed a source of pain, each nerve root generally manifests with a unique symptom location that allows clinicians to discern the location of the disorder (Table 10-2). Other than symptom patterns, the presence of neurologic signs such as hypoactive deep tendon reflexes, diminished sensation, and motor impairments alludes to a nerve root disorder.20 The etiology of nerve root–related pain is multifactorial, and in the case of pain referring into the hip, this pain is often the result of a lumbar disk herniation or foraminal stenosis present at the upper lumbar spine. The following section outlines the expected clinical presentation of the various nerve roots that may be affected in patients with lumbosacral disorders.
Physical Examination Findings for Lumbar Segmental Nerve Root Lesions
|T12||None||Lower abdominal and inguinal area||None|
|L1||None||Back, anterior thigh, as well as medial upper thigh||None|
|L2||Psoas and hip adductors||Back to anterolateral to proximal medial thigh||None|
|L3||Psoas and quadriceps||Back, upper buttock to anterior and medial thigh to knee||Diminished or absent patellar reflex|
|L4||Tibialis anterior and extensor hallucis||Medial buttock, lateral thigh to medial lower leg and medial aspect of foot||Diminished or absent patellar reflex|
|L5||Extensor hallucis, peroneals, gluteus medius, and dorsiflexors||Buttock, posterior and lateral thigh to anterolateral aspect of leg to the dorsum of foot||None|
|S1||Ankle plantar flexors, hamstrings, and peroneals||Buttock, thigh, and posterior leg and lateral foot||Diminished or absent Achilles reflex|
|S2 to S4||Diminished control of the pelvic floor muscles contributing to inhibited control of bowel and bladder control||Perineum, genitals, and lower sacrum||Absent or diminished anal wink|
Nerve Root Lesions
Nerve root lesions of the lower thoracic and lumbar spine typically refer pain distally into the hip, thigh, lower leg, and foot5 (Fig. 10-2). Symptoms distributed in these regions may give the impression of hip pain in some cases; however, a clear description of referral patterns for each nerve root may provide the clinician with insight into potential sources of pain. Moreover, nerve root lesions produce a host of signs and symptoms (paresthesia, myotomal weakness, sensory disturbance) not commonly encountered in hip disorders. When a nerve root is chemically irritated or mechanically compressed in the absence of neurapraxia or axonotmesis (temporary or more permanent loss of conduction with degeneration), only nerve root symptoms would be expected during the clinical examination.
T12 Nerve Root Lesion
The twelfth thoracic nerve root exits between the twelfth thoracic and first lumbar vertebrae. Nerve lesions at this level often refer symptoms from the midback coursing around the torso to the lower abdominal region. Ventrally, the symptoms would manifest proximal to the iliac crest to the region just superior to the public symphysis (see Fig. 10-2, A). Generally, no myotomes or deep tendon reflexes are attributed to this level. A key differentiating factor here is the pain pattern. Symptoms associated with thoracic nerve root disorders manifest around the thorax at the approximate level of the lesion.
L1 Lumbar Nerve Root Lesion
The first lumbar nerve root exits between the first and second lumbar vertebrae. A lesion of the first lumbar nerve root would refer symptoms from the midback, around the torso to the lower abdominal region and proximal medial thigh. Ventral symptoms would reside over the pubic symphysis (see Fig. 10-2, B). Generally, no myotomes or deep tendon reflexes are attributed to this level.
L2 Lumbar Nerve Root Lesion
The second nerve root exits between the second and third lumbar vertebrae. A lesion at this level would refer symptoms from the midback, around the torso to the proximal anterior and medial thigh (see Fig. 10-2, C). Examination may reveal weakness of the psoas and hip adductors.
L3 Lumbar Nerve Root Lesion
A third lumbar nerve root lesion often refers symptoms along the midlumbar spine that extend to the upper buttock, coursing in an oblique pattern to anterior and medial thigh, ending at the knee medial to the patella (see Fig. 10-2, D). Examination findings may include a weakness of the psoas and quadriceps, as well as diminished patellar tendon reflexes.
L4 Lumbar Nerve Root Lesion
The L4 nerve root exits between the fourth and fifth vertebrae. Patients with a fourth lumbar nerve root lesion may describe pain located in the midlumbar spine, outer thigh, and leg extending to the medial foot and great toe (see Fig. 10-2, E). They may also demonstrate weakness of the tibialis anterior and possibly great toe extension. Furthermore, the patellar tendon reflex may be diminished or absent.
L5 Lumbar Nerve Root Lesion
The L5 nerve root lies between L5 and the first sacral vertebra. Patients with a fifth lumbar nerve root lesion generally describe pain in the sacroiliac region, as well as the lower buttock, lateral thigh, down to the anterolateral leg and dorsum of foot excluding the first and fifth toes (see Fig. 10-2, F). Weakness of the extensor hallucis longus, peroneals, gluteus medius, and dorsiflexor muscles may be present.
S1 Nerve Root Lesion
First sacral nerve root lesions refer symptoms, which may be described as low back and buttock pain that extends to the plantar aspect of the foot and heel (see Fig. 10-2, G). On examination, myotomal weakness of the gastrocnemius-soleus complex, peroneals, and hamstring muscles may be identified. On further examination, the patient may also have atrophy of the gluteal and intrinsic foot muscles, as well as hypoesthesia of the calf and lateral foot. The Achilles deep tendon reflex may be diminished or absent.
S2 to S4 Nerve Root Lesion
Although a lesion of the second, third, or fourth sacral nerve root is rare, it may be present as a result of disk herniations, cyst formation, malignant disease, or trauma. These lesions are often described as pain in the lower sacral or peritoneal and genital area (see Fig. 10-2, H). In addition, patients may describe saddle paresthesia and demonstrate a diminished or absent anal wink. Irrespective of the specific diagnosis, neuropathic pain manifests as radiculopathy, and each nerve root has a relatively consistent clinical presentation, as outlined in Table 10-2.
Changes in bowel or bladder function, as well as saddle region sensory changes, are pathognomonic for cauda equina syndrome. Cauda equina syndrome, when suspected, is a medical emergency because of the potential for incomplete neurologic recovery. Patients suspected of having cauda equina syndrome should be referred for emergency medical care immediately. Depending on the cause of symptoms, patients may benefit from surgical intervention to relieve pressure on the involved nerve root. Ahn and colleagues21 published a metaanalysis of surgical outcomes after cauda equina syndrome secondary to lumbar disk herniation. When disk herniation was involved, the most common levels were L1 to L2 (27%), L3 to L4 (26%), and L5 to S1 (22%), whereas levels least often involved were L4 to L5 (16%) and L2 to L3 (9%). The findings of this study reinforce the importance of immediate medical care. A significant difference was found when comparing patients receiving surgical decompression before and after the 48-hour mark. Patients who underwent surgical treatment within 48 hours demonstrated greater resolution of sensory and motor deficits, as well as better urinary and rectal function.
Further to pain location, changes in response to testing may assist in the clinical evaluation and decision-making process. As stated previously, activity isolated to a particular region that provokes concordant symptom reproduction adds to the diagnostic process from a face validity perspective. Moreover, symptoms originating from the lumbar spine that change in response to movement may provide insight into the cause. Primary reference to a change in symptoms in response to testing involves the concepts of centralization and peripheralization, which are invariably linked to diskogenic disorders.11 Patients with spinal stenosis are more likely to peripheralize with extension or ipsilateral lumbar flexion and to report symptom resolution with lumbar flexion or contralateral lateral flexion. More importantly, when a patient’s symptoms centralize or peripheralize in response to lumbar movements, the clinician may eliminate hip disease as the source of symptoms. Furthermore, evidence suggests that symptoms arising from the sacroiliac joint and facet disorders neither peripheralize nor centralize in response to movements.7
Although pain sources and associated referral patterns have been defined in the literature, clinicians should not solely rely on location (in lieu of a prudent clinical examination) as their source for diagnosis because overlap exists. The next section of this chapter presents clinical characteristics for the more common sources of lumbosacral disorders that may refer pain to the hip and pelvis. Although a baseline discussion of pathologic features for each condition is given, the objectives reside in providing content imperative to the differential diagnosis. A discussion of interventions for treating lumbosacral conditions is beyond the scope of this chapter.
The differential diagnosis of pelvic and hip disorders is often complicated by competing pathologic conditions with a similar pain referral location, as well the prevalence of concurrent disease. This section discusses selected lumbosacral disorders that should be considered when a patient presents with hip pain and the underlying cause is not clear. Information is provided in the context of the differential diagnosis of lumbosacral disorders from an evidence-based perspective using studies that are inclusive of diagnostic reference standards where applicable. In cases where there is a paucity of evidence, a pragmatic approach grounded in biologic plausibility is presented.
Trigger Points and Myofascial Pain
Although evidence from pain pattern and diagnostic studies rarely implicate muscle or fascia as a source of chronic pain, muscle or fascia is nevertheless an established source of clinical symptoms. Some reports suggest (based on the clinical examination) that approximately 85% of the population will report myofascial pain during their lifetime.22 Myofascial pain syndrome (MPS) is characterized by the presence of a myofascial trigger point, which has been defined as a tender point in a taut band of muscle.23 Trigger points typically are characterized by an area of muscle tenderness that can be provoked by palpation or mechanical stimulation.24 This stimulation also produces referred pain that is perceived at a location distal from the trigger point.25 Two primary types of trigger points are active and latent trigger points.24 Active trigger points contribute to symptoms at rest, and the familiar symptoms are reproduced when pressure is placed on them. Latent trigger points generally are not symptomatic at rest and cause symptoms only when pressure is placed over the offending area.24
The pathogenesis of myofascial pain is not fully understood. Mechanical stress, metabolic deficiencies, and psychological influences have all been found to interact with myofascial pain.26 Several contributing factors to the pathophysiology of myofascial tenderness have been suggested, including trauma, overuse, poor posture, psychological stress, mechanical overload, growth hormone deficiency, inflammatory diseases, alcohol toxicity, and constrictive clothing.27,28 Maintaining prolonged postures and repetitive activities with light loads may be mechanisms of injury that a patient would not recognize as readily as he or she would a specific traumatic event.29
Patients with myofascial pain and trigger points in the lumbopelvic region generally report pain without a specific mechanism of injury. Symptoms are often provoked with prolonged static positions and are generally referred to distal locations.25 Patients describe muscular pain as being steady, aching, and deep, whereas examination findings reveal specific tenderness that provokes familiar symptoms with focal pressure. Patients also may have a taut band and “twitch response” to palpation. Referral patterns vary; however, those muscles with the most common referral patterns in the lumbopelvic hip complex are the iliopsoas, gluteus medius, quadratus lumborum, piriformis, erector spinae, and hamstring muscles (Fig. 10-3). Although some of the trigger points and structures responsible for myofascial pain may indeed be anatomically classified with the hip itself, myofascial disorders can be differentiated from other competing disorders such as extraarticular strains or nerve root disorders based on both symptom location and areas of tenderness. Moreover, an absence of macrotrauma or microtrauma may help steer the clinician away from extraarticular pathologic conditions.
Diskogenic disorders are significant contributors to LBP and are the primary source of pathologic conditions in many studies investigating sources of lumbosacral disorders.5–8 Descriptions of diskogenic disorders range from internal disk derangements to annular tears and extrusions. Diskogenic disorders with external morphologic changes such as protrusions, extrusions, and sequestrations may produce symptoms stemming from the annulus itself or from contact with structures such as the dura matter and nerve roots.
The mechanism of injury is variable, ranging from no apparent reason to activities such as combined flexion with rotation or lifting. During rotation, a majority of force is accommodated or resisted by the contralateral facet joint, as well as by the supraspinous ligament. Therefore, the disk alone provides a minority of resistive force during rotation. However, when rotation is coupled with other movements, such as flexion and rotation, the disk may be at greater risk for injury. The annulus is most susceptible in the posterior or posterolateral fibers.30 This again is another reason that specific combined movements such as flexion and rotation may be caustic to disk function.
The degenerative process can contribute to diskogenic disorders as well. Normally, the intervertebral disk is a closed system, and compressive forces expand the nuclear material outward, thereby placing greater internal pressure on the annulus. During the degenerative process, the annular fibers degrade and become unable to accommodate these forces. This desiccation of the disk leads to narrowing disk height and the potential for encroachment of key spaces in the spinal column. In time, the degenerative sequelae of the disk itself may lead to spondylosis or degenerative changes in the spine.
Box 10-1 provides an overview of characteristics of diskogenic disorders. Patients with diskogenic symptoms may report pain that is isolated to the lower back or may describe referred or radicular symptoms. Diskogenic symptoms may manifest in the midline, bilaterally or unilaterally, and referral depends on structures mechanically compressed. In the early stages or in less complex cases of diskogenic disorders, patients often report central or unilateral LBP. Diskogenic lesions on the right side of disk tend to produce right-sided symptoms, whereas central disease tends to produce central or bilateral LBP.5 Pain referral is often from the posterior annulus and posterior longitudinal ligament and in some cases may refer to the buttock region. If the diskogenic lesion contacts the dura, symptoms may be referred to the thigh; however, pain that follows a specific nerve root pattern (as described in the pain referral section of this chapter) suggests nerve root compression. Nonetheless, as the degenerative condition progresses, key spaces in the spine may be compromised, and patients may have a clinical presentation of foraminal stenosis (discussed in next section). If the lateral foraminal canal is occupied by disk herniation, patients may present with unilateral symptoms in a distribution consistent with the involved nerve root level.31
Generally, patients with diskogenic disorders describe some positions or movements that decrease symptoms and others that provoke them, a situation that indicates a directional preference. A directional preference is present when movements or positions in a particular direction decrease or abolish pain or cause referred pain emanating from the spine to centralize or retreat in a proximal direction.32 The previous section on centralization and peripheralization provides insight into more common symptom responses to movement. In particular, evidence suggests that these patients will have pain with sitting to standing or with prolonged sitting and generally can walk off their symptoms (see Box 10-1).
On examination, these patients often have positive neural tension signs assessed by the straight leg raise (Fig. 10-4), crossover sign (Fig. 10-5), or Slump sit test (Fig. 10-6) if compression of lower lumbosacral nerve roots (or dura matter) exists, whereas a prone knee flexion test (Fig. 10-7) would predict upper lumbar dura or root compression.33 In particular, a positive straight leg raise result has an odds ratio of 3.7 for disk herniation, whereas a positive crossover sign demonstrates an odds ratio exceeding 4.0. Reduced deep tendon reflexes and motor or sensory loss may exist in cases of prolonged compression when a neurapraxia has developed. Additionally, patients with a loss of extension during the physical examination are thought to have a presentation associated with diskogenic symptoms.12 Patients with diskogenic disorders who centralize in response to lumbar movements in a particular direction (e.g., directional preference) are thought to have a good prognosis, whereas those who peripheralize in response to movements in all directions are more likely to have a poor prognosis. In particular, patients with diskogenic disorders often experience centralization with lumbar extension with or without laterally directed movements of positioning.
A study by Donelson and colleagues11 compared the clinical examination with the diagnostic gold standard for disk disease (i.e., diskography) and found that patients with diskogenic disorders were likely to centralize, with the exception of those patients with a disk extrusion or incompetent annulus, who were likely to peripheralize in response to both flexion and extension.
Spondylosis refers to spinal degenerative osteoarthritis that begins at the disk and progresses along the articulation between the neural foramina or zygapophysial joints.34 If the condition is advanced, it may compromise the central or lateral foraminal canal and contribute to motor or sensory disturbances, which include muscle weakness, pain, or paresthesia.35 The end progression of spondylosis is spinal stenosis. Spinal stenosis is a narrowing of specific spaces in the spine that include the lateral foraminal or central canal. Narrowing of these spaces often contributes to LBP and leg pain, which are exacerbated with activities such as standing or walking. It is most common in patients older than 48 years of age and is one of the primary reasons for surgical treatment in patients older than the age of 65 years.30,36
Activities that compromise the posterior spinal elements include standing or walking and may contribute to exacerbation of symptoms. Conversely, flexion-biased activities such as sitting or leaning forward generally ease symptoms.37 Two primary types of foraminal canal narrowing are recognized. Central canal narrowing is often associated with conditions such as facet arthrosis, thickening of the ligamentum flavum, or a central intervertebral disk bulge,38 whereas lateral foraminal canal stenosis may compromise the spinal nerve roots as they exit the lateral space between adjacent vertebrae. A loss of intervertebral disk height may contribute to narrowing of this space.
Box 10-2 lists common characteristics associated with degenerative disorders. Because of the degenerative and progressive nature of spondylosis, the condition often has no specific mechanism of injury, and symptoms manifest insidiously.39 Patients with spondylosis generally describe symptoms that include a deep ache and morning stiffness. Depending on the severity, symptoms may ease with activity throughout the course of the day. However, in advanced cases, compromise of the central or lateral foraminal canal may result in neurologic symptoms or signs.40 Symptoms include referred pain and paresthesia into the lower extremity and are exacerbated with activities that further compromise the neural canal such as prolonged standing or walking.35 Moreover, activities such as slouched sitting and bending are likely to relieve symptoms.6,30,41
Changes in pain location are based on morphologic changes to the lateral foramen with movements.42 Specifically, evidence suggests that extension and ipsilateral lateral flexion narrow the foramen by 12% and 8%, respectively.42 Conversely, flexion and contralateral lateral flexion increase the foraminal space by 11% and 8%, respectively.42 Examination findings for spondylosis consist of localized pain in the early stages. In advanced cases (because of the compressive origin), however, neurologic findings may be present including altered deep tendon reflexes, sensory anesthesia, ataxia, and motor weakness.
On examination, the patient may present with a positive treadmill test result, which requires the patient to walk on a level treadmill at a comfortable pace until symptoms manifest. The amount of time to onset of symptoms is recorded. The patient then sits down, the time until symptoms return to baseline is recorded, and the test is then repeated with the patient walking on the treadmill at a 15-degree incline. Again, the time to onset of symptoms and the time to resolution of symptoms while sitting are recorded. Researchers found that earlier onset of symptoms with level walking to be consistent with a clinical diagnosis of lumbar spinal stenosis (sensitivity, 68%; specificity, 83%).43 In addition, a longer total treadmill walking time during incline when compared with level walking was indicative of lumbar spinal stenosis (sensitivity, 50%; specificity, 92%). Finally, prolonged recovery after level walking was also consistent with the clinical diagnosis of stenosis (sensitivity, 82%; specificity, 68%).