9.1 Failed Back Surgery Syndrome
Recurrent or residual low back pain after lumbar disc surgery; incidence ranges between 5 and 40%
Permanent nerve root injury from the original disc herniation
Deafferentation pain which is usually constant and burning
i. Permanent injury to the nerve roots from surgery
Deafferentation pain which is usually constant and burning and is responsible for 6–16% of persistent symptoms in postoperative patients
Due to a dural tear at the time of surgery; the differential includes postoperative serous fluid collections and infected collections
Scar or granulation tissue formation causing compression and mechanical distortion of the nerve root
Once very common after contrast myelography, particularly with the combination of hemorrhage from myelography/surgery and retained contrast material. The differential includes: (a) intradural mass, (b) cerebrospinal fluid (CSF) tumor spread and (c) spinal stenosis
Incidence after lumbar discectomy 0.2%; intractable back pain 1–4 weeks postop after a period of symptomatic relief. The differential includes: (a) neoplasm, (b) degenerative disease, and (c) osteomyelitis
Insufficient root decompression by residual soft tissue or bone (i.e., stenosis of exit foramen, residual soft tissue such as a synovial cyst)
Disc herniation at another level
Mechanical segmental instability
Recurrence at operated level many years later, secondary stenosis after surgery at adjacent level or at level fused in the midline
Causes of back pain unrelated to the original condition (i.e., myofascial syndrome, paraspinal muscle spasm
Psychological factors such as secondary gains, drug addiction, poor motivation, psychological problems
9.3 Scar versus Residual Disc
MRI without intravenous contrast is at least equivalent to contrast CT in distinguishing scar tissue from disk material and yielding an accuracy of 83%. The addition of Gadolinium (Gd)-DTPA increases further the diagnostic accuracy from 89 to 96%. Overall sagittal and axial T1-weighted preand post-Gd-DTPA MRI remains the single most effective method of evaluating the postoperative lumbar spine patient (▶Fig. 9.1). The important criteria for evaluating of scar tissue versus disk material in the postoperative patient based on Gd-DTPA-enhanced MRI can be summarized as follows:
Fig. 9.1 (a–d) Radiologic characteristics between scar versus disc material. The hallmark sign distinguishing scar from recurrent or residual disc herniation is the pattern of enhancement. Scar tissue tends to enhance homogeneously, while disc herniation tends to enhance peripherally. In the early postoperative period (less than 3–6 months) it may be impossible to distinguish peripherally enhancing scar type changes from recurrent/residual disc herniation.
Scar tissue enhances immediately after injection, irrespective of the time since surgery (some scars continue to enhance for more than 20 years).
Disk material does not enhance immediately following injection.
Smoothly marginated, polypoid anterior epidural mass showing continuity with the parent disc space (except for free fragments) is disk material.
Scar tissue can have mass effect and be contiguous to the disk space.
Retraction of the thecal sac toward aberrant epidural soft tissue can be a helpful sign of scar tissue when present.
Note: The presence or absence of mass effect should be a secondary consideration when compared to the presence or absence of enhancement.
9.4 Multiple Lumbar Spine Surgery (Failed Back Syndromes)
A history of failed lumbar spine surgery is a diagnostic and therapeutic challenge to a physician. The first step is to differentiate those patients whose back or leg pain originates from a systemic cause (e.g., pancreatitis, diabetes, abdominal aneurysm) from those with a mechanical problem, and therefore, a thorough medical evaluation should be undertaken in this group at the same time the neurosurgical evaluation is done.
Patients with profound emotional disturbances and instability (e.g., alcoholism, drug abuse, depression) and those involved with compensation and litigation should undergo a thorough psychiatric evaluation. Even if they are found to have a genuine neurosurgical problem, their psychosocial problem should be dealt with first, because additional low back surgery would fail again. After exclusion of the psychosocial group of patients, a smaller group of patients with back and/or leg pain due to mechanical instability or scar tissue is separated; only the patients with mechanical instability will benefit from additional surgery.
9.4.1 Causes of failed back syndromes
These affect 10–40% of patients following low back surgery. Recurrent or residual back and/or leg pain after lumbar disc surgery constitutes the “failed back syndrome” (excluding secondary gain, and other nonmedical causes).
9.4.2 Differential diagnosis
i. Original disc not removed: This may occur if a disc fragment is left in the intervertebral disc space or if the wrong disc level was removed. Patients will continue to have the preoperative leg pain because of continued mechanical compression and inflammation of the same nerve root. Patients will wake up from surgery complaining of the same preoperative pain and will continue without ever being pain free. Patients will benefit from reoperation.
ii. Recurrent disc at the same level: Patients will develop a sudden onset of leg pain as preoperatively, following a pain-free period of greater than months. An additional operation is indicated. In the case of a recurrent disc at different level, patients will have a painfree interval greater than 6 months, and suffer a sudden onset of leg and/or back pain. The neurologic symptoms and the radiologic findings, however, will be at different level than preoperatively. Reoperation will yield very good results.
i. Without enhancement: Recurrent disc material causes a nonspecific mass effect, density greater than 90 Hounsfield units, may reveal gas or calcium collection, and nodularity, does not conform to the margins of the thecal sac, and the margins tend to be sharp. The majority of the disc material is centered at the intervertebral disc space.
ii. With intravenous contrast enhancement: Herniated disc material does not enhance early on following contrast administration. The disc material, however, enhances on the delayed CT scan images (e.g., 40 minutes after injection of the contrast material). Discs are typically seen as areas of decreased attenuation with a peripheral rim of enhancement, whereas epidural scar enhances homogeneously.
MRI: Within 6 weeks following surgery at the operative site, there is a large amount of tissue disruption and edema (producing mass effect on the anterior thecal wall) that is heterogeneously isointense to muscle on T1-WI and increased on T2-WI. These disruptions will heel within 2–6 months postoperatively. MRI may be used in the immediate postoperative period for a more gross view of the thecal sac and epidural space, to exclude significant hemorrhage, pseudomeningocele, or disc space infection. Even with the use of CT-myelography, distinction between these entities on MRI is extremely difficult, as all will appear as nonspecific extradural mass effects. Herniated disks will show contiguity with the parent disc space (except for free fragments) and mass effect. Small protruded discs are low in signal intensity on T2-WI, whereas larger protruded, extruded, and free fragments can show central high-signal intensity on T2-WI. Recurrent herniations display a smooth polyploid configuration, and an hypointense rim outlining the high-signal intensity herniations, which helps to separate the herniated material from the adjacent CSF on T2-WI.
Six weeks to 6 months following lumbar spina surgery, there is gradual replacement of the immediate postoperative changes by posterior scar tissue. Fibrosis can be extradural (most common type) and intradural (arachnoiditis). Patients with arachnoiditis have a history of multiple lumbar spine surgeries, with pain-free intervals ranging between 1 and 6 months. They usually complain of both back and leg pain in varying degrees and the neurological evaluation is inconclusive.
The diagnosis of scar tissue versus disc is extremely important. Surgery is not indicated for scar (epidural fibrosis) but would be beneficial if disc can be diagnosed as a cause of the radiculopathy.
The definitive study for diagnosing arachnoiditis is:
i. Myelographic findings of mild arachnoiditis are blunting of the caudal nerve root sleeves, segmental nerve root fusion, and small irregularities of the thecal sac margin. Multisegmental nerve root fusion with root sleeve obliteration, intradural scarring, and loculation is seen with moderate arachnoiditis. Severe adhesive arachnoiditis may cause a myelographic block.
ii. Postmyelogram CT scan reveals nodular, or cordlike intradural masses with moderate disease. Sometimes the nerve roots are annealed against the dura and the thecal sac appears empty or featureless.
iii. MRI findings of arachnoiditis include intradural fibrosis, nerve root clumping, loculation and sacculation, root retraction, and adhesions.
The best means of trying to identify epidural scar tissue are:
i. CT scan with and without enhancement
CT without contrast was correct 43% of the time, while CT with contrast was correct 74% of the time in differentiating scar tissue from disc material
Scar tissue causes retraction of the thecal sac to the surgical site and conforms to the thecal sac margin.
Linear strandlike densities occur within scar tissue
The majority of the scar tissue is seen above or below the particular disc level
Scar tissue shows attenuation of 75 Hounsfield units or less and shows contrast enhancement
Preand postcontrast MRI gives 96% accuracy in differentiating scar tissue from disc material
Scar tissue is consistently enhancing immediately following injection on T1-WI. This enhancement occurs regardless of the time since surgery; even when surgery was more than 20 years ago.
Scar tissue may occasionally show mass effect and should not be used as a major discriminator of epidural fibrosis versus disc material
Cauda equina compression from central spinal stenosis results in neurogenic claudication with bilateral leg pain that begins after walking a short distance. The pain is not well localized and often is more of a dysesthesia than true pain.
Plain X-rays: The interpediculate distance increases from T12 to L5. Interpediculate measurements of less than 16 mm at the L4–5 or less than 20 mm at L5–S1 and canal cross-sectional areas of less than 1.45 cm2 are considered abnormal.
CT scanning will show bony encroachment upon the neural elements and is especially useful in evaluating the lateral recesses and foraminae. A cross-sectional area of less than 100 mm2 is abnormal.
MRI is useful as soft tissue, such as the intervertebral disc and ligamentum flavum, contributes significantly to most cases of stenosis. Sclerotic bone will have low signal intensity on T1-WI and T2-WI, and is recognized by the encroachment upon the epidural and foraminal fat. Osteophytes containing fatty marrow are recognized by their high signal intensity on T1-WI. Sagittal images are most useful in defining bony foraminal stenosis or more generalized stenosis secondary to disc degeneration with lost disc space height and rostrocaudal subluxation of the facets.
Instability of the lumbar spine will cause pain on a mechanical basis in the multiple spine surgery patient. A coexisting spondylolisthesis, pseudoarthrosis, or an excessively wide bilateral laminectomy can cause spinal instability. These patients complain of back pain associated with activity (mechanical) and their physical examination may be negative. The diagnosis of lumbar spinal instability is based on plain X-ray features.
Wong CB, Chen WJ, Chen LH, Niu CC, Lai PL. Clinical outcomes of revision lumbar spinal surgery: 124 patients with a minimum of two years of follow-up. Chang Gung Med J 2002;25(3):175–182
Arts MP, Kols NI, Onderwater SM, Peul WC. Clinical outcome of instrumented fusion for the treatment of failed back surgery syndrome: a case series of 100 patients. Acta Neurochir (Wien) 2012;154(7): 1213–1217
Walker BF. Failed back surgery syndrome. COMSIG Rev 1992;1(1):3–6
Long DM. Failed back surgery syndrome. Neurosurg Clin N Am 1991;2(4):899–919
Guyer RD, Patterson M, Ohnmeiss DD. Failed back surgery syndrome: diagnostic evaluation. J Am Acad Orthop Surg 2006;14(9):534–543
Block AR, Gatchel RJ, Deardorff WW, Guyer RD. The Psychology of Spine Surgery. Washington DC: American Psychological Association; 2003
Louw JA. The differential diagnosis of neurogenic and referred leg pain. SA Orthop J 2014;13(2)
Mavrocordatos P, Cahana A. Minimally invasive procedures for the treatment of failed back surgery syndrome. In: Pickard JP, ed. Advances and Technical Standard in Neurosurgery. Vol. 31. Springer-Verlag; 2006:212–247
Bundschuh CV, Modic MT, Ross JS, et al. Epidural fibrosis and recurrent disk herniation in the lumbar spine: MR imaging assessment AJNR Am J Neuroradiol 2009;30:1082–1097
Small J, Schaefer W. Neuroradiology:Key differential diagnosis and clinical questions. Elsevier-Saunders; 2013
9.5 Low Back Pain
In the vast majority of patients (> 80%) no specific pathoanatomical diagnosis can be made. Low back pain is the second most common reason for people to seek medical help; its prevalence ranges from 60–90% and has an incidence rate of approximately 5%. Only 1% will develop nerve root symptoms and only 1–3% of patients have lumbar disc herniation. Low back pain is only a symptom which can result from several conditions and therefore, the term should not be equated with herniated lumbar disc.
Acute and subacute low back pain
Acute low back pain is self-limited and the majority of patients start getting better within 6 weeks. Approximately 10% of patients will persist having symptoms for more than 6 weeks thus entering a subacute phase
i. Musculoligamentous sprain/lumbosacral strain
A localized pain complaint associated with a tense muscle containing a very tender spot, i.e. trigger point, identifiable by palpation and which may be distant to the source of pain.
iii. Spondylolysis and spondylolisthesis
Overuse injuries secondary to repetitive, unrepaired microtrauma are frequent particularly to athletes engaging in high-impact sports)
iv. Posttraumatic disc herniation
Immunocompromised and debilitated patients, drug abusers, diabetics, and alcoholics are at increased risk. Local spinal tenderness to percussion has 80% sensitivity with bacterial pyogenic infections, but a low specificity.
Staphylococcus aureus is the most common organism accounting for 60% of infections; Enterobacter for 30%; other organisms are Escherichia coli, Salmonella, Pseudomonas aeruginosa, and Klebsiella pneumoniae.
Granulomatous and miscellaneous spondylitis
Granulomatous spondylitis—Mycobacterium tuberculosis most commonly involved; Brucella melitensis. Fungal spondylitis—blastomycosis, aspergillosis, actinomycosis, cryptococcosis, and coccidioidomycosis. Parasitic spondylitis—Echinococccus.)
ii. Epidural and subdural abscesses (S. aureus is by far the most common organism)
Spinal meningitis can be caused by bacterial, fungal, parasitic, or viral organisms, often as a manifestation of cerebral meningitis.
Viral infections such as herpes, coxsackie, and polio viruses are the most common organisms, and the HIV-related myelitis is increasing recently.
Patients aged > 50 years with an unexplained weight loss and relentless pain of > 4–5 months (range 3 days to 3.8 years) not responding to bed rest or other conservative treatment may have spinal tumors.
i. Extradural spinal cord tumors (55%)
ii. Intradural spinal cord tumors (40%)
iii. Intramedullary spinal cord tumors (5%)
An acute inflammatory disorder which may be seen early in ankylosing spondylitis. It causes morning back stiffness, hip pain and swelling, failure to get relief at rest and improvement with exercise
Referred pain of visceral origin
Patients writhing in pain should be evaluated for an intra-abdominal or vascular pathology; e.g., in aortic dissection the pain is described as a “tearing” pain whereas in patients with neurogenic low back pain it tends to remain still and moving only to change positions at intervals.
i. Abdominal aortic aneurysm eroding the vertebrae
ii. Occlusive vascular disease causing radicular or plexus ischemia
iii. Direct involvement of lumbosacral plexus or sciatic nerve (e.g., trauma, tumors, injections into or close to the sciatic nerve)
Patients at risk for osteoporosis or with known cancer.
From all patients with an acute low back pain, 5% of them will continue having persistent symptoms and fall into chronicity after 3 months. These patients account for 85% of the cost in lost work and line-up in the workman’s compensation list.
All causes of acute and subacute low back pain listed earlier.
i. Spondylosis, spondylolysis, and spondylolisthesis
Spondylosis refers to osteoarthritis involving the articular surfaces (joints and discs) of the spine, often with osteophyte formation and cord or root compression. Spondylolysis refers to a separation at the pars articularis which permits the vertebrae to slip. Spondylolisthesis is defined as the anterior subluxation of the suprajacent vertebra, often producing central stenosis; it is the slipping of one vertebra forward on the one below.
Multiple nerve roots are involved and the pain in the spine is significantly greater than that in the limb. Symptoms aggravate when standing or walking. Impairment in the bowel, bladder, or sexual function may occur.
Single or multiple nerve roots on one or both sides become compressed. Pain in the limb is usually equal to or greater than that in the spine. Symptoms are brought on by either walking or standing and are relieved with sitting. Testing by straight leg raising may be negative.
iv. Facet arthrosis and synovial cysts
v. Lumbar disc disease (bulge-herniation)
Clinical features include positive straight leg raising and radicular pain in the limb disproportionate to that in the spine. Loss of strength, reflex, and sensation occurs in that root’s territory.
Inflammatory disorders involving
Werneke M, Hart DL. Centralization phenomenon as a prognostic factor for chronic low back pain and disability. Spine 2001;26(7):758–764, discussion 765
Kinkade S. Evaluation and treatment of acute low back pain. Am Fam Physician 2007;75(8):1181–1188
Rush AJ, Polatin P, Gatchel RJ. Depression and chronic low back pain: establishing priorities in treatment. Spine 2000;25(20):2566–2571
Patrick N, Emanski E, Knaub MA. Acute and chronic low back pain. Med Clin North Am 2014;98(4):777–789, xii
Atlas SJ, Deyo RA. Evaluating and managing acute low back pain in the primary care setting. J Gen Intern Med 2001;16(2):120–131
Rives PA, Douglass AB. Evaluation and treatment of low back pain in family practice. J Am Board Fam Pract 2004;17(Suppl):S23–S31
Chou R, Qaseem A, Snow V, et al. Prognosis and treatment of low back pain: A joint clinical practice. Guideline from the American College of Physicians and the American Pain Society clinical guidelines Ann Intern Med 2007;147:478–491
9.6 Claudication Pain
Claudication pain is a cramp-like pain that is always induced by exercise at a constant distance that the patient walks; it can be either unilateral or bilateral and is relieved by rest. The most important disorder of claudication is that of peripheral arterial disease and must be distinguished from pseudoclaudication caused by lumbar spinal stenosis. Intermittent claudication must also be differentiated from lower extremity pain caused by nonvascular etiologies that may include neurologic, musculoskeletal, and venous pathologies.
9.6.1 Differential diagnosis
9.6.2 Differentiating signs and symptoms
Lumbar spinal stenosis claudication
Lumbar spinal stenosis is due to nerve root compression by herniated disks or osteophytes and the pain typically follows the dermatome of the affected root.
The pain usually begins immediately upon walking and may be felt in the calf or in the lower leg and it is associated sometimes with numbness and paresthesia.
The pain is not quickly relieved by rest and may even be present at rest.
A sensation of pain running down the back of the leg as well as a history of back problems may be present.
Symptoms are usually associated with walking; however, upright standing may produce pain, weakness, or discomfort in the hips, thighs and buttocks.
Symptoms are alleviated by sitting or flexing the lumbar spine forward as opposed to standing which alleviates pain caused by intermittent claudication.
In patients with cauda equina syndrome, upright positioning aggravates the narrowing of the spinal canal and therefore causes the symptoms.
Venous claudication occurs in patients with chronic venous insufficiency and those who develop postthrombotic syndrome after deep venous thrombosis. Baseline venous hypertension in the obstructed veins worsens with exercise.
Venous claudication produces a tight bursting pressure in the limb following exercise, usually worse in the thigh and uncommonly in the calf.
It is usually associated with venous edema in the leg.
Leg elevation helps in relieving the symptoms.
Venous claudication tends to improve with cessation of exercise but total resolution takes much longer time than the resolution of intermittent claudication.
Chronic compartment syndrome is an uncommon cause of exercise-induced leg pain, which results from thickened fascia, muscular hypertrophy or when external pressure is applied to the leg. It occurs in young athletes who develop increased pressure within a fixed compartment which compromises the perfusion and the function of the tissues within that space. The diagnosis is based on testing the intercompartmental pressure before and after exercise.
Chronic compartment syndrome presents as tight bursting pressure in the calf or foot after endurance sports or other robust exercise.
Osteoarthritis in joints is typically worse in the morning or at the initiation of movement and does not cease upon stopping exercise or standing.
The pain improves after sitting, lying down, or leaning against an object to alleviate weight-bearing on the joint.
The pain may be affected by weather changes and may be present at rest.
Mufson I. Intermittent limping—intermittent claudication: their differential diagnosis. Ann Intern Med 1941;14(12):2240–2245
Comer CM, Redmond AC, Bird HA, Conaghan PG. Assessment and management of neurogenic claudication associated with lumbar spinal stenosis in a UK primary care musculoskeletal service: a survey of current practice among physiotherapists. BMC Musculoskelet Disord 2009;10:121
Weinberg I, Jaff MR. Nonatherosclerotic arterial disorders of the lower extremities. Circulation 2012;126(2):213–222
9.7 Differential Diagnosis of Claudicant Leg Pain
Both the backache and the leg symptoms of lumbar spinal canal stenosis are considered mechanical in nature. That is, they are aggravated by activity and often relieved significantly by rest. They are distinguished from vascular claudication in that the rest required for relief is usually of many minutes rather than a brief interruption in activities.
It is important to remember that spinal stenosis has many ways of presentation, some not clearly defined until the end of complete vascular and spinal examination. Although vascular claudication is the number one differential diagnosis, other conditions that cause upset in walking also have to be included in the differential diagnosis. These include:
Pain in groin along with the thigh (both aggravated by walking)
Inability to rotate the hip for daily tasks (e.g., putting on socks and shoes) and an associated loss of hip range of motion
Although it may occur with walking, it does not limit walking distance
It rarely goes below the knees
It is not associated with neurologic symptoms (numbness, paresthesia)
Peripheral neuropathy (PN) is the most difficult differential diagnosis of all and missing it has to be the most common reason for a failed outcome following surgery for lumbar spinal stenosis.
Spinal stenosis and PN coexist in the same age group
PN is dominated by neurologic symptoms more than pain
PN produces a more uniform distal stocking pattern on neurologic deficits
Walking does not necessarily aggravate the pain in the patients with PN, but they do experience unsteadiness that interferes with walking
Electrophysiologic testing is required to differentiate among these conditions
9.8 Thoracic Pain
Metastatic tumors are more common (66%) than primary spinal tumors (30%); the remaining 4% were prevertebral tumors invading the spinal canal. The frequency of skeletal metastases was much higher for some tumors: 84% for prostatic cancer and 74% of breast cancer.
Comprise approximately 25% of primary spinal tumors; 90% of spinal meningiomas are purely intradural and the remaining 7–10% may be extradural. Among the spinal meningiomas, 17% were in the cervical spine, 75–81% in the thoracic spine, and 2–7% in the lumbar region
Nerve sheath tumors (e.g., schwannoma, neurofibroma, neurinoma, and neurilemoma perineurofibroblastoma)
Spinal vascular malformations (e.g., dural/intradural arteriovenous malformations, cavernous angioma, capillary telangiectasia, venous malformation)
Spinal vascular tumors (e.g., hemangioblastomas)
Epidermoid and dermoid cysts and teratomas
iii. Intramedullary spinal cord tumors
Intramedullary lesions (excluding spinal cord tumors)
Heart (T 1–5 roots; pain referred to: chest and arm)
Stomach (T 5–9 root; pain referred to manubrial xiphoid)
Duodenum (T 6–10 root; pain referred to xiphoid to umbilicus)
Pancreas (T 7–9 root; pain referred to upper abdomen or back)
Gallbladder (T 6–10; right upper abdomen)
Appendix (T11–L2; right lower quadrant)
Kidney, glans (T9–L2; costovertebral angle, penis)
Fruth SJ. Differential diagnosis and treatment in a patient with posterior upper thoracic pain. Phys Ther 2006;86(2):254–268
van Kleef M, Stolker RJ, Lataster A, Geurts J, Benzon HT, Mekhail N. 10. Thoracic pain. Pain Pract 2010;10(4):327–338
Sizer PS Jr, Phelps V, Dedrick G, Matthijs O. Differential diagnosis and management of spinal nerve root-related pain. Pain Pract 2002;2(2):98–121
9.9 Thoracic Outlet Syndrome
(Scalenus anterior syndrome, cervical rib syndrome, costoclavicular syndrome, hyperabduction syndrome, upper thoracic neurovascular syndrome; ▶Fig. 9.2)
Neurovascular compression occurs in three possible spaces:
Scalene triangle: Most common site of brachial plexus compression
Costoclavicular space: Area between first rib and clavicle.
Pectoralis minor space: Area between pectoralis minor and chest wall.
Group of poorly categorized syndromes that include a variety of pain, motor loss (wasting and weakness of muscles in the hand) and paresthesias in the neck, shoulder, arms, and hand (4th and 5th digits). Symptoms and signs emanate from continuous or intermittent pressure on portions of the brachial plexus (C8, and T1 nerve roots, and lower trunk) and the auxiliary or subclavian vessels by anatomical structures (cervical rib, an enlarged first thoracic rib, fibrous bands, and hypertrophic scalenus muscles). Rare causes include a poor posture, head or neck trauma, repetitive occupational movements, atherosclerotic plaque formation, a Pancoast tumor. Rarely found under the age of 20 years.
Neurologic type (95% of cases): 20–60 years
Caused by compression of the lower portion of the brachial plexus by a band of tissue that joins the transverse process at C7 to the first rib. Women are most commonly affected. Characterized by a variety of pain and paresthesias in the head, neck, arms, and hand.
Venous type (4% of cases): 20–35 years
Results from the compression of the subclavian vein. Young men are most often affected. Characterized by arm claudication, edema, cyanosis, and venous dilatation.
Arterial type (1% of cases; atherosclerosis): older than 50 years
Caused by the compression of the subclavian artery by a cervical rib, and it is the most serious form of the syndrome. Men and women are equally affected. Characterized by digital vasospasm, potential thrombosis or embolism, aneurysm, muscle atrophy, and gangrene.
Cooke RA. Thoracic outlet syndrome—aspects of diagnosis in the differential diagnosis of hand-arm vibration syndrome. Occup Med (Lond) 2003;53(5):331–336
Stallworth JM, Horne JB. Diagnosis and management of thoracic outlet syndrome. Arch Surg 1984;119(10):1149–1151
Dragu A, Lang W, Unglaub F, Horch RE. [Thoracic outlet syndrome: differential diagnosis and surgical therapeutic options] Chirurg 2009;80(1):65–76
Hooper TL, Denton J, McGalliard MK, Brismée JM, Sizer PS Jr. Thoracic outlet syndrome: a controversial clinical condition. Part 1: anatomy, and clinical examination/diagnosis. J Manual Manip Ther 2010;18(2): 74–83
9.10 Cervical Radiculopathy
Patients with a cervical radiculopathy usually report axial spine and upper extremity pain that often is accompanied by numbness, paresthesias, and weakness. A number of musculoskeletal disorders, however, generate pain referral and weakness patterns similar to radicular patterns and may be present in individuals with or without radiculopathy.
It is frequently difficult to differentiate whether the pain source is secondary to cervical nerve root compression or secondary to a soft-tissue disorder. Upper extremity musculoskeletal disorders and cervical radiculopathy may present with similar pain-referral patterns, in a similar patient population, and may be present concomitantly.
9.10.1 Differential diagnosis
Differential diagnosis of entities causing upper extremity pain, weakness, and sensory changes:
Peripheral mononeuropathy (suprascapular, long thoracic, accessory, musculocutaneous, or ulnar neuropathy, carpal tunnel syndrome, etc.)
Radhakrishnan K, Litchy WJ, O’Fallon WM, Kurland LT. Epidemiology of cervical radiculopathy. A population-based study from Rochester, Minnesota, 1976 through 1990. Brain 1994;117(Pt 2):325–335
Rubinstein SM, Pool JJ, van Tulder MW, Riphagen II, de Vet HC. A systematic review of the diagnostic accuracy of provocative tests of the neck for diagnosing cervical radiculopathy. Eur Spine J 2007;16(3):307–319
Rao R. Neck pain, cervical radiculopathy, and cervical myelopathy: pathophysiology, natural history, and clinical evaluation. J Bone Joint Surg Am 2002;84-A(10):1872–1881
Jackson R. The classic: the cervical syndrome. 1949. Clin Orthop Relat Res 2010;468(7):1739–1745
9.11 Mononeuropathy of the Lower Extremity
Mononeuropathies are common clinical entities and may result from pathology located anywhere along the course of the peripheral nerve. Dysfunction can lead to weakness, pain, or sensory deficits. As individual nerves are affected, one does not see the distal and symmetric (stocking-glove type) distribution of deficits typical of a generalized polyneuropathy, at least early on.
Mononeuropathies are thought of as compressive or noncompressive. Compressive neuropathies produce symptoms in the distribution of the affected nerve root, plexus, or individual nerve. Noncompressive neuropathies may be sequelae of underlying systemic disease (e.g., diabetes, malignancy, infection, and inflammatory conditions). Viral infections such as herpes zoster, herpes simplex virus (HSV), Epstein–Barr virus (EBV), and cytomegalovirus can involve nerve roots, leading to painful radiculitis, or may trigger a Guillain–Barre syndrome 1–3 weeks after infection, usually in individuals with a reduced immune function (e.g., older people, or in HIV). Cancer can produce nerve dysfunction secondary to compression by solid tumors, infiltration by malignant cells, or paraneoplastic immune-mediated attack.
Vasculitic neuropathy usually occurs suddenly and is painful. The typical vasculitic picture is stepwise involvement of multiple individual nerves (mononeuritis multiplex) rather than an isolated mononeuropathy.
9.11.1 Differential diagnosis
Technically a radiculoplexopathy; a common clinical entity in diabetic patients with some immune-mediated microvasculitic component.
Uncommon neuropathies that may mimic a mononeuropathy. Causes include compression from a solid tumor, abscess, hematoma, or infiltrating malignancies.
The lower nerve roots L5/S1 followed by L4/L5 are most commonly affected. The most common causes are disk herniation, chronic degenerative changes, metastatic tumors (if known primary malignancy)
The most common mononeuropathy affecting the lower extremity, manifesting as a foot drop. Most often the nerve is injured at the fibular neck due to compression (e.g., surgical positioning, crossing legs, or trauma).
Due to compression of the lateral femoral cutaneous nerve. Often seen in overweight people, but patients who wear tight-fitting clothes and workers using heavy tool belts are also at risk.
Morton neuroma (metatarsalgia)
This is a relatively common source of foot pain at the base of the third and fourth toes, and is due to perineural fibrosis of an intermetatarsal nerve.
Seen most commonly in women who have undergone obstetric/gynecologic procedures.
The sciatic nerve arises from the L4–S2 nerve root and lumbosacral plexus before exiting through the greater sciatic foramen.
The tibial nerve is rarely involved in isolation, and when involved it usually occurs distally at the level of the ankle.
Tarsal tunnel syndrome (distal tibial neuropathy)
Compression of the distal tibial nerve as it passes through the tarsal tunnel (flexor retinaculum, at the medial side of the ankle), manifesting as perimalleolar pain.
The femoral nerve originates from the posterior divisions of the L2, L3, and L4 nerve roots. This can result in weakness when walking and falls due to buckling of the knee.
Hereditary neuropathy with liability to pressure palsies (HNPP) Dominantly inherited condition producing relapsing and remitting episodes of painless compression neuropathy at the common sites of entrapment (e.g., peroneal neuropathy at the fibular head).
It is an important cause of compression lower extremity mononeuropathies, following trauma or injury.
Patients with HIV can present with a mononeuritis multiplex pattern as well as a length-dependent sensorimotor polyneuropathy.
Caused by reactivation of a primary varicella zoster virus infection due to lowering of the cell-mediated immunity. Presents with burning or stabbing pain followed by a vesicular rash in the affected dermatomes.
Infection with HSV1 and HSV2 manifests with symptoms and signs ranging from tingling and burning with eruptions of vesicular lesions to painful oral, genital, and ocular ulcerations.
Infectious mononucleosis is the clinical syndrome caused by EBV, and also can cause a myriad of neurologic illness. Pain and weakness may indicate the presence of EBV radiculopathy, especially in patients with AIDS.
Affects the immunocompromised patients and manifests with fever, bone marrow suppression, and tissue-invasive disease such as pneumonia, hepatitis, colitis, nephritis, and retinitis.
Patients can present with a mononeuritis multiplex or polyradicular pattern.
Unknown etiology, possibly multifactorial including genetic, immunologic, and infectious causes (e.g., viruses, Borrelia burgdorferi, Mycobacterium tuberculosis, and Mycoplasma).
Chronic inflammatory and autoimmune disorder characterized by diminished lacrimal and salivary gland secretion.
The most common inflammatory arthritis characterized by symmetric arthritis of the small joints of the hands and feet.
Acquired demyelinating sensory motor polyneuropathy
Autoimmune disorder supported by pathology changes in peripheral nerve biopsies.
Neoplastic compressive lumbosacral radiculopathy
Direct compression from a malignancy, usually metastatic and can occur acutely. Suspected on cases with a known primary tumor.
Neoplastic compressive lumbosacral plexopathy
Direct compression from malignancy, mostly due to intra-abdominal extension, but growth from metastases is also possible.
Radiation may give rise to localized ischemia and fibrosis because of microvascular insufficiency.
Group of malignancies of the lymphoid system linked to infectious causes with bacteria and viruses, autoimmune disorders, immunodeficiency states, and environmental factors
An amyloid protein deposition disease that may have a primary cause or be secondary to other diseases, it can be localized, systemic, inherited, senile systemic, or dialysis amyloidosis.
Paraneoplastic immune-mediated attacks
Tumor-induced autoimmunity against the nervous system can cause lumbosacral plexopathy.
Neurofibrosarcoma is probably the most important death-causing complication of neurofibromatosis type 1.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
