Spinal Column

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Spinal Column C E N T E R F O R S P I N E H E A LT H

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MASQUERADERS

Masqueraders — You will never establish the diagnosis of a process or disease that you did not think of A Message from Edward C. Benzel, MD Masqueraders of spine pathology — what’s that all about? Spine pathology is spine pathology — isn’t it? As you will read, perhaps not. Edward C. Benzel, MD Dr. Benzel can be contacted at 216.445.5514 or [email protected].

IN THIS ISSUE: When Back Pain Stems from Something Worse p. 2 Rheumatologic Causes p. 5 Musculoskeletal Causes p. 6 Metabolic Bone Disorders p. 8 Brachial Plexopathies p. 10

Spine diagnostics and therapeutics are not, in general, analytical processes. The utilization of the best medical evidence is obviously a critical component of the diagnostic and decision-making process. Without equivocation, however, the medical literature is flawed. Therefore, common sense and, most importantly, wisdom play an obligatorily large role in both the diagnostic and decision-making processes. With all that said, spine disorders are often both difficult to accurately diagnose and difficult to treat. Complicating this overall picture is the fact that multiple masqueraders of spine pathology do, indeed, exist. It has been shown that approximately one out of three patients seeking care from a spine surgeon does not have a spine-related etiology of his/her complaint or pain. It, therefore, is incumbent on the spine physician, as well as referring physicians, to understand the complexity of ‘spine-related’ complaints and the importance of their identification. Arriving at an accurate diagnosis is critical. More often than not, however, it is impossible to identify the precise etiology of pain. This is particularly true for the majority of cases of episodic back pain. With this group of patients, spontaneous resolution is the norm. What is critical, however, is the fact that overlooking a non-spine etiopathology may be associated with a serious diagnostic and even prognostic impact. The

fact remains: You will never establish the diagnosis of a process or disease that you did not think of. The obvious solution here is to increase our fund of knowledge regarding the myriad diagnostic possibilities. With this in mind, our skilled team of clinician-educators have compiled information that is critical to all physicians and other practitioners who interface with spine patients. This issue has been crafted to help us call to mind such tangential diagnoses. Perhaps we should consider this issue a lesson in ‘clinical out-ofthe-box thinking.’ Tools to be learned herein include the critical assessment of the patient’s symptoms and findings, a heightened awareness of non-spine pathologies and the suspicion that ineffective prior therapies may be related to the fact that such therapies may have been directed toward the wrong diagnosis. Regardless, read on, think out of the box and look under the mask.

FO R M O RE INFO RM AT I O N To learn more about the Center for Spine Health, please contact Dr. Benzel at 216.445.5514 or our administrator, Susan Rossi, at 216.444.6890. To refer patients, call 216.444.2225 or 800.553.5056, ext. 4225.

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When Back Pain Stems from Something Worse By Robert F. McLain, MD

Back pain affects so many of us that it’s often dismissed as a normal part of aging and activity. And, since the common causes of pain are typically age-related degenerative changes or minor trauma, 90 percent of patients improve with simple supportive care and physical therapy. Yet, when pain persists, or presents in an unusual way, most physicians begin to worry that they may be missing something more serious.

Robert F. McLain, MD Guest Medical Co-Editor Dr. McLain can be contacted at 216.444.2744 or [email protected].

While serious, unrecognized diseases are uncommon causes of back pain. Their impact on health and survival is well out of proportion to their prevalence. Even experienced practitioners often harbor concerns about the possibility of overlooking more serious or life-threatening pathology. Fortunately, these kinds of disorders almost always offer a few clear clues to their diagnosis. A careful history and physical examination, which includes looking for specific signs and symptoms, as well as proper selection of diagnostic studies, will allow physicians to confidently rule out more ominous underlying diseases. Cancer of the spine Unremitting pain often raises the same fear in patients and caregivers — a fear of cancer. Back pain is the presenting symptom in most patients with spinal cancer. Spinal cancer pain differs from common back pain in several ways. Benign back pain is activity related, relieved by rest and often is associated with a recognized injury. It typically begins to get better after four to six weeks. Pain caused by a spinal tumor is more persistent, progressively getting worse, and is not relieved by rest (see figure 1). It often worsens at night, which is a key point to the history. Spinal tumor back pain may be associated with belt-like thoracic pain or radicular symptoms of pain or weakness in the legs, depending on the location of the tumor. Pathologic fractures resulting from vertebral destruction may be the first presentation of a tumor. The physician should always look for hallmark signs and symptoms of systemic disease — fatigue, weight loss, abnormal bleeding, abdominal swelling, subcutaneous masses or lymphadenopathy. Symptoms associated with common adenocarcinomas, such as hematochezia, hemoptysis, nipple discharge or breast

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mass or change in bowel habits should prompt a more complete evaluation. The most common cause of spinal cancer is metastatic disease, and the most common sources of that metastasis comes from carcinomas of the lungs, breasts, prostate, kidneys, colon and thyroid. These diseases, along with multiple myeloma and lymphoma, account for 90 percent of all spinal tumors. These organs and systems should be thoroughly examined when cancer is suspected. Nonspinal pelvic or abdominal malignancies also may cause low back pain. The pain is typically non-mechanical, i.e., constant and unrelieved by positional change. Night pain disrupting sleep also is typical. Primary tumors of the ovary, uterus, pancreas, kidney and colon are most commonly associated with back pain. Infection Spinal infections can be either acute or chronic problems. Acute infections are most often pyogenic, while chronic infections may result from pyogenic, fungal or granulomatous disease. Infections always start somewhere else, and the most frequent sources are urinary tract infections, dental abscesses, pneumonia and any wound. Patients with infection usually have focal pain that is made worse by weight bearing and activity. Exquisite pain may be relieved only by laying down (see figure 2). Fever, chills, headache and systemic illness are not always present even with advanced infection, but weight loss and fatigue, fevers, chills and night sweats should raise suspicion. Severe pain may be elicited in patients with discitis simply by sitting the patient up or by changing posi-

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tion. If the vertebra has collapsed, focal kyphosis may be detected. Neurological signs should be carefully sought. Patients who initially complain of focal spine pain, followed by progressive radicular pain, weakness and incipient paralysis may have an infection within the canal, with development of an epidural abscess. Visceral Disease Mimicking Back Pain There are a number of disorders involving the abdominal viscera that can produce back pain symptoms, and some of these disorders are imminently life-threatening. Although rare, they cannot be overlooked. The most serious vascular disorder presenting as back pain is the abdominal aortic aneurysm. Patients with abdominal aortic aneurysm often are misdiagnosed on initial presentation, as initial symptoms may be subtle and nonspecific. The pain of the aneurysm can be generated by compression of adjacent structures by the expanding aorta or, in late stages, by distension or dissection of the arterial wall. Pain is deep seated and referred to the thoracic or thoracolumbar segments of the spine. The pain of aortic dissection is particularly intense and undiminished by narcotics. A palpable pulsatile abdominal mass is found in almost all cases. Lower extremity pulses may be diminished or asymmetrical.

Back pain also can be triggered by disorders of the gastrointestinal tract. Ulcers, especially those involving the posterior duodenal wall, may cause upper lumbar pain. A perforated ulcer may trigger intense pain and spasm, as well as signs of systemic illness and an acute abdomen. Pyelonephritis, renal artery occlusion or nephrolisthiasis may all cause severe, colicky back pain. Renal pain usually is referred to the thoracolumbar junction and flank. Bladder disorders may cause low back symptoms, usually concurrent with suprapubic discomfort and urinary symptoms. Pancreatic disease produces pain in the upper lumbar region, which worsens when laying down. A history of pancreatitis, jaundice or alcoholism — in association with increased amylase and lipase — differentiates pancreatic pain from primary spinal pain. An expanding pancreatic tumor may cause upper lumbar or thoracolumbar pain, irritating the peritoneal lining or directly distorting the nerve endings encapsulating the pancreas. Back pain caused by visceral sources is not activity related, and may be colicky or throbbing in nature. If pain is aggravated by eating, the menstrual cycle, is colicky or cramping in nature, or reproduced by abdominal palpation, it is unlikely to originate from spinal pathology.

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Figure 2: Focal collapse and disc destruction are hallmarks of infection in this patient who complained of pain for PRQWKVSULRUWRDQ\HYDOXDWLRQ2QSUHVHQWDWLRQSDWLHQW was experiencing fevers, chills, night sweats and weight loss. TB test was positive, and MRI revealed extensive abscess requiring surgical treatment.

Percussion over the costovertebral angle of the back reproduces pain caused by pyelonephritis or renal stone. Deep palpation of the abdomen may reveal guarding, rebound or focal tenderness. Signs of an acute abdomen, or palpation of a pulsatile mass should generate an urgent surgical evaluation. Rectal examination will reveal guaiac-positive stool in cases of peptic ulcer or colorectal disease. The key to identifying any of these disorders is a proper abdominal exam — meaning getting the patient into a gown, down on an exam table, and carefully assessing each aspect of the exam: tenderness, mass, organomegaly, rebound and guarding, and auscultating for bowel sounds and bruits. An abdominal flat-plate radiograph will reveal evidence of free air, small bowel obstruction, biliary disease, stones or aortic aneurysm. Abdominal CT can further elucidate these findings, if needed. The Spinal Work-up Diagnostic Studies: Nonspecific, but highly sensitive, erythrocyte sedimentation rate (ESR) is almost always elevated in cases of systemic neoplasia or infection. If a tumor is suspected, a workup including chest radiography, mammography, measurement of prostate-specific antigen and abdominal CT usually reveals the underlying primary malignancy, if one exists.

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In infections, C-Reactive Protein will be elevated, but 40 percent of patients will have a normal white blood count. Remaining labs are typically normal. A TB skin test should be placed, with appropriate controls, in at-risk patients (emigrants from areas of endemic disease, immunocompromised patients and patients with known exposure). If the abdomen itself is the source of concern, a complete metabolic panel is a must, and amylase and lipase levels should be included. Urinalysis, WBC level and stool guaiac should be obtained routinely. CT, ultrasound or MRI may each be helpful in completing the assessment if physical findings suggest an intraabdominal condition. Imaging: Spinal tumors are only visualized on initial X-rays when significant bone destruction has occurred. A bone scan is positive earlier and serves as a good screening test. MRI can screen the whole spine, shows the soft tissue elements inside and outside the spinal column, and reveals marrow replacement disease in vertebrae that would appear perfectly normal on plain X-ray. MRI is the study of choice to assess any patient with suspected tumor or infection (see figure 1). The sensitivity of MRI in infected patients is further increased by gadolinium enhancement.

In tumor patients, basic laboratory studies may reveal anemia, hypercalcemia and elevated levels of alkaline phosphatase. Serum and urine protein electrophoresis (SPEP and UPEP) are specific for myeloma or plasmacytoma. Urinalysis may reveal hematuria, associated with renal cell carcinoma.

Robert McLain, MD, is a spine surgeon with the Cleveland Clinic Center for Spine Health. His specialty interests include back and neck surgery, cervical and lumbar artificial disc replacement, reconstruction and disc surgery, minimally invasive disc and fusion surgery, treatment of spinal tumors and deformity, X-stop and kyphoplasty.

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Rheumatologic Causes of Spinal Pain By Daniel Mazanec, MD

When considering evaluation of rheumatologic causes of back or neck pain, the differential diagnosis is somewhat age-dependent. In general, diabetic polyradiculopathy and polymyalgia rheumatica (PMR) are much more common in persons over 40 years of age. In contrast, spondyloarthropathy (ankylosing VSRQG\OLWLV DQGÀEURP\DOJLDDUHH[DPSOHVRIFRQGLWLRQVWKDWVKRXOGEHFRQVLGHUHGLQHYDOXDWLQJ\RXQJHU patients with chronic spinal pain.

Daniel Mazanec, MD Guest Medical Co-Editor Dr. Mazanec can be contacted at 216.444.6191 or [email protected].

Polymyalgia rheumatica (PMR) is a disorder that often presents with dominant symptoms of pain and stiffness in the neck, shoulders, low back and hip girdle. Virtually all patients are over 50 years of age and most over age 65. Characteristically, symptoms begin abruptly — literally overnight. Prolonged, immobilizing morning stiffness or “gel” is usual. Clinical findings are sparse, but the key diagnostic study is the Westegren erythrocyte sedimentation rate (WESR), which is usually greater than 50 mm/ hour and often is much higher. The diagnosis is further confirmed by a dramatic and prompt response to modest doses of prednisone (10–15 mg). Diabetic polyradiculopathy (also known as proximal motor neuropathy or diabetic amyotrophy) is a somewhat uncommon form of diabetic neuropathy that most commonly affects older male patients with type 2 diabetes. Symptoms include unilateral or bilateral leg pain that may resemble lumbar radiculopathy. The pain is often worst at night and may be associated with proximal muscle weakness and atrophy. The associated diabetes may be very mild or even unrecognized prior to the onset of leg pain. Electrodiagnostic testing confirms this diagnosis. Diabetic polyradiculopathy is a self-limited disorder with resolution of pain and weakness over several months. Ankylosing spondylitis (AS) is the prototype of a group of disorders known as “seronegative spondyloarthropathies” (SNSA). AS is characterized by inflammatory spinal disease involving the entheses — ligamentous attachments at bone — with diverse extraspinal manifestations and a clear association with HLA-B27. Patients usually describe the insidious onset of dull, aching pain in the lower lumbosacral area with marked stiffness in the back as well, particularly in the morning or after prolonged rest. Inflammatory pain and stiffness improves with exercise or activity, in contrast to typical mechanical or degenerative spinal pain. Patients often note symptoms during the night, which disrupts sleep. As the

name implies, the disease leads to variable degrees of spinal ankylosis with loss of spinal motion and decreased chest expansion. AS typically begins before age 30, often in adolescence. Extra-articular manifestations, particularly iritis, should raise suspicion of the diagnosis in patients with associated back symptoms. With the recent development of effective drug treatments for AS, which may prevent ankylosis and deformity, earlier recognition of patients with inflammatory spinal disease is of increased importance. Fibromyalgia (FMS) is a very common syndrome of chronic, widespread musculoskeletal pain and stiffness, usually associated with fatigue, nonrestorative and fragmented sleep, and discrete myofascial tender points. Though the syndrome may present at any age, many patients are under age 40. Nearly 80 percent of patients with FMS report low back pain and, in a rheumatology spine practice, 12 percent of persons evaluated for back pain were found to have previously unrecognized FMS. The condition is identified clinically with findings of widespread tenderness in characteristic muscle points. Laboratory and imaging studies are normal. Often patients exhibit an array of other symptoms or conditions, including depression, fatigue, cognitive impairment, tempormandibular joint syndrome, irritable bowel syndrome, headache and nondermatomal paresthesias or numbness. Patients presenting with symptoms and findings suggestive of FMS should be evaluated for other medical causes of widespread myofascial pain, such as hypothyroidism, polymyalgia rheumatica, vitamin D deficiency (osteomalacia) or statin therapy.

Daniel Mazanec, MD, is Associate Director of the Cleveland Clinic Center for Spine Health and Head of Spine Medicine. He specializes in evaluation and medical management of spinal disorders, medical acupuncture and adult rheumatology.

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Musculoskeletal Causes of Back and Neck Pain By Gordon R. Bell, MD

Some common musculoskeletal conditions can pose a diagnostic dilemma in patients presenting with back and neck pain. It is important, therefore, for the clinician to ask the patient to describe the character of the pain. Most back conditions presenting with either back or leg pain have a mechanical component to the pain. In other words, there are usually clear provocative and palliative factors associated with the pain. Pain that is present constantly, regardless of position or activities, is rarely from mechanical neural compression (“pinched nerve”). Gordon R. Bell, MD Dr. Bell can be contacted at 216.444.8126 or [email protected].

Constant leg pain, for example, should alert the clinician to the possibility of neuropathic pain. Such neuropathic pain usually is not helped by surgery and often requires medical management. Noctural pain is common with arthritic pain, so that patients with hip arthritis commonly are awakened with pain. Other features of the pain that suggest a hip etiology include a limp, difficulty in putting on shoes and socks due to pain and limitation of hip motion, and difficulty in climbing stairs. In addition to the character of the pain, it is important for the clinician to listen to the patient’s description of the location of the pain. The most common sites of clinical lumbar disc disease are the L4-5 and L5-S1 levels, so most leg pain has either an L5 or an S1 dermatomal distribution, characterized by pain that radiates below the knee into the calf. More proximal leg pain should alert the clinician to the possibility of other etiologies besides radiculopathy. Proximal anterior thigh and groin pain could indicate a high lumbar radiculopathy with an L4 or L3 dermatomal distribution. Such pain could also, however, come from the hip. Indeed, most hip pain is associated with groin pain. Another diagnostic possibility associated with groin pain includes inguinal hernia. Patients with a lumbar radiculopathy rarely limp from the pain. They might limp due to leg weakness from a neurogenic cause, but rarely from radicular pain. Therefore, a musculoskeletal cause of the pain should be suspected in a patient with an antalgic (painful) gait. An antalgic gait is characterized by a shortened stance phase of the gait cycle as the patient tries to limit the amount of time that he or she is standing on the affected leg.

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The clinical exam should include both a neurologic and a musculoskeletal component. A patient who presents with groin pain and an antalgic gait should be suspected of having a hip etiology for the pain, such as avascular necrosis (AVN) or arthritis, until proven otherwise. Clinical affirmation of a hip cause for the pain comes from reproducing the patient’s typical pain by hip rotation. Patients with arthritic hip pain commonly exhibit a painful restriction of hip motion, particularly with flexion and internal rotation.

Patients with arthritic hip pain commonly exhibit a painful restriction of hip motion, SDUWLFXODUO\ZLWKÁH[LRQDQGLQWHUQDOURWDWLRQ

Another common masquerader of back and leg pain is greater trochanteric bursitis. The greater trochanter is the bony projection on the lateral aspect of the hip that serves as an attachment for some of the hip muscles. As with other such bony projections, a bursa develops in order to minimize the friction of the muscles and other structures that glide over the bone. If the bursa becomes inflamed, it can be painful. A patient with trochanteric bursitis typically describes pain directly over the tip of the greater trochanter and commonly gives a history of night pain when they lie on the affected side. The diagnosis is made by reproducing the patient’s pain by direct palpation of the trochanter. The diagnosis can be confirmed by injecting the trochanteric bursa with a combination of a local anesthetic agent and a corticosteroid.

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As with the lumbar spine, conditions emanating from structures other than the cervical spine can mimic cervical spine conditions. Pain from the shoulder commonly is mistaken for either neck pain or cervical radiculopathy. It is important for the clinician to have the patient accurately describe the character and location of the pain. Nocturnal pain that awakens the patient is uncommon with a cervical radiculopathy, although such pain can certainly make it difficult for the patient to get to sleep. Shoulder pain from either glenohumeral arthritis, AVN or rotator cuff disease commonly presents with night pain that awakens the patient. Patients with rotator cuff disease and other painful shoulder conditions often have pain with overhead reaching. Patients with a cervical radiculopathy, on the other hand, usually obtain relief of their arm pain by elevating their affected arm behind their head. This maneuver is called the shoulder abduction relief sign and provides relief of radicular pain by enlarging the neural foramen. This maneuver is nearly pathognomonic of cervical radiculopathy and should always be sought in the clinical history.

Any complaint primarily involving the shoulder or proximal arm mandates a careful shoulder exam and, if suspicious of shoulder pathology, appropriate shoulder radiographs. Rotator cuff tears commonly are associated with supraspinatus and infraspinatus muscle atrophy and weakness of external rotation. These findings should be specifically sought. As noted above, patients with adhesive capsulitis have restricted active and passive motion and commonly have severe restriction of internal rotation to the extent that they may not be able to put their affected hand in their rear pocket.

Gordon R. Bell, MD, is Associate Director of the Cleveland Clinic Center for Spine Health and Vice Chair of the Department of Orthopaedic Surgery. His interests include degenerative conditions of the lumbar and cervical spine, spine fractures and athletic spine injuries.

Patients presenting with complaints of restricted shoulder motion, often associated with pain in the shoulder, may have primary shoulder pathology rather than cervical radiculopathy. This condition can be due to adhesive capsulitis (“frozen shoulder”) and commonly is seen in diabetic patients. Any diabetic patient with a primary shoulder region complaint associated with both active and passive restricted motion, particularly internal rotation, should be suspected of having a frozen shoulder.

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Metabolic Bone Disorders of the Spine By Augusto Hsia Jr., MD

Metabolic bone diseases can involve any bone in the body and often disrupt one or more of the four major FRPSRQHQWVRIERQHPLQHUDOVPDLQO\FDOFLXPDQGSKRVSKDWH PDWUL[FROODJHQÀEHUV RVWHRFODVWERQH remodeling cells) and osteoblast (bone-producing cells). The spine can be more greatly affected than other ERQHVEHFDXVHLWPDNHVXSDVLJQLÀFDQWSRUWLRQRIWKHERG\·VERQHPDVVDQGDOZD\VKDVVRPHVRUWRI bone remodeling and repair process going on.

Augusto Hsia Jr., MD Dr. Hsia can be contacted at 216.445.3450 or [email protected].

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Major metabolic bone disorders that can affect the spine include Paget’s disease, primary hyperparathyroidism, osteomalacia and osteoporosis. Paget’s disease is a localized disorder of bone remodeling. The process is initiated by an increase in osteoclast-related bone resorption with subsequent compensatory increase in disorganized new bone formation. The structural change produces bone that is expansive in size, less compact and more susceptible to fracture than normal bone. Patients generally are asymptomatic and often diagnosed incidentally when an elevated serum alkaline phosphatase is noted on routine laboratory screening or when an X-ray is taken for an unrelated problem. The pathognomonic radiographic findings include expansion of bone, cortical thickening, coarsening of trabecular markings and typical lytic changes.

lates the release of calcium and phosphate from bone, as well as resorption of calcium from the kidneys, and increases intestinal absorption of calcium and phosphate by stimulating synthesis of 1,25 dihydroxy vitamin D. The result is heightened levels of serum calcium. Osteitis fibrosa is seen in hyperparathyroidism and often is a result of aggressive bone resorption. It appears microscopically as microfractures and microhemorrhages with hemosiderin-filled macrophages and osteoclasts that become dispersed throughout fibrous tissues. Progressive focal bone resorption and fibrosis results in macroscopically visible cysts that coalesce to form brown tumors or osteoclastomas. Nonspecific back and joint pains may then develop. Spinal pain also can result from associated compression fractures. There is a rare association with gait disturbances, hyperreflexia and muscle atrophy mimicking cervical myelopathy that resolves after correction of hyperparathyroidism.

Symptomatic patients can have mechanical back pain from an enlarged pagetic vertebra and accelerated degeneration. Microfractures frequently occur, causing back discomfort. Hypervascularity in pagetic bones causes an increased sensation of warmth in the spine. Neurologic compromise from compression of neural tissues adjacent to pagetic bone can cause radicular and central stenosis symptoms. Rare sarcomatous degeneration leading to osteosarcoma also has been reported.

Osteomalacia is softening of the bones caused by Vitamin D deficiency. Vitamin D encourages absorption of calcium and phosphate from the intestines. In osteomalacia, the bones have a normal amount of collagen in the matrix, but have insufficient calcium (poor mineralization). In children, osteomalacia is called rickets.

Primary hyperparathyroidism is a relatively common disorder with an incidence of one in 500. It usually is a result of increased secretion of PTH — which regulates the level of calcium and phosphate in the blood — by a solitary benign adenoma. Primary hyperparathyroidism, metastatic disease and certain immunologic disorders like sarcoidosis account for the majority of clinical hypercalcemia. PTH stimu-

Other causes of osteomalacia are renal and liver failure leading to altered Vitamin D metabolism, hypophosphatemia (Fanconi’s Syndrome), and as a side effect from taking drugs like Dilantin® and phenobarbital. Osteomalacia causes a vague, dull, achy pain primarily in the lower back, pelvis and lower extremities, which worsens with physical activity. Vertebral fractures can occur as a result of bone

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Patient presented with focal back pain brought RQE\PLQRUWUDXPD3DLQSURJUHVVHGRYHUWLPH UDWKHUWKDQLPSURYLQJDQGZDVFRQVLVWHQWO\ DJJUDYDWHGE\DFWLYLW\3DWLHQW·VNQRZQ osteoporosis was a reason for further evaluation. The progressive collapse of the compression IUDFWXUHZDVDFOHDULQGLFDWLRQIRUN\SKRSODVW\ which gave good pain relief.

softening. In more severe cases, widespread pain can occur that mimics a diffuse pain syndrome like fibromyalgia. Osteomalacia can cause proximal extremity weakness that worsens with walking. Extremity pain and numbness has been reported, which can be confused with lumbar radiculopathy. Osteoporosis is characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a subsequent increased risk for fractures. It is the most prevalent metabolic bone disease; four out of 10 White women in the United States will experience a hip, spine or wrist fracture sometime during their lives. A bone mineral density test is used to definitely diagnose osteoporosis, assess fracture risk and measure response to treatment. Osteoporosis is asymptomatic until a fracture arises. Most vertebral fractures are stable because posterior spinal elements are intact.

paraspinal muscles. Significant thoracic kyphosis can result from multiple compression fractures. An osteoporotic spine is specifically problematic in spinal instrumentation with potentially higher rates of fusion failures. IV bisphosphonates and IV analog of PTH (Forteo®) that build up bone quickly have been used in these cases.

Augusto Hsia Jr., MD, is a medical spine specialist with the Cleveland Clinic Center for Spine Health. His specialty interests include acute and chronic low back pain, osteoporosis, spondyloarthropathy and lumbar canal stenosis.

Spine pain not only relates to the fracture itself, but also to stresses on the ligaments, facet joints and

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%UDFKLDO3OH[RSDWKLHV By Andrew Utter, MD

,QHYDOXDWLRQRIQHFNDQGDUPSDLQDQGZHDNQHVVGLVRUGHUVRIWKHEUDFKLDOSOH[XVDUHFKDOOHQJLQJIRU PDQ\SK\VLFLDQV1HXURORJLFORFDOL]DWLRQPD\VHHPLQWLPLGDWLQJGXHWRWKHFRPSOH[DQDWRP\RIWKH region. After localization, diagnosis involves consideration of a wide variety of unusual and interesting disorders responsible for these lesions (see table on page 12). The prognosis for neurological recovery PD\EHH[FHOOHQWRUH[WUHPHO\SRRUGHSHQGLQJRQWKHXQGHUO\LQJFDXVHRIWKHSOH[RSDWK\

Andrew Utter, MD Dr. Utter can be contacted at [email protected].

The brachial plexus is composed of five nerve roots uniting above the clavicle to form three trunks: the upper (C5 and C6), middle (C7) and lower (T1 and C8). Beneath the clavicle, the trunks separate to form six divisions and three cords, which then form the major nerves of the upper extremity. Lesions of the brachial plexus typically are unilateral and can be divided into upper or lower plexus lesions depending on the predominate trunk involved. Upper plexus lesions involve the C5 and C6 nerve roots and affect the rhomboids, deltoid, biceps, supinator, supraspinatus and infraspinatus muscles. The paralyzed muscles cause the arm to internally rotate and extend at the elbow with the palm facing upwards, sometimes called the “Waiter’s tip” position. In closed traumatic lesions of the upper trunk, the injury occurs with forceful lateral bending of the neck and downward displacement of the opposing shoulder, causing traction on the upper trunk of the brachial plexus. The classic example is shoulder dystocia during delivery, causing Erb-Duchenne palsy. Heavy backpacks in college students or soldiers also have led to weakness from excessive stretch on the upper trunk of the brachial plexus. Acute Idiopathic Brachial Plexitis is an illness of obscure nature first described in Parsonage and Turner in 1948 and is easily confused with cervical radiculopathy. The ventral nerve roots that contribute to the upper trunk are often involved, although Parsonage Turner Syndrome also may be isolated to a single nerve, particularly the long thoracic or phrenic nerve. The classic case involves an antecedent event such as an upper respiratory infection, flu-like illness, vaccination, pregnancy, child birth, trauma or surgery at a remote site. The illness begins two to three weeks later with an abrupt onset of intense burning pain

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or deep ache in the shoulder, upper arm or scapular area that lasts several days to several weeks before gradually resolving. Profound weakness of the deltoid, infraspinatus, supraspinatus and/or winging of the scapula follows as the pain subsides. Sensory and reflex changes occur thereafter. The evaluation of Parsonage Turner syndrome may involve MRI and EMG. If obtained early, MRI of the brachial plexus or shoulder girdle will reflect the acute denervation with increased T2 signal changes within the affected muscles without structural changes in the brachial plexus.1 MRI can rule out rotator cuff tears or impingement syndrome and can be useful if an early, specific diagnosis would be beneficial. Symptomatic treatment usually takes the form of narcotics acutely, amitryptiline or gabapentin and physical therapy to prevent adhesive capsulitis or “frozen shoulder” in this self-limited condition. Lower plexus lesions generally involve the C8 and T1 nerve roots and cause weakness and wasting of the intrinsic hand muscles and a characteristic clawhand deformity. Sensory loss is limited to the ulnar border of the hand and inner forearm. Traumatic injury to the lower trunk of the brachial plexus can occur as a consequence of traction on the adducted arm during a fall. Traumatic injury may also occur during birth, especially breech delivery — classically called Dejerine-Klumpke’s paralysis. Lastly, the lower trunk may be affected by compression from displaced fractures or callus formation of the first rib and/or clavicle or by an accessory cervical rib, as in the case of neurogenic thoracic outlet syndrome. Tumors infiltrating or compressing the brachial plexus often affect the lower trunk. The pain often is described as a constant, severe burning or freezing

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plexus. Relative sparing of the lower trunk may be due to shielding by the clavicle in radiation plexopathy. The pain is generally a minor complaint, unlike plexus invasion by metastasis. Radiation plexopathy characteristically shows myokymic discharges and fasciculations by EMG.

shoulder pain that radiates to the elbow and is made worse with shoulder movement. Pancoast’s tumor generally is a non-small-cell bronchogenic carcinoma occurring in smokers (see figure). Pancoast’s syndrome manifests as the tumor causes Horner’s syndrome and lower plexus injury by direct extension of the tumor from the pulmonary apex to the sympathetic chain and Stellate ganglion, posterior chest wall and C8 and T1 nerve roots. The treatment of these tumors involves fractionated radiation of 30-50 Gray, which produces pain relief in 40 percent to 70 percent of patients, but only a third has improvement in motor or sensory deficits.2 Breast cancer also may spread to the lower trunk via lymphatics adjacent to the axially lymph nodes, but infrequently causes Horner’s syndrome, unlike a lung carcinoma. The prognosis generally is better than lung cancer as well. It must be differentiated from radiation plexopathy, which generally requires a latency of at least one year except in patients receiving more than 6,000 cGy.3 Radiation plexopathy involves paresthesias of the first two digits with weakness and numbness of the C5-6 distribution or the upper

Benign nerve sheath tumors such as schwannomas and neurofibromas can affect any part of the brachial plexus and are amenable to surgical excision. Symptoms are generally pain and paresthesias. A Tinel’s sign is characteristic where lightly percussing over the mass elicits a tell-tale sensation of “pins and needles.” Schwannomas and solitary or fusiform neurofibromas can be resected completely, with pain relief and preservation of function in the large majority of cases with meticulous intrafascicular dissection. Plexiform neurofibromas in Neurofibromatosis type 1 generally require subtotal resection to preserve function as the tumor involves a large amount of functioning neural tissue. Plexiform neurofibromas, however, have a lower threshold to operate due to the 15 percent of these tumors that undergo malignant degeneration and the need to obtain tissue diagnosis.4 Panplexus lesions cause a flail arm where the entire arm is paralyzed, hanging uselessly at the side with a complete sensory loss only sparing the axilla and medial aspect of the upper arm. The usual cause is a motor vehicle collision. Evaluation may involve CT myelography and EMG to determine if the lesion is preganglionic or postganglionic. Preganglionic injury will show nerve root avulsion from the spinal cord and pseudomeningocele formation on CT myelography. In preganglionic injuries, EMG will show preservation of sensory nerve action potentials and normal conduction velocities due to the survival of the dorsal root ganglion.

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In contrast, postganglionic injuries cause Wallerian degeneration and diminished or absent sensory nerve action potentials and reduced conduction velocities. Postganglionic lesions when the nerve remains in continuity should show signs of improvement in three months with some chance for reasonable recovery. Postganglionic injuries with loss of continuity are surgical candidates for brachial plexus reconstruction. Following reconstruction, the prognosis is best for the upper plexus with return of shoulder and arm strength as compared with hand re-animation.

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Andrew Utter, MD, is a spine fellow in the Cleveland Clinic Center for Spine Health. He completed a neurosurgery residency at the Mayo Clinic in Rochester, Minnesota.

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REFERENCES

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1. Scalf RE, Wenger DE, Frick MA, Mandrekar JN, Adkins

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MC. MRI findings of 26 patients with Parsonage Turner

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Syndrome. AJR. 2007;189:W39-44. 2. Kori SH, Foley KM, Posner JB. Brachial plexus lesions in

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patients with cancer: 100 cases. Neurology. 1981;31:45-50.

‡ +HDY\EDFNSDFNV ‡ 7KRUDFLFRXWOHWV\QGURPH ‡ 'LVSODFHGIUDFWXUHVRUFDOOXVRIWKHFODYLFOHRUÀUVWULE

3. Johansson S, Svensson H, Denkeamp J. Timescale of evolution of late radiation injury after postoperative radiotherapy of breast cancer patients. Int J Radiat Oncol Biol Phys. 2000;48:745-750.

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4. Das S, Ganju A, Tiel R, Klein DG. Tumors of the brachial

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plexus. Neurosurgery Focus. 2007;22:1-5.

‡ 5DGLDWLRQXVXDOO\!F*\ ‡ 6WHUQRWRP\ZLWKH[FHVVLYHWUDFWLRQRQORZHUWUXQN ‡ 1HUYHEORFNVHVSHFLDOO\LQWUDVFDOHQHDQGD[LOODU\LQMHFWLRQV I N F L A M M AT O R Y ‡ 'LDEHWLFDP\RWURSK\ ‡ $FXWHLGLRSDWKLFEUDFKLDOSOH[LWLV3DUVRQDJH7XUQHUV\QGURPH H E R E D I TA R Y ‡ +HUHGLWDU\QHXUDOJLFDP\RWURSK\+1$  ‡ +HUHGLWDU\QHXURSDWK\ZLWKOLDELOLW\WRSUHVVXUHSDOV\+133

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February 20-22, 2009 3rd Annual International Symposium on Stereotactic Body Radiation Therapy and Stereotactic Radiosurgery Course Directors: Lilyana Angelov, MD, Gene Barnett, MD, Edward Benzel, MD, Sam Chao, MD, and John Suh, MD The Grand Floridian Resort and Spa Lake Buena Vista, Fla.

July 22-28, 2009 Spine Review Course Course Directors: Edward Benzel, MD, Doug Orr, MD, Lars Gilbertson, PhD, Greg Trost, MD, and Marc Eichler, MD Lutheran Hospital Castele Learning and Conference Center Cleveland, Ohio

Contact Martha Tobin at 216.445.3449 or 800.223.2273, ext. 53449, or at [email protected] for seminar details.

UPCOMING

Symposia C L E V E L A N D C L I N I C .O R G / S P I N E

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CLEVELAND CLINIC CENTER F O R S P I N E H E ALT H

CLEVELAND CLINIC CENTER FOR SPINE HEALT H

Locations

Clinical Trials

Cleveland Clinic 9500 Euclid Ave. Cleveland, Ohio 44195 216.444.BACK (2225) ,QGHSHQGHQFH)DPLO\+HDOWK&HQWHU 5001 Rockside Road Independence, Ohio 44131 216.986.4000 Lutheran Hospital 1730 West 25th St. Cleveland, Ohio 44113 216.363.2410 6RORQ)DPLO\+HDOWK&HQWHU 29800 Bainbridge Road Solon, Ohio 44139 440.519.6800

Prospective outcomes evaluation of decompression with or without instrumented fusion for lumbar stenosis ZLWKGHJHQHUDWLYHJUDGH,VSRQG\OROLVWKHVLV

6WURQJVYLOOH)DPLO\+HDOWKDQG6XUJHU\&HQWHU 16761 SouthPark Center Strongsville, Ohio 44136 440.878.2500 :HVWODNH)DPLO\+HDOWK&HQWHU 30033 Clemens Road Westlake, Ohio 44145 440.899.5555

Edward Benzel, MD 216.445.5514

Ajit Krishnaney, MD 216.445.3777

Randomized, controlled trial of Duragen plus adhesion barrier matrix to minimize DGKHVLRQVIROORZLQJOXPEDUGLVFHFWRP\ Edward Benzel, MD 216.445.5514

:LOORXJKE\+LOOV)DPLO\+HDOWK&HQWHU 2570 SOM Center Road Willoughby Hills, Ohio 44094 440.943.2500

A prospective, multicenter, randomized FRQWUROOHGVWXG\WRFRPSDUHWKHVSLQDO VHDODQWDVDQDGMXQFWWRVXWXUHGGXUDO repair with standard of care methods GXULQJVSLQDOVXUJHU\

$QDVVHVVPHQWRI3ERQHSXWW\ in anterior cervical fusion with instrumentation

&60VWXG\ Edward Benzel, MD 216.445.5514

7KHHIIHFWLYHQHVVRISK\VLFDOWKHUDS\IRU patients with lumbar spinal stenosis Daniel Mazanec, MD 216.444.6191

Iain Kalfas, MD 216.444.9064

23SXWW\ Michael Steinmetz, MD 216.445.4633

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Spinal Column SPRIN G 20 0 9 Co-Editor:

Edward C. Benzel, MD Director, Cleveland Clinic Center for Spine Health Co-Editor: Daniel J. Mazanec, MD, FACP Associate Director, Cleveland Clinic Center for Spine Health Head, Section of Spine Medicine Guest Medical Editors: Robert F. McLain, MD Daniel J. Mazanec, MD, FACP Marketing: Colleen Burke Kim Kerver Managing Editor: Christine Coolick Art Director: Anne Drago

Spinal Column is published by Cleveland Clinic’s Center for Spine Health to provide up-to-date information about the center’s research and services. The information contained in this publication is for research purposes only and should not be relied upon as medical advice. It has not been designed to replace a physician’s independent medical judgment about the appropriateness or risks of a procedure for a given patient.

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The Cleveland Clinic Foundation Spinal Column 9500 Euclid Avenue / AC311 Cleveland, OH 44195 For referrals to Cleveland Clinic’s Center for Spine Health, call 216.444.2225

S PIN A L C O LU MN | S P RIN G 20 0 9 | M A S Q U E R A D E R S

Dr.Connect ONLINE ACCESS TO YOUR PATIENT’S MEDICAL RECORD Whether you are referring from near or far, our new eCleveland Clinic service, Dr.Connect, can streamline your communication with our specialists. This new online tool offers you secure access to your patient’s Cleveland Clinic medical record. You can track your patient’s care in real time, without additional software or hardware other than an Internet connection. To establish a Dr.Connect account, please call 877.224.7367 or e-mail [email protected].

08-NEU-005

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