Version May 2024
INTRODUCTION — Polyradiculopathy refers to damage to multiple nerve roots sufficient to produce neurologic symptoms and signs such as pain, weakness, and sensory loss. This topic will review the signs and symptoms of polyradiculopathy by spinal region, and provide an overview of the most common etiologies. Diagnostic testing and the differential diagnosis are also discussed.
Cervical and lumbosacral radiculopathy are discussed in greater detail separately. (See "Clinical features and diagnosis of cervical radiculopathy" and "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis".)
CLINICAL PRESENTATION — The main feature that distinguishes radiculopathy from other neurologic disorders is that the symptoms and signs of radiculopathy follow sensory and motor nerve root distributions (figure 1 and figure 2 and figure 3 and table 1).
Because polyradiculopathy affects multiple nerve roots, it can mimic conditions such as polyneuropathy, plexopathy, and mononeuropathy multiplex, making the diagnosis quite challenging. Often, objective signs such as weakness, sensory loss, and reflex change are mild in comparison with complaints of pain and paresthesia. Although there are certainly exceptions to this rule, the subtlety of physical examination findings in polyradiculopathy is a consequence of collateral motor and sensory innervation and incomplete nerve root damage.
Although precise details as to the prevalence of polyradiculopathy by spinal region are not readily available, 60 to 90 percent of single-level radiculopathies occur in the lumbosacral levels. Cervical radiculopathy accounts for most of the balance, with thoracic radiculopathy representing only a small minority of cases [1]. It is likely that polyradiculopathy also follows a similar prevalence by region.
●Cervical polyradiculopathy – Cervical polyradiculopathy presents with neck pain radiating unilaterally or bilaterally into the arms with associated paresthesia, weakness, and sensory loss. The most common cause of cervical polyradiculopathy is degenerative cervical spondylosis, which can be accompanied by signs of cervical myelopathy such as spasticity and weakness in the lower extremities and bladder incontinence. (See "Clinical features and diagnosis of cervical radiculopathy" and "Cervical spondylotic myelopathy".)
●Thoracic polyradiculopathy – Thoracic polyradiculopathy is the least common of the polyradiculopathies, mainly because spinal stenosis and associated foraminal narrowing in this region is generally modest, even in older adults [2,3]. Symptoms include pain and paresthesia in the chest and abdomen and, occasionally, abdominal wall weakness with herniation of abdominal contents [4,5].
●Lumbosacral polyradiculopathy – Lumbosacral polyradiculopathy accounts for the majority of polyradiculopathy cases. Central canal spinal stenosis in this region classically presents as neurogenic claudication, characterized by an aching that begins in the buttocks and descends into the knees, is brought on by walking or exercise, and is relieved by forward flexion (see "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Symptoms'). Spinal stenosis may also affect the lateral recesses, producing compression of multiple nerve roots without claudication symptoms. Diabetic amyotrophy is another well-known, but less common cause of lumbosacral polyradiculopathy-like symptoms, although the exact localization of this disorder remains unresolved. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)
●Cauda equina syndrome – A variant of lumbosacral polyradiculopathy is the cauda equina syndrome, in which the cauda equina itself is compressed within the spinal canal. The most common cause for this is a large, central disc herniation or central spinal canal stenosis [6]. Cauda equina syndrome is generally considered a neurologic emergency characterized by progressive lower extremity weakness, sphincter dysfunction, and saddle anesthesia. Other causes of cauda equina syndrome include epidural abscess, epidural tumor, intradural extramedullary tumor, the tethered cord syndrome, inflammatory conditions including spinal arachnoiditis, chronic inflammatory demyelinating polyneuropathy, and sarcoidosis. The cauda equina syndrome can also be caused by infection with cytomegalovirus, herpes simplex virus, herpes zoster virus, Epstein-Barr virus, Lyme disease, mycoplasma, and tuberculosis. In the case of acute disk herniation, cauda equina syndrome may require urgent surgical evaluation and treatment to preserve neurologic function. (See "Anatomy and localization of spinal cord disorders", section on 'Cauda equina syndrome' and "Clinical features and diagnosis of neoplastic epidural spinal cord compression".)
ETIOLOGIES — The etiologies of polyradiculopathy can generally be divided into structural (or surgical) and nonstructural (or medical) categories (table 2). The most common etiologies, along with their evaluation and treatment, will be discussed in this section.
Spinal stenosis — Spinal stenosis refers to the narrowing of the spinal canal or intervertebral foramina. The majority of cases of spinal stenosis are caused by degenerative change (spondylosis), which is reviewed here briefly and discussed in detail separately. (See "Clinical features and diagnosis of cervical radiculopathy", section on 'Pathophysiology' and "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis", section on 'Degenerative spondylosis' and "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Pathophysiology'.)
Presenting with increasing frequency in the sixth and seventh decades, the initiating change in degenerative spinal stenosis is desiccation of the intervertebral discs. As a result of disc desiccation and loss of disc height, the posterior elements of the spine, including the facet joints and ligamentum flavum, become increasingly involved in axial load bearing. The stress placed on these structures results in compensatory bony and ligamentous hypertrophy and osteophyte formation, which narrows both the diameter of the central spinal canal and the neural foramina. Because the degenerative process occurs at multiple levels, polyradiculopathy often results.
Additional causes of spinal stenosis (table 2) include congenital conditions, such as hereditary spinal stenosis or achondroplasia, systemic conditions such as ankylosing spondylitis or Paget disease, and excess accumulation of epidural fat (epidural lipomatosis), which can be seen in patients with Cushing disorder, exogenous glucocorticoid exposure, or obesity [7-12].
The symptoms and signs of polyradiculopathy due to spinal stenosis vary according to spinal level:
●At the cervical level, symptoms of polyradiculopathy in isolation include arm pain, paresthesias, weakness, and sensory loss (see "Clinical features and diagnosis of cervical radiculopathy"). More worrisome is adjacent spinal cord dysfunction (ie, cervical myelopathy), characterized by leg weakness, gait difficulty, and incontinence of bowel or bladder. This condition is a potential neurologic emergency and may require urgent decompressive surgery. (See "Cervical spondylotic myelopathy".)
●Lumbar spinal stenosis may produce lower back pain radiating into the leg (similar to that which occurs in herniated nucleus pulposus) or may produce the clinical syndrome of neurogenic claudication [13]. Patients with neurogenic claudication characteristically experience aching that begins in the buttocks and descends to the knees, is brought on by walking or exercise, and is relieved by forward flexion. This can be distinguished from the symptoms of vascular claudication of the lower extremities, which is also characterized by pain with exercise. True vascular claudication is relieved by shorter rest periods, is not aggravated by lumbar extension, is accompanied by diminished or absent lower extremity pulses, and is often quite asymmetric. Central canal stenosis of the lumbar spine may also produce the cauda equina syndrome. (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Clinical presentation'.)
Magnetic resonance imaging (MRI) has become the test of choice in the evaluation of spinal stenosis (image 1), although bony changes such as osteophyte formation are better demonstrated by computed tomography (CT). (See "Clinical features and diagnosis of cervical radiculopathy", section on 'Imaging studies' and "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Neuroimaging'.)
Because the radiographic changes of spinal stenosis are so common in older patients, the history and physical examination remain critical in establishing the relevance of neuroimaging findings and determining appropriate therapy. Electrodiagnostic studies are often required to confirm the diagnosis when the clinical presentation is ambiguous. (See "Clinical features and diagnosis of cervical radiculopathy", section on 'Electrodiagnostic studies' and "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis", section on 'Neurodiagnostic testing'.)
The management of spinal stenosis and its associated manifestations is discussed separately in appropriate topic reviews. (See "Treatment and prognosis of cervical radiculopathy" and "Cervical spondylotic myelopathy", section on 'Treatment' and "Acute lumbosacral radiculopathy: Treatment and prognosis" and "Lumbar spinal stenosis: Treatment and prognosis".)
Tethered cord syndrome — The tethered cord syndrome is a developmental anomaly usually seen in children (see "Closed spinal dysraphism: Pathogenesis and types", section on 'Tethered cord syndrome'). It can also produce polyradiculopathy in adults. During early development, a defect in the dura mater allows communication of the spinal cord with subcutaneous tissues, anchoring the conus medullaris and preventing the normal upward migration of the spinal cord [14].
The tethered cord syndrome presents in childhood or in adulthood as pain in the lower extremities and perianal region, progressive weakness, sensory disturbances, and sphincter dysfunction [15-17]. Because the cauda equina and conus medullaris are affected, both spastic and flaccid bowel and bladder dysfunction may be noted [16]. In most adult cases, motor weakness does not follow a strict myotomal pattern [18].
In tethered cord syndrome, cutaneous signs of spinal dysraphism such as sacral dimples or tufts of hair over the lumbosacral spine are very frequent in pediatric-onset cases but present in only approximately 35 percent of adults [17].
MRI usually demonstrates a low-lying termination of the conus medullaris below the inferior aspect of the L2 vertebral body (image 2), but occasionally the conus level is at or above L2/L3 [17]. Associated structural abnormalities on MRI may include a thickened filum terminale, an intradural or extradural lipoma, a myelomeningocele, fibrous adhesions around the conus or the filum, a split cord malformation, and various types of cyst (eg, arachnoid, dermoid, enteric).
Surgical treatment of tethered cord syndrome involves lumbar or sacral laminectomy with sectioning of the thickened filum terminale [16]. A systematic review of 451 adult cases of tethered cord syndrome published in 2008 reported that surgery was associated with improvement in pain and motor deficits in 83 and 59 percent of patients, respectively, while sphincter and sensory deficits improved in 46 and 43 percent [17]. Most of the included studies were uncontrolled series or case reports, and few patients were followed beyond two years after surgery. Thus, the benefit of surgery for tethered cord syndrome is uncertain.
Primary tumors — A variety of primary tumors may cause polyradiculopathy (table 2) [19,20]. The one that most characteristically does so is ependymoma, classically presenting as a cauda equina syndrome [21]. Surgery is the preferred treatment for most primary tumors that produce polyradiculopathy, with the need for postoperative radiotherapy and chemotherapy dictated by tumor histology and the completeness of the surgical resection. (See "Intracranial ependymoma and other ependymal tumors" and "Spinal cord tumors" and "Clinical features and diagnosis of neoplastic epidural spinal cord compression".)
Leptomeningeal metastases — Cancer arising outside the central nervous system can metastasize to any structure of the central nervous system, including the membranes covering the brain and spinal cord, which are the dura mater, the arachnoid mater, and the pia mater. The last two are together called the leptomeninges. Tumor involvement of the leptomeninges is a condition termed "leptomeningeal metastases." It is also known by a variety of synonyms, including meningeal carcinomatosis, carcinomatous meningitis, and neoplastic meningitis. This disorder is reviewed here briefly and discussed in detail elsewhere. (See "Clinical features and diagnosis of leptomeningeal disease from solid tumors" and "Treatment of leptomeningeal disease from solid tumors".)
The cluster of symptoms related to leptomeningeal metastases is widespread (table 3) [22]. Leptomeningeal metastases can cause polyradiculopathy by direct involvement of the spinal nerve roots, and radicular pain is the most common presenting symptom. The primary malignancies that most frequently produce this syndrome are leukemia, lymphoma, breast cancer, lung cancer, melanoma, and gastrointestinal cancers.
The classic cerebrospinal fluid (CSF) findings of leptomeningeal metastases include a high opening pressure, low glucose concentration, high protein concentration, lymphocytic pleocytosis, and positive cytology for malignant cells [22-25]. Although most patients do not have all of these features, an entirely normal CSF examination is uncommon. Initial CSF examination reveals a mildly increased cell count in 50 to 60 percent of patients, elevated protein in a large majority, and low glucose in approximately 30 percent. In most cases, a positive cytology can be obtained with two separate samplings. However, CSF cytology is persistently negative in as much as 20 percent of patients with clinically or radiographically unequivocal leptomeningeal metastases. MRI may reveal contrast enhancement of the meninges and nerve roots in a diffuse or nodular pattern (image 3).
The diagnosis of leptomeningeal metastases is straightforward in the patient with advanced cancer, multifocal signs and symptoms, typical imaging findings by MRI, and positive CSF cytology. A contrast-enhanced MRI of the symptomatic region of brain or spine should be obtained prior to obtaining CSF by lumbar puncture or ventricular tap, because CSF removal can cause iatrogenic meningeal enhancement. A positive CSF cytology establishes the diagnosis of leptomeningeal metastases. At least two CSF samples, with a combined total of 30 mL, should be evaluated. However, obtaining CSF for cytology may be unnecessary in patients with typical signs and symptoms, characteristic MRI findings, and known widespread malignancy. (See "Clinical features and diagnosis of leptomeningeal disease from solid tumors", section on 'Diagnostic evaluation'.)
The treatment of leptomeningeal metastases arising from solid tumors is reviewed separately. (See "Treatment of leptomeningeal disease from solid tumors".)
The treatment of leptomeningeal metastases in hematologic malignancies, especially large cell lymphomas and acute leukemias, is also discussed elsewhere. (See "Treatment of leptomeningeal disease from solid tumors" and "Secondary central nervous system lymphoma: Clinical features and diagnosis", section on 'Leptomeningeal dissemination' and "Involvement of the central nervous system (CNS) with acute myeloid leukemia (AML)".)
Diabetic thoracic radiculopathy — Diabetic thoracic radiculopathy is an uncommon syndrome that tends to affect patients with poorly controlled diabetes of long duration [2]. The main clinical features are severe, sharp, or burning pain and paresthesias in the abdominal or chest well [2,3]. Some patients may have associated abdominal muscle weakness with abdominal wall herniation [4,5]. Polyradiculopathy occurs in approximately 60 percent of patients [2]. The diagnostic electromyographic (EMG) findings are fibrillation potentials in the abdominal oblique muscles, rectus abdominis, intercostal muscles, and thoracic paraspinal muscles [2,3]. In general, the prognosis for patients with diabetic thoracic polyradiculopathy is good, with 11 of 12 patients in one series achieving remission within two years, the majority of these within the first year [2]. Spontaneous resolution is also noted in patients with abdominal wall bulging [4]. During the acute phase of illness, however, pain control may be challenging.
Patients with suspected thoracic radiculopathy should undergo EMG and nerve conduction studies to confirm the localization. Although disc herniations and spinal stenosis are uncommon at thoracic levels, MRI of the thoracic spine should be performed to exclude structural causes of radiculopathy. We suggest treatment with agents for neuropathic pain administered in the acute phase, such as tricyclic agents, dual reuptake inhibitors of serotonin and norepinephrine, or calcium channel alpha 2-delta ligands (gabapentin and pregabalin).
Our preferred agents are gabapentin titrated to 1200 mg three times daily or nortriptyline titrated to 100 mg daily at bedtime. In our clinical experience, patients often have a prompt and dramatic reduction in pain with this approach. For patients who do not improve with these agents, we also consider a short course of oral glucocorticoids (eg, prednisone at a dose of 60 mg daily for one to two weeks, followed by a taper) with careful glycemic control being maintained throughout the treatment period. However, there is no study clearly supporting the use of oral glucocorticoids for this indication.
Diabetic amyotrophy — Diabetic amyotrophy is reviewed here briefly and discussed in detail elsewhere. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)
Diabetic amyotrophy is a condition referred to by many names, including diabetic lumbosacral polyradiculoneuropathy, proximal diabetic neuropathy, diabetic lumbosacral plexopathy, and Bruns-Garland syndrome. It is not a pure lumbosacral plexopathy because it also affects the lumbosacral nerve roots and peripheral nerves. The most likely cause of diabetic amyotrophy and the clinically similar condition of idiopathic lumbosacral radiculoplexus neuropathy is ischemic injury from a nonsystemic microvasculitis [26,27]. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)
Diabetic amyotrophy usually affects patients with type 2 diabetes of middle or older age [26,27]. Diabetic amyotrophy may be the first symptom of diabetes, and most patients who develop the condition do not have poorly controlled diabetes. The traditional features include the acute, asymmetric, focal onset of pain followed by weakness involving the proximal leg. However, onset in the distal leg is not uncommon. Furthermore, the condition becomes more widespread and symmetric with time. In many cases, the symptoms and signs progress to affect the contralateral limb and the distal legs. There are associated symptoms including fever, weight loss, malaise, and autonomic failure. Progression occurs over months and is followed by partial recovery in most patients. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Clinical features'.)
The diagnosis of diabetic amyotrophy is based upon the presence of suggestive clinical features in a patient with known or newly diagnosed diabetes mellitus. Appropriate laboratory investigations, particularly electrodiagnostic studies, and neuroimaging in select patients are useful to exclude other peripheral and central nervous system etiologies as a cause of the neurologic symptoms and signs. Abnormalities on electrodiagnostic studies typically involve the lumbar and sacral roots, the lumbosacral plexus, and the peripheral nerves [27]. Nerve conduction studies show markedly reduced amplitudes of the compound muscle action potentials and sensory nerve action potentials (SNAPs), while conduction velocities show only mild slowing. Needle EMG shows fibrillation potentials, decreased motor unit recruitment, and long-duration, high-amplitude motor unit action potentials. Paraspinal muscles are typically involved; this finding demonstrates that pathology must exist outside of the lumbosacral plexus. In patients who do not have diabetes, idiopathic lumbosacral radiculoplexus neuropathy is the primary consideration in the differential diagnosis. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Diagnostic evaluation'.)
While some clinical improvement is the rule with diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy, most patients do not recover completely. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Prognosis'.)
No treatments are proven to be effective for diabetic amyotrophy or for idiopathic lumbosacral radiculoplexus neuropathy. Symptomatic management is the mainstay of treatment. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Treatment'.)
Diabetic cervical radiculoplexus neuropathy — Polyradiculopathy due to diabetes at the cervical level was postulated as early as the late 19th century, but was more precisely characterized only in the modern era [28]. Typical features include subacute development of weakness, pain, and numbness, usually with focal onset, sometimes evolving into a multifocal or bilateral process.
The upper, middle, and lower trunks of the brachial plexus are clinically involved with equal frequency, and panplexopathy may occur. Simultaneous involvement of the thoracic, lumbosacral, or contralateral cervical segments is frequent. In the largest series of patients with diabetic cervical radiculoplexus neuropathy, MRI of the brachial plexus was abnormal in 47 of 48 patients who underwent imaging [28].
The pathology of diabetic polyradiculopathy is mainly ischemic injury from microvasculitis. These findings are similar in many respects to those described for diabetic amyotrophy with lower limb involvement. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Cervical and thoracic involvement'.)
Lyme disease — Lyme radiculoneuritis is one of the three most common presentations of acute, early neurologic Lyme disease. Lyme radiculoneuritis is reported in approximately 3 percent of Lyme disease cases in the United States.
Lyme radiculoneuritis can mimic a mechanical radiculopathy (eg, sciatica) with radicular pain in one or several dermatomes, accompanied by corresponding sensory, motor, and reflex changes. This disorder should be considered in patients in endemic areas presenting in spring through autumn with severe limb or truncal radicular pain without an apparent mechanical precipitant.
The evaluation includes electrodiagnostic testing and imaging as outlined below to confirm the neurologic localization and exclude mechanical and structural disease. The diagnosis of Lyme rests on serologic testing, which is highly sensitive and specific.
Lyme radiculoneuritis is discussed in detail separately. (See "Nervous system Lyme disease", section on 'Radiculoneuritis (Bannwarth syndrome)'.)
Polyradiculopathy in HIV and AIDS — Rapidly progressing lumbosacral polyradiculopathy (cauda equina syndrome) occurs mainly in HIV-infected patients with severe immunosuppression. The most common cause is cytomegalovirus infection, followed by neurosyphilis and lymphomatous meningitis [29-31]. Since the advent of highly active antiretroviral therapy, this clinical entity is uncommonly seen, except in the untreated patient with advanced AIDS.
The clinical picture is dominated by the subacute onset of lower extremity weakness and numbness in a patient with advanced HIV-related immunosuppression and often a prior diagnosis of cytomegalovirus disease in other sites [32]. Sensory dysesthesia can begin in the feet or in the saddle region from involvement of sacral roots. Symptoms can be asymmetric, especially early in the course of the disease. Clinical progression occurs rapidly over days, leading to flaccid paraparesis or paraplegia with urinary retention and sphincter dysfunction. A less fulminant, more slowly progressing variant has also been described. On examination, a lumbar sensory level and lower extremity areflexia with saddle anesthesia can be demonstrated. Sacral radiculomyelitis can also be seen secondary to genital herpes simplex virus infection; this syndrome can occur at any stage of HIV disease. Radiculomyelitis has also been reported rarely with syphilis and tuberculosis infection in HIV-infected patients.
Lumbar puncture characteristically shows CSF pleocytosis, frequently predominated by polymorphonuclear cells, elevated protein, and, in a minority of patients, decreased glucose [33,34]; with lymphomatous meningitis, the CSF typically reveals a lymphocytic pleocytosis. Cytomegalovirus can be cultured from the CSF in some cases. Viral culture cannot be used as the sole means of diagnosis because of false-negative results and the fact that viral cultures may not turn positive for up to a week [30,35]. Polymerase chain reaction testing for cytomegalovirus DNA in the CSF can provide a more rapid diagnosis [36]. Testing for syphilitic polyradiculopathy in these cases is also recommended; a negative treponemal serologic test in the serum or CSF renders this diagnosis unlikely.
Electrophysiologic studies can help confirm the presence of polyradiculopathy and exclude a polyradiculoneuropathy; sensory action potentials are present in patients with a polyradiculopathy but are abnormal in patients with a polyradiculoneuropathy. MRI of the spine should be performed mainly to exclude structural lesions and cauda equina compression. Cauda equina root enhancement with contrast-enhanced MRI is seen in many, but not all, patients with cytomegalovirus-related polyradiculopathy. However, this finding is not specific and is seen in other inflammatory and neoplastic conditions involving the cauda equina.
Diagnosis and management of AIDS-related neurologic disease caused by cytomegalovirus (CMV), syphilis, tuberculosis, and lymphoma are reviewed in detail elsewhere. (See "AIDS-related cytomegalovirus neurologic disease" and "Syphilis in patients with HIV" and "Central nervous system tuberculosis: An overview" and "HIV-related lymphomas: Primary central nervous system lymphoma".)
DIAGNOSTIC TESTING — A diagnosis of polyradiculopathy can be made on purely clinical grounds in most cases. However, localization of the problem to multiple nerve roots is often challenging, because lesions of the brachial or lumbosacral plexus, peripheral nerves, or central nervous system can present similarly. The tests that are most useful in establishing a diagnosis of polyradiculopathy are the following:
●Electromyography (EMG) and nerve conduction studies
●Magnetic resonance imaging (MRI) with and without contrast
●Lumbar puncture for cerebrospinal fluid (CSF) analyses
Electrodiagnostic studies — Electrodiagnostic studies allow the differentiation between radiculopathy and other neurologic conditions such as polyneuropathy, compression neuropathy, myopathy, plexopathy, and motor neuron disease. (See "Overview of electromyography" and "Overview of nerve conduction studies".)
The most useful electrodiagnostic finding in patients with radiculopathy is an abnormal needle EMG. Needle EMG can provide evidence for physiologic abnormalities consistent with a radiculopathy, grade the extent and severity of injury, and determine its duration [37]. One major limitation to needle EMG is in patients with polyradiculopathy predominantly affecting the dorsal roots, in whom there may be no abnormalities on needle EMG despite substantial pain.
Needle EMG findings follow the distribution of a nerve root and include the following:
●Acute (less than one week): reduced recruitment
●Subacute (between one week and three months): reduced recruitment, fibrillation potentials, and positive sharp waves
●Chronic (greater than three months): increased motor unit potential amplitude, duration, and polyphasic motor unit potentials
The sensitivity of the needle EMG in patients with cervical radiculopathy varies from 50 to 72 percent, while in patients with suspected lumbosacral radiculopathy, needle EMG has a sensitivity of 36 to 64 percent [38-41]. Several limitations of the technique explain these modest sensitivities:
●Many patients with radiculopathy have pain and paresthesias alone and lack the motor involvement required to produce needle EMG abnormalities
●Abnormal spontaneous activity requires at least seven days before it appears in paraspinal muscles and several weeks to appear in limb muscles [37]
●Fibrillation potentials and positive sharp waves will disappear with time as reinnervation leads to recovery or chronic injury leads to loss of some muscle reactivity [37]
Nerve conduction studies are routinely performed in conjunction with EMG. They are most effective in eliminating polyneuropathy, plexopathy, and compression neuropathy as diagnostic considerations. However, nerve conduction studies have several limitations in establishing the diagnosis of polyradiculopathy:
●Conventional nerve conduction studies assess a small number of spinal levels, predominantly C8-T1 in the upper extremities and L5-S1 in the lower extremities.
●Compound motor action potential (CMAP) amplitude abnormalities are relatively uncommon in radiculopathy: for patients with L5/S1 radiculopathies, CMAPs were absent from the extensor digitorum brevis or flexor digitorum brevis muscles in only 6 percent, and amplitudes were decreased in just 24.1 percent [42]. The likelihood of finding CMAP abnormalities in patients with radiculopathy is reduced by overlapping nerve root innervation and the usually incomplete nature of root injury. For similar reasons, slowing of motor conduction velocities between proximal and distal stimulation sites is uncommon and, if present, limited in degree [37].
●Normal sensory nerve action potential (SNAP) amplitudes favor a diagnosis of radiculopathy rather than plexopathy or polyneuropathy because nerve root injury in radiculopathy is most often proximal to the dorsal root ganglion [37]. Nerve fiber degeneration therefore occurs in the axon that projects centrally from the dorsal root ganglion rather than from the one that projects peripherally. However, in inflammatory and neoplastic lesions, damage may occur distal to the dorsal root ganglion and consequently produce abnormal SNAPs. In addition, the SNAP amplitude may be reduced in a subset of patients with L5 nerve root involvement due to the dorsal root ganglia being located within the spinal canal itself [43].
The late responses known as the H reflex and F wave may be useful in the evaluation of polyradiculopathy.
●The H reflex is similar to a deep tendon reflex (see "Overview of nerve conduction studies", section on 'Late responses'). The main limitation of the H reflex test is that it is commonly obtainable only from the soleus and occasionally from the flexor carpi radialis, which restricts the number of spinal levels that it can assess. It is also somewhat nonspecific, being affected in disorders that injure the neurons anywhere along their path. However, one study that evaluated normal controls and those with an L5 or S1 radiculopathy found that the H reflex for S1 radiculopathy had a sensitivity and specificity of 50 and 91 percent, respectively [44]. In a broader patient population referred for polyradiculopathy, in whom polyneuropathy, cervical monoradiculopathy, and plexopathy are the main considerations in the differential diagnosis, the sensitivity of the H reflex would likely increase while the specificity would likely decrease.
●F waves are produced by antidromic activation of motor neurons (see "Overview of nerve conduction studies", section on 'Late responses'). F response latency was abnormal in 69 percent of 39 tibial and peroneal nerves in one study of patients with spinal stenosis [45]. Other studies reported that the sensitivity of prolonged F response latency was 70 to 80 percent in patients with L5-S1 monoradiculopathy [37]. Although the sensitivity of F response abnormalities for radiculopathy is relatively high, the specificity is limited, as any injury along the entirety of the nerve that is being stimulated may produce prolonged F responses.
Magnetic resonance imaging — MRI is the single best test for demonstrating structural pathology responsible for polyradiculopathy. Although spinal stenosis is readily identifiable on MRI, because degenerative changes of the spine are so common with age, the clinical history and examination are often the crucial factors in making a diagnosis of polyradiculopathy. Polyradiculopathy of infectious, inflammatory, or neoplastic origin may be accompanied by abnormal contrast enhancement of the nerve roots or may be entirely normal, but when these conditions are suspected, a contrast-enhanced MRI is essential to exclude more common structural causes [46,47].
Lumbar puncture — When no clear structural source for polyradiculopathy is identified on MRI, lumbar puncture is often the next step in evaluation. Although lumbar puncture may not establish a specific diagnosis, CSF abnormalities may guide further testing:
●In leptomeningeal metastases, the CSF white blood cell count is increased in >50 percent, the CSF protein is increased in approximately 80 percent, the CSF glucose is <40 mg/dL in 25 to 30 percent, and CSF cytology is positive for malignant cells in 80 to 90 percent with sufficient CSF sampling. (See 'Leptomeningeal metastases' above.)
●In Lyme meningitis, with or without radiculoneuritis, the CSF white count is elevated, predominated by lymphocytes or monocytes; the CSF protein is usually elevated; and the CSF glucose concentration is usually normal. However, CSF analysis is of limited utility if disease is limited to the peripheral nervous system. (See 'Lyme disease' above.)
●In lumbosacral polyradiculopathy associated with HIV/AIDS, the CSF white blood cell count is increased, frequently predominated by polymorphonuclear cells; the CSF protein is increased; the CSF glucose is normal or decreased; and CSF cultures are positive for cytomegalovirus in approximately 50 percent of cases. (See 'Polyradiculopathy in HIV and AIDS' above.)
DIFFERENTIAL DIAGNOSIS — As noted above, the multiple nerve roots that are affected in polyradiculopathy may lead to widespread complaints that can be confused with a variety of neurologic, musculoskeletal, and vascular disorders.
Although most polyradiculopathies produce pain and paresthesias, pure motor presentations can mimic central nervous system conditions including cerebrovascular infarction or hemorrhage, demyelinating disease, and brain neoplasms. These conditions can be differentiated from polyradiculopathy by increased tone, hyperactive reflexes, and abnormal neuroimaging findings. (See "Evaluation of peripheral nerve and muscle disease", section on 'Distinguishing peripheral from central nervous system disease'.)
Motor neuron disease is a neurodegenerative disorder of upper and lower motor neurons that can be difficult to distinguish from polyradiculopathy. Careful physical examination and electromyography (EMG) to detect abnormalities of bulbar muscles and midthoracic paraspinal muscles help to establish this diagnosis. The absence of any sensory complaints and pain is also suggestive of motor neuron disease over polyradiculopathy. (See "Clinical features of amyotrophic lateral sclerosis and other forms of motor neuron disease" and "Diagnosis of amyotrophic lateral sclerosis and other forms of motor neuron disease".)
A variety of peripheral nervous system disorders can imitate polyradiculopathy, and electrodiagnostic testing is often required to establish a clear diagnosis.
●Plexopathy is most often characterized by weakness and pain affecting multiple myotomes and dermatomes, and may be the single condition that most closely resembles polyradiculopathy on a clinical level. (See "Brachial plexus syndromes" and "Lumbosacral plexus syndromes".)
●Myopathy is usually symmetric, and rarely produces the same degree of pain, and never the same objective sensory findings that are seen in polyradiculopathy. (See "Approach to the patient with muscle weakness".)
●Polyneuropathy is typically distal and symmetric, but exceptions to these rules can produce a presentation similar to polyradiculopathy. (See "Overview of polyneuropathy".)
Musculoskeletal conditions such as tendonitis, myofascial pain syndrome, fibromyalgia, and bursitis can occasionally be confused with polyradiculopathy. Although they are characterized by pain without sensory loss or weakness, the pain produced by these conditions can result in functional weakness. (See "Overview of soft tissue musculoskeletal disorders".)
As noted above, vascular disease of the lower extremities can produce claudication symptoms that can be differentiated from neurogenic claudication by improvement after shorter rest periods, prominent asymmetry, lack of aggravation by lumbar spine extension, and diminution or absence of peripheral pulses. (See "Clinical features and diagnosis of lower extremity peripheral artery disease".)
Thoracic polyradiculopathy is often not initially suspected until more common intrathoracic and abdominal processes such as cardiac ischemia or gastrointestinal disease are eliminated.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Radiculopathy".)
SUMMARY
●Clinical features – The main feature that distinguishes radiculopathy from other neurologic disorders is that the symptoms and signs of radiculopathy follow sensory and motor nerve root distributions (figure 1 and figure 2 and figure 3 and table 1). (See 'Clinical presentation' above.)
•Cervical polyradiculopathy presents with neck pain radiating unilaterally or bilaterally into the arms with associated paresthesia, weakness, and sensory loss.
•Thoracic polyradiculopathy is the least common of the polyradiculopathies; symptoms include pain and paresthesia in the chest and abdomen and, occasionally, abdominal wall weakness with herniation of abdominal contents.
•Lumbosacral polyradiculopathy accounts for the majority of polyradiculopathy cases. Central canal spinal stenosis in this region classically presents as neurogenic claudication, characterized by an aching that begins in the buttocks and descends into the knees, is brought on by walking or exercise, and is relieved by forward flexion.
•The cauda equina syndrome, a variant of lumbosacral polyradiculopathy, is characterized by progressive lower extremity weakness, sphincter dysfunction, and saddle anesthesia.
●Etiologies – The etiologies of polyradiculopathy can generally be divided into structural (or surgical) and nonstructural (or medical) categories (table 2). (See 'Etiologies' above.)
•Structural causes
-Spinal stenosis refers to the narrowing of the spinal canal or intervertebral foramina. The majority of cases of spinal stenosis are caused by degenerative change (spondylosis). (See 'Spinal stenosis' above.)
-The tethered cord syndrome is a developmental anomaly usually seen in children that can also produce polyradiculopathy in adults. (See 'Tethered cord syndrome' above.)
-A variety of primary tumors may cause polyradiculopathy. (See 'Primary tumors' above.)
-Leptomeningeal metastases can cause polyradiculopathy by direct involvement of the spinal nerve roots; radicular pain is the most common presenting symptom. (See 'Leptomeningeal metastases' above.)
•Nonstructural causes
-Diabetic thoracic radiculopathy is an uncommon syndrome that tends to affect patients with poorly controlled diabetes of long duration. (See 'Diabetic thoracic radiculopathy' above.)
-Diabetic amyotrophy is a type of lumbosacral plexopathy that also affects the lumbosacral nerve roots and peripheral nerves. (See 'Diabetic amyotrophy' above.)
-Lyme disease may affect the nervous system; the classic manifestations are lymphocytic meningitis, cranial neuropathy, and radiculoneuritis, alone or in combination. (See 'Lyme disease' above.)
-A rapidly progressing lumbosacral polyradiculopathy (cauda equina syndrome) occurs mainly in HIV-infected patients with severe immunosuppression. (See 'Polyradiculopathy in HIV and AIDS' above.)
●Diagnosis and evaluation – A diagnosis of polyradiculopathy can be made on purely clinical grounds in most cases. However, localization of the problem to multiple nerve roots is often challenging because lesions of the brachial or lumbosacral plexus, peripheral nerves, or central nervous system can present similarly. The tests that are most useful for establishing a diagnosis of polyradiculopathy are electromyography (EMG) and nerve conduction studies, magnetic resonance imaging (MRI) of the relevant spinal level with and without contrast, and lumbar puncture for cerebrospinal fluid (CSF) analyses. (See 'Diagnostic testing' above.)
●Differential diagnosis – The multiple nerve roots that are affected in polyradiculopathy may lead to widespread complaints that can be confused with a variety of neurologic, musculoskeletal, and vascular disorders. (See 'Differential diagnosis' above.)
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟
