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Spinal Cord Compression and Myelopathies 1 3 Spinal Cord Compression and Myelopathies 1 3 William F. Schmalstieg and Brian G. Weinshenker Abstract Patients with signs and symptoms of acute myelopathy require urgent neurologic evaluation focused upon the identifi cation and management of treatable disorders. MRI of the spine is the imaging modality of choice to evaluate for a compressive lesion. When cord compression is present, sur- gical treatment is usually indicated. When compression is not detected, an analysis of precise lesion localization, nonneurological clinical features, MRI fi ndings, and serologic studies narrow the differential diagnosis. The key diagnostic considerations include demyelinating, vascular, infl amma- tory, infectious, and paraneoplastic disorders. Empiric high-dose corticos- teroid treatment is often indicated in noncompressive myelopathy; additional investigations are important to identify patients with relapsing or progressive disorders who may benefi t from preventive therapies. Patients whose symptoms continue to progress after initial immunosup- pressive treatment may benefi t from plasmapheresis and occasionally from biopsy for defi nitive diagnosis. Keywords CNS • Demyelinating autoimmune disease • Magnetic resonance imaging • Myelitis • Spinal cord compression • Spinal cord diseases • Transverse Acute myelopathies are potentially devastating etiologies of acute myelopathy are treatable, conditions that may result in irreversible loss of and rapid diagnosis and institution of appropri- mobility and control of bodily functions. Many ate treatment can prevent or reduce the extent of permanent damage to the spinal cord. Delays in the diagnosis and treatment of acute cord syn- W. F. Schmalstieg , MD (*) dromes are frequent and may contribute to loss Neurology , Mayo Clinic , of neurologic function [ 1 ] . Furthermore, some Rochester , MN , USA e-mail: [email protected] infl ammatory conditions that cause myelopathy may stabilize or remit but later relapse; patients B. G. Weinshenker , MD, FRCP(C) Neurology , Mayo Clinic , Rochester , MN , USA with such conditions may benefi t from mainte- e-mail: [email protected] nance prophylactic therapies, and therefore, K.L. Roos (ed.), Emergency Neurology, DOI 10.1007/978-0-387-88585-8_13, 235 © Springer Science+Business Media, LLC 2012 236 W.F. Schmalstieg and B.G. Weinshenker Fig. 13.1 Approach to diagnosis and management of acute and subacute myelopathies ( NMO neuromyelitis optica; LETM longitudinally extensive transverse myelitis; MS multiple sclerosis) consideration of the risk of relapse is important subacute spinal cord disorders and includes a even when spontaneous or treatment-induced diagnostic algorithm to distinguish compressive remission occurs. and noncompressive myelopathies and also to This chapter considers the clinical presenta- distinguish among the various noncompressive tion, evaluation, and management of acute and etiologies (Fig. 13.1 ). The key elements are high 13 Spinal Cord Compression and Myelopathies 237 index of suspicion and confi rmation, primarily infl ammation then leads to localized demyelina- with neuroimaging, but occasionally supported tion and frank ischemia of the cord [ 2 ] . by other laboratory studies. This chapter con- Vascular occlusions or other vascular anoma- cludes with treatment recommendations. lies can cause acute cord injury. The portion of the cord supplied by the anterior spinal artery is particularly vulnerable. Restricted fl ow of the Pathophysiology feeding vessels to this artery may produce water- shed ischemia, particularly at the terminal regions A review of spinal anatomy informs a discussion supplied by the dominant radicular artery of of the pathophysiology and clinical presentation Adamkiewicz as may occur during surgical cross- of acute disorders of the cord. The spinal cord clamping of the aorta. Other potential causes of extends between the medulla and the conus med- anterior spinal artery obstruction include aortic ullaris, the terminus of which ends opposite the dissection, atherosclerosis, cardiac embolism, L1 vertebral body. Much of the substance of the hypercoagulable states, and fi brocartilaginous cord is composed of large myelinated tracts, the embolism from intervertebral disk fragments. most clinically relevant of which include: Another uncommon but important vascular 1. Lateral corticospinal tracts carrying ipsilateral anomaly associated with myelopathy is the dural motor fi bers arteriovenous fi stula. In this condition, an abnor- 2. Spinothalamic tracts carrying contralateral mal connection of a dural artery to a vein results pain and temperature sensation in venous hypertension, resulting in damage to 3. Dorsal columns carrying ipsilateral joint posi- the cord and leading to the telltale distension of tion and vibratory sensation the epidural venous plexus that is an important The arterial vascular supply of the spinal cord radiologic sign of this entity. includes a single anterior spinal artery and two As elaborated in the section on differential posterior spinal arteries, which originate from the diagnosis, a wide variety of demyelinating, vertebral arteries. The anterior spinal artery is infl ammatory, and infectious conditions can pro- also supplied by multiple segmental arteries aris- duce intrinsic damage to the substance of the spi- ing from the thoracic and abdominal aorta. The nal cord. A detailed description of the underlying anterior spinal artery supplies the lateral corti- pathophysiology of each of these conditions is cospinal and spinothalamic tracts, whereas the beyond the scope of this text, and in many of dorsal columns are supplied by the posterior spi- these conditions the pathogenesis is poorly nal arteries. The venous drainage of the cord is understood. through the epidural venous plexus. One recent noteworthy discovery is that the The cord is surrounded by the meninges (pia, NMO-IgG antibody, a clinically validated bio- arachnoid, and dura mater), which are in turn marker of neuromyelitis optica (NMO), may be encircled by the vertebrae. The vertebral bodies responsible for an important portion of what had are anterior to the cord, the pedicles lateral, and been previously regarded as “idiopathic trans- the laminae and spinous processes posterior. verse myelitis.” NMO is an infl ammatory demy- In compressive lesions, such as epidural elinating disease characterized by recurrent, abscess or metastatic disease, obstruction of the severe attacks of optic neuritis and longitudinally epidural venous plexus initiates spinal cord extensive transverse myelitis [3 ] . The target of the injury. Impairment of venous drainage causes NMO-IgG antibody is the aquaporin-4 (AQP4) vasogenic edema, which is in turn followed by an water channel, which is highly expressed at the infl ammatory cascade mediated, in part, by pros- astrocytic end feet of the blood–brain barrier. taglandins and other infl ammatory cytokines. Current evidence suggests that this antibody is Simultaneously, the combination of external pathogenic and not merely a marker of autoim- mechanical compression and internal swelling of munity or disease severity. Brain MRI lesions in the cord disrupts axonal conduction. Subsequent patients with NMO occur in regions known to 238 W.F. Schmalstieg and B.G. Weinshenker express high levels of AQP4 [ 4 ] . Additionally, Table 13.1 (continued) transfer of pooled IgG antibodies from NMO-IgG Infectious-bacterial positive patients to rats reproduces lesions similar – Mycoplasma to those seen in human NMO [5, 6 ] . Antibody- – Chlamydia – Syphilis and complement-mediated cytotoxicity to astro- – Tuberculosis cytes occurs in vitro in the presence of AQP4 – Lyme disease (rare) autoantibodies and active complement and may Infectious-parasitic account for the tissue damage seen in pathologic – Schistosomiasis samples from patients with NMO [ 7 ] . Additional – Strongylosis mechanisms that may contribute to injury caused Infl ammatory – Sjögren syndrome by AQP4 specifi c autoantibodies include disrup- – Systemic lupus erythematosus tion of potassium and glutamate homeostasis due – Wegener granulomatosis to the physical association of AQP4 with an – Behçet disease inward rectifying potassium channel and the Sarcoidosis excitatory amino acid transporter EAAT2. Toxic/metabolic – Nitrous oxide toxicity – Copper defi ciency – Vitamin B12 defi ciency (rare) Differential Diagnosis Iatrogenic – Radiation myelitis The differential diagnosis of acute myelopathy is – Postvaccination myelitis – Intrathecal chemotherapy extensive, including structural, vascular, demy- Neoplasia elinating, infectious, infl ammatory, neoplastic, – Intradural, extramedullary tumors (meningioma, and paraneoplastic conditions (Table 13.1 ). neurofi broma) – Intramedullary tumors (astrocytoma, ependymoma) Table 13.1 Etiologies of acute and subacute myelopathies – Lymphomatoid granulomatosis – Intravascular lymphoma External compression Paraneoplastic myelitis – Metastatic spinal cord compression – Epidural abscess – Spinal stenosis – Disk herniation – Spinal fracture Structural – Extramedullary hematopoiesis – Epidural lipomatosis External compression of the spinal cord is an – Atlantoaxial instability important and treatable cause of acute myelopa- Syrinx Vascular thy. Recognition of these conditions with MR – Spinal cord infarct imaging is usually considered straightforward. A – Intraspinal hematoma typical example of cord compression in the set- – Dural arteriovenous fi stula ting of vertebral metastasis from a primary lung Demyelinating carcinoma is displayed
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