What does interruption of the dorsal spinal cord columns cause in a client with spinal cord injury?

SA-CME LEARNING OBJECTIVES

After completing this journal-based SA-CME activity, participants will be able to:

■ Describe the anatomy and function of the major neuronal pathways involved in incomplete cord syndromes.
■ Localize ISCS lesions in the spinal cord according to the associated clinical findings.
■ Cite examples of common diseases associated with each of the six incomplete cord syndromes described in this review.

Introduction

The spinal cord serves as a highway for information to travel between the brain and peripheral nervous system. The information is transmitted by way of highly specialized afferent (traveling toward the cord and relaying sensory information) and efferent (predominantly motor, traveling away from the cord) pathways, relay neurons, and interconnections. Interruption of these pathways results in development of spinal cord syndromes, which are classified neurologically as complete or incomplete. Each of these syndromes has a variety of causes and clinical manifestations.

Complete cord syndrome is caused by lesions involving a whole spinal cord segment and will cause complete motor, sensory, and autonomic dysfunction below the level of the lesion (1,2). It has the worst prognosis for recovery and is due to entities such as cord transection secondary to trauma, severe tumor compression of the cord, epidural abscess, and acute inflammatory processes such as transverse myelitis.

Incomplete spinal cord syndrome (ISCS) occurs when lesions involve specific structural and/or functional anatomic regions of the cord, with some preservation of sensory and/or motor function below the lesion. There are six basic types of ISCS based on clinical findings: (a) central cord syndrome (CCS), (b) Brown-Séquard syndrome, (c) ventral (anterior) cord syndrome (VCS), (d) dorsal (posterior) cord syndrome (DCS), (e) cauda equina syndrome (CES), and (f) conus medullaris syndrome (CMS) (1,3). Table 1 summarizes these syndromes, including tracts involved, location of involved lesions, common causes, and typical clinical manifestations.

Table 1: Summary of ISCS Features

Knowledge of the spinal cord anatomy and the ability to recognize the typical clinical findings of common spinal cord syndromes are essential for patient examination and treatment. Imaging plays a pivotal role in localizing disease and determining the cause, treatment, and prognosis. Herein, we review the relevant anatomy of three important white matter tracts—corticospinal tract (CST), spinothalamic tract (STT), and dorsal (posterior) columns—the understanding of which is crucial for determining the type of ISCS.

Spinal Cord Anatomy

The spinal cord, which is contained within the thecal sac, begins below the foramen magnum and ends at the tip of the conus medullaris (between the T12 and L2-3 disk level), typically ending around the L1 or L1-2 disk level (4). The cord has a tubular shape that on a cross section is elliptical in the cervical region and round in the thoracic region. The cord is thickest in two areas that innervate the limbs: a cervical enlargement at the C5-T1 spinal level that innervates the upper extremities, and a smaller lumbar enlargement at the T9-L2 spinal level that innervates the lower extremities and pelvis (5). The spinal cord is divided along its length into 31 spinal segments that give rise to the spinal nerves: eight cervical, 12 thoracic, five lumbar, and five sacral segments, and one coccygeal segment. A thin band of connective tissue, the filum terminalis, extends from the tip of the conus medullaris through the caudal end of the thecal sac and attaches to the first coccygeal segment (6).

The spinal cord is nearly completely separated into right and left halves by a deep ventral median fissure anteriorly and a shallower dorsal median sulcus and septum posteriorly (6). Dorsal nerve roots enter the cord on the posterior cord surface through dorsolateral sulci. Ventral nerve roots emerge from the anterior cord surface through the ventrolateral sulci (Fig 1) (6). The cord surface topography is best demonstrated on axial T2-weighted magnetic resonance (MR) images (Fig 1b)—especially those obtained with heavily T2-weighted gradient-echo sequences (eg, fast imaging employing steady-state acquisition, constructive interference in steady state, balanced fast field echo, and driven equilibrium)—and computed tomographic (CT) myelograms.

Figure 1a. Axial anatomy of the spinal cord. (a) Drawing illustrates a cross section of the thoracic cord, with central H- or butterfly-shaped gray matter and peripheral white matter. The central gray matter has a dorsal (posterior) horn (dark blue) involved in sensory processing, a lateral horn (yellow) containing interneurons and autonomic nuclei, and a ventral (anterior) horn (pink) that contains motor neurons. White matter tracts—specifically the dorsal columns (DC), lateral CST, and STT—are located at the periphery. Note the somatotropic organization of fibers in the CST and STT, from medial to lateral: thoracic (T), lumbar (L), and sacral (S) fibers. Ten percent of the CST fibers do not decussate and continue ipsilaterally as the anterior CST (★). Dorsal and ventral nerve roots enter the spinal cord at the dorsolateral (straight arrow) and ventrolateral (curved arrow) sulci, respectively. (Reprinted, with permission, from Jill K. Gregory.) (b) Axial T2-weighted fast imaging employing steady-state acquisition MR image of the cervical cord shows dorsal nerve roots (arrowheads) at the dorsolateral sulci and ventral nerve roots (arrows) at the ventrolateral sulci.

Figure 1a.

Figure 1b. Axial anatomy of the spinal cord. (a) Drawing illustrates a cross section of the thoracic cord, with central H- or butterfly-shaped gray matter and peripheral white matter. The central gray matter has a dorsal (posterior) horn (dark blue) involved in sensory processing, a lateral horn (yellow) containing interneurons and autonomic nuclei, and a ventral (anterior) horn (pink) that contains motor neurons. White matter tracts—specifically the dorsal columns (DC), lateral CST, and STT—are located at the periphery. Note the somatotropic organization of fibers in the CST and STT, from medial to lateral: thoracic (T), lumbar (L), and sacral (S) fibers. Ten percent of the CST fibers do not decussate and continue ipsilaterally as the anterior CST (★). Dorsal and ventral nerve roots enter the spinal cord at the dorsolateral (straight arrow) and ventrolateral (curved arrow) sulci, respectively. (Reprinted, with permission, from Jill K. Gregory.) (b) Axial T2-weighted fast imaging employing steady-state acquisition MR image of the cervical cord shows dorsal nerve roots (arrowheads) at the dorsolateral sulci and ventral nerve roots (arrows) at the ventrolateral sulci.

Figure 1b.

In contrast to the gray matter in the brain, the gray matter in the spinal cord is located centrally and surrounded by white matter columns. The gray matter appears as an H- or butterfly-shaped region in the center of the cord that is relatively hypointense on T1-weighted MR images and hyperintense on T2-weighted and other fluid-sensitive MR images. The peripherally located ascending and descending white matter columns appear hyperintense to gray matter on T1-weighted MR images. The central gray matter has ventral and dorsal extensions (ie, horns) along the entire length of the cord, with small lateral horns extending from approximately the T1-L1 spinal segments (Fig 1a) (6). Dorsal horns are primarily involved in sensory processing and receive primary afferent fibers from the dorsal roots of spinal nerves. Ventral horns contain motor neurons, and lateral horns contain autonomic nuclei and interneurons (6). The ventral and dorsal gray matter commissures form a horizontal line connecting the arms of the “H” around the central canal. When visible at MR imaging, the central canal appears as a thin longitudinally oriented, nonenhancing fluid-signal-intensity structure between the ventral one-third and dorsal two-thirds of the cervical or thoracic cord or more centrally in the lumbar region (7,8).

White matter in the spinal cord consists of three columns or funiculi—the ventral (anterior), lateral, and dorsal (posterior) columns—which are bundles of nerve axons that make up the neural pathways. The ventral columns are between the ventral median septum and ventral nerve roots. The lateral columns are between the ventrolateral and dorsolateral sulci, where ventral and dorsal nerve roots enter and exit, respectively. The dorsal columns are between the dorsal median sulcus and dorsolateral sulci on each side (6,9). Ascending sensory and descending motor pathways travel in these columns. It is important to know the location, function, and somatotopic organization of three specific spinal pathways when examining patients who have incomplete cord syndromes: the CST, dorsal columns, and STT. Knowing the sites at which these pathways decussate and their location within the cord cross section is key to identifying, at imaging, which of them are involved.

Corticospinal Tract

The CST is a descending motor tract that controls fine movements and the most important motor pathway in humans. It consists of axons from upper motor neurons (UMNs), more than 50% of which arise from the primary motor cortex (ie, precentral gyrus), with the remainder contributed by the premotor cortex, supplementary motor area, and sensory cortex. These fibers descend through the cerebral white matter, posterior limb of the internal capsule, cerebral peduncle, and ventral pons. In the medulla, 75%–90% of the fibers in the CST decussate in the pyramid and continue as the lateral CST in the lateral column (Fig 2). The neurons of the lateral CST synapse in the ventral horn before exiting the cord. Ten percent of the axons do not decussate but rather continue as the anterior CST, crossing over to the opposite side in each spinal cord segment supplying motor neurons in the ventral horn (Fig 1a).

Damage to neurons in the motor cortex and CST causes UMN deficits. Injury to neurons in the ventral horns and peripheral nerves results in lower motor neuron (LMN) deficits.

The important differences between UMN and LMN deficits are outlined in Table 2 (10).

Figure 2. Descending (green arrow) CST. Drawing depicts axons from the primary motor cortex in the cerebral hemisphere coursing through the internal capsule (thin black arrows), midbrain (not shown), ventral pons (not shown), and medullary pyramids. Ninety percent of the fibers cross to the opposite side at the pyramidal decussation (thick black arrow) and continue as the lateral CST. The somatotopic organization of fibers in the CST, from medial to lateral, is as follows: cervical (C, blue), thoracic (T, pink), lumbar (L, red), and sacral (S, purple) fibers. (Reprinted, with permission, from Jill K. Gregory.)

Figure 2.

Table 2: Findings of UMN versus LMN Deficits

Axons in the CST and STT have a similar laminar somatotopic arrangement. Axons from the cervical and thoracic segments, which innervate the upper extremities and thorax, are located medially, and axons from the lumbar and sacral segments, which innervate the abdomen and lower extremities, are positioned laterally

(6).Therefore, disease originating in the central spinal cord affects the upper extremities initially, as the lesion grows outward (Figs 1a, 2) (3,6,10).

Dorsal Columns

Information about proprioception, vibrating sensation, and fine-touch sensation travels in the dorsal (posterior) column. This column consists of two large ascending tracts: the medial fasciculus gracilis and lateral fasciculus cuneatus. The fasciculus gracilis begins at the distal cord and consists of fibers carrying sensory input from the lower extremities and lower trunk—specifically, the medial sacral and lumbar fibers. The fasciculus cuneatus carries sensory input from the upper extremities and upper trunk (lateral thoracic and cervical fibers) and begins in the thoracic region. Fibers from the dorsal column receive input from the dorsal root ganglion, ascend on the same side of the cord, synapse in their respective nuclei (gracilis or cuneatus), and decussate in the medulla. After crossing over, fibers of the dorsal column form the medial lemniscus, ascend within the brainstem, synapse in the ventral posterior nucleus of the thalamus, and terminate in the primary somatosensory cortex of the postcentral gyrus (Fig 3). Figures 1a and 3 illustrate the somatotopic arrangement of these fibers.

Figure 3. Ascending (orange arrow) dorsal column. Drawing depicts axons of first-order neurons of the dorsal root ganglion (small straight black arrows) that carry information about proprioception, vibration, and fine touch and ascend in the ipsilateral posterior columns. Medial sacral and lumbar fibers terminate in the nucleus gracilis (large straight black arrow). Lateral thoracic and cervical fibers project to the nucleus cuneatus (arrowhead). Axons from second-order neurons in the nucleus gracilis and nucleus cuneatus decussate in the medulla and travel to the contralateral ventral posterolateral nucleus of the thalamus (not shown). Third-order neurons from the ventral posterolateral nucleus of the thalamus terminate in the primary sensory cortex (curved arrow). The somatotopic organization of fibers in the dorsal columns, from medial to lateral, is as follows: sacral (S, purple), lumbar (L, red), thoracic (T, pink), and cervical (C, blue) fibers. (Reprinted, with permission, from Jill K. Gregory.)

Figure 3.

Spinothalamic Tract

The STT carries information about pain, temperature, and crude touch. Small-diameter unmyelinated axons from the dorsal root ganglion that carry pain, temperature, and crude-touch sensation information enter the cord and synapse immediately in the dorsal horn.

The second-order neurons in the dorsal horn carrying pain and temperature sensation cross at the anterior spinal commissure and ascend as the STT in the contralateral anterolateral white matter (3). Among the tracts described, the STT is the only one that decussates at the level of the spinal cord.

The decussating fibers must ascend at least two to three spinal segments before reaching the opposite side; therefore, a lesion affecting the STT causes contralateral loss of pain and temperature sensations, beginning a few segments below the level of the lesion (10). Like the nerve fibers in the CST, the axons in the STT also have a somatotopic arrangement (Figs 1a, 4).

Figure 4. Ascending (blue arrow) STT. Drawing depicts axons from first-order neurons of the dorsal root ganglion (arrowheads) that carry information about crude touch, pain, and temperature and synapse immediately into the dorsal horn. Axons from second-order neurons of the dorsal horn cross over into the anterior commissure (small black arrows) at each segment and ascend as the STT into the anterolateral white matter of the contralateral cord. The STT terminates in the primary sensory cortex (large black arrow) via the thalamus (second-order neurons not shown). The somatotopic organization of fibers in the STT, from medial to lateral, is as follows: cervical (C, blue), thoracic (T, pink), lumbar (L, red), and sacral (S, purple) fibers. (Reprinted, with permission, from Jill K. Gregory.)

Figure 4.

Spinal Cord Blood Supply

The spinal cord is supplied by a single anterior spinal artery (ASA) and paired posterior spinal arteries (PSAs) (Fig 5a). The ASA is formed by the fusion of vertebral artery branches, while the PSAs arise from either the posterior inferior cerebellar artery or vertebral arteries. The ASA runs in the ventral midline sulcus of the cord, and the PSAs run along the right and left dorsolateral sulci. Both vessels form a vascular pial plexus that surrounds the cord and is reinforced by medullary branches of radicular arteries from the posteroinferior cerebellar, vertebral, deep cervical, intercostal, and lumbar arteries (Fig 5b). The largest radicular artery usually arises off the left side of the aorta between the T9 and L2 vertebral levels and is called the artery of Adamkiewicz. This artery provides the primary blood supply to the lumbar and sacral cord segments and commonly demonstrates a “hairpin” loop before joining the ASA (5).

Figure 5a. Spinal cord blood supply. (a) Drawing depicts a single ASA and paired PSAs forming a pial plexus around the spinal cord. The ASA supplies the anterior two-thirds of the cord (shaded tan), and PSAs supply the posterior one-third (shaded dull pink). (b) Drawing depicts the major branches reinforcing the pial plexus via medullary branches of radicular arteries. A large radicular artery—the artery of Adamkiewicz—arises from the left side of the aorta, commonly between the T9 and L2 vertebral levels, and has a characteristic hairpin bend before it joins the ASA. The watershed regions in the cord are typically located in the middle to lower region (oval) of the thoracic cord. (Reprinted, with permission, from Jill K. Gregory.)

Figure 5a.

Figure 5b. Spinal cord blood supply. (a) Drawing depicts a single ASA and paired PSAs forming a pial plexus around the spinal cord. The ASA supplies the anterior two-thirds of the cord (shaded tan), and PSAs supply the posterior one-third (shaded dull pink). (b) Drawing depicts the major branches reinforcing the pial plexus via medullary branches of radicular arteries. A large radicular artery—the artery of Adamkiewicz—arises from the left side of the aorta, commonly between the T9 and L2 vertebral levels, and has a characteristic hairpin bend before it joins the ASA. The watershed regions in the cord are typically located in the middle to lower region (oval) of the thoracic cord. (Reprinted, with permission, from Jill K. Gregory.)

Figure 5b.

The ASA supplies the anterior two-thirds of the spinal cord, and the PSA supplies the posterior one-third. Watershed regions in the spinal cord depend on the number of radicular branches and the level of the origin of these vessels. However, they are typically located around the middle to lower thoracic cord. These regions are susceptible to ischemia during hypoperfusion states such as that induced by major cardiac aortic surgery or shock (11–13).

Incomplete Cord Syndromes

Dorsal Cord Syndrome

A lesion in the posterior one-third of the spinal cord that involves primarily the posterior column can cause DCS that results in loss of fine-touch, vibration, and proprioception sensations (Fig 6). Patients present with sensory ataxia, usually in association with a history of dizziness, unsteady gait, and frequent falls, especially during activities in the dark or when the eyes are closed (3,14). At clinical examination, patients have a positive Romberg sign—that is, a loss of balance or swaying when standing erect with the eyes closed. For normal balance, three sensory inputs—vestibular, visual, and proprioception—are required. Dark environments and activities involving closed eyes, such as showering, remove visual input, and a lack of proprioception due to dorsal column involvement results in a loss of balance. Large lesions can also affect the lateral CST and autonomic tracts to the sacral cord. Involvement of these tracts causes weakness and spasticity (involving the CST), bowel and bladder incontinence, erectile dysfunction, and orthostatic hypotension (involving the autonomic tracts) (3,14).

Figure 6a. DCS. (a) Drawing depicts the cross section of the spinal cord at the level of the upper thoracic spinal cord. The patchy shaded area represents the region involved in DCS. As the lesion grows, it may affect the CST and autonomic center in the lateral horn (arrow). The thoracic (T), lumbar (L), and sacral (S) fibers are illustrated. DC = dorsal columns. (b) Drawing depicts the areas affected by the clinical features of DCS involving a lesion at the T1 spinal level. These features include bilateral loss of fine-touch, proprioception, and vibration sensations. (Reprinted, with permission, from Jill K. Gregory.)

Figure 6a.

Figure 6b. DCS. (a) Drawing depicts the cross section of the spinal cord at the level of the upper thoracic spinal cord. The patchy shaded area represents the region involved in DCS. As the lesion grows, it may affect the CST and autonomic center in the lateral horn (arrow). The thoracic (T), lumbar (L), and sacral (S) fibers are illustrated. DC = dorsal columns. (b) Drawing depicts the areas affected by the clinical features of DCS involving a lesion at the T1 spinal level. These features include bilateral loss of fine-touch, proprioception, and vibration sensations. (Reprinted, with permission, from Jill K. Gregory.)

Figure 6b.

The causes of DCS include subacute combined degeneration due to vitamin B12 deficiency, multiple sclerosis, tabes dorsalis, cervical spondylotic myelopathy, acquired immunodeficiency syndrome–related myelopathy, Friedreich ataxia, and external compression from epidural or intradural extramedullary tumors (3,15). Posterior spinal cord infarction can manifest in association with unilateral DCS and is rare, compared with anterior spinal cord infarction, owing to a rich vascular pial plexus and paired posterior spinal cord arteries (16).

The classic imaging appearance of subacute combined degeneration on axial T2-weighted MR images is increased signal intensity in the posterior columns, with the configuration of an inverted V (Fig 7) (14). Increased signal intensity in the CST is seen at T2-weighted MR imaging in more severe cases (Fig 8). These imaging changes are reversible with use of vitamin B12 therapy. MR imaging can be used to monitor the clinical response to treatment (14). Patients with multiple sclerosis who are found to have DCS after presenting have demyelination plaques in the dorsal cord. With active demyelination, a T2-hyperintense signal that is disproportionate to the lesion size (secondary to edema) (Fig 9a), with variable contrast material enhancement (Fig 9b), is seen at MR imaging (15,17).

Figure 7. Subacute combined degeneration in a 42-year-old man who had been on a vegan diet for the past 2 years and had a history of frequent falls, most recently while showering. Axial T2-weighted MR image shows a hyperintense signal, with the classic inverted V configuration (arrows), in the dorsal columns.

Figure 7.

Figure 8a. Subacute combined degeneration in a 58-year-old man with ataxia and mild weakness in the upper extremities, which was greater on the right than on the left. (a) Axial T2-weighted MR image shows increased signal intensity (arrow) in the dorsal columns and subtle increased signal intensity (arrowheads) in the lateral CST. (b) Sagittal T2-weighted MR image shows linear increased signal intensity (arrows) in the dorsal columns.

Figure 8a.

Figure 8b. Subacute combined degeneration in a 58-year-old man with ataxia and mild weakness in the upper extremities, which was greater on the right than on the left. (a) Axial T2-weighted MR image shows increased signal intensity (arrow) in the dorsal columns and subtle increased signal intensity (arrowheads) in the lateral CST. (b) Sagittal T2-weighted MR image shows linear increased signal intensity (arrows) in the dorsal columns.

Figure 8b.

Figure 9a. Active demyelination in a 35-year-old woman with multiple sclerosis and paresthesia in the upper extremities. Sagittal T2-weighted (a) and contrast material–enhanced (b) MR images show a hyperintense signal and focal enhancement (arrow) in the dorsal cord.

Figure 9a.

Figure 9b. Active demyelination in a 35-year-old woman with multiple sclerosis and paresthesia in the upper extremities. Sagittal T2-weighted (a) and contrast material–enhanced (b) MR images show a hyperintense signal and focal enhancement (arrow) in the dorsal cord.

Figure 9b.

Ventral Cord Syndrome

Lesions that involve the anterior two-thirds of the cord and spare the dorsal columns cause VCS (Fig 10a) (3,18). The most common cause of VCS, also known as ASA syndrome, is spinal cord ischemia or infarction. Other common causes include trauma with disk herniation, cord impingement by fracture fragments, and multiple sclerosis (3,19). Among all of the incomplete cord syndromes, VCS is associated with the worst prognosis (18).

Figure 10a. VCS. (a) Drawing shows a patchy shaded area, representing the region involved in VCS, with sparing of the dorsal columns (DC). The lesion affects the CST, STT, anterior horn motor neurons (*), and autonomic center (★). (b) Drawing depicts the areas affected by the clinical features of VCS. These features include motor deficit involving the CST and loss of pain and temperature sensations involving the STT. (Reprinted, with permission, from Jill K. Gregory.)

Figure 10a.

Figure 10b. VCS. (a) Drawing shows a patchy shaded area, representing the region involved in VCS, with sparing of the dorsal columns (DC). The lesion affects the CST, STT, anterior horn motor neurons (*), and autonomic center (★). (b) Drawing depicts the areas affected by the clinical features of VCS. These features include motor deficit involving the CST and loss of pain and temperature sensations involving the STT. (Reprinted, with permission, from Jill K. Gregory.)

Figure 10b.

Spinal cord ischemia accounts for 6% of acute myelopathies and has a poor prognosis. Common causes of spinal cord ischemia in children are hypotension and hypoxemia secondary to cardiac malformations and trauma. In adults, the most common cause of spinal cord infarction is stenosis or an embolic phenomenon secondary to atherosclerosis. Other causes include aortic dissection, aortic aneurysm, aortic surgery, systemic hypotension or shock, major thoracic surgery such as coronary artery bypass graft placement, disk compression of the radicular artery, cocaine abuse, and sickle cell disease. Venous hypertension or occlusion secondary to coagulopathies, epidural infection with subsequent epidural venous thrombosis, and spinal arteriovenous malformations also can cause spinal cord ischemia (13,20).

Patients present with complete motor deficiency below the level of the lesion due to involvement of the CST and anterior horn cells; loss of pain, temperature, and crude-touch sensations (involving the STT); and orthostatic hypotension, bladder and/or bowel incontinence, and sexual dysfunction (involving the autonomic center) (Fig 10b). The sensations of fine touch, proprioception, and vibration are preserved. Early motor deficits due to spinal shock include flaccidity with absent reflexes, followed by a gradual return of the reflexes and increased tone or spasticity. Bilateral sensory deficits start two to three segments below the level of the lesion, since the STTs ascend at least two to three segments before crossing to the opposite side at the anterior commissure.

MR imaging is the imaging modality of choice for evaluation of spinal cord ischemia, which should include axial and sagittal diffusion-weighted MR imaging examinations. Characteristic MR imaging features of acute spinal cord ischemia include diffusion restriction in the ASA territory on diffusion-weighted images (Fig 11a, 11b) and a pencil-like hyperintense signal on sagittal T2-weighted images, with or without cord enlargement (Fig 11c). Axial MR images show a central T2-hyperintense signal on either side of the median fissure because there is relative sparing of the peripheral and posterior cords due to collateral vessels from the vascular pial plexus and both PSAs (13,20,21). In some cases, a central T2-hyperintense signal resembling snake eyes is seen in the anterior spinal cord on either side of the median fissure (Fig 12) (13,21). Although this finding is considered specific for spinal cord infarction, it can also appear in association with compression myelopathy and various infectious or inflammatory spinal conditions (13,22–25).

Figure 11a. Acute spinal cord ischemia in a 66-year-old man who presented with acute paraplegia 2 days after undergoing coronary artery bypass graft placement. (a, b) Axial diffusion-weighted MR image (a) and corresponding apparent diffusion coefficient map (b) show restricted diffusion (arrow). (c) Sagittal T2-weighted MR image shows a linear pencil-like hyperintense signal (arrows) in the lower thoracic cord.

Figure 11a.

Figure 11b. Acute spinal cord ischemia in a 66-year-old man who presented with acute paraplegia 2 days after undergoing coronary artery bypass graft placement. (a, b) Axial diffusion-weighted MR image (a) and corresponding apparent diffusion coefficient map (b) show restricted diffusion (arrow). (c) Sagittal T2-weighted MR image shows a linear pencil-like hyperintense signal (arrows) in the lower thoracic cord.

Figure 11b.

Figure 11c. Acute spinal cord ischemia in a 66-year-old man who presented with acute paraplegia 2 days after undergoing coronary artery bypass graft placement. (a, b) Axial diffusion-weighted MR image (a) and corresponding apparent diffusion coefficient map (b) show restricted diffusion (arrow). (c) Sagittal T2-weighted MR image shows a linear pencil-like hyperintense signal (arrows) in the lower thoracic cord.

Figure 11c.

Figure 12. Spinal cord infarction in a 53-year-old woman with a history of sepsis and severe hypotension, who presented with paraparesis and urinary incontinence after recovering from shock. Axial T2-weighted MR image shows a hyperintense signal (arrows) resembling snake eyes in the anterior spinal cord.

Figure 12.

Central Cord Syndrome

CCS is the most common ISCS. It occurs secondary to injury or lesions around the central canal (18,26,27). Trauma is the most common cause of CCS.

Hyperextension is the classic mechanism of injury in elderly patients with underlying spinal stenosis secondary to cervical spondylosis. With this condition, the spinal cord is pinched between a posterior buckled ligamentum flavum and anterior disk-osteophyte complexes (19,26–28) (Figs 13, 14). In young patients, the most common mechanism of injury is fracture dislocation or herniation secondary to hyperflexion injury, with associated cord compression (Fig 15) (26). Congenital spinal canal stenosis predisposes individuals to CCS (29–31). Other causes of CCS include intramedullary spinal cord tumors and syringohydromyelia.

Figure 13. Drawing depicts the hyperextension injury seen in older patients with CCS secondary to underlying cervical spondylosis. Note the pinching of the spinal cord between the anterior disk-osteophyte complexes (arrows) and buckled posterior ligamentum flavum (arrowheads). (Reprinted, with permission, from Jill K. Gregory.)

Figure 13.

Figure 14. Cervical spondylosis with cervical stenosis in a 73-year-old man who presented with a burning sensation and weakness in the upper extremities 2 years after a fall. Sagittal T2-weighted MR image shows severe cervical spondylotic changes (arrow), with a disk-osteophyte complex and buckled ligamentum flavum (white arrowheads). Note the mild increased signal intensity (black arrowhead) in the cord secondary to myelomalacia.

Figure 14.

Figure 15a. Hyperflexion distraction injury in a 21-year-old man involved in a motor vehicle accident. (a) Three-dimensional volume-rendered CT image shows anterior translation of C5 over C6 (single arrow), distraction of the posterior elements with perched facets (arrowhead), and an increased posterior interspinous distance (double-headed arrow). (b) Sagittal T2-weighted MR image obtained in the immediate postoperative period shows a hyperintense signal (white arrows) at the C4-C7 spinal level (secondary to cord contusion), disruption of the posterior ligaments (black arrow), and anterior fusion changes (arrowhead).

Figure 15a.

Figure 15b. Hyperflexion distraction injury in a 21-year-old man involved in a motor vehicle accident. (a) Three-dimensional volume-rendered CT image shows anterior translation of C5 over C6 (single arrow), distraction of the posterior elements with perched facets (arrowhead), and an increased posterior interspinous distance (double-headed arrow). (b) Sagittal T2-weighted MR image obtained in the immediate postoperative period shows a hyperintense signal (white arrows) at the C4-C7 spinal level (secondary to cord contusion), disruption of the posterior ligaments (black arrow), and anterior fusion changes (arrowhead).

Figure 15b.

The clinical manifestations of CCS correlate with the lesion size. Small lesions in the central cord region involve the STT, where they cross to the contralateral side in the anterior commissure (Fig 16a) and cause bilateral segmental loss of pain and temperature sensations. Since the decussating fibers must ascend at least two to three spinal segments before reaching the opposite side, loss of pain and temperature sensations begins two to three segments below the level of the lesion. Sensations above and below this level are normal, with a band of sensory loss in between (suspended sensory loss) (Fig 16b). Patients who have cervical spinal cord lesions caused by either canal stenosis and underlying cervical spondylosis, or syringohydromyelia in the cervical spinal cord present with loss of pain and temperature sensations in the upper thorax, both shoulders, and upper arms—in a classic “cape” distribution (Fig 16b) (3).

Figure 16a. Small-lesion CCS. (a) Drawing shows a small patchy shaded area (arrows) that represents a small lesion involving the SSTs at the anterior commissure. The cervical (C), thoracic (T), lumbar (L), and sacral (S) fiber segments are illustrated. Light blue line and arrow illustrate the path of the STT on the right side, crossing over to the opposite side and ascending in the STT location in the anterolateral tract. Dark blue line and arrow illustrate this path on the left side. (b) Drawing depicts the region classically affected by the clinical features of CCS. These features include bilateral suspended sensory loss of pain and temperature sensations at the level of the lesion. The affected region manifests in the classic cape distribution of sensory loss that is seen with lesions in the cervical cord. (Reprinted, with permission, from Jill K. Gregory.)

Figure 16a.

Figure 16b. Small-lesion CCS. (a) Drawing shows a small patchy shaded area (arrows) that represents a small lesion involving the SSTs at the anterior commissure. The cervical (C), thoracic (T), lumbar (L), and sacral (S) fiber segments are illustrated. Light blue line and arrow illustrate the path of the STT on the right side, crossing over to the opposite side and ascending in the STT location in the anterolateral tract. Dark blue line and arrow illustrate this path on the left side. (b) Drawing depicts the region classically affected by the clinical features of CCS. These features include bilateral suspended sensory loss of pain and temperature sensations at the level of the lesion. The affected region manifests in the classic cape distribution of sensory loss that is seen with lesions in the cervical cord. (Reprinted, with permission, from Jill K. Gregory.)

Figure 16b.

Large central cord lesions can involve the anterior horn cells, CST, posterior columns, STT, and autonomic centers in the lateral horn (Fig 17a). Owing to the somatotopic organization of fibers in the CST and STT (Fig 17a), sensory and motor deficits are disproportionately severe in the upper compared with lower extremities (3,19) (Fig 17b). LMN motor deficits occur at the level of the lesion owing to involvement of anterior horn cells, whereas UMN deficits occur below the level of the lesion owing to CST involvement. Mixed sensory loss with sacral sparing occurs below the level of the lesion owing to variable involvement of the STT and posterior columns (Fig 17b) (3).

Figure 17a. Large-lesion CCS. (a) Drawing shows a patchy shaded area that represents a large lesion causing CCS. The dorsal columns (DC), CST, STT, and ventral horn neurons (★) at the level of the lesion are affected. Note the sparing of the sacral (S) fiber segments (arrows) in the CST and STT. The cervical (C), thoracic (T), lumbar (L), and sacral fiber segments are illustrated. (b) Drawing depicts the areas affected by the clinical features of large-lesion CCS. These features include UMN deficit involving the CST; loss of fine-touch, proprioception, and vibration sensations involving the dorsal columns; and loss of crude-touch, pain, and temperature sensations involving the STT, with sacral sparing (★). (Reprinted, with permission, from Jill K. Gregory.)

Figure 17a.

Figure 17b. Large-lesion CCS. (a) Drawing shows a patchy shaded area that represents a large lesion causing CCS. The dorsal columns (DC), CST, STT, and ventral horn neurons (★) at the level of the lesion are affected. Note the sparing of the sacral (S) fiber segments (arrows) in the CST and STT. The cervical (C), thoracic (T), lumbar (L), and sacral fiber segments are illustrated. (b) Drawing depicts the areas affected by the clinical features of large-lesion CCS. These features include UMN deficit involving the CST; loss of fine-touch, proprioception, and vibration sensations involving the dorsal columns; and loss of crude-touch, pain, and temperature sensations involving the STT, with sacral sparing (★). (Reprinted, with permission, from Jill K. Gregory.)

Figure 17b.

MR imaging is the primary imaging modality for evaluation of acute traumatic CCS. In the acute setting, there is an increased T2 signal secondary to cord edema (Fig 15b). Thinning of the cord and myelomalacia are seen with chronic cord injuries (Fig 14). Low signal intensity on gradient-echo MR images suggests intramedullary hemorrhage. However, this finding is uncommon in patients with CCS; if present, it portends a poor prognosis (27,28,31). Relatively new techniques such as quantitative diffusion-tensor MR imaging and fiber tractography show promise as examinations that will enable better delineation of white matter lesions in the spinal cord (32).

Intramedullary spinal cord tumors (IMSCTs) can also manifest in association with symptoms of CCS. Glial tumors (ependymoma and astrocytoma) are the most common IMSCTs (33). Ependymomas, which arise from ependymal cells lining the central canal, are common in adults and account for 60% of all glial tumors. These tumors are slow-growing, relatively well-circumscribed expansile lesions that typically occur in the cervical cord. They demonstrate cord expansion, an isointense to slightly hypointense signal on T1-weighted MR images, a hyperintense signal on T2-weighted MR images (Fig 18a), and contrast enhancement (Fig 18b, 18c). A T1-hypointense signal can be seen in tumors with internal hemorrhage. Cysts, either polar nontumoral cysts (60%) (Fig 18a, 18b) or less frequently intratumoral cysts with an enhancing wall, are common with ependymomas (78%–84% of cases) (34). Twenty percent to 33% of ependymomas have a rim of very low T2 signal intensity at the pole secondary to hemorrhage—that is, a tumor cap sign (Fig 18a) (34).

Figure 18a. Ependymoma in a 45-year-old man with numbness, tingling, and weakness in both upper extremities, as well as mild ataxia. (a) Sagittal T2-weighted MR image shows an expansile lesion (thick straight white arrows) with a heterogeneous mild hyperintense signal at the C7-T1 spinal level, a focal hypointense signal (black arrow) due to hemorrhage, polar cysts (thin straight white arrows) at the C4-C6 spinal level, and cord edema (curved arrows). Note the “tumor cap” sign—that is, the hypointense signal (white arrowhead) along the cranial margin of the lesion. There is a fluid-fluid level (black arrowheads) in the cyst at the C5-C6 level. (b) Sagittal contrast-enhanced MR image shows an intensely enhancing expansile mass (large white arrow), with a focal hypointense signal (arrowhead) secondary to hemorrhage and polar cysts (small white arrows). (c) Axial contrast-enhanced MR image shows an intensely enhancing lesion with focal hemorrhage (arrowhead). The lesion nearly replaces the entire cord.

Figure 18a.

Figure 18b. Ependymoma in a 45-year-old man with numbness, tingling, and weakness in both upper extremities, as well as mild ataxia. (a) Sagittal T2-weighted MR image shows an expansile lesion (thick straight white arrows) with a heterogeneous mild hyperintense signal at the C7-T1 spinal level, a focal hypointense signal (black arrow) due to hemorrhage, polar cysts (thin straight white arrows) at the C4-C6 spinal level, and cord edema (curved arrows). Note the “tumor cap” sign—that is, the hypointense signal (white arrowhead) along the cranial margin of the lesion. There is a fluid-fluid level (black arrowheads) in the cyst at the C5-C6 level. (b) Sagittal contrast-enhanced MR image shows an intensely enhancing expansile mass (large white arrow), with a focal hypointense signal (arrowhead) secondary to hemorrhage and polar cysts (small white arrows). (c) Axial contrast-enhanced MR image shows an intensely enhancing lesion with focal hemorrhage (arrowhead). The lesion nearly replaces the entire cord.

Figure 18b.

Figure 18c. Ependymoma in a 45-year-old man with numbness, tingling, and weakness in both upper extremities, as well as mild ataxia. (a) Sagittal T2-weighted MR image shows an expansile lesion (thick straight white arrows) with a heterogeneous mild hyperintense signal at the C7-T1 spinal level, a focal hypointense signal (black arrow) due to hemorrhage, polar cysts (thin straight white arrows) at the C4-C6 spinal level, and cord edema (curved arrows). Note the “tumor cap” sign—that is, the hypointense signal (white arrowhead) along the cranial margin of the lesion. There is a fluid-fluid level (black arrowheads) in the cyst at the C5-C6 level. (b) Sagittal contrast-enhanced MR image shows an intensely enhancing expansile mass (large white arrow), with a focal hypointense signal (arrowhead) secondary to hemorrhage and polar cysts (small white arrows). (c) Axial contrast-enhanced MR image shows an intensely enhancing lesion with focal hemorrhage (arrowhead). The lesion nearly replaces the entire cord.

Figure 18c.

Astrocytoma is the most common IMSCT in children, with ependymoma following as the next most common (34). In adults, astrocytoma is the second most common IMSCT (34). The thoracic cord is the most frequent location for astrocytoma, with the cervical cord being the second most frequent location (34). These slightly eccentric tumors have no surrounding capsule and cause diffuse fusiform enlargement of the cord. At MR imaging, these lesions are ill defined, with a T1-isointense to T1-hypointense signal, a T2-hyperintense signal (Fig 19a), and variable enhancement (33,34) (Fig 19b). Other IMSCTs, such as ganglioglioma and metastases, also can manifest in association with CCS. Metastases usually have cord edema that is disproportionate in size compared with the lesion, and cysts are less frequently encountered than are primary tumors (33,34).

Figure 19a. Findings in a 10-year-old boy with a grade III astrocytoma who presented with neck and bilateral shoulder pain, difficulty gripping a pen, and a change in handwriting. Sagittal T2-weighted (a) and contrast-enhanced (b) MR images show an expansile lesion (arrows) with a homogeneous hyperintense signal and mild diffuse enhancement.

Figure 19a.

Figure 19b. Findings in a 10-year-old boy with a grade III astrocytoma who presented with neck and bilateral shoulder pain, difficulty gripping a pen, and a change in handwriting. Sagittal T2-weighted (a) and contrast-enhanced (b) MR images show an expansile lesion (arrows) with a homogeneous hyperintense signal and mild diffuse enhancement.

Figure 19b.

Hemangioblastoma is the third most common IMSCT, and it frequently (in 50% of cases) involves the thoracic cord, followed closely by the cervical cord (in 40% of cases) (34). One-third of patients with hemangioblastoma have von Hippel–Lindau syndrome (34). These slow-growing, highly vascular tumors cause cord expansion and are frequently associated with cystic changes or syringohydromyelia (Fig 20a). At MR imaging, they have variable signal intensity on T1-weighted images and high signal intensity on T2-weighted images, with flow voids, diffuse cord edema, and intense homogeneously enhancing tumor nodules (Fig 20) (33,34).

Figure 20a. Hemangioblastoma in a 16-year-old girl with a history of neck pain. (a) Sagittal T2-weighted MR image shows an expansile lesion with a heterogeneous hyperintense signal (long straight arrows) from the C4 through C6 level, diffuse edema (short straight arrows), cystic changes (curved arrows), and foci of hypointense signal (arrowhead) due to hemorrhage or flow voids. (b) Sagittal contrast-enhanced MR image shows an intensely enhancing expansile lesion (arrows) and foci of hypointense signal (arrowhead) due to hemorrhage or flow voids.

Figure 20a.

Figure 20b. Hemangioblastoma in a 16-year-old girl with a history of neck pain. (a) Sagittal T2-weighted MR image shows an expansile lesion with a heterogeneous hyperintense signal (long straight arrows) from the C4 through C6 level, diffuse edema (short straight arrows), cystic changes (curved arrows), and foci of hypointense signal (arrowhead) due to hemorrhage or flow voids. (b) Sagittal contrast-enhanced MR image shows an intensely enhancing expansile lesion (arrows) and foci of hypointense signal (arrowhead) due to hemorrhage or flow voids.

Figure 20b.

Syringohydromyelia is a fluid-filled cavity in the spinal cord; it can be classified as primary or secondary. Primary causes of syringohydromyelia include basilar invagination, Chiari malformation (Fig 21), and idiopathic entities. Trauma, infection, and tumor are secondary causes (35,36).

Figure 21a. Chiari I malformation with syringohydromyelia in a 7-year-old girl with recurrent headaches, frequent cuts to both hands, bilateral upper-extremity weakness, and mild ataxia. (a) Sagittal T2-weighted MR image shows pointed cerebellar tonsils (double-headed arrow) below the plane of the foramen magnum (white line) and interrupted syringohydromyelia, which is greater in the cervical cord (arrow) than in the thoracic cord (arrowhead). (b) Axial T2-weighted MR image of the cervical cord shows a large syrinx (arrow).

Figure 21a.

Figure 21b. Chiari I malformation with syringohydromyelia in a 7-year-old girl with recurrent headaches, frequent cuts to both hands, bilateral upper-extremity weakness, and mild ataxia. (a) Sagittal T2-weighted MR image shows pointed cerebellar tonsils (double-headed arrow) below the plane of the foramen magnum (white line) and interrupted syringohydromyelia, which is greater in the cervical cord (arrow) than in the thoracic cord (arrowhead). (b) Axial T2-weighted MR image of the cervical cord shows a large syrinx (arrow).

Figure 21b.

Brown-Séquard Syndrome

Brown-Séquard syndrome, also known as hemicord syndrome, occurs with lesions that affect one-half of the spinal cord (Fig 22a) (21). Penetrating trauma, such as knife or bullet injury, is the most common cause of this syndrome (37,38). Other causes include idiopathic spinal cord herniation, blunt trauma, cord ischemia, disk herniation, spinal cord tumors, epidural hematoma, intramedullary hemorrhage, and arteriovenous malformations (3,38–42).

Figure 22a. Brown-Séquard syndrome. (a) Drawing shows a patchy shaded area representing the region involved in Brown-Séquard syndrome. The dorsal columns (DC), CST, STT, ventral horn (*), and dorsal horn (★) are affected. (b) Drawing depicts the areas affected by the clinical features of Brown-Séquard syndrome. These features include ipsilateral spastic paralysis (UMN type involving the CST); ipsilateral loss of fine-touch, proprioception, and vibration sensations involving the dorsal columns; and contralateral loss of pain and temperature sensations involving the STT. The loss of contralateral pain and temperature sensations starts two to three segments below the level of the motor deficit because STT fibers ascend two to three segments before crossing to the opposite side. A small segmental ipsilateral region of combined LMN deficit and complete sensory deficit (arrow) is present at the level of the lesion. (Reprinted, with permission, from Jill K. Gregory.)

Figure 22a.

Figure 22b. Brown-Séquard syndrome. (a) Drawing shows a patchy shaded area representing the region involved in Brown-Séquard syndrome. The dorsal columns (DC), CST, STT, ventral horn (*), and dorsal horn (★) are affected. (b) Drawing depicts the areas affected by the clinical features of Brown-Séquard syndrome. These features include ipsilateral spastic paralysis (UMN type involving the CST); ipsilateral loss of fine-touch, proprioception, and vibration sensations involving the dorsal columns; and contralateral loss of pain and temperature sensations involving the STT. The loss of contralateral pain and temperature sensations starts two to three segments below the level of the motor deficit because STT fibers ascend two to three segments before crossing to the opposite side. A small segmental ipsilateral region of combined LMN deficit and complete sensory deficit (arrow) is present at the level of the lesion. (Reprinted, with permission, from Jill K. Gregory.)

Figure 22b.

At clinical examination, patients with Brown-Séquard syndrome are found to have an ipsilateral UMN deficit secondary to interruption of the CST. Damage to the posterior columns causes ipsilateral loss of proprioception and vibration sensations. Injury to the STT results in contralateral loss of crude-touch, pain, and temperature sensations (3,18,19). Contralateral sensory deficit starts two to three segments below the level of the lesion, as STT fibers ascend at least two to three segments before crossing over to the opposite side (Fig 22b). At the level of the lesion, a small band of combined ipsilateral segmental loss of motor function and total sensory deficit occurs owing to damage to the anterior horn cells and dorsal horn, respectively (Fig 22b).

In the evaluation of penetrating trauma, CT and MR images provide valuable and complementary information. CT best depicts bone injury, the knife or bullet path, and free fracture or bullet fragments or air in the spinal canal (Fig 23a). MR imaging is the modality of choice for evaluating the extent of injury to the spinal cord, nerve roots, soft tissues, ligaments, and/or paraspinal musculature and detecting epidural or subdural hematomas (Figs 23b, 24). It is also useful in the evaluation of postoperative complications such as infection, cerebrospinal fluid leakage, and pseudomeningocele (37,43,44) (Fig 24).

Figure 23a. Penetrating injury with hemicord transection, leading to Brown-Séquard syndrome, in a 32-year-old woman. (a) Three-dimensional volume-rendered CT image shows a knife traversing the right lamina and hemicord. (b) Axial T2-weighted MR image obtained in the immediate postoperative period shows asymmetric increased signal intensity (arrow) on the right side of the cord, as compared with the signal intensity on the left, and a defect (arrowheads) in the right lamina.

Figure 23a.

Figure 23b. Penetrating injury with hemicord transection, leading to Brown-Séquard syndrome, in a 32-year-old woman. (a) Three-dimensional volume-rendered CT image shows a knife traversing the right lamina and hemicord. (b) Axial T2-weighted MR image obtained in the immediate postoperative period shows asymmetric increased signal intensity (arrow) on the right side of the cord, as compared with the signal intensity on the left, and a defect (arrowheads) in the right lamina.

Figure 23b.

Figure 24a. Penetrating injury with hemicord transection and a pseudomeningocele in a 23-year-old man. (a) Axial T2-weighted MR image shows a hyperintense signal (arrow) in the right hemicord and a knife tract (arrowheads) with signal intensity similar to that of cerebrospinal fluid. (b) Sagittal T2-weighted MR image shows a hyperintense signal (arrowhead) in the cord at the C2 level and a knife tract (arrow) communicating with the spinal canal.

Figure 24a.

Figure 24b. Penetrating injury with hemicord transection and a pseudomeningocele in a 23-year-old man. (a) Axial T2-weighted MR image shows a hyperintense signal (arrow) in the right hemicord and a knife tract (arrowheads) with signal intensity similar to that of cerebrospinal fluid. (b) Sagittal T2-weighted MR image shows a hyperintense signal (arrowhead) in the cord at the C2 level and a knife tract (arrow) communicating with the spinal canal.

Figure 24b.

Idiopathic spinal cord herniation is a rare condition that involves the thoracic cord, typically between the T4 and T7 spinal levels. This condition can manifest in association with Brown-Séquard syndrome (45). The cord protrudes ventrally through an anterior or lateral defect in the dura (Fig 25a). On MR images, the cord at the level of herniation has an anterolateral kink and an increase in the dorsal cerebrospinal fluid space (Fig 25). The cord appears narrowed or deformed, and it may have increased signal intensity on T2-weighted MR images. Increased turbulence in the dorsal cerebrospinal fluid space may mimic a flow void on T2-weighted MR images and help differentiate cord herniation from a type III meningeal (intradural arachnoid) cyst (45). Rarely, arteriovenous malformations manifest in association with hemicord syndrome secondary to cord ischemia from venous hypertension or the steal phenomenon.

Figure 25a. Idiopathic transdural spinal cord herniation in a 38-year-old woman with right lower-extremity weakness and a chronic nonhealing ulcer of the left foot. (a) Axial T2-weighted MR image shows herniation of the right hemicord through a focal anterolateral dural defect (arrow), as well as an increase in the dorsal and left lateral cerebrospinal fluid space (arrowheads). (b) Sagittal T2-weighted MR image shows a kinked or S-shaped cord (arrow) at the T6 level, with an associated increase in the dorsal cerebrospinal fluid space (arrowheads).

Figure 25a.

Figure 25b. Idiopathic transdural spinal cord herniation in a 38-year-old woman with right lower-extremity weakness and a chronic nonhealing ulcer of the left foot. (a) Axial T2-weighted MR image shows herniation of the right hemicord through a focal anterolateral dural defect (arrow), as well as an increase in the dorsal and left lateral cerebrospinal fluid space (arrowheads). (b) Sagittal T2-weighted MR image shows a kinked or S-shaped cord (arrow) at the T6 level, with an associated increase in the dorsal cerebrospinal fluid space (arrowheads).

Figure 25b.

Conus Medullaris Syndrome

Injury or lesions involving the tapered distal end of the spinal cord (T12 through L2) can lead to CMS. Common causes of this syndrome include disk herniation in the lower thoracic and upper lumbar spine, trauma resulting in a compression or burst fracture with retropulsed fragments causing cord compression, intramedullary tumor (metastasis or primary tumor), infection (ie, epidural abscess), spinal dural arteriovenous fistulas, and cord infarction (18,33,34,46–49). The clinical features of CMS are severe back pain, lower-extremity weakness (mixed UMN and LMN deficit), saddle anesthesia or hypoesthesia (Fig 26), early bladder and rectal sphincter dysfunction, and impotence (18,19).

Figure 26. CMS with a saddle anesthesia or hypoesthesia pattern. Drawing depicts the areas affected by the clinical features of this syndrome. These features include bilateral symmetric sensory deficit in the buttocks, perineum, and inner thighs. With CES, asymmetric loss of sensation in these regions occurs when there is involvement of the sacral nerve roots. (Reprinted, with permission, from Jill K. Gregory.)

Figure 26.

The lumbar and sacral nerve roots that form the cauda equina also arise from this region. Therefore, the pathologic entities that cause CMS can also affect the cauda equina and result in an overlap in the clinical findings of CMS and CES.

The primary difference between CMS and CES is in the type of motor deficit. CMS causes mixed UMN and LMN deficits, while CES causes a purely LMN deficit (18).

Both CT and MR imaging should be used to examine patients who present with symptoms of CMS following trauma. CT is used to evaluate bone injury (Fig 27a), and MR imaging is used to assess the cord, disk, and soft tissues (Fig 27b) (18,46,49). Early surgical intervention substantially improves the patient’s prognosis.

Figure 27a. CMS secondary to burst fracture in a patient who presented with paraparesis, saddle anesthesia, and urinary incontinence. (a) Sagittal CT image shows a burst fracture (arrow) at the T12 vertebral level, with a retropulsed component (arrowhead) in the spinal canal causing severe canal stenosis. (b) Sagittal T2-weighted MR image shows a compression fracture at the T12 vertebral level with retropulsion (arrow), and a mild hyperintense signal (arrowhead) in the conus medullaris due to edema.

Figure 27a.

Figure 27b. CMS secondary to burst fracture in a patient who presented with paraparesis, saddle anesthesia, and urinary incontinence. (a) Sagittal CT image shows a burst fracture (arrow) at the T12 vertebral level, with a retropulsed component (arrowhead) in the spinal canal causing severe canal stenosis. (b) Sagittal T2-weighted MR image shows a compression fracture at the T12 vertebral level with retropulsion (arrow), and a mild hyperintense signal (arrowhead) in the conus medullaris due to edema.

Figure 27b.

Myxopapillary ependymoma, a variant of ependymoma arising from the ependymal glia of the filum terminale, is the most common neoplasm in this region (33,34). These soft, lobulated, encapsulated mucin-producing tumors are slow growing, are more common in males, appear in persons at an earlier age compared with typical ependymomas, and can cause widening of the spinal canal (33,34). Clinically, these tumors manifest with various combinations of CMS and CES symptoms. At MR imaging, these lesions demonstrate an isointense signal on T1-weighted images, high signal intensity on T2-weighted images, and intense contrast enhancement (Fig 28). Other IMSCTs that manifest with CMS include astrocytoma (Fig 29), hemangioblastoma, lipoma, and metastasis (33,34).

Figure 28. Myxopapillary ependymoma in a 20-year-old woman with bilateral lower-extremity weakness, back pain, and urinary incontinence. Sagittal contrast-enhanced MR image shows an intensely enhancing expansile lesion (arrows) in the region of the conus medullaris and cauda equina, with mild scalloping of the posterior vertebral bodies (arrowheads).

Figure 28.

Figure 29. Juvenile pilocytic astrocytoma in a 5-year-old girl with difficulty walking, bilateral leg pain, and urinary and fecal incontinence. Sagittal T2-weighted MR image shows an expansile lesion with solid (large arrow) and cystic (small arrows) components in the conus medullaris and edema (arrowhead) in the adjacent cord. This solid component exhibited intense enhancement (not shown).

Figure 29.

Spinal dural arteriovenous fistulas, or type I spinal arteriovenous fistulas, are the most common vascular malformations of the spinal cord and are frequently located in the thoracolumbar region; 80% of them are located between the T6 and L2 spinal levels (50). These abnormal arteriovenous shunts occur at the junction of bridging or radicular veins and the epidural venous plexus in the lateral epidural space, close to the nerve root, and are fed by radiculomeningeal arteries. Chronic venous hypertension or congestion of intramedullary veins secondary to these shunts results in chronic hypoxia and progressive myelopathy, with patients presenting with clinical features of CMS (47,50).

On T2-weighted MR images, the conus medullaris and distal spinal cord show a diffuse ill-defined central hyperintense signal due to edema, a peripheral rim of hypointense signal due to chronic venous hypertension (ie, deoxygenated blood), and multiple flow voids along the dorsal surface of the cord (Fig 30a). Contrast-enhanced spinal MR angiography or CT angiography can be used to localize a shunt, which is commonly located below the pedicle, and the spinal cord may show variable enhancement (Fig 30b). Digital subtraction angiography enables the confirmation and endovascular management of these lesions (50).

Figure 30a. Spinal dural arteriovenous fistula in a 45-year-old man with progressive weakness, tingling and numbness in the bilateral lower extremities, and urinary incontinence. (a) Sagittal T2-weighted MR image shows a central hyperintense signal in the conus medullaris and lower thoracic cord (straight arrows), a peripheral hypointense signal (arrowheads), and flow voids (curved arrows) along the dorsal surface of the cord. (b) Sagittal contrast-enhanced MR image shows tortuous enhancing vessels (arrows) along the dorsal surface and variable contrast enhancement (arrowheads) of the cord.

Figure 30a.

Figure 30b. Spinal dural arteriovenous fistula in a 45-year-old man with progressive weakness, tingling and numbness in the bilateral lower extremities, and urinary incontinence. (a) Sagittal T2-weighted MR image shows a central hyperintense signal in the conus medullaris and lower thoracic cord (straight arrows), a peripheral hypointense signal (arrowheads), and flow voids (curved arrows) along the dorsal surface of the cord. (b) Sagittal contrast-enhanced MR image shows tortuous enhancing vessels (arrows) along the dorsal surface and variable contrast enhancement (arrowheads) of the cord.

Figure 30b.

Cauda Equina Syndrome

Compression of the lower lumbar and sacral nerve roots in the vertebral canal below the level of the conus medullaris can cause CES. Although this is not a true ISCS, it is included in this discussion because there is substantial overlap between the clinical features of CES and those of CMS. The most common cause of CES is disk herniation secondary to degenerative disease (51,52). Other causes include trauma, lumbar spinal stenosis, arachnoiditis, and epidural abscess. The neoplastic processes that lead to CES include primary tumors such as myxopapillary ependymoma (Fig 28) and astrocytoma involving the cauda equina; space-occupying extramedullary intradural tumors such as schwannoma, meningioma, and neurofibroma; and rarely, extradural tumors such as vertebral metastases (51–55).

Arachnoiditis is inflammation of the meninges and subarachnoid space secondary to a broad group of pathologic entities that include infectious, inflammatory, or neoplastic processes. The infectious causes of arachnoiditis can be viral, bacterial, mycobacterial, fungal, or parasitic (53,54,56,57). Inflammatory causes of arachnoiditis include autoimmune diseases such as Guillain-Barré syndrome, subarachnoid hemorrhage, recent spinal surgery, and administration of intrathecal agents (eg, steroids, anesthetics, contrast media, epidural anesthetic) (51,52,57). Neoplastic causes include primary tumors with intrathecal spread, such as ependymoma, and secondary metastasis or leptomeningeal carcinomatosis from breast carcinoma, lung carcinoma, melanoma, or non-Hodgkin lymphoma (51,52,55).

Clinically, CES is classified as incomplete or complete. Incomplete CES manifests with unilateral or bilateral sciatica, back pain, variable sensory deficit in the lower extremities, saddle anesthesia (at S4 and the S5 nerve roots), and asymmetric unilateral or bilateral LMN-type motor deficit in the lower extremities, depending on the level of compression and the nerve roots involved. Complete CES manifests with urinary and bowel retention or incontinence, in addition to the aforementioned clinical features of incomplete CES (18,51,52).

MR imaging is the imaging modality of choice for evaluation of CES. Lumbar canal stenosis—either primary or congenital, or acquired owing to degenerative disease and disk herniation—is best depicted on MR images (Fig 31).

Figure 31a. Lumbar spondylosis with canal stenosis and CES in a 72-year-old man with increasing bilateral lower-extremity weakness and right lower-extremity paresthesia. (a) Sagittal T2-weighted MR image shows a multilevel disk bulge or herniation (arrowheads) and ligamentum flavum buckling (thin arrows). The combination of these findings can lead to an hourglass appearance of the spinal canal. Crowded redundant cauda equina nerve roots (thick arrows) have a serpiginous appearance. (b) Axial T2-weighted MR image shows a “trefoil” configuration (arrows) of the central canal and buckling (arrowheads) of the ligamentum flavum.

Figure 31a.

Figure 31b. Lumbar spondylosis with canal stenosis and CES in a 72-year-old man with increasing bilateral lower-extremity weakness and right lower-extremity paresthesia. (a) Sagittal T2-weighted MR image shows a multilevel disk bulge or herniation (arrowheads) and ligamentum flavum buckling (thin arrows). The combination of these findings can lead to an hourglass appearance of the spinal canal. Crowded redundant cauda equina nerve roots (thick arrows) have a serpiginous appearance. (b) Axial T2-weighted MR image shows a “trefoil” configuration (arrows) of the central canal and buckling (arrowheads) of the ligamentum flavum.

Figure 31b.

Arachnoiditis is classified into three types on the basis of the MR imaging appearance: Type I arachnoiditis involves central clumping or conglomeration of the roots (Fig 32). With type II arachnoiditis, the nerve roots are adherent to the periphery of the thecal sac, creating the “empty thecal sac” sign on MR or CT myelograms (Fig 33). With type III, a large central soft-tissue mass replaces the thecal sac (57,58). Rarely, chronic inflammation and fibrosis can progress to arachnoiditis ossificans, which involves intradural calcification and clumped nerve roots (Fig 34) (59).

Figure 32. Type I arachnoiditis in a 32-year-old man who had a history of meningitis and presented with back pain, bilateral lower-extremity weakness, and urinary and fecal incontinence. Axial T2-weighted MR image shows central conglomeration (arrow) of the nerve roots.

Figure 32.

Figure 33a. Type II arachnoiditis in a 40-year-old woman who had a history of prior spinal surgery and presented with lower-extremity weakness (greater on the left than on the right) and altered sensation. (a) Sagittal T2-weighted MR image shows an empty thecal sac (arrow). (b) Axial T2-weighted MR image shows an empty thecal sac (arrow), with peripheral clumping of the nerve roots (arrowheads).

Figure 33a.

Figure 33b. Type II arachnoiditis in a 40-year-old woman who had a history of prior spinal surgery and presented with lower-extremity weakness (greater on the left than on the right) and altered sensation. (a) Sagittal T2-weighted MR image shows an empty thecal sac (arrow). (b) Axial T2-weighted MR image shows an empty thecal sac (arrow), with peripheral clumping of the nerve roots (arrowheads).

Figure 33b.

Figure 34. Arachnoiditis ossificans in a 35-year-old woman who had a history of arachnoiditis after spinal anesthesia, with increasing weakness in the lower extremities during the next 2 years. Sagittal nonenhanced CT image shows clumps of intradural calcification (arrows) along the cauda equina.

Figure 34.

Conclusion

An understanding of the spinal cord anatomy and clinical features of spinal cord syndromes aids in the imaging and localization of cord abnormalities that manifest with classic incomplete cord syndromes. A summary of the six basic types of ISCS is provided in Table 1.

Acknowledgment

The authors thank Jill K. Gregory, MFA, Certified Medical Illustrator, for creating the drawn illustrations included in this article.

Recipient of a Certificate of Merit award for an education exhibit at the 2016 RSNA Annual Meeting.

For this journal-based SA-CME activity, the authors, editor, and reviewers have disclosed no relevant relationships.

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Received: Aug 11 2017
Revision requested: Oct 13 2017
Revision received: Dec 11 2017
Accepted: Dec 20 2017
Published online: July 11 2018
Published in print: July 2018

What would happen if you had an injury in the dorsal region of the spinal cord?

Spinal cord injuries can cause one or more of the following signs and symptoms: Loss of movement. Loss of or altered sensation, including the ability to feel heat, cold and touch. Loss of bowel or bladder control.

What is the most common complication of spinal cord injury?

Abnormally low blood pressure is a common SCI complication, particularly in people whose injury is in their cervical (neck) or thoracic (mid-back) spine.

What are the possible consequences of an injury to the spinal cord?

Spinal cord injury is associated with a risk of developing secondary conditions that can be debilitating and even life-threatening—e.g. deep vein thrombosis, urinary tract infections, muscle spasms, osteoporosis, pressure ulcers, chronic pain, and respiratory complications.

Which signals will get disrupted in case of a spinal cord injury?

In case of a spinal cord injury, the signals coming from the receptors as well as the signals sent to the effectors will be disrupted. As both of these signals meet in a bundle in the spinal cord, so, if there is any spinal cord injury then both of these signals will be disrupted.