The central nervous system (CNS) comprises the brain and the spinal cord. The spinal cord plays a particularly important role in relaying sensorimotor signals between the brain and the body. An understanding of the anatomic arrangement of cord structures can help an examiner to localize related lesions.

ANATOMY

The spinal cord extends from the medulla, through the foramen magnum, and down the spinal canal. The filum terminale, a connective tissue band, anchors the cord to the end of the canal. Anterior to the cord are 7 cervical, 12 thoracic, 5 lumbar, and 5 sacral vertebral bodies. These vertebral bodies are related to the motor and sensory nerve roots that emerge from the ventral and dorsal aspects of the cord along its length. Both the vertebral bodies and nerve roots are numbered, but those sets of numbers do not match consistently. Most cervical nerve roots (i.e., C1 to C7) emerge above the corresponding cervical vertebral bodies (e.g., the C6 nerve root traverses between the C5 and C6 vertebral bodies), but the C8 nerve roots exit between the seventh cervical and first thoracic vertebral bodies (i.e., at the C7-T1 level), because there is no C8 vertebral body. Distal to the T1 level, nerve roots are located below the corresponding vertebral body so the L3 nerve root is located between the L3 and L4 vertebral bodies, or at the L3-4 level (Fig. 22-1). The spinal cord extends to approximately the level of the L1 vertebral body. Accordingly, safe lumbar punctures can be performed below this level because there is no spinal cord in the canal there.

In cross section, the spinal cord contains the “central gray” matter and neuron cell bodies, distributed in the shape of an H (Fig. 22-2). Each side of this central gray has an anterior and posterior (dorsal) horn. The anterior horns contain primarily the alpha motor neurons and motor nerve fibers innervating skeletal muscles. The dorsal horns represent the gateway for sensory information. The right and left aspects of the central gray matter are connected by the transverse commissure.

Surrounding the gray matter are white matter tracts traveling to and from the brain. The most important descending motor tract is the corticospinal tract (CST) (Fig. 22-3). After descending from the cortex, the CST crosses at the medulla before descending in the lateral aspect of the cord. Accordingly, fibers from the left motor cortex cross at the medullary pyramids before descending on the right side of the spinal cord to serve the right limbs, and vice versa. Thus, spinal cord injuries that involve the right CST cause right body (ipsilateral) motor deficits.

The lateral aspect of the cord also contains autonomic fibers from the hypothalamus and brainstem. Sympathetic fibers course from T1 to L2 where they exit the spinal cord. Injuries to autonomic fibers proximal to S2 can result in a “neurogenic bladder.” This term describes automatic, involuntary bladder emptying when a certain level of distention occurs. Parasympathetic nerve fibers leave the spinal cord in the S2 to S4 cord segments. Injuries to peripheral nerve fibers at these distal levels can result in overflow incontinence from a flaccid bladder.

There are two important ascending sensory tracts: the dorsal column and the spinothalamic tracts (Fig. 22-2). The dorsal columns refer to the heavily myelinated tracts in the posterior aspect of the spinal cord that mediate joint position, discriminative touch, and, to some degree, vibration sense. These tracts are arranged with fibers ascending from the cervical spinal cord (fasciculus cuneatus) lateral to the fibers ascending from the lumbosacral segments (fasciculus gracilis) medially. These ascending fibers remain ipsilateral to their site of origin until they cross at the level of the medulla, en route to the ventroposterolateral nucleus of the thalamus. Thus, spinal cord injuries affecting the right dorsal columns may impair proprioception in the right limbs. The lateral spinothalamic tracts are unmyelinated and carry pain and temperature sensory information. After these fibers enter the spinal cord and ascend about two levels, they cross in the ventral white commissure. Thus, a spinal cord lesion involving the right lateral spinothalamic tracts may impair pain and temperature sensation starting a few levels below the level of the lesion on the left (because these ascending fibers have already crossed).

FIGURE 22-1. Posterior view of vertebral bodies in the cervical (A) and lumbar (B) regions showing the relationship that can exist between a herniated nucleus pulposus (pink) and the spinal nerve roots. (Note that there are eight cervical nerves and only seven cervical vertebrae.) In the lumbar region, the emerging L4 nerve roots emerge laterally, close to the pedicles of the fourth lumbar vertebra, and are not closely related to the intervertebral disk between the fourth and fifth lumbar vertebrae. Pressure on the L5 motor nerve root can prvoduce weakness of dorsiflexion at the ankle. (From Snell RS. Clinical Neuroanatomy. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.)

FIGURE 22-2. Transverse section of the spinal cord showing the sensory pathways. The posterior columns relay information concerning proprioception and two-point discrimination. The spinothalamic tracts relay pain and temperature information. (From Ginsberg L. Lecture Notes: Neurology. 8th ed. Oxford: Blackwell Publishing; 2005:122. Copyright © 2005 L Ginsberg. Reprinted by permission of John Wiley & Sons, Inc.)

The blood supply for the anterior two-thirds of the spinal cord comes primarily from a single anterior spinal artery (ASA) running along most of the ventral surface of the cord. The cephalad portion of the ASA arises from branches of the two vertebral arteries. The caudal portion of the ASA originates as aortic branches that form the artery of Adamkiewicz. The anterior horns, spinothalamic tracts, and lateral corticospinal tracts, are perfused by the ASA. There are two posterior arteries that perfuse the dorsal columns.

FIGURE 22-3. The corticospinal tract from the cortex to the ventral horn. [Copyright © 2012 Dr. Juan Acosta, MD.]

The spinal cord is protected chemically by the blood–brain (or blood–CNS) barrier and structurally by the resilient connective tissue of the dura mater and surrounding vertebrae. Importantly, related spinal structures, such as the intervertebral disks, can cause neurologic dysfunction when out of place.For example, herniated disks can cause potentially serious “extradural” compression of the cord. Compressive lesions can also occur within the dura but outside of the spinal cord itself (“intradural, extramedullary” lesions); examples include meningiomas and neurofibromas. Finally, lesions within the cord itself (“intramedullary” lesions), such as gliomas, can cause cord impingement and dysfunction. Spinal cord compression causes weakness, incoordination, and sphincter dysfunction below the level of the lesion and often causes a sensory level at or below the lesion. Spinal cord compression is a neurologic emergency, although related symptoms and signs can evolve over time.

LOCALIZATION OF SPINAL CORD DYSFUNCTION

The symptoms of spinal cord dysfunction can be protean, but the patient’s history and a careful neurologic examination can help point to a lesion in this region of the CNS. Patients may report sensorimotor symptoms. Bowel and bladder dysfunction often accompanies cord dysfunction. A girdle or band-like sensation around the torso can reflect cord dysfunction with involvement of the dorsal columns, as can a sensation of limb swelling in the absence of visible edema. In classic, chronic spinal cord dysfunction, “long tract signs” such as limb spasticity and hyperreflexia may be present. Indeed, the combination of increased reflexes and weakness in the same somatic territory (such as a motor root distribution) are a common finding in the setting of cord dysfunction. By performing a sensory (e.g., pinprick) examination of the limbs and posterior trunk bilaterally, a “level” demarcating the boundary between normal and abnormal sensation can be sought. Such a finding indicates a cord lesion at or above the identified level. (Because of the laminated organization of fibers in the cord, this level can rise over time.) It is important to remember that acute cord lesions (e.g., spinal shock) can be associated with paralysis and a loss of, rather than increase in, reflexes and tone. In this scenario, the more characteristic signs of cord dysfunction may emerge only after a period of weeks.

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The Sensory System The Approach to Coma and Altered Consciousness Head Trauma Radiculopathy, Plexopathy, and Peripheral Neuropathy The Approach to Weakness Demyelinating Diseases of the Central Nervous System

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