External Structure

The spinal cord has major functional and teleologic importance, yet it is almost paradoxical that its total mass represents just 2% of the entire central nervous system volume. The spinal canal dimensions are slightly larger, allowing the cord to move freely within the canal during neck and back flexion/extension as its perspective changes with movement. The spinal cord per se is a cylindrical elongated structure flattened dorsoventrally, having a length of 42–45 cm (Fig. 44-1). It lies within the vertebral canal extending from the atlas, continuous with the medulla through the foramen magnum, to the level of the 1st and 2nd lumbar vertebra. Here it tapers into the conus medullaris and terminates as the cauda equina (Fig. 44-1). In conditions such as meningitis, one must not place the spinal needle above the L3 vertebra in order not to specifically damage the underlying spinal cord. It is safe to enter the spinal canal distal to this level because the spinal nerves originating from the distal cord and forming the cauda equina, as nerve roots L2-S5, are anatomically arranged so that they are gently moved aside by the passage of the needle in contrast to the fixed spinal cord that may be easily pierced by the needle insertion and thus cause significant damage.

Figure 44-1 Spinal Cord and Vental Rami in Situ.

The cervical and lumbar enlargements of the spinal cord provide the nerve roots innervating, respectively, the upper and lower limbs. There are 31 pairs of spinal nerves, each having dorsal sensory and ventral motor roots that exit the cord (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal). Although there are 7 cervical vertebrae, there are 8 cervical nerve roots (Fig. 44-2). The C1-7 roots exit above their respective vertebrae whereas C8 exits below the 7th cervical vertebra and all thoracic, lumbar, and sacral roots exit below their specific vertebrae.

Figure 44-2 Relation of Spinal Nerve Roots to Vertebrae.

Three protective membranes, the meninges including the dura mater, being the outer layer, then the arachnoid, and the most inner one, the pia, surround the cord (Fig. 44-2). Cerebrospinal fluid flows between the arachnoid and pia. Epidural fat is present in the epidural space between the spinal canal and dura mater. When clinical myelopathies develop, these various disorders are classically categorized as intramedullary, that is, intrinsic to the cord, or extramedullary, occurring secondary to disorders extrinsic to the cord. Extramedullary disorders are further subdivided into those with either an intradural extramedullary locus or a purely extradural site of pathology.

Internal Structure

White matter, consisting of myelinated fibers, surrounds the butterfly or H-shaped gray matter that contains cell bodies and their processes within the cord’s center. These include both primary ascending sensory fibers and descending motor fibers. The sensory pathways are most superficial, while the motor fibers such as the corticospinal fibers are more deeply situated but still superficial and superior to the ventral horn containing the anterior horn cells that are the primary receptors for the corticospinal tract fibers. Longitudinal furrows on the cord’s surface divide the white matter into columns or funiculi that are large bundles of nerve fibers having diverse functions. The anterior median fissure, posterior median, posterior intermediate, and the anterolateral sulci divide the dorsal or posterior, lateral, and anterior columns. The posterior columns are further divided into two fasciculi, gracilis medially (present at all spinal levels) and cuneatus laterally (T6 and above).

Specific Spinal Tracts

Ascending and descending tracts within the cord are interrupted at sites of cord damage (Figs. 44-3 to 44-5). The subsequent clinical sequelae develop based on the specific tracts that are affected.

Figure 44-3 Principal Fiber Tracts of Spinal Cord.

Figure 44-4 Spinal Cerebral Afferent Systems.

Figure 44-5 Cerebral Cortex: Efferent Pathways.

Spinal Gray Matter

The gray matter within the central cord from dorsal to ventral respectively includes the dorsal horn, the medial commissure, and the anterior horn. Various types of sensory fibers end in different layers of the dorsal horn. The high-threshold, very thin, and unmyelinated A delta and C fibers, conducting impulses from the nociceptors, end almost exclusively in the substantia gelatinosa (lamina I and II). In contrast, nerves carrying the low-threshold mechanoreceptors subserving A beta fibers terminate in the deeper layers of the dorsal horn Rexed layers III-V. Lastly the largest, A alpha joint position sensory nerves end in the deepest layer VI of the dorsal horn (see Fig. 44-4).

Motor neurons are primarily contained within the anterior horn. The preponderant numbers of these somatic efferent neurons are primarily located within the cervical and lumbosacral enlargements (see Fig. 44-5). Here these provide the motor innervation for their respective extremities. In contrast, the ventral horn areas subsume a much smaller portion of the thoracic cord. Here the lateral horn of the gray matter becomes preeminent, where it includes the intermediolateral nucleus. Here the preganglionic sympathetic neuron perikarya are located; similar neurons are also found within the brainstem (Fig. 44-6).

Figure 44-6 Spinal Cord Cross Sections: Fiber Tracts.

Vascular Supply

Arterial

One anterior and two posterior spinal arteries course the length of the cord supplying the anterior two thirds and posterior one third of the cord, respectively (Fig. 44-7). Sulcal or central branches of the anterior spinal artery supply the central cord, whereas coronal or circumferential branches supply the ventral and lateral columns (Fig. 44-8).

Anterior spinal artery supplies the anterior horn, spinothalamic tract, and corticospinal tract.

Posterior spinal artery supplies the dorsal column, dorsal gray matter, and superficial dorsal aspect of lateral columns.

Vertebral artery medullary branches join the anterior and posterior spinal arteries to supply the cervical cord.

Aortic segmental arteries provide the supply for the remainder of the cord by branching into dural arteries that supply the dura and nerve root sleeve. Radicular branches supply the anterior and posterior nerve roots, and medullary branches join the anterior and posterior spinal arteries to supply the cord. Adamkiewicz’s artery, at the lumbar enlargement, usually arises from the left side between T6 and L4. It provides the major arterial supply to the lower cord. The cord levels of C1–T2 and T9 caudally have excellent vascular supplies. In contrast, the T3–T8 arterial vasculature is more limited in number of vessels. Thus, this is usually considered a watershed area that is quite vulnerable to ischemic events.

Figure 44-7 Arteries of Spinal Cord: Schema.

Figure 44-8 Arteries of Spinal Cord: Intrinsic Distribution.

Venous

The anteromedial cord (anterior horns and white matter) is drained by the central or sulcal veins into the anterior median spinal vein that extends the length of the cord. The anterolateral, peripheral, and dorsal cord capillary plexus drains into the radial veins. The radial veins subsequently drain into the coronal venous plexus on the spinal cord surface (Fig. 44-9). This plexus, with superficial spinal cord veins (anterior median, anterolateral, posterior median, posterior intermediate), drains into medullary veins. These are anatomically linked to the nerve roots traveling through the intervertebral foramen forming the epidural venous plexus. Subsequent drainage is to the inferior vena cava, azygous, and hemizygous veins.

Figure 44-9 Veins of Spinal Cord and Vertebrae.

Intramedullary Loci

Syringomyelia, or more rarely either an intramedullary cord tumor or a central hemorrhagic spinal necrosis present with a classic dissociated sensory syndrome. Classically these patients have a “cape loss” of pain and temperature modalities. That is, the patient may note loss of temperature and pain sensation limited to their hands, arms, and shoulders with preservation of same on the trunk and lower extremities. In this instance, the decussating pain and temperature fibers, such as C5-8 fibers, are damaged as they pass under the spinal cord’s expanding central canal. Normally, these fibers join the ascending spinothalamic tracts from the legs and trunk to ascend to the brain (Fig. 44-14). Here temperature and pain sensation are intact distal to the site of the intramedullary lesion; thus there is a dissociation in the patient’s ability to perceive these basic modalities proximally at the midcervical levels but preserving same below the affected areas. Light touch and proprioception are typically preserved. Extension of the lesion into the anterior horn cells leads to segmental neurogenic atrophy, paresis, and areflexia. As the corticospinal tracts become involved, a spastic paresis develops below the level of the syrinx.

Figure 44-14 Syringomyelia.

Another form of dissociated sensory loss occurs in the rare instance of an intramedullary spinal tumor that expands from within destroying fiber tracts that are deep within the cord while it leaves intact the most peripheral portions of the spinothalamic tract carrying pain and temperature sensation from the S1-S5 regions, that is, the posterior thighs and buttocks. In this instance, when one examines the buttocks, a “saddle sparing” is present.

The posterior-lateral columns and often the adjacent corticospinal tracts may also be preferentially affected. Common examples include multiple sclerosis, vitamin B₁₂ (cyanocobalamin) or copper deficiency, and HIV-associated vacuolar myelopathy. Here position and usually vibration modalities are primarily affected concomitant with impaired corticospinal tract function. Vibration and proprioception are impaired in the lower extremities. Paresthesiae may be more pronounced in the feet, although the hands are often earlier affected with cyanocobalamin deficiency.

Occasionally a patient presents with a primary intramedullary lesion that primarily affects the anterior spinal cord. The primary damage occurs within the spinal cord anatomy dependent on anterior spinal artery supply. In this instance, the patient experiences damage to the lateral spinothalamic and anterior and lateral spinothalamic tracts as well as the relevant anterior horn cells (see Fig. 44-12). Typically these patients become paraparetic or paraplegic, with a complete pain and temperature sensory loss below the level of the lesion. In essence, this is an anterior two thirds transverse spinal cord lesion. Therefore, these patients characteristically have preservation of proprioception modalities (position sense) as the posterior columns remain intact. Very rarely, weakness occurs in all four extremities when the cervical cord is infarcted; however, the abundance of collateral circulation at this level makes this an exceedingly rare clinical scenario. A posterior one-third myelopathy would be expected to lead to a sensory ataxia, spasticity, and hyperreflexia with preserved pain and temperature and corticospinal tract function; however, this clinical picture is extremely rare.

Intradural Extramedullary

Hemi-cord lesions: The Brown-Sequard syndrome is a classic example. The corticospinal tract subserves the ipsilateral extremities, as its decussation has previously occurred at the cervical medullary junction. Therefore, these patients have weakness appropriate to the side of the spinal lesion. In contrast, pain and temperature loss is confined to the contralateral body as the fibers composing the spinothalamic tract have already decussated as it ascends within the cord. Thus, a left-sided lesion affects the right side’s ability to perceive these modalities, whereas the motor loss is ipsilateral to the lesion site.

This combination of incongruous motor and sensory dysfunction is known as a dissociated clinical pattern. A good illustration is a 40-year-old woman who noted that her left leg was occasionally scuffing somewhat when she played tennis. Subsequently, she did not recognize having cut her right leg while shaving. Thus, she was developing a hemicord Brown-Sequard syndrome that proved to be at the thoracic spine level (Fig. 44-15).

Figure 44-15 Intradural Extramedullary Tumors of Spinal Cord.

As a lesion such as this increases in size, the other sensory modalities are sometimes affected ipsilateral to the spinal lesion. These include loss of position, that is, proprioceptive function. Sometimes vibration and touch modalities are also affected.

Extradural Extramedullary

Patients with this type of pathologic process may have either a diffuse or a solitary lesion. Many extradural processes are manifested by a widespread “seeding” representing an extension of some systemic process, including metastatic tumors, various parameningeal infections, or very rare granulomatous processes.

Focal bony lesions, often from metastases, are the typical example of an extramedullary extradural lesion. These may present subacutely or relatively acutely from pathologic fracture dislocation and extension of the tumor leading to rapid cord compromise (Fig. 44-16). Characteristically, these patients experience pain secondary to involvement of the pain-sensitive meninges, its adjacent sensory nerve roots, or the concomitant bone as occurs with metastatic cancers. Therefore, pain is one of the hallmarks of many extradural extramedullary disorders. As the size of the lesion increases, direct pressure is applied to the adjacent spinal cord, or the primary vascular supply is compromised, predominantly affecting the anterior two thirds of the cord, or both. Often these lesions expand or displace cord tissue acutely, essentially leading to a pathophysiologic cord transection. Thus, the final clinical picture may mimic a traumatic myelopathy; it is therefore of paramount importance to expeditiously evaluate these patients in order to preserve cord function.

Figure 44-16 Extradural Tumors.

More chronically, a progressive cervical spondylosis will produce spinal stenosis leading to a gradual relatively symmetric cord compression. Typically, these patients evidence posterior column and corticospinal tract dysfunction. This is manifested by numbness in the feet and tendency to a spastic gait.

Transverse Myelopathy, Complete Spinal Cord Lesions

When one is faced with lesions extensively damaging the entire spinal cord, the resultant clinical picture is characterized by total interruption of all sensory and motor functions below the damaged level. An acute insult causes flaccid paralysis and areflexia secondary to “spinal shock”; subsequently, spasticity and hyperreflexia develop, as in more ingravescent lesions. These chronic lesions are associated with a slowly evolving weakness. If the anterior horn cells, ventral roots, or both are also involved, lower motor neuron signs, including fasciculations, atrophy, areflexia, and weakness, occur at the lesion level. An extensive cord insult is necessary to completely affect touch sensation as both the posterior columns and spinothalamic tracts provide touch. The demonstration of a sensory level, assessed by testing pain and temperature (spinothalamic tract), segmental paresthesiae, or radicular pain, often helps to localize the spinal cord level.