Chapter 5 - Spinal Cord

Topographic anatomy

The cervical and lumbar enlargements of the spinal cord result from enlargement of the gray matter that contains the neural machinery necessary to operate the limbs. The cord ends in the upper lumbar region (L1-2) at the conus medullaris (see figure). Of course there are nerves to the lower extremities that exit the spine all the way down to the sacrum. Therefore, the lower lumbar and sacral nerve roots must leave the spinal cord in the lower thoracic/upper lumbar regions and course within the canal made by the vertebrae down to their point of exit. This bundle of nerve roots is called the "cauda equina" and can be injured in the low back with catastrophic consequences (including loss of bladder and bowel control). The filum terminale interna is a continuation of pia matter that continues to the lower end of the thecal sac (around S2). It then continues, along with a contribution from the dura matter, the filum terminale externa, to attach to the coccyx, anchoring the lower end of the spinal cord.

The spinal cord is composed of a core of gray matter surrounded by white matter. The white matter appears in three locations: lateral, anterior and posterior to the gray matter (the lateral, ventral and dorsal funiculi, respectively). The white matter consists of tracts that interconnect segments of the spinal cord or connect the spinal cord with the brain. The gray matter appears in a "butterfly shape", with ventral and dorsal horns, an intermediate gray matter and, in the thoracic cord, a lateral horn (sympathetic neurons). The dorsal horn contains neurons that represent some of the processing mechanisms for sensory signals and the ventral horn contains motor neurons.

The gray mater of the spinal cord has layers (Rexed's lamina), which basically progress from posterior to anterior. (lamina I-IX). Laminae I-III are usually included in the “substantia gelatinosa”. This is where many sensory fibers terminate and are initially processed. Laminae IV and V includes the neurons that give rise to the spinothalamic tract. Lamina IX is the location of the alpha motor neurons. There is a topographic organization of motor neurons, with motor neurons to extensor muscles placed more anteriorly and flexor motor neurons more posteriorly in Lamina IX of the anterior horn.

Laminae VII and VIII are often included in the “intermediate gray matter” of the spinal cord. This is where most of the interneurons that are part of reflex pathways are located. These interneurons often interconnect with one another and receive processed signals from sensory systems and eventually (often through some chain of interneurons) connect with motor neurons. Interneurons mostly use gutamate as excitatory transmitter or glycine for inhibition. There are interneurons that have axons cross the spinal cord, synapsing on the contralateral side of the cord and others that travel for many segments, contributing to intersegmental reflexes and motor patterns (such as normal locomotor patterns or reciprocal arm and leg swing). Most of the axons that travel between segments travel in the white matter immediately adjacent to the gray matter (so-called propriospinal fibers). Interneurons of the intermediate gray are under descending control via descending tracts. Most of this descending control is inhibitory.

Lamina X is the small area of gray matter around the central canal of the cord.

Spinal reflexes

Reflexes, at a minimum, require a sensory signal and a motor response of some type. There are often interneurons present that pattern the reflex response. In the case of spinal reflexes, the intermediate gray (Rexed's laminae VII and VIII) contains these interneurons.

An understanding of reflexes requires some appreciation of normal muscle contraction. Muscles contract by activation of alpha motor neurons. Each alpha motor neuron synapses on a large number of extrafusal muscle fibers (the “motor unit”). The motor unit does not consist of a clump of adjacent muscle fibers, but rather consists of muscle fibers spread over a large portion of the muscle, interspersed with muscle fibers belonging to other motor units. Small motor neurons contact “red” muscle (Type I, sometimes called “slow-twitch”) fibers and are activated first as the muscle barely begins to contract. These muscle fibers are very oxidatively active and can sustain tonic contraction. The “white” (Type II, fast-twitch) muscle fibers are connected to large motor neurons and are only recruited with stronger contractions (“size principle” of contraction). There is a class of muscle fibers that is “in between” the classic white and red fibers and humans have no muscles that are purely made up of one fiber type.

With minimal contraction, only one small motor neuron is activated (with its motor unit). This motor unit initially fires at a very low rate, which increases as the contraction gradually builds. A second motor unit than begins to fire and it, too, gradually buids its rate of fire until a third (and so on) unit is added. Eventually, large motor neurons, connected to white muscle fibers, are added to the contraction. Of course, this buildup occurs quite quickly when rapid, forceful contractions are attempted.

Muscle stretch (myotatic) reflexes are mediated purely at the spinal cord level, with monosynaptic connections between muscle spindle afferents and motor neurons to the muscle that was stretched. The muscle spindle consists of specially modified muscle fibers (“intrafusal fibers”) that are arranged in parallel with extrafusal fibers in the muscle. When the muscle is stretched, not only are extrafusal muscle fibers stretched, but also the intrafusal muscle fibers. The intrafusal muscle fibers have a sensory nerve fiber that is wrapped around the central portion of the fiber. This “annulospiral” ending is activated by stretch of the muscle fibers. There are some other sensory endings (“flowrspray”) that can also be activated by stretch but are not as important. The annulospral endings are attached to the largest sensory axons in the body (so-called Ia afferent nerve fibers).

The intrafusal muscle fibers have contractile elements in the ends of the fiber. These intrafusal fibers are contracted by activation of gamma motor neurons (extremely small motor neurons, also located in the ventral horn of the spinal cord). When the intrafusal muscle fibers are contracted, since the contractile elements are in the ends of the fibers, the center of the intrafusal fiber is stretched and this can activate the annulospiral sensory receptor. This is important since, when the muscle is contracted (i.e., when the extrafusal fibers are shortened), all tension would come off of the muscle spindle if the intrafusal fibers were not also contracted. This would make the muscle spindle useless for sensing length and stretch of the contracted muscle.

When the annulospral ending is stimulated by stretch of the muscle spindle, a reflex is elicited. There is monosynaptic activation of motor neurons to the muscle that is stretched. There is also polysynaptic facilitation of agonist muscles and polysynaptic inhibition of antagonist muscles. This coordinated response readjusts the tension of the muscle to resist displacement from the set point of the muscle spindle. The sensitivity of this reflex can be adjusted by activation of the gamma motor neurons. This reflex is under a constant degree of inhibition via descending tracts (particularly medullary reticulospinal tracts). The activity of the gamma motor neuron sets the length that the stretch reflex will attempt to cause the muscle to assume. More activity of gamma motor neurons in a muscle will cause the muscle to contract reflexly. In fact many normal movements are produced by activation of a gamma motor neuron to a muscle, which will trigger action potentials in annulosprial endings and reflex activation of many motor neurons to the muscle in question (as well as contraction in agonists and relaxation of antagonists). This method of contracting muscles is termed the “gamma loop” and is a very efficient way of causing a movement.

In individuals with over-activity of gamma motor neurons (seen in patients with interruption of descending pathways), there is resistance to movement in all directions (stiffness) that is called spasticity.

The "inverse myotatic" reflex involves inhibition of muscles as a result of very forceful stretching of the muscle. This involves massive activation of Golgi tendon organs. These sensory organs consist of nerve endings located in the regions where muscles connect to tendons. When the muscle is contracted, the sensory fibers are activated and there is transmission of this information about tension back to the spinal cord. The afferent fibers are slightly slower than the muscle spindle afferents, falling into the Ib category. Potentially damaging levels of tension in the muscle results in massive activation of the Golgi tendon organs result in a reflex that includes polysynaptic inhibition of the of the motor neurons to the muscle (and contraction of antagonists). This is probably protective, preventing the muscle from tearing. It is only normally seen when a muscle is stretched to the breaking point although it is seen as the "give-way" portion of the "clasp-knife" response seen in patients with spasticity.

The third type of reflex is the withdrawal reflex to noxious stimuli. These are protective and are mediated via polysynaptic pathways that involve both sides of the cord and many levels of the nervous system. This reflex response includes withdrawal (physiologic flexion) evoked by activation of nociceptive nerve fibers. This information is primarily resulting from activation of the fast pain fibers (of the A? type). In addition to activation of the physiologic flexors of this limb, it activates extensors of the contralateral limb. In fact, there is some effect on all four limbs when this reflex is activated, making this a very complicated reflex. Spinal reflexes are normally kept in check by descending pathways. Damage to the spinal cord usually results in exaggerated reflexes below the level of the lesion after a brief period of "shock". The Babinski response is over-activity of this reflex.

Jump to: