10.4: The Spinal Cord

Spinal cord anatomy

The spinal cord extends posteriorly from the brain stem, surrounded by the vertebrae. In a typical human, the spinal cord is about 1 cm in diameter. Generally, the diameter of the spinal cord decreases from anterior to posterior, with two exceptions: an enlargement in the mid-cervical region to accommodate the extra nerves of the arms and hands, and a smaller enlargement in the lumbar region to accommodate extra nerves of the legs and feet (chapter 2.1).

The output neurons of the motor cortex carry voluntary motor information and send their axons down through two major descending communication routes. At the level of the brain stem, both pass through the medullary pyramids, paired anatomical structures found on the ventral surface of the medulla. Because of this, both descending axonal tracts are also called the pyramidal tracts.

The corticobulbar tract is made up of axons that terminate in various brain stem motor nuclei. These nuclei communicate directly with several cranial nerves, particularly those with motor function: The trigeminal nucleus (CN V) modulates muscles of chewing, the facial nucleus (CN VII) regulates facial expressions, the glossopharyngeal nucleus (CN IX) controls the muscles involved in speech and swallowing, and the hypoglossal nucleus (CN XII) controls the muscles of the tongue.

The other major output of M1 are the upper motor neurons whose axons are the corticospinal tract, which runs down the spinal cord through white matter. This pathway has two different communication components.

Upwards of 90% of the corticospinal tract are axons of the lateral corticospinal tract, which sends voluntary motor control to the contralateral distal limbs, such as in the arms, hands, legs, and feet. Some neurons of M1 are Betz cells, the largest known neurons in the brain. Most of this tract crosses hemispheres at the pyramidal decussation, runs down the contralateral spinal cord, then forms synapses onto the lower motor neurons in the ventral horn. These lower motor neurons then send nerve rootlets out of the ventral surface of the spinal cord, then form a neuromuscular junction with the muscles.

The remaining output is the anterior corticospinal tract, which carries information to the muscles of the trunk, such as our shoulders or pectorals. This signaling from the brain stem descends ipsilaterally, but eventually decussates at the spinal cord, resulting in contralateral control. Here, as above, the neuron forms synapses with the lower motor neurons found in the ventral horn.

Reflexes

Reflexes are involuntary motor responses that are performed automatically and independent of brain signals (although some can be suppressed voluntarily, with extra effort). Reflexes involve very simple circuits, sometimes consisting of only two populations of neurons: Sensory information comes in from the periphery, synapsing onto motor neurons in the brainstem or spinal cord. Reflexes can take place as quickly as 1/100th of a second!

A simple reflex is the patellar reflex, or the “knee-jerk” or myotatic reflex (described in more depth in chapter 8; figure 8.27). The stretching of the tendon causes the muscle to elongate, sensory receptors detect this change in muscle length, and the corresponding signal is sent into the spinal cord. This sensory neuron synapses directly onto a motoneuron, which then tells the thigh muscle to contract, making the kicking “knee-jerk” movement. Since only one synapse is involved in producing this response, this is an example of a monosynaptic reflex arc.

The reflexive kick is controlled at the level of the spinal cord and cannot be intentionally suppressed by descending motor pathways no matter how hard you concentrate.

Central pattern generators (CPG)

Central pattern generators (CPGs) are networks of cells that are capable of producing intrinsic motor responses even in the absence of sensory or brain inputs. These motor responses are usually well-rehearsed, repetitive, and happen at the unconscious level, meaning that certain behavioral outputs can be performed independently of signals upstream in the motor cortex. Some example motor responses driven by CPGs include diaphragm movement (respiration), alternating leg swinging and foot flexing (walking), and the progressive contraction of up to 25 pairs of muscles in the tongue and mouth (swallowing). Some CPGs are located in the brain stem (respiration) and others throughout the spinal cord (locomotion).

CPGs have been observed in several organisms, ranging from insects, crayfish, birds, and mammals including humans, hinting that their evolution was highly adaptive for survival. Imagine how difficult it would be to survive if every breath required a conscious thought!

The CPG is not a standalone driver of motor activity, however. The circuits receive signals from higher brain areas which can modify their characteristics. Imagine that you want to consciously hold your breath, or intentionally walk in some unusual or goofy way. In both cases, the descending signals from the brain are able to override the output motor command pattern that the CPG normally produces. Once you stop intentionally changing your motor behavior, the muscles return to their normal activity in response to CPG output.

CPGs of respiration

Getting oxygen is one of the most essential functions that an animal needs to perform for survival. As such, involuntary control of respiratory muscles through CPG activation is likely an evolutionary older mechanism. Respiratory control circuits are found at the level of the brain stem, specifically, the medulla and pons. One suspected CPG is a population of medullary cells called the pre-Bötzinger complex, which contains cells that change their activity in a cyclic pattern. Neurons in these areas are also sensitive to changes in blood chemistry (Chapter 9.3).

The major nerves involved with respiration are the phrenic nerve, which innervates the diaphragm, and the intercostal nerves, which predictably innervate the intercostal muscles. When we inhale (inspiration), the diaphragm contracts and the intercostals move the rib cage to increase the volume of the chest cavity, which allows the lungs to expand. During exhalation, the reverse process is true. These nerves receive innervation from neurons of the CPGs in the respiratory centers of the hindbrain (medulla and pons, specifically.)

The activity of the respiratory CPGs is so potent, that they can sometimes function while unconscious. Some deficits in respiratory CPGs are believed to be one cause of central sleep apnea, a disorder where a person stops breathing while asleep (chapter 12).

CPGs of locomotion

It is much more complex to describe the action of the muscle groups needed for a simple behavior of just walking down the sidewalk: the ankle dorsiflexors, the hamstrings, hip flexors, gluteus maximus and many more function at very precise moments, allowing us to propel ourselves forward. Importantly, this pattern of activity is rhythmic, and repeats at the frequency of stepping.

Many earlier studies of spinal cord CPGs were conducted in different animal groups with unique locomotor patterns. Mollusks have crawling activity that is rhythmic, fish swim by sending alternative patterns of muscle activity through their body, and birds fly by rhythmic flapping of their wings.

In mammals, spinal CPGs were demonstrated in cats with a thoracic-level spinal cord transection. Following this surgery, the signals from the brain were unable to be communicated down to the hind legs, eliminating voluntary movement. They exhibited weakened muscular power, but were still able to stand for short times. If their front paws were put onto a stable platform while their hindlegs were put on a moving treadmill, the cat would involuntarily walk to keep up.

Humans also have CPGs for movement. One remarkable study looked at 37-year-old man who had injured his spinal cord in a football accident as a young man. His injury was at the level of C5, resulting in complete paralysis and a loss of sensation from the neck down. Over the following years, he gradually recovered a small amount of function. Fine manipulation skills and bladder bowel control never recovered, and he had not walked unassisted for ten years, experiencing tremendous weakness after taking a few steps.

Just days after beginning a physical therapy regimen consisting of assisted upright walking, upon lying down, the man reported alternating muscle flexion and relaxation of the hips, knees, and ankles similar to the pattern of activity seen in locomotion. He was unable to voluntarily stop these motions, and could only get some rest by turning to the side. This muscle activity was smooth and rhythmic, as would be seen in a healthy person walking.