There is considerable information concerning the neurochemistry of motor neurons. The large neurons of the anterior horns of the spinal cord contain high concentrations of choline acetyltransferase and use acetylcholine as their transmitter at the neuromuscular junction. The main neurotransmitters of the descending corticospinal tract, in so far as can be determined in humans, are aspartate and glutamate. Glycine is the neurotransmitter released by Renshaw cells, which are responsible for recurrent inhibition, and by interneurons that mediate reciprocal inhibition during reflex action. Gamma-aminobutyric acid (GABA) serves as the inhibitory neurotransmitter of interneurons in the posterior horn. There are also descending cholinergic, adrenergic, and dopaminergic axons, which play a less well-defined role in reflex functions.
Paralysis due to Lesions of the Lower Motor Neurons
If all, or practically all, peripheral motor fibers supplying a muscle are interrupted, the voluntary, postural, and reflex movements of that muscle are abolished. The muscle becomes lax and soft and does not resist passive stretching, a condition known as flaccidity. Muscle tone—the slight resistance that normal relaxed muscle offers to passive movement—is reduced (hypotonia or atonia). The denervated muscle undergoes extreme atrophy, being reduced to 20 or 30 percent of its original bulk within 3 to 4 months. The reaction of the muscle to sudden stretch, as by tapping its tendon, is lost (areflexia). Damage restricted to only a portion of the motor fibers supplying the muscle results in partial paralysis, or paresis, and a proportionate diminution in the force and speed of contraction. The atrophy will be less and the tendon reflex reduced instead of lost. The electrodiagnosis of denervation depends upon finding fibrillations, fasciculations, and other abnormalities on needle electrode examination as mentioned in the previous chapter. However, some of these abnormalities do not appear until several days or a week or two after nerve injury.
Lower motor neuron (infranuclear) paralysis is the direct result of loss of function or destruction of anterior horn cells or their axons in anterior roots and nerves. The signs and symptoms vary according to the location of the lesion. In any individual case, the most important clinical question is whether sensory changes coexist. The combination of a flaccid, areflexic paralysis, and sensory changes usually indicates involvement of mixed motor and sensory nerves or of both anterior and posterior roots. If sensory changes are absent, the lesion must be situated in the anterior gray matter of the spinal cord, in the anterior roots, in a purely motor branch of a peripheral nerve, or in motor axons alone (or in the muscle itself). At times it may be impossible to distinguish between nuclear (spinal) and anterior root (radicular) lesions.
Preserved and often heightened tendon reflexes and spasticity in muscles weakened by lesions of the corticospinal systems attest to the integrity of the spinal segments below the level of the lesion. However, acute and profound spinal cord lesions and, to a lesser extent, corticospinal lesions in the brainstem and cerebrum, may temporarily abolish spinal reflexes (“spinal shock”; see Chap. 42). This is probably caused by the interruption of descending tonic excitatory impulses, which normally maintain a sufficient level of excitation in spinal motor neurons to permit the peripheral activation of segmental reflexes. The attenuation of spinal shock by opiate antagonists, such as naloxone, suggests that the phenomenon is at least in part mediated by the release of previously stored endogenous opiates from the distal terminals of neurons in the periaqueductal gray matter. Once the stored opiates are depleted, the presynaptic inhibition of motor neurons ceases, heralding the end of spinal shock and the beginning of the period of spasticity.