The many investigations of the biochemical changes that underlie spasticity and the mechanisms of action of antispasticity drugs have been reviewed by Davidoff. Because glutamic acid is the neurotransmitter of the corticospinal tracts, one would expect its action on inhibitory interneurons to be lost. As mentioned earlier, GABA and glycine are the major inhibitory transmitters in the spinal cord; GABA functions as a presynaptic inhibitor, suppressing sensory signals from muscle and cutaneous receptors. Baclofen, a derivative of GABA, is thought to act by reducing the release of excitatory transmitters from the presynaptic terminals of primary afferent terminals. Diazepam and other benzodiazepines have a similar effect but by a different mechanism of potentiating postsynaptic GABA receptors. Actually, none of these agents is entirely satisfactory in the treatment of spasticity when administered orally; the administration of baclofen intrathecally at times has a more beneficial effect. The antispasticity agent tizanidine acts by yet another mechanism as an alpha-2 adrenergic agonist, which increases presynaptic inhibition. Glycine is the transmitter released by inhibitory interneurons and is measurably reduced in quantity, uptake, and turnover in the spastic animal. There is some evidence that the oral administration of glycine reduces experimentally induced spasticity. Interruption of descending noradrenergic, dopaminergic, and serotonergic fibers is undoubtedly involved in the genesis of spasticity, although the exact mode of action of these neurotransmitters on the various components of spinal reflex arcs remains to be defined.
Table 3-1 summarizes the main attributes of upper motor neuron lesions and contrasts them with those of the lower motor neuron discussed above.
Motor Disturbances Caused by Lesions of the Parietal Lobe
As indicated earlier in this section, a significant portion of the pyramidal tract originates in neurons of the parietal cortex. Also, the parietal lobes are important sources of visual and tactile information necessary for the control of movement. Pause and colleagues have described the motor disturbances caused by lesions of the parietal cortex. The patient is unable to maintain stable postures of the outstretched hand when his eyes are closed and cannot exert a steady contraction. Exploratory movements and manipulation of small objects are impaired, and the speed of tapping is diminished. Posterior parietal lesions (involving areas 5 and 7 in Fig. 3-3) are more detrimental in this respect than anterior ones (areas 1, 3, and 5), but both regions are affected in patients with the most severe deficits.
All that has been said about the cortical and spinal control of the motor system gives one only a limited idea of human motility. Viewed objectively, the conscious and sentient human organism is continuously active—fidgeting, adjusting posture and position, sitting, standing, walking, running, speaking, manipulating tools, or performing the intricate sequences of movements involved in athletic or musical skills. Some of these activities are relatively simple, automatic, and stereotyped. Others have been learned and mastered through intense conscious effort and with long practice have become habitual—that is, reduced to an automatic level—a process not at all understood physiologically. Still others are complex and voluntary, parts of a carefully formulated plan, and demand continuous attention and thought. What is more remarkable, one can be occupied in several of these variably conscious and habitual activities simultaneously, such as driving through heavy traffic while dialing a cellular phone (not endorsed) and engaging in animated conversation. Moreover, when an obstacle prevents a particular sequence of movements from accomplishing its goal, a new sequence can be undertaken automatically for the same purpose.