The one place where corticospinal fibers are entirely isolated is the pyramidal tract in the medulla. In humans, there are a few documented cases of a lesion more or less confined to this location. The result of such lesions has been an initial flaccid hemiplegia (with sparing of the face), from which there is considerable recovery. Similarly in monkeys—as was shown by Tower in 1940 and subsequently by Lawrence and Kuypers and by Gilman and Marco—interruption of both pyramidal tracts results in a hypotonic paralysis; ultimately, these animals regain a wide range of movements, although slowness of all movements and loss of individual finger movements remain as permanent deficits. Also, the cerebral peduncle had in the past been sectioned in patients in an effort to abolish involuntary movements (Bucy et al). In some of these patients, a slight degree of weakness or only a Babinski sign was produced but no spasticity developed. These observations indicate that a pure pyramidal tract lesion does not result in spasticity. Animal experiments suggest that the corticoreticulospinal pathways are particularly important in this respect, because their fibers are arranged somatotopically and influence stretch reflexes. Further studies of human disease, possibly using diffusion tensor imaging techniques, are necessary to settle problems related to volitional movement and spasticity.
The distribution of the paralysis caused by upper motor neuron (supranuclear) lesions varies with the locale of the lesion, but certain features are characteristic of all of them. A group of muscles is always involved, never individual muscles, and if any movement is possible, the proper relationships between agonists, antagonists, synergists, and fixators are preserved. On careful inspection, the paralysis never involves all the muscles on one side of the body, even in the severest forms of hemiplegia. Movements that are invariably bilateral—such as those of the eyes, jaw, pharynx, upper face, larynx, neck, thorax, diaphragm, and abdomen—are affected little or not at all. This occurs because these muscles are bilaterally innervated; that is, stimulation of either the right or left motor cortex results in contraction of these muscles on both sides of the body. Upper motor neuron paralysis is rarely complete for any long period of time; in this respect it differs from the absolute paralysis that results from destruction of anterior horn cells or interruption of their axons.
Upper motor neuron lesions are characterized further by certain peculiarities of retained movement. There is decreased voluntary drive on spinal motor neurons (fewer motor units are recruitable and their firing rates are slower), resulting in a slowness of movement. There is also an increased degree of cocontraction of antagonistic muscles, reflected in a decreased rate of rapid alternating movements. These abnormalities probably account for the greater sense of effort and the manifest fatigability in effecting voluntary movement of the weakened muscles. Another phenomenon is the activation of paralyzed muscles as parts of certain automatisms (synkinesias). For example, the paralyzed arm may move suddenly during yawning and stretching. Attempts by the patient to move the hemiplegic limbs may also result in a variety of associated movements. Thus, flexion of the arm may result in involuntary pronation and flexion of the leg or in dorsiflexion and eversion of the foot. Also, volitional movements of the paretic limb often evoke imitative (mirror) movements in the normal one or vice versa. Mirror movements are also a feature of Parkinson disease and of lesions in the upper cervical spinal cord. In some patients, as they recover from hemiplegia, a variety of movement abnormalities emerge, such as tremor, athetosis, and chorea on the affected side. These are expressions of damage to basal ganglionic and thalamic structures and are discussed in Chap. 4.