A common cause of motor impairment in humans is interruption of the cerebral cortical efferent fibers in the internal capsule; such interruptions occur in capsular strokes. The resulting disorder is often termed a pyramidal tract syndrome, or upper motor neuron disease, although these names are misnomers. Motor changes characteristic of this disorder include (1) increased phasic and tonic stretch reflexes (spasticity); (2) weakness, usually of the distal muscles, especially the finger muscles; (3) pathological reflexes, including the sign of Babinski (dorsiflexion of the big toe and fanning of the other toes when the sole of the foot is stroked); and (4) a reduction in superficial reflexes, such as the abdominal and cremasteric reflexes. Of importance is that if only the corticospinal tract is interrupted, as can occur with a lesion of the medullary pyramid, most of these signs are much reduced or absent. In this situation, the most prominent deficits are weakness of the distal muscles, especially those of the fingers, and a Babinski sign. Spasticity does not occur; instead, muscle tone may actually decrease. Evidently, the presence of spasticity requires the disordered function of other pathways, such as the reticulospinal tracts, as would occur after loss of the descending cortical influence to the brainstem nuclei of origin of these tracts.
The effects of interruption of the medial system pathways are quite different from those produced by corticospinal tract lesions. The main deficits associated with medial system interruption are an initial reduction in the tone of postural muscles and loss of righting reflexes. Long-term effects include locomotor impairment and frequent falling. However, manual manipulation of objects is perfectly normal.
The Decerebrate Preparation
The decerebrate preparation has been useful for experimentally investigating how various descending pathways interact with the spinal cord circuitry. Surgical decerebration is achieved either by transection of the midbrain, often at an intercollicular level, or by occlusion of the blood vessels feeding this area. In the latter case, a lesion also occurs in the anterior vermis of the cerebellum, an important distinction.
With the intercollicular transection, some descending pathways, such as those originating in the cerebral cortex, are interrupted, whereas others, such as those originating in the brainstem, remain intact.
However, remember that the corticospinal tract is only one component of the cortical descending fibers. Many other cortical fibers project to locations throughout the brainstem, including the nuclei of origin for the medial descending pathways. Loss of these cortical control systems results in altered activity in the intact descending pathways. As a result, affected animals show hypertonia and suppression of some spinal reflexes, such as the flexion reflex, and exaggeration of others, such as the stretch reflex; this condition is called decerebrate rigidity. Decerebrate animals maintain a posture that has been called exaggerated standing. Human patients with brainstem damage may also develop a decerebrate state that has many of the same reflex features as animal preparations. The prognosis in such patients is poor if signs of decerebration appear.
Loss of descending control on the reticular formation results in increased activity in the pontine reticulospinal pathway and decreased activity in the medullary reticulospinal pathway. Such increase and decrease in activity, respectively, produces increased excitation and decreased inhibition (disinhibition) of the motor neurons, which explains the observed rigidity. Interestingly, this hypertonia can be relieved by cutting the dorsal roots, which indicates that the reticulospinal tracts have a major effect on γ motor neurons. This is because γ motor neuron activity alters muscle stiffness by increasing muscle spindle sensitivity and thereby causes increased activity in the group Ia and group II afferent fibers, which travel through the dorsal roots into the spinal cord in order to innervate the α motor neurons.