The terms hypokinesia and akinesia (the extreme form of hypokinesia) refer to a reduction in the spontaneous movements of an affected part and a failure to engage it freely in the natural actions of the body. In contrast to what occurs in paralysis (the primary symptom of corticospinal tract lesions), strength is not significantly diminished. Also, hypokinesia is unlike apraxia, in which a lesion erases the pattern of movements necessary for an intended act, leaving other actions intact. Hypokinesia is expressed most clearly in the parkinsonian patient where it takes the form of an extreme underactivity (“poverty”) of movement. The frequent automatic, habitual movements observed in the normal individual—such as putting the hand to the face, folding the arms, or crossing the legs—are absent or greatly reduced. In looking to one side, the eyes move, but not the head. In arising from a chair, there is a failure to make the usual small preliminary adjustments, such as pulling the feet back, putting the hands on the arms of the chair, and so forth. Blinking is infrequent. Saliva is swallowed less frequently and drooling results. The face lacks expressive mobility (“masked facies,” or hypomimia). Speech is rapid, mumbling (or “cluttered”), and monotonic, and the voice is soft.
Bradykinesia connotes slowness of movement, another aspect of the same physiologic difficulty as reflected in hypokinesia. Not only is the parkinsonian patient slightly “slow off the mark” (displaying a longer-than-normal interval between a command and the first contraction of muscle—that is, increased reaction time), but the velocity of movement, or the time from onset to completion of movement, is slower than normal. The extremes of hypokinesia or of bradykinesia can result in a complete impediment of movement, akinesia, a sign that may also result from several other disorders of motor function and volitional motor initiation. Hallett equates akinesia with a prolonged reaction time and bradykinesia with a prolonged time of execution. For a time, bradykinesia was attributed to the frequently associated rigidity, which could reasonably hamper all movements, but the limitation of this explanation became apparent when it was discovered that an appropriately placed stereotactic lesion in a patient with Parkinson disease may abolish rigidity while leaving the hypokinesia unaltered. Thus it appears that apart from their contribution to the maintenance of posture, the basal ganglia provide an essential element for the performance of the large variety of voluntary and semiautomatic actions required for the full repertoire of natural human motility. That cells in the basal ganglia participate in the initiation of movement is also evident from the fact that the firing rates in these neurons increase before movement is detected clinically.
Hallett and Khoshbin, in an analysis of ballistic (rapid) movements in the parkinsonian patient, found that the normal triphasic sequence of agonist–antagonist–agonist activation, as described in the next chapter, is intact but lacks the amplitude (number of activated motor units) to complete the movement normally. Several smaller triphasic sequences are then needed, which slow the movement. The patient experiences these phenomena as not only slowness but also a perceived weakness.