Bradykinesia, or slowness of movement, is often used interchangeably with hypokinesia (poverty of movement) and akinesia (absence of movement). Bradykinesia is the most characteristic symptom of basal ganglia dysfunction in PD (19). It may be manifested by a delay in the initiation and slowness of execution of a movement. Other aspects of bradykinesia include a delay in arresting movement, decrementing amplitude and speed of repetitive movement, and an inability to execute simultaneous or sequential actions. In addition to whole body slowness and impairment of fine motor movement, other manifestations of bradykinesia include drooling due to impaired swallowing of saliva (20), monotonous (hypokinetic) dysarthria, loss of facial expression (hypomimia), and reduced arm swing when walking (loss of automatic movement). Micrographia has been postulated to result from an abnormal response due to reduced motor output or weakness of agonist force coupled with distortions in visual feedback (21). Bradyphrenia is slowness of thought and does not always correlate with bradykinesia. Therefore, different biochemical mechanisms may underlie these two parkinsonian disturbances (22).
After recording electromyographic (EMG) patterns in the antagonistic muscles of parkinsonian patients during a brief ballistic elbow flexion, Hallett and Khoshbin
(23) concluded that the most characteristic feature of bradykinesia was the inability to "energize" the appropriate muscles to provide a sufficient rate of force required for the initiation and the maintenance of a large, fast (ballistic) movement. Therefore, PD patients need a series of multiple agonist bursts to accomplish a larger movement. Micrographia, a typical PD symptom, is an example of a muscle-energizing defect (23). The impaired generation and velocity of ballistic movement can be ameliorated with levodopa (24,25).
Bradykinesia, more than any other cardinal sign of PD, correlates well with striatal dopamine deficiency. Measuring brain dopamine metabolism of rats running on straight and circular treadmills, Freed and Yamamoto (26) found that dopamine metabolism in the caudate nucleus was more affected by posture and direction of movement. Dopamine metabolism in the nucleus accumbens was more linked to the speed and direction of the antagonists, appears to be normal in PD, and is probably more under cerebellar than basal ganglia control (23). In other words, in PD, the simple motor program to execute a fast ballistic movement is intact, but it fails because the initial agonist burst is insufficient. The degree of bradykinesia correlates with a reduction in the striatal fluorodopa uptake measured by positron emission tomography (PET) scans and with nigral damage (27). Studies performed in monkeys made parkinsonian with the toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (28), and in patients with PD provide evidence that bradykinesia results from excessive activity in the subthalamic nucleus (STN) and the internal segment of the globus pallidus (GPi) (29). Thus, there are both functional and biochemical evidence of increased activity in the outflow nuclei, particularly STN and GPi, in patients with PD. As a result of the abnormal neuronal activity at the level of the GPi, the muscle discharge in patients with PD changes from the normal high (40 Hz) to pulsatile (10 Hz) contractions. These muscle discharges can be auscultated with a stethoscope (30). More recent studies suggest that the observed 15 to 30 Hz oscillations of the STN may reflect synchronization with cortical beta oscillation via the cortico-subthalamic pathway and may relate to mechanisms of bradykinesia. Stimulation at the 15 Hz rate worsens bradykinesia, and dopaminergic drugs promote faster oscillations (about 70 Hz) and improve bradykinesia—similar to the high frequency stimulation associated with deep brain stimulation (31,32).
Bradykinesia, like other parkinsonian symptoms, is dependent on the emotional state of the patient. With a sudden surge of emotional energy, the immobile patient may catch a ball or make other fast movements. This curious phenomenon, called "kinesia paradoxica," demonstrates that the motor programs are intact in PD, but that patients have difficulty in utilizing or accessing the programs without the help of an external trigger (33). Therefore, parkinsonian patients are able to make use of prior information to perform an automatic or a preprogrammed movement, but they cannot use this information to initiate or select a movement. Another fundamental defect in PD is the inability to execute learned sequential motor plans automatically (34). This impairment of normal sequencing of motor programs probably results from a disconnection between the basal ganglia and the supplementary motor cortex, an area that subserves planning function for movement. The supplementary motor cortex receives projections from the motor basal ganglia (via the GPi and ventrolateral thalamus) and, in turn, projects to the motor cortex. In PD, the early component of the premovement potential (Bereitschaftspotential) is reduced, probably reflecting inadequate basal ganglia activation of the supplementary motor area (35,36). Recording from the motor cortex of MPTP monkeys, Tatton et al. (37) showed markedly increased gain of the long-latency (M2) segments of the mechanoreceptor-evoked responses. This and other findings indicate that PD patients have an abnormal processing of sensory input necessary for the generation and execution of movement.
Most neurophysiologic and neurobehavioral studies in PD have concluded that the basal ganglia (and possibly the supplementary motor cortex) play a critical role in planning and sequencing voluntary movements (38). For example, when a patient arises from a chair, he/she may "forget" any one of the sequential steps involved in such a seemingly simple task: to flex forward, place hands on the arm rests, place feet under the chair, and then push out of the chair into an erect posture. Similar difficulties may be encountered when sitting down, squatting, kneeling, turning in bed, and walking. Lakke (33) suggests that since the patient can readily perform these activities under certain circumstances, such as when emotionally stressed, the intrinsic program is not disturbed, and, therefore, these axial motor abnormalities are a result of apraxia. Thus, the PD patient has an ability to "call up" the axial motor program on command.
The inability to combine motor programs into complex sequences seems to be a fundamental motor deficit in PD. The study of reaction time and velocity of movement provides some insight into the mechanisms of the motor deficits at an elementary level. Evarts et al. (39) showed that both reaction and movement times are independently impaired in PD. In patients with asymmetrical findings, reaction time is slower on the more affected side (40). Reaction time is influenced not only by the degree of motor impairment but also by the interaction between cognitive processing and motor response. This is particularly evident when choice reaction time is used and compared to simple reaction time (22). Bradykinetic patients with PD have more specific impairment in choice reaction time, which involves a stimulus categorization and a response selection, and reflects disturbance at more complex levels of cognitive processing (41). Reduced dopaminergic function has been hypothesized to disrupt normal motor cortex activity leading to bradykinesia. While recording from single cortical neurons in free-moving rats, a decrease in firing rate correlated with haloperidol-induced bradykinesia, demonstrating that reduced dopamine action impairs the ability to generate movement and causes bradykinesia (42). Bereitschaftspotential, a premovement potential, has been found to be abnormal in PD patients and to normalize with levodopa (43). The movement time, particularly when measured for proximal muscles, is less variable than the reaction time and more consistent with the clinical assessment of bradykinesia. Both movement and reaction times are better indicators of bradykinesia than the speed of rapid alternating movements. Ward et al. (44) attempted to correlate the median movement and reaction times with tremor, rigidity, and manual dexterity in 10 patients. The only positive correlations were found between movement time and rigidity and between reaction time and manual dexterity. Of the various objective assessments of bradykinesia, movement time correlated best with the total clinical score, but it was not as sensitive an indicator of the overall motor deficit as the clinical rating. Ward et al. (44) concluded that although movement time was a useful measurement, it alone did not justify the use of elaborate and expensive technology. The clinical rating scale probably more accurately reflects the patient's disability, because it includes more relevant observations.
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