A generalized slowness of movement is arguably the defining feature of PD and other parkinsonian disorders, and this phenomenon has been termed bradykinesia. Bradykinesia is often used interchangeably with two other terms, akinesia (absence of movement) and hypokinesia (poverty of movement), and is a major cause of disability in PD. It is eventually seen in all patients and is a requirement for diagnosis of PD in many published diagnostic criteria.5-7 Patients often have a difficult time describing symptoms of bradykinesia, instead using "weakness," "incoordination," and even "fatigue" or "tiredness" to describe the difficulty and extreme effort of initiating movement. In general, patients first notice a delay in the initiation of voluntary movement, with difficulty multitasking or executing sequential actions. Family members will first notice a decrease of spontaneous associated movements, such as loss of gestures during conversation, decreased eye blinking or facial masking, which may cause family to think that the patient is unhappy, angry, or not paying attention. The voice may become softer (hypophonia), with the patient frequently needing to repeat sentences. Swallowing may also be impaired but is only rarely a source of major disability in early stage disease. Parkinsonian dysphagia is due to bradykinesia of the pharyngeal musculature, which can lead to pooling of saliva in the mouth and drooling (sialorrhea),13 even though the amount of saliva produced in PD is normal.
Bradykinesia usually starts distally in the limbs, with decreased dexterity of fingers and hand. One side is often more affected than the other, and this pattern does not change throughout the course of the disease.14 Patients often complain of difficulty buttoning buttons, tying shoelaces, double clicking a computer mouse, or typing. Handwriting is usually small (micrographia) and cramped. Complaints of difficulty lifting the legs when walking, shuffling steps, and easy fatigability are common and plaintively expressed. Patients or family members observe that one or both arms become involuntarily flexed when walking or that the arms hang by their side without swinging. A sensation of unsteadiness without falling is common in some cases as the disease progresses and, in advanced stages, patients have difficulty standing up from a chair, getting out of a car, or maintaining upright posture without leaning or falling.
Freezing is a phenomenon that is poorly understood and contributes to the gait difficulty seen in PD, but it can also be considered a manifestation of bradykinesia. It generally does not occur until the advanced stages of PD and may be seen as patients begin walking after standing up from a chair or bed (start hesitation), when open space is narrowed or constricted (e.g., approaching a doorway or in a crowd of people), or just before reaching a targeted destination (chair or bed).
In addition to careful clinical observation of the signs described above, bedside examination of bradykinesia includes evaluation of speed, amplitude, and rhythm of sequential movements on each side of the body through finger taps, opening and closing fists, pronation-supination of the hands, and heel or toe tapping. In early disease, these tasks usually show mild slowing and decreased amplitude the longer the movements are performed. As the disease progresses, these movements become less coordinated, with frequent hesitation or arrests. Fortunately, bradykinesia responds well to dopaminergic medications and deep brain stimulation (DBS) surgery. Stimulation of both the globus pallidus pars interna (GPi) and subthalamic nucleus (STN) seem to be equally effective for bradykinesia.1516
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