Rick, there's more going on than inhibiting movement. Part of bradykinesia is the inability to do two things at once well.

For example, I can draw, or write in print, with my right hand (though after too much repetition, my hand cramps up). BUT if I simple squeeze my left hand into a fist, I have great difficulty using my right hand immediately. I can't do both at once.

It seems to be partly a control and feedback problem. And a problem handling internally prompted movements.

There's a great review article about bradykinesia that is worth reading:

Pathophysiology of bradykinesia in Parkinson's disease

http://brain.oxfordjournals.org/cgi/...ll/124/11/2131

From the article:

Simultaneous, sequential or repetitive movements

Simultaneous, sequential or repetitive movements
If any additional complexity is added to a simple movement, either by repeating the movement or by combining it with other tasks, bradykinesia becomes more prominent.

Clinical tests of bradykinesia often make use of this phenomenon. Repetitive sequential movement involving isolated finger movements, hand opening/closing or wrist pronation/supination become smaller (hypokinesia) and slower with repetition of the movement (`fatigue') (Agostino et al., 1998Go).

Schwab and colleagues asked patients to squeeze a sphygmomanometer bulb in one hand and outline a drawing with the other (Schwab et al., 1954Go). They had much more difficulty if they had to do both tasks together than if each one was performed alone. Indeed, in most cases, patients tended to alternate between the tasks rather than perform them at the same time.

Experimental studies have analysed these features of bradykinesia in some detail. In essence, they show that bradykinesia is more than the slowness seen in simple single movements. There are additional problems in combining or sustaining complex movements. Benecke and colleagues examined rapid elbow flexion movements combined with a simultaneous or sequential hand movement performed with either the same or the opposite arm (Benecke et al., 1986Go, 1987Go).

In contrast to normal subjects, in whom there was no decrement of performance when two tasks were combined, patients with Parkinson's disease showed (i) a marked slowing of movement over and above that seen in each task alone when both had to be performed together, and (ii) a longer pause between each element of a sequential task.

Indeed, these two extra deficits correlated better with clinical measures of bradykinesia than the slowness in each simple movement........

Conclusion


The term `bradykinesia' is often used to cover a range of related problems in the control of movement. However, in all cases the principal deficit is that movements are slow. The data reviewed here suggest that, although secondary factors such as muscle weakness, tremor and rigidity may contribute, the principal deficit is due to insufficient recruitment of muscle force during the initiation of movement.

The result is that patients' movements undershoot their targets and end by approaching it in several smaller steps.

The two distinguishing features of parkinsonian bradykinesia are (i) that patients underscale muscle force and (ii) that the deficit is often ameliorated when external cues (vision, sound) are given to guide the movement.

The former has led to the suggestion that bradykinesia is a problem of scaling motor output appropriately to the task rather than to any intrinsic limitation in motor execution.

The latter is usually interpreted in terms of the preferential access of basal ganglia motor output to medial rather than lateral motor cortical areas. Medial cortical areas are more active in association with internally generated movements, whilst lateral areas are more active during externally cued movement.

In summary, bradykinesia seems to result primarily from the underscaling of movement commands in internally generated movements.

This may well reflect the role of the basal ganglia in selecting and reinforcing appropriate patterns of cortical activity during movement preparation and performance.

Recent imaging and EEG studies have shown that other regions of the CNS can adapt to the primary basal ganglia deficit of Parkinson's disease.

Thus, the clinical presentation of bradykinesia may be a mixture of the primary deficit and compensatory processes.

We raise the possibility that some aspects of bradykinesia, such as the long intervals between successive elements of a sequence, difficulty in doing two things at the same time and the progressive slowing of long sequences of movement, are the result of this interaction.

This line of argument can be followed further. One of the new understandings of basal ganglia pathophysiology is that disease may make the basal ganglia output noisy. Surgical interventions may work in part by removing or reducing this noise.

The implication is that surgery improves function both by normalizing basal ganglia output and by allowing other structures to compensate better for the underlying deficit