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

(performing sequential finger movements)

Brain, Vol. 123, No. 2, 394-403, February 2000
© 2000 Oxford University Press
Cortical motor reorganization in akinetic patients with Parkinson's disease
A functional MRI study
U. Sabatini1,5, K. Boulanouar1, N. Fabre1,2, F. Martin1, C. Carel1,2, C. Colonnese5, L. Bozzao5, I. Berry1,3, J. L. Montastruc4, F. Chollet1,2 and O. Rascol1,4


Using functional MRI (fMRI), we have studied the changes induced by the performance of a complex sequential motor task in the cortical areas of six akinetic patients with Parkinson's disease and six normal subjects. Compared with the normal subjects, the patients with Parkinson's disease exhibited a relatively decreased fMRI signal in the rostral part of the supplementary motor area (SMA) and in the right dorsolateral prefrontal cortex, as previously shown in PET studies.

Concomitantly, the same patients exhibited a significant bilateral relative increase in fMRI signal in the primary sensorimotor cortex, lateral premotor cortex, inferior parietal cortex, caudal part of the SMA and anterior cingulate cortex.

These fMRI data confirm that the frontal hypoactivation observed in patients with Parkinson's disease is restricted to the rostral part of the SMA and to the dorsolateral prefrontal cortex.

These results also show that, apart from the lateral premotor and parietal cortices, increased fMRI signals can be found in other cortical motor areas of these patients, including the posterior SMA, the anterior cingulate cortex and the primary sensorimotor cortices, which are then likely to participate in the same putative attempt by the dopamine-denervated brain to recruit parallel motor circuits in order to overcome the functional deficit of the striatocortical motor loops.....

Conclusions
The present fMRI neuroimaging study shows that the subcortical putaminal dopamine deficit which characterizes Parkinson's disease disorganizes the cortical motor pathways in a complex way.

It induces a focal `underactivation' restricted to the rostral SMA and DLPC, possibly responsible for the patients' akinesia.

It also induces an abnormal pattern of `overactivation' in most of the other known motor cortical areas, including the caudal SMA, the anterior cingulate cortex, the lateral premotor, the primary sensorimotor and the parietal cortices.

This reorganization, which involves parallel-acting multiple motor areas, can be seen as an attempt at motor recovery. The general aspect of this reorganization resembles what has been described previously with PET in other motor diseases, such as paresis induced by acute stroke (Chollet et al., 1991Go; Weiller, 1995Go; Chollet and Weiller, 1997). It is also interesting to compare the present results with those reported in patients with cerebellar degeneration (Wessel et al., 1995Go). The pattern of motor activation in this last condition appeared to be the opposite to what we observed in Parkinson's disease: several areas of the lateral motor circuit, including the lateral premotor cortex and the lobus parietalis inferior, were less activated in the cerebellar patients than in the normal controls, probably as a result of defective cerebellar inputs, while, in contrast, other premotor systems, including the SMA, were used more heavily in the cerebellar patients than in the controls. It is thus tempting to speculate that these phenomena illustrate the capacity of the adult human brain for functional plasticity in compensating for one motor circuit deficit by recruiting another parallel one. The exact mechanisms of these phenomena remain to be understood.


http://brain.oxfordjournals.org/cgi/...full/123/2/394

Motor task

The activation paradigm consisted of a sequential movement performed with the right hand. This sequential task had been chosen among several others, according to preliminary fMRI data from our laboratory, because it induces a clear activation signal in areas known to be involved in both motor programming and motor execution. To perform this task, the subjects had to (i) make finger-to-thumb opposition movements in the specified order of the index, middle, ring and little finger; (ii) open and clench the fist twice; (iii) complete finger-to-thumb oppositions in the opposite order (i.e. little, ring, middle and index finger); (iv) open and clench the fist twice again; and finally (v) repeat the same series of movements during the 30 s of data acquisition. This was intentionally a more complex and cognitively demanding task than generally used in previously published SPECT and PET studies performed in patients with Parkinson's disease.

As I explain to my wife, when I am off I can walk or I can talk but I can't do both.

In a tight space or crowded room I get an overstimulated sensation very similar to that I get when on and dealing with a traffic crossing as a pedestrian. Multiple input streams leading to freezing.

Interestingly enough, one of the ways they assess the effects of prenatal insults to rats is how they react to being in an alien environment with one of the critical measures being "freezing".

I'm never bored.

Rick, that's a good way to describe it, and it's the reason I avoid traveling on the train during 'rush hour'. When people cross in front of me, or even come up beside me, I get discombobulated real fast! If they're moving too close to me, I freeze. Even on an empty sidewalk, if someone passes me and feels too close, I come to a stop.

I think our compensatory mechanisms work, but in a minimal way, so it's hard to do multiple things using the new circuits. I bet the new circuits can only handle so much, and then they crash, momentarily, when asked to do too much.

...it is pretty silly to say that the problem is a net lack of dopamine making it difficult to initiate movement. For example, when off I can't take a normal step but I can take that step if I exaggerate as though I were walking in mud. It involves the same muscles and similar motions. So, once again, the current model is just too simplistic.