Hi Jeremy

Thanks very much for the references. I have had a quick look at the Stolze et al 2001 article and this looks really interesting. I probably need to digest it a bit more. Could you give me the full reference for the Kuba, et al. 2002 study?

I understand this to mean that perhaps the problem is not in the BG itself (as in PD) which could influence the SMA, but rather in the SMA itself or some other area of the frontal lobe or its pathways.
This is a very interesting idea. It is feasible isn’t it. Given the wider damage inflicted on the brain with NH than with PD it seems likely the cortex takes a direct assault – the fact that these patients often have dementia to go with it suggests a cortical involvement.

As I said I probably need to read the paper in more detail but it did get me thinking:

1. Maybe the SMA hypothesis is a bit overstated. Would it not be more likely that there is both the SMA (other cortical areas) and the Basal ganglia damage? The nature of the pathophysiology and clinical features (eg concurrent dementia) reflects this. When you look at those CTs or Wikipedia reference-linkMRIs of NH with those grossly dilated ventricles it is hard not to see how the BG adjacent to the ventricles would not be majorly disrupted.

2. In the study the authors admitted the NH patients were more severe the NH patients were also on average 10 years older than the PD patients.The NH patients did actually increase step length but it wasn’t translated into increased velocity

3. Based on these points it could be the poorer responsiveness of the NH patients to cues could be just due to more advanced disease and age rather primarily a circuitry issue. In PD the cueing approach also only works within a “window of opportunity” and becomes less effective as the disease becomes more severe and age could also be a factor.

4. The time between doing the CSF cueing intervention was only 24 hours. This isn’t much time for the CNS to recover. Wouldn’t it be better to see the participants later down the track after tapping when there has been time for more recovery, beneficial neuroplastic changes etc. Perhaps this isn’t feasible due to the temporary nature of the procedure and in a clinical trial you would need look at patients who have undergone shunting.

I suppose until we have a some decent RCTs of gait cueing in NH we won’t really know if cueing is helpful or not. However I do agree that this casts a bit of a shadow on using cueing.

Yes do keep me posted. I do find it interesting.

Geoff