Although the spasticity could be due to the facilitatory supraspinal pathways, it might not be necessarily so. Undergoing unilateral rhizotomy does not mean there are no spinal loops at all, it only means that the dorsal root input to the segmental interneurons is affected, leaving all the other inputs and internal loops intact. When dorsal roots are cut, part of the interneurons loose their excitatory innervation. The result might be a reduction in spinal inhibitory mechanisms.

I would recommend this review on neuronal mechanisms of spasticity:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3009478/pdf/fneur-01-00149.pdf

Hope this will help you. Good luck with your project.

Matija.

Hello Daniel Teodoru 

please check the resources related to your topic .

regards

http://link.springer.com/chapter/10.1007/978-3-642-65942-3_13#page-1

http://www.ncbi.nlm.nih.gov/pubmed/11219613

http://archneur.jamanetwork.com/article.aspx?articleid=566231

https://books.google.co.in/books?id=E4F5AgAAQBAJ&pg=PA187&lpg=PA187&dq=Spasticity+after+dorsal+rhizotomy+in+monkeys?&source=bl&ots=ClYSKRVLq8&sig=_3bp2uRbG2mljV8gqdez2gS2HTM&hl=en&sa=X&ved=0ahUKEwjTu5TMxsjOAhVMPo8KHZB5DIAQ6AEIRzAG#v=onepage&q=Spasticity%20after%20dorsal%20rhizotomy%20in%20monkeys%3F&f=false

You have been most kind and i am very grateful. I am familiar with all those older studies and reviews. My main concern is in explaining the propensity for ventroflextion of the wrist and flexion at the elbow. The former cause the monkeys to put weight on the deaff hand dorsum, severely iinjuring the wrist so that hand can no longer be used, and forearm extention is greatly impeded, discouraging use and maximal recovery. The relief of reflex spasticity with rhizotomy we see clinically but massive deaff as we did in monkeys assures no reflex role and presumes descending tonic effects. Our hoped for studies back in the 70s hoped to look at striatal inhibition resulting from PARTIAL deaff as in DORSAL COLUMN NUCLEI lesion where maipulative skill becomes irretrivable but after bilat C2 to T5 rhizotomy recovers astonishinly. Of course, if cenrtal spasticity impedes recovery

I'm no expert in animal experiments, but more or less fixed postures may correpond rather to dystonia or dystonic hemiparesis, respectively. At least, the pathophysiologic hypothesis suggest a deficit in sensorimotor intergration. The same should hold true for peripherically induced dystonia, as suggested by the mechanism the abnormal posture / pattern is provoked.