Is there a rationale for these? I’d a thought reflexes were more likely to be retarded by neural damage.
Different reflexes mean damage in different parts of the nervous system. That’s why how the patient responds to tests tells a neuro where lesions are. If you google “neurological clinical examination” or something like that, you’ll be able to find out loads about it.
Thanks karen, I think I get it; that there are normal inhibitory processes that serve to block/dampen neuronal signalling, which can be affected by lesions in particular areas (UMN or pyramidal tract), resulting in a ‘hyperactive’ reflex response, whereas lesions elsewhere can have the opposite effect (anterior horn, LMN, nerve or motor end plate). Does that sound right?
Sounds good to me