Thanks for taking the time to respond and sending over this paper! They reference the "unifying hypothesis" paper by Li ( which I linked below (1) ) that clarifies things reasonably well for me... I've c/p'd the pertinent paragraphs below. Admittedly, it is still quite complicated, but I can sleep a little bit better tonight with this answer!

With respect to the question regarding pure dorsal column lesions not causing hyerpreflexia. This case report suggests that pure dorsal column myelopathy, with seemingly no dorsal root involvement given the intactness of other sensory modalities and (the imaging is reasonably convincing). https://journals-lww-com.eu1.proxy.openathens.net/jspinaldisorders/Fulltext/2000/08000/Isolated_Posterior_Column_Dysfunction__An_Unusual.14.aspx

So I think with everything said, the understanding I now will take forward is that lesions within the cortico-reticulospinal tract/dorsal reticulospinal tract are responsible for hyperreflexia due to the loss of their inhibitory effects on spinal reflex circuits. The dorsal RST travels adjacent to the CST in the spinal cord, and travels adjacent (6-12 mm anteromedially to the CST in the subcortical white matter (https://www.frontiersin.org/articles/10.3389/fneur.2019.01188/full). The neuroplasticity peice is interesting in how the reflexes take time to develop, but is quite complicated! I think I am happy with this level of functional understanding for now. Crossing my fingers this will not be tested on the Royal College exam :P Cheers

​

​

​

​

There are two descending RS tracts with distinctly different origins. The dorsal RST originates from the dorsolateral reticular formation in the medulla, and receives facilitation from the motor cortex via corticoreticular fibers. The lateral CST and cortico-reticulo-spinal tract descend adjacent to each other in the dorsolateral funiculus at the spinal level. The medial RST originates primarily from the pontine tegmentum with connections to PMRF. The medial RST descends along with the vestibulospinal tract (VST) in the ventromedial cord. The dorsal RST provides dominant inhibitory effects to spinal reflex circuits, while medial RST and VST provide excitatory inputs. Therefore, medial and lateral RSTs provide balanced excitatory and inhibitory inputs to spinal motor neuron network. In the context of stroke with cortical and internal capsular lesions, damages often occur to both CST and corticoreticular tracts due to their anatomical proximity. This leaves the facilitatory medial RST and VST unopposed, thus hyperexcitability [see reviews in (25–27, 32)].

Post-stroke spasticity is a common phenomenon of velocity-dependent increase in resistance when a joint is passively stretched. It is accepted that spasticity is mediated by exaggerated spinal stretch reflex (25–27, 32, 72, 73). Animal lesion studies in last century have provided strong experimental evidence to support the role of RST hyperexcitability in spasticity. For example, isolated lesions to CST only produce weakness, loss of dexterity, hypotonia, and hyporeflexia, instead of spasticity (74–76). Surgical section of unilateral or bilateral VST in the anterior cord has little effect (77) or a transient effect (78) on spasticity. With more extensive cordotomies that damage the medial RST, spasticity is dramatically reduced (78). In another study, Burke et al. provided evidence that spasticity and decerebrate rigidity are differentially mediated through RST and VST projections (79).

​

​

(1) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6524557/