These days the process and passage of laminitis is extremely well understood .
Elevated levels of catecholamines (adrenaline and noradrenaline ) which are released into the circulatory system in response to stress , diseases and other altered physiological states , result in the opening of arteriovenous (AV) bypasses or shunts at the hoof level thence depriving the laminar microvasculature of oxygen. Tissue changes resulting from oxygen deprivation lead to inflammation of these laminar .The severity and longevity of these vascular changes will ultimately determine the extent of permanent tissue damage.
These processes are being continually researched and a more detailed microscopic and pharmacological appreciation of these processes is being gained daily.
However the factor which has not been well understood is why certain individuals within a population seem more susceptible and also why individual digits (hooves) within an individual appear more susceptible to these abnormal increases in catecholamines.
A theory is that in some individuals hooves (extremities) or in an individual extremity the receptors which are normally triggered by catecholamines (neurtransmittors) are already hypersensitised and therefore appear to overreact to elevations in these chemicals causing microvascular shutdown. This phenomena has been demonstrated in humans experiencing symptoms of hand or foot pain. These syndromes are referred to as expressions of neuropathic pain or reflex sympathetic dystrophies.
Anecdotal findings (not scientifically validated) with clinical assessments of alterations in the progress of cases of laminitis following cervical vertebral mobilisation under anaesthetic CVMUA have suggested that this phenomena may also exist in the equine species. Formal clinical studies are required to either validate or refute these theories. Hopefully in time these will be carried out !!