It has been hypothesized that peripheral nerve injury alters the neurochemical features of dorsal root ganglia (DRGs) neurons ('phenotypic change') in both damaged and intact neurons, and results in disordered sensory processing (Zimmermann, 2001; Luo et al., 2002; Obata et al., 2003, 2004a, b; Ji & Strichartz, 2004; Yamanaka et al., 2004).
It can be hypothesized that peripheral vasoconstriction, induced by hyperoxia, may be beneficial in septic and hemorrhagic shock, reducing the need for intravenous volume resuscitation and vasopressor requirements.
Although the mechanism by which Tregs exert their function via these chemokine/chemokine receptors remains elusive, it could be hypothesized that peripheral Tregs and leukocytes (especially anti-inflammatory leukocytes) may be recruited to VAT based on their unique pattern of chemokine-chemokine receptor expression.
It has been hypothesized that a peripheral and/or central sensitization is one of the main reasons for these decreased pain thresholds in migraine patients [3, 13 15].
It is believed that brain and peripheral soluble amyloid-β are in equilibrium and it has previously been hypothesized that a reduction in peripheral amyloid-β can lower brain amyloid-β, thereby reducing formation of plaques predominantly composed of insoluble amyloid-β; the so-called peripheral sink hypothesis.
It also has been hypothesized that the complications of diabetes (peripheral neuropathy, peripheral vascular disease), diabetes treatment (insulin), or both could increase the risk of falls and fractures (14, 26).
It has been hypothesized that the paranodal disruptions in peripheral nerves could be due to heat generation at the node from repetitive action potentials [11].
It can be hypothesized that the combination of peripheral vascular disease (which was significantly more frequent in TA patients) and severe anaemia might be responsible for the higher extent of renal damage after TA TAVI.
It is hypothesized that dendritic cells are activated by unknown stimuli in peripheral tissues, and migrate into the lymph nodes, where they induce T cells to proliferate.
In addition, it can be hypothesized that pain interferes with the motor control both at peripheral and supraspinal level (avoidance reflex).
