(a) High-level (Th1) SCI interrupts neural vegetative innervation of the adrenal glands from the spinal cord via splanchnic and adrenal nerves. (b) Adrenal denervation results in a drop of CA release and in disinhibition of GC release. Increased GCs then suppress ACTH production (primary hypercortisolism). Dysfunctional neuro-endocrine signaling leads to high GC and low NE levels which promote infections via pathways including reduced cardiac output, disturbed lymphocyte trafficking, or increased immune cell apoptosis. (c) The susceptibility to pneumonia was reversed if GC levels remained balanced in adrenotransplanted animals. The figure additionally shows how further pathways of immune dysfunction after SCI interfere with the here presented cascade. For example, vagus nerve-mediated parasympathetic innervation of the cardiovascular system (top) or spleen and liver (bottom) intersect with the sympathetic route. This might be of particular relevance to lesions of the central nervous system, which are located above the originating vagus fibers in the brainstem, such as in stroke.