Neurogenic Orthostatic Hypotension (NOH) Following Brainstem Infarction: An Underrecognized Consequence of Central Baroreflex Failure

Neurogenic orthostatic hypotension (NOH) is a well-documented consequence of peripheral autonomic dysfunction in conditions such as Parkinson’s disease, multiple system atrophy, and diabetic neuropathy. However, NOH resulting from acute brainstem infarction through damage to central baroreflex control centers remains significantly underrepresented in clinical literature. This review examines the neuroanatomical substrate of baroreflex control, presents evidence for brainstem stroke as a cause of severe NOH through baroreflex failure, and highlights the therapeutic challenges unique to this etiology. The nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM) serve as critical integration centers for blood pressure regulation. Infarction affecting these structures results in catastrophic loss of baroreflex function, manifesting as severe orthostatic hypotension with potentially life-threatening consequences. Recognition of this mechanism is essential for appropriate clinical management, as standard NOH therapies may be insufficient in the context of central baroreflex failure. We argue that brainstem infarction should be explicitly recognized as a primary cause of NOH in clinical classification systems and treatment guidelines.