Just like solving a complex puzzle, scientists are tirelessly working to unravel the secrets of idiopathic normal pressure hydrocephalus (iNPH). This baffling disorder, which leads to dementia, remains enigmatic. Recent research has revealed that multiple systems within the brain are involved in the development of iNPH, but a definitive cause has yet to be pinpointed. By delving into the intricacies of cerebrovasculature, including the formation of hydrocephalus, disruptions in cerebral blood flow, breakdown of the blood-brain barrier, and dysfunction in the glymphatic pathway, researchers have gained valuable insights into the iNPH phenotype. These insights not only shed light on the inner workings of this condition but also provide useful information for predicting treatment outcomes with cerebrospinal fluid diversion. While there is still much to learn, scientists are optimistic about uncovering more about how iNPH arises and progressing towards effective interventions.

The pathophysiologic mechanisms underpinning idiopathic normal pressure hydrocephalus (iNPH), a clinically diagnosed dementia-causing disorder, continue to be explored. An increasing body of evidence implicates multiple systems in the pathogenesis of this condition, though a unifying causative etiology remains elusive. Increased knowledge of the aberrations involved has shed light on the iNPH phenotype and has helped to guide prognostication for treatment with cerebrospinal fluid diversion. In this review, we highlight the central role of the cerebrovasculature in pathogenesis, from hydrocephalus formation to cerebral blood flow derangements, blood-brain barrier breakdown, and glymphatic pathway dysfunction. We offer potential avenues for increasing our understanding of how this disease occurs.

Read Full Article (External Site)