The pathophysiology of NPH continues to provoke debate. Although guidelines and best-practice recommendations are well established, there remains a lack of consensus about the role of individual imaging modalities in characterizing specific features of the condition and predicting the success of CSF shunting. Variability of clinical presentation and imperfect responsiveness to shunting are obstacles to the application of novel imaging techniques. Few studies have sought to interpret imaging findings in the context of theories of NPH pathogenesis. In this paper, the authors discuss the major streams of thought for the evolution of NPH and the relevance of key imaging studies contributing to the understanding of the pathophysiology of this complex condition.
Keywords: CBF = cerebral blood flow; DESH = disproportionately enlarged subarachnoid-space hydrocephalus; DTI; DTI = diffusion tensor imaging; ICP = intracranial pressure; NPH; NPH = normal pressure hydrocephalus; PET = positron emission tomography; REM = rapid eye movement; ROI = region of interest; Rcsf = resistance to CSF outflow; SINPHONI = Study of Idiopathic Normal Pressure Hydrocephalus on Neurological Improvement; SPECT = single photon emission computed tomography; VP = ventriculoperitoneal; [11C]PiB = carbon 11 labeled Pittsburgh Compound B; iNPH = idiopathic NPH; imaging; rCBV = regional cerebral blood volume; theories.