**3. Pathophysiology**

There are two main mechanisms involved in the pathogenesis of NPH [13, 14], that is, increased venous resistance and altered production and absorption of CSF. Studies

have found that in patients with NPH, there is reduction in vascular compliance particularly involving superior sagittal sinus. Hakim and Adam's hypothesized [4] that in NPH reduced CSF absorption leads to raised intracranial pressure and over a period leading to compensatory ventricular enlargement. This new intracranial pressure state directs more CSF flow toward the Virchow-Robin spaces and thus into the brain parenchyma [15]. These metabolic and mechanical changes further leads to periventricular damage and raised myelin basic protein (a possible biomarker) elevated in these patients [16]. This leads to tissue compression, white matter ischemia and parenchymal changes characterized by myelin pallor. These changes further lead to periventricular damage, reduced cellular metabolism, clearance of toxins, and their sequel [15, 17]. Studies have shown that following CSF diversion, there is normalization in global brain stiffness and elasticity on magnetic resonance studies [18].
