Introduction

Normal pressure hydrocephalus (NPH) is characterized by pathological intracranial accumulation of cerebrospinal fluid (CSF) in the brain, resulting in enlarged ventricles. It is a chronically progressive condition that primarily affects the elderly, leading to gait disturbance and ultimately immobility, dementia, and urinary incontinence (Adams et al., 1965; Vanneste, 2000). Population-based prevalence rates have been estimated to range from 0.2/100.000 in subjects aged 70-79 years, to 5.9/100.000 in those aged over 80 years (Jaraj et al., 2014). However, recent studies have reported significantly higher prevalence rates (Thavarajasingam et al., 2024), and a systematic survey suggests NPH prevalence to be even higher than generally assumed (Brean and Eide, 2008). This indicates that patients may often remain undiagnosed. Considering the demographic changes, with elderly subjects (>65 years) being the world wide fastest-growing age group expected to even outnumber people aged 15-24 years by 2050 (Chang et al., 2025), the prevalence of NPH is expected to increase dramatically in the coming decades, placing a greater burden on caregivers, and putting additional socioeconomic strain on health care systems. Therefore, improving the understanding of the pathophysiology of this condition and enhancing treatment outcomes for NPH patients is highly relevant.

Although the efficacy of CSF-diversion procedures has been demonstrated in numerous NPH patients (Pearce et al., 2024), shunt failure remains a prevalent occurrence (Williams et al., 1998), and disease progression continues unabated despite treatment. Unlike secondary NPH, which is caused by preceding or underlying pathologies such as hemorrhage or inflammatory conditions that alter CSF reabsorption and/or CSF flow-dynamics, the etiology of idiopathic NPH remains unclear. However, multiple factors have been suggested to alter CSF equilibrium (Das and Biagioni, 2025): These include an increase in CSF pulse pressure during blood pressure systole due to reduced CSF outflow and/or reabsorption, loss of the Windkessel effect in skull base arteries due to arterial hypertension, altered transependymal flow, and changes within the glymphatic system (Bubenikova et al., 2025). Decreases in CSF-efflux via the lymphatic system (Back et al., 2025) have also been reported as pathophysiological contributing factors. Furthermore, increasing evidence suggests, that the spinal compartment may be more relevant to NPH pathophysiology than is commonly acknowledged: Traditionally, it has been believed that CSF-reabsorption mainly occurs at the arachnoid villi as the interface between the subarachnoid and the venous space, mediating CSF-reabsorption along the pressure gradient between the two compartments (Bradley, 2015). However, it is also important to consider the role of CSF reabsorption and flow within the intraspinal compartment for maintaining intracranial CSF homeostasis (Maillot, 1991). In particular, the spinal compartment seems to be crucial for intracranial volume-pressure compensation, a process known as craniospinal compliance. Recent in vitro simulation studies provided evidence that intracranial CSF flow-dynamics and dynamic craniospinal compliance are altered by narrowing of the spinal canal (Benninghaus et al., 2026).

We therefore hypothesized that degenerative spine disease, which induces rigidity and narrowing of the spinal canal, may influence NPH by decreasing CSF reabsorption and altering CSF flow dynamics. However, there is a lack of patient data in support of this hypothesis. As a first exploratory step, we conducted a retrospective analysis of potential associations between cervical and lumbar spinal canal stenosis and NPH imaging characteristics in patients admitted for shunt surgery.