Normal Pressure Hydrocephalus: A Syndrome, Not a Disease.
Neill Graff-Radford1, Gregory Day1, Philip Tipton1, Olga Fermo1, Christian Lachner1, Sanjeet Grewal1, Kaisorn Chaichana1, Lauren Haydu1, Yoav Piura1
1Mayo Clinic Jacksonville
Objective:

Assess the frequency of congenital, genetic, vascular, impaired CSF absorption and degenerative contributors in patients with clinical diagnoses of normal pressure hydrocephalus (NPH).

Background:

Recent research suggests that multiple factors contribute to the NPH phenotype. However, we do not know how frequently these factors occur and overlap.

Design/Methods:

Clinical data, genetic variants, neuroimaging, and blood/CSF-biomarkers of Alzheimer disease (AD) were systematically measured in patients with NPH diagnosed at our tertiary care center (03-2020 to 07-2024). Brain MRIs were independently reviewed by two neurologists for presence/absence of disproportionately enlarged subarachnoid space hydrocephalus (DESH) and white matter hyperintensities (Fazekas score).

Results:

Sixty-five patients were diagnosed with NPH (mean age 71.3±8.7 years; 45% females). Average head circumference was 57.3±2.1 cm. Head circumference was >98th percentile of expected in 20/58 (35%) patients, suggesting a congenital contribution. Loss of function mutations in the CWH43 gene were detected in 5/43 (12%) patients. Neuroimaging revealed DESH in 45/65 (69%) patients, indicating impaired CSF absorption above the Sylvian fissures; moderate-to-severe white matter disease (Fazekas score of 2-3) in 30/65 (45%) patients; and both in 27/65 (41%) patients (p<0.001). Plasma pTau217 levels were increased (>0.185 pg/mL) in 19/61 (31%) patients, suggesting concurrent AD neuropathologic change. Plasma pTau217 levels were inversely associated with performance on bedside tests of cognition (Spearman Rho = -0.56; p=<0.001), supporting a contribution of concurrent AD to cognitive impairment in NPH.  Multiple factors (i.e., large head circumference, CWH43 mutations, DESH, white matter disease, AD pathology) were present in 62% of participants, with a median of 2 (range 0-4) factors per patient.

Conclusions:

Clinical, genetic, neuroimaging, and biomarker data suggest multiple factors contribute to NPH. The myriad potential contributors suggest that NPH is a syndrome. These findings emphasize the value of comprehensive assessments across multiple domains when evaluating suspected NPH patients and suggest potential benefits of multifaceted management approaches.

 

 

 

 

10.1212/WNL.0000000000210771
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