Abstract Details

Title A Novel Paradigm of Normal Pressure Hydrocephalus (NPH) as a Disorder of Intracranial Thermodynamics

Topic Movement Disorders

Presentation(s) P1 - Poster Session 1 (11:45 AM-12:45 PM)

Poster/Presentation
Number 5-032

Objective We seek to simulate NPH as a disorder of intracranial thermodynamics using an electrical tank circuit.

Background

The cranium encases pulsatile and smooth energy flow through the cerebrovasculature and cerebrospinal fluid (CSF). The cerebral windkessel mechanism separates this pulsatile and smooth flow, using the CSF path as a hydraulic link to protect intracranial capillaries from this pulsatility while maintaining perfusion. This is reflected in the windkessel effectiveness (W) equation:

??=????/?? (I represents CSF path inertance (pulse magnitude), K is CSF path elastance, and R is resistance in the CSF path.)

In NPH, we posit that the windkessel is impaired via a blunted CSF pulse in the subarachnoid space (SAS) secondary to arteriosclerosis (lowering I) and reduced SAS CSF path elastance secondary to age-related, brain tissue softening (lowering K). Ventriculomegaly and shunting may improve windkessel effectiveness by reducing resistance (R) in the CSF path.

Design/Methods We utilize a tank circuit with parallel inductance and capacitance to simulate pulsatile flow of blood and CSF as alternating current (AC) and smooth flow as direct current (DC). We model NPH by decreasing windkessel inertance (I) and intracranial elastance (K) each two-fold. We simulate ventriculomegaly and shunting by lowering R of this circuit two- and four-fold, respectively.

Results In simulating NPH, we noted significant elevations in the amplitude and power of AC in the CSF and capillary paths with decreased inertance and elastance. This pulse power decreased with reduced CSF path resistance.

Conclusions Simulations of NPH demonstrated increased pulse redistribution to the CSF and capillary paths. We posit that this pulsatile stress is diverted to the periventricular leg and bladder fibers, which may explain NPH symptomatology. Ventricular dilation lowers CSF path resistance and may be an adaptive response to windkessel impairment. Shunting provides a low resistance conduit to drain AC power in the CSF path to restore windkessel effectiveness.

Authors/Disclosures
Racheed M. Mani, MD PRESENTER	Dr. Mani has nothing to disclose.
Liu Yang, PhD	Dr. Yang has nothing to disclose.
Jade Basem, BA	Ms. Basem has nothing to disclose.
Susan M. Fiore (Stony Brook University Medical Center)	No disclosure on file
Petar M. Djuric, PhD	The institution of Prof. Djuric has received research support from NSF.
Michael Egnor, MD	Dr. Egnor has nothing to disclose.

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