A Novel Paradigm of Normal Pressure Hydrocephalus (NPH) as a Disorder of Intracranial Thermodynamics
Racheed Mani1, Liu Yang3, Jade Basem4, Susan Fiore2, Petar Djuric3, Michael Egnor2
1Department of Neurology, 2Department of Neurological Surgery, Stony Brook University Hospital, 3Department of Electrical and Computer Engineering, Stony Brook University, 4Renaissance School of Medicine at Stony Brook University
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:
π=πΌπΎ/π
(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.
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