Abstract Details

Title Simulating Low-pressure Hydrocephalus as a Disorder of Intracranial Pulse Redistribution From Low Intracranial Elastance Using an Electric Circuit Model

Topic Neuro Trauma and Critical Care

Presentation(s) P6 - Poster Session 6 (5:00 PM-6:00 PM)

Poster/Presentation
Number 19-002

Objective We simulate the pathophysiology of low-pressure hydrocephalus (LPH) using an electric circuit model of the cerebral windkessel system.

Background LPH represents a rare syndrome of symptomatic hydrocephalus in a shunted patient with coma, bradycardia, ventriculomegaly, and paradoxically low intracranial pressure (ICP). With many neurologists still unfamiliar with this condition, LPH is characterized by low brain turgor, and its treatment includes prolonged ventricular drainage with siphoning and jugular vein compression. Physiologically, the cranium consists of a cerebral windkessel mechanism, which serves as a band-stop filter to dampen the arterial blood pressure (ABP) pulse in the cranium, transmitting this pulse from arteries to veins via the cerebrospinal fluid (CSF) path, bypassing the microvasculature to render capillary flow smooth. We propose that LPH reflects cerebral windkessel impairment due to low brain elastance, which increases the impedance to pulsatility in the CSF path.

Design/Methods We simulated LPH using a current divider model of the cerebral windkessel system with circuit values derived from published flow magnetic resonance imaging (MRI) of normal and hydrocephalic patients. We lowered direct current (DC) to reflect lowered cerebral blood flow (CBF), reduced the frequency from the alternating current (AC) source to simulate bradycardia, and lowered circuit resistance to simulate ventricular dilatation. To simulate treatment, we lowered circuit resistance even further to simulate siphoning and increased elastance to simulate jugular venous compression via neck wrapping.

Results Our electric circuit model successfully simulated both the pertinent characteristics of LPH and its positive response to siphoning and neck wrapping.

Conclusions LPH reflects windkessel impairment due to low brain elastance in the setting of intracranial energy depletion from CSF shunting and is mitigated by siphoning and neck wrapping. Our circuit model elegantly demonstrated the proof-of-concept of LPH as a manifestation of windkessel impairment caused by low intracranial elastance, thus providing a novel understanding of this paradoxical condition.

Authors/Disclosures
Racheed M. Mani, MD PRESENTER	Dr. Mani has nothing to disclose.
Nahid Shirdel Abdolmaleki	Mrs. Shirdel Abdolmaleki has nothing to disclose.
Anand Ravishankar	Mr. Ravishankar has nothing to disclose.
Liu Yang, PhD	Dr. Yang has nothing to disclose.
Tingchang Wang, PhD	Mr. Wang has nothing to disclose.
Chiemeka D. Uwakwe, MS	Mr. Uwakwe has nothing to disclose.
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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