Simulating Low-pressure Hydrocephalus as a Disorder of Intracranial Pulse Redistribution From Low Intracranial Elastance Using an Electric Circuit Model
Racheed Mani1, Nahid Shirdel Abdolmaleki4, Anand Ravishankar4, Liu Yang5, Yicun Wang2, Chiemeka Uwakwe3, Petar Djuric4, Michael Egnor3
1Department of Neurology, 2Department of Radiology, 3Department of Neurological Surgery, Stony Brook University Hospital, 4Department of Electrical and Computer Engineering, Stony Brook University, 5Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University
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.
Disclaimer: Abstracts were not reviewed by Neurology® and do not reflect the views of Neurology® editors or staff.