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Zhe Wang, Liu Yang, Petar M. Djurić, and Michael R. Egnor

OBJECTIVE

Pseudotumor cerebri is a disorder of intracranial dynamics characterized by elevated intracranial pressure (ICP) and chronic cerebral venous hypertension without structural abnormalities. A perplexing feature of pseudotumor is the absence of the ventriculomegaly found in obstructive hydrocephalus, although both diseases are associated with increased resistance to cerebrospinal fluid (CSF) resorption. Traditionally, the pathophysiology of ventricular dilation and obstructive hydrocephalus has been attributed to the backup of CSF due to impaired absorption, and it is unclear why backup of CSF with resulting ventriculomegaly would not occur in pseudotumor. In this study, the authors used an electrical circuit model to simulate the cerebral windkessel effect and explain the presence of ventriculomegaly in obstructive hydrocephalus but not in pseudotumor cerebri.

METHODS

The cerebral windkessel is a band-stop filter that dampens the arterial blood pressure pulse in the cranium. The authors used a tank circuit with parallel inductance and capacitance to model the windkessel. The authors distinguished the smooth flow of blood and CSF and the pulsatile flow of blood and CSF by using direct current (DC) and alternating current (AC) sources, respectively. The authors measured the dampening notch from ABP to ICP as the band-stop filter of the windkessel.

RESULTS

In obstructive hydrocephalus, loss of CSF pathway volume impaired the flow of AC power in the cranium and caused windkessel impairment, to which ventriculomegaly is an adaptation. In pseudotumor, venous hypertension affected DC power flow in the capillaries but did not affect AC power or the windkessel, therefore obviating the need for adaptive ventriculomegaly.

CONCLUSIONS

In pseudotumor, the CSF spaces are unaffected and the windkessel remains effective. Therefore, ventricles remain normal in size. In hydrocephalus, the windkessel, which depends on the flow of AC power in patent CSF spaces, is impaired, and the ventricles dilate as an adaptive process to restore CSF pathway volume. The windkessel model explains both ventriculomegaly in obstructive hydrocephalus and the lack of ventriculomegaly in pseudotumor. This model provides a novel understanding of the pathophysiology of disorders of CSF dynamics and has significant implications in clinical management.

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Grant A. Bateman

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Mark E. Wagshul, John J. Chen, Michael R. Egnor, Erin J. McCormack, and Patricia E. Roche

Object

A recently developed model of communicating hydrocephalus suggests that ventricular dilation may be related to the redistribution of pulsations in the cranium from the subarachnoid spaces (SASs) into the ventricles. Based on this model, the authors have developed a method for analyzing flow pulsatility in the brain by using the ratio of aqueductal to cervical subarachnoid stroke volume and the phase of cerebrospinal fluid (CSF) flow, which is obtained at multiple locations throughout the cranium, relative to the phase of arterial flow.

Methods

Flow data were collected in a group of 15 healthy volunteers by using a series of images acquired with cardiac-gated, phase-contrast magnetic resonance imaging.

The stroke volume ratio was 5.1 ± 1.8% (mean ± standard deviation). The phase lag in the aqueduct was −52.5 ± 16.5° and the phase lag in the prepontine cistern was −22.1 ± 8.2°. The flow phase at the level of C-2 was +5.1 ± 10.5°, which was consistent with flow synchronous with the arterial pulse. The subarachnoid phase lag ventral to the pons was shown to decrease progressively to zero at the craniocervical junction. Flow in the posterior cervical SAS preceded the anterior space flow.

Conclusions

Under normal conditions, pulsatile ventricular CSF flow is a small fraction of the net pulsatile CSF flow in the cranium. A thorough review of the literature supports the view that modified intracranial compliance can lead to redistribution of pulsations and increased intraventricular pulsations. The phase of CSF flow may also reflect the local and global compliance of the brain.

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Rui Zou, Eun-Hyoung Park, Erin McCormack Kelly, Michael Egnor, Mark E. Wagshul, and Joseph R. Madsen

Object

The relationship between the waveform of intracranial pressure (ICP) and arterial blood pressure can be quantitatively characterized using a newly developed technique in systems analysis, the time-varying transfer function. This technique considers the arterial blood pressure as an input signal composed of multiple frequencies represented in the output ICP according to the transfer function imposed by the intracranial system on the input signal. The transfer function can change with time and with physiological manipulations. The authors examined data obtained from canine experiments involving manipulations of ICP.

Methods

The authors analyzed 11 experiments from 3 normal mongrel dogs under conditions of normal ICP and with changes in ICP made by bolus injection, infusion, or withdrawal of cerebrospinal fluid by using time-varying transfer function.

Results

During normal ICP periods, the gain of the transfer function displayed a deep notch (≥ 1 log unit) centered at or near the cardiac frequency. In systems terms, the intracranial compartment under normal conditions appears to act as a notch filter attenuating the cardiac frequency input relative to other frequencies. Epochs of ICP elevation showed suppression of the notch, and the notch was restored when ICP returned to normal.

Conclusions

The intracranial system in these animals could be considered to include a pulsation absorber for which the target frequency appears to be close to the cardiac frequency. One possible source for such an absorber mechanism might be the free movement of cerebrospinal fluid, implying that impairment of this motion may have important clinical implications in various neurological conditions such as hydrocephalus.

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Mark E. Wagshul, Erin J. Kelly, Hui Jing Yu, Barbara Garlick, Tom Zimmerman, and Michael R. Egnor

Object

The intracranial pulse pressure is often increased when neuropathology is present, particularly in cases of increased intracranial pressure (ICP) such as occurs in hydrocephalus. This pulse pressure is assumed to originate from arterial blood pressure oscillations entering the cranium; the fact that there is a coupling between the arterial blood pressure and the ICP is undisputed. In this study, the nature of this coupling and how it changes under conditions of increased ICP are investigated.

Methods

In 12 normal dogs, intracarotid and parenchymal pulse pressure were measured and their coupling was characterized using amplitude and phase transfer function analysis. Mean intracranial ICP was manipulated via infusions of isotonic saline into the spinal subarachnoid space, and changes in transfer function were monitored.

Results

Under normal conditions, the ICP wave led the arterial wave, and there was a minimum in the pulse pressure amplitude near the frequency of the heart rate. Under conditions of decreased intracranial compliance, the ICP wave began to lag behind the arterial wave and increased significantly in amplitude. Most interestingly, in many animals the pulse pressure exhibited a minimum in amplitude at a mean pressure that coincided with the transition from a leading to lagging ICP wave.

Conclusions

This transfer function behavior is characteristic of a resonant notch system. This may represent a component of the intracranial Windkessel mechanism, which protects the microvasculature from arterial pulsatility. The impairment of this resonant notch system may play a role in the altered pulse pressure in conditions such as hydrocephalus and traumatic brain swelling. New models of intracranial dynamics are needed for understanding the frequency-sensitive behavior elucidated in these studies and could open a path for development of new therapies that are geared toward addressing the pulsation dysfunction in pathological conditions, such as hydrocephalus and traumatic brain injury, affecting ICP and flow dynamics.

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Marvin Bergsneider, Michael R. Egnor, Miles Johnston, Dory Kranz, Joseph R. Madsen, James P. Mcallister II, Curt Stewart, Marion L. Walker, and Michael A. Williams

✓In an effort to identify critical gaps in the prevailing knowledge of hydrocephalus, the authors formulated 10 key questions. 1) How do we define hydrocephalus? 2) How is cerebrosinal fluid (CSF) absorbed normally and what are the causes of CSF malabsorption in hydrocephalus? 3) Why do the ventricles dilate in communicating hydrocephalus? 4) What happens to the structure and function of the brain when it is compressed and stretched by the expanding ventricles? 5) What is the role of cerebrovenous pressure in hydrocephalus? 6) What causes normal-pressure hydrocephalus? 7) What causes low-pressure hydrocephalus? 8) What is the pathophysiology of slit ventricle syndrome? 9) What is the pathophysiological basis for neurological impairment in hydrocephalus, and to what extent is it reversible? 10) How is the brain of a child with hydrocephalus different from that of a young or elderly adult? Rigorous answers to these questions should lead to more effective and reliable treatments for this disorder.