Intracranial hypertension

Modeling intracranial pressures in microgravity: the influence of the blood-brain barrier

Authors: Lakin WD, Stevens SA, Penar PL.

INTRODUCTION: A majority of astronauts experience symptoms of headache, vomiting, nausea, lethargy, and gastric discomfort during the first few hours or days after entering a microgravity environment. Due to similarities in symptoms and their time evolution, it has been hypothesized that some of these conflicts are related to the development of benign intracranial hypertension in these individuals in microgravity.

METHODS: This hypothesis was tested using a validated mathematical model that embeds the intracranial system in whole-body physiology. This model was used to predict steady-state intracranial pressures in response to various cardiovascular stimuli associated with microgravity, including changes in arterial pressure, central venous pressure, and blood colloid osmotic pressure. The model also allowed alterations of the blood-brain barrier due to factors such as gravitational unloading and increased exposure to radiation in space to be considered.

RESULTS: Simulations predicted that intracranial pressure will increase significantly if, combined with a drop in blood colloid osmotic pressure, there is a reduction in the integrity of the blood-brain barrier in microgravity.

DISCUSSION: These results suggest that in some otherwise healthy individuals microgravity environments may elevate intracranial pressure to levels associated with benign intracranial hypertension, producing symptoms that can adversely affect crew health and performance.

Can chronic increased intracranial pressure or exposure to repetitive intermittent intracranial pressure elevations raise your risk for Alzheimer’s disease?

Author: Wostyn P

Over a decade ago, I formulated the hypothesis that cumulative effects of exposure to high intracranial pressure (ICP) may contribute to the development of Alzheimer's disease (AD), though not necessarily in an exclusive way. In addition to individual ICP characteristics (high 'physiological' ICP) and diseases causing ICP elevation, various activities with significant Valsalva effort, such as weightlifting and wind instrument playing, can generate very high ICPs. Recent studies of normal-pressure hydrocephalus (NPH), glaucoma and Alzheimer's disease provide supportive evidence for this hypothesis. A number of studies have shown a high incidence of AD related lesions in patients with NPH, which is known to be associated with prolonged elevation of ICP in a majority of cases. In both NPH and AD, an important decrease in cerebrospinal fluid (CSF) production was calculated. According to researchers in the US, the resulting CSF stagnation with impaired clearance and accumulation of neurotoxic substances may play an important role in the onset and progression of AD. They tested the hypothesis that improving CSF turnover by means of an investigational low-flow ventriculoperitoneal shunt will delay the progression of dementia in patients with Alzheimer's disease. With regard to the observed decrease in CSF production in patients suffering from NPH, it was postulated that chronic increased ICP causes downregulation of CSF production. It is hypothesized here that repetitive intermittent ICP elevations also may lead to downregulation of CSF production due to long-term cumulative effects. If the latter proves to be true, then both chronic increased ICP and repeated exposures to increased ICP (e.g., repetitive Valsalva maneuvers) may cause a similar cascade of CSF circulatory failure events leading to AD over time. Furthermore, AD may be causally related to increased ICP through other pathomechanisms. Additional supportive evidence for the role of a pressure factor in the pathogenesis of AD comes from studies concerning glaucoma. Elevated intraocular pressure (IOP) is a hallmark of glaucoma. Recently, similarities in pathophysiology between glaucoma and AD have been noted, with increased processing of amyloid precursor protein (APP) and up-regulation of beta-amyloid protein expression in retinal ganglion cells (RGCs). Given this link between AD and glaucoma, evidence for a causal relationship between repetitive intermittent ICP elevations and AD is gained from research indicating that high resistance wind instrument playing raises IOP and may result in glaucomatous damage. To test the validity of the hypothesis that exposure to repetitive but nonsustained ICP elevations may predispose to AD a non-invasive, epidemiological study is proposed in this paper.

Intracranial hypertension in acute liver failure

Authors: Donald Richardson 1 and Mark Bellamy 2 

1Department of Nephrology, York District Hospital, York and
2Department of Anaesthesia, St James University Hospital, Leeds, UK

The development of liver failure is a medical emergency requiring specialist assessment and care. The development of renal failure in the patient with hepatic failure is one of the few prognostic indicators of poor outcome. Its presence is associated with prolonged intensive care unit (ICU) stay, prolonged hospitalization and death . The high incidence of renal failure with necessity for dialysis support requires the nephrologist to have an understanding of liver failure and its concomitant complications. Indeed the nephrologist may be called upon outside of a liver centre to provide advice and may be in a position to guide subsequent management and referral to an appropriate centre or within that centre may be asked to assist with investigation and management. An understanding of the causes and treatments of intracranial hypertension will better arm the nephrologist in the management of this syndrome.

Benign intracranial hypertension and chronic renal failure

Authors: Chang D, Nagamoto G, Smith WE.

Department of Nephrology, Medical College of Virginia, Richmond 23298-0160.

Benign intracranial hypertension (also called pseudotumor cerebri, otitic hydrocephalus, or meningeal hydrops) is a syndrome of markedly elevated intracranial pressure in the absence of intracranial mass, inflammation, or obstruction. Numerous disease processes and medications have been associated with it. However, renal failure has not been documented as an associated condition. In this report, the case of a 27-year-old Native American man with chronic renal failure of unknown etiology is described, with new-onset headache, papilledema, and elevated intracranial pressure. After normal cerebrospinal fluid, computed tomography, and magnetic resonance imaging studies, a diagnosis of benign intracranial hypertension was made. Despite repeated lumbar punctures with cerebrospinal fluid removal, the patient's headaches persisted, and intracranial pressures remained in the 200 to 400 mm H2O range. After initiation of hemodialysis due to progressive deterioration of renal function, the patient's headaches became less severe and eventually disappeared. This case represents a unique association of chronic renal failure with benign intracranial hypertension.

Intracranial pressure and glaucoma

Authors: Berdahl, John Pa; Allingham, R Randb

Current Opinion in Ophthalmology: March 2010 - Volume 21 - Issue 2 - p 106–111 doi: 10.1097/ICU.0b013e32833651d8 Glaucoma: Edited by Donald L. Budenz

Purpose of review: Glaucoma remains a disease with an unclear basic pathophysiology. The optic nerve travels through two pressurized regions: the intraocular space and the intracranial space. Some authors have suggested that the relationship between intraocular pressure and intracranial pressure may play a fundamental role in the development of glaucoma.

Recent findings: Recent studies have shown that intracranial pressure is lower in patients with glaucoma and normal-tension glaucoma. Conversely, intracranial pressure appears to be elevated in patients with ocular hypertension. Early mathematical modeling studies have suggested that the counterbalance provided by intracranial pressure would be an important factor in the development of glaucoma.

Summary: The relationship between intraocular pressure and intracranial pressure may play an important role in the development of glaucoma.

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