Background: Pathologic signs in orbital phlebographies have been reported in various neurological diseases.
Purpose: To study if pathologic signs in orbital phlebography may be markers of inflammation primarily affecting intracranial capillaries, which would cause intracranial hypertension.
Material And Methods: Two groups with different intracranial cerebrospinal fluid pressures (Pcsf) were compared as to inflammatory markers in serum and pathologic signs in orbital phlebographies.
Objective: This study aims to question the generally accepted cerebrospinal fluid (CSF) bulk flow theory suggesting that the CSF is exclusively absorbed by the arachnoid villi and that the cause of hydrocephalus is a CSF absorption deficit. In addition, this study aims to briefly describe the new hydrodynamic concept of hydrocephalus and the rationale for endoscopic third ventriculostomy (ETV) in communicating hydrocephalus.
Critique: The bulk flow theory has proven incapable of explaining the pivotal mechanisms behind communicating hydrocephalus.
Neuroradiol J
October 2006
It is almost a century since Dandy made the first experimental studies on hydrocephalus, but its underlying mechanism has been unknown up to now. The conventional view is that cerebrospinal fluid (CSF) malabsorption due to hindrance of the CSF circulation causes either obstructive or communicating hydrocephalus. Analyses of the intracranial hydrodynamics related to the pulse pressure show that this is an over-simplification.
View Article and Find Full Text PDFThe pathophysiology of syringomyelia development is not fully understood. Current prevailing theories suggest that increased pulse pressure in the subarachnoid space forces cerebrospinal fluid (CSF) through the spinal cord into the syrinx. It is generally accepted that the syrinx consists of CSF.
View Article and Find Full Text PDFSyringomyelia is a condition that results in fluid-containing cavities within the parenchyma of the spinal cord as a consequence of altered cerebrospinal fluid dynamics. This review discusses the history and the classification of the disorder, the current theories of pathogenesis, and the advanced imaging modalities used in the diagnosis. The intramedullary pulse pressure theory (a new pathophysiologic concept of syringomyelia) also is presented.
View Article and Find Full Text PDFPurpose: To detect skeletal muscle ischemia with first-pass gadolinium (Gd) kinetics after exercise.
Materials And Methods: Eleven subjects with intermittent claudication performed a symptom-limited bilateral plantar flexion exercise in the magnet. Regional ROIs were placed bilaterally in the gastrocnemius and soleus muscles, and a signal intensity (SI) time-curve analysis was performed.
Objective: To present a patient with symptoms similar to those of superior canal dehiscence syndrome due to another cause.
Study Design: Case report.
Setting: University hospital, tertiary referral center.
Neurosurg Rev
July 2004
It is almost a century since Dandy made the first experimental studies on hydrocephalus, but its underlying mechanism has been unknown up to now. The conventional view is that cerebrospinal fluid (CSF) malabsorption due to hindrance of the CSF circulation causes either obstructive or communicating hydrocephalus. Analyses of the intracranial hydrodynamics related to the pulse pressure show that this is an over-simplification.
View Article and Find Full Text PDFAccording to Starling's hypothesis, the osmotic pressure of plasma proteins in the capillary is the principal force for fluid absorption. The leakage of plasma proteins from capillaries to tissue during 24 h accounts for the total amount of plasma proteins in the vascular system. The same amount must therefore be reabsorbed by the lymphatic system, which is considered to be the sole absorber of proteins from tissue.
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