Brain Collateral Perfusion Augmentation by Cerebral Venous Pressure Modulation

Can be used in both an emergency situation (outside of a hospital) and within a hospital settingProvides for control over the rate of collateral CBF to avoid reperfusion injuryEase of administration to permit rapid and wide spread adoptionAdaptable to use access routes currently familiar to health care professionalsDoes not produce backflow of blood to the brain, eliminating retroperfusion injuryEliminates the need for inferior vena cava (IVC) clamping, eliminating damage to the IVCProvides accurate measurement of the jugular venous pressureSimple; low complication ratesCan be combined with IVC catheterization procedures to administer fluids, medications, and other deliverable agentsCan be used in combination with all antegrade perfusion enhancement methodsEffective in both acute and chronic timeframes

Ameliorate ischemiaProtect the brain and cerebral vasculature of patients suffering from global or local ischemiaEnable control over the rate of collateral CBF and/or cessation of collateral CBF to the ischemic regionProvide access for performing other therapeutic interventions

UCLA researchers have designed a device and corresponding method to use applied pressure to artificially achieve collateral circulation in the brain. Their method and device both capitalize on a biological phenomenon where flow rate through a collapsible tube will depend only on an upstream pressure at the feeding segment and will be independent of pressure downstream. To increase cerebral venous pressure and therefore, redirect maldistributed blood flow, they invented a novel device to create an occlusion of one or more veins coupled to the collapsed vessel. The device consists of an elongated tubular member with proximal and distal ends for insertion into a patient's superior vena cava (or other vein), an expandable occluder located at the distal end of the tubular member (the occluder has an expanded and a collapsed state), a device to measure pressure at the distal end of the tubular member, a device to measure cerebral blood flow in the patient, and a controller programmed to actuate the expandable occluder as a function of the measured venous pressure and the measured cerebral blood flow. This method and device are intended to treat patients suffering from blood flow diversion due to vessel collapse and rapidly restore CBF to about 50% of normal.

Patent Number: CN1218114C
Application Number: CN2001140858A
Inventor: YUE Z | LI Z | LUO J
Priority Date: 22 Sep 2000
Priority Number: CN1218114C
Application Date: 21 Sep 2001
Publication Date: 7 Sep 2005
IPC Current: E21B000100 | E21B004400 | E21B004500 | E21B004704
Assignee Applicant: The University of Hong Kong
Title: Monitor system for drilling procedure | Drilling process monitoring system
Usefulness: Monitor system for drilling procedure | Drilling process monitoring system
Summary: For monitoring borehole drilling operation.
Novelty: Borehole drilling monitoring device measures movement of drill feed with respect to fixed points on ground and pressure of compressed air from drilling machine controller to drilling rig

Disease Diagnostic/Treatment

Other Disease

9833598

State Of Development

The researchers developed several variations of their general method, creating the occlusion in a number of possible veins depending on the patient. The researchers are working to develop a clinically applicable device, based on their method, to be used for stroke treatment. Clear evidence exists that the device will effectively treat strokes

Background

Cerebral ischemia, or damage to tissue due to reduced blood supply, can quickly lead to organ dysfunction and cell death. Cerebral ischemia can lead to stroke, which when not treated in a timely fashion, can cause permanent neurological impairments and death. Normal cerebral blood flow (CBF), when at rest and awake, is around 45 to 60 mL/100g/min. When CBF drops below 10 mL/100g/min, the threshold for energy and ion homeostasis, a cascade of metabolic events is induced, ultimately leading to cellular death. If regional CBF (rCBF) stays below this threshold for prolonged periods the brain damage can be irreversible, but if rCBF is increased before such progression to necrosis then proper brain function and structure can be restored. Therefore, this clinically relevant "therapeutic window" allows the opportunity to improve the outcome of stroke by increasing CBF. 

Current options for stroke treatment include maintaining cerebral perfusion pressure (CPP), augmenting blood flow, and lowering cerebral metabolic rate. These are all, however, limited by a specific clinical context and inconclusive efficacies. None directly addresses enhancement of penumbral blood flow, the blood flow in the area surrounding the damaged tissue. Additionally, none of the methods considers cerebral vascular collapse as the mechanism for restricted arterial blood flow to the brain nor do they aim to minimize the effects of vascular collapse or cerebral blood flow diversion. Cerebral vessels collapse when external pressure exceeds intravascular pressure. Accordingly, when the intravascular pressure rises, the vessels reopen and their diameter increases. Although the concept of abolishing blood diversion by increasing venous pressure has been previously described it has never been applied to patients where venous steal exists, that is, where blood has been diverted from where it is needed such as occurs in a stroke. It would be desirable to improve existing methods and apparatus for treating acute and chronic ischemic conditions in the brain, particularly acute ischemic stroke.

Tech ID/UC Case

21548/2009-224-0

Related Cases

2009-224-0

USA

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