Change of cerebral blood volume over the respiratory cycle during elevated intracranial pressure

2002 ◽  
Author(s):  
M.L. Daley ◽  
M. Griffith ◽  
J.T. Robertson
Keyword(s):  
Intracranial Pressure ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Respiratory Cycle ◽  
Elevated Intracranial Pressure

Rheographic assessment of cerebral blood volume and correlations with changes in intracranial pressure

1976 ◽  
Vol 34 (1-4) ◽  
pp. 287-294 ◽  
Author(s):  
A. L. Benabid ◽  
J. C. Persat ◽  
J. F. Piquard ◽  
M. Barge ◽  
J. P. Chirossel
Keyword(s):  
Intracranial Pressure ◽  
Blood Volume ◽  
Cerebral Blood Volume

Effects of increased intracranial pressure on cerebral blood volume, blood flow, and oxygen utilization in monkeys

1975 ◽  
Vol 43 (4) ◽  
pp. 385-398 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
Michael E. Phelps ◽  
Robert A. Ratcheson
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Metabolic Rate ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Blood Volume ◽  
Cerebral Perfusion ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Cerebral Metabolic Rate

✓ The relationship of cerebral blood volume (CBV) to cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and the cerebral metabolic rate for oxygen (CMRO2) was examined in rhesus monkeys. In vivo tracer methods employing radioactive oxygen-15 were used to measure CBV, CBF, and CMRO2. Cerebral perfusion pressure was decreased by raising the intracranial pressure (ICP) by infusion of artificial cerebrospinal fluid (CSF) into the cisterna magna. The production of progressive intracranial hypertension to an ICP of 70 torr (CPP of 40 torr) caused a rise in CBV accompanied by a steady CBF. With a further increase in ICP to 94 torr, CBV remained elevated without change while CBF declined significantly. Cerebral metabolic rate for oxygen did not change significantly during intracranial hypertension. For comparison, CPP was lowered by reducing mean arterial blood pressure in a second group of monkeys. Only CBF was measured in this group. In this second group of animals, the lower limit of CBF autoregulation was reached at a higher CPP (CPP ∼ 80 torr) than when an increase in ICP was employed (CPP ∼ 30 torr).

scholarly journals Intracranial pressure dynamics in patients with acute brain damage

1997 ◽  
Vol 82 (4) ◽  
pp. 1270-1282 ◽  
Author(s):  
M. Ursino ◽  
C. A. Lodi ◽  
S. Rossi ◽  
N. Stocchetti
Keyword(s):  
Intracranial Pressure ◽  
Brain Damage ◽  
Blood Volume ◽  
Time Constant ◽  
Cerebral Blood Volume ◽  
Volume Index ◽  
Parameter Estimates ◽  
Time Pattern ◽  
Pressure Dynamics ◽  
Parameter Values

Ursino, M., C. A. Lodi, S. Rossi, and N. Stocchetti.Intracranial pressure dynamics in patients with acute brain damage. J. Appl. Physiol. 82(4): 1270–1282, 1997.—The time pattern of intracranial pressure (ICP) during pressure-volume index (PVI) tests was analyzed in 20 patients with severe acute brain damage by means of a simple mathematical model. In most cases, a satisfactory fitting between model response and patient data was achieved by adjusting only four parameters: the cerebrospinal fluid (CSF) outflow resistance, the intracranial elastance coefficient, and the gain and time constant of cerebral autoregulation. The correlation between the parameter estimates was also analyzed to elucidate the main mechanisms responsible for ICP changes in each patient. Starting from information on the estimated parameter values and their correlation, the patients were classified into two main classes: those with weak autoregulation (8 of 20 patients) and those with strong autoregulation (12 of 20 patients). In the first group of patients, ICP mainly reflects CSF circulation and passive cerebral blood volume changes. In the second group, ICP exhibits paradoxical responses attributable to active changes in cerebral blood volume. Moreover, in two patients of the second group, the time constant of autoregulation is significantly increased (>40 s). The correlation between the parameter estimates was significantly different in the two groups of patients, suggesting the existence of different mechanisms responsible for ICP changes. Moreover, analysis of the correlation between the parameter estimates might give information on the directions of parameter changes that have a greater impact on ICP.

Management of Elevated Intracranial Pressure

2002 ◽  
Vol 15 (2) ◽  
pp. 167-185 ◽  
Author(s):  
Beth A. Vanderheyden ◽  
Brian D. Buck
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Blood Volume ◽  
Vital Signs ◽  
Elevated Intracranial Pressure ◽  
Neurologic Injury ◽  
Barbiturate Coma ◽  
Therapeutic Modalities ◽  
Neurologic Disorders ◽  
Pharmacologic Management ◽  
The Relationship

Elevated intracranial pressure (ICP) is a primary cause of morbidity and mortality for many neurologic disorders. The relationship between ICP and brain volume is influenced by autoregulatory processes that can become dysfunctional. As a result, neurologic damage can occur by systemic and intracranial insults such as ischemia and excitatory amino acids. Therefore, survival is dependent on optimizing ICP and cerebral perfusion pressure. Treatment of intracranial hypertension requires intensive monitoring and aggressive therapy. Intracranial pressure monitoring techniques such as intraventricular catheters are useful for determining ICP elevations before changes in vital signs and neurologic status. Therapeutic modalities, generally aimed at reducing cerebral blood volume, brain tissue, and cerebrospinal fluid (CSF) volume, include nonpharmacologic (CSF removal, controlled hyperventilation, and elevating the patient’s head) and pharmacologic management. Mannitol and sedation are first-line agents used to lower ICP. Barbiturate coma may be beneficial in patients with elevated ICP refractory to conventional treatment. The use of prophylactic antiseizure therapy and optimal nutrition prevents significant complication. Currently, investigations are directed at discovering useful neuroprotective agents that prevent secondary neurologic injury.

scholarly journals Increased cerebral blood volume pulsatility during head-down tilt with elevated carbon dioxide: the SPACECOT Study

2017 ◽  
Vol 123 (1) ◽  
pp. 62-70 ◽  
Author(s):  
Gary E. Strangman ◽  
Quan Zhang ◽  
Karina Marshall-Goebel ◽  
Edwin Mulder ◽  
Brian Stevens ◽  
...  
Keyword(s):  
Infrared Spectroscopy ◽  
Intracranial Pressure ◽  
Blood Volume ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Cerebral Blood Volume ◽  
Optic Disk ◽  
Fluid Shifts ◽  
Mayer Wave ◽  
Over Time

Astronauts aboard the International Space Station (ISS) have exhibited hyperopic shifts, posterior eye globe flattening, dilated optic nerve sheaths, and even optic disk swelling from spaceflight. Elevated intracranial pressure (ICP) consequent to cephalad fluid shifts is commonly hypothesized as contributing to these ocular changes. Head-down tilt (HDT) is frequently utilized as an Earth-based analog to study similar fluid shifts. Sealed environments like the ISS also exhibit elevated CO2, a potent arteriolar vasodilator that could further affect cerebral blood volume (CBV) and cerebral blood flow, intracranial compliance, and ICP. A collaborative pilot study between the National Space Biomedical Research Institute and the German Aerospace Center tested the hypotheses that 1) HDT and elevated CO2 physiologically interact and 2) cerebrovascular pulsatility is related to HDT and/or elevated CO2. In a double-blind crossover study ( n = 6), we measured CBV pulsatility via near-infrared spectroscopy, alongside noninvasive ICP and intraocular pressure (IOP) during 28-h −12° HDT at both nominal (0.04%) and elevated (0.5%) ambient CO2. In our cohort, CBV pulsatility increased significantly over time at cardiac frequencies (0.031 ± 0.009 μM/h increase in total hemoglobin concentration pulsatility amplitude) and Mayer wave frequencies (0.019 ± 0.005 μM/h increase). The HDT-CO2 interaction on pulsatility was not robust but rather driven by one individual. Significant differences between atmospheres were not detected in ICP or IOP. Further work is needed to determine whether individual differences in pulsatility responses to CO2 relate to visual changes in space. NEW & NOTEWORTHY Cerebral blood volume (CBV) pulsatility—as measured by near-infrared spectroscopy—increases over time during −12° head-down tilt at both cardiac and Mayer wave frequencies. CBV pulsatility appeared to increase more under elevated (0.5%) CO2 at Mayer wave frequencies in some individuals. If similar dynamic pulsatility increases occur in astronauts, there is the potential to initiate vascular and possibly other remodeling processes that lead to symptoms associated with sustained increases in intracranial pressure.

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