Dynamic response of the intracranial system in the conscious dog to papaverine hydrochloride. (1/760)

The influence of papaverine on the intracranial system of the dog was studied by measuring the pressure-depth-time response for the intact intracranial system, i.e., for the subarachnoid and subpial compartments. This was accomplished by a measurement system which provided an accurate pressure-depth determination and a uniform rate of transducer insertion. Distinct regions of the intracranial system (subarachnoid, transitional, and subpial) were identified from inflections in the pressure response curve. The test parameter, brain relative stiffness (BRS), was obtained by determining the slope of the pressure response values within the subpial region. This parameter is a measure of the "stiffness" or elasticity of bring tissue within the test configuration. A bolus injection of papaverine (1 mg per kilogram, i.v.) caused an increase in the transitional region, a compensatory reduction in the subarachnoid space, and an increase in BRS. It is postulated that at normotensive arterial blood pressure, cerebrovascular expansion caused by papaverine resulted in increased brain tissue elasticity, i.e., an increase in the pressure-depth response for the subpial region. Possible implications for this increase are discussed. Experiments should be conducted in which local blood flow studies are coupled with measurements of brain elastic response.  (+info)

Cerebral blood flow in the monkey after focal cryogenic injury. (2/760)

A focal cryogenic lesion was made in the left superior frontal gyrus of the anesthetized macaque brain. Cerebral blood flow (CBF) was determined by the hydrogen clearance technique before and during the 4 hours following trauma. Local CBF in tissue adjacent to the lesion increased in the first half hour after the lesion was made and then decreased during the ensuing 3 1/2 hours. Local CBF in the contralateral superior frontal gyrus, as well as total CBF and oxygen consumption, were unchanged by cryogenic trauma. The spread of vasogenic edema into uninjured tissue probably accounts for the observed decrease in local CBF. This experimental model may assist in discovering therapy to alter favorably the spatial and temporal profile of pathologic CBF changes in tissue surrounding an acute lesion of the brain.  (+info)

Evaluation of the pressure transfer system in the intracranial cavity by coherency. (3/760)

Coherency provides a method to evaluate model linearity. The characteristics of pressure wave transmission in the intracranial cavity were studied by coherency in 16 cats with hydrostatic pressure loading to assess the linearity of the system, which is an assumption for use of the transfer function. Linearity was observed in only the fundamental waves of the respiration-induced component and the cardiac-induced component of intracranial pressure oscillation, and in the second harmonic wave of the latter. Linearity at the other frequencies was close to zero. The pressure transfer system in the intracranial cavity was basically a non-linear system. As intracranial pressure rose, the increase in the pressure transfer efficiency was largest in the low-frequency domain and smallest in the high-frequency domain, indicating that the cerebral blood vessels are characterized by inferior transmission of high frequency due to increased intracranial pressure. In addition, the correlation between the coherencies of the cardiac-induced fundamental wave component and intracranial pressure, and between those of the cardiac-induced second harmonic wave component and intracranial pressure, showed that the slope of the straight line was greater between 45 and 70 mmHg than between 10 and 45 mmHg. This suggests that there is a break point, located between 45 and 70 mmHg, where the increase in the coherency values is accelerated, caused by an increase in the intracranial elastance, as well as an increase in the cerebrovascular compliance due to the reduced vascular transmural pressure.  (+info)

Phase-contrast MRI measurement of systolic cerebrospinal fluid peak velocity (CSFV(peak)) in the aqueduct of Sylvius: a noninvasive tool for measurement of cerebral capacity. (4/760)

BACKGROUND: Cerebrospinal fluid (CSF) outflow to intra- and extracranial subarachnoid spaces caused by arterial inflow to the brain predominantly compensates systolic increases in cerebral blood volume. Phase-contrast magnetic resonance imaging is a new tool for noninvasive assessment of CSF displacement by measuring CSF peak velocity (CSFV(Peak)). The authors tested this new tool in an experimental human model of increased intracranial pressure and reduced cerebral capacity by means of continuous positive airway pressure (CPAP) breathing. METHODS: The authors investigated systolic CSFV(Peak) in the aqueduct of Sylvius in 11 awake, normocapnic (end-tidal carbon dioxide [ET(CO2)] = 40 mmHg) volunteers without CPAP and at two different CPAP levels (6 and 12 cm H2O) by means of electroencephalography-gated phase-contrast magnetic resonance imaging. RESULTS: Administration of 6 cm H2O CPAP did not change systolic CSFV(Peak) (-4.9+/-2.8 cm/s vs. control: -5.1+/-2.7 cm/s), whereas 12 cm H2O CPAP significantly reduced systolic CSFV(Peak) (-4.0+/-1.8 cm/s vs. control: -5.1+/-2.7 cm/s; P < 0.05). CONCLUSIONS: These findings in awake volunteers show that monitoring CSFV(Peak) in the aqueduct of Sylvius is a sensitive method for detecting even minor impairment of cerebral capacity caused by experimentally induced increases in intracranial pressure.  (+info)

Intracranial pressure changes with different doses of lignocaine under general anaesthesia. (5/760)

The effect of intravenous lignocaine on intracranial pressure (ICP) was studied on thirty patients of either sex, aged above 5 years and scheduled for elective ventriculoperitoneal shunt surgery. The patients were randomly divided into 3 groups, which received intravenous lignocaine in the dose of 1 mg, 1.5 mg and 2 mg/kg body weight respectively. Intracranial pressure, heart rate, ECG, arterial pressure and arterial blood gases were monitored at various intervals for a period of 30 minutes. Maximum decrease in ICP was seen at 2 minutes after IV lignocaine in all the three groups (p<0. 001). The fall in ICP was significantly more in group II and group III (35.65% and 37.5% respectively) as compared to group I (17.47%) (p<0.001). This fall in ICP in all the three groups persisted below the basal level, throughout the study period. None of the groups showed any significant change in the heart rate, but a statistically significant fall in arterial pressure was observed in group III (p<0. 05). In conclusion intravenous lignocaine, in a dose of 1.5 mg/kg, causes significant fall in ICP without causing any untoward cardiovascular effects and is recommended for routine clinical use.  (+info)

Sevoflurane increases lumbar cerebrospinal fluid pressure in normocapnic patients undergoing transsphenoidal hypophysectomy. (6/760)

BACKGROUND: The data on the effect of sevoflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that sevoflurane would increase intracranial pressure as compared to propofoL METHODS: In 20 patients with no evidence of mass effect undergoing transsphenoidal hypophysectomy, anesthesia was induced with intravenous fentanyl and propofol and maintained with 70% nitrous oxide in oxygen and a continuous propofol infusion, 100 microg x kg(-1) x min(-1). The authors assigned patients to two groups randomized to receive only continued propofol infusion (n = 10) or sevoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the sevoflurane group received, in random order, two concentrations (0.5 times the minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of sevoflurane for 10 min each. The authors continuously monitored lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations. RESULTS: Lumbar CSF pressure increased by 2+/-2 mmHg (mean+/-SD) with both 0.5 MAC and 1 MAC of sevoflurane. Cerebral perfusion pressure decreased by 11+/-5 mmHg with 0.5 MAC and by 15+/-4 mmHg with 1.0 MAC of sevoflurane. Systolic blood pressure decreased with both concentrations of sevoflurane. To maintain blood pressure within predetermined limits (within+/-20% of baseline value), phenylephrine was administered to 5 of 10 patients in the sevoflurane group (range = 50-300 microg) and no patients in the propofol group. Lumbar CSF pressure, cerebral perfusion pressure, and systolic blood pressure did not change in the propofol group. CONCLUSIONS: Sevoflurane, at 0.5 and 1.0 MAC, increases lumbar CSF pressure. The changes produced by 1.0 MAC sevoflurane did not differ from those observed in a previous study with 1.0 MAC isoflurane or desflurane.  (+info)

Decreases in blood pressure and sympathetic nerve activity by microvascular decompression of the rostral ventrolateral medulla in essential hypertension. (7/760)

BACKGROUND: Neurovascular compression of the rostral ventrolateral medulla, a major center regulating sympathetic nerve activity, may be causally related to essential hypertension. Microvascular decompression of the rostral ventrolateral medulla decreases elevated blood pressure. CASE DESCRIPTION: A 47-year-old male essential hypertension patient with hemifacial nerve spasms exhibited neurovascular compression of the rostral ventrolateral medulla and facial nerve. Microvascular decompression of the rostral ventrolateral medulla successfully reduced blood pressure and plasma and urine norepinephrine levels, low-frequency to high-frequency ratio obtained by power spectral analysis, and muscle sympathetic nerve activity. CONCLUSIONS: This case suggests not only that reduction in blood pressure by microvascular decompression of the rostral ventrolateral medulla may be mediated by a decrease in sympathetic nerve activity but also that neurovascular compression of this area may be a cause of blood pressure elevation via increased sympathetic nerve activity.  (+info)

Cerebral vasodilatation causing acute intracranial hypertension: a method for noninvasive assessment. (8/760)

Deep spontaneous vasodilatatory events are frequently recorded in various cerebral diseases, causing dramatic increases (A-waves) in intracranial pressure (ICP) and subsequently provoking ischemic brain insults. The relationship between fluctuations in CBF, ICP, and arterial blood pressure (ABP) is influenced by properties of cerebrovascular control mechanisms and the cerebrospinal pressure-volume compensation. The goal of this study was to construct a mathematical model of this relationship and to assess its ability to predict the occurrence and time course of A-waves. A group of 17 severely head-injured patients were included in the study. In our model ICP was derived from the ABP waveform using a linear signal transformation. The transformation was modified during the simulation by a relationship between ABP and flow velocity, i.e., by the characterization of the cerebrovascular bed. In this way the ICP could be calculated from the ABP waveform. This model was verified by comparison of simulated and directly measured ICP during A-waves recorded in seven of the patients. In all simulations, plateau elevations of ICP were well replicated. The mean absolute error between real and simulated ICP was 8.3 +/- 5.4 mm Hg at the baseline and 7.9 +/- 4.3 mm Hg at the top of plateau waves. The correlation coefficient between real and simulated increase in ICP was R = 0.98; P < .001. Similarly, correlation between real and simulated increase in pulse amplitude of ICP was highly significant (R = 0.94; P < .001). The mathematical model of the relationship between ABP, flow velocity, and ICP is of potential clinical use for the noninvasive detection of A-waves in patients in whom invasive ICP assessment is not conducted.  (+info)