Disease relevance of Intracranial Pressure

• We have investigated the influence of TGF-beta on regional cerebral blood flow (rCBF), intracranial pressure (ICP), and brain edema formation during the early phase of experimental meningitis [1].
• In a rat model of meningococcal meningitis, intracisternal injection of heat-killed meningococci caused a disruption of the blood-brain barrier (BBB), an increase in intracranial pressure, and CSF pleocytosis paralleled by the occurrence of MMP-9 activity in the CSF 6 hours after meningococcal challenge [2].
• Indomethacin normalizes intracranial pressure in acute liver failure: a twenty-three-year-old woman treated with indomethacin [3].
• Thiopental, an effective anesthetic agent that effectively lowers intracranial pressure, was not used in 25 of 35 stable patients with isolated head injury (71.4%) [4].
• The osmotic diuretic mannitol may be used in diverse clinical settings, such as providing "renal protection" in patients at risk for acute renal failure, decreasing intracranial pressure in patients with intracranial trauma, and preventing the dialysis-disequilibrium syndrome [5].

Psychiatry related information on Intracranial Pressure

• MEASUREMENTS AND RESULTS: Admission Glasgow Coma Scale score, survival, need for cardiopulmonary resuscitation, presence of shock, peak intracranial pressure, duration of coma, Glasgow Outcome Scale score, and the results of neuropsychologic tests were analyzed [6].

High impact information on Intracranial Pressure

• A previous study showed that cerebrospinal fluid from the lateral ventricle of patients without disturbance of sensorium or intracranial pressure contains 15 to 30 nm 3', 5' cyclic adenosine monophosphate [7].
• Increased intracranial pressure, which releases vasopressin by altering normal hypothalamic anatomy, may represent a unique type of stress to neuroendocrine systems and may contribute to adrenal secretion by a mechanism that requires intact brainstem function [8].
• Reduction in oxygen uptake and increases in intracranial pressure and CSF lactate were blocked by pretreatment with L-NAME, an inhibitor of nitric oxide synthase [9].
• Intracranial pressure was continuously monitored, and cortical water and glutamine contents were measured after the rats were killed [10].
• Intravenous bolus injection of bethanechol reversed the suppression of gastric antral contractility induced by increased intracranial pressure [11].

Chemical compound and disease context of Intracranial Pressure

• Brain edema in rabbits with galactosamine-induced fulminant hepatitis. Regional differences and effects on intracranial pressure [12].
• Cerebral oedema is the commonest immediate cause of death in fulminant hepatic failure and an investigation was carried out to determine the value of monitoring intracranial pressure (ICP) and to examine the effects of ICP of dexamethasone therapy and mannitol administration [13].
• Two young adult women are described in whom headache and papilloedema in association with raised intracranial pressure occurred during prednisolone treatment for inflammatory bowel disease [14].
• We investigated the effect of CO2 changes on cerebral blood flow velocity in patients with severe intracranial hemorrhage and evaluated the relation between CO2 reactivity, intracranial pressure, and outcome [15].
• Incomplete cerebral ischemia was produced by intracranial pressure elevation for 30 minutes with plasma glucose at 540 +/- 15 mg/dL [16].

Biological context of Intracranial Pressure

• Cerebral infection in wild-type (WT) mice caused an increase in vascular permeability and intracranial pressure (ICP), which were significantly reduced in IL-6-/- mice [17].
• Furosemide did not significantly reduce mean arterial blood pressure but slightly reduced mean intracranial pressure in each group [18].
• Since both alpha 1 and alpha 2 adrenoceptor agonists are less potent constrictors of pial veins than norepinephrine in vivo, a preferential use of alpha 1 or alpha 2 adrenoceptor agonists cannot be recommended from these experiments, if a therapeutic reduction of intracranial pressure or blood volume is desired [19].
• Autoregulation of cerebral blood flow remained unimpaired and intracranial pressure remained stable during nitroglycerin infusion [20].
• METHODS: Nine adult mongrel dogs were anesthetized with isoflurane and their rectal temperatures maintained at 37 degrees C. Electrocardiogram, heart rate, mean arterial pressure, mean pulmonary artery pressure, and intracranial pressure were continuously measured [21].

Anatomical context of Intracranial Pressure

• A significant relationship was found between intracranial pressure and the cerebrospinal fluid vasopressin concentration within all groups of patients and in the whole sample as well (r = 0.79; p less than 0.001) [22].
• N-Nitro-L-arginine treatment (5 mg/kg intravenously, followed by 5 mg/kg/hour) reversed the increase in regional cerebral blood flow; prevented an increase in brain water content, intracranial pressure, and cerebrospinal fluid nitrite concentrations; and reduced cerebrospinal fluid white blood cell count [23].
• Patients with normal intracranial pressure (ICP) and normal brain stem function (group 1) had decreased plasma cortisol levels (less than or equal to 5 micrograms/dl) within 36 h (mean +/- SEM, 2.4 +/- 0.3 microgram/dl; t 1/2, 18 h) [24].
• Thus, granulocytes may contribute to brain edema during meningitis if adequately stimulated, but intracranial pressure and CSF protein and lactate concentrations appear independent of granulocytes [25].
• In a well-established rat model, intracisternal injection of purified pneumococcal cell walls induced meningitis characterized by increases in the regional cerebral blood flow and intracranial pressure, an influx of leukocytes, and high concentrations of tumor necrosis factor alpha (TNF-alpha) in the cerebrospinal fluid [26].

Associations of Intracranial Pressure with chemical compounds

• Intravenous methylprednisolone (2.0 g initially followed by 0.5 g every 2 hr) administered immediately before and after hepatic devascularization prevented rises in intracranial pressure but had no effect when given 4 hr after operation [27].
• gamma-Hydroxybutyric acid and intracranial pressure [28].
• Treatment with MSO prevented ammonia-induced increases in intracranial pressure [29].
• Ten patients required preoperative medical therapy with mannitol, barbiturates or both for a rise in intracranial pressure above 25 mm Hg [30].
• The dosage of thiopental was adjusted incrementally until intracranial pressure, measured by extradural transducers, fell to within normal limits or adverse hemodynamic changes occurred [31].

Gene context of Intracranial Pressure

• In addition to enhanced leukocyte infiltration into the CSF, meningitis-associated intracranial complications including blood-brain barrier disruption and the rise in intracranial pressure were significantly augmented in infected eNOS-deficient mice [32].
• Thus, we investigated early changes in the concentrations of CSF S100B and various cytokines after TBI and evaluated the relations of both S100B and cytokines to intracranial pressure (ICP) and prognosis [33].
• The dynamics of the ET-1 concentration changes observed in rats with blocked ETA receptor suggests that SAH is an ET-1 production stimulator significantly more potent than other factors assessed in the study, such as a rise in the intracranial pressure resulting from administering aCSF to CM [34].
• However, at 3 days the AQP4 null mice had significantly higher intracranial pressure (mean +/- SEM 27 +/- 2 vs. 17 +/- 2 mmHg; p < 0.001) and brain water content (81.0 +/- 0.3 vs. 79.3 +/- 0.5 % water by weight in the abscess-containing hemisphere; p < 0.01) than wild-type mice [35].
• Serum gastrin levels were normal in both groups and did not correlate with intracranial pressure [36].

Analytical, diagnostic and therapeutic context of Intracranial Pressure

• The intracranial pressure was reduced, in each case, by 185 to 500 mg (median: 250 mg) thiopental given over 15 min, and in eight cases continuing infusion achieved stable normal intracranial pressure and cerebral perfusion pressure [31].
• The following outcome variables were assessed: intracranial pressure, Glasgow Outcome Scale score, pneumonia, cardiac arrhythmia, prothrombin time, and partial thromboplastin time [37].
• When the variables were combined into a stepwise logistic regression model, Glasgow Coma Scale score at admission, age, mean arterial pressure <70 mm Hg, fluid balance lower than -594 mL, and intracranial pressure > 25 mm Hg, in that order, were the most powerful variables in determining outcome [38].
• OBJECTIVE: Intravenous lidocaine commonly is used to treat ventricular arrhythmias and to attenuate reflex airway constriction and intracranial pressure elevation during airway manipulation in intensive care units [39].
• INTERVENTIONS: In 11 anesthetized pigs, intracranial pressure and brain oxygenation were measured with microsensor technology, brain glucose/lactate by microdialysis, and electroencephalograph by conventional methods [40].

References