PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Intracranial”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1999

Intracranial cavity volume can be accurately estimated from the weights of intracranial contents: confirmation by the dental plaster casting method.

Intracranial cavity volume is used to evaluate brain size relative to the intracranial space. This volume can theoretically be obtained from the weights and densities of the brain and surrounding cerebrospinal fluid (weight method). However, the accuracy of this method has not been examined. In this study, we examined the reliability of the weight method, by comparing the intracranial cavity volumes of 41 post-mortem cases obtained by the weight method (ICVw) with those obtained by a dental plaster casting method (ICVcast) which was shown to be unbiased. The ICVw was not significantly different from the ICV cast (P=0.49, paired t-test), and the standard error of difference was 18 ml (1.3% of ICVcast). These results show that the weight method is reliable, and applicable to routine autopsies.

Aged↗
PubMed1988

Correlations among intracranial pulsatility, intracranial hemodynamics, and transcranial Doppler wave form: literature review and hypothesis for future studies.

In the present work, the major correlations among cerebrospinal fluid (CSF) pulsatility, cerebral hemodynamic changes, the action of mechanisms regulating cerebral blood flow and cerebral blood volume, and the main aspects of the intracranial basal artery transcranial Doppler wave form are critically examined. CSF pulsatility is a consequence of rigidity of the craniospinal compartment and the pulsating changes in cerebral blood volume. At low and medium intracranial pressures (ICPs), changes in CSF pulsatility are mainly the result of changes in craniospinal elastance. During severe intracranial hypertension, however, CSF pulse pressure reflects an abrupt increase in cerebrovascular (i.e., cerebral vessel) compliance. The mechanisms controlling cerebral blood flow and cerebral blood volume affect CSF pulsatility through both an alteration in craniospinal blood volume and a change in vascular wall pulsatility. Examination of the main parameters of the Doppler velocity pattern (maximal systolic blood velocity, diastolic blood velocity, and peak to peak pulsatility index) in cerebral basal arteries reveals a significant alteration in the velocity wave form during severe ICP increase (above 60 mm Hg). During moderate ICP increase, when cerebral regulatory mechanisms are effective, the Doppler velocity pattern is not significantly affected by ICP changes.

Brain↗
PubMed1979

Acute intracranial hypertension and auditory brain-stem responses. Part 1: Changes in the aduitory brain-stem and somatosensory evoked responses in intracranial hypertension in cats.

Changes in auditory brain-stem responses (BER's) and somatosensory evoked responses (SER's) were investigated to correlate mass volume, intracranial pressure, and neurological dysfunction in mass-induced intracranial hypertension in cats. As the intracranial pressure was raised by expansion of a supratentorial balloon, the late components of the SER's were suppressed first, followed by the early components of the SER's, then Wave V and Wave IV of the BER's, in that order. This suggests that the nonspecific reticular projections are most vulnerable to compression ischemia, and the specific somatosensory pathways are the next most vulnerable. Neural activity of the auditory pathways in the upper brain stem was also gradually suppressed, but less so than that of the somatosensory pathways. After complete transtentorial herniation, in spite of immediate mass evacuation, the function of the somatosensory pathways was greatly impaired, often irreversibly. The neural activity of the auditory pathways in the upper brain stem revealed progressive recovery during a 3-hour period. The measurements of BER Wave V is thought to be useful in predicting transtentorial herniation.

Animals↗
PubMed1984

Changes in intracranial stenotic lesions after extracranial-intracranial bypass surgery.

The natural history of intracranial arterial stenosis is not well understood. The lesions are pathologically quite diverse, and are subject to resolution, progression, or occlusion. The authors undertook an investigation to examine what effects, if any, extracranial-intracranial (EC-IC) bypass surgery had on the evolution of intracranial arterial stenosis in 18 patients undergoing EC-IC bypass procedures for ipsilateral hemispheric ischemia. There was inaccessible internal carotid artery stenosis in 14 patients, and middle cerebral artery stenosis in four patients. Early (within 2 weeks) and late (at 6 months) postoperative angiography was performed in all patients. During the period of the study, there was a significant change in the arterial stenosis in 50% of the patients (nine of 18). The stenotic artery became occluded in four patients while the grafts were widely patent. The occlusion occurred within a few days after the operation in three of the four cases, and was accompanied by an ischemic stroke in these patients. There was improvement or resolution of the stenotic lesion in five patients; the graft became occluded in two of these cases and was patent but showed poor cortical artery filling in the other three. All these patients remained asymptomatic and the change was detected on routine late postoperative angiograms. It is concluded that arterial stenoses should not be viewed as static or inflexible lesions, and that EC-IC bypass procedures can modify the hemodynamic parameters across stenotic lesions, predisposing them to improvement or worsening. This, in turn, may affect bypass patency. Such hemodynamic interactions are accompanied by ischemic symptoms in some patients, and contribute to the relatively higher morbidity associated with EC-IC bypass surgery in the setting of arterial stenosis.

Adult↗
PubMed2003

Intracranial stent placement for the treatment of a carotid-cavernous fistula associated with intracranial angioplasty. Case report.

The authors report a case of an iatrogenic carotid-cavernous fistula (CCF) associated with intracranial angioplasty. Angioplasty was performed using a 3 x 10-mm Open Sail coronary balloon in a patient with high-grade stenosis of the left cavernous internal carotid artery (ICA). After angioplasty, a perforation developed in the cavernous ICA, resulting in a CCF. A 3.5 x 9-mm S670 coronary stent was used to treat the fistula. To the authors' knowledge, this is the first reported case in which a CCF developed after angioplasty was performed using a coronary balloon. Long-term angiographic and clinical evaluation is needed to test the suitability and durability of intracranial angioplasty and stent placement in the treatment of symptomatic intracranial stenosis.

Aged↗
PubMed2000

Effect of hyperventilation on brain tissue oxygen pressure, carbon dioxide pressure, pH value and intracranial pressure during intracranial hypertension in pigs.

OBJECTIVE: To study the effect of hyperventilat ion on brain tissue oxygen pressure (P(ti)O(2)), brain tissue carbon dio xide pressure (P(ti)O(2)), pH value and intracranial pressure (ICP) dur ing intracranial hypertension in pigs. METHODS: Autologous arterial blood (5.5 mlplus minus0.5 ml) was injected into the left frontal lobe by micropump to establish the model of intr acerebral hematoma in pigs. After blood injection, the animals were hyperventila ted for 15 minutes to decrease the pressure of carbon dioxide in arterial blood (P(a)CO(2)) to 27.35 mm Hgplus minus11.97 mm Hg (1 mm Hg=0.133 kPa). The mean arterial pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), P(ti)O(2), (P(ti)CO(2)), pH value and [HCO(3)(-)] were continuously monitored and the blood gas was analyzed. RESULTS: After hyperventilation, the ICP significantly decr eased (P<0.01), the CPP significantly increased (P<0.05), while the P(ti)O(2) greatly decreased to t he ischemic level (8.20 mm Hgplus minus2.50 mm Hg) (P<0.01), the P(ti)CO(2) decreased (P<0.01) and the pH value increased (P<0.01). At the same time, bl ood gas analysis showed that the P(a)CO(2) greatly decreased and the pH valu e increased. CONCLUSIONS: Hyperventilation can decrease the ICP and the P(ti)O(2) significantly. Therefore, hyperventilation should be avoided earl y after brain injury. The P(ti)O(2) monitoring will be helpful for detec ting cerebral ischemia early.

Journal Article↗
PubMed1993

[Diagnosis of intracranial occlusive vascular disease and evaluation of extracranial-intracranial (EC/IC) arterial bypass using three-dimensional magnetic resonance angiography].

The three-dimensional time-of-flight (TOF) magnetic resonance angiograms (MRA) were studied to evaluate its accuracy in the assessment of the intracranial carotid occlusive lesions, collateral circulation and also the patency of extracranial-intracranial (EC/IC) arterial bypass surgery. All occlusive lesions of the intracranial major arteries seen in conventional angiograms were revealed clearly with MRA. However MRA had its practical limitation in the evaluation of the leptomeningeal anastomosis (collateral circulation) probably due to the deterioration of contrast in its slow flow and saturation effect of the magnetization. In addition to that, MRA often exaggerated the severity of the stenotic lesions, mostly in severe cases. The post-operative state of collateral flow and the patency of EC/IC bypass could be evaluated as properly with MRA as with conventional angiography, although MRA was limited in spatial resolution and evaluation of flow direction. In conclusion, MRA was considered t be a reliable non-invasive modality as a screening examination for the evaluation of the carotid occlusive disease and as the follow-up study of the post-operative patients with EC/IC bypass surgery.

Carotid Artery Diseases↗
PubMed1978

Intracranial pressure in patients with diffuse cerebral arterial spasm following ruptured intracranial aneurysms.

Intracranial pressure (ICP) was recorded continuously in 12 pre-operative patients with angiographic evidence of diffuse cerebral arterial spasm due to a ruptured intracranial aneurysm. Recordings were made for 1 to 7 days, starting within 13 days after the haemorrhage. 1. An increased ICP was observed in the first week after subarachnoid haemorrhage (SAH) in 4 of the patients without any signs of angiographic arterial spasm. 2. This initial increase was regularly followed by a depression of ICP in between 7--12 days after SAH. In 11 out of 12 patients such a depression was concomitant with the beginning of arterial spasm. During the period of depressed ICP pattern, 6 patients showed little or no neurological deterioration, whereas 5 patients showed impaired consciousness or neurological deficits. 3. A secondary rise of ICP thereafter always followed due to ischaemic brain swelling or infarction, and was usually associated with a serious neurological deterioration. 4. Continuous ventricular drainage was performed to control the secondary increased ICP in 7 patients who survived, 4 of them with good clinical improvement and 3 with severe neurological deficits. 5. In the stage of depressed ICP, the administration of isoproterenol and steroids is recommended in order to try to alleviate the secondary rise of ICP.

Acute Disease↗
PubMed2001

Assessment of intracranial pressure volume relationships in childhood: the lumbar infusion test versus intracranial pressure monitoring.

OBJECT: This study was undertaken to compare the results of two tests that are widely used to assess intracranial pressure-volume relationships in children: the lumbar steady state infusion test providing information about the resistance to cerebrospinal fluid (CSF) outflow (Rout), and continuous intracranial pressure (ICP) monitoring. METHODS: The study included 28 children aged 5-91 months, on whom both tests were performed. The median duration between the tests was 1 month. With the child in general narcosis, the lumbar CSF pressure was recorded before and during infusion of artificial CSF, and the Rout was calculated on the basis of the opening (Po) and plateau (Pp) pressures (Rout=Pp-Po/infusion rate). ICP was recorded every 5 s using a computer-based system. CONCLUSIONS: We found no significant correlation between Rout and mean ICP asleep. There were no significant relationships between abnormal mean ICPs during sleep (defined as either 10 or 15 mmHg) and abnormally high Rout values (defined as either 10 or 12 mmHg/ml/min), and no significant relationships between abnormally high Rout values (10 or 12 mmHg ml(-1) min(-1)) and the presence of abnormal ICP elevations (defined as either 20 or 25 mmHg and lasting 5 min). Therefore the calculation of Rout by the infusion test performed on children under general anesthesia gave no reliable prediction of abnormal ICP.

Cerebrospinal Fluid Pressure↗
PubMed1999

Rebound intracranial hypertension in dogs after resuscitation with hypertonic solutions from hemorrhagic shock accompanied by an intracranial mass lesion.

We compared intracranial pressure (ICP) and cerebral blood flow (CBF) in dogs after inflating a subdural intracranial balloon to increase ICP to 20 mm Hg, inducing hemorrhagic shock (mean arterial pressure [MAP] of 55 mm Hg), and infusing a single bolus of fluid consisting of either 54 mL/kg of 0.8% saline (SAL), 6 mL/kg of 7.2% hypertonic saline (HS), 20% hydroxyethyl starch (HES) in 0.8% SAL, or a combination fluid (HS/HES) containing 20% HES in 7.2% saline. Twenty-six dogs were ventilated with 0.5% halothane in N2O and O2 (60:40 ratio). As ICP was maintained at 20 mm Hg, rapid hemorrhage reduced MAP to 55 mm Hg (time interval of zero [T0]) which was maintained at that level for 30 minutes (until T30). Subsequently, over a 5-minute interval (T30-T35), one of the four randomly assigned resuscitation fluids was infused. Data were collected at baseline; after subdural balloon inflation; at T0, T30, T35, and 30-minute intervals thereafter for 2 hours (T65, T95, T125, and T155). CBF and ICP were compared using repeat-measure ANOVA. Cerebral blood flow was greater at T35 in the HS and HS/HES groups than in the HES group (P = .025). In the SAL group, ICP increased significantly from T0 to T35, remaining unchanged thereafter. At T35, ICP in the HS group was significantly lower than in the SAL group (P < .05) but subsequently increased. ICP in the HS/HES group exceeded that in all other groups at T95 and T125 (P < .05). After a severe reduction in cerebral perfusion pressure (CPP), HS solutions (both HS and HS/HES) were associated with a delayed rise in ICP and did not improve global forebrain CBF in comparison with conventional saline solutions.

Animals↗
PubMed2002

Phenylephrine increases cerebral perfusion pressure without increasing intracranial pressure in rabbits with balloon-elevated intracranial pressure.

Using a rabbit model of intracranial hypertension, we studied the effects of infusion of phenylephrine on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Seven New Zealand white rabbits were anesthetized with isoflurane and normocapnia was maintained. An extradural balloon was used to raise ICP to 25 +/- 1 mm Hg. Infusion of phenylephrine increased mean arterial blood pressure (MAP) (77 +/- 6 --> 95 +/- 8 mm Hg) and CPP (52 +/- 7 --> 70 +/- 7 mm Hg). ICP was unchanged during infusion of phenylephrine (25 +/- 1 vs. 25 +/- 2 mm Hg). The phenylephrine infusion was stopped after 45 minutes and MAP returned to baseline (76 +/- 8 mm Hg). We conclude that phenylephrine increased CPP because of its effect on MAP, but did not alter ICP. Phenylephrine may be used to increase CPP without raising ICP when autoregulation is intact.

Animals↗
PubMed2004

Desflurane increases intracranial pressure more and sevoflurane less than isoflurane in pigs subjected to intracranial hypertension.

Desflurane and sevoflurane may have advantages over isoflurane in neuroanesthesia, but this is still under debate. A porcine model with experimental intracranial hypertension was used for paired comparison of desflurane, sevoflurane, and isoflurane with respect to the effects on cerebral blood flow (CBF), cerebrovascular resistance (CVR), and intracranial pressure (ICP). The agents, given in sequence to each of six pigs, were compared at 0.5 and 1.0 minimal alveolar concentrations (MAC) and three mean arterial blood pressure (MAP) levels (50, 70, and 90 mm Hg) at normocapnia and one MAP level (70 mm Hg) at hypocapnia. MAC for each agent had been previously determined in a standardized manner for comparison reliability. CBF was measured with Xe. MAP was lowered by inflation of a balloon catheter in the inferior caval vein and raised by inflation of a balloon catheter in the descending aorta. ICP was measured intraparenchymally. Two Fogarty catheters positioned extradurally were inflated to a baseline ICP of 20 to 22 mm Hg at 0.2 MAC of each agent. CBF and ICP with the three agents at normocapnia and MAP 70 and 90 mm Hg at both 0.5 and 1.0 MAC were as follows (P < 0.05): desflurane > isoflurane > sevoflurane. None of the agents abolished CO2 reactivity. High-dose desflurane resulted in a higher CBF at hypocapnia than corresponding doses of sevoflurane or isoflurane, but there were no significant differences between the agents in ICP at hypocapnia. The present study showed that desflurane increased ICP more and sevoflurane less than isoflurane during normoventilation, but the differences disappeared with hyperventilation.

Anesthetics, Inhalation↗
PubMed2006

The effects of indomethacin on intracranial pressure and cerebral hemodynamics during isoflurane or propofol anesthesia in sheep with intracranial hypertension.

The effect of indomethacin in reducing intracranial pressure (ICP) may be dependent on the choice of anesthetic regimen. We studied the effects of indomethacin on ICP and cerebral blood flow (CBF) during isoflurane or propofol anesthesia in a sheep model of intracranial hypertension. A crossover design was applied in which six sheep were anesthetized with isoflurane and propofol in a random order. Anesthetic depth was measured with response and state entropy. Changes in CBF, ICP, mean arterial blood pressure, arterio-venous oxygen difference, and Paco2 were measured at specific times before and after an IV indomethacin bolus (0.2 mg/kg). Response and state entropy values during anesthesia were similar in both groups. Isoflurane and propofol reduced CBF by 11% and 34%, respectively. Indomethacin caused a reduction in ICP within 15 s during both anesthetic regimens, with the decrease in ICP being significantly more pronounced during isoflurane (P = 0.009). In both anesthetic groups, indomethacin caused a simultaneous increase in mean arterial blood pressure and a further 17% versus 14% decrease in CBF from predrug values for isoflurane and propofol, respectively. The reduction in CBF was significantly more pronounced for propofol (P = 0.02). The effect on ICP, however, was most pronounced during isoflurane anesthesia. We suggest that the effect of indomethacin is partly mediated by an autoregulatory response.

Anesthesia, Inhalation↗
PubMed1983

Can a patent extracranial-intracranial bypass provoke the conversion of an intracranial arterial stenosis to a symptomatic occlusion?

Although extracranial-intracranial (EC-IC) artery anastomosis seems to result in symptomatic improvement in certain types of cerebrovascular ischemic disease, this procedure can also be associated with significant morbidity, some of which paradoxically may be the direct result of a patent bypass. A review of the last 51/2 years at the Oregon Health Sciences University shows that 50 patients underwent 51 superficial temporal artery to middle cerebral artery bypass procedures with an angiographic patency rate of 91%. Of the 50 patients, 17 had intracranial stenotic lesions of either the middle cerebral artery (7 patients) or the internal carotid artery (10 patients). One patient had posterior cerebral artery stenosis. Five of the 18 patients with stenosis and a patent bypass developed a symptomatic occlusion of the stenotic lesion within 30 days after the anastomosis. It is hypothesized that the EC-IC bypass may have contributed to the occlusion in some of these patients by causing a change in the hemodynamic state. Possibly the bypass reversed the direction of flow distal to the stenosis to result in stasis and subsequent occlusion at the site of the stenosis or in some other manner affected hemostasis (i.e., the coagulation cascade).

Aged↗
PubMed1977

Intracranial hypertension in patients with ruptured intracranial aneurysm.

Simultaneous continuous recording of intracranial pressure (ICP) and systemic blood pressure was carried out in 26 patients admitted within 1 week after subarachnoid hemorrhage (SAH) due to a ruptured intracranial aneurysm. The patients were graded as described by Hunt and Hess. Recordings were made for 1 to 5 days. The more impaired the consciousness, the higher the rate of ICP. In Grade III, IV, and V patients, the mean ICP level was in the range of 15 to 40 mm Hg, 30 to 75 mm Hg, and exceeded 75 mm Hg, respectively. A definite correlation between vasospasm shown by cerebral arteriogram and the clinical grade was not observed. In our series of ICP recordings, we never observed a typical plateau wave. The variations of ICP seen in Grade III and IV patients were the B- and C-waves (15 to 45 mm Hg in amplitude) described by Lundberg, and those in Grade V patients were the high amplitude monotonous waves synchronous with the arterial pulses (15 to 40 mm Hg in amplitude). These phenomena may indicate that Grade III and IV patients with SAH are in a condition of cerebral vasomotor instability, and Grade V patients have cerebral vasomotor paralysis.

Adult↗
PubMed1994

Intracranial dural arteriovenous fistulae: angiographic predictors of intracranial hemorrhage and clinical outcome in nonsurgical patients.

This long-term follow-up study of 54 patients clarifies the angiographic predictors of intracranial hemorrhage (ICH) and clinical outcome in individuals with unoperated intracranial dural arteriovenous fistulae (AVF's). All of these patients were examined at the Mayo Clinic between 1976 and 1989, and all available cerebral arteriograms were reviewed by a neuroradiologist. Follow-up information was obtained for 52 patients (96%) until death or treatment intervention, or for at least 1 year after diagnosis, with a mean follow-up period of 6.6 years. Throughout this 6.6-year follow-up period, ICH related to dural AVF occurred in five of the 52 patients, for a crude risk of hemorrhage of 1.6% per year. The risk of hemorrhage at the time of mean follow-up examination was 1.8% per year. Angiographic examination revealed several characteristics that were considered potential predictors of ICH during the follow-up period. Lesions of the petrosal sinus and straight sinus had a higher propensity to bleed, although the small numbers in the series precluded a definite conclusion. A person suffering from a dural AVF with a venous varix on a draining vein had an increased risk of hemorrhage, whereas no hemorrhage was seen in the 20 patients without a varix (p < 0.05). Lesions draining into leptomeningeal veins had an increased occurrence of hemorrhage, although this increased risk was not statistically significant. Patients' initial symptoms were compared to those at follow-up evaluation. Pulsatile tinnitus improved in more than half of the 52 patients, and resolved in 75% of those showing some improvement. Individuals without a sinus or venous outflow occlusion at initial cerebral angiography were more likely to improve or remain stable (89%), whereas patients with an occlusion showed infrequent improvement (11%; p < 0.05).

Adult↗
PubMed1990

[Treatment of ischemic cerebral edema with intracranial hypertension after neurosurgery of intracranial aneurysms].

Ischemic cerebral edema frequently develops after aneurysm surgery and may lead to severe intracranial hypertension. Of prime importance are reducing the level of ICP and preserving oligemic areas from becoming infarcted. Besides correction of factors known to worsen intracranial hypertension, several therapeutics may be of value: external CSF drainage, perfusion of mannitol, induced arterial hypertension and use of anesthetic agents with cerebral vasoconstricting capability. Hyperventilation is not recommended. Arterial hypotension and hypovolemia certainly contribute to aggravate cerebral ischemia and must be corrected. Cerebral ischemia may be reduced by two specific approaches: by improving cerebral oxygen transport in ischemic areas using arterial hypertension and calcium blockers rather than hemodilution or hypervolemia; by reducing cerebral metabolic rates with heavy anesthesia under the cover of a complete cardiovascular monitoring. In view of the large heterogenicity in cerebral lesions and physiopathological stages, a therapeutical trial appears suitable in each individual case. Criteria allowing to know if any therapeutic, used alone or in association, is beneficial include increase in blood flow in ischemic areas, reduction of ICP level and normalizing of indices like CSF or venous jugular blood lactate.

Blood Pressure↗