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MR-Intracranial pressure (ICP): a method to measure intracranial elastance and pressure noninvasively by means of MR imaging: baboon and human study.

PURPOSE: To develop a noninvasive method for intracranial elastance and intracranial pressure (ICP) measurement. MATERIALS AND METHODS: Intracranial volume and pressure changes were calculated from magnetic resonance (MR) imaging measurements of cerebrospinal fluid (CSF) and blood flow. The volume change was calculated from the net transcranial CSF and blood volumetric flow rates. The change in pressure was derived from the change in the CSF pressure gradient calculated from CSF velocity. An elastance index was derived from the ratio of pressure to volume change. The reproducibility of the elastance index measurement was established from four to five measurements in five healthy volunteers. The elastance index was measured and compared with invasive ICP measurements in five patients with an intraventricular catheter at MR imaging. False-positive and false-negative rates were established by using 25 measurements in eight healthy volunteers and six in four patients with chronically elevated ICP. RESULTS: The mean of the fractional SD of the elastance index in humans was 19.6%. The elastance index in the five patients with intraventricular catheters correlated well with the invasively measured ICP (R:(2) = 0.965; P: <.005). MR imaging-derived ICPs in the eight healthy volunteers were 4.2-12.4 mm Hg, all within normal range. Measurements in three of the four patients with chronically elevated ICP were 20.5-34.0 mm Hg, substantially higher than the normal limit. CONCLUSION: MR imaging-derived elastance index correlates with ICP over a wide range of ICP values. The sensitivity of the technique allows differentiation between normal and elevated ICP.

Adult↗

CSF hypovolemia vs intracranial hypotension in "spontaneous intracranial hypotension syndrome".

OBJECTIVES: To investigate the role of CSF hypovolemia in spontaneous intracranial hypotension (SIH) syndrome because so-called SIH syndrome sometimes lacks intracranial hypotension. METHODS: Ten women (aged from 28 to 49 years) with characteristic orthostatic headache without a previous history of dural tear were investigated. In addition to gadolinium (Gd)-enhanced brain MRI, spinal MRI with and without Gd enhancement was performed. RESULTS: Gd-enhanced brain MRI demonstrated diffuse pachymeningeal enhancement in all patients. Sagittal T2-weighted spinal MRI revealed a variable amount of CSF in the extradural space in all patients. Sagittal T2-weighted MRI or axial Gd-enhanced T1-weighted MRI showed dilated epidural veins located in the high cervical portion in each patient. The intensity of dilatation of the epidural veins correlated significantly with the amount of CSF in the epidural space. This suggested that the Monro-Kellie doctrine was applicable in this circumstance. CONCLUSIONS: Since some patients with SIH syndrome have normal CSF pressure and since a downward displacement of the brain due to a reduction of the buoyant action of CSF may induce symptoms, CSF hypovolemia, not intracranial hypotension, may be the cause. Based on the Monro-Kellie doctrine, detecting leaked CSF and venous engorgement (epidural vein dilatation and pachymeningeal enhancement) is an important clue to diagnose so-called SIH syndrome. Dilatation of epidural veins suggests CSF hypovolemia in appropriate conditions.

Adult↗

Long-term observations of intracranial pressure after severe head injury. The phenomenon of secondary rise of intracranial pressure.

The long-term course of intracranial pressure (ICP) was studied in 53 patients from a group of 90 patients with severe head injury treated over a 3-year period. In 49 of these, ICP was significantly elevated during the observation period. The maximum in ICP was usually observed 24 to 96 hours posttrauma. A subgroup of patients developed a second rise of ICP. Such a course was observed in 15 (31%) of the 49 patients with intracranial hypertension. In these cases, ICP increased initially to 20 to 30 mm Hg but could be controlled. Thereafter, ICP was decreased again for at least 12 hours. The secondary ICP rise occurred 3 to 10 days after trauma. In six patients, intracranial hypertension became uncontrollable and eventually caused brain death. The outcome of patients with a secondary rise of ICP was worse when compared with that of patients without this complication. A cause of the secondary ICP rise could only be identified in some cases. Delayed traumatic intracerebral hemorrhage, traumatic vasospasm, hypoxia, and hyponatremia were diagnosed in seven cases. In seven other patients, the secondary ICP rise coincided with a pronounced leukocytosis, which was not associated with apparent infections. Because the occurrence and degree of a secondary rise of ICP after severe head injury are important factors affecting outcome, monitoring of ICP after severe head injury should be prolonged.

Adolescent↗

Intracranial pressure changes induced by sodium nitroprusside in patients with intracranial mass lesions.

Because of the ability of sodium nitroprusside (SNP) to dilate cerebral blood vessels, intracranial pressure (ICP) should increase with its use. In patients with vascular intracranial tumors following SNP (0.01%) infusion, ICP increased from 14.58 +/- 1.85 to 27.61 +/- 3.33 torr (p greater than 0.0005) and cerebral perfusion pressure decreased from 89.32 +/- 3.5 to 43.23 +/- 4.60 torr (p less than 0.0005) when the mean arterial pressure had reduced by 33%. These results suggest that SNP not be used in patients with raised ICP unless previous measures have been taken to improve intracranial compliance.

Blood Pressure↗

Effects of positive end-expiratory pressure on intracranial pressure in dogs with intracranial hypertension.

Positive end-expiratory pressure (PEEP) is used to improve oxygenation in patients with the adult respiratory distress syndrome. Nevertheless, this treatment may increase intracranial pressure (ICP) and be detrimental to certain neurosurgical patients. This clinical situation was simulated by administering PEEP to dogs with normal and elevated ICP. Increases in PEEP increased ICP in all animals. However, the presence of intracranial hypertension diminished the increase in ICP seen at a given level of PEEP. Cerebral perfusion pressure also fell less in the presence of intracranial hypertension than it did in the absence, although in the former situation cerebral perfusion pressure was at the lower limits of the range of cerebral autoregulation. These findings suggest that PEEP is no more detrimental to patients with elevated ICP than it is to patients whose ICP is normal, assuming that their cerebral autoregulation is not impaired.

Animals↗

Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography.

Previous studies have suggested that only a small proportion (< 15%) of comatose head-injured patients whose initial computerized tomography (CT) scan was normal or did not show a mass lesion, midline shift, or abnormal basal cisterns develop intracranial hypertension. The aim of the present study was to re-examine this finding against a background of more intensive monitoring and data acquisition. Eight severely head-injured patients with a Glasgow Coma Scale score of 8 or less, whose admission CT scan did not show a mass lesion, midline shift, or effaced basal cisterns, underwent minute-to-minute recordings of arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) derived from blood pressure minus ICP. Intracranial hypertension (ICP > or = 20 mm Hg lasting longer than 5 minutes) was recorded in seven of the eight patients; in five cases the rise was pronounced in terms of both magnitude (ICP > or = 30 mm Hg) and duration. Reduced CPP (< or = 60 mm Hg lasting longer than 5 minutes) was recorded in five patients. Severely head-injured (comatose) patients whose initial CT scan is normal or does not show a mass lesion, midline shift, or abnormal cisterns nevertheless remain at substantial risk of developing significant secondary cerebral insults due to elevated ICP and reduced CPP. The authors recommend continuous ICP and blood pressure monitoring with derivation of CPP in all comatose head-injured patients.

Adolescent↗

Experimental evaluation of the Spiegelberg intracranial pressure and intracranial compliance monitor. Technical note.

The goal of this study was to compare the Spiegelberg intraventricular intracranial pressure (ICP)/intracranial compliance monitoring device, which features an air-pouch balloon catheter, with existing gold-standard methods of measuring ICP and intracranial compliance. A Spiegelberg intraventricular catheter, a standard intraventricular catheter, and a Codman intraparenchymal ICP microsensor were placed in five sheep, which previously had been given anesthetic and paralytic agents, to allow comparative measurement of ICP at incremental levels (range 5-50 mm Hg). Intracranial pressure measured using the Spiegelberg intraventricular air-pouch balloon catheter displayed a linear correlation with ICP measured using the standard intraventricular fluid-filled catheter (r2 = 0.9846, p < 0.001; average bias -0.74 mm Hg), as well as with ICP measured using the Codman intraparenchymal strain-gauge sensor (r2 = 0.9778, p < 0.001; average bias 0.01 mm Hg). Automated measurements of intraventricular compliance obtained using the Spiegelberg compliance device were compared with compliance measurements that were made using the gold-standard manual cerebrospinal fluid bolus injection technique at ICPs ranging from 5 to 50 mm Hg, and a linear correlation was demonstrated between the two methods (r2 = 0.7752, p < 0.001; average bias -0.019 ml/mm Hg). The Spiegelberg air-pouch ICP/compliance monitor provides ICP and compliance data that are very similar to those obtained using both gold-standard methods and an intraparenchymal ICP monitor over a range of pathophysiological ICPs. The automated closed Spiegelberg system offers practical advantages for the measurement of intraventricular compliance. Assessment of the clinical utility and robustness of the Spiegelberg system, together with the development of an intraparenchymal device, would enhance the clinical utility of automated compliance measurement and expand the range of its applications.

Animals↗

Enigma of raised intracranial pressure in patients with complex craniosynostosis: the role of abnormal intracranial venous drainage.

OBJECT: In this study the authors investigated whether patterns of intracranial venous drainage in children with complex craniosynostosis associated with raised intracranial pressure (ICP) were abnormal and, thus, could support the theory that venous hypertension is a major contributor to raised ICP that can lead to impaired visual function or even blindness in these patients. METHODS: The authors analyzed the anatomy of intracranial venous drainage as demonstrated in the results of 24 angiography studies obtained in 23 patients, all of whom had either a craniosynostosis-related syndrome (18 patients) or a nonsyndromic multisutural synostosis (five patients). Twenty-one patients had experienced raised ICP (in 19 patients diagnosis was based on invasive ICP monitoring and in two patients on clinical grounds alone) 1 to 6 weeks before undergoing angiography. Of the two remaining patients (both with Apert syndrome) whose ICP monitoring was normal immediately before angiography, each had undergone two previous cranial vault expansion procedures. On results of 18 angiography studies a 51 to 99% stenosis or no flow at all could be observed in the sigmoid-jugular sinus complex either bilaterally (11 patients) or unilaterally (seven patients). In 11 of these patients a florid collateral circulation through the stylomastoid emissary venous plexus was also seen. Two angiography studies were performed in one patient with Crouzon syndrome. A comparison of the two studies demonstrated a progression of the abnormal venous anatomy in that case. The authors found no obvious correlation between each patient's baseline ICP and the degree of abnormality of their venous anatomy, as judged on the basis of a venous-phase angiography severity score. CONCLUSIONS: Based on their findings, the authors assert that in children with complex forms of craniosynostosis in whom other factors, such as hydrocephalus, are absent, abnormalities of venous drainage that particularly affect the sigmoid-jugular sinus complex produce a state of venous hypertension that, in turn, is responsible for the majority of cases of raised ICP. The incidence of these changes is unknown, but an analysis of the ages of the children in this study indicated that the period of particular vulnerability to the effects of venous hypertension lasts until the affected child is approximately 6 years old. After that age the collateral venous drainage through the stylomastoid plexus will likely become sufficient to allow ICP to normalize.

Acrocephalosyndactylia↗

Overnight recordings of intracranial pressure and electroencephalography in neurosurgical patients. Part II: Changes in intracranial pressure during sleep.

Changes in intracranial pressure (ICP) during sleep were investigated in 37 patients with chronic intracranial hypertension or chronic hydrocephalus, in whom episodic pressure waves characterized by A-waves or episodic B-waves were seen in Part I of this paper. The patients were conscious, and sleep stages including REM sleep were observed in all of them. During non-REM sleep, ICP significantly rose in Stage II on many occasions, and was always lower in Stage IV than in other sleep stages. A marked elevation of ICP was seen in REM sleep. ICP changes during REM sleep were characterized by frequent appearances of the pressure waves; 88.9% of A-waves and 95.1% of episodic B-waves appeared during REM sleep. The initiation of REM sleep scored on EEG began 1 to 2 minutes prior to or at the onset of the episodic pressure waves. The episodic pressure waves are assumed to be induced by the intracranial conditions in REM sleep, when increased brain activity and reduced sympathetic tone are known to occur simultaneously.

Adolescent↗

[The use of trans-cranial Doppler sonography in a neurosurgical intensive care unit. Intracranial pressure, intracranial circulatory arrest].

Transcranial Doppler Sonography (TCD) is a noninvasive simple bedside procedure to control continuously cerebral blood flow velocity in basal brain arteries in comatose patients of an intensive care unit (ICU). This measure can already be performed at ICU, to determine timing of angiography for confirming intracranial circulatory arrest when an organ explantation of patients judged clinically brain-dead is intended. TCD is also carried out to assess cerebral circulation in patients with intracranial hypertension. 64 patients are repeatedly evaluated by TCD and have been continuously monitored for ICP at the same time. According to our results a strong correlation between the flow parameters derived from TCD and the ICP exists when the ICP surpasses the level of 25 mmHg. Furthermore repeated control-TCD-examinations of 150 comatose patients in our ICU have elucidated the significant prognostic value of the pulsatility index representing the cerebrovascular resistance. Thereby important informations concerning further clinical course of patients suffering from intracranial hypertension are available. Additionally a clinical example of complete failure of cerebrovascular autoregulation shortly after hypoxic brain damage is demonstrated.

Blood Flow Velocity↗

[The behavior of intracranial pressure and intracranial compliance in nifedipine-induced hypotension].

The influence of nifedipine induced hypotension on intracranial pressure (ICP) and intracranial compliance (ICC) was investigated in dogs without (group I, n = 8) and with (group II, n = 8) intracranial hypertension. ICP in group II was raised by gradual inflation of an epidurally placed balloon catheter. A volume-pressure-response curve (VPR) was established before and during the administration of nifedipine. In group II dogs angiotensin was infused before and during infusion of nifedipine in a dose sufficient to raise mean arterial pressure (MAP) by 30-40 mm Hg. An infusion of nifedipine (2 micrograms X kg-1 X min-1) subsequent to a bolus injection of nifedipine (10 micrograms X kg-1) resulted in a significant and sustained decrease in MAP (p less than 0.05) by 25% and 35% resp. due to a significant reduction in total peripheral resistance (p less than 0.05). ICP increased from 8.7 +/- 3.0 mm Hg to a maximum of 12.5 +/- 5.2 mm Hg in group I animals (p less than 0.05) and from 19.8 +/- 2.6 mm Hg to 24.8 +/- 7.2 mm Hg not significantly in group II dogs. The pressure-volume-index revealed a slight reduction of ICC in group I and a slight increase of ICC in group II resp. during nifedipine as compared to before nifedipine. When angiotensin was being administered in group II dogs before nifedipine was given, MAP increased by 40 +/- 5.8 mm Hg while ICP did not change significantly (+2 +/- 2.4 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

[Effect of furosemide on intracranial pressure in patients with intracranial hypertension].

Furosemid administration to patients with intracranial hypertension of tumour genesis was associated with temporal regression of general cerebral symptoms, coinciding in time with the period marked by a decrease in cerebrospinal fluid pressure. A correlation between the magnitude of this decrease and the furosemid-induced elevated secretion of urine containing chlorine and sodium was established. Restoration of the liquid lost from the body following drug administration was not accompanied by either a fall in the cerebrospinal fluid pressure or a change in the intensity of general cerebral symptoms. The action of furosemid on intracranial pressure is explained by a reduction in the central venous pressure, by an increased outflow of the venous blood from the cranial cavity as well as by its diminished volume. Concomitant administration of large quantities of water lowers or completely precludes the hypotensive action of the agent on intracranial pressure and, thus, is considered unadvisable.

Brain Diseases↗

[Intracranial hemorrhage and hemostasis. Monitoring patients after intracranial hemorrhage by determination and follow-up of activation products of blood coagulation].

OBJECTIVE: The aim of the study was to improve the detection of small hemorrhages with minimal symptoms and of unruptured aneurysms after a subdural and subarachnoid bleeding by the control of the intravascular hemostatic system. DESIGN: Prospective, open study. SETTING: Neurosurgical intensive care unit of a university hospital. PATIENTS: 44 patients undergoing a cranial trepanation. Patients of group 1 (control n = 11) had an intrasellar hypophysoma, patients of group 2 (n = 12) a chronic subdural hematoma without a previous traumatic incident and patients of group 3 (n = 15) a subarachnoid hemorrhage caused by an intracranial aneurysm. INTERVENTIONS: After cranial trepanation changes of plasmatic hemostasis have been assessed by means of immunologically determined parameters of coagulation. The investigation included blood parameters (hemoglobin, hematocrit, thrombocytes), clotting status (prothrombin time, partial thromboplastin time, thrombin time, fibrinogen, plasminogen, antithrombin III [AT III] activity and proteinase inhibitors), as well as immunological methods such as fibrinopeptide A (FPA), thrombin-antithrombin III (TAT), protein C and factor XIII activity (F XIII activity). RESULTS: In comparison to group 1 (control) a significant difference (p < 0.001) was seen in groups 2 and 3 for thrombin-antithrombin III (TAT), fibrinopeptide A (FPA), protein C, and the antithrombin III activity. Intra- and postoperatively increased TAT levels in groups 2 (16.9 ng/ml) and 3 (21.1 ng/ml) and decreased protein C levels (group 2: 61% and group 3: 58%) demonstrated an intravascular thrombin generation. On account of the elevated FPA levels in groups 2 (6.5 ng/ml) and 3 (5.7 ng/ml) and decreased AT III activity in groups 2 (58%) and 3 (62%), this thrombin generation was only incompletely compensated. Caused by proteolytic thrombin effects, another sign for a thrombin-induced turnover of clotting factors is the significant reduction (p < 0.001) of F XIII activity in groups 2 (40%) and 3 (44%). In comparison to group 1 this significantly reduced F XIII activity in groups 2 and 3 was correlated (r = 0.99) to changes in FPA and TAT plasma levels, an indication of latent chronic clotting activity. No significant difference was found concerning total amount of infusion, intra- and postoperative blood loss and blood parameters. Eight patients (group 2: 5 patients, group 3: 3 patients) showed a rebleeding episode without operative interventions. In these patients increased clotting activity (TAT, FPA, protein C) caused by proteolytic thrombin effects was combined with a factor XIII activity smaller than 40%. CONCLUSION: The results of the recent study indicated that immunologically determined TAT, FPA, protein C, factor XIII and AT III activities might serve to improve management in patients with intracranial bleeding events. In view of these parameters the evaluation of risks for a rebleeding is improved. A decrease of the plasma factor XIII activity under 40% associated with a latent clotting activity induced by a thrombin generation caused a higher risk of rebleeding after an initial intracranial bleeding event. The necessity of substituting factor XIII in such cases should be elucidated to minimize risks of rebleeding.

Aneurysm, Ruptured↗

[Evaluation of intracranial volume compensation analyzing changes of harmonic components of intracranial pressure pulse wave].

Intracranial pressure (ICP) pulse wave was analysed during infusion tests performed in hospital (hydrocephalus) and in cats. Pulse wave changes were evaluated calculating the high frequency centroid index (HFC) in the HFC, found to be a very valuable parameter in intracranial volume-pressure situation evaluation. The HFC decrease occurred much earlier than the rise of ICP in both clinical and experimental studies. Thus the HCF index should be very usefull in clinical evaluation of intracranial volume-pressure relation disturbances.

Adolescent↗

Interobserver variability in angiographic measurement and morphologic characterization of intracranial aneurysms: a report from the International Study of Unruptured Intracranial Aneurysms.

PURPOSE: To determine the variability in assessment of the principal inherent characteristics of intracranial aneurysms through the evaluation of interobserver variability for material with uniform quality. METHODS: Blinded interpretations of a single set of cerebral arteriograms of 55 aneurysms were evaluated by several statistical approaches. RESULTS: Excellent correlations were found for the detection and measurement of aneurysms after adjusting for geometric distortion caused by magnification. Progressively decreasing correspondence was found for factors that characterized morphology, including, in order, determination of margins, assessment of accessory appendages, and identification of a neck. DISCUSSION: Correction for geometric distortion was the most critical factor that influenced uniform measurement of size. Standards for measurement and morphologic characteristics were subsequently established for use in the International Study of Unruptured Intracranial Aneurysms.

Adult↗

Wilms' tumor with intracranial metastases presenting with intracranial hemorrhage.

Intracranial metastasis of Wilms' tumor is very rare. Furthermore, intracerebral hemorrhage is an unusual presentation of metastases. We report the case of a 4-year-old girl who had multiple intracranial metastatic lesions, initially presenting as an intracranial hemorrhage. Removal of the tumors and hematoma was followed by radiation therapy and chemotherapy. Thereafter, complete remission occurred. It is thought that this malignant tumor with metastases may be curable through combined therapy.

Antineoplastic Combined Chemotherapy Protocols↗

On the pattern of reticular fibers in the intracranial arteries of mature newborn with and without intracranial hemorrhage.

A detailed histological study was carried out on the major intracranial arteries of 20 mature newborn. A substantial reduction of the reticular fiber content within the wall of the cerebral arteries was observed in all samples originating from infants with intracranial hemorrhage. No other differences occurred when comparisons were made using the conventional staining methods on the vessels from the ten newborn with hemorrhage and the ten others without bleeding. These data indicate that the structural deficiency of the brain vasculature provides the morphological basis for the development of intracranial hemorrhages in the term newborn.

Arteries↗

Comparison of the effects of succinylcholine and atracurium on intracranial pressure in monkeys with intracranial hypertension.

The effects of succinylcholine (1.5 mg X kg-1 IV) administered five minutes after a defasciculating dose of curare (0.05 mg X kg-1 IV), were compared with the effects of atracurium (0.5 mg X kg-1 IV) on intracranial pressure (ICP) in 13 cynomolgus monkeys with intracranial hypertension (ICP approximately 25 mmHg). Neither succinylcholine nor atracurium increased ICP during general anaesthesia with 60 per cent N2O/O2, 0.5-1 per cent halothane. During a rapid sequence induction and intubation with thiopentone 5 mg X kg-1 IV, ICP increased equally with intubation following both atracurium (25 +/- 1 to 32 +/- 2 mmHg) and succinylcholine (25 +/- 1 to 31 +/- 2 mmHg) (p less than 0.05). Intubation was also associated with significant increases in PaCO2, CVP and MAP. We conclude that in this primate model of intracranial hypertension, neither atracurium nor succinylcholine (when given following a defasciculating dose of curare) elevates ICP. In terms of the elevation of ICP associated with intubation, atracurium was found to offer no advantage over succinylcholine.

Anesthesia, Endotracheal↗