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PubMedDate not supplied

Assessment of childhood intracranial pressure recordings using a new method of processing intracranial pressure signals.

BACKGROUND: Intracranial compliance may be more reliably predicted by the pulsatile component (pulse pressure) than the steady (mean pressure) component of intracranial pressure (ICP). A new method of processing continuous ICP signals assessing both components of ICP is described and applied to the ICP recordings of 6 pediatric cases. METHOD: The new method was applied to each subsequent 6-second time sequence window of a continuous ICP signal. For time sequence windows including single ICP waves, the following time sequence (TS.x)-related parameters were computed: (a) mean ICP (i.e. TS.MeanP) was computed according to the currently used and known technology; (b) the mean ICP wave was computed according to the new method, characterized by mean wave amplitude (i.e. TS.MeanWavedP) and mean wave latency (i.e. TS.MeanWavedT). Cases No. 1-4 were treated for hydrocephalus and cases No. 5 and 6 for craniosynostosis. RESULTS: In 5 children, clinical intracranial hypertension was associated with elevations of mean ICP above 15-20 mm Hg of variable durations. The ICP recordings of the 5 children with intracranial hypertension and successful outcome after surgery revealed mean wave amplitude values above 5 mm Hg. Mean wave latency was more variable, ranging between 0.10 and 0.25 s. CONCLUSIONS: In the children with intracranial hypertension and successful outcome after surgery, mean wave amplitude was variably above 5 mm Hg. It is suggested that mean wave amplitude may be a useful parameter by more directly predicting cerebral compliance than mean ICP.

Cerebrospinal Fluid Shunts↗

PubMed2002

Treatment of giant intracranial aneurysms with saphenous vein extracranial-to-intracranial bypass grafting: indications, operative technique, and results in 29 patients.

OBJECTIVE: The treatment of giant intracranial aneurysms is a challenge because of the limitations and difficulty of direct surgical clipping and endovascular coiling. We describe the indications, surgical technique, and complications of saphenous vein extracranial-to-intracranial bypass grafting followed by acute parent vessel occlusion in the management of these difficult lesions. METHODS: Between January 1990 and December 1999, 29 patients with giant intracranial aneurysms underwent 30 saphenous vein bypass grafts followed by immediate parent vessel occlusion. There were 11 men and 18 women with a mean follow-up period of 62 months. Twenty-five patients harbored aneurysms involving the internal carotid artery, 2 had middle cerebral artery aneurysms, and 2 had aneurysms in the basilar artery. Serial cerebral or magnetic resonance angiograms were obtained to assess graft patency and aneurysm obliteration. RESULTS: All 30 aneurysms were excluded from the cerebral circulation, with 28 vein grafts remaining patent. Two patients had graft occlusions: one because of poor runoff and the other because of misplacement of a cranial pin during a bypass procedure on the contralateral side. Other surgical complications included one death from a large cerebral infarction, homonymous hemianopsia from thrombosis of an anterior choroidal artery after internal carotid artery occlusion, and temporary hemiparesis from a presumed perforator thrombosis adjacent to a basilar aneurysm. CONCLUSION: With appropriate attention to surgical technique, a saphenous vein extracranial-to-intracranial bypass followed by acute parent vessel occlusion is a safe and effective method of treating giant intracranial aneurysms. A high rate of graft patency and adequate cerebral blood flow can be achieved. Thrombosis of perforating arteries caused by altered blood flow hemodynamics after parent vessel occlusion may be a continuing source of complications.

Cerebral Arteries↗

PubMed1992

Intracranial pressure and intracranial volume in children with craniosynostosis.

Intracranial volume and intracranial pressure have been measured in 66 children with craniosynostosis, 48 boys and 18 girls. The premature fusion of skull sutures is assumed to restrict skull growth and predispose to elevated intracranial pressure. Thirteen children (20 percent) had raised intracranial pressure and demonstrated a significant restriction of skull growth. In this series, volume measurement alone, however, did not serve as a reliable predictor that the intracranial pressure was raised.

Adolescent↗

PubMed1982

Intracranial pressure in patients with the empty sella syndrome without benign intracranial hypertension.

The intracranial pressure was monitored continuously for at least 48 hours in five patients with empty sella syndrome, who did not have clinical benign intracranial hypertension (BIH). It has been suggested that the empty sella syndrome is a result of chronically elevated intracranial pressure in the presence of a congenitally deficient diaphragma sellae. However, whilst the intracranial pressure in two of the five patients was abnormally high, in three patients in whom it was monitored, the CSF pressure was normal. Although these cases may represent "burnt out" forms of intracranial pressure problems, it might be that the normal pulsations of CSF are sufficient to produce the empty sella in the presence of a deficient diaphragma sella.

Adult↗

PubMed1993

Falling intracranial pressure: an important element in the genesis of intracranial hemorrhage in the beagle puppy.

To study the role of extravascular intracranial pressure (ICP) in the genesis of intracranial hemorrhage in the beagle puppy, we measured ICP in animals on the day of birth, untreated 3-day-old controls, and 3-day-old animals treated from birth with prolactin. Baseline ICP varied substantially in all 3 groups. Only 8% of this variability was attributable to variability in mean arterial pressure and central venous pressure. ICP was lower in the 3-day-old controls, animals at high risk for intracranial hemorrhage after a hypovolemic/hypotensive insult followed by rapid volume expansion, than in the other groups which are at lower risk. Administration of a hyperosmolar insult, intraperitoneal glycerol, to animals whose ICP was relatively high promptly lowered ICP. After this treatment, the risk of intracranial hemorrhage was markedly increased in these previously low-risk groups. We conclude that the normal neonatal decrease in brain water content and the consequent fall in ICP substantially increase the risk of intracranial hemorrhage in the beagle puppy, a model which appears similar in pathophysiology to hemorrhage in the preterm human infant.

Age Factors↗

PubMed1999

[Evolution of angiographic signs of venous hypertension and clinical signs of intracranial hypertension in intracranial dural arteriovenous fistulas].

Dural arteriovenous fistulas (dAVFs) can cause cerebral venous hypertension (VHT). The most common mechanism is due to the fact that some dAVFs can drain retrogradelly in cortical (better defined as leptomeningeal) veins (directly or after drainage in a dural sinus) causing venous engorgement and consequently an impairment of the cerebral venous drainage. However, more rarely, dAVFs without a cortical venous drainage can also be responsible for VHT probably due to dAVF shunts causing insufficient antegrade cerebral venous drainage. In addition, dAVFs are often associated with stenosis and/or thrombosis of dural sinus(es) which can worsen the VHT. Raised pressure within the superior sagittal sinus causes impeded cerebrospinal reabsorption in the arachnoid villi allowing increased intracranial pressure. The venous engorgement in the cortical veins can cause a venous congestive encephalopathy analogous to the venous congestive myelopathy of the spinal dural AVFs. Clinically VHT can cause not only symptoms related to increased intracranial pressure but also seizures, neurological deficits, impairment of the cognitive functions and dementia. An important aspect is the risk of hemorrhage in dAVFs with a leptomeningeal venous drainage leading to VHT. Although the term VHT sensu strictu should be used if venous pressure measurements are performed, angiographic criteria for VHT such as delayed circulation time, venous engorgement and abnormal visualization of the cerebral veins are well established. The purpose of our study was to evaluate the angiographic signs of VHT in patients with dAVF and to study the course of the VHT and of the clinical signs of increased intracranial pressure before and after dAVF endovascular treatment. A retrospective chart analysis of 22 patients (13 males, 9 females) ranging in age from 20 to 87 years (mean: 53 ys.) with a dAVF associated with angiographic signs of VHT was performed. Ten dAVFs were located on the transverse/sigmoid sinus(es), 6 on the superior sagittal sinus, 3 on the petro-tentorial incisura, 1 on the inferior petrosal sinus, 1 on the anterior ethmoidal region and 1 on the Galen vein region. All dAVFs had a retrograde leptomeningeal venous drainage. Stenosis or thrombosis of the dural AVF sinus was observed in 17 cases and stenosis or thrombosis of another sinus(es) and/or of the jugular vein in 8 cases. In 11 patients, the angiographic signs of VHT were global affecting the entire cerebral venous drainage and, in the other 11 patients, the VHT was focal. The VHT caused clinical symptoms of increased intracranial pressure in 18 patients. Other clinical findings included: bruit (11 cases), seizures (3 cases), vertigo (3 cases), visual deficits (2 cases) and impairment of cognitive functions (4 cases). Three patients presented hemorrhage (one parenchymal hematoma, one hemorrhagic infarction and one subarachnoid hemorrhage). The 4 patients without clinical symptoms of increased intracranial pressure presented only bruit in 2 cases, bruit and vertigo in 1 case, bruit and hemorrhagic infarction in another one. The dAVFs were treated by endovascular therapy (arterial approach: 3 cases, venous approach: 6 cases and both arterial and venous approach: 13 cases). Endovascular sessions ranged from 1 to 7 (mean: 2.8) for each patient. After the endovascular treatment, in 12 patients with complete occlusion of the dAVF, the disappearance of angiographic signs of VHT and clinical cure were observed. In 8 patients with partial occlusion of the dAVF, the disappearance of angiographic signs of VHT and clinical cure were observed in 4 cases (almost complete dAVF occlusion in 2 cases); in the other 4 cases, only reduction the angiographic signs of VHT and clinical improvement were obtained. In all 16 patients who were clinically cured angiographic signs of VHT disappeared despite the persistence of dAVF shunts as observed in 4 cases. (ABSTRACT TRUNCATED)

Adult↗

PubMed2003

Optimal temperature for the management of severe traumatic brain injury: effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism.

OBJECTIVE: We studied the effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism in patients with severe traumatic brain injury to clarify the optimal temperature for hypothermia, with a view toward establishing the proper management techniques for such patients. METHODS: The study was performed in 31 patients with severe head injury (Glasgow Coma Scale score as high as 5). All patients were sedated, paralyzed, ventilated, and cooled to 33 degrees C. Brain temperature, core temperature, intracranial pressure, cerebral perfusion pressure, jugular venous oxygen saturation, mixed venous oxygen saturation, cardiac output, oxygen delivery, oxygen consumption, and resting energy expenditure were monitored continuously. RESULTS: Intracranial pressure decreased significantly at brain temperatures below 37 degrees C and decreased more sharply at temperatures 35 to 36 degrees C, but no differences were observed at temperatures below 35 degrees C. Cerebral perfusion pressure peaked at 35.0 to 35.9 degrees C and decreased with further decreases in temperature. Jugular venous oxygen saturation and mixed venous oxygen saturation remained in the normal range during hypothermia. Resting energy expenditure and cardiac output decreased progressively with hypothermia. Oxygen delivery and oxygen consumption decreased to abnormally low levels at rectal temperatures below 35 degrees C, and the correlation between them became less significant at less than 35 degrees C than that when temperatures were 35 degrees C or higher. Brain temperature was consistently higher than rectal temperature by 0.5 +/- 0.3 degrees C. CONCLUSION: These results suggest that, after traumatic brain injury, decreasing body temperature to 35 to 35.5 degrees C can reduce intracranial hypertension while maintaining sufficient cerebral perfusion pressure without cardiac dysfunction or oxygen debt. Thus, 35 to 35.5 degrees C seems to be the optimal temperature at which to treat patients with severe traumatic brain injury.

Adolescent↗

PubMedDate not supplied

[Intracranial pressure instability index as a new method of evaluating the capacity of intracranial volume compensation].

An index of intracranial pressure instability is calculated as a new way to evaluate the capacity of intracranial voluminal compensation in patients suffering from cranio-cerebral trauma. The value of the index is determined by mutual relations of intracranial pressure standard deviations measured during 3-minute periods before and after intracranial administration of 2 ml of 0.9% NaCl. Normal physiological range of the index was evaluated in controls without intracranial pathology.

Adolescent↗

PubMed2000

Gamma knife radiosurgery as a primary treatment for prolactinomas.

OBJECT: The purpose of this study was to estimate the efficacy of gamma knife radiosurgery (GKS) in controlling tumor growth and endocrinopathy associated with prolactinomas. METHODS: Between 1993 and 1997, 164 of 469 patients with pituitary adenomas treated by GKS harbored prolactinomas. The dose to the tumor margin ranged from 9 to 35 Gy (mean 31.2 Gy), and the visual pathways were exposed to a dose of less than 10 Gy. The mean tumor diameter was 13.4 mm. The mean follow-up time for 128 cases was 33.2 months (range 6-72 months). Tumor control was observed in all but two patients who underwent surgery 18 and 36 months, respectively, after GKS. Clinical cure was achieved in 67 cases. Clinical improvement was noted with a decrease in the hyperprolactinemia after GKS. Nonetheless, in 31 (29%) of 108 patients who were followed for more than 2 years no improvement in serum prolactin levels was demonstrated, although this could be normalized by bromocriptine administration after treatment. Nine infertile women became pregnant 2 to 13 months after GKS and all gave birth to normal children. There was no visual deterioration related to GKS. Five women experienced premature menopause. In these patients there was subtotal disappearance of the tumor and an empty sella developed. CONCLUSIONS: Gamma knife radiosurgery as a primary treatment for prolactinomas can be safe and effective both for controlling tumor growth and for normalization of prolactin hypersecretion. A higher margin dose (> or = 30 Gy) seemed to be associated with a better clinical outcome. Gamma knife radiosurgery may make prolactinomas more sensitive to the bromocriptine.

Humans↗

PubMed2003

Automatic segmentation of the brain and intracranial cerebrospinal fluid in T1-weighted volume MRI scans of the head, and its application to serial cerebral and intracranial volumetry.

A new fully automatic algorithm for the segmentation of the brain and total intracranial cerebrospinal fluid (CSF) from T(1)-weighted volume MRI scans of the head, called Exbrain v.2, is described. The algorithm was developed in the context of serial intracranial volumetry. A brain mask obtained using a previous version of the algorithm forms the basis of the CSF segmentation. Improved brain segmentation is then obtained by iterative tracking of the brain-CSF interface. Gray matter (GM), white matter (WM), and intracranial CSF volumes and probability maps are calculated based on a model of intensity probability distribution (IPD) that includes two partial volume classes: GM-CSF and GM-WM. Accuracy was assessed using the Montreal Neurological Institute's (MNI) digital phantom scan. Reproducibility was assessed using scan pairs from 24 controls and 10 patients with epilepsy. Segmentation overlap with the gold standard was 98% for the brain and 95%, 96%, and 97% for the GM, WM, and total intracranial contents, respectively; CSF overlap was 86%. In the controls, the Bland and Altman coefficient of reliability (CR) was 35.2 cm(3) for the total brain volume (TBV) and 29.0 cm(3) for the intracranial volume (ICV). Scan-matching reduced CR to 25.2 cm(3) and 17.1 cm(3) for the TBV and ICV, respectively. For the patients, similar CR values were obtained for the ICV.

Adult↗

PubMed2006

Management of pseudoaneurysms in the intracranial segment of the internal carotid artery with covered stents specially designed for use in the intracranial vasculature: technical notes.

Vascular diseases like aneurysms, pseudoaneurysms and direct high-flow carotid-cavernous fistulas on the intracranial segment of the internal carotid artery are usually managed through transarterial embolization with detachable coils or balloons. Utility of covered stents has been reported with good results in the treatment of selective cases. But the current generation of covered stents for coronary use is rather stiff and difficult to navigate in tortuous vessels particularly in the intracranial vasculature. Herein, we report on the use and technical respects of balloon-expanded covered stents specially designed for intracranial vasculature in the treatment of two pseudoaneurysms secondary to the successful obliteration of direct CCFs on the intracranial segment of the internal carotid artery. This is the first report of covered stents specially developed for use in intracranial vasculature.

Adult↗

PubMed1985

Histopathological study of major intracranial arteries in premature infants related to intracranial hemorrhage.

The incidence of various types of intracranial hemorrhage (ICH) and the microscopic appearance of the major intracranial arteries were investigated in 112 premature infants, and related to birth weight. In none of the premature newborns, regardless of the presence of ICH, did the intracranial arteries contain true elastic elements. The wall of the basilar artery was significantly thinner in all premature infants with any kind of ICH. Within each body-weight group those with ICH had intracranial arteries with fewer reticular fibers than did those without ICH. The density of the reticular fibers in the cerebral arteries of premature neonates without ICH did not seem to depend on maturity. The authors believe that the hypoplasia of the major intracranial arteries and the reticular fiber deficiency most probably involve the whole vascular system of the brain and may predispose to hemorrhage.

Cerebral Arteries↗

PubMed1988

Transcranial Doppler ultrasonography in raised intracranial pressure and in intracranial circulatory arrest.

Transcranial Doppler ultrasonography was used to monitor 71 patients suffering from intracranial hypertension with subsequent brain death. Among these, 29 patients were also assessed for systemic arterial pressure and epidural intracranial pressure, so that a correlation between cerebral perfusion pressure and the Doppler ultrasonography waveforms could be established. Four-vessel angiography was also performed in 33 patients after clinical brain death. With increasing intracranial pressure, the transcranial Doppler ultrasonography waveforms exhibited different characteristic high-resistance profiles with first low, then zero, and then reversed diastolic flow velocities, depending on the relationship between intracranial pressure and blood pressure (that is, cerebral perfusion pressure). This study shows that transcranial Doppler ultrasonography may be used to assess the degree of intracranial hypertension. This technique further provides a practicable, noninvasive bedside monitor of therapeutic measures.

Adolescent↗

PubMed1977

Intracranial pulse pressure dynamics in patients with intracranial hypertension.

The pulsative inflow of blood to the brain causes fluctuations in the cerebral blood volume, and this is considered to be the main cause of the pulsations of the intracranial pressure (ICP). This statement allows discrimination between two different factors that influence the pulse amplitude of the ICP: 1. The pulsatile pattern of the cerebral arterial blood flow. 2. The slope of the intracranial pressure-volume curve. In order to clarify the relative contributions of the two factors we have developed a simulation model of the intracranial pressure-volume curve and the cerebral blood flow. Measurements from clinical practice and data from other authors can be interpreted with reference to this model. The increase in the pulse amplitude due to a moderate increase in the ICP is mainly explained by the decrease of the intracranial compliance. However, it is recognized that, when the ICP approaches the arterial blood pressure, the ICP amplitude increases disproportionally with increasing ICP. In this situation the transmural pressure of the cerebral arteries approaches zero, and the compliance relevant to the arterial flow system is no longer that of the vessel wall but the compliance of the craniospinal compartment.

Adult↗

PubMed2005

Interpretation of approximate entropy: analysis of intracranial pressure approximate entropy during acute intracranial hypertension.

We studied changes in intracranial pressure (ICP) complexity, estimated by the approximate entropy (ApEn) of the ICP signal, as subjects progressed from a state of normal ICP (< 20-25 mmHg) to acutely elevated ICP (an ICP "spike" defined as ICP > 25 mmHg for < or = 5 min). We hypothesized that the measures of intracranial pressure (ICP) complexity and irregularity would decrease during acute elevations in ICP. To test this hypothesis we studied ICP spikes in pediatric subjects with severe traumatic brain injury (TBI). We conclude that decreased complexity of ICP coincides with episodes of intracranial hypertension (ICH) in TBI. This suggests that the complex regulatory mechanisms that govern intracranial pressure are disrupted during acute rises in ICP. Furthermore, we carried out a series of experiments where ApEn was used to analyze synthetic signals of different characteristics with the objective of gaining a better understanding of ApEn itself, especially its interpretation in biomedical signal analysis.

Adolescent↗

PubMed1990

Unruptured intracranial aneurysms and arteriovenous malformations: frequency of intracranial hemorrhage and relationship of lesions.

Among 91 patients with unruptured intracranial arteriovenous malformations (AVM's), 16 patients had 26 unruptured intracranial saccular aneurysms. An actuarial analysis showed the risk of intracranial hemorrhage among patients with coexisting aneurysm and AVM to be 7% per year at 5 years following diagnosis compared to 1.7% for patients with AVM alone. The difference in length of survival free of hemorrhage was significant (log-rank, p less than 0.0007). Several angiographic and clinical parameters were investigated to better understand the relationship of these lesions. The aneurysms occurred in similar percentages in patients with small, medium, and large AVM's. Twenty-five aneurysms were on arteries feeding the malformation system, almost equally distributed proximally and distally. Eleven aneurysms were atypical in location, and all arose from primary or secondary branch feeders to the malformation; 24 were on enlarged feeding arteries. Eleven (16%) of the 67 patients with high-flow AVM's had associated aneurysms, compared with five (21%) of the 24 patients with low-flow AVM's. Four (16%) of 25 low-shunt malformations and 12 (18%) of 65 high-shunt malformations had associated aneurysms. All five aneurysms associated with low-shunt malformations were on a direct arterial feeder of the malformation. These data suggest that the intracranial AVM's predispose to aneurysm formation within AVM feeding systems and that the mechanism is not simply based upon the high blood flow or high arteriovenous shunt in these systems.

Adolescent↗

PubMed1985

Intracranial pressure, conductance to cerebrospinal fluid outflow, and cerebral blood flow in patients with benign intracranial hypertension (pseudotumor cerebri).

Intracranial pressure, conductance to cerebrospinal fluid outflow, and cerebral blood flow were investigated in 14 patients with benign intracranial hypertension (pseudotumor cerebri). Intracranial pressure was increased in 9 patients (20 to 30 mm Hg), borderline in 4 patients (15 to 18 mm Hg), and normal in 1 patient (8 mm Hg). Six patients had plateau waves, and all had B waves in more than 50% of the monitored time. Conductance to cerebrospinal fluid outflow, measured by a lumbo-lumbar perfusion method, was significantly reduced: 0.042 ml X mm Hg-1 X min-1 (+/- 0.004 [SEM]; normal, more than 0.080 ml X mm Hg-1 X min-1). Cerebral blood flow was measured by xenon 133 inhalation and single photon emission computer tomography. Mean hemispheric flow was normal in all cases, averaging 59 +/- 9 ml X 100 gm-1 X min-1. Only 2 patients showed focal low-flow areas. Thus, a disturbance of cerebrospinal fluid circulation seems to be of pathogenetic significance in benign intracranial hypertension.

Adolescent↗

PubMed1978

Preliminary observations on the use of Corynebacterium parvum in patients with primary intracranial tumors: effect on intracranial pressure.

It has been observed that patients with metastatic brain lesions developed neurologic symptoms when given Corynebacterium parvum. To obtain more information in patients with intracranial mass lesions, intracranial pressures (ICP) were measured or observed in six patients undergoing C. parvum therapy. All patients except two (one previously shunted, one recently operated) demonstrated a profound increase in ICP. It is presumed that either edema is formed within brain and tumor tissue (inasmuch as neurologic deterioration has not been observed in patients without an intracranial lesion) or transient increases in cerebral blood flow adversely alter an already compromised intracranial volume. Surgical decompression of tumor volume or use of Lasix may abort this response to C. parvum infusion.

Adolescent↗