Role Of Intracranial Pressure Research Articles

Estimated intracranial pressure in glaucoma patients and its correlation with disease severity

Purpose To compare the intracranial pressure (ICP) and the translaminar pressure difference (TLPD) between primary open-angle glaucoma (POAG) patients and non-glaucoma subjects and to assess the correlation between the ICP (and TLPD) and glaucoma severity. Methods This was a cross-sectional study. Patients with POAG and age-matched controls were included. ICP was calculated using proxy algorithm to attain indirect surrogate parameter values. Differences were compared between groups. The correlation between ICP (and TLPD) and both structural and functional variables was evaluated using linear and non-linear regression analysis and estimated with Pearson’s correlation coefficient. Results Fifty patients with POAG and 25 normal controls were included. The mean estimated ICP was lower in POAG (10.9 ± 3.2 mmHg) as compared to controls (15.0 ± 3.7 mmHg, p < 0.001). The TLPD was higher in POAG (2.6 ± 4.1 mmHg) when compared to non-glaucoma (−0.3 ± 3.6 mmHg, p = 0.002). ICP displayed a negative correlation with cup-to-disk ratio (r = −0.566; 95% CI, −0.699 to −0.369, p’0.000) and a positive correlation with retinal nerve fiber layer thickness (r = 0.441; 95% CI, 0.230 to 0.612; p’0.000). There was a positive correlation between ICP and mean deviation (r = 0.280; 95% CI, 0.05 to 0.482, p = 0.017). Conclusion Glaucoma patients presented lower ICP values; lower ICP values were associated with more advanced disease. These observations strengthen the role of ICP as a potential player on the glaucoma pathogeny.

Historical aspects of the problem of surgical treatment of hemorrhagic stroke. The role of intracranial pressure in the choice of treatment tactics (review of literature)

This article provides a literature review of the past 60 years, conducted using keywords through the PubMed Internet resource, dedicated to the methods of surgical treatment of hemorrhagic stroke. The existing published results of clinical studies do not allow us to draw unambiguous conclusions about the superiority of conservative or neurosurgical treatment in relation to the functional recovery of patients. There is a statistical significance of the advantages of surgery based on the prevention of dislocation syndrome, control of intracranial hypertension, and prevention or at least reduction of the effect of blood and its degradation products on the surrounding healthy tissue. However, large randomized controlled trials have failed to demonstrate this benefit in terms of mortality or functional outcome.There are two main areas of hemorrhagic stroke surgery – open surgery and minimally invasive methods. The practice of open surgery is associated with high trauma rates, as well as with certain risks and complications. However, craniotomy is a lifesaving measure in critical situations with signs of persistent increased intracranial pressure leading to neurological impairment. The ability to control intracranial pressure provides a chance for the choice of more optimal tactics of surgical treatment.Today, the gold standard for intracranial pressure monitoring is the installation of invasive intraventricular or intraparenchymal transducers. The method is appreciated for its accuracy, however, there are a number of disadvantages in the form of the possibility of hemorrhagic and infectious complications, as well as the high cost of the sensor itself, which limits its routine use. The inability to measure intracranial pressure before surgery causes an unreasonable expansion of indications for choosing an open method of surgery, which reduces the possibility of a better functional outcome.All of these points make it urgent to search for a non-invasive method for measuring intracranial pressure, which would contribute to the timely choice of a surgical method without the danger of worsening the clinical outcome.

A Retrospective Analysis of Intracranial Pressure Monitoring and Outcomes in Adults after Severe Traumatic Brain Injury at Kaiser Permanente Trauma Centers.

The role of intracranial pressure (ICP) monitoring in improving outcomes after severe traumatic brain injury especially at level II trauma centers remains controversial. A retrospective analysis was undertaken to assess the impact of ICP monitoring on mortality and long-term functional outcome in adults after severe traumatic brain injury at level II trauma centers. The data were extracted from the Kaiser Permanente trauma database. Inclusion criteria were adults (≥ 18 years) with severe traumatic brain injury (Glasgow Coma Scale score, < 9) admitted to 2 level II trauma centers in Northern California from 2014 to 2019. Of 199 patients, 58 (29.1%) underwent ICP monitoring. The monitored subgroup was significantly younger (< 65 years), had lower Glasgow Coma Scale scores (3-5), underwent cranial procedures (craniotomy or decompressive craniectomy) more often, and had greater injury severity scores (≥ 15). Despite monitored patients being more severely injured, there was no significant difference in mortality or 6-month favorable outcomes between monitored and nonmonitored patients, including patients who underwent cranial procedures. Increased monitoring frequency and reduction in overall mortality was seen throughout the study period yet with a parallel reduction in both groups. ICP monitoring may not impact in-patient mortality or long-term outcomes at level II trauma centers. Improved outcomes may be more related to identifying patients who may benefit from ICP-guided therapy rather than simply increasing the overall use of it. Last, our pattern of care and outcomes are comparable to level I trauma centers and our findings may serve as a benchmark for future studies.

Intracranial Pressure and Its Relationship to Glaucoma

While the pathophysiology of glaucoma remains elusive, a growing body of evidence suggests that intracranial pressure may play a significant role. This review aims to highlight recent findings on the role of intracranial pressure in the development of glaucomatous optic neuropathy. The translaminar pressure gradient is defined as intraocular pressure (IOP) minus intracranial pressure (ICP) divided by the thickness of the lamina cribrosa. Prior research has demonstrated the effect of elevated IOP of ganglion cell apoptosis, but newer research shows that ganglion cell death may occur with normal IOP but reduced ICP. Additionally, patients with normal tension glaucoma have lower ICPs than controls. Stresses and strains on the lamina cribrosa may be responsible for some of the development of glaucomatous optic neuropathy. The pathophysiology of glaucomatous optic neuropathy may include a delicate balance of the translaminar pressure differential involving intraocular pressure, intracranial pressure, and lamina cribrosa biomechanics.

Quantitative magnetic resonance image assessment of the optic nerve and surrounding sheath after spaceflight

A subset of long-duration spaceflight astronauts have experienced ophthalmic abnormalities, collectively termed spaceflight-associated neuro-ocular syndrome (SANS). Little is understood about the pathophysiology of SANS; however, microgravity-induced alterations in intracranial pressure (ICP) due to headward fluid shifts is the primary hypothesized contributor. In particular, potential changes in optic nerve (ON) tortuosity and ON sheath (ONS) distension may indicate altered cerebrospinal fluid dynamics during weightlessness. The present longitudinal study aims to provide a quantitative analysis of ON and ONS cross-sectional areas, and ON deviation, an indication of tortuosity, before and after spaceflight. Ten astronauts undergoing ~6-month missions on the International Space Station (ISS) underwent high-resolution magnetic resonance imaging (MRI) preflight and at five recovery time points extending to 1 year after return from the ISS. The mean changes in ON deviation, ON cross-sectional area, and ONS cross-sectional area immediately post flight were −0.14 mm (95% CI: −0.36 to 0.08, Bonferroni-adjusted P = 1.00), 0.13 mm2 (95% CI −0.66 to 0.91, Bonferroni-adjusted P = 1.00), and −0.22 mm2 (95% CI: −1.78 to 1.34, Bonferroni-adjusted P = 1.00), respectively, and remained consistent during the recovery period. Terrestrially, ONS distension is associated with increased ICP; therefore, these results suggest that, on average, ICP was not pathologically elevated immediately after spaceflight. However, a subject diagnosed with optic disc edema (Frisen Grade 1, right eye) displayed increased ONS area post flight, although this increase is relatively small compared to clinical populations with increased ICP. Advanced quantitative MRI-based assessment of the ON and ONS could help our understanding of SANS and the role of ICP.

Do Most Patients With a Spontaneous Cerebrospinal Fluid Leak Have Idiopathic Intracranial Hypertension?

The association between cerebrospinal fluid (CSF) leaks at the skull base and raised intracranial pressure (ICP) has been reported since the 1960s. It has been suggested that spontaneous CSF leaks might represent a variant of idiopathic intracranial hypertension (IIH). We review the evidence regarding the association between spontaneous CSF leaks and IIH, and the role of ICP in the pathophysiology of nontraumatic skull base defects. We also discuss the management of ICP in the setting of CSF leaks and IIH. References were identified by searches of PubMed from 1955 to September 2018 with the terms "idiopathic intracranial hypertension" and "cerebrospinal fluid leak." Additional references were identified using the terms "pseudotumor cerebri," "intracranial hypertension," "benign intracranial hypertension," and by hand search of relevant articles. A CSF leak entails the egress of CSF from the subarachnoid spaces of the skull base into the surrounding cavitary structures. Striking overlaps exist regarding demographic, clinical, and radiological characteristics between IIH patients and those with spontaneous CSF leaks, suggesting that some (if not most) of these patients have IIH. However, determining whether a patient with spontaneous CSF leak may have IIH may be difficult, as signs and symptoms of raised ICP may be obviated by the leak. The pathophysiology is unknown but might stem from progressive erosion of the thin bone of the skull base by persistent pulsatile high CSF pressure. Currently, there is no consensus regarding the management of ICP after spontaneous CSF leak repair when IIH is suspected. IIH is becoming more widely recognized as a cause of spontaneous CSF leaks, but the causal relationship remains poorly characterized. Systematic evaluation and follow-up of patients with spontaneous CSF leaks by neuro-ophthalmologists will help clarify the relation between IIH and spontaneous CSF leaks.

The role of intracranial pressure in glaucoma and therapeutic implications.

Despite glaucoma being the second leading cause of blindness globally, its pathogenesis remains incompletely understood. Although intraocular pressure (IOP) contributes to glaucoma, and reducing IOP slows progress of the disease, some patients progress despite normal IOP (NTG). Glaucomatous damage causes characteristic cupping of the optic nerve where it passes through the lamina cribrosa. There is evidence that cerebrospinal fluid (CSF) within the optic nerve sheath has a different composition from CSF surrounding the brain. Furthermore, fluctuations in CSF flow into the optic nerve sheath may be reduced by trabeculae within the sheath, and on standing intracranial pressure (ICP) within the sheath is stabilised at around 3 mmHg due to orbital pressure. Blood pressure has been linked both to glaucoma and ICP. These facts have led some to conclude that ICP does not play a role in glaucoma. However, according to stress formulae and Laplace's Law, stress within the lamina cribrosa is dependent on the forces on either side of it, (IOP and ICP), and its thickness. On lying flat at night, ICP between the brain and optic nerve sheath should equalise. Most evidence suggests ICP is lower in glaucoma than in control groups, and that the lamina cribrosa is thinner and more posteriorly displaced in glaucoma. Subjects who have had ICP reduced have developed signs of glaucoma. This review finds most evidence supports a role for low ICP in the pathogenesis of glaucoma. Caffeine, theophylline and vitamin A may increase ICP, and could be new candidates for an oral treatment.

The Role of Intracranial Pressure and Subarachnoid Blood Clots in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats

Early brain injury after subarachnoid hemorrhage (SAH), which is considered a main factor leading to poor outcome, is believed to be caused by the increase of intracranial pressure (ICP) and/or the presence of subarachnoid blood clots (SBC) itself. The purpose of this study was to examine whether ICP or SBC is more important to neurologic deficit in the presence of apoptosis or edema. A total of 50 rats were allocated to 3 groups: an endovascular perforation SAH model (the SAH group), a cisterna magna saline injection model (the saline injection group), and a cisterna magna sham injection model (the sham injection group). Statistical analysis of correlations among the ICP, the grade of clot volume, neuronal apoptosis, brain water content (brain edema), and neurologic deficit was performed. In the SAH group, each of increased ICP and clot volume was correlated with neuronal apoptosis and brain edema. In the saline injection group, increased ICP was associated with apoptosis, but it did not correlate with brain edema. Neuronal apoptosis (r= 0.75; P < 0.01) and brain edema (r= 0.89; P < 0.01) correlated independently with neurologic deficit in the SAH group. The present study suggests that neuronal apoptosis is caused mainly by increased ICP, whereas brain edema is induced by SBC, and increased ICP could aggravate it in the presence of SBC. Brain edema could affect neurologic deficit, but apoptosis alone may be less influential. Not only ICP but also SBC seem important for brain damage in the acute stage of SAH.

Intracranial pressure monitoring following decompressive hemicraniectomy for malignant cerebral infarction

Randomized controlled trials have demonstrated the efficacy of decompressive craniectomy in substantially decreasing mortality and improving functional outcome in middle cerebral artery infarction. The role of intracranial pressure (ICP) monitoring following decompressive craniectomy for stroke has not been well studied. We present a retrospective review of our experience with postoperative ICP monitoring in 12 stroke patients who underwent decompressive craniectomy. All elevations of ICP above a 20mmHg threshold were noted. ICP was recorded for 1417 hours during which 68 ICP elevations were seen. Nine out of 12 patients had events of raised ICP, including eight with more than three elevations. A total of 81 interventions were employed to treat elevated ICP; 71 were effective in reducing ICP below the 20mmHg threshold. The most frequent intervention was cerebrospinal fluid drainage via an external ventricular drain, which was effective in 85.4% of cases. Eleven out of 12 patients survived (92%) and attained a median modified Rankin Scale score of 4 (interquartile range 4–5) at a mean 15month follow-up. In our experience, elevated ICP may commonly occur following decompressive craniectomy for stroke. Monitoring ICP influenced postoperative management and standard measures for reducing ICP were usually effective in the current series.

The role of low intracranial pressure in the development of glaucoma in patients with Alzheimer's disease

October 22, 2013Dear Editor,We read with great interest the paper by Janssen et al. (2013)entitled ‘The vast complexityof primaryopen angle glaucoma: Dis-ease genes, risks, molecular mechanisms and pathobiology.’ Theauthors deserve appreciation for their very informative reviewarticle.However,wewishtomakeacommentconcerningtheirdis-cussion of the potential role of intracranial pressure (ICP) in Alz-heimer’s disease (AD) and glaucoma.In the last section of their paper, Janssen and colleaguesdiscuss the potential relation between primary open angle glau-coma (POAG) and AD. As the authors mention, several studieshave found an increase in the occurrence of glaucoma in AD pa-tients. The authors state: “In our view, POAG damage could becaused by the net pressure over the optic disk, involving boththe aqueous humor pressure of the eye and cerebrospinal fluid(CSF) pressure of the brain, as described above. Also, CSF pressurechanges have been described in AD (Silverberg et al., 2006).Could these pressure changes underlie a relationship betweenPOAG and AD, and at the same time explain the apparently con-flicting association studies?” Further, the authors state: “We hy-pothesize that there is a strong association between normalpressure glaucoma and late AD, since both disease stages,following the ‘net pressure on the optic disk hypothesis’,arecharacterized by one single disease mechanism: an abnormallylow ICP.”Janssen et al. (2013) thus hypothesize that low ICP may play arole in the association between glaucoma and AD. We fully agreewith the authors since our group has previously presented this hy-pothesisforthefirsttime(Wostynetal.,2008,2009a).Intwoofourearlier manuscripts published in 2008 (Wostyn et al., 2008) and2009 (Wostyn et al., 2009a), we proposed low ICP occurring inAD as a factor leading to increased risk of glaucoma. Evidence forthishypothesiswasgainedfromCSFpressuremeasurementstudiesin AD patients and patients with glaucoma. The finding of a highoccurrence of reduced CSF pressure among patients with AD(Silverberg et al., 2006; Wostyn et al., 2009b) could be linked tothe high rate of reported comorbidity between AD and glaucoma(Bayer et al., 2002; Tamura et al., 2006), since it has been shownthat CSF pressure is lower in patients with glaucoma (Berdahlet al., 2008a, 2008b; Ren et al., 2010). This could result in anabnormally high trans-lamina cribrosa pressure difference andlead to glaucomatous damage. Given this previously advanced hy-pothesis, it was a great surprise when Janssen et al. (2013) recentlyhypothesized about the potential role of low ICP in glaucoma andAD without citing our earlier work (Wostyn et al., 2008, 2009a)or making clear the relevant precedents. The authors did cite oneof our papers, one largely focused on the high occurrence rate ofglaucoma among patients with normal pressure hydrocephalus(Wostyn et al., 2010), but this paper has no direct relevance tothe above hypothesis.Sincerely yours,Peter Wostyn, MDVeva De Groot, MD, PhDDebby Van Dam, PhDKurt Audenaert, MD, PhDPeter Paul De Deyn, MD, PhDReferences

Aetiology of herniation of the hindbrain in craniosynostosis. An investigation incorporating intracranial pressure monitoring and magnetic resonance imaging.

The occurrence and extent of herniation of the hindbrain has been evaluated in a population of children with craniosynostosis by means of magnetic resonance imaging of the craniocervical junction. The role of intracranial pressure (ICP), posterior fossa size and hydrocephalus in the development of this deformity has also been assessed. Magnetic resonance imaging (Siemens Magnetom 1.5T) was reviewed in 27 cases of craniosynostosis in whom there had been no previous cranial vault surgery. The position of the cerebellar tonsils in relation to the plane of the foramen magnum was measured and an index of the size of the posterior fossa relative to the rest of the cranial vault was also calculated for each case. The presence of hydrocephalus (requiring a cerebrospinal fluid diversion procedure) was documented. In 22 of these cases overnight, subdural ICP monitoring using the Camino fibre optic device had also been performed. Herniation of the hindbrain below the plane of the foramen magnum occurred in 10 of 27 cases (37%). The level of ICP showed a significant correlation with the extent of hindbrain herniation (p < 0.001) as did small posterior fossa size (p = 0.0035). Hydrocephalus was present in 4 patients, all of whom had hindbrain herniation. The extent of hindbrain herniation did not correlate with age (p = 0.48). We propose that herniation of the hindbrain in craniosynostosis is a consequence of brain deformation occurring in response to the physical forces imposed by a combination of the anatomical deformity at the skull base and intracranial hypertension rather than a primary malformation of brain development as commonly supposed.

Relationship between chronic raised intracranial pressure and empty sella presenting hormonal disturbances

The role of intracranial pressure in the development and maintenance of the primary empty sella has been pointed out in the literature previously. The hormonal changes and clinical features have been evaluated in a 30 year-old female patient examined for a convexity meningioma and a 20 year-old patient examined for chronic hydrocephalus caused by cured meningitis. Histories and investigations revealed an empty sella turcica associated with primary amenorrhoea and delayed puberty. The removal of the convexity meningioma resulted in loss of amenorrhoea and a rise in plasma gonadotrophins. The establishment of a ventriculo-peritoneal shunt did not bring about any changes in hormonal values and clinical features except the subjective headache disappeared. The importance of consideration of intracranial causes in patients who have delayed puberty or absence of menstrual history is briefly emphasized in light of the literature. Our data also demonstrated a correlation between an increase in intracranial pressure and a deficiency of hormonal secretion by the hypophysis.

The Role of Intracranial Pressure (ICP) Monitoring after Cardio-pulmonary Resuscitation (CPR)

The Role of Intracranial Pressure (ICP) Monitoring after Cardio-pulmonary Resuscitation (CPR)

Chronic cerebral arterial spasm. The role of intracranial pressure.

The author used isolated rabbit common carotid and femoral arteries perfused at a constant pressure of 90 mm Hg to examine the variation of flow (F) with transmural pressure (TMP). When the TMP was reduced below 50 to 60 mm Hg in arteries with normal smooth muscle tone, arterial resistance increased significantly causing a reduction in flow. It is suggested that the diffuse arterial narrowing that occurs in patients with severe intracranial hypertension may be the result of a similar reduction in TMP. In the presence of active vasoconstriction, any increase in extraluminal (intracranial) pressure (ICP) resulted in a substantial increase in arterial resistance and subsequent reduction of flow. This F-TMP relationship depended only on the initial degree of constriction and was independent of the vasoconstrictor used to achieve this constriction and of the artery in which this constriction was produced. A review of the literature suggests that human cerebral arteries normally exhibit only mild constrictions in response to subarachnoid blood during the chronic phase of spasm. In the present study, a mild constriction in the absence of increased ICP or a moderate increase in ICP (45 mm Hg) in the absence of constriction produced minor reductions in arterial diameter and an average flow reduction of only 5% to 10%. However, when ICP was increased to 45 mm Hg in the presence of a mild constriction, severe arterial narrowing resulted and flow was reduced by 50%. Therefore, it is suggested that chronic arterial spasm is the result of a mild constriction which is amplified by the simultaneous occurrence of increased ICP. Phenoxybenzamine was found to be effective in reversing and preventing these contractions. The improvement in flow produced by phenoxybenzamine decreased as the TMP was reduced below 60 mm Hg. The effects of both diffuse and local spasm on cerebral blood flow are discussed.

The role of intracranial pressure in the arrest of hemorrhage in patients with ruptured intracranial aneurysm.

✓ Intracranial epidural pressure (EDP) was recorded in 29 patients admitted with ruptured saccular aneurysms, but unfit for immediate surgery. In 10 patients a total of 13 recurrent hemorrhages were recorded; the average time before rerupture was 7.7 days after the last hemorrhage. Ten of the rebleedings started from intracranial pressure levels at or below 400 mm H2O whereas three started from higher prerupture levels. The observations indicate an increasing risk of rebleeding as the epidural pressure decreases toward normal pressure. Most repeat hemorrhages are arrested at EDP levels about that of the diastolic blood pressure. The resulting reduced pressure gradient across the aneurysm wall is important in the arrest of hemorrhage and the maintenance of hemostasis. Measurement of internal carotid artery blood flow during the acute stage of recurrent hemorrhage shows marked changes in blood flow pattern. Arrest of blood flow occurred only at the end of diastole; forward flow occurred only during systole. The effect of intracranial-pressure-buffering mechanisms on the increased EDP after rupture is discussed. Activation of these mechanisms may reduce the EDP to acceptable pressure levels within minutes and should be awaited before decompressive management is considered. Continuous recording of the EDP in patients unfit for immediate aneurysm surgery is important in the selection of the optimal time for operation.