scholarly journals Intracranial pressure elevation alters CSF clearance pathways

2019 ◽  
Author(s):  
Vegard Vinje ◽  
Anders Eklund ◽  
Kent-Andre Mardal ◽  
Marie E. Rognes ◽  
Karen-Helene Støverud
Keyword(s):  
Intracranial Pressure ◽  
Mathematical Models ◽  
Subarachnoid Space ◽  
Compartment Model ◽  
Normal Pressure ◽  
Cribriform Plate ◽  
Relative Distribution ◽  
Common Procedure ◽  
Arachnoid Granulations ◽  
Intracranial Pressure Elevation

AbstractBackgroundInfusion testing is a common procedure to determine whether shunting will be beneficial in patients with normal pressure hydrocephalus. The method has a well-developed theoretical foundation and corresponding mathematical models that describe the CSF circulation from the choroid plexus to the arachnoid granulations. Here, we investigate to what extent the proposed glymphatic or paravascular pathway (or similar pathways) modifies the results of the traditional mathematical models.MethodsWe used a two-compartment model consisting of the subarachnoid space and the paravascular spaces. For the arachnoid granulations, the cribriform plate, capillaries and paravascular spaces, resistances were calculated and used to estimate flow before and during an infusion test. Next, pressure in the subarachnoid space and paravascular spaces were computed. Finally, different variations to the model were tested to evaluate the sensitivity of selected parameters.ResultsAt baseline, we found a very small paravascular flow directed into the subarachnoid space, while 60% of the fluid left through the arachnoid granulations and 40% left through the cribriform plate. However, during the infusion, paravascular flow reversed and 25% of the fluid left through these spaces, while 60% went through the arachnoid granulations and only 15% through the cribriform plate.ConclusionsThe relative distribution of CSF flow to different clearance pathways depends on intracranial pressure (ICP), with the arachnoid granulations as the main contributor to outflow. As such, ICP increase is an important factor that should be addressed when determining the pathways of injected substances in the subarachnoid space.

scholarly journals Intracranial pressure elevation alters CSF clearance pathways

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Vegard Vinje ◽  
Anders Eklund ◽  
Kent-Andre Mardal ◽  
Marie E. Rognes ◽  
Karen-Helene Støverud
Keyword(s):  
Intracranial Pressure ◽  
Mathematical Models ◽  
Subarachnoid Space ◽  
Compartment Model ◽  
Normal Pressure ◽  
Lymphatic Drainage ◽  
Cribriform Plate ◽  
Relative Distribution ◽  
Common Procedure ◽  
Arachnoid Granulations

Abstract Background Infusion testing is a common procedure to determine whether shunting will be beneficial in patients with normal pressure hydrocephalus. The method has a well-developed theoretical foundation and corresponding mathematical models that describe the CSF circulation from the choroid plexus to the arachnoid granulations. Here, we investigate to what extent the proposed glymphatic or paravascular pathway (or similar pathways) modifies the results of the traditional mathematical models. Methods We used a compartment model to estimate pressure in the subarachnoid space and the paravascular spaces. For the arachnoid granulations, the cribriform plate and the glymphatic circulation, resistances were calculated and used to estimate pressure and flow before and during an infusion test. Finally, different variations to the model were tested to evaluate the sensitivity of selected parameters. Results At baseline intracranial pressure (ICP), we found a very small paravascular flow directed into the subarachnoid space, while 60% of the fluid left through the arachnoid granulations and 40% left through the cribriform plate. However, during the infusion, 80% of the fluid left through the arachnoid granulations, 20% through the cribriform plate and flow in the PVS was stagnant. Resistance through the glymphatic system was computed to be 2.73 mmHg/(mL/min), considerably lower than other fluid pathways, giving non-realistic ICP during infusion if combined with a lymphatic drainage route. Conclusions The relative distribution of CSF flow to different clearance pathways depends on ICP, with the arachnoid granulations as the main contributor to outflow. As such, ICP increase is an important factor that should be addressed when determining the pathways of injected substances in the subarachnoid space. Our results suggest that the glymphatic resistance is too high to allow for pressure driven flow by arterial pulsations and at the same time too small to allow for a direct drainage route from PVS to cervical lymphatics.

Can Medial Temporal Impairment Be an Imaging Red Flag for Neurodegeneration in Disproportionately Enlarged Subarachnoid Space Hydrocephalus?

2021 ◽  
pp. 1-11
Author(s):  
Keita Sakurai ◽  
Daita Kaneda ◽  
Yuto Uchida ◽  
Shohei Inui ◽  
Masahiko Bundo ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Subarachnoid Space ◽  
Lewy Bodies ◽  
Normal Pressure ◽  
Temporal Horn ◽  
Red Flag ◽  
Argyrophilic Grain ◽  
Magnetic Resonance Imaging Mri ◽  
Specific Symptoms ◽  
Multiple Cerebral Infarctions

Background: The differentiation of idiopathic normal pressure hydrocephalus (iNPH) from neurodegenerative diseases such as Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB) is often challenging because of their non-specific symptoms. Therefore, various neuroradiological markers other than ventriculomegaly have been proposed. Despite the utility of disproportionately enlarged subarachnoid-space hydrocephalus (DESH) for the appropriate selection of shunt surgery candidates, the specificity and neuropathology of this finding have not been sufficiently evaluated. Objective: Investigation of the clinicopathological features and comparison of the neuroradiological findings between DESH with postmortem neuropathological diagnoses (pDESH) and clinically-diagnosed iNPH (ciNPH) patients are the main purposes of this study. Method: In addition to the retrospective evaluation of clinicopathological information, quantitative, semiquantitative, and qualitative magnetic resonance imaging (MRI) indices were compared between pathologically-investigated 10 patients with pDESH and 10 patients with ciNPH Results: Excluding one patient with multiple cerebral infarctions, the postmortem neuropathological diagnoses of the pathologically-investigated patients were mainly neurodegenerative diseases (five AD, one DLB with AD pathologies, one DLB, one argyrophilic grain disease, and one Huntington’s disease). In addition to the common neuroradiological features Conclusion: Hippocampal atrophy and deformation with temporal horn enlargement seem to be characteristic neuroradiological findings of long-standing severely demented patients with DESH and neurodegenerative diseases, mainly advanced-stage AD.

Increased Intracranial Pressure

1981 ◽  
Vol 2 (9) ◽  
pp. 269-276
Author(s):  
John F. Griffith ◽  
Jimmy C. Brasfield
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Subarachnoid Space ◽  
Buffering Capacity ◽  
Raised Intracranial Pressure ◽  
Cranial Cavity ◽  
Increased Intracranial Pressure ◽  
Underlying Process ◽  
Spinal Subarachnoid Space ◽  
Rate Of Absorption

The infant or child with increasing pressure within the cranial cavity must be identified early and treated promptly in order to prevent serious complications or death. When the pressure elevation is gradual it is frequently well tolerated, and the patient may seem deceptively well. There is a critical point, however, beyond which any further increase in pressure leads to a catastrophic deterioration in the patient's condition.1 When this occurs, the outlook for quality survival is poor despite the best therapy. Unfortunately, this can occur when the underlying process is benign and would have been reversible if recognized and treated promptly. For prompt recognition and treatment, the physician must be familiar with the pathophysiology of raised intracranial pressure. PATHOPHYSIOLOGY The intracranial compartment contains blood vessels, cerebrospinal fluid (CSF), brain, and leptomeninges which include the rigid dural membranes forming the falx and tentorium. Whenever there is an increase in the volume of any one of these intracranial components (brain, CSF, blood) there must be a corresponding reduction in the size of the others in order for the intracranial pressure to remain normal. This type of compensation or buffering capacity is particularly important in the early stages of intracranial disease. As the pressure mounts from any type of mass lesion, the CSF is displaced caudally into the spinal subarachnoid space and there is a corresponding increase in the rate of absorption of CSF.2

Controlled Evaluation of Muscle Relaxation in the Ventilated Neonate

PEDIATRICS ◽  
1981 ◽  
Vol 67 (5) ◽  
pp. 641-646
Author(s):  
N. N. Finer ◽  
P. M. Tomney
Keyword(s):  
Birth Weight ◽  
Intracranial Pressure ◽  
Low Birth Weight ◽  
Muscle Relaxation ◽  
Control Period ◽  
Pancuronium Bromide ◽  
Intracranial Pressure Elevation ◽  
Controlled Evaluation ◽  
And Control ◽  
Inspiratory Oxygen

To assess the effects of muscle relaxation on the critically ill ventilated neonate, pancuronium bromide was administered for a 12-hour period to ten low-birth-weight neonates (960 to 2,000 gm) of 26 to 34 weeks gestation, all of whom required mechanical ventilation and were studied within 48 hours of birth (six to 39 hours). The infants were also studied for a 12-hour period during which no pancuronium bromide was administered. During both study periods, the order of which was randomized, heart rate, blood pressure, Po2, and intracranial pressure were continuously measured. The amounts of handling during the pancuronium and control periods were similar. The results revealed a significantly greater duration of hypoxia (P02 < 50 torr) (56.1 vs 23.6 minutes, P < .001) and hyperoxia (Po2 > 70 torr) during the control period (92.5 vs 13 minutes, P < .001). Durations of intracranial pressure elevation 10 cm H2O above the infant's baseline were significantly less during paralysis (6.7 vs 58.8 minutes, P < .001) as were spikes of intracranial pressure to greater than 25 cm H2O (1.6 vs 24.4, P < .05). There was no significant improvement in blood gas values, fractional inspiratory oxygen, or ventilator settings during muscle relaxation. Pancuronium reduced periods of nonoptimal oxygenation and elevated intracranial pressure and may therefore help to decrease adverse sequelae for the low-birth-weight, ventilated neonate.

Abstract W P211: Investigating the Cause for “Collateral Failure” in Stroke-in-Progression: Intracranial Pressure Elevation Reduces Flow Through Collateral Vessels

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Daniel Beard ◽  
Damian McLeod ◽  
Neil J Spratt
Keyword(s):  
Intracranial Pressure ◽  
Flow Velocity ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Minor Stroke ◽  
Collateral Flow ◽  
Mca Occlusion ◽  
Intracranial Pressure Elevation ◽  
Flow Through ◽  
Collateral Vessels

Background: Adequacy of the collateral circulation is a major determinant of outcome in stroke patients. Recent human imaging data indicates that collateral failure, rather than reperfusion-reocclusion is the most common cause for early progression in minor stroke. Our previous experimental data shows that intracranial pressure (ICP) rises transiently 24 h after even minor stroke. Herein, we investigated the effect of ICP manipulation on blood flow through collateral vessels during MCA occlusion. Methods: We developed and validated a method to quantify flow velocity and vessel diameter of anterior-middle cerebral artery (ACA-MCA) leptomeningeal collaterals in rats during stroke, using fluorescent microspheres. BIood flow velocity and diameter was quantified in individual collateral vessels and used to calculate absolute flow during MCA occlusion and reperfusion (n = 6). In separate experiments, ICP was increased after MCA occlusion by fluid infusion into the lateral ventricles and effects on relative collateral flow were determined (n = 4). Results: In vitro validation indicated accurate flow quantification (R 2 = 0.99, P<0.0001). Collateral flow was seen to switch from bidirectional to unidirectional flow (toward occluded vessel) and increase by 595 ± 134 % within 10 min of vessel occlusion. Direction and flow changes were variable after MCA reperfusion, however there was a mean flow reduction of 52 ± 15 % by 5 mins. Artificially elevating ICP during MCA occlusion caused a reduction of cerebral perfusion pressure which was strongly correlated with collateral flow reduction (R 2 = 0.90, p<0.0001). Discussion: Our method permits real time quantification of flow through individual collateral vessels during stroke and reperfusion. Intracranial pressure elevation reduced collateral flow, proportional to its effect on cerebral perfusion pressure. Coupled with our previous data indicating significant ICP elevation after even minor stroke, this suggests that transient ICP elevation is the possible cause of the collateral failure recently described in patients with stroke-in-progression.

Serial Lumbar Punctures for at Least Temporary Amelioration of Neonatal Posthemorrhagic Hydrocephalus

PEDIATRICS ◽  
1985 ◽  
Vol 75 (4) ◽  
pp. 719-724
Author(s):  
Katherine L. Kreusser ◽  
Theodore J. Tarby ◽  
Edward Kovnar ◽  
Donald A. Taylor ◽  
Alan Hill ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Lumbar Puncture ◽  
Subarachnoid Space ◽  
Ventricular Size ◽  
Anterior Fontanel ◽  
Posthemorrhagic Hydrocephalus ◽  
Before And After ◽  
Cranial Ultrasonography ◽  
Lumbar Subarachnoid Space

Serial lumbar punctures for the management of neonatal posthemorrhagic hydrocephalus without intracranial hypertension were evaluated in 16 infants. Cranial ultrasonography to evaluate ventricular size and the Ladd monitor at the anterior fontanel to measure intracranial pressure were utilized immediately before and after lumbar puncture. In 12 patients, a decrease in ventricular size and in anterior fontanel pressure could be effected with each lumbar puncture. In these infants, cessation of progression of the hydrocephalus and intermittent decreases in ventricular size were accomplished. In four patients, lumbar punctures were not successful in decreasing ventricular size or lowering intracranial pressure. Two criteria could be defined to determine whether lumbar puncture could provide at least temporary benefit for the treatment of posthemorrhagic hydrocephalus. The first of these is to establish the presence of communication between lateral ventricles and lumbar subarachnoid space by effecting a decrease in ventricular size and a decrease in intracranial pressure by removal of CSF. The second criterion is to ascertain a critical volume of CSF (usually relatively large) that must be removed in order to effect the above changes. Cranial ultrasonography and measurement of intracranial pressure by application of the Ladd monitor to the anterior fontanel are extremely valuable in the evaluation of lumbar punctures in the management of posthemorrhagic hydrocephalus.

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