scholarly journals Spinal cerebrospinal fluid flow is increased in rats with elevated intracranial pressure 18 hours after cortical ischaemic stroke

2020 ◽  
Author(s):  
Steven William Bothwell ◽  
Daniel Omileke ◽  
Debbie-Gai Pepperall ◽  
Adjanie Patabendige ◽  
Neil J Spratt
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Infarct Volume ◽  
Compensatory Mechanism ◽  
Tracer Transport ◽  
Cerebrospinal Fluid Flow ◽  
Post Stroke ◽  
Spinal Subarachnoid Space ◽  
Infarct Expansion ◽  
Underlying Mechanisms

Abstract Background A dramatic oedema-independent intracranial pressure (ICP) rise occurs 24 hours post-stroke in rats and may explain infarct expansion. Underlying mechanisms of this rise are unknown but evidence suggests cerebrospinal fluid (CSF) dynamics are involved. Methods We investigated how CSF flow changes post-stroke and how this relates to ICP by infusing CSF tracer into the lateral ventricles of rats and assessing transport time and total tracer transport to the spinal subarachnoid space over a 90 minute period. Results Stroke animals with ICP rise had faster tracer transit when compared with stroke animals without ICP rise (27.6 ± 4, n = 6, vs 48.6 ± 4.5 mins, n = 6) or animals subjected to a sham procedure (47.9 ± 4 mins, n = 8), F(2,17) = 0.1, p≤0.01. There was a correlation between tracer transit time and ΔICP (R = -0.52, p=0.02) and infarct volume (R = -0.6, p=0.04). There was no difference in total tracer observed. Conclusions Faster tracer transit in stroke animals may be explained by impairment of other CSF outflow pathways, whereby, spinal drainage acts as a compensatory mechanism. Investigation into the disruption of other CSF drainage routes post-stroke may offer insight into the underlying mechanisms of infarct expansion post-stroke.

scholarly journals Altered Cerebrospinal Fluid Clearance and Increased Intracranial Pressure in Rats 18 h After Experimental Cortical Ischaemia

2021 ◽  
Vol 14 ◽  
Author(s):  
Steven W. Bothwell ◽  
Daniel Omileke ◽  
Rebecca J. Hood ◽  
Debbie-Gai Pepperall ◽  
Sara Azarpeykan ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Lymph Nodes ◽  
Subarachnoid Space ◽  
Ex Vivo ◽  
Bimodal Distribution ◽  
Cervical Lymph Nodes ◽  
Post Stroke ◽  
Spinal Subarachnoid Space

Oedema-independent intracranial pressure (ICP) rise peaks 20–22-h post-stroke in rats and may explain early neurological deterioration. Cerebrospinal fluid (CSF) volume changes may be involved. Cranial CSF clearance primarily occurs via the cervical lymphatics and movement into the spinal portion of the cranio-spinal compartment. We explored whether impaired CSF clearance at these sites could explain ICP rise after stroke. We recorded ICP at baseline and 18-h post-stroke, when we expect changes contributing to peak ICP to be present. CSF clearance was assessed in rats receiving photothrombotic stroke or sham surgery by intraventricular tracer infusion. Tracer concentration was quantified in the deep cervical lymph nodes ex vivo and tracer transit to the spinal subarachnoid space was imaged in vivo. ICP rose significantly from baseline to 18-h post-stroke in stroke vs. sham rats [median = 5 mmHg, interquartile range (IQR) = 0.1–9.43, n = 12, vs. −0.3 mmHg, IQR = −1.9–1.7, n = 10], p = 0.03. There was a bimodal distribution of rats with and without ICP rise. Tracer in the deep cervical lymph nodes was significantly lower in stroke with ICP rise (0 μg/mL, IQR = 0–0.11) and without ICP rise (0 μg/mL, IQR = 0–4.47) compared with sham rats (4.17 μg/mL, IQR = 0.74–8.51), p = 0.02. ICP rise was inversely correlated with faster CSF transit to the spinal subarachnoid space (R = −0.59, p = 0.006, Spearman’s correlation). These data suggest that reduced cranial clearance of CSF via cervical lymphatics may contribute to post-stroke ICP rise, partially compensated via increased spinal CSF outflow.

scholarly journals Decreased Intracranial Pressure Elevation and Cerebrospinal Fluid Outflow Resistance: A Potential Mechanism of Hypothermia Cerebroprotection Following Experimental Stroke

2021 ◽  
Vol 11 (12) ◽  
pp. 1589
Author(s):  
Daniel Omileke ◽  
Steven W. Bothwell ◽  
Debbie Pepperall ◽  
Daniel J. Beard ◽  
Kirsten Coupland ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Ischaemic Stroke ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Experimental Stroke ◽  
Outflow Resistance ◽  
Hypothermia Treatment ◽  
Post Stroke ◽  
Intracranial Pressure Elevation

Background: Elevated intracranial pressure (ICP) occurs 18–24 h after ischaemic stroke and is implicated as a potential cause of early neurological deterioration. Increased resistance to cerebrospinal fluid (CSF) outflow after ischaemic stroke is a proposed mechanism for ICP elevation. Ultra-short duration hypothermia prevents ICP elevation 24 h post-stroke in rats. We aimed to determine whether hypothermia would reduce CSF outflow resistance post-stroke. Methods: Transient middle cerebral artery occlusion was performed, followed by gradual cooling to 33 °C. At 18 h post-stroke, CSF outflow resistance was measured using a steady-state infusion method. Results: Hypothermia to 33 °C prevented ICP elevation 18 h post-stroke (hypothermia ∆ICP = 0.8 ± 3.6 mmHg vs. normothermia ∆ICP = 4.4 ± 2.0 mmHg, p = 0.04) and reduced infarct volume 24 h post-stroke (hypothermia = 78.6 ± 21.3 mm3 vs. normothermia = 108.1 ± 17.8 mm3; p = 0.01). Hypothermia to 33 °C did not result in a significant reduction in CSF outflow resistance compared with normothermia controls (0.32 ± 0.36 mmHg/µL/min vs. 1.07 ± 0.99 mmHg/µL/min, p = 0.06). Conclusions: Hypothermia treatment was protective in terms of ICP rise prevention, infarct volume reduction, and may be implicated in CSF outflow resistance post-stroke. Further investigations are warranted to elucidate the mechanisms of ICP elevation and hypothermia treatment.

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

Mumps as a Cause of Hydrocephalus

PEDIATRICS ◽  
1972 ◽  
Vol 50 (2) ◽  
pp. 346-347
Author(s):  
J. Hower ◽  
H. E. Clar ◽  
M. Düchting
Keyword(s):  
Cerebrospinal Fluid ◽  
Fluid Flow ◽  
Intracranial Pressure ◽  
Head Circumference ◽  
Aqueductal Stenosis ◽  
Sudden Increase ◽  
Increased Intracranial Pressure ◽  
Cerebrospinal Fluid Flow ◽  
Human Pathology ◽  
Experimental Findings

We read Dr. Bray's communication with great interest. With actually three cases of aqueductal stenosis after mumps being recorded we cannot doubt that the experimental findings of Johnson and Johnson have a bearing on human pathology. Our patient, a 6½-year-old boy, underwent evaluation of his megacephalus five months before the onset of mumps. At that time a pneumoencephalogram could be obtained by lumbar filling. Cerebrospinal fluid flow was considered marginally adequate. Three months after mumps meningoencephalitis the patient presented with symptoms of increased intracranial pressure (papilledema, sudden increase in head circumference, and widening of the coronar suture).

Management of proximal shunt obstruction

1988 ◽  
Vol 68 (5) ◽  
pp. 817-819 ◽  
Author(s):  
Charles C. Duncan
Keyword(s):  
Cerebrospinal Fluid ◽  
Fluid Flow ◽  
Intracranial Pressure ◽  
Signs And Symptoms ◽  
Ventricular Catheter ◽  
Shunt Failure ◽  
Content Type ◽  
Cerebrospinal Fluid Flow ◽  
Shunt Obstruction ◽  
Fine Print

✓ Proximal shunt obstruction or obstruction of the ventricular catheter may present with signs and symptoms of shunt failure with either no cerebrospinal fluid flow or a falsely low intracranial pressure (ICP) upon shunt tap. The author reports a technique for lowering the ICP and for measuring the pressure in patients with such obstruction by cannulation of the reservoir and ventricular catheter to penetrate into the ventricle with a 3½-in. No. 22 spinal needle. The findings in 20 cases in which this approach was utilized are summarized.

Three-Dimensional Computational Modeling of Subject-Specific Cerebrospinal Fluid Flow in the Subarachnoid Space

2008 ◽  
Vol 131 (2) ◽  
Author(s):  
Sumeet Gupta ◽  
Michaela Soellinger ◽  
Peter Boesiger ◽  
Dimos Poulikakos ◽  
Vartan Kurtcuoglu
Keyword(s):  
Fluid Dynamics ◽  
Computational Fluid Dynamics ◽  
Cerebrospinal Fluid ◽  
Subarachnoid Space ◽  
Three Dimensional ◽  
Volumetric Flow Rate ◽  
Cerebrospinal Fluid Flow ◽  
Spinal Subarachnoid Space ◽  
Subject Specific ◽  
Foramen Of Luschka

This study aims at investigating three-dimensional subject-specific cerebrospinal fluid (CSF) dynamics in the inferior cranial space, the superior spinal subarachnoid space (SAS), and the fourth cerebral ventricle using a combination of a finite-volume computational fluid dynamics (CFD) approach and magnetic resonance imaging (MRI) experiments. An anatomically accurate 3D model of the entire SAS of a healthy volunteer was reconstructed from high resolution T2 weighted MRI data. Subject-specific pulsatile velocity boundary conditions were imposed at planes in the pontine cistern, cerebellomedullary cistern, and in the spinal subarachnoid space. Velocimetric MRI was used to measure the velocity field at these boundaries. A constant pressure boundary condition was imposed at the interface between the aqueduct of Sylvius and the fourth ventricle. The morphology of the SAS with its complex trabecula structures was taken into account through a novel porous media model with anisotropic permeability. The governing equations were solved using finite-volume CFD. We observed a total pressure variation from −42Pato40Pa within one cardiac cycle in the investigated domain. Maximum CSF velocities of about 15cm∕s occurred in the inferior section of the aqueduct, 14cm∕s in the left foramen of Luschka, and 9cm∕s in the foramen of Magendie. Flow velocities in the right foramen of Luschka were found to be significantly lower than in the left, indicating three-dimensional brain asymmetries. The flow in the cerebellomedullary cistern was found to be relatively diffusive with a peak Reynolds number (Re)=72, while the flow in the pontine cistern was primarily convective with a peak Re=386. The net volumetric flow rate in the spinal canal was found to be negligible despite CSF oscillation with substantial amplitude with a maximum volumetric flow rate of 109ml∕min. The observed transient flow patterns indicate a compliant behavior of the cranial subarachnoid space. Still, the estimated deformations were small owing to the large parenchymal surface. We have integrated anatomic and velocimetric MRI data with computational fluid dynamics incorporating the porous SAS morphology for the subject-specific reconstruction of cerebrospinal fluid flow in the subarachnoid space. This model can be used as a basis for the development of computational tools, e.g., for the optimization of intrathecal drug delivery and computer-aided evaluation of cerebral pathologies such as syrinx development in syringomelia.

Normal pressure hydrocephalus

2019 ◽  
pp. 1083-1092
Author(s):  
Nicole Keong
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Fluid Flow ◽  
Surgical Management ◽  
Normal Pressure Hydrocephalus ◽  
Clinical Presentation ◽  
Normal Pressure ◽  
Cerebrospinal Fluid Flow ◽  
Underlying Mechanisms

This chapter is on normal pressure hydrocephalus (NPH) and deals with aspects from theories of pathogenesis, clinical presentation, and management, surgical management, and complications, as well as the assessment of outcome. It provides a concise overview of a challenging topic; many theories have been advanced to explain the underlying mechanisms by which the NPH syndrome develops. However, the basic pathophysiological processes still remain unclear. The major theory streams proposed for the pathogenesis of NPH can be loosely organized into structural, cerebral blood flow, and cerebrospinal fluid flow subgroups. The components of each theory stream are expanded in this chapter, although the list of studies supporting each section is by no means exhaustive.

scholarly journals Short-duration hypothermia completed prior to reperfusion prevents intracranial pressure elevation following ischaemic stroke in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Daniel Omileke ◽  
Sara Azarpeykan ◽  
Steven W. Bothwell ◽  
Debbie Pepperall ◽  
Daniel J. Beard ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Ischaemic Stroke ◽  
Short Duration ◽  
Infarct Volume ◽  
Arterial Occlusion ◽  
Reperfusion Therapy ◽  
Artery Occlusion ◽  
Experimental Stroke ◽  
Stroke Patients ◽  
Post Stroke

AbstractReperfusion therapies re-establish blood flow after arterial occlusion and improve outcome for ischaemic stroke patients. Intracranial pressure (ICP) elevation occurs 18–24 h after experimental stroke. This elevation is prevented by short-duration hypothermia spanning the time of reperfusion. We aimed to determine whether hypothermia-rewarming completed prior to reperfusion, also prevents ICP elevation 24 h post-stroke. Transient middle cerebral artery occlusion was performed on male outbred Wistar rats. Sixty-minute hypothermia to 33 °C, followed by rewarming was induced prior to reperfusion in one group, and after reperfusion in another group. Normothermia controls received identical anaesthesia protocols. ΔICP from pre-stroke to 24 h post-stroke was measured, and infarct volumes were calculated. Rewarming pre-reperfusion prevented ICP elevation (ΔICP = 0.3 ± 3.9 mmHg vs. normothermia ΔICP = 5.2 ± 2.1 mmHg, p = 0.02) and reduced infarct volume (pre-reperfusion = 78.6 ± 23.7 mm3 vs. normothermia = 125.1 ± 44.3 mm3, p = 0.04) 24 h post-stroke. There were no significant differences in ΔICP or infarct volumes between hypothermia groups rewarmed pre- or post-reperfusion. Hypothermia during reperfusion is not necessary for prevention of ICP rise or infarct volume reduction. Short-duration hypothermia may be an applicable early treatment strategy for stroke patients prior to- during-, and after reperfusion therapy.

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