Intraoperative Ventricular Puncture

Neurosurgery ◽  
1988 ◽  
Vol 22 (6P1-P2) ◽  
pp. 1107-1109 ◽  
Author(s):  
Jonathan T. Paine ◽  
H. Hunt Batjer ◽  
Duke Samson

Abstract Modem neuroanesthetic techniques frequently provide the neurosurgeon with adequate brain relaxation for an atraumatic frontotemporal or transylvian dissection. Circumstances such as recent subarachnoid hemorrhage with brain edema and acute hydrocephalus can mandate significant frontal lobe retraction before access to cerebrospinal fluid (CSF) drainage from the basal cisterns is gained. A simple technique can give the “early” aneurysm surgeon reliable access to the frontal horn of the lateral ventricle for intraoperative drainage of CSF before brain retraction.

Neurosurgery ◽  
1982 ◽  
Vol 10 (1) ◽  
pp. 50-54 ◽  
Author(s):  
H. E. James ◽  
H. D. Wilson ◽  
J. D. Connor ◽  
J. W. Walsh

Abstract The antibiotic concentration of the fluid from either lateral ventricle was determined 104 times in 37 patients through direct ventricular puncture, external ventricular drainage (EVD). or cerebrospinal fluid shunt sampling. The patients were 1 month to 12 years old. When the patients were receiving maximal intravenous antibiotic therapy alone, the concentrations for the most part were below 5 μg/ml. whereas patients receiving an antibiotic through direct ventricular puncture, EVD. or a shunt reservoir usually had concentrations over 5 μ/ml. However, wide variations from patient to patient were found with all forms of treatment despite similar dosages. Clustering of the concentration tended to occur in each individual patient. The authors conclude that, to obtain a high concentration of an antibiotic in the ventricular fluid, one should administer it directly into the ventricle.


1984 ◽  
Vol 61 (3) ◽  
pp. 604-605 ◽  
Author(s):  
Robert Howman-Giles ◽  
Andrew McLaughlin ◽  
Ian Johnston ◽  
Ian Whittle

✓ A simple technique for the evaluation of shunt function and cerebrospinal fluid (CSF) circulation in hydrocephalic patients is described. The method utilizes clearance rates of a radionuclide tracer injected into the lateral ventricle via an indwelling frontal catheter which is separate from the shunt apparatus. This permits an accurate assessment of drainage of ventricular CSF via the shunt, or the patency of normal or alternative CSF pathways where the shunt is malfunctioning.


2008 ◽  
Vol 63 (suppl_1) ◽  
pp. ONS162-ONS167 ◽  
Author(s):  
Udaya K. Kakarla ◽  
Louis J. Kim ◽  
Steven W. Chang ◽  
Nicholas Theodore ◽  
Robert F. Spetzler

Abstract Objective: To study the safety and accuracy of ventriculostomy by neurosurgical trainees. Methods: Initial computed tomographic studies of 346 consecutive patients who underwent bedside ventriculostomy were reviewed retrospectively. Diagnosis, catheter tip location, midline shift, and procedural complications were tabulated. To analyze catheter placement, we used a new grading system: Grade 1, optimal placement in the ipsilateral frontal horn or third ventricle; Grade 2, functional placement in the contralateral lateral ventricle or noneloquent cortex; and Grade 3, suboptimal placement in the eloquent cortex or nontarget cerebrospinal fluid space, with or without functional drainage. Statistical analysis was performed using Fisher's exact test and a weighted k coefficient. Results: Diagnoses included the following: subarachnoid hemorrhage, n = 153 (44%); trauma, n = 64 (18%); intracerebral hemorrhage/intraventricular hemorrhage, n = 63 (18%); and other, n = 66 (20%). There were 266 (77%) Grade 1, 34 (10%) Grade 2, and 46 (13%) Grade 3 catheter placements. Hemorrhagic complications occurred in 17 (5%). Four patients (1.2%) were symptomatic, with two (0.6%) requiring surgery. Interand intraobserver agreement was almost perfect (k = 0.846 and 0.922, respectively) as applied to our grading system. Rates of suboptimal placement were highest in patients with midline shift (P = 0.059) and trauma (P = 0.0001). Rates of optimal placement were highest in patients with subarachnoid hemorrhage (P = 0.003) and when the catheter was placed ipsilateral to the side of midline shift (P = 0.063). Neither the resident's training experience nor the side of placement seemed to affect accuracy. Conclusion: Bedside ventriculostomy is a safe and accurate procedure for intracranial pressure monitoring and cerebrospinal fluid drainage.


1990 ◽  
Vol 122 (2) ◽  
pp. 191-200 ◽  
Author(s):  
C. G. J. Sweep ◽  
Margreet D. Boomkamp ◽  
István Barna ◽  
A. Willeke Logtenberg ◽  
Victor M. Wiegant

Abstract The effect of intracerebroventricular (lateral ventricle) administration of arginine8-vasopressin (AVP) on the concentration of β-endorphin immunoreactivity in the cerebrospinal fluid obtained from the cisterna magna was studied in rats. A decrease was observed 5 min following injection of 0.9 fmol AVP. No statistically significant changes were found 5 min after intracerebroventricular treatment of rats with 0.09 or 9 fmol. The decrease induced by 0.9 fmol AVP was of short duration and was found 5 min after treatment but not 10 and 20 min. Desglycinamide9-AVP (0.97 fmol), [pGlu4, Cyt6]-AVP-(4–9) (1.44 fmol), Nα-acetyl-AVP (0.88 fmol), lysine8-vasopressin (0.94 fmol) and oxytocin (1 fmol) when intracerebroventricularly injected did not affect the levels of β-endorphin immunoreactivity in the cerebrospinal fluid 5 min later. This suggests that the intact AVP-(1–9) molecule is required for this effect. Intracerebroventricular pretreatment of rats with the vasopressin V1-receptor antagonist d(CH2)5Tyr(Me)AVP (8.63 fmol) completely blocked the effect of AVP (0.9 fmol). In order to investigate further the underlying mechanism, the effect of AVP on the disappearance from the cerebrospinal fluid of exogenously applied β-endorphin was determined. Following intracerebroventricular injection of 1.46 pmol camel β-endorphin-(1–31), the β-endorphin immunoreactivity levels in the cisternal cerebrospinal fluid increased rapidly, and reached peak values at 10 min. The disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid then followed a biphasic pattern with calculated half-lifes of 28 and 131 min for the initial and the terminal phase, respectively. Treatment of rats with AVP (0.9 fmol; icv) during either phase (10, 30, 55 min following intracerebroventricular administration of 1.46 pmol β-endorphin-(1–31)) significantly enhanced the disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid. The data suggest that vasopressin plays a role in the regulation of β-endorphin levels in the cerebrospinal fluid by modulating clearance mechanisms via V1-receptors in the brain.


Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 921-928 ◽  
Author(s):  
Yoshihiro Yamamoto ◽  
David H. Bernanke ◽  
Robert R. Smith

Abstract The cause of chronic cerebral vasospasm after subarachnoid hemorrhage has been studied intensively, but it is still controversial whether the observable luminal narrowing should be attributed to the contraction of vascular smooth muscle cells or whether it results from some organic change in the wall. A proliferation of myointimal cells, accompanied by increased deposition of collagen, as well as myonecrosis, have been frequently observed several days after aneurysm rupture. Studies from our laboratory showed that these myointimal cells had characteristics identical to myofibroblasts. In this study, we quantitatively and morphologically examined the effect of cerebrospinal fluid on the ability of myofibroblasts to alter collagen matrices using an in vitro model. Myofibroblasts contract the collagen matrix by rearranging or compacting the framework of collagen fibers. Cerebrospinal fluid obtained from patients with recently ruptured aneurysms significantly accelerated lattice contraction, especially when the patient developed symptomatic vasospasm. This study suggests that myofibroblasts in the spastic artery can produce a contractile force that contributes to chronic vasospasm, tightening the proliferated collagen. Some unknown agent present in bloody cerebrospinal fluid accelerates the rearrangement of the collagen lattice by myofibroblasts, both of which have, until now, been considered non-contractile components.


Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Yonatan Hirsch ◽  
Joseph R Geraghty ◽  
Eitan A Katz ◽  
Jeffrey A Loeb ◽  
Fernando Testai

Introduction: The role of neuroinflammation following aneurysmal subarachnoid hemorrhage (SAH) and its relationship to outcome is the subject of many ongoing studies. The proteolytic enzyme, caspase-1, activated by the inflammasome complex, is known to contribute to numerous downstream pro-inflammatory effects. In this study, we investigated caspase-1 activity in the cerebrospinal fluid (CSF) of SAH patients and its association to outcome. Methods: SAH patients were recruited from a regional stroke referral center. CSF samples from 18 SAH subjects were collected via an external ventricular drain and obtained within 72 hours of the onset of symptoms. For control subjects, we collected the CSF from 9 patients undergoing lumbar puncture with normal CSF and normal brain MRI. Caspase-1 activity was measured using commercially available luminescence assays. SAH subjects were categorized at hospital discharge into those with good outcomes (Glasgow Outcome Scale, GOS, of 4-5) and poor outcomes (GOS of 1-3). The levels of caspase-1 activity in various groups were analyzed using Mann-Whitney and Pearson correlation tests. Caspase-1 activity was also adjusted by initial severity of bleed using analysis of covariance (ANCOVA). Results: Caspase-1 levels from SAH patients were significantly higher than that measured from the control group (mean 1.06x10-2 vs 1.90x10-3 counts per second (CPS)/μl*min), p = 0.0002). Within the SAH group, 10 patients (55.6%) had good outcomes and 8 patients (44.4%) had poor outcomes. Caspase-1 activity was significantly higher in the poor outcome group (mean 1.54x10-2 vs 1.60x10-3 CPS/μl*min), p = 0.0012). Additionally, caspase-1 activity had a statistically significant correlation with GOS score (r = -0.60; p = 0.0100). When adjusted for initial severity of bleed, the difference in caspase-1 activity in good vs. poor outcome remained significant (adjusted mean 7.10x10-3 vs. 2.54x10-2 CPS/μl*min, p=0.004). Conclusions: The inflammasome-dependent protein caspase-1 is elevated in CSF early after SAH and higher in those with poor functional outcome. Inflammasome activity therefore may serve as a novel biomarker to predict outcome shortly after aneurysm rupture.


Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Lauren Koffman ◽  
Gabor Toth ◽  
M. Shazam Hussain ◽  
Magdy Selim ◽  
Peter Rasmussen ◽  
...  

Introduction: Iron-dependent formation of reactive oxygen species has been implicated in the development of vasospasm (VSP) and neuronal injury following experimental subarachnoid hemorrhage (SAH). We report the association between unbound (“free”) iron in CSF of SAH patients and the risk of angiographic vasospasm and cerebral infarcts (CI) on neuroimaging from a recently completed pilot study. Methods: Samples of cerebrospinal fluid (CSF) were obtained on days 1, 3, and 5. A fluorometric assay that relies on an oxidation sensitive probe was used to measure redox active iron (REDOX-Fe). Ceruloplasmin (Cp) concentration and levels of malondialdehyde (MDA), a marker of lipid peroxidation were also measured. We prospectively collected and recorded demographic, clinical, and radiological data. Logistic regression and Wilcoxon Rank Sum test were used. Results: Five of 12 patients developed angiographic VSP (41.6%) and eight developed CI (66.6%). Mean REDOX-Fe was higher in patients with CI (3.96 ± 0.97 Vs. 2.77 ± 0.87 mcg/dl, p 0.07), particularly in patients with deep-seated strokes (4.56 ± 0.67 Vs. 3.35 ± 0.89, p 0.03). Levels of Cp at day 3 were lower in patients with deep strokes (34,092 ± 23,780 Vs. 86,045 ± 34,752 ng/ml, p 0.03). A trend towards higher REDOX-Fe on day 3 in patients who developed VSP (4.52 ± 1.16 Vs. 2.96 ± 0.71, p 0.07), and lower Cp levels on day 5 (45,033 ± 29,079 Vs. 63,044 ± 24,821, p 0.1) was found. Levels of MDA were higher in patients who developed CI (10.36 ± 4.36 Vs. 5.9 ± 4.2 nmol, p 0.08). Conclusions: In this preliminary study we found higher concentrations of redox active iron in CSF of SAH patients who develop deep-seated CI on neuroimaging. Evidence of increased oxidative damage correlated with development of CI. A possible association between non-protein bound iron and angiographic VSP is suggested as well. Ceruloplasmin may exert a protective effect in this setting. Further studies are needed to validate these findings.


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