Cerebral oxygen and microdialysis monitoring during aneurysm surgery: effects of blood pressure, cerebrospinal fluid drainage, and temporary clipping on infarction

2002 ◽  
Vol 96 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Rupert Kett-White ◽  
Peter J. Hutchinson ◽  
Pippa G. Al-Rawi ◽  
Marek Czosnyka ◽  
Arun K. Gupta ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Brain Tissue ◽  
Total Duration ◽  
Wilcoxon Test ◽  
Fisher Exact Test ◽  
Content Type ◽  
The Impact ◽  
Temporary Clipping ◽  
Fine Print

Object. The aim of this study was to investigate potential episodes of cerebral ischemia during surgery for large and complicated aneurysms, by examining the effects of arterial temporary clipping and the impact of confounding variables such as blood pressure and cerebrospinal fluid (CSF) drainage. Methods. Brain tissue PO2, PCO2, and pH, as well as temperature and extracellular glucose, lactate, pyruvate, and glutamate were monitored in 46 patients by using multiparameter sensors and microdialysis. Baseline data showed that brain tissue PO2 decreased significantly, below a mean arterial pressure (MAP) threshold of 70 mm Hg. Further evidence of its relationship with cerebral perfusion pressure was shown by an increase in mean brain tissue PO2 after drainage of CSF from the basal cisterns (Wilcoxon test, p < 0.01). Temporary clipping was required in 31 patients, with a mean total duration of 14 minutes (range 3–52 minutes), causing brain tissue PO2 to decrease and brain tissue PCO2 to increase (Wilcoxon test, p < 0.01). In patients in whom no subsequent infarction developed in the monitored region, brain tissue PO2 fell to 11 mm Hg (95% confidence interval 8–14 mm Hg). A brain tissue PO2 level below 8 mm Hg for 30 minutes was associated with infarction in any region (p < 0.05 according to the Fisher exact test); other parameters were not predictive of infarction. Intermittent occlusions of less than 30 minutes in total had little effect on extracellular chemistry. Large glutamate increases were only seen in two patients, in both of whom brain tissue PO2 during occlusion was continuously lower than 8 mm Hg for longer than 38 minutes. Conclusions. The brain tissue PO2 decreases with hypotension, and, when it is below 8 mm Hg for longer than 30 minutes during temporary clipping, it is associated with increasing extracellular glutamate levels and cerebral infarction.

Effect of systemic arterial hypotension on the rate of cerebrospinal fluid formation in dogs

1974 ◽  
Vol 41 (3) ◽  
pp. 350-355 ◽  
Author(s):  
Michael E. Carey ◽  
A. Richard Vela
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Mean Arterial Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Ventriculocisternal Perfusion ◽  
Fluid Formation ◽  
The Mean ◽  
Csf Production ◽  
Fine Print

✓The rate of cerebrospinal fluid (CSF) production in dogs was measured by ventriculocisternal perfusion with artificial CSF containing inulin. In normotensive animals, the average CSF production was 36 ± 6 µl/min. When the mean arterial blood pressure was reduced to 62 ± 1 mm Hg, the CSF production fell to 22 ± 5 µl/min, a 39% reduction in fluid formation. The authors briefly discuss various hypotheses to explain this reduction.

The effect of nimodipine on cerebral oxygenation in patients with poor-grade subarachnoid hemorrhage

2004 ◽  
Vol 101 (4) ◽  
pp. 594-599 ◽  
Author(s):  
Michael F. Stiefel ◽  
Gregory G. Heuer ◽  
John M. Abrahams ◽  
Stephanie Bloom ◽  
Michelle J. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Brain Tissue ◽  
Cerebral Oxygenation ◽  
Content Type ◽  
Poor Grade ◽  
Physiological Variables ◽  
Arterial Blood ◽  
End Tidal ◽  
Fine Print

Object. Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2. Methods. Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4 ± 10.9 mm Hg. The baseline MABP and CPP were 90 ± 20 and 84 ± 19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9 ± 7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5 ± 7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7 ± 11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2. Conclusions. Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.

Posttraumatic intradiploic meningoencephalocele

1996 ◽  
Vol 84 (2) ◽  
pp. 284-287 ◽  
Author(s):  
Arun-Angelo Patil ◽  
Hamid Etemadrezaie
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cerebrospinal Fluid ◽  
Magnetic Resonance ◽  
Brain Tissue ◽  
Blunt Trauma ◽  
Arachnoid Membrane ◽  
Resonance Imaging ◽  
Content Type ◽  
Parietal Area ◽  
Fine Print

✓ A case of posttraumatic intradiploic meningoencephalocele is reported. The patient presented with a progressively enlarging lump in the left parietal area approximately 8 months after a blunt trauma. Magnetic resonance imaging showed an intradiploic cyst containing cerebrospinal fluid and brain tissue. These findings were confirmed at surgery. In addition, the cyst was found to have a lining of arachnoid membrane.

Experimental intracranial hypertension due to vascular blockade

1970 ◽  
Vol 33 (2) ◽  
pp. 156-166 ◽  
Author(s):  
J. Donald McQueen ◽  
Lawrence F. Jelsma ◽  
Fernando Bacci ◽  
Isauro Pereira
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Edema ◽  
Content Type ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Pressure Transmission ◽  
Fine Print

✓ High intracranial hypertension was induced in dogs by intracarotid injections of oil. Cerebrospinal fluid pressures continued to rise as Cushing pressor responses were evoked, but were not exceeded by the blood pressure. Transmission of blood pressure through a dilated vascular bed has been suggested as the mechanism. There was no correlation between levels of cerebral edema and the rise in intracranial pressure. This increase in pressure due to vascular blockade has been differentiated from that caused by subarachnoid blockade.

Changes in extracellular potassium concentration in cortex and brain stem during the acute phase of experimental closed head injury

1981 ◽  
Vol 55 (5) ◽  
pp. 708-717 ◽  
Author(s):  
Hiroshi Takahashi ◽  
Shinya Manaka ◽  
Keiji Sano
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Low Voltage ◽  
Potassium Concentration ◽  
Control Level ◽  
Extracellular Potassium ◽  
Content Type ◽  
The Impact ◽  
The Brain ◽  
Fine Print

✓ A high potassium concentration ([K+]o) in brain tissue impedes neuronal activity, as observed in spreading cortical depression. Experimental studies were performed on mice and rats to determine the role of changes of [K+]o in cerebral concussion. In the first experiment, a 600 gm-cm impact was delivered to the vertex of the mouse skull. This impact induced arrest of spontaneous movement for 465 ± 55.9 seconds (mean ± SD), accompanied by apnea, bradycardia, and low-voltage electroencephalographic recordings (EEG). The injury was also frequently followed immediately by epilepsy. This impact induced an increase of cortical [K+]o from the control level of 4.1 ± 1.8 mM to 20–30 mM, with gradual recovery within 30 minutes to the control level. In the second experiment, an impact of 9000 gm-cm was delivered to the midline parieto-occipital area of the rat and produced concussion-like phenomena similar to those elicited in mice. This level of trauma induced a significant increase of cortical [K+]o from the control level of 4.2 ± 0.8 mM to 20–50 mM in all of the rats, and also a significant increase of brain-stem [K+]o from 3.9 ± 0.6 to 20–30 mM in 73% of the rats. In these latter rats, the impact also induced apnea and a transient elevation of blood pressure, and resulted in low-voltage EEG recordings. In 23% of the rats in which [K+]o changes in the brain stem were not significant, the impact caused a transient reduction of blood pressure. The present study disclosed that an increase of [K+]o in the cerebral cortex and also in the brain stem is an important element in the phenomenon of concussion.

Role of dural fenestrations in acute subdural hematoma

2001 ◽  
Vol 95 (2) ◽  
pp. 263-267 ◽  
Author(s):  
Joseph N. Guilburd ◽  
Gil E. Sviri
Keyword(s):  
Brain Tissue ◽  
Surgical Decompression ◽  
Acute Subdural Hematoma ◽  
Intensive Care Treatment ◽  
Content Type ◽  
Poor Outcomes ◽  
Dural Opening ◽  
The Impact ◽  
The Brain ◽  
Fine Print

Object. Patients with acute subdural hematomas (ASDHs) have higher mortality and lower functional recovery rates compared with those of other head-injured patients. Early surgical decompression and active intensive care treatment represent, so far, the best way to assist these patients. Paradoxically, one of the factors contributing to poor outcomes in cases of ASDHs could be rapid surgical decompression, owing to the severe extrusion of the brain through the craniotomy defect in response to acute brain swelling. To avoid the deleterious consequences of abrupt decompression of the subdural space with disruption of brain tissue, the authors have adopted a new surgical technique for evacuation of ASDHs. This procedure consists of creating multiple fenestrations of the dura (MFD) in a meshlike fashion and removing clots through the small dural openings that are left open, avoiding the creation of a wide dural opening and the disruption of and additional damage to brain tissue. Methods. Thirty-one patients (26 male and five female patients with a mean age of 32.5 years) harboring ASDHs were treated using this method. On admission there were 16 patients (51.5%) with Glasgow Coma Scale (GCS) scores of 3 to 5, 11 patients (35.5%) with GCS scores of 6 to 8, and four patients (12.9%) with GCS scores of 9 to 12. Postoperative computerized tomography scans of the brain revealed evacuation of more than 80% of the hematoma in 29 of 31 patients. The overall mortality rate in this group was 51.6%. Conclusions. This preliminary report of a new surgical approach for patients who have sustained ASDHs should be considered to avoid abrupt disruption of the brain and to allow the gradual and gentle release of subdural clots. This is especially important in cases in which there are severe midline shifts and a tight brain. Further clinical studies should be conducted in a more selected series to estimate the impact of this new procedure on morbidity and mortality rates.

Vascular components of cerebrospinal fluid compensation

1999 ◽  
Vol 90 (4) ◽  
pp. 752-759 ◽  
Author(s):  
Marek Czosnyka ◽  
Hugh K. Richards ◽  
Zofia Czosnyka ◽  
Stefan Piechnik ◽  
John D. Pickard
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Arterial Blood Pressure ◽  
Outflow Resistance ◽  
Content Type ◽  
Arterial Blood ◽  
New Zealand White Rabbits ◽  
Vascular Component ◽  
Resistance To Csf Outflow ◽  
Fine Print

Object. The aim of the study was to assess how cerebrospinal fluid (CSF) pressure—volume compensation depends on cerebrovascular tone.Methods. In 26 New Zealand White rabbits, intracranial pressure (ICP), arterial blood pressure, and basilar artery blood flow velocity were measured continuously. Saline was infused into the cranial subarachnoid space to assess CSF compensatory parameters: the resistance to CSF outflow, the elastance coefficient, and the amplitude of the ICP pulsatile waveform. Infusions were repeated on two different levels of CO2 concentration in the arterial blood (PaCO2), at normotension and hypotension, and after the death of the animal.An increase in PaCO2 from a mean of 27 to 48 mm Hg was accompanied by an 18% increase in the resistance to CSF outflow (p < 0.005) and a 64% increase (p < 0.05) in the elastance coefficient. A decrease in arterial blood pressure from a mean of 100 to 51 mm Hg caused a 25% decrease in CSF outflow resistance (p < 0.01) but did not affect the elastance coefficient. Postmortem, a 23% decrease in the CSF outflow resistance was associated with a 102% decrease in the elastance coefficient.Conclusions. Cerebrovascular parameters have a limited but significant impact on CSF infusion studies. The vascular component of ICP may be identified as a significant factor contributing to this phenomenon. During infusion studies, physiological parameters influencing vascular conditions should be maintained as stable as possible.

Recurrent intracranial solitary fibrous tumor with cerebrospinal fluid dissemination

2004 ◽  
Vol 101 (6) ◽  
pp. 1045-1048 ◽  
Author(s):  
Katsuyoshi Miyashita ◽  
Yutaka Hayashi ◽  
Hironori Fujisawa ◽  
Mitsuhiro Hasegawa ◽  
Junkoh Yamashita
Keyword(s):  
Cerebrospinal Fluid ◽  
Malignant Transformation ◽  
Solitary Fibrous Tumor ◽  
S100 Protein ◽  
Spinal Tumors ◽  
Content Type ◽  
Csf Dissemination ◽  
Fibrous Tumor ◽  
Fine Print ◽  
Mib 1

✓ Solitary fibrous tumor (SFT) is a benign and rare neoplasm. To date, only 37 patients with intracranial SFTs have been reported. Although a number of the tumors were recurrent and some later underwent malignant transformation, none of these lesions progressed to cerebrospinal fluid (CSF) dissemination. In this paper the authors report a case of SFT in which the lesion recurred several times and ultimately was disseminated by the CSF. The patient was a 63-year-old woman with multiple intracranial and spinal tumors. Fifteen years before this presentation, at the age of 48 she had been hospitalized for resection of a falcotentorial tumor. During the ensuing 15 years she underwent multiple surgeries and sessions of radiation therapy for recurrent lesions. The exclusive location of her tumors in the subarachnoid space at the end of this 15-year period indicate CSF dissemination of the tumor. The tumor that was resected when the patient was 48 years old and the latest resected lesion were analyzed by performing immunohistological CD34, epithelial membrane antigen, vimentin, S100 protein, and reticulin staining, and determining the MIB-1 labeling index (LI). Most of the results were identical, and both tumors were diagnosed as SFT according to a staining pattern that showed a strong and diffuse positive reaction for CD34. Nevertheless, the authors noted that the MIB-1 LI increased from less than 1% in the original tumor to 13% in the latest tumor. The increased proliferation of MIB-1 indicates that the malignant transformation could have occurred during tumor recurrence with CSF dissemination.

Evaluation of endorphin content in the CSF of patients with trigeminal neuralgia before and after Gasserian ganglion thermocoagulation

1981 ◽  
Vol 55 (6) ◽  
pp. 935-937 ◽  
Author(s):  
Giuseppe Salar ◽  
Salvatore Mingrino ◽  
Marco Trabucchi ◽  
Angelo Bosio ◽  
Carlo Semenza
Keyword(s):  
Cerebrospinal Fluid ◽  
Trigeminal Neuralgia ◽  
Control Group ◽  
Gasserian Ganglion ◽  
Content Type ◽  
Group Of Seven ◽  
Idiopathic Trigeminal Neuralgia ◽  
Significant Difference ◽  
Before And After ◽  
Fine Print

✓ The β-endorphin content in cerebrospinal fluid (CSF) was evaluated in 10 patients with idiopathic trigeminal neuralgia during medical treatment (with or without carbamazepine) and after selective thermocoagulation of the Gasserian ganglion. These values were compared with those obtained in a control group of seven patients without pain problems. No statistically significant difference was found between patients suffering from trigeminal neuralgia and those without pain. Furthermore, neither pharmacological treatment nor surgery changed CSF endorphin values. It is concluded that there is no pathogenetic relationship between trigeminal neuralgia and endorphins.

Acquired Chiari I malformation secondary to spontaneous spinal cerebrospinal fluid leakage and chronic intracranial hypotension syndrome in seven cases

1998 ◽  
Vol 88 (2) ◽  
pp. 237-242 ◽  
Author(s):  
John L. D. Atkinson ◽  
Brian G. Weinshenker ◽  
Gary M. Miller ◽  
David G. Piepgras ◽  
Bahram Mokri
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Hypotension ◽  
Chiari I Malformation ◽  
Csf Leak ◽  
Cerebrospinal Fluid Leakage ◽  
Content Type ◽  
Intracranial Hypotension Syndrome ◽  
Csf Leakage ◽  
Chiari I ◽  
Fine Print

Object. Spontaneous spinal cerebrospinal fluid (CSF) leakage with development of the intracranial hypotension syndrome and acquired Chiari I malformation due to lumbar spinal CSF diversion procedures have both been well described. However, concomitant presentation of both syndromes has rarely been reported. The object of this paper is to present data in seven cases in which both syndromes were present. Three illustrative cases are reported in detail. Methods. The authors describe seven symptomatic cases of spontaneous spinal CSF leakage with chronic intracranial hypotension syndrome in which magnetic resonance (MR) images depicted dural enhancement, brain sagging, loss of CSF cisterns, and acquired Chiari I malformation. Conclusions. This subtype of intracranial hypotension syndrome probably results from chronic spinal drainage of CSF or high-flow CSF shunting and subsequent loss of brain buoyancy that results in brain settling and herniation of hindbrain structures through the foramen magnum. Of 35 cases of spontaneous spinal CSF leakage identified in the authors' practice over the last decade, MR imaging evidence of acquired Chiari I malformation has been shown in seven. Not to be confused with idiopathic Chiari I malformation, ideal therapy requires recognition of the syndrome and treatment directed to the site of the spinal CSF leak.

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