Recent research into the nature of cerebrospinal fluid formation and absorption

1983 ◽  
Vol 59 (3) ◽  
pp. 369-383 ◽  
Author(s):  
J. Gordon McComb

✓ Recent information regarding the nature of bulk cerebrospinal fluid formation and absorption is reviewed, integrated with previous knowledge, and applied to the clinical setting.

1974 ◽  
Vol 41 (3) ◽  
pp. 350-355 ◽  
Author(s):  
Michael E. Carey ◽  
A. Richard Vela

✓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.


1980 ◽  
Vol 53 (5) ◽  
pp. 652-655 ◽  
Author(s):  
K. Gwan Go ◽  
Gerald M. Hochwald ◽  
Lenie Koster-Otte ◽  
Annie K. van Zanten ◽  
Mysore Gandhi

✓ The net contribution of vasogenic brain edema to cerebrospinal fluid (CSF) formation was studied by ventriculocisternal perfusion. Individual cats were perfused both before and 2 ½ hours after a severe cold-induced injury to the cerebral cortex, and the results were compared. Although the edema had occupied the larger part of the hemispheric white matter and bordered the lateral ventricle, a decrease rather than an increase in CSF formation rate was observed. This decrease was related to a decrease in the cerebral perfusion pressure by a regression equation that was not affected by the cold injury.


1976 ◽  
Vol 44 (6) ◽  
pp. 735-739 ◽  
Author(s):  
Thomas H. Milhorat ◽  
Mary K. Hammock ◽  
Techen Chien ◽  
Donald A. Davis

✓ A ventricular perfusion technique was used to determine the rate of cerebrospinal fluid (CSF) formation in a 5-year-old child who had undergone bilateral choroid plexectomy for communicating hydrocephalus during infancy. At the time of the study, the patient had a failed ventriculoperitoneal shunt and was suffering from progressive ventriculomegaly. The calculated rate of CSF formation, 0.35 ml/min, ± 0.02 standard deviation, was within normal limits.


1972 ◽  
Vol 37 (2) ◽  
pp. 177-181 ◽  
Author(s):  
Michael D. F. Deck ◽  
V. Deonarine ◽  
D. Gordon Potts

✓ Experiments were performed on dogs to estimate the effect of intraventricular air on the rate of cerebrospinal fluid formation. The rate of formation was measured satisfactorily in eight beagle dogs before and after the introduction of air using ventriculocisternal perfusion of artificial cerebrospinal fluid containing 14C-labelled inulin. Statistical analysis of rates of cerebrospinal fluid formation estimated half hourly indicated that there was little or no change after the introduction of air.


1975 ◽  
Vol 42 (6) ◽  
pp. 674-678 ◽  
Author(s):  
Warren E. Lux ◽  
Joseph D. Fenstermacher

✓ The authors perfused rhesus monkeys from lateral ventricles to lumbar sac with an artificial cerebrospinal fluid (CSF) containing a Blue Dextran 2000 marker. Analysis of marker dilution at steady state showed ventricular CSF formation occurring at a rate of 28.3 ± 2.5 µ1/min. No significant CSF formation was found in the spinal subarachnoid space.


1972 ◽  
Vol 36 (3) ◽  
pp. 276-282 ◽  
Author(s):  
Osamu Sato ◽  
Takahiko Asai ◽  
Yoshiyuki Amano ◽  
Makoto Hara ◽  
Ryuichi Tsugane ◽  
...  

✓ The spinal subarachnoid space of the dog was perfused with an artificial cerebrospinal fluid containing inulin as a tracer. The experimental procedures were based upon the concept that the decrease in inulin concentration occurring during the perfusion was exclusively a function of the volume of newly formed cerebrospinal fluid in the system.


2004 ◽  
Vol 101 (6) ◽  
pp. 1045-1048 ◽  
Author(s):  
Katsuyoshi Miyashita ◽  
Yutaka Hayashi ◽  
Hironori Fujisawa ◽  
Mitsuhiro Hasegawa ◽  
Junkoh Yamashita

✓ 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.


1981 ◽  
Vol 55 (6) ◽  
pp. 935-937 ◽  
Author(s):  
Giuseppe Salar ◽  
Salvatore Mingrino ◽  
Marco Trabucchi ◽  
Angelo Bosio ◽  
Carlo Semenza

✓ 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.


1998 ◽  
Vol 88 (2) ◽  
pp. 237-242 ◽  
Author(s):  
John L. D. Atkinson ◽  
Brian G. Weinshenker ◽  
Gary M. Miller ◽  
David G. Piepgras ◽  
Bahram Mokri

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.


1981 ◽  
Vol 55 (6) ◽  
pp. 877-883 ◽  
Author(s):  
Lennart Brandt ◽  
Bengt Ljunggren ◽  
Karl-Erik Andersson ◽  
Bengt Hindfelt ◽  
Tore Uski

✓ In small human cerebral arteries preincubated with indomethacin, contractions induced by cerebrospinal fluid (CSF), from patients with subarachnoid hemorrhage were markedly increased. Also contractions induced by noradrenaline, but not 5-hydroxytryptamine, were augmented. Prostacyclin and its metabolite 6-keto-prostaglandin (PG)E1 reversed the contractions induced by CSF, as well as by noradrenaline, 5-hydroxytryptamine, and PGF2α. The findings suggest that these substances are able to counteract the influence of vasoconstrictor material in hemorrhagic CSF. If the capacity to synthesize these “protective” arachidonic acid metabolites is reduced, the resulting imbalance between contractile and relaxant forces acting on the vessel wall may lead to sustained cerebral vasoconstriction.


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