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[Production and absorption rate of cerebrospinal fluid in the spinal subarachnoid space of the dog (author's transl)].

Adult mongrel dogs, weighing 10-17 kg. were anesthetized with Nembutal and cervical and lumbosacral laminectomy was performed. The spinal subarachnoid space was blocked by extradural ligation at the level of the C4 to interrupt CSF communication between the cranial and spinal space. Polyethylene catheters were placed in the cervical and lumbosacral subarachnoid space, and artificial Mock CSF buffer, pH 7.35-7.40, containing inulin of 25 mg/dl or 14C-inulin of 1.5-2 muCi/dl as a tracer was perfused in the sacro-cervical direction through the catheter. After a steady state of perfusion was acommplished, the CSF was collected from the outlet catheter. Production and absorption rate of the CSF were calculated after Pappenheimer and Heisey's equation. 1) Effects of CSF pressure on the rate of production (Vf) and absorption (Va) of CSF and on the difference between outflow fluid rate (Vo) and inflow fluid rate (Vi) were studied within the pressure range of -100 to +600 mmH2O. Then, regression lines were calculated by means of the least square method. See Article. Vf was little affected by changes in CSF pressure, while Va increased linearly as CSF pressure elevated. This suggests that the spinal subarachnoid space plays an important role as a site of CSF absorption when the intracranial pressure increases. Vo-Vi, that is difference between absorption and production rate, decreased linearly as the CSF pressure increased. 2) Under a constant CSF pressure of +200 mmH2O, the effects of glucocorticoids (dexamethasone, 0.25 mg/kg and hydrocortisone, 4.15 mg/kg) and a carbonic anhydrase inhibitor (acetazolamide, 10 mg/kg) upon the production and absorption rate of CSF were determined 1/2, 1, 2 and 3 hours after intravenous administration. a) Effect of dexamethasone: The rate of CSF production was reduced to 60.5 +/- 2.4% (p less than 0.001) of the control level. The absorption rate of CSF also decreased to 59.2 +/- 6.09% (p less than 0.001) of the control. b) Effect of hydrocortisone: The production rate of CSF decreased to 67.4 +/- 6.61% (p less than 0.001), and the absorption rate to 76.5 +/- 3.94% (p less than 0.001) of the control level. c) Effect of acetazolamide: The production and absorption rate also decreased to 57.2 +/- 5.61% (p less than 0.001) and to 56.9 +/- 7.02% (p less than 0.001), respectively. 3) Pentration of tritiated dexamethasone and tritiated hydrocortisone from plasma to CSF. The penetration of tritiated dexamethasone and tritiated hydrocortisone from plasma to CSF in the spinal and cranial subarachnoid space was observed after the intravenous administration. The CSF/Plasma ratio of dexamethasone was 30.9% at 15 minutes and gradually increased to 91.5% and 93.5%, respectively, in the cranial and spinal CSF at 3 hours after the injection.

Acetazolamide↗

Perfusion of the subarachnoid space in cadavers: a technique applicable for prevention of paraplegia in surgery of the thoracic aorta.

BACKGROUND: No safe technique of subarachnoid perfusion during thoracoabdominal aneurysm surgery has been described. We tested the hypothesis that in cold cadavers, perfusion of the subarachnoid space at the lumbar level with warm solution is feasible and increases the temperature at the thoracic level without an increase in cerebrospinal fluid (CSF) pressure. METHODS: Six cadavers were used. A 5 Fr silastic catheter in the subarachnoid space between the second and third lumbar vertebra (L2-3) was used as an inflow and a 16-gauge catheter at L4-5 as an outflow. Normal saline at 38 degrees C was infused at 999 mL/h. Temperatures of inflow and outflow, of the thoracic subarachnoid space (T8), and of the cisterna magna, were recorded. CSF pressures were measured from the outflow catheter. RESULTS: Outflow temperature was 9+/-1 degrees C at 10 minutes. At 15 minutes it was 27+/-4 degrees C, and thoracic subarachnoid temperatures was 22+/-5 degrees C. There was no statistical difference between the temperatures recorded at 10 and 15 minutes. The temperature of the cisterna magna was 8.5+/-1.2 degrees C at 15 minutes, significantly higher than the baseline (p=0.01), but lower than that at the T8 level (p=0.0001). CSF pressures during the experiment did not changed significantly from baseline and remained below 10 cm H20. CONCLUSIONS: The technique described is simple to implement, and effective in changing the temperature of the subarachnoid space at the thoracic level. Whether spinal cord cooling by this technique safely reduces the risk of paraplegia remains to be established in an animal model.

Aged↗

Comparison of MR signal intensities of cerebral perivascular (Virchow-Robin) and subarachnoid spaces.

PURPOSE: The purpose of this work was to compare quantitatively the T2-weighted MR signal intensity values of the perivascular (Virchow-Robin) spaces and the cerebrospinal fluid (CSF). METHOD: Coronal 3D T2-weighted turbo spin echo MR images of the brain were evaluated in 44 subjects without any significant cerebral pathology. MR signal intensity values of the perivascular spaces around the anterior commissure and the CSF in the ventricles and the subarachnoid space were measured. RESULTS: A statistically significant difference between the mean MR signal intensity values of the perivascular spaces and the CSF both in the ventricles and in the subarachnoid space was found. The intensity values in the ventricles and in the subarachnoid space were not statistically significantly different. CONCLUSION: The perivascular spaces have a different MR signal intensity than the CSF-containing structures within and around the brain. This finding is in keeping with the statement that the perivascular spaces represent entrapments of interstitial fluid and are not the invagination of CSF-filled subarachnoid sheaths.

Cerebral Cortex↗

Cerebrospinal fluid dynamics between the intracranial and the subarachnoid space of the optic nerve. Is it always bidirectional?

CSF is thought to flow continuously from the site of production in the ventricles into interconnected spaces; i.e. cisterns and subarachnoid spaces (SASs). Since the SAS of the optic nerve is defined by a cul-de-sac anatomy, it is not evident how local CSF might recycle from that region to the general SAS. The concept of free communication of CSF has recently been challenged by the description of a concentration gradient of beta-trace protein, a lipocalin-like prostaglandin d-synthase (L-PGDS), between the spinal CSF and that in the SAS of the optic nerve, indicating diminished local clearance or local overproduction of L-PGDS here. In fact, computed cisternography with a contrast agent in three patients with idiopathic intracranial hypertension and asymmetric papilloedema demonstrate a lack of contrast-loaded CSF in the SAS of the optic nerve despite it being present in the intracranial SAS, thus suggesting compartmentation of the SAS of the optic nerve. The concept of an optic nerve compartment syndrome is further supported by a concentration gradient of brain-derived L-PGDS between the spinal CSF and the CSF from the optic nerve SAS in the same patients.

Adult↗

Non-hindbrain-related syringomyelia. Obstruction of the subarachnoid space and the central canal in rats. An experimental study.

BACKGROUND: The aim is to determine the mechanism of non-hindbrain-related syringomyelia in experimental models. The effects of obstruction of central canal and subarachnoid space on occurrence of cavities were discussed. METHODS: 31 Sprague-Dawley rats were used with eight (Group D) as a control. In 10 rats (Group A) 1.5 microl kaolin was microinjected into the dorsal columns and central gray matter of the spinal cord at the level of Th6-10. In 10 rats (Group B) 0.1 cc kaolin was injected into the subarachnoid space at the same level. In 3 rats (Group C), 1.5 microl kaolin was administered into both dorsal midline of the spinal cord and the subarachnoid space. RESULTS: In Group A, histological examination revealed cystic cavity and dilatation of the central canal in five rats; denuded ependymal line and multicystic formations in ependymal and periependymal areas in seven rats. In Group B, denuded ependymal line in three rats and microcystic formations in ependymal and periependymal areas in four rats were revealed. In Group C, there were microcystic formations in two rats and syrinx cavity in one rat. CONCLUSIONS: Developments leading to occurrence of cavities are focused on the central canal in all groups. These models indicate that the CSF-flow is from the subarachnoid space to the central canal leading to changes of cavities. In cases of obstruction of the subarachnoid space or the central canal, the occurrence of syrinx cavity initially is due to increased CSF (cerebrospinal fluid) pressure in the central canal. Flow changes in spinal cord is indicated by this study.

Animals↗

Alleviation of neuropathic pain symptoms by xenogeneic chromaffin cell grafts in the spinal subarachnoid space.

Recent data have suggested that adrenal medullary tissue allografts in the spinal cord subarachnoid space, by releasing catecholamines and opioid peptides, attenuate responses to various acute noxious stimuli and chronic pain-related behaviors. However, the application of this approach is limited by the low availability of allogeneic donor material. Alternatively, chromaffin cells from xenogeneic sources such as the bovine adrenal medulla are plentiful and simple to extract. The goal of this study was to evaluate the potential for bovine chromaffin cell xenografts in the rat spinal subarachnoid space to alleviate chronic pain. This was assessed in an animal model of neuropathic pain induced by loose ligation of the sciatic nerve, which resulted in allodynia, hyperalgesia, and skin temperature abnormalities. Two weeks after nerve injury, animals were implanted with either isolated bovine chromaffin cells or control bovine adrenal fibroblasts in the spinal subarachnoid space at the level of lumbar enlargement and immunosuppressed with cyclosporine A. In animals with chromaffin cell implants, but not fibroblast implants, both cold allodynia and thermal hyperalgesia were markedly reduced or eliminated as early as 1 week following implantation and hind paw skin temperature asymmetry was also normalized. These beneficial effects were maintained without decrement or apparent tolerance for the 9 week course of the symptomology. The analgesic effects of chromaffin cell grafts were partially attenuated following i.t. injection of naloxone and phentolamine separately and in combination, suggesting involvement of spinal opioid and alpha-adrenergic receptors. Following termination of behavioral studies, immunocytochemical analysis revealed robust survival of chromaffin cells in the implants. These results demonstrate that chromaffin cell xenografts may be effective in alleviating pain of neurogenic origin.

Adrenal Medulla↗

Metrizamide demonstration of the subarachnoid space surrounding the Gasserian ganglion.

The chance opacification of the subarachnoid space surrounding the Gasserian ganglion, observed during metrizamide basal cisternography, is reported. This is compared to similar demonstrations of the optic subarachnoid space. Such infrequently observed images should be known because they may be related to the occurrence of trigeminal neuralgia.

Adult↗

Focal spinal arachnoiditis increases subarachnoid space pressure: a computational study.

BACKGROUND: Enlarging fluid filled cystic cavitations form within the spinal cord in up to 28% of spinal cord injured patients. These post-traumatic syrinxes can cause neurological deterioration and current treatment results are unsatisfactory. Localized scar tissue (arachnoiditis) within the subarachnoid space at the level of injury has been suggested to be involved in the pathogenesis of syrinx formation. This study tests the hypothesis that pressure pulses in the subarachnoid space are accentuated adjacent to regions of arachnoiditis, which may drive fluid into the spinal cord and contribute to syrinx formation. METHODS: An axisymmetric, cylindrical computational fluid dynamics model was developed to represent the subarachnoid space under normal physiological conditions and in the presence of arachnoiditis. Cerebrospinal fluid flow into the model was estimated from magnetic resonance imaging flow studies. Arachnoiditis was modelled as a porous obstruction in the subarachnoid space. FINDINGS: Peak fluid pressures were higher above the obstruction than in the absence of obstruction. The peak pressures were strongly dependent on the permeability of the obstruction. INTERPRETATION: Elevations in subarachnoid space pressures due to arachnoiditis may facilitate fluid flow into the spinal cord, enhancing syrinx formation. This suggests that it may be worthwhile to investigate strategies that inhibit arachnoiditis or minimize systolic pressure peaks for treating or preventing syringomyelia.

Arachnoiditis↗

Microsurgical anatomy of spinal subarachnoid space.

The anatomy of the spinal subarachnoid space is reviewed with special reference to the work of Key and Retzius, the authors' own cadaver dissections, and experience from operative cases. It appears that despite some variations in the spinal arachnoid anatomy, there are many consistent features that can serve to guide the operating neurosurgeon.

Adult↗

Metrizamide CT cisternography and perioptic subarachnoid space imaging.

Opacification of the perioptic subarachnoid space (PSAS) is a normal occurrence. Opacification depends on the anatomy of the meningeal layers surrounding the optic nerves. To determine the reliability and the most efficacious technique for opacifying the PSAS, a retrospective study of 200 computed tomographic cisternography studies with water soluble contrast medium (metrizamide or iopamidol) was undertaken. Of these patients, 32.5% had opacification of the PSAS. Opacification was facilitated by examining the patients in the prone position. Demonstration of the PSAS was frequently noted in patients with empty sella and rhinorrhea.

Adult↗

Scanning electron microscopy of Acanthamoeba culbertsoni as observed in the subarachnoid space.

Scanning electron microscopy was used to study the pathogenic protozoan, Acanthamoeba culbertsoni, in the leptomeningeal subarachnoid space surrounding the spinal cord of the experimentally inoculated dog. Know to inhabit such areas as moist soils, stagnant waters, and sewage around the world, these protozoans have been identified as etiologic agents in numerous cases of meningoencephalitis. Infection occurs via a nasopharyngeal inoculation, through penetration of the olfactory mucosal epithelium and cribriform plate, into the subarachnoid space, whence it gains access to the central nervous system. Stock preparations of these amebae extracted directly from their culture medium for scanning microscopic study provided an index for their identification within the subarachnoid space and also permitted a heretofore unobserved survey of their pleomorphic surface features. From the observations of others, it had appeared that the ultimate portal of entry into the central nervous system involved some type of cytolytic process; however, this study illustrates an action of simple diapedesis in which the organisms seek a pathway of least resistance; namely the naturally-occurring pial fenestrations.

Animals↗

Induction of tolerance and withdrawal in rats receiving morphine in the spinal subarachnoid space.

Rats implanted with chronic catheters in the spinal subarachnoid space were given twice daily injections for 7 days of morphine sulfate, either intrathecally into the lumbar subarachnoid space (15 or 50 microng) or i.p. (20 mg/kg). The development of tolerance, as manifested in a reduction of the analgetic efficacy of these injections on the hot plate and tail flick, occurred in a dose dependent fashion over a period of 7 days. At this time, injections of i.p. morphine into animals which had received spinal morphine and vice versa revealed the existence of a two way cross tolerance between spinal and systemically administered morphine. Injection of naloxone into the spinal cord of animals exposed to i.p. morphine or conversely, i.p. naloxone in animals tolerant to intrathecal morphine, yielded a hyperreflexia and extreme sensitivity to handling. Other signs commonly observed in percipitated withdrawal, however, such as wet shakes and weight loss, were not observed.

Analgesics, Opioid↗

Hyperintense signal abnormality in subarachnoid spaces and basal cisterns on MR images of children anesthetized with propofol: new fluid-attenuated inversion recovery finding.

BACKGROUND AND PURPOSE: MR imaging is the method of choice for pediatric neuroimaging. Sedation is often needed to suppress patient motion and ensure diagnostic image quality, and propofol is rapidly becoming the preferred anesthetic. The purpose of this study was to document a new finding on fast fluid-attenuated inversion recovery (fast-FLAIR) MR images of children anesthetized with propofol that can be mistaken for subarachnoid space pathologic abnormality. METHODS: A retrospective analysis was conducted of 55 MR images of the brain for children who ranged in age from 1 week to 12 years. Forty-two patients received chloral hydrate, and 13 received propofol anesthetic. Multiplanar MR images were studied to detect the presence or absence of hyperintense signal (artifact) in the subarachnoid spaces and basal cisterns. The T1 values and null times of chloral hydrate, propofol, and CSF were determined in vitro at room temperature by using an inversion recovery pulse sequence at 1.5 T. RESULTS: The fast-FLAIR images of all 13 patients who received propofol had hyperintense signal abnormality. For 10 (77%) of 13 patients, this artifact was in the basal cisterns and subarachnoid spaces overlying the brain convexity. For three (23%) of 13 patients, this artifact was in the convexity region only. Two patients underwent follow-up MR imaging with a nonpropofol anesthetic agent, and the artifact resolved. None of the images of the children who received chloral hydrate had this artifact. The T1 value of chloral hydrate was 0.2 s, of propofol was 1.86 s, and of CSF was 2.32 s at room temperature. CONCLUSION: The fast-FLAIR images of children anesthetized with propofol have artifactual hyperintense signal in the basal cisterns and subarachnoid spaces, and this artifact mimics disease of the subarachnoid space. The T1 value of propofol approaches that of CSF. Depending on the chosen null time, there may be incomplete nulling of signal coming from propofol. To account for this observation, other possible causes include increased CSF pulsation in children creating motion artifact, changes in arterial oxygen concentration intrinsic to propofol or related to the supplemental oxygen normally administered, or changes in CSF protein levels related to propofol binding to proteins for uptake into CSF.

Anesthesia↗

Differential diagnosis of arachnoid cyst from subarachnoid space enlargement by phase-contrast cine MRI.

OBJECTIVES: To reveal the relationship of brain motion and cerebrospinal fluid (CSF) flow by phase-contrast cine MRI, and to evaluate this technique in differentiating between arachnoid cysts and subarachnoid space enlargement. METHODS: Using a phase-contrast cine MRI pulse sequence, we measured brain motion and CSF flow during the cardiac cycle in 10 healthy volunteers and 10 patients with MRI-suspected arachnoid cyst or subarachnoid space enlargement. CSF stroke volume curve was illustrated according to flow quantification, and time-signal intensity curve was traced. The two curves were compared. RESULTS: This study showed that brain motion was due to the volume difference between arterial and venous blood flow during a cardiac cycle, and thus drives CSF pulsation. Arachnoid cysts and subarachnoid space enlargement carried different curve patterns, demonstrating that phase-contrast MRI and flow quantification can be a useful and reliable technique for non-invasive evaluation of brain motion and CSF flow. CONCLUSION: Arachnoid cysts can be successfully differentiated using phase-contrast cine MRI from subarachnoid space enlargement.

Adult↗

Cortical dysplasia associated with massive ectopia of neurons and glial cells within the subarachnoid space.

A detailed neuropathological study of the brain of a 31-day-old premature newborn infant revealed the presence of massive ectopia of neurons and glial cells within the subarachnoid space. The extrusion of neural tissue into the subarachnoid space appeared to have taken place through multiple pial-glial bridges. The laminar cortical pattern was also severely disturbed at these sites. Narrow strips of normal and dysplastic cortex alternated in direct relationship to the presence or absence of the pial-glial gaps. Migration of postmitotic neurons and the final positioning of postmigratory neurons appear to take place within highly specified and restricted pathways entrained in a radial direction. Our findings suggest that the pial-glial barrier plays an important role in the control of neuronal migration, and that its disruption may lead to the development of neuronal and glial cell ectopias in the subarachnoid space. The crucial role played by radial glia, the glia limitans and the basal lamina during cortical neurogenesis is emphasized.

Cerebral Cortex↗

[Treatment of chronic leptomeningitis (arachnoiditis) by administration of ozone into the subarachnoid space].

The authors report of ozone administration into the subarachnoid space for the treatment of chronic scarring--adhesive processes in the pial membrane. Among the 104 studied patients, 62 had convexital leptomeningitis, 7--basal, 3--of the posterior cavity and 28 diffuse forms. In patients with leptomeningitis of the posterior cavity in the absence of an engorged papilla of the eyeground, ozone was introduced by occipital punctures, in convexital and basal leptomeningitis--by lumbar puncture. An introduction of ozone into the subarachnoid space was conducted in combination with resorptive and general therapy.

Adolescent↗

6-OHDA-induced ectopia of external granule cells in the subarachnoid space covering the cerebellum. Genesis and topography.

The present report describes the genesis, development and topographical distribution of ectopic cells of the external granular layer in the subarachnoid space covering the rat cerebellum. Following one intracisternal injection to newborn rats of 100 micrograms 6-hydroxydopamine (6-OHDA), the meningeal cells degenerate and are removed by phagocytosis within 24 h post injection (p.i.), leaving the cerebellar cortex without a pia-arachnoid cover. Defects appear in the basal lamina investing the cerebellar cortex 3 to 5 days p.i., and both external granule cells and 'sprouts' from Bergmann-glia endfeet grow into the subarachnoid space. The latter form large, flat glial lamellae and cover extensive areas of the denuded cerebellar surface, although they do not form a glial scar over the exposed neuropil of the cerebellar cortex. The numbers of ectopic external granule cells increase within the subarachnoid space both by proliferation and a continuous efflux of cells from the cerebellar cortex. They migrate, aggregate, and ultimately develop into granule, stellate and basket cells, the morphology of which is indistinguishable from their counterparts in situ; they make specific afferent and efferent connections, both among themselves and with the underlying cerebellar cortex and brainstem. The distribution of ectopic external granule cells and their derivatives is restricted to the anterior vermal fissures and the vermal-hemispheric junctions. The present results indicate that external granule cells and their derivatives are capable of both differentiating normally and surviving in the subarachnoid space if they become associated with glial cells and establish synaptic connections.

Animals↗

Developmental morphology of the subarachnoid space and contiguous structures in the mouse.

Development of pia-arachnoidal membranes in the mouse occurs in four stages: the first (prenatal days 10-13) follows closure of the neural tube and is a period of initial vascularization of the developing telencephalon; the second (prenatal days 14-16) is a period of delineation during which the limits of the subarachnoid space are defined; the third (prenatal day 17 to birth) is a period of ensheathment of pia-arachnoidal blood vessels; and the fourth (birth to postnatal day 21) includes addition of smooth muscle to larger vessels, the appearance of macrophages in the subarachnoid space, and a general increase in extracellular collagenous and elastic fibers. The mesenchyme over the telencephalic surface in the 10-day fetus has a typically large extracellular space. By the 13th fetal day cerebrospinal fluid begins to seep into and replace it. The mesenchymal extracellular compartment is reduced peripherally, resulting in a compacted pia-arachnoidal tissue which limits the peripheral extent of the subarachnoid space. By the 21st postnatal day a subarachnoid space typical of the adult animal has been established.

Animals↗