Reduction In Cerebrospinal Fluid Pressure Research Articles

The association of cerebrospinal fluid pressure with optic nerve head and macular vessel density.

The present study aims to investigate the effect of temporary cerebrospinal fluid pressure (CSFP) reduction on optic nerve head (ONH) and macular vessel density (VD) using optical coherence tomography angiography. Forty-four eyes of 44 adults with diagnostic lumbar puncture and CSFP reduction were recruited. Thirty-two eyes of 32 healthy volunteers were controls. ONH and macular VD images were evaluated differences between baseline and after CSFP reduction. The results showed that the mean CSFP decreased from (11.6±2.1) mmHg to (8.2±3.4) mmHg (P<0.001). VD in the macular regions decreased significantly after CSFP reduction in the study group (all P<0.05). The control group showed no significant changes in macular VD (all P>0.05). In the study group, decreased VD in the macular parainferior region was associated with CSFP reduction (R2=0.192, P=0.003), the reduction of macular VD in parafoveal (R2=0.098, P=0.018), parainferior (R2=0.104, P=0.021), parasuperior (R2=0.059, P=0.058), paranasal (R2=0.057, P=0.042), paratemporal (R2=0.079, P=0.026) was associated with mean ocular perfusion pressure decrease following CSFP reduction. ONH vessel density did not differ after CSFP reduction (all P>0.05). In conclusion, macular vessel density decreased in association with CSFP reduction. Retinal vessel density in the macular region is more sensitive than that in peripapillary region after CSFP reduction.

The Association of Acute Cerebrospinal Fluid Pressure Reduction with Choroidal Thickness

ABSTRACT Purpose To investigate the changes in choroidal thickness (CT) after acute cerebrospinal fluid pressure (CSFP) reduction in human subjects. Methods Before and 15 minutes after diagnostic lumbar puncture (LP), 44 patients underwent measurement of CT by swept-source optical coherence tomography. Thirty-two healthy volunteers imitated the body posture of LP procedure and underwent the same measurement before and 15 minutes after body posture change. Results After CSFP reduction from 10.9 ± 2.1 mmHg at baseline to 8.1 ± 1.5 mmHg (p < 0.001), CT decreased in subfoveal region (p = 0.005), small to medium vessel layer (SMVL, p < 0.001), peripapillary regions in temporal (p = 0.001), nasal (p < 0.001), superior (p < 0.001) and inferior (p < 0.001), respectively. However, no significant change in CT in the control group after body posture change (all p > 0.05). A significant association between CSFP and the ratio of small to medium vessel layer to total choroidal thickness was found (p = 0.009). The CSFP reduction rate was associated with the change rate of SMVL to total CT portion, for each percent decrease in CSFP was associated with a decrease by 0.22% in the rate of SMVL to total CT portion (R2 = 0.125, p = 0.018). Conclusions A significant decrease in subfoveal CT, small to medium vessel layer and peripapillary region were observed following acute CSFP reduction. The CSFP reduction rate was associated with the change rate of small to medium vessel layer to total CT portion.

Time-Dependent Effects of Reduced Cerebrospinal Fluid Pressure on Optic Nerve Retrograde Axonal Transport

PurposeTo study the time-dependent effects of reduced cerebrospinal fluid pressure (CSFP) on axonal transport in the rat optic nerve.MethodsSeventy-two adult Sprague Dawley rats were used for this study. Fluoro-Gold was injected into the superior colliculi to study axonal transport. CSFP was reduced to 1.5 to 2.9 mm Hg by continuous aspiration of cerebrospinal fluid. In the sham control group (n = 18), a trocar was implanted in the cisterna magna, but cerebrospinal fluid was not released. CSFP and intraocular pressure (IOP) were continually monitored. CSFP was reduced for 1 hour (low-CSFP-1h study group; n = 18), 3 hours (low-CSFP-3h study group; n = 18), or 6 hours (low-CSFP-6h study group; n = 18) before the animals were euthanized. Confocal microscopy was used to compare axonal transport in different quadrants of the retina between control and low-CSFP eyes.ResultsChanges in axonal transport were observed only after 3 hours of CSFP reduction and not in the low-CSFP-1h study group. These changes occurred in a time-dependent manner, with 6 hours of CSFP reduction producing the longest lasting and most severe reduction in fluorescence.ConclusionsThe time-dependent changes observed in axonal transport in the optic nerve provide further evidence regarding the pathogenesis of axonal damage caused by reduced CSFP.

The Effect of Acetazolamide and Weight Loss on Intraocular Pressure in Idiopathic Intracranial Hypertension Patients.

Acetazolamide (ACZ) lowers intraocular pressure (IOP), acutely in normal eyes and both acutely and chronically in eyes with glaucoma, and cerebrospinal fluid pressure (CSFp), chronically in patients with idiopathic intracranial hypertension (IIH). We hypothesize chronic daily ACZ would significantly reduce IOP and contribute to a translaminar pressure gradient change reflected by alteration in the CSFp-IOP difference and the deformation of the neural canal in patients with IIH and no glaucoma. Before randomization to ACZ or placebo treatment for 6 months, 165 participants in the IIH Treatment Trial had evaluations that included Goldmann applanation, CSFp measurement, and optical coherence tomography determination of the neural canal deformation. These measures were repeated at the 6-month outcome. The IOP was not significantly decreased from baseline at 1, 3, or 6 months in eyes in both treatment groups. At month 6, the amount of ACZ or weight modification did not correlate with any IOP change. The 6-month mean change in neural canal deformation was 0.96 and -0.04 (P=0.001) and in CSFp was -128 and -38 mm H2O (P=0.001), but CSFp-IOP difference change was not significant, in the ACZ and placebo groups, respectively. ACZ does not reduce the IOP in eyes without glaucoma but does decrease the pathologic elevated CSFp, providing evidence that normal systems can compensate for chronic medication effects. The CSFp-IOP is not a direct marker of translaminar pressure gradient and the ACZ normalization of the neural canal deformation appears due to CSFp reduction alone.

Ultrasonic measurement of optic nerve sheath diameter: a non-invasive surrogate approach for dynamic, real-time evaluation of intracranial pressure

The current study aimed to identify whether ultrasonographic measurements of optic nerve sheath diameter (ONSD) could dynamically and sensitively evaluate real-time intracranial pressure (ICP). ONSD measurements were performed approximately 5 min prior to and after a lumbar puncture (LP). A total of 84 patients (mean±SD age, 43.5±14.7 years; 41 (49%) men; 18 patients with elevated ICP) were included in the study. The Spearman correlation coefficients between the two observers were 0.779 and 0.703 in the transverse section and 0.751 and 0.788 in the vertical section for the left and right eyes, respectively. The median (IQR) change in ONSD (ΔONSD) and change in ICP (ΔICP) were 0.11 (0.05–0.21) mm and 30 (20–40) mmH2O, respectively, for all participants. With a reduction in cerebrospinal fluid pressure, 80 subjects (95%) showed an immediate drop in ONSD; the median (IQR) decreased from 4.13 (4.02–4.38) mm to 4.02 (3.90–4.23) mm (p<0.001). Significant correlations were found between ONSD and ICP before LPs (r=0.482, p<0.01) and between ΔONSD and ΔICP (r=0.451, p<0.01). Ultrasonic measurement of ONSD can reflect the relative real-time changes in ICP.

Selective Early Glial Reactivity in the Visual Pathway Precedes Axonal Loss, Following Short-Term Cerebrospinal Fluid Pressure Reduction.

To examine the early glial reactivity and neuron damage in response to short-term cerebrospinal fluid pressure (CSFp) reduction, as compared with intraocular pressure (IOP) elevation. The experiment included 54 male Sprague-Dawley rats with elevated translaminar cribrosa pressure difference (TLPD), defined as IOP minus CSFp. These rats underwent either continuous CSF drainage for 6 hours (n = 18), or unilateral IOP elevation to 40 mm Hg for 6 hours (n = 18). For control, 18 normal rats were anesthetized for 6 hours. Orthograde axonal transport was examined by intravitreal injection of 3% rhodamine-β-isothiocyanate. We also used transmission electron microscopy to display the ultrastructural features of retinal ganglion cell axons in the optic nerve head. Early glial reactivity in the retina, lateral geniculate nucleus (LGN), and superior colliculus (SC) was detected by immunostaining and Western blot for the glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS). We also observed the glial reactivity in the inferior colliculus and hippocampus to rule out possible influences of CSF dynamics and composition. Anterograde staining with 3% rhodamine-β-isothiocyanate revealed decreased fluorescence intensity of the SC and LGN projected from both lower CSFp and higher IOP eyes. Transmission electron microscopy showed loss of axons from the optic nerve head in the high-IOP group, but not in the low-CSFp group. Compared with the anesthesia control group, GFAP expression was significantly increased in the retina, LGN, and SC, whereas GS expression was only increased in the retina following CSFp reduction. However, their expressions were not significantly elevated in the inferior colliculus and hippocampus. In the high-IOP group, expressions of GFAP and GS were significantly increased in the retina, LGN, and SC. Visual system neurons may be much more sensitive than other nervous tissues. Following short-term CSFp reduction, early glial reactivity may precede axonal loss. Changes of translaminar cribrosa pressure difference in both experimental low-CSFp and high-IOP groups induce selective early glial reactivity. The neuron damage from abnormally low CSFp may be pathogenetically similar to high IOP.

Long-term Response of Cerebrospinal Fluid Pressure in Patients with Idiopathic Intracranial Hypertension - A Prospective Observational Study.

Background:Idiopathic intracranial hypertension (IIH) is increased intracranial pressure (ICP) with normal cerebrospinal fluid (CSF) contents, in the absence of an intracranial mass, hydrocephalus, or other identifiable causes. The current knowledge of the treatment outcome of IIH is limited, and the data on the natural history of this entity are scant.Objective:The objective of the study is to study the treatment response of IIH by serially measuring the CSF opening pressure and to delineate the factors influencing the same.Materials and Methods:A prospective observational study in a cohort of fifty patients with IIH in whom CSF opening pressure was serially measured at pre-specified intervals.Results:The mean CSF opening pressure at baseline was 302.4 ± 51.69 mm of H2O (range: 220–410). Even though a higher body mass index (BMI) showed a trend toward a higher CSF opening pressure, the association was not significant (P = 0.168). However, the age of the patient had a significant negative correlation with the CSF pressure (P = 0.006). The maximum reduction in CSF pressure occurred in the first 3 months of treatment, and thereafter it plateaued. Remission was attained in 12 (24%) patients. BMI had the strongest association with remission (P = 0.001).Conclusions:In patients with IIH, treatment response is strongly related to BMI. However, patients with normal BMI are also shown to relapse and hence should have continuous, long-term follow-up. The reduction in CSF pressure attained in the first 3 months could reflect the long-term response to treatment.

Translamina Cribrosa Pressure Difference as Potential Element in the Pathogenesis of Glaucomatous Optic Neuropathy.

The main proven risk factor for glaucomatous optic neuropathy (GON) is an intraocular pressure (IOP) higher than the pressure sensibility of the optic nerve head allows. Fulfilling Koch postulates, numerous studies have shown that the presence of high IOP leads to GON, that lowering IOP stops the progression of GON, and that a re-increase in IOP again causes the progression of GON. There are, however, many patients with glaucoma who have statistically normal or low IOP, and despite low IOP values, they develop progressing GON. These observations led to findings that IOP is only 1 of 2 determinants of the translamina cribrosa pressure difference (TLCPD), which is the main pressure-related parameter for the physiology and pathophysiology of the optic nerve head. The second parameter influencing TLCPD is orbital cerebrospinal fluid pressure (CSFP) as the counter pressure against IOP across the lamina cribrosa. Recent experimental and clinical studies have suggested that a low CSFP could be associated with GON in normal-pressure glaucoma. These investigations included studies with an experimental long-term reduction in CSFP in monkeys, population-based studies, and clinical retrospective and prospective investigations on patients with normal-pressure glaucoma. Besides TLCPD, other ocular parameters influenced by CSFP may be choroidal thickness, retinal vein pressure and diameter, occurrence of retinal vein occlusions, and occurrence and severity of diabetic retinopathy.

Interventions for idiopathic intracranial hypertension.

Interventions for idiopathic intracranial hypertension.

Dynein, kinesin and morphological changes in optic nerve axons in a rat model with cerebrospinal fluid pressure reduction: the Beijing Intracranial and Intraocular Pressure (iCOP) study.

To examine the influence of experimentally reduced cerebrospinal fluid pressure (CSFP) as compared to elevated intraocular pressure (IOP) on axonal morphology and axonal motor proteins in retinal ganglion cells (RGCs). The experimental study included 39 rats which underwent cerebrospinal fluid drainage for 6 hr, 30 rats which unilaterally underwent IOP elevation for 6 hr and 30 rats in a control group. Six hours after baseline, the animals were killed and the eyes were histologically and immunohistochemically examined. In experimental models in the high-IOP group and the low-CSFP group as compared to the control group, RGC axons became abnormally dilated and accumulated vesicles. Both groups as compared to the control group showed an accumulation of dynein IC (intermediate chain) at the optic nerve head and retina and a reduction in kinesin HC (heavy chain) immunoreactivity in the optic nerve fibre axons. As a corollary, Western blot analysis revealed an elevation of dynein IC protein levels in the optic nerve head and retina and a decrease in kinesin HC protein levels in the optic nerve. Experimental models with an acute IOP rise or with an acute CSFP reduction showed similar morphologic changes in the retinal ganglion cell axons and similar immunohistochemical changes in the axonal motor proteins kinesin HC and dynein IC. It supports the hypothesis that an experimental model with an acute reduction in CSFP as well as an experimental model with an acute rise in IOP may share similarities in the process of optic nerve damage.

Axonal Transport in the Rat Optic Nerve Following Short-Term Reduction in Cerebrospinal Fluid Pressure or Elevation in Intraocular Pressure.

To examine the influence of short-term reduction in cerebrospinal fluid pressure (CSFP) as compared with short-term elevation in IOP on axonal transport. The study included 111 adult Sprague-Dawley rats. For 6 hours, IOP was unilaterally elevated to 40 mm Hg (IOP40-group; n = 27), IOP was unilaterally increased to a value of 25 mm Hg below the mean blood pressure (PP25-group; n = 27), or CSFP was reduced by continuous aspiration of cerebrospinal fluid (Low-CSFP-group; n = 27). A sham control group (with a trocar in cisterna magna without cerebrospinal fluid release) included 24 rats. The left eyes of the IOP40 study group and PP25 study group served as additional contralateral control group. Orthograde axonal transport was examined by intravitreally injected rhodamine-β-isothiocyanate; retrograde axoplasmic flow was assessed by fluorogold injected into the superior colliculi. At 24 hours after baseline, rhodamine-β-isothiocyanate (RITC) staining intensity of the optic nerve was lower (P < 0.05) in the IOP40-group, PP25-group, and Low-CSFP-group than in the control groups. At 6 hours after the fluorogold injection, fluorogold fluorescence was significantly lower in the IOP40-group, the PP25-group, and the Low-CSFP-group than in the control groups. At 5 days after baseline, the fluorogold fluorescence no longer differed significantly between the IOP40-group or the Low-CSFP-group and the control groups. At 1 week after baseline, retinal ganglion cell density was markedly reduced only in the PP25-group. Both short-term lowering of CSFP and short-term rise in IOP were associated with a disturbance of both the orthograde and retrograde axonal transport. The findings support the notion of an association between abnormally low CSFP and optic nerve damage.

Facts and myths of cerebrospinal fluid pressure for the physiology ofthe eye.

The orbital cerebrospinal fluid pressure (CSFP) represents the true counter-pressure against the intraocular pressure (IOP) across the lamina cribrosa and is, therefore, one of the two determinants of the trans-lamina cribrosa pressure difference (TLPD). From this anatomic point of view, an elevated TLPD could be due to elevated IOP or abnormally low orbital CSFP. Both experimental and clinical studies have suggested that a low CSFP could be associated with glaucomatous optic neuropathy in normal-pressure glaucoma. These included monkey studies with an experimental long-term reduction in CSFP, and clinical retrospective and prospective studies on patients with normal-pressure glaucoma. Since the choroidal blood drains via the vortex veins through the superior ophthalmic vein into the intracranial cavernous sinus, anatomy suggests that the CSFP could influence choroidal thickness. A population-based study revealed that thicker subfoveal choroidal thickness was associated with higher CSFP. Since the central retinal vein passes through the orbital CSF space, anatomy suggests that the retinal venous pressure should be at least as high as the orbital CSFP. Other experimental, clinical or population-based studies suggested an association between higher CSFP and higher retinal venous pressure and wider retinal veins. Consequently, a higher estimated CSFP was associated with arterial hypertensive retinopathy (with respect to the dilated retinal vein diameter and higher arterial-to-venous diameter) and with the prevalence, severity and incidence of diabetic retinopathy. Physiologically, CSFP was related with higher IOP. The influence of the CSFP on the episcleral venous pressure and/or a regulation of both CSFP and IOP by a center in the dorsomedial/perifornical hypothalamus may be responsible for this. Insummary, the CSFP may be an overlooked parameter in ocular physiology and pathology. Abnormal changes in the CSFP, in particular in relationship to the IOP, may have pathophysiologic importance.

Mechanism study on trans-lamina cribrosa pressure difference correlated with optic neuropathy in glaucoma

Glaucomatous optic neuropathy is among the most common causes of blindness worldwide. Elevated intraocular pressure (IOP) has long being considered to be the major risk factors for the development and progression of glaucomatous optic nerve damage. However, numerous studies have shown that a relatively large number of patients with typical glaucomatous optic neuropathy, in whom the IOP measurements have always been in the normal range (<21 mmHg, 1 mmHg = 0.133 kPa). Thus, the role of IOP in the pathogenesis of POAG becomes vague and controversial. Based on prospective clinical observations, Beijing iCOP (Intracranial and Intraocular Pressure) Study has found that the orbital cerebrospinal fluid pressure (CSF-P) may be of importance for the physiology and patho-physiology of the optic nerve head and may play a role in the pathogenesis of glaucomatous optic neuropathy. A low CSF-P in the retrobulbar region of the orbit may act as the counter-pressure against IOP and theoretically have a similar effect as an increased IOP on the trans-lamina cribrosa pressure difference which may be more relevant to the glaucomatous optic neuropathy than IOP alone. Moreover, an experimental and chronic reduction in CSF-P in monkeys was associated with the development of optic nerve damage morphologically typical for glaucomatous optic neuropathy. The findings support the hypothesis the CSF-P may play a role in the pathogenesis of glaucomatous optic neuropathy.

Cerebrospinal fluid pressure decreases with older age.

PurposeClinical studies implicate low cerebrospinal fluid pressure (CSFP) or a high translaminar pressure difference in the pathogenesis of primary open angle glaucoma (POAG) and normal tension glaucoma (NTG). This study was performed to examine the effect of age, sex, race and body mass index (BMI) on CSFP.MethodsElectronic medical records from all patients who had a lumbar puncture (LP) performed at the Mayo Clinic from 1996–2009 were reviewed. Information including age, sex, race, height and weight, ocular and medical diagnoses, intraocular pressure (IOP) and LP opening pressure was obtained. Patients using medications or with medical diagnoses known to affect CSFP, and those who underwent neurosurgical procedures or where more than one LP was performed were excluded from analysis.ResultsElectronic medical records of 33,922 patients with a history of having an LP during a 13-year period (1996–2009) were extracted. Of these, 12,118 patients met all entry criteria. Relative to mean CSFP at age group 20–49 (mean 11.5±2.8 mmHg), mean CSFP declined steadily after age 50, with percent reduction of 2.5% for the 50–54 age group (mean 11.2±2.7 mmHg, p<0.002) to 26.9% for the 90–95 group (mean 8.4±2.4 mmHg, p<0.001). Females had lower CSFP than males throughout all age groups. BMI was positively and independently associated with CSFP within all age groups.ConclusionThere is a sustained and significant reduction of CSFP with age that begins in the 6th decade. CSFP is consistently lower in females. BMI is positively and independently associated with CSFP in all age groups. The age where CSFP begins to decline coincides with the age where the prevalence of POAG increases. These data support the hypothesis that reduced CSFP may be a risk factor for POAG and may provide an explanation for the mechanism that underlies the age-related increase in the prevalence of POAG and NTG.

Effect of cerebrospinal fluid drainage and/or partial exsanguination on tolerance to prolonged aortic cross-clamping.

Paraplegia as a consequence of spinal cord ischemia associated with procedures on the thoracic and thoracoabdominal aorta has been linked to the interaction of proximal hypertension with elevated cerebrospinal fluid pressure (CSFP) during aortic cross-clamping (AXC). CSFP reduction via cerebrospinal fluid (CSF) drainage is thought to significantly prolong the cord's tolerance to AXC. Likewise, partial exsanguination is reported to effectively reduce ischemic injury by controlling proximal hypertension. To evaluate the individual and collective efficacy of both techniques, 18 mongrel dogs (25 to 35 kg), divided into three equal groups, underwent a fourth interspace left thoracotomy AXC. Baseline proximal arterial blood pressure (PABP), distal arterial blood pressure (DABP), and CSFP were established and monitored at 5-minute intervals during 120 minutes of AXC, and for 30 minutes thereafter. Group I animals were partially exsanguinated prior to AXC to maintain PABP at a mean of 115 to 120 mmHg. Group II animals had sufficient (16 +/- 5 cc) CSF withdrawn to maintain a DABP-CSFP gradient, i.e., spinal cord perfusion pressure (SCPP) of 20 mmHg. Group III animals were treated with both CSF drainage and partial exsanguination in the same manner as groups I and II, respectively. Perioperative somatosensory evoked potential (SEP) monitoring evaluated cord function. Postoperative neurological outcome was assessed with Tarlov's criteria. SEPs degenerated approximately 22 minutes following AXC for groups II and III. In contrast, group I exhibited rapid (10 +/- 7 min) SEP loss. All five surviving group I animals displayed paralysis 48 hours postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of exsanguination and sodium nitroprusside on compliance of the spinal canal during aortic occlusion

To evaluate the effects of sodium nitroprusside (SNP) and partial exsanguination (EXS) on systemic hemodynamics and cerebrospinal fluid dynamics, we monitored proximal and distal blood pressure (BP), cerebrospinal fluid pressure (CSFP), spinal cord perfusion pressure (SCPP), and compliance of the spinal canal (CSC) in 10 mongrel dogs during aortic cross-clamping of the descending thoracic aorta. CSC was measured by serial injections of 2 ml of saline solution into the cisterna cerebellomedullaris via a percutaneously placed catheter with simultaneous measurements of CSFP. Data were acquired at baseline (BL), during aortic cross-clamping with proximal hypertension (AXC), and after control of proximal hypertension with EXS and SNP. During the cross-clamp interval, mean proximal aortic pressure (PxBP) rose from 114 ± 6 to 150 ± 3 mm Hg ( P < 0.001), whereas mean blood pressure decreased to 88 ± 5 and 82 ± 4 mm Hg during the SNP and EXS intervals, respectively ( P < 0.05 vs BL). EXS and SNP were equally effective in controlling PxBP (82 ± 4 vs 88 ± 5 mm Hg, P > 0.05). Mean distal aortic pressure (DsBP) decreased from systemic values to 21.5 ± 1.9 mm Hg during AXC, and to 12.4 ± 1.0 and to 8 ± 0.8 mm Hg during EXS and SNP, respectively ( P < 0.05 AXC vs EXS and SNP). SNP lowered DsBP significantly more than EXS, 8 ± 0.8 vs 12.4 ± 1.0 mm Hg ( P < 0.05). CSFP decreased significantly during EXS compared with BL, AXC, and SNP (4.0 ± 1.32 vs 7.0 ± 0.87, 12.5 ± 1.43, and 18.8 ± 1.46 mm Hg, respectively, P < 0.05). As a result of the detrimental effects of SNP on DsBP and CSFP, SCPP was significantly lower during the infusion of SNP than during AXC and EXS (−10 ± 1 vs 10 ± 2 and 8 ± 1 mm Hg, respectively, P < 0.05). CSC increased significantly during EXS as compared with AXC (0.69 ± 0.04 to 1.15 ± 0.24 ml/mm Hg) whereas it decreased, although not significantly, during SNP compared with AXC and BL (0.55 ± 0.8 vs 1.15 ± 0.24 and 0.69 ± 0.04 ml/mm Hg, respectively, P > 0.05; AXC vs BL, P > 0.05). This study shows that the decrease in SCPP caused by SNP is caused by an increase in CSFP and a decrease in DsBP: however, the rise in CSFP does not appear to be caused solely by a decrease in CSC. The effects of reduction in CSFP observed with EXS are associated with an increase in CSC. Based on the results of this study, we conclude that the beneficial effects of EXS on SCPP may be mediated by an improvement in CSC.

Reduction of cerebrospinal fluid pressure by hypocapnia: changes in cerebral blood volume, cerebrospinal fluid volume and brain tissue water and electrolytes. II. Effects of anesthetics.

Part I of these studies (Artru, 1987) examined how cerebral blood volume (CBV), CSF volume, and brain tissue water and electrolytes determined CSF pressure during 4 h of hypocapnia in sedated dogs. The three groups reported were: hypocapnia (PaCO2 20 mm Hg) with no intracranial mass (group 1), intracranial mass (epidural balloon, CSF pressure 35 cm H2O) but no hypocapnia (group 2), and intracranial mass with hypocapnia used to lower CSF pressure (group 3). It was found that in dogs with an intracranial mass (group 3) the CSF pressure-lowering effect of hypocapnia was sustained for 4 h due to improved reabsorption of CSF, decrease of CSF volume to offset reexpansion of CBV and no increase in the sum of CSF volume and CBV. The present Part II studies (groups 4-8) examine the effects of anesthetics on CSF pressure during conditions like those used for group 3, namely, intracranial mass present and hypocapnia used to lower CSF pressure. When halothane or enflurane were used for anesthesia, the CSF pressure-lowering effect of hypocapnia was not sustained. CSF pressure increased from 17.3 +/- 4.7 and 19.0 +/- 4.1 cm H2O, respectively (mean +/- SD), at 10 min to 50.3 +/- 12.8 and 43.2 +/- 12.8 cm H2O, respectively at 4 h. Increase of CSF pressure was associated with increased resistance to reabsorption of CSF (Ra) and increase in the sum of CSF volume and CBV. With halothane the intracranial volume increase was comprised chiefly of cerebral blood and with enflurane the intracranial volume increase was comprised chiefly of CSF. When isoflurane, fentanyl, or thiopental were used for anesthesia, the CSF pressure-lowering effect of hypocapnia was sustained. Ra did not increase and the sum of CBV and CSF volume remained reduced.

Reduction of cerebrospinal fluid pressure by hypocapnia: changes in cerebral blood volume, cerebrospinal fluid volume, and brain tissue water and electrolytes.

The study examined the role of cerebral blood volume (CBV), cerebrospinal fluid (CSF) volume, and brain tissue water and electrolytes on CSF pressure during 4 h of hypocapnia in dogs. Group I (n = 6) was examined during hypocapnia (PaCO2 20 mm Hg), with no intracranial mass being present. Group II (n = 6) was examined with an intracranial mass present (epidural balloon, CSF pressure 35 cm H2O), but no hypocapnia. In group III (n = 6), an intracranial mass was present, and hypocapnia was used to lower CSF pressure. In group I, hypocapnia initially reduced CBV from 3.4 to 2.4 ml. With continued hypocapnia, CBV reexpanded to 3.4 ml by 4 h. CSF volume changed reciprocally, so that intracranial CSF pressure remained constant. In group II, CBV remained steady (2.7 ml), and CSF volume fell only slightly, so that CSF pressure remained elevated. In group III, hypocapnia initially reduced CBV from 2.8 to 2.2 ml, and CSF pressure fell from 35 to 19 cm H2O. With continued hypocapnia, CBV rose to 2.8 ml by 4 h, but CSF volume fell from 6.1 to 5.0 ml, so that CSF pressure remained low. Net intracranial absorption of CSF did not exceed net intracranial CSF production, suggesting that CSF volume fell because hypocapnia improved access of intracranial CSF to spinal sites of CSF reabsorption. Brain tissue composition was not different among groups. The results indicate that hypocapnia lowers elevated CSF pressure initially by lowering CBV. This CSF pressure-lowering effect is sustained (despite reexpansion of CBV) by a further reduction of CSF volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Spinal cord compression and blood flow. I. The effect of raised cerebrospinal fluid pressure on spinal cord blood flow.

The effect of cerebrospinal fluid pressure (CSFP) on spinal cord blood flow (SCBF), measured by the hydrogen clearance technique, was studied in dogs. CSFP was altered by the infusion of mock CSF into the lumbar subarachnoid space. Occluding snares at T-13 limited the effect of raised pressure on the brain. As the perfusion pressure was reduced when the CSFP was increased, flow remained constant up to a perfusion pressure of approximately 50 mm Hg. Below this value, flow decreased with decreasing perfusion pressure. Normal flow values could be reestablished even at a raised CSFP if the perfusion pressure was increased by raising the arterial blood pressure. Rapid reduction of CSFP was accompanied by reactive hyperemia. The autoregulation of flow down to a perfusion pressure of 50 mm Hg was due to progressive decrease in vascular resistance. Carbon dioxide-responsiveness of the vessels was decreased markedly as the perfusion pressure was reduced.

Cerebral and blood flow and cerebral blood volume in communicating hydrocephalus (author's transl)

Regional cerebral blood flow (rCBF) and regional cerebral blood volume (rCBV) were estimated in patients with communicating hydrocephalus, arteriosclerotic and presenile dementia. In all groups ischemic patterns were detected which did not allow any differential diagnostic separation between the patients. In some patients with communicating hydrocephalus reduction of cerebrospinal fluid pressure by lumbar puncture or ventriculoperipheral shunt respectively resulted in increase of rCBF and rCBV. This was not achieved in the other patients with dementia. Predominantly areas with ischemic flow values gained profit from reduction of CSF pressure. This was interpreted as a sign of regional damage to the autoregulation.