Loss Of CSF Research Articles

Postoperative epidural hematoma as a rare complication after intracranial tumor resection: a case series report and causes analysis

BackgroundTo review the treatment and the causes of postoperative epidural hematoma (PEDH) after intracranial tumor resection.MethodA retrospective case study was conducted to examine a series of patients who developed PEDH as a complication following intracranial tumor resection between January 2016 and June 2021. The study collected data from hospital charts, including clinical status at admission, imaging results, histopathologic findings, surgical management, complications, and outcomes. Causes of PEDH were evaluated through a review of operative notes and discussions with the surgical team.ResultsTwenty-five patients (10 males, 15 females; median age 42 years, range 11–61 years; median medical history 27 months, range 1–96 months) were enrolled in the study. Regarding tumor location, 16 cases exhibited supratentorial brain tumors, 4 cases had infratentorial brain tumors, 2 cases of tumors occurred in the petroclival region, 2 cases in the peritorcular region, and 1 case in the pineal region. Four of these cases were complicated with supratentorial hydrocephalus. The 25 cases in this study were classified into four types based on location. Type 1 refers to EDHs that occur at the adjacent site of the operative field without involvement of the surgical area. Type 2 includes hematomas that occur at the adjacent site of the surgical area and the surgical area. Type 3 includes EDHs that occur in distant areas, and type 4 involves EDHs in the surgical field. The numbers of cases of types 1, 2, 3, and 4 PEDHs were 16, 2, 3, and 4 cases, respectively. Most PEDHs were associated with reduced ICP after craniotomy due to intracranial tumor resection and substantial loss of CSF. All patients achieved satisfactory outcomes after hematoma evacuation.ConclusionThe decrease in ICP resulting from intracranial tumor resection and CSF loss might lead to PEDHs. By employing optimized surgical techniques and meticulous patient management to prevent rapid decreases in ICP and dural detachment, we can potentially lower the incidence of PEDHs. Additionally, prompt evacuation of hematomas can contribute to positive outcomes.

Diphtheria toxin induced but not CSF1R inhibitor mediated microglia ablation model leads to the loss of CSF/ventricular spaces in vivo that is independent of cytokine upregulation

BackgroundTwo recently developed novel rodent models have been reported to ablate microglia, either by genetically targeting microglia (via Cx3cr1-creER: iDTR + Dtx) or through pharmacologically targeting the CSF1R receptor with its inhibitor (PLX5622). Both models have been widely used in recent years to define essential functions of microglia and have led to high impact studies that have moved the field forward.MethodsUsing either Cx3cr1-iDTR mice in combination with Dtx or via the PLX5622 diet to pharmacologically ablate microglia, we compared the two models via MRI and histology to study the general anatomy of the brain and the CSF/ventricular systems. Additionally, we analyzed the cytokine profile in both microglia ablation models.ResultsWe discovered that the genetic ablation (Cx3cr1-iDTR + Dtx), but not the pharmacological microglia ablation (PLX5622), displays a surprisingly rapid pathological condition in the brain represented by loss of CSF/ventricles without brain parenchymal swelling. This phenotype was observed both in MRI and histological analysis. To our surprise, we discovered that the iDTR allele alone leads to the loss of CSF/ventricles phenotype following diphtheria toxin (Dtx) treatment independent of cre expression. To examine the underlying mechanism for the loss of CSF in the Cx3cr1-iDTR ablation and iDTR models, we additionally investigated the cytokine profile in the Cx3cr1-iDTR + Dtx, iDTR + Dtx and the PLX models. We found increases of multiple cytokines in the Cx3cr1-iDTR + Dtx but not in the pharmacological ablation model nor the iDTR + Dtx mouse brains at the time of CSF loss (3 days after the first Dtx injection). This result suggests that the upregulation of cytokines is not the cause of the loss of CSF, which is supported by our data indicating that brain parenchyma swelling, or edema are not observed in the Cx3cr1-iDTR + Dtx microglia ablation model. Additionally, pharmacological inhibition of the KC/CXCR2 pathway (the most upregulated cytokine in the Cx3cr1-iDTR + Dtx model) did not resolve the CSF/ventricular loss phenotype in the genetic microglia ablation model. Instead, both the Cx3cr1-iDTR + Dtx ablation and iDTR + Dtx models showed increased activated IBA1 + cells in the choroid plexus (CP), suggesting that CP-related pathology might be the contributing factor for the observed CSF/ventricular shrinkage phenotype.ConclusionsOur data, for the first time, reveal a robust and global CSF/ventricular space shrinkage pathology in the Cx3cr1-iDTR genetic ablation model caused by iDTR allele, but not in the PLX5622 ablation model, and suggest that this pathology is not due to brain edema formation but to CP related pathology. Given the wide utilization of the iDTR allele and the Cx3cr1-iDTR model, it is crucial to fully characterize this pathology to understand the underlying causal mechanisms. Specifically, caution is needed when utilizing this model to interpret subtle neurologic functional changes that are thought to be mediated by microglia but could, instead, be due to CSF/ventricular loss in the genetic ablation model.

Growth mechanism and thermal behavior of electroless Cu plating on short carbon fibers

Short carbon fibers (Csf), when used at 550–650 °C, often suffer from oxidization and mass loss during the preparation of Csf reinforced magnesium matrix composites (Csf/Mg composites). Here, a Cu coating is deposited on the Csf by using electroless plating to address this long-standing issue. The growth mechanism of the Cu coating, as well as its protection capability, is investigated. FT-IR suggests a proper pretreatment on the Csf provides favorable nucleation sites for subsequent electroless plating. SEM images show that, initially, a thin Cu coating with a thickness of 0.30 μm is grown on nucleation sites during electroless plating, and the Cu nanoparticles appear to be deposited on such Cu coating afterwards. With the electroless plating time increasing, the Cu particles are accumulated and become massive and flaky, then some holes and cracks appear. More importantly, TG conducted at 600 °C reveals that the mass loss of the Cu-coated Csf (4 min) is 8%, which is 4 times lower than that of the Csf without Cu coating. The optimal electroless plating time is 3–4 min for the Cu coating, which can effectively protect the Csf at high temperature for preparing Csf/Mg composites. More importantly, TG conducted at 600 °C reveals that the mass loss of the Cu-coated Csf (4 min) is 8%, which is 4 times lower than that of the Csf without Cu coating.

Intraocular pressure during neurosurgical procedures in context of head position and loss of cerebrospinal fluid.

Perioperative visual loss (POVL) is a rare but serious complication in surgical disciplines, especially in spine surgery. The exact pathophysiology of POVL remains unclear, but elevated intraocular pressure (IOP) is known to be part of it. As POVL is rarely described in patients undergoing intracranial or intradural surgery, the aim of this study was to investigate the course of IOP during neurosurgical procedures with opening of the dura mater and loss of CSF. In this prospective, controlled trial, 64 patients fell into one of 4 groups of 16 patients each. Group A included patients undergoing spine surgery in the prone position, group B patients had intracranial procedures in the prone position, and group C patients were treated for intracranial pathologies in a modified lateral position with the head rotated. In groups A-C, the dura was opened during surgery. Group D patients underwent spine surgeries in the prone position with an intact dura. IOP was measured continuously pre-, peri-, and postoperatively. In all groups, IOP decreased after induction of anesthesia and increased time dependently after final positioning for the operation. The maximum IOP in group A prior to opening of the dura was 28.6 ± 6.2 mm Hg and decreased to 23.44 ± 4.9 mm Hg directly after dura opening (p < 0.0007). This effect lasted for 30 minutes (23.5 ± 5.6 mm Hg, p = 0.0028); after 60 minutes IOP slowly increased again (24.5 ± 6.3 mm Hg, p = 0.15). In group B, the last measured IOP before CSF loss was 28.1 ± 5.0 mm Hg and decreased to 23.5 ± 6.1 mm Hg (p = 0.0039) after dura opening. A significant IOP decrease in group B lasted at 30 minutes (23.6 ± 6.0 mm Hg, p = 0.0039) and 60 minutes (23.7 ± 6.0 mm Hg, p = 0.0189). In group C, only the lower eye showed a decrease in IOP up to 60 minutes after loss of CSF (opening of dura, p = 0.0007; 30 minutes, p = 0.0477; 60 minutes, p = 0.0243). In group D (control group), IOP remained stable throughout the operation after the patient was prone. This study is the first to demonstrate that opening of the dura with loss of CSF during neurosurgical procedures results in a decrease in IOP. This might explain why POVL predominantly occurs in spinal but rarely in intracranial procedures, offers new insight to the pathophysiology of POVL, and provides the basis for further research and treatment of POVL.German Clinical Trials Register (DRKS) no.: DRKS00007590 (drks.de).

Bilateral remote cerebellar hemorrhage following surgical clipping a ruptured supratentorial aneurysm

Remote cerebellar hemorrhage (RCH) is a rare and severe complication after supratentorial surgery, with various risk factors and mechanisms remaining uncertain. Herein, we report a 64-year-old female patient suffered bilateral RCH following surgical clipping a ruptured aneurysm of internal carotid artery bifurcation. RCH is considered as venous in origin, and is likely the result of intra-operative or post-operative loss of CSF. Thus, appropriate control and close monitor the intra-operative and post-operative loss of CSF is of great importance for preventing the occurrence of RCH.

Lateral petrosectomy with obliteration cavity for spontaneous cerebrospinal otorrhea in children

PurposeThe most common causative factors of CSF otorrhea in children are injuries and congenital abnormalities of the temporal bone. Spontaneous CSF leak as a consequence of congenital temporal bone defects may result in recurrent meningitis. Diagnosis and management of such an entity are particularly difficult in early childhood. Materials and methodsThe aim of this study was to investigate clinical features and to discuss possible methods of treatment of spontaneous CSF otorrhea in children. ResultsSevere unilateral sensorineural hearing loss or total deafness was found in children with CSF otorrhea. CT and MRI of the temporal bones revealed dehiscences in the walls of the tympanic cavity and defects of the inner ear, which were confirmed intraoperatively. Lateral petrosectomy and closure of the fistula with muscle tissue and fat obliteration cavity were performed. The children remain free of otorrhea and recurrences of meningitis. ConclusionThe diagnosis of spontaneous otorrhea in children is based on the severe unilateral sensorineural hearing loss and presence of CSF in the middlę ear cavity. It may be successfully treated by means of lateral petrosectomy with obliteration of the vestibule with muscle tissue and tympanic cavity with fat tissue.

Radioisotope Cisternography: A Potentially Useful Tool for Headache Diagnosis in Patients with an IDD Pump

Background: Spontaneous intracranial hypotension (SIH) and related headache after intrathecal pump implantation is a possibility. Knowing the exact location of the cerebrospinal fluid (CSF) leak is mandatory for managing with interventional therapies. Objectives: Radioisotope cisternography (RICG) is a common procedure in nuclear medicine and may be used as an additional procedure in the differential diagnosis of headaches due to intracranial liquor hypotension syndrome caused by microleakage of CSF. Study Design: We report an imaging case of complex chronic headache in a patient with an implanted drug delivery pump. The symptomatology of the patient was considered typical of spontaneous intracranial hypotension (SIH). Therefore, the initial suspicion was the loss of CSF due to the implanted pump catheter. The negativity of the routine headache test can exclude any leakage of CSF at the site of catheter insertion. Setting: Anesthesia, Critical Care, and Multidisciplinary Pain Management Department, General University General Hospital, Valencia, Spain. Results: Many patients are treated with implanted intrathecal infusion systems. In these patients, any neurological symptoms are readily attributed to the invasive neuroaxial system, especially severe cephalalgia. RICG was helpful in this particular case to make a diagnosis of exclusion of the diagnosis of SIH due to CSF leakage. Conclusion: RICG may be considered as an additional diagnostic technique in patients with chronic pain and implanted spinal infusion devices for whom standard detection procedures have been exhausted. Key words: Intrathecal drug delivery (IDD), chronic headache (CH), radiosotope cisternography (RICG), cerebrospinal fluid leakage, spontaneous intracranial hypotension (SIH)

Incidence of high-frequency hearing loss after microvascular decompression for hemifacial spasm

The primary aim of this study was to evaluate the incidence and discuss the pathogenesis of high-frequency hearing loss (HFHL) after microvascular decompression (MVD) for hemifacial spasm (HFS). Preoperative and postoperative audiogram data and brainstem auditory evoked potentials (BAEPs) from 94 patients who underwent MVD for HFS were analyzed. Pure tone audiometry at 0.25-2 kHz, 4 kHz, and 8 kHz was calculated for all individuals pre- and postoperatively ipsilateral and contralaterally. Intraoperative neurophysiological data were reviewed independently. An HFHL was defined as a change in pure tone audiometry of more than 10 dB at frequencies of 4 and 8 kHz. The incidence of HFHL was 50.00% and 25.53% ipsilateral and contralateral to the side of surgery, respectively. The incidence of HFHL adjusted for conductive and nonserviceable hearing loss was 26.6% ipsilaterally. The incidence of HFHL at 4 and 8 kHz on the ipsilateral side was 37.23% and 45.74%, respectively, and it was 10.64% and 25.53%, respectively, on the contralateral side. Maximal change in interpeak latency Waves I-V compared with baseline was the only variable significantly different between groups (p < 0.05). Sex, age, and side did not increase the risk of HFHL. Stepwise logistic regression analysis did not find any changes in intraoperative BAEPs to increase the risk of HFHL. High-frequency hearing loss occurs in a significant number of patients following MVD surgery for HFS. Drill-induced noise and transient loss of CSF during surgery may impair hearing in the high-frequency ranges on both the ipsilateral and contralateral sides, with the ipsilateral side being more affected. Changes in intraoperative BAEPs during MVD for HFS were not useful in predicting HFHL. Follow-up studies and repeat audiological examinations may be helpful in evaluating the time course and prognosis of HFHL. Prospective studies focusing on decreasing intraoperative noise exposure, as well as auditory shielding devices, will establish causation and allow the team to intervene appropriately to decrease the risk of HFHL.

Spinal level of myelomeningocele lesion as a contributing factor in posterior fossa volume, intracranial cerebellar volume, and cerebellar ectopia

McLone and Knepper's unified theory of Chiari malformation Type II (CM-II) describes how the loss of CSF via the open posterior neuropore fails to create adequate distending pressure for the developing rhomboencephalic vesicle. The authors of the present article describe the relationship between the posterior fossa volume and intracranial cerebellar volume as being related to the distance from the obex of the fourth ventricle to the myelomeningocele lesion using a common mathematical model, the Hagen-Poiseuille law. All newborns who required closure of a myelomeningocele at the authors' institution between 2008 and 2011 and who were between 4 weeks premature and 2 months, corrected gestational age, at the time of MRI were included in this study. Volumes and measurements were obtained from axial and sagittal T2-weighted MR images of the brain and spine. A total of 56 newborn infants met the inclusion criteria. There was a direct linear relationship between both posterior fossa volume and cerebellar volume and the spinal level of the myelomeningocele lesion (p = 0.0012 and p = 0.0041, respectively). There was a negative linear relationship between the cerebellar descent, the spinal level of the lesion, and posterior fossa volume and cerebellar volume. These relationships strengthen in patients with no syringomyelia and are not significant in those groups with syringomyelia. The results of a 1-way ANOVA for the 3 groups did not reach significance. Using a linear equation derived from the Hagen-Poiseuille law that describes pressure in the fourth ventricle as being directly related to the length of the central canal from the obex to the myelomeningocele lesion, the authors were able to explain the directly observed linear relation between posterior fossa volume, intracranial cerebellar volume, and cerebellar descent to the level of the spinal lesion. As this model assumes a uniform radius of the central canal they were able to validate this model when they observed a strengthening in relationships in the no syringomyelia group and statistically insignificant correlations in the groups with syringomyelia. They therefore propose that the spinal level of the lesion is one of the major determinants of posterior fossa volume, intracranial cerebellar volume, and cerebellar ectopia.

Skull base cerebrospinal fluid fistula

A skull base CSF fistula occurs when there is a defect at the skull base and the subarachnoid space communicates with the extracranial space. Galen in the 2nd century aD was the first to describe leakage of CSF after cranial trauma.5 The term “rhinorrhea” was coined by Thomson3 while describing spontaneous nasal CSF leaks in patients. There exist a number of constants in neurosurgery with respect to achieving good outcomes for our patients. These include an intimate knowledge of surgical anatomy, meticulous technique to avoid injury to vital tissue, sharp attention to hemostasis, and so forth. This issue of Neurosurgical Focus deals with one of these constants that is paramount in cranial, skull base, and spinal neurosurgery, that is, exclusion of the CSF space from the external environment. Failure to obtain adequate closure, resulting in the loss of CSF and the communication of privileged internal space with the exterior milieu, can have a disastrous influence on the eventual outcome of an otherwise uneventful operation. Techniques to restore or maintain seclusion of the space occupied by CSF around the brain and spinal cord is the subject of this issue. The importance of closing the dural defect was put forward by Grant in 1923.2 Walter Dandy,1 in 1926, published the first report on the surgical repair of CSF rhinorrhea. He used muscle and fascia to close a frontal sinus defect. Using an endoscope in the repair of a skull base defect was proposed by Wigand in 1981.4 In recent years endonasal endoscopic approaches to the cranial base have been particularly in vogue. Therefore, it should come as no surprise that this issue has a particular emphasis on techniques applied in these procedures to achieve satisfactory closure. This aspect of contemporary cranial base surgery has taken advantage of the unique expertise of neurosurgeons and our otorhinolaryngology colleagues. Our ability to traverse the nasoand oropharyngeal spaces to reach the skull base and intracranial compartment has realized significant advancements in the past years. New biological and structural materials as well as innovative vascularized tissue transfer techniques have contributed equally to an enhanced ability to create seals that prevent egress of CSF. The level of facility with these techniques, built on the collective experience of others in our field, is demonstrated in this issue. Treating CSF fistulas, whether from surgical or accidental trauma, remains a critical clinical and surgical challenge. Our results are certainly not perfect; however, a high standard is reachable with adherence to certain principles and proficiency with contemporary techniques. (http://thejns.org/doi/abs/10.3171/2012.5.FOCUS12164)

Congenital hydrocephalus associated with myeloschisis

Neural tube defects (NTDs) can be divided into two main groups, one being open NTDs wherein visible neural tissue and cerebrospinal fluid leakage are present and the other, closed NTDs without exposed neural tissue and no drainage of CSF. This communication is devoted to open NTDs that can be further subdivided into myelomeningoceles, myeloschisis, and hemimyelomeningoceles. Common to all these is the loss of CSF during fetal development that leads to an extensive malformation of the central nervous system with hydrocephalus being a frequent feature. The only known difference between a newborn with myelomeningocele versus a newborn with myeloschisis is the initial presence (myelomeningocele) or absence (myeloschisis) of a cystic component with the overall clinical picture the same for these two forms of open neural tube defects.

Evaluation of beta amyloid loss to CSF sample collection and storage containers

Evaluation of beta amyloid loss to CSF sample collection and storage containers

Intrathecal Gadolinium-Enhanced MR Myelography Showing Multiple Dural Leakages in a Patient with Marfan Syndrome

oss of CSF or imbalance of its turnover can cause symptoms such as orthostatic headaches, nausea, and neck pain. These symptoms are frequently the result of CSF leakage from the dura and can occur spontaneously or after trauma, lumbar puncture, or neurosurgery. It has been suggested that disorders of the connective tissues predispose patients to spontaneous CSF leaks [1]. Hence, localization and identification of dural leakages are crucial for satisfactory treatment. We present the case of a patient with Marfan syndrome and multiple dural leaks. The exact site of CSF leakage was not apparent on conventional myelography or high-resolution CT myelography, but was shown using intrathecal contrast-enhanced MR myelography. Case Report A 19-year-old man with Marfan syndrome presented with severe headaches, neck pain, and nausea. These symptoms were triggered by orthostatic conditions involving an erect posture (e.g., sitting, standing, or walking). However, the symptoms resolved after lying down for several minutes. Blood analysis and neurologic examinations presented normal parameters. Intrathecal pressure was not measurable after lumbar puncture. Spontaneous intracranial hypotension (SIH) and chronic loss of CSF were assumed to be responsible for the symptoms. MR images using T1- and T2-weighted and constructive interference in steady-state 3D imaging showed dural ectasia at different levels of the lumbosacral spine and extradural fluid with CSF-like signal performance dorsally to L5 and S1, but no connection to the subarachnoid space was proven. A CT scan of the brain showed normal cisterns, no caudal displacement of the brainstem, and no evidence of low intracranial pressure. Myelography, a postmyelography high-resolution CT scan, and T2

Effects on intracranial pressure of dural puncture in supine and head‐elevated positions. A study on the cat

Lumbar dural puncture may reduce intracranial pressure (ICP) due to a hydrostatic pressure gradient created by distal opening of the spinal fluid column towards the atmosphere. The magnitude of the reduction in hydrostatic force on the brain should depend on the vertical distance between the brain and the dural opening, and thus will increase by head elevation. No studies have analyzed ICP after dural puncture in supine and upright positions. This study on the cat records ICP, mean arterial pressure, and central venous pressure before and after dural puncture in supine and head-elevated positions. The dural puncture was performed at a level corresponding to the lumbar region. Initially ICP was 10.9 +/- 1.9 mmHg (mean +/- SD), which decreased to 5.1 +/- 2.0 mmHg after 24.5 cm (18 mmHg) of head elevation (n = 7). Intracranial pressure decreased to 5.2 +/-3.5 mmHg following dural puncture in the supine position and to -11.3 +/- 4.2 mmHg after the head elevation (n = 7). Active drainage of CSF fluid in the supine position in a volume similar to that spontaneously drained after head elevation reduced ICP by 2.0 +/- 0.5 mmHg (n = 3). The results show that a significant ICP reduction may occur following opening of the spinal canal. The reduction can be explained more by hydrostatic forces than by loss of CSF; also explaining why it is more significant when upright than supine. The decrease in ICP increases transvascular pressure, which may induce the disappearance of the normally present subdural venous collapse with an increase in venous blood volume.

Cervical MRI Findings in Intracranial Hypotension

Intracranial hypotension is characterised by a fall in intracranial pressure presenting clinically with postural headache and cervical pain. The syndrome may arise after lumbar puncture, surgery, trauma, severe dehydration or spontaneously. We studied two patients with intracranial hypotension presenting hallmark intracranial MR features of the syndrome with different involvement of the cervical spine in terms of MR features and clinical presentation and course. MR imaging of the cervical and dorsal spine in both patients was carried out using T1, T2 and T2-FLAIR weighted sagittal spin echo sequences and T2 weighted axial turbo spin echo (TSE) sequences. In the first patient, MR disclosed an area of altered signal intensity within the cerebral canal in an extradural, anterior and lateral location both right and left, symmetrical with craniocaudal extension from C1 to D2. The area was strongly hyperintense in T2-FLAIR sequences compressing the anterolateral surface of the dura mater and was ascribed to an enlargement of the anterior vertebral venous plexus. MR examination four days later showed an almost complete resolution of the previous picture. In the second patient, MR imaging showed a fluid collection in the subdural space in the cervicodorsal spine in sagittal FLAIR and axial TSE images wth a hyperintense signal consistent with hygroma. Follow-up disclosed slow gradual resolution of the previous changes. The dilated epidural venous plexuses in the first patient could compensate the loss of CSF, as occurs intracranially where CSF volume is balanced with blood volume (Monro-Kellie's theory). The spinal hygroma evident in the second patient may have been a transudate secondary to meningeal hyperaemia. This hypothesis is supported by the raised proteins and cells found in the CSF and the meningeal enhancement after contrast administration. Intracranial hypotension is characterized not only by well-known changes in intracranial MR signal, but also by specific MR findings in the cervicodorsal spine. Knowledge of these MR features allows prompt recognition and adoption of the most suitable MR sequence with due assessment of the morphology of areas of altered signal intensity to disclose the pathogenesis.

硬膜穿刺後の一過性感音難聴例

We report a case of temporary decrease in bilateral hearing after a lumbar puncture. A 46-year-old female underwent extradural anesthesia for vaginal hysterotomy. During administration of the extradural anesthesia between lumbar vertebra No. 4 and 5 using a 17-gauge needle, the dura mater was damaged, resulting in leakage of cerebrospinal fluid. Lumbar puncture was then performed between lumbar vertebra No. 3 and 4 and the operation was performed. On the following day, the patient complained of bilateral hearing loss, headache, and tinnitus. The audiometry showed a hearing loss of 20-50dB mainly in the low frequency range. The patient was treated with lactated Ringer's injection and vitamin B12. An audiogram on the seventh postoperative day showed improvement. Normal hearing returned 4 weeks later. Seven months later, the patient underwent spinal anesthesia again for fracture dislocation of the left ankle. A 25-gauge needle was used for this anesthesia. She did not complain of headache and hearing loss, but minor hearing deficits were found by audiometry. We speculate that the hearing loss could be due to endolymphatic hydrops resulting from perilymphatic hypotonia due to loss of CSF.

Changes in intracranial CSF volume after lumbar puncture and their relationship to post-LP headache.

Post-lumbar puncture (LP) headache may be due to "low CSF pressure", leading to stretching of pain sensitive intracranial structures. The low intracranial pressure is secondary to net loss of intracranial CSF. It has, however, not been possible to measure intracranial CSF volume accurately during life until recently. Intracranial CSF volume can now be measured non-invasively by a MRI technique. The changes in intracranial CSF volume were studied in 20 patients who had LP. Total intracranial CSF volume was reduced in 19 of the 20 patients 24 hours after LP (range -1.8 mls to -158.6 mls). Most of the CSF was lost from the cortical sulci. Very large reductions in intracranial CSF volume were frequently related to post-LP headache but some patients developed headache with relatively little alteration in the intracranial CSF volume. There was not a measurable change in position of the intracranial structures following LP.

Brain water and ion content during progressive water loading in the newborn puppy.

Speculation: The relative absence of apparent brain volume regulation in response to acute water loads in the newborn in comparison to the adult is due to mechanical factors, namely the more compliant newborn skull. The more compliant skull allows a greater increase in intracranial volume before intracranial pressure values are reached that are critical for pressure-dependent brain volume regulatory processes, e.g. bulk flow loss of brain ecf and CSF via arachnoid villi.