Decrease In Cerebrospinal Fluid Pressure Research Articles

Modeling the impact of thoracic pressure on intracranial pressure

A potential contribution to the progression of Spaceflight Associated Neuro-ocular Syndrome is the thoracic-to-spinal dural sac transmural pressure relationship. In this study, we utilize a lumped-parameter computational model of human cerebrospinal fluid (CSF) systems to investigate mechanisms of CSF redistribution. We present two analyses to illustrate potential mechanisms for CSF pressure alterations similar to those observed in microgravity conditions. Our numerical evidence suggests that the compliant relationship between thoracic and CSF compartments is insufficient to solely explain the observed decrease in CSF pressure with respect to the supine position. Our analyses suggest that the interaction between thoracic pressure and the cardiovascular system, particularly the central veins, has greater influence on CSF pressure. These results indicate that future studies should focus on the holistic system, with the impact of cardiovascular changes to the CSF pressure emphasized over the sequestration of fluid in the spine.

Association between cerebrospinal fluid pressure and cognition in patients with Alzheimer’s disease and Lewy body dementia

BackgroundThe relationship between cerebrospinal fluid pressure (CSFP) and cognition has received little research attention. The purpose of this study was to explore the relationship between CSFP and cognition in patients with Alzheimer’s disease (AD) and patients with Lewy body dementia (LBD).MethodWe included 178 participants, including 137 patients with AD and 41 patients with LBD (including dementia with Lewy bodies (DLBs) and Parkinson’s disease dementia (PDD)). CSFP was measured by lumbar puncture, and a patient-reported history and laboratory test data were collected. Logistic and linear regression analyses were used to evaluate the associations between CSFP and cognition, the cerebrospinal fluid (CSF) / serum albumin ratio (Qalb), and CSF biomarkers of AD.ResultsThe mean age of the included patients was 63.58 ± 8.77 years old, and the mean CSFP was 121 ± 33.72 mmH2O. A total of 76.9% of the patients had a CSFP distribution of [90–170) mmH2O, 46 patients (25.8%) had severe dementia, 83 patients (46.6%) had moderate dementia, 28 patients (15.7%) had mild dementia, and 21 patients (11.8%) had mild cognitive impairment (MCI) (including 16 patients with MCI due to AD and 5 patients with MCI due to LBD). In all patients (p value < 0.001) and in patients with AD (p value = 0.01), the mean cerebrospinal fluid pressure (CSFP) was higher in patients with MCI than in patients with dementia. In multivariate analysis, in all patients (OR: 6.37, 95% confidential interval (CI): 1.76–23.04, p = 0.005) and patients with AD (odds ratio (OR): 5.43, 95% CI: 1.41–20.87, p = 0.005), a CSFP in the lowest quartile ([50–90) mmH2O) was associated with a higher level of severe dementia than a CSFP in the highest quartile ([170–210) mmH2O). In addition, there was a significant linear correlation between CSFP and the Mini-Mental State Examination (MMSE) score in all patients with dementia (r = 0.43, p = 0.04, Durbin-Watson test (D-W test) = 0.75).ConclusionIn patients with AD, the mean cerebrospinal fluid pressure was higher in patients with MCI than in patients with dementia, and the decrease in CSFP was related to a more serious dementia level. However, no such relationship was found in patients with LBD.

Abstract Number ‐ 12: First‐In‐Human Endovascular Treatment of Idiopathic Intracranial Hypertension Using a Miniature Biomimetic Transdural Shunt.

Introduction Successful percutaneous transvenous deployment of a miniature valved biomimetic transdural endovascular shunt (CereVasc eShunt, Auburndale, MA, USA) via an inferior petrosal sinus approach was recently described for treatment of post‐subarachnoid hemorrhage communicating hydrocephalus.The endovascular shunt replicates the function of the arachnoid granulation by draining cerebrospinal fluid (CSF) from the cerebello‐pontine angle cistern to the ipsilateral internal jugular vein. Idiopathic intracranial hypertension (IIH), usually resulting from venous transverse sinus stenosis, can be treated with pharmacological inhibition of CSF production, surgical ventriculoperitoneal shunting, or using venous stent angioplasty. In IIH, elevated CSF pressure can act to exacerbate venous sinus stenosis, resulting in worsening CSF reabsorption, thereby perpetuating a vicious cycle. The authors sought to evaluate the role of the minimally invasive eShunt approach in IIH management. Methods A 50‐year‐old male patient with history of dyslipidemia and IIH initially presented 6 years ago with diplopia initially treated with poorly tolerated acetazolamide and periodic lumbar punctures with subsequent symptom improvement. The patient was admitted following rapid evolution of sudden onset horizontal diplopia and headache. Brain magnetic resonance revealed flattening of the posterior sclera, partially empty Sella Turcica, enhancement of the prelaminar optic nerves and enlarged Meckel´s cave. Lumbar puncture was performed with opening pressure of 28 cmH2O. Cerebral angiography with 3D venography confirmed bilateral transverse sinus stenosis, though without a significant pressure gradient. Results The patient declined surgical ventriculoperitoneal shunting and was approved for compassionate use of eShunt by regulatory and bioethics committees.He underwent successful endovascular transdural deployment of the eShunt, which he tolerated well and was discharged at 48 hours post‐procedure with rapid symptomatic headache relief. Upon 30‐day follow‐up repeat brain MRI showed improvement of the prominent subarachnoid space around both optic nerves and sustained improvement of his pre‐procedural headache and diplopia.A repeat lumbar puncture revealed a lowed opening pressure of 20 cmH2O and MRI cisternography confirmed maintained patency of the biomimetic valve with accumulation of Gadolinium‐enhanced CSF drainage through the eShunt into the jugular bulb. Conclusions The current report describes the first‐in‐human use of the eShunt device for treatment of IIH resulting in sustained symptomatic relief along with decrease in CSF pressure and pre‐laminar optic nerve edema. The current results, which require confirmation in a larger cohort with longer follow‐up, are encouraging and suggest a possible role for minimally invasive endovascular transdural eshunt placement in the management of IIH.

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.

Complications Associated With Transsphenoidal Pituitary Surgery: Review of the Literature.

Complications Associated With Transsphenoidal Pituitary Surgery: Review of the Literature.

Post-Spinal a Rare Complication and Treatment: Tinnitus and Epidural Blood Patch.

Dear Editor, Rare auditory symptoms such as tinnitus after spinal anaesthesia have been observed (1–4). It can be accompanied by headache (1, 4) and can become chronic and affect a patient’s quality of life. In this case, we aimed to present our clinical experience regarding the relief of symptoms by an epidural blood patch in a patient who developed headache and bilateral tinnitus following spinal anaesthesia. A 31-year-old female patient, who was 58 kg in weight and 169 cm in height, was scheduled for operation under spinal anaesthesia due to venous stasis. Informed written consent was obtained. The spinal space was accessed with a 25-G Quincke needle on the first try through the L4–5 interspinous space. On observing a clear cerebrospinal fluid leak, 12.5 mg of hyperbaric bupivacaine and 15 μg of fentanyl were intrathecally administered in a volume of approximately 3 mL. The patient was admitted to the hospital on the first postoperative day due to severe headache that started from the nape of the neck and that involved the entire head. The headache was accompanied by tinnitus (ringing in both ears and motor noise) and nausea–vomiting and was more prominent in the standing and sitting positions. The patient was chiefly discomforted by the tinnitus. The headache diminished while in the lying position, but the tinnitus did not subside. An intravenous access was established in the patient, and she was hydrated. An oral caffeinated analgesic and antiemetic were started. The headache alleviated on the second day of admission, but the tinnitus remained. The patient was unable to sleep and expressed that she was extremely discomforted by this. Given that it was accompanied by headache, we thought that the patient could benefit from an epidural blood patch. Following appropriate site cleaning, approximately 12 mL of the blood patch was epidurally administered by accessing the same space. The tinnitus in the left ear immediately improved following the injection, while it disappeared within approximately 12 h in the right ear. Additionally, the complaint of pain, which lost its severity with the medical treatment, completely disappeared. Aetiology regarding symptoms related to hearing following spinal anaesthesia is not very clear. One of the proposed hypotheses is the decrease in intra-labyrinth pressure. The cochlear duct provides an anatomical connection between the cochlea and the subarachnoid distance. The composition of the perilymph in the cochlea closely resembles the cerebrospinal fluid. One of the proposed views is that a decrease in cerebrospinal fluid pressure causes a decrease in intra-labyrinth pressure and that this causes functional inability in the ear in transmitting sounds (5). Symptoms could spontaneously subside; however, there are patients who became chronic. The relationship of chronic cases with spinal anaesthesia can only be revealed by obtaining a good medical history. These patients can benefit from an epidural blood patch (1, 2, 4). In a patient who developed tinnitus following spinal anaesthesia (4 years), it was learned, upon obtaining medical history by the ear, nose and throat specialist, that the complaint started 24 h after spinal anaesthesia, and the patient was directed to an anaesthetist. The tinnitus was successfully treated by administering 20 mL of an epidural blood patch to the patient (2). A patient with postspinal 8 years tinnitus complaint underwent epidural anaesthesia for another surgical operation. The tinnitus recovered by the epidural administration of 27 mL of bolus, followed by a local anaesthetic performed by continuous infusion (3). Due to the high rate of success and ease of application, an epidural blood patch is the accepted gold standard treatment in treating postspinal headache when conservative treatments have failed. It is a treatment whose major side effects are (usually temporary) rare, and it is safe and effective. Side effects are low back pain or radicular pain during injection, generally related to the administered volume (6). For evaluating these cases, the epidural administration of any application-blood, normal saline or local anaesthetics-appears to be effective in improving auditory symptoms. In conclusion, the accompaniment of nausea–vomiting and tinnitus with headache that develops after spinal anaesthesia negatively affects the quality of life. Therefore, we think that administering an epidural blood patch without delay in the presence of auditory symptoms accompanying headache will improve the comfort of patients.

Comments: New approach to treat an old problem: Mannitol for post dural puncture headache.

Sir, We read with great interest the article, ‘New approach to treat an old problem: Mannitol for post-dural puncture headache (PDPH)’.[1] PDPH is a low pressure headache. The role of cerebrospinal fluid (CSF) leak and lowering CSF pressure are the causes for the headache. Two theories are postulated in this regard.[2,3] First, decrease in CSF pressure leading to the traction on the pain sensitive parietal dura and intracranial structures leading to the headache. The second theory is based on the Monro Kellie doctrine[2] which states that the sum of volume of brain, CSF and intracranial blood is kept constant; loss of CSF leads to increase in the blood volume due to venodilatation. This venodilatation is attributed as the cause of the headache. As rightly mentioned in the article, there is no evidence suggesting a role for use of mannitol in relieving PDPH which is a low pressure headache. Mannitol is a drug commonly used for lowering high intracranial pressure (ICP). The mechanism leading to reduction in PDPH may be explained as below: ICP reduction can be due to two mechanisms, the early reduction being due to plasma expansion and late, due to diuresis.[4] Plasma expansion reduces the blood viscosity and increases the cerebral blood flow and oxygenation. This eventually leads to a probable reduction in the headache due to cerebral vasoconstriction as a compensatory mechanism. This may be cited as the reason behind the improvement of the headache. As far as the osmotic action of mannitol is concerned, an intact blood brain barrier is a prerequisite, and frequent dosing would cause dyselectrolytaemia and dehydration which would worsen the situation.[4] Another theory can be related to the rebound increase in ICP that can occur after the initial reduction because of the eventual passage of mannitol into the brain. This rebound phenomenon[4,5] is particularly associated with mannitol administration in a patient without an intact blood brain barrier which is possibly the case here. But utilising this disadvantage of mannitol to get relief from a self-limiting headache which is expected to resolve in 50% of the patients in 3–4 days[2] and as well as subjecting them to the risk of dehydration and electrolyte imbalance may not be acceptable.

Neurogenic Shock Immediately following Posterior Lumbar Interbody Fusion: Report of Two Cases

Study Design Case report. Objective To present two cases of neurogenic shock that occurred immediately following posterior lumbar interbody fusion (PLIF) and that appeared to have been caused by the vasovagal reflex after dural injury and incarceration of the cauda equina. Case Report We present two cases of neurogenic shock that occurred immediately following PLIF. One patient had bradycardia, and the other developed cardiac arrest just after closing the surgical incision and opening the drainage tube. Cardiopulmonary resuscitation was performed immediately, and the patients recovered successfully, but they showed severe motor loss after awakening. The results of laboratory data, chest X-ray, electrocardiogram, computed tomography, and echocardiography ruled out pulmonary embolism, hemorrhagic shock, and cardiogenic shock. Although the reasons for the postoperative shock were obscure, reoperation was performed to explore the cause of paralysis. At reoperation, a cerebrospinal fluid collection and the incarceration of multiple cauda equina rootlets through a small dural tear were observed. The incarcerated cauda equina rootlets were reduced, and the dural defect was closed. In both cases, the reoperation was uneventful. From the intraoperative findings at reoperation, it was thought that the pathology was neurogenic shock via the vasovagal reflex. Conclusion Incarceration of multiple cauda equina rootlets following the accidental dural tear by suction drainage caused a sudden decrease of cerebrospinal fluid pressure and traction of the cauda equina, which may have led to the vasovagal reflex.

Does the treatment of normal pressure hydrocephalus put the retinal ganglion cells at risk? A brief literature review and novel hypothesis

Normal pressure hydrocephalus (NPH) is a poorly understood entity as well as a source of continuous controversy in the neuroscientific community. The surgical management of this disease requires that intracranial pressure (ICP), also referred to as the cerebrospinal fluid pressure (CSFP), be lowered using a cerebrospinal fluid (CSF) diversion procedure. Numerous complications are linked with this procedure; we believe that new evidence suggests that the induction or acceleration of glaucomatous optic neuropathy are possible sequelae that warrant further investigation. We also suggest potential solutions derived from the increased understanding of the disease's pathophysiology and new advances in imaging of the optic nerve head complex. The recent inclusion of the translaminar gradient (TLG) (the difference between the intraocular pressure (IOP) and the ICP/CSFP across the thickness of the lamina cribrosa in the optic nerve head complex) in the pathogenesis of normal tension glaucoma (NTG) suggests that the disease may be a complication encountered during the treatment of NPH with CSF diversion procedures. The significant decrease in CSFP required to treat NPH increases this gradient. In addition, there have been recent observations of an increased prevalence of NTG, as well as other forms of glaucoma, among patients with NPH, thought to be due to inherently fragile neurons in these patients. This new data suggest that patients who undergo ICP lowering therapy for their NPH may be at a higher risk of developing or accelerating already present NTG. We present the clinical and theoretical basis for our hypothesis after reviewing the relevant literature linking the two entities. We also propose a possible solution, as we believe that treatment guidelines for NPH should take the TLG into account. Indeed, recent advances in the imaging of the optic nerve head complex may provide an opportunity to detect the mechanical sequelae of an increased TLG in the preclinical stage, i.e., prior to optic nerve damage. If we are able to determine safe parameters for the TLG in this population, we may be able to recommend the initiation of prophylactic glaucoma therapy for selected patients.

Intracranial hypotension syndrome in a patient due to suboccipital craniectomy secondary to Chiari type malformation

Intracranial hypotension syndrome (IHS) is a rare disorder characterized by a decrease in cerebrospinal fluid pressure to less than 60 mm H2O. The syndrome is associated with occipital headache radiating to the frontal and temporal zones. The current clinical case describes the manifestation of IHS in a twenty-five year old female with a history of suboccipital craniectomy due to Chiari I malformation nine years earlier. The patient was admitted to the hospital complaining about postural, mainly occipital, headache during the last three months, aggravated by being in an upright position. The magnetic resonance imaging (MRI) revealed engorgement of the dural venous sinuses, significant enlargement of the pituitary gland and download displacement or sagging of the brain with effacement of the perichiasmatic cisterns and the prepontine cistern, while the spinal T2W MRI revealed a 7 mm × 2.5 mm dural defect with an extradural cerebrospinal fluid collection at the dorsal soft tissues of the cervical spine. The previous imaging did not reveal subdural effusions.

Post-dural puncture headache.

Dear Editor, August Bier’s first report of spinal anesthesia in August 1898 impressively described the development of a postdural puncture headache (PDPH) (1). When asked for complications of spinal anesthesia today, patients often respond with PDPH. PDPH is defined as a constant headache that worsens in the sitting or upright position following lumbar puncture (LP). Its incidence after spinal anesthesia in obstetric anesthesia is 1% to 6% (2) and 30% to 50% after a diagnostic LP (3) and can reach 80% after inadvertent LP during epidural obstetric anesthesia (4). Many theories exist regarding the pathophysiology of PDPH, but it appears to be related to the loss of cerebrospinal fluid into the epidural space with a decrease in cerebrospinal fluid pressure and downward movement of the brain and traction on the dura (5). Spontaneous recovery within 5 days occurs in most cases, but PDPH can last up to many months, like the case report of Barbosa et al. demonstrated (6). During this time, patients suffer and rehabilitation is restricted. Pharmacological therapy is seldom a complete success (5), but an epidural blood patch can resolve the issue in many cases (7). Due to the frequency of occurrence and the resulting physical limitations of patients, every effort should be made to learn about the risk factors of PDPH and how to avoid it. Nonmodifiable risk factors include gender, age, pregnancy, previous history of PDPH or chronic headache, and low body mass index (BMI). However, of modifiable risk factors, such as needle shape, bevel orientation, number of LP attempts, and prelumbar puncture positioning (8, 9), the most relevant appears to be needle size the smaller the size, the lower the PDPH incidence. Nevertheless, the approach may be considerable. Median, paramedian, and Taylor´s approaches have been advocated as the primary method in different settings, whereas the median approach may be easier for trainees, because the primary orientation seems straightforward. If cerebrospinal fluid cannot be detected, many choose the paramedian approach as a second strategy. With regard to the angled paramedian approach as the primary method, Mossafa et al. show that there is no difference in the incidence of PDPH compared with the median approach. In their study, the number of attempts to puncture is restricted to only one. This may not reflect clinical reality but may be part of the reason for these interesting results, demonstrating this kind of approach is not a risk factor for PDPH.

Is Multiple Sclerosis a Risk for Hypercoagulation States or Breast Cancer? A Case Report and a Literature Review to Assess Options

Abstract 4665 Introduction:Multiple sclerosis (MS) is an autoimmune inflammatory and chronic demyelinating disease. Occurrence of hypercoagulable states and breast cancer in patients with multiple sclerosis (MS) has not been extensively reported. We report a case of a female MS patient with recurrent DVTs, elevated factor VIII levels, and advanced breast cancer with aggressive biologic phenotypes. Case report:A 45-year-old Caucasian female with a history of MS had a breast mass diagnosed on a screening mammogram. She was diagnosed with right breast carcinoma (2.5 × 2.5 × 1.6 cm), T2 N3 M0, which correlated to stage IIIC. She underwent a right modified radical mastectomy with 16/25 lymph nodes involved, ER/PR status was positive, HER-2/neu 0 with high Ki67. Her post-surgery treatment plan included 4 cycles of Cyclophosphamide and Taxotere chemotherapy. She also received chest wall radiation as well as tamoxifen and aromatase inhibitor (Femara) therapy. The patient had never been on hormone replacement therapy or oral contraceptives. She had bilateral salpingo-oophorectomy and hysterectomy and pathology was unremarkable. Patient was diagnosed with Multiple Sclerosis at age 27. She was treated with intermittent courses of steroids, Interferon b-1b, Interferon b-1a, and Mitoxantrone (MTX) for relapsing/remitting MS for several years until she developed left hemiparesis, hypoesthesias, and residual visual dysfunction that prompted her to start IVIG therapy and plasmapheresis. Past medical history presents recurrent DVT (in 2006) and elevations of coagulation factor VIII (355%). The patient also developed superior vena cava thrombosis in the presence of Lovenox and coumadin therapy. Discussion:Multiple sclerosis (MS) is an autoimmune inflammatory disease of the central nervous system, frequently complicated by devastating neurologic symptoms and progressive disability. Risks of DVT in bedridden or wheelchair-bound MS patients have been suggested. Previous studies show that the frequency of DVT in late-stage MS may be over 40%. Additionally, in MS patients without risk factors, it has been suggested with an autoimmune inflammatory disease that the inflammatory infiltration in MS plaques located close to small or medium-sized veins could have a role as well. The lumbar puncture could also be one of other thrombophilic factor in MS, since after dural puncture the decrease of cerebrospinal fluid pressure induces a rostrocaudal sagging effect with traumatic damage to the fragile venous endothelial wall and may trigger a venous vasodilatation with resultant stasis. Elevated factor VIII levels are a risk factor for venous thrombosis and may also be associated with the risk of arterial thrombosis in coronary heart disease. Studies show that factor VIII levels may be increased by chronic inflammation. However, elevated factor VIII levels in patients with MS have never been reported.There is no cure for MS, though there are several drugs such as immunomodulatory agents that can slow or stop its progress. However, current data show a small increased risk of breast cancer in women with MS. The size of the breast tumor was also larger for woman with MS. More specifically, the proportions of biologically aggressive phenotypes that can worsen the prognosis of breast cancer incrementally despite the biologic phenotype at diagnosis also were investigated in this group of patients. One hypothesis linking breast cancer and MS involves long-term use of immunomodulatory agents including IFNs and glatiramer. Immunomodulatory therapy may impart immune system alterations that promote enhancement of cancer cells' ability to evade immune recognition and cancer metastasis by altering the body's ability to conduce immunosurveillance. However, consistent with previous observations, this remains unexplained and warrants further attention. Conclusion:The Female patient with MS described in this article presents an example of recurrent DVT, Superior Vena Cava thrombosis, elevated factor VIII levels, and breast cancer with stage IIIC and biologically aggressive phenotypes. The authors concern is that there is an increased risk of hypercoagulation states and breast cancer development in patients with MS. The systematic application of long-term preventive DVT may be considered for this group of patients. Disclosures:No relevant conflicts of interest to declare.

More advanced Alzheimer's disease may be associated with a decrease in cerebrospinal fluid pressure

In a recent article, elevated cerebrospinal fluid pressure (CSFP) consistent with very early normal pressure hydrocephalus (NPH), was found in a small subset of Alzheimer's disease (AD) patients (possible AD-NPH hybrids) enrolled in a clinical trial for chronic low-flow cerebrospinal fluid drainage. Also in the same study, was another interesting finding that merits further discussion: a substantial proportion of AD patients had very low CSFP. Based on the characteristics of these subjects, we hypothesize that more advanced AD may be associated with a decrease in CSFP. Reduced CSFP among a group of AD patients could provide a clue towards a better understanding of the high rate of comorbidity reported between AD and glaucoma since it has been shown that mean CSFP is lower in subjects with primary open-angle glaucoma. This could result in an abnormally high trans-lamina cribrosa pressure difference and lead to glaucomatous damage.

Hearing Loss and Cerebrospinal Fluid Pressure: Case Report and Review of the Literature

A decrease in cerebrospinal fluid pressure may result in an endolymphatic hydrops through a patent cochlear aqueduct or through the fundus of the internal auditory canal. This hydrops typically leads to low-frequency sensorineural hearing loss. We describe the case of a man who presented with a subjective and objective hearing loss in addition to a headache 4 days after he had undergone a dural puncture. We treated him with a standard epidural blood patch. Immediately after treatment, his hearing improved and his headache resolved.

Perioperative Hearing Impairment

Perioperative Hearing Impairment

Myth: fluids, bed rest, and caffeine are effective in preventing and treating patients with post-lumbar puncture headache.

Myth: fluids, bed rest, and caffeine are effective in preventing and treating patients with post-lumbar puncture headache.

Intracranial Volume/Pressure Relationship During Desflurane Anesthesia in Dogs

Desflurane-induced increase of intracranial pressure (ICP) does not appear to be completely explained by desflurane-induced changes in cerebral blood flow, cerebrospinal fluid (CSF) formation and reabsorption, or brain tissue water content. The present study was designed to determine whether desflurane alters intracranial volume/pressure relationships sufficiently to account for desflurane-induced increase of ICP. In 24 dogs, infusions of mock CSF were used to determine the CSF pressure increase due to increase of CSF volume, and the capacity of CSF pressure to return to baseline after a CSF pressure increase (CSF pressure normalization). CSF pressure increase was assessed by determining (a) CSF pressure prior to volume infusion (P(o)), (b) peak CSF pressure (Pp) caused by volume injection, (c) intracranial compliance (C, calculated as the ratio of change of intracranial volume [delta V] to change of CSF pressure [delta P]), (d) the volume pressure response (VPR, a measure of elastance, calculated as the ratio of delta P to delta V, (e) the pressure/volume index (PVI, calculated as the ratio of delta V to log Pp/P(o)), and (f) estimated intracranial compliance (C(e), calculated from PVI as 0.4343PVI/P(o)). CSF pressure normalization was assessed by determining the first (S1) and second (S2) phase slopes of decrease of CSF pressure from Pp, the duration of S1 (DS1), and the intersection of extrapolated S2 with the P(o) to Pp slope (delta Ps). During normocapnia (Group 1, n = 6) and hypocapnia (Group 2, n = 6), two infusions were made at each of four experimental conditions: 0.5 minimum alveolar anesthetic concentration (MAC) desflurane and normal or increased CSF pressure, and 1.0 MAC desflurane and normal or increased CSF pressure. For comparison to these two desflurane-anesthetized groups, intracranial volume/pressure values were determined at the same experimental conditions during 0.5 MAC isoflurane (Group 3, n = 6) and in controls (Group 4, n = 6) anesthetized with thiopental 12 mg/kg then 12 mg.kg-1.h-1 intravenously combined with halothane 0.5% inspired. In comparison to controls, both desflurane and isoflurane decreased Ce at normal CSF pressure but not at increased CSF pressure. However, desflurane and isoflurane had no consistent effect on the other measures of CSF pressure increase caused by increase of CSF volume. Isoflurane also decreased the capacity for CSF pressure normalization at normal CSF pressure as indicated by decreased S1 and increased delta Ps. It is concluded that, under conditions of normal ICP, desflurane may decrease Ce, favoring an increase of ICP.

Limiting ischemic spinal cord injury using a free radical scavenger 21-aminosteroid and/or cerebrospinal fluid drainage.

Traumatic spinal cord injury occurs in two phases: biomechanical injury, followed by ischemia and reperfusion injury. Biomechanical injury to the spinal cord, preceded or followed by various pharmaceutical manipulations or interventions, has been studied, but the ischemia/reperfusion aspect of spinal cord injury isolated from the biomechanical injury has not been previously evaluated. In the current study, ischemia to the lumbar spinal cord was induced in albino rabbits via infrarenal aortic occlusion, and two interventions were analyzed: the use of U74006F (Tirilazad mesylate), a 21-aminosteroid, and cerebrospinal fluid (CSF) drainage. These treatment modalities were tested alone or in combination. In Phase 1 of this study, the rabbits received 1.0 mg/kg of Tirilazad or an equal volume of vehicle (controls) prior to the actual occlusion, three doses of Tirilazad (1 mg/kg each) during the occlusion, then several doses after the occlusion. Of the Tirilazad-treated animals, 30% became paraplegic while 70% of the control animals became paraplegic. Phase 2 involved the same doses of Tirilazad as in Phase 1 and, in addition, CSF pressure monitoring and drainage were performed. The paraplegia rate was 79% in the control animals, 36% in the group receiving Tirilazad alone, 25% in the group with CSF drainage alone, and 20% in the Tirilazad plus CSF drainage group. This rate also correlated with changes noted in CSF pressure; both Tirilazad administration alone and CSF drainage alone induced a decrease in CSF pressure and the two combined produced a further decrease. There was marked improvement in the perfusion pressure when using Tirilazad alone, CSF drainage alone, and Tirilazad therapy in combination with CSF drainage, with the last group producing the largest increase. This change in CSF pressure and perfusion pressure correlated with improved functional neurological outcome. Pathological examination revealed that Tirilazad therapy reduced the extensive and diffuse neuronal, glial, and endothelial damage to (in its most severe form) a more patchy focal region of damage in the gray matter. Cerebrospinal fluid drainage resulted in pyknosis of some motor neurons, and some eosinophilia. The combination of CSF drainage and Tirilazad administration resulted in the least abnormality, with either normal or near-normal spinal cords. It is concluded that Tirilazad administration decreased CSF pressure during spinal cord ischemia and reperfusion and, like CSF drainage, increased and improved the perfusion pressure to the spinal cord, decreased spinal cord damage, and improved functional outcome.(ABSTRACT TRUNCATED AT 400 WORDS)

Cerebello-Pontine Angle and Brain-Stem Tumors with Fluctuating Hearing Loss (5 Case Report)

Five cases of cerebello-pontine angle and brain-stem tumors with fluctuating hearing loss were reported. They were consisted of two cases of acoustic neurinomas, one of cerebello-pontine angle meningioma, one of hemangioblastoma of brain-stem, and one of supra- and sub-tentorial dumb-bell type astrocytoma.Their fluctuating hearing losses occurred predominantly on the range of low frequencies. They were observed paroxysmal fluctuation in the hearing losses during their clinical courses. In two cases of them, deafness occurred and improved abruptly, and we found a cyst in a part of these tumors.The mechanisms of the fluctuating phenomenon were explored from the operative and audiological findings, and following causes were presumed.The first, in the courses of growths of the tumors, it may act as reversible invasion to acoustic nerve or acoustic tracts in the brain-stem, within a certain period of time. The second, as a result of that cerebello-pontine angle tumor may exert pressure upon the labyrinthine artery, it may cause the reversible of the inner ear function to make change in some instances. The third, the rapid increase or decrease in cerebro-spinal fluid pressure may cause the change of pressure of the tumor on acoustic nerve or brain-stem.

Decrease in cerebrospinal fluid-pressure induced by cervical sympathetic stimulation

Summary In cats monolateral and bilateral stimulation of the cervical sympathetic trunks causes a reduction of the cerebrospinal fluid-pressure, the responses being evident also within the range of physiological frequencies. Neither cocaine nor guanethidine and nicergoline, an alpha-receptor blocking agent, influenced the responses to nerve stimulation at doses which per se did not markedly change CSF-pressure or systemic blood pressure.