Visualization of intravenously administered contrast material in the CSF on fluid-attenuated inversion-recovery MR images: an in vitro and animal-model investigation.
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BACKGROUND AND PURPOSE: The FLAIR (fluid-attenuated inversion-recovery) pulse sequence has been shown to be sensitive to abnormalities of the subarachnoid space. Our clinical experience led us to investigate whether intravenously injected contrast material can affect the appearance of the subarachnoid space on FLAIR MR images. METHODS: After noting unexplained high signal in the subarachnoid space on FLAIR images in a patient, we studied two dogs with sequential FLAIR MR imaging after i.v. administration of contrast material. A third dog was studied with a 6-hour delayed FLAIR sequence after triple-dose (0.3 mmol/kg) i.v. contrast administration. CSF was obtained from two animals for measurement of gadolinium concentration. A phantom was developed to determine the lowest concentration at which the effects of gadolinium were evident on FLAIR images in vitro. RESULTS: In all three animals, the appearance of the CSF in the ventricles or subarachnoid space was modified after administration of i.v. contrast. This was most evident on delayed images. The CSF samples showed a gadolinium concentration of 0.007 mmol/L in the dog who received the 0.1 mmol/kg dose and 0.02 mmol/L in the dog who received a triple dose. In our in vitro phantom experiments, gadolinium effects were evident on FLAIR images at a concentration four times lower than those on T1-weighted images. CONCLUSION: I.v. contrast material can cross into the CSF in sufficient concentration to alter the appearance of the subarachnoid space on FLAIR images in normal dogs. Although we encountered two patients with CNS disease in whom enhancement of the CSF was seen on postcontrast FLAIR images, additional investigation is needed in humans to determine whether enhancement may occur at triple dose in healthy subjects. (+info)
Influence of sex on cerebrospinal fluid density in adults.
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The extent of sensory block during spinal anaesthesia is unpredictable and is influenced by many factors, mainly patient position, site of injection, baricity and the dose of drug injected. Among other factors, cerebrospinal fluid (CSF) density has been advocated to affect subarachnoid distribution of local anaesthetics. In this study, we have investigated the influence of patient characteristics such as sex, age, weight and height on variations in the density of CSF in more than 46 consecutive patients undergoing spinal anaesthesia. CSF 2 ml was obtained after spinal puncture and before injection of local anaesthetic. Mean CSF density measured at 37 degrees C was mean 1.00054 (SD 0.00017) g ml-1, with significantly lower CSF densities in women (1.00049 (0.00011) g ml-1) than in men (1.00058 (0.00011) g ml-1) (P = 0.024). In contrast, there was no correlation between age, weight or height, and CSF density. These results suggest that sex significantly influenced CSF density and may therefore modify subarachnoid distribution of local anaesthetics. (+info)
Computerized axial tomography: the normal EMI scan.
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Computerized axial tomography using the EMI scanner as a new method of using x-rays in diagnosis. The technique displays intracranial and orbital structures in the transverse plane. The appearances of normal EMI Scans are described and correlated with cerebral and orbital anatomy seen in transverse section. (+info)
Computerized tomography (the EMI Scanner): a comparison with pneumoencephalography and ventriculography.
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Computerized tomography, using the EMI Scanner, allows the diagnosis of cerebral atrophy or hydrocephalus to be made with the same degree of accuracy as conventional neuroradiological methods. Ventricular measurements made on EMI scans have been compared with those from pneumoencephalograms and ventriculograms. A range of normal ventricular measurements for the EMI scan is suggested. (+info)
Regulation of proprioceptive memory by subarachnoid regional anesthesia.
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BACKGROUND: Patient perception of limb position during regional anesthesia is frequently incorrect. The existing model ascribes this misperception, or phantom sensation, as a reversion to a fixed, slightly flexed, body schema. A model was developed to evaluate the influence of limb position changes on the incidence of incorrect or phantom sensations during regional anesthesia. METHODS: Forty American Society of Anesthesiologists physical status I-III adult patients undergoing genitourinary procedures under subarachnoid anesthesia were assigned to a lidocaine or bupivacaine treatment group and randomly assigned to one of four time groups (1, 4, 7, and 10 min). After blockade, patients were placed supine and blinded to limb positioning manipulations. One leg was flexed and the contralateral leg extended, with leg positions subsequently reversed at the assigned time point. At 10 min, patients were asked to identify the position of each leg. Percentage of incorrect response was analyzed using a logistic regression model with two independent variables: treatment and time. A supplemental study was undertaken to evaluate the observed difference in incorrect perceptions relative to flexed first versus extended limb first sequencing. RESULTS: The inability to perceive a change in limb position under regional anesthesia is dependent on the time after the block that the position change is initiated in relation to the onset characteristics of the local anesthetic. A phantom sensation of an extended leg position clearly exists. The flexed-first limb has a significantly higher incidence of incorrect or phantom perceptions. CONCLUSION: Proprioceptive memory involves a dynamic neuroplastic imprinting process that is influenced by limb or joint position prior to onset of regional anesthesia. This contrasts with previously held beliefs of a purely fixed body schema. (+info)
Subarachnoid meperidine (Pethidine) causes significant nausea and vomiting during labor. The Duke Women's Anesthesia Research Group.
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BACKGROUND: The combined spinal-epidural (CSE) technique using bupivicaine-fentanyl has become an established method of pain control during parturition. One limitation is the relatively short duration of effective analgesia produced by bupivicaine-fentanyl. In contrast, subarachnoid meperidine has been shown to provide a long duration of anesthesia in nonobstetric patients. Therefore, the authors tested the hypothesis that subarachnoid meperidine produces a significant increase in the duration of analgesia compared with bupivicaine-fentanyl. METHODS: Based on a power analysis of preliminary data, the authors intended to recruit 90 patients for the study, randomized to three groups: 2.5 mg bupivicaine-25 microg fentanyl, 15 mg meperidine, or 25 mg meperidine. However, after enrolling 34 patients, the study was discontinued because of a significant increase in nausea or vomiting in the study patients. RESULTS: Nausea or vomiting was substantially increased in both meperidine groups compared with the bupivicaine-fentanyl group: 16 with nausea or vomiting in the meperidine groups (n = 21), compared with 1 in the bupivicaine-fentanyl group (n = 11), P = 0.0011. The mean duration of analgesia provided by 25 mg meperidine was 126 +/- 51 min, compared with 98 +/- 29 min for bupivicaine-fentanyl and 90 +/- 67 min for 15 mg meperidine. These data were not significant (P = 0.27). CONCLUSIONS: Although intrathecal meperidine could potentially prolong subarachnoid analgesia during labor, its use was associated with a significant incidence of nausea or vomiting. These data do not support the use of subarachnoid meperidine in doses of 15 or 25 mg for labor analgesia. (+info)
Analgesia produced by morphine when acting from the liquor space.
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1 In cats analgesia was produced by morphine sulphate introduced into different parts of the liquor space in doses too small to be effective on intravenous injection. Analgesia was measured with the tail pinch method of Russell & Tate (1975). 2 On infusion into the fourth ventricle or into the subarachnoid space beneath the ventral surface of the brain stem caudal to the pons, doses of 100 to 200 mug of morphine sulphate were sufficient to produce strong long-lasting analgesia. On injection into the cisterna magna somewhat larger doses (400 to 800mug) were required. 3 It is concluded that the site where morphine acts when producing analgesia in all three circumstances is at the ventral surface of the brain stem. 4 The possibility is discussed that the structures acted upon are tryptaminergic nerve fibres. They arise from the raphe nuclei, belong to a descending inhibitory pathway, and on their way to the spinal cord, reach the ventral surface of the brain stem lateral to each pyramid, where they could be reached and acted upon by the morphine. This theory postulates a morphine sensitivity of tryptaminergic nerve fibres. (+info)
Alterations in endogenous brain beta-endorphin release by adrenal medullary transplants in the spinal cord.
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While transplants of adrenal medullary cells into the spinal subarachnoid space may produce antinociception via inhibition of spinal pain transmission pathways, alterations at higher central nervous system (CNS) centers have not been addressed. Recent findings suggest that prolonged noxious stimulation results in release of endogenous beta-endorphin in the brain, possibly as a compensatory mechanism to reduce nociception. The goal of this study was to determine whether adrenal medullary transplants in the spinal subarachnoid space alter endogenous beta-endorphin secretion in the hypothalamic arcuate nucleus, its principal CNS source. Pain behaviors and arcuate beta-endorphin secretion by microdialysis were monitored during the formalin pain test in animals with spinal adrenal medullary or control transplants. Basal levels of extracellular beta-endorphin were 3-fold higher in adrenal medullary-implanted than in controls. In control animals, formalin induced robust pain behaviors and a marked transient increase in beta-endorphin release 30-60 min following injection. In contrast, pain behaviors were attenuated and the formalin-induced increase in beta-endorphin was completely blocked in adrenal medullary implanted animals. Findings from these studies indicate that adrenal medullary transplants in the spinal subarachnoid space can alter beta-endorphin release in the arcuate nucleus both basally and in response to noxious stimuli. Thus, spinally placed adrenal medullary transplants not only alter local spinal cord pharmacology, but can alter endogenous neurochemistry at higher pain processing centers as well. (+info)