Brown-Séquard syndrome: a rare manifestation of decompression sickness.

Neurological decompression sickness (DCS) is a rare condition that commonly leads to spinal cord injury. We report the case of a 30-year-old man who developed left-sided weakness and numbness after diving to a maximum depth of 15 m with a total dive time of 205min (10 repetitive dives). To the best of our knowledge, only six cases diagnosed as Brown-Séquard syndrome caused by DCS have been reported in the literature. Divers should be aware of the risk factors of DCS before diving and clinicians should make the diagnosis of spinal cord DCS based primarily on clinical symptoms, not on magnetic resonance imaging findings.

Minimizing shoulder syndrome with intra-operative spinal accessory nerve monitoring for neck dissection.

The objective of this study was to analyze the safety and results of intra-operative SAN (spinal accessary nerve) monitoring during selective neck dissection, with emphasis on shoulder syndrome. Twenty-five consecutive patients with head and neck cancer were studied. Selective neck dissection was performed by a single clinical fellow under the supervision of the department chief using an intra-operative SAN monitor. Electrophysiological data were recorded after initial identification of the SAN and continued until just before closure. Electromyographic evaluation was carried out to assess SAN function one month postoperatively. Shoulder disability was also evaluated at this time using a questionnaire for shoulder syndrome (shrug, flexion, abduction, winging, and pain). No patients had postoperative shoulder syndrome involving shrug, flexion, abduction, or winging. Twenty-two of the 25 (88%) patients had shoulder pain, but the average pain score was low (2.3 ± 1.3). No patients had neck recurrence during at least 1 year of follow up. By using nerve monitoring during selective neck dissection, no patient developed significant "shoulder syndrome", with the exception of slight pain.

Cloning and functional characterization of an Arabidopsis nitrate transporter gene that encodes a constitutive component of low-affinity uptake.

The Arabidopsis CHL1 (AtNRT1) gene encodes an inducible component of low-affinity nitrate uptake, which necessitates a "two-component" model to account for the constitutive low-affinity uptake observed in physiological studies. Here, we report the cloning and characterization of a CHL1 homolog, AtNRT1:2 (originally named NTL1), with data to indicate that this gene encodes a constitutive component of low-affinity nitrate uptake. Transgenic plants expressing antisense AtNRT1:2 exhibited reduced nitrate-induced membrane depolarization and nitrate uptake activities in assays with 10 mM nitrate. Furthermore, transgenic plants expressing antisense AtNRT1:2 in the chl1-5 background exhibited an enhanced resistance to chlorate (7 mM as opposed to 2 mM for the chl1-5 mutant). Kinetic analysis of AtNRT1:2-injected Xenopus oocytes yielded a K(m) for nitrate of approximately 5.9 mM. In contrast to CHL1, AtNRT1:2 was constitutively expressed before and after nitrate exposure (it was repressed transiently only when the level of CHL1 mRNA started to increase significantly), and its mRNA was found primarily in root hairs and the epidermis in both young (root tips) and mature regions of roots. We conclude that low-affinity systems of nitrate uptake, like high-affinity systems, are composed of inducible and constitutive components and that with their distinct functions, they are part of an elaborate nitrate uptake network in Arabidopsis.

Rapid and continuous monitoring of cerebral perfusion by magnetic resonance line scan assessment with arterial spin tagging.

A new approach is presented for rapid and continuous monitoring of cerebral perfusion which is based upon line-scan MR column imaging with arterial spin tagging (AST) of endogenous water. Spin tagging of arterial water protons is accomplished using adiabatic fast passage inversion, followed by acquisition of the perfusion sensitive MR signal from a column placed at the desired level through the brain using line scan localization techniques. A perfusion sensitive line scan is followed by a non-perfusion sensitive line scan, and perfusion is calculated pixel-by-pixel from the intensity difference of the two lines. Continuous perfusion measurements are reported with temporal resolution of 10 s in pixels of volume 0.027 cm3 or less. Examples of the methodology are given during hypercapnic challenge induced with carbon dioxide, and during an ischemic event induced by reversible middle cerebral artery occlusion. The method is also used to characterize the signal response as a function of arterial inversion time and post inversion acquisition delay. These methods permit rapid and continuous monitoring of cerebral perfusion with high spatial resolution, and can be interleaved with MR measurements of diffusion and T1 to follow the progression of cerebral events during physiological or pharmacological intervention.

The influence of preischemic hyperglycemia on acute changes in brain water ADCw following focal ischemia in rats.

The effect of preischemic hyperglycemia on the acute decline of brain apparent diffusion coefficient of water (ADCw) following cerebral ischemia was studied in a rat model of middle cerebral artery occlusion (MCAO). ADCw was measured by NMR with a newly developed spin-echo line-scan protocol that provides for an ADCw calculation every 15 s at a spatial resolution of 3.4 microl/pixel. A remote controlled occluding device was used to initiate ischemia from outside the magnet, allowing for continuous monitoring of ADCw before, during and after MCAO. Preischemic hyperglycemia (25-30 mM) was achieved via i.v. infusion of 50% glucose. The decline in ADCw following ischemia was analyzed to obtain three-time constants: the time from onset of ischemia to initial significant ADCw decline below baseline level (i.e., 20% of maximal decline, T0.20), the time to decline by 50% (T0.50), and the time to decline by 95% (T0.95). Mean (+/-S.D.) values for T0.20, T0.50, T0.95 were: 39.6+/-7.2, 54. 0+/-7.8, 105.0+/-15.0 s for the normoglycemic group (n=7), and 49. 2+/-33.0, 116.4+/-2.4, 351.0+/-189.0 s for the hyperglycemic group (n=6), respectively. Hyperglycemia significantly prolongs T0.50 and T0.95 but does not affect T0.20. The temporal profiles of ADCw decline following ischemia under normo- and hyperglycemia are distinctively different from the known time course of membrane depolarization under similar experimental conditions, suggesting that mechanisms other than membrane depolarization and cell swelling may contribute to changes in ADCw in cerebral ischemia.

H2-uptake activity, spectra, reduction potentials, and kinetics of iron release on the surface of iron core from Azotobacter vinelandii bacterial ferritin.

Bacterial ferritin from Azotobacter vinelandii (AvBFo) has a function in H2 uptake. The Fe3+ reduction on the surface of the iron core from AvBFo is accompanied simultaneously by H2 uptake, with a maximum activity of H2 uptake of 450 H2/AvBFo. A reduction potential of -402 mV for iron reduction on the surface of the core is found. A shift to the red the protein absorbance peaks ranging from 280 to 290 nm is observed between pH 5 and 9 under 100% H2 reduction. The reduction potential for iron release becomes negative at a rate of 0.025 mV/Fe2+ released. The kinetics of iron release on the surface of the core is a first-order reaction.

The influence of preischemic hyperglycemia on acute changes in the apparent diffusion coefficient of brain water following global ischemia in rats.

We report the effect of increased plasma glucose levels on changes in the apparent diffusion coefficient of brain water (ADCw) during the first few minutes of global ischemia in rats. Brain ADCw values were acquired every 15 s using a diffusion-weighted line-scan MR pulse sequence. Preischemic hyperglycemia was achieved by infusion of 50% dextrose (i.v.) prior to KCl-induced cardiac arrest global ischemia. Analysis based on single voxels (3.4 microl) in brain demonstrated significant differences in the time course of ADCw decline between normoglycemic (n = 8) and hyperglycemic (n = 6) groups. Mean data from the hyperglycemic group indicated a biphasic decline of ADCw that was characterized by an initial rapid drop followed by a plateau of approximately 1 min before gradually declining and leveling off to its minimum value. In the normoglycemic group, ADCw declined to the same value as in the hyperglycemic group, but without a notable plateau. In the cerebral cortex, the times to maximal and half maximal ADCw drop following global ischemia in the hyperglycemic group were 3.96 and 2.26 min respectively. Corresponding time intervals for the normoglycemic group were 1.86 and 1.14 min, respectively. The time course for changes in ADCw demonstrated here is significantly different than that for anoxic depolarization reported under similar experimental conditions and suggests that events other than the complete loss of membrane ionic homeostasis and subsequent cell swelling may be involved in the initial decline of ADCw in global cerebral ischemia.

Perfusion deficit parallels exacerbation of cerebral ischemia/reperfusion injury in hyperglycemic rats.

Magnetic resonance imaging (MRI) techniques were used to determine the effect of preexisting hyperglycemia on the extent of cerebral ischemia/reperfusion injury and the level of cerebral perfusion. Middle cerebral artery occlusion (MCAO) was induced by a suture insertion technique. Forty one rats were divided into hyperglycemic and normoglycemic groups with either 4 hours of continuous MCAO or 2 hours of MCAO followed by 2 hours of reperfusion. Diffusion-weighted imaging (DWI) was performed at 4 hours after MCAO to quantify the degree of injury in 6 brain regions. Relative cerebral blood flow (CBF) and cerebral blood volume (CBV) were estimated using gradient echo (GE) bolus tracking and steady-state spin echo (SE) imaging techniques, respectively. Brain injury correlated with the perfusion level measured in both SE CBV and dynamic GE CBF images. In the temporary MCAO model, mean lesion size in DWI was 118% larger and hemispheric CBV was reduced by 37% in hyperglycemic compared with normoglycemic rats. Hyperglycemia did not significantly exacerbate brain injury or CBV deficit in permanent MCAO models. We conclude that preexisting hyperglycemia increases acute postischemic MRI-measurable brain cellular injury in proportion to an associated increased microvascular ischemia.

The application of diffusion-weighted line-scanning for the rapid assessment of water ADC changes in stroke at high magnetic fields.

Rapid changes in the apparent diffusion coefficient of water following brain ischemia have been extensively studied using echo planar diffusion imaging at low fields (2.0 T). There is a desire to perform these studies at higher fields (> 3.0 T) where the benefits of improved signal-to-noise can be exploited. Unfortunately, EPI diffusion is technically difficult to implement at high fields because of large magnetic susceptibility effects. This article demonstrates the feasibility of employing a line-scan diffusion protocol for ADCw measurements in stroke. The technique was applied on a 4.0 T system to monitor the decline in ADCw following the induction of focal cerebral ischemia in rat. ADCw data were acquired every 15 s with 10 b-values or every 22.5 s with 15 b-values, with a cubic spatial resolution of 1.5 mm. The results demonstrate that estimates of ADCw can be acquired with coefficients of variation under 3.0%, and with a combination of spatial and temporal resolution comparable to that previously reported for EPI.

Perfusion imaging by un-inverted flow-sensitive alternating inversion recovery (UNFAIR).

A new pulse sequence for estimating cerebral blood flow called UNFAIR, which uses a combination of sequential hyperbolic secant preparatory pulses, is introduced. This sequence is based on the same generalized conditions as previously introduced inversion recovery techniques except that the spins in the image slice of interest always have +z magnetization and the in-flowing spins are alternately inverted and uninverted. CBF-weighted images of rat brain under conditions of normocpnia and hypercapnia are presented and demonstrate the expected CBF response. A model describing the signal response to this pulse sequence is also presented and compared with in-vivo data acquired from gray and white matter.

Hydroxyl radical formation in hyperglycemic rats during middle cerebral artery occlusion/reperfusion.

Preexisting hyperglycemia is associated with enhanced reperfusion injury in the postischemic rat brain. The goal of this study was to evaluate whether the hyperglycemic exacerbation of brain injury is associated with enhanced generation of hydroxyl radicals in rats subjected to middle cerebral artery occlusion (2 h), followed by reperfusion (2 h). Magnetic resonance images revealed the exacerbation of focal brain injury in hyperglycemic rats. The salicylate trapping method was used in conjunction with microdialysis to continuously estimate hydroxyl radical production by measurement of the stable adducts 2,3- and 2,5-dihydroxybenzoic acid (DHBA) during ischemia/reperfusion. In normoglycemic rats, from a mean baseline level of 130 nmol/l, 2,3-DHBA levels surged to peak levels of 194 nmol/l 45 min into ischemia and to 197 nmol/l 15-30 min into the reperfusion period, returning to baseline by 2 h into reperfusion. A similar temporal profile was observed in hyperglycemic rats, except that absolute 2,3-DHBA levels were higher (165 nmol/l at baseline, 317 nmol/l peak during ischemia, 333 nmol/l peak during reperfusion), and levels remained significantly high (p < .05) throughout the reperfusion period. These results suggest that hydroxyl radical is an important contributor to the exacerbation of neuronal and cerebrovascular injury after focal ischemia/reperfusion in hyperglycemic rats.

CHL1 encodes a component of the low-affinity nitrate uptake system in Arabidopsis and shows cell type-specific expression in roots.

The Arabidopsis CHL1 (AtNRT1) gene confers sensitivity to the herbicide chlorate and encodes a nitrate-regulated nitrate transporter. However, how CHL1 participates in nitrate uptake in plants is not yet clear. In this study, we examined the in vivo function of CHL1 with in vivo uptake measurements and in situ hybridization experiments. Under most conditions tested, the amount of nitrate uptake by a chl1 deletion mutant was found to be significantly less than that of the wild type. This uptake deficiency was reversed when a CHL1 cDNA clone driven by the cauliflower mosaic virus 35S promoter was expressed in transgenic chl1 plants. Furthermore, tissue-specific expression patterns showed that near the root tip, CHL1 mRNA is found primarily in the epidermis, but further from the root tip, the mRNA is found in the cortex or endodermis. These results are consistent with the involvement of CHL1 in nitrate uptake at different stages of root cell development. A functional analysis in Xenopus oocytes indicated that CHL1 is a low-affinity nitrate transporter with a K(m) value of approximately 8.5 mM for nitrate. This finding is consistent with the chlorate resistance phenotype of chl1 mutants. However, these results do not fit the current model of a single, constitutive component for the low-affinity uptake system. To reconcile this discrepancy and the complex uptake behavior observed, we propose a "two-gene" model for the low-affinity nitrate uptake system of Arabidopsis.

A comparison of the early development of ischemic brain damage in normoglycemic and hyperglycemic rats using magnetic resonance imaging.

The early evolution of ischemic brain injury under normoglycemic and streptozotocin-induced hyperglycemic plasma conditions was studied using magnetic resonance imaging (MRI). Male Sprague-Dawley rats were subjected to either permanent middle cerebral artery occlusion (MCAO), or 1-h MCAO followed by reperfusion using the intraluminal suture insertion method. The animals were divided into four groups each with eight rats: normoglycemia with permanent MCAO, normoglycemia with 1-h MCAO, hyperglycemia with permanent MCAO, and hyperglycemia with 1-h MCAO. Diffusion-weighted images (DWIs) and T2-weighted images (T2WIs) were aquired every 1 h from 20 min until 6 h after MCAO, at which time cerebral plasma volume images (PVIs) were acquired. Tissue infarction was determined by triphenyltetrazolium chloride staining at 7 h after MCAO. The ischemic damage, measured as the area of DWI and T2WI hyperintensity and tissue infarction, increased significantly in hyperglycemic rats in both permanent and transient MCAO models. In the permanent MCAO model, the maximal apparent water diffusion coefficient (ADC) decline under either normo- or hyperglycemia was about 40%, but the speed of ADC drop was faster in hyperlgycemic rats than in normoglycemic rats. Reperfusion after 1 h of MCAO in normoglycemic rats partly reversed the decline in ADC, whereas the low ADC area continued to expand after reperfusion in the hyperglycemic group. Between the two hyperglycemic groups with either permanent MCAO or reperfusion, no significant difference was found in the infarct volume measured at 7 h after MCAO. However, reperfusion dramatically increased the extent and accelerated the development rate of vasogenic edema. ADC in the hyperglycemic reperfusion group also dropped to a lower level. A large "no-reflow" zone was found in the ischemic hemisphere in the hyperglycemic reperfusion group. This study provides strong evidence to support that preischemic hyperglycemia exacerbates ischemic damage in both transient and permanent MCAO models and demonstrates, using MRI, that reperfusion under preischemic hyperglycemia accelerates the evolution of early ischemic injury.

Nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester decreases ischemic damage in reversible focal cerebral ischemia in hyperglycemic rats.

We tested the hypothesis that the exacerbation of post-ischemic brain tissue injury associated with hyperglycemia in rats is due to toxic metabolism of nitric oxide. We used magnetic resonance imaging (MRI) techniques to measure neuronal and cerebrovascular injury in a 2-h transient focal cerebral ischemia model in normoglycemic and hyperglycemic rats at 3 and 24 h post-ischemia onset. We determined the effect of low dose (3 mg/kg i.p.) treatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Compared to normoglycemia, preexisting hyperglycemia increased the volume of brain tissue exhibiting hyperintensity in diffusion weighted MRI (DWI) by factors of 5.6 and 6.2 at 3 h and 24 h post-ischemia, respectively. A similar increase in tissue volumes exhibiting hyperintense signal in T2-weighted MRI (T2WI) (3.3-fold and 5.6-fold) was observed. Cerebral blood volume MRI indicated a large focal no-reflow zone in hyperglycemic rats. Treatment with L-NAME eliminated the no-reflow zone in the hyperglycemic rats, and reduced tissue volumes of DWI hyperintensity by 86% and 93% at 3 h and 24 h, respectively. Similarly, tissue volumes of T2WI hyperintensity were reduced by 80% and 94% at 3 h and 24 h, respectively. Thus, nitric oxide is an important mediator in the exacerbation of post-ischemic brain injury in hyperglycemic rats. Inhibition of nitric oxide synthase limits edema formation, improves perfusion and reduces infarct volume.

The evolution of acute stroke recorded by multimodal magnetic resonance imaging.

Events associated with an evolving cerebral infarction were studied using multiple magnetic resonance imaging (MRI) techniques at 4.7 T in a rat model of middle cerebral artery occlusion. High resolution perfusion images revealed a core of absent perfusion surrounded by a zone of slow, but measurable perfusion. Only the core of severest perfusion deficit demonstrated restricted water diffusion as early as 1 hr, consistent with "cytotoxic" cellular edema in the most vulnerable region. Within 24 hours, the area of restricted diffusion encompassed the entire region destined to become infarcted. In spin-echo images, hypointensity, likely reflecting deoxygenated hemoglobin, was visible in the ischemic hemisphere. Edema accumulated over 72 hr primarily in the surrounding slowly perfused rim, consistent with the concept of "vasogenic" edema. These studies demonstrate that multimodal MRI can visualize events which define the ischemic penumbra--deoxygenation, maintenance of transmembrane ionic gradients, reduced flow, and delayed cell death. These experiments noninvasively visualized differential hemodynamic and biochemical processes within the core and perifocal penumbra and will allow quantitation over time of the relationship between blood flow, cytotoxicity and edema in stroke.