Corpus callosum damage and interhemispheric transfer of information following closed head injury in children.

We evaluated the relationship of corpus callosum atrophy and/or lesions on magnetic resonance imaging (MRI) to functional hemispheric disconnection following closed head injury (CHI) in 51 pediatric patients, including mild CHI, moderate to severe CHI with extracallosal lesions, and moderate to severe CHI with callosal atrophy and/or lesions. Interhemispheric transfer of information was assessed using auditory, motor, tactile, and visual tests in patients and in 16 uninjured children. Total and regional callosal areas were measured from the midsagittal MRI slice by morphometry. The corpus callosum lesion group demonstrated a greater right ear advantage on verbal dichotic listening than all other groups. Areas of the posterior corpus callosum were negatively correlated with laterality indices of verbal dichotic listening performance and tachistoscopic identification of verbal material. The relationship of corpus callosum atrophy and/or lesions to asymmetry in dichotic listening is consistent with previous investigation of posttraumatic hemispheric disconnection effects in adults.

Magnetic fields from human prefrontal cortex differ during two recognition tasks.

The present study represents our second successful use of magnetoencephalography to identify different sources of human prefrontal activity corresponding to subjects' engagement in different tasks. We used two visual recognition tasks: a familiar person recognition and an abstract pattern recognition task in the context of a design suitable for eliciting Contingent Negative Variations (CNVs) and their concurrent slow magnetic fields in this preliminary study of 5 subjects. Each trial of either task was started by one of two specific warning symbols (S1), indicating whether a person's picture or an abstract pattern should be attended during the presentation of a second stimulus (S2), and compared to the corresponding person's picture or pattern contained in the third stimulus, (S3) that followed. The S2 and S3 stimuli were common to both tasks, and were composed of patterns made with four line traces superimposed on photographs of persons familiar to each subject. Subjects responded with a right hand button press, following S3, indicating their judgments regarding the identity of the patterns or persons' pictures contained in the S2 and the S3 stimuli, for the two tasks, respectively. Results showed that the sources of the CNV equivalent magnetic fields were localized in different cortical regions depending on the task and that this difference was consistent across all subjects. The sources were localized in the right hemisphere, in medial areas of the prefrontal cortex for the person recognition task and in the dorsolateral prefrontal cortex for the pattern recognition task. The same degree of consistency was not found for the left hemisphere sources. Moreover, as in our previous study, we found no difference between the sources active during the first and the second CNV periods (occurring during the S1-S2 and the S2-S3 intervals, respectively), within each task condition.

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.

Magnetic resonance imaging quantitation of changes in muscle volume during 7 days of strict bed rest.

BACKGROUND: Prolonged bed rest results in a loss of leg lean body mass. Previous studies using bed rest as a model for microgravity have shown decreases in leg mass after 12 and 14 d, 5 and 17 wk. HYPOTHESIS: As magnetic resonance imaging (MRI) can provide a precise and non-invasive means of determining muscle volume, we sought to determine if changes in leg muscle volume could be detected in bed rest periods as short as 7 d. METHODS: Five young, healthy, male volunteers were subjected to 7 d of absolute bed rest. Each subject underwent MRI quantitation of segmental muscle volumes of the calves and thighs before and after bed rest. Eleven (calf) and nine (thigh) contiguous 1-cm thick transaxial images were generated over prescribed regions using a Technicare MRI imager with a 0.6T superconducting magnet and body coil. Image processing was performed using a generalized 8-bit medical image analysis package developed at University of Texas Medical Branch. Images were analyzed for muscle and non-muscle volumes (including fat, blood vessel, and bone marrow volumes). RESULTS: The MRI quantitation demonstrated bed rest-induced significant decreases in segmental thigh muscle (approximately 3.0%, p < 0.05) volume. CONCLUSIONS: We conclude that computerized image analysis of MRI images provides a sensitive tool capable of detecting leg volume changes of as little as 3.0% over a 7-d period of strict bed rest.

Frontal lobe changes after severe diffuse closed head injury in children: a volumetric study of magnetic resonance imaging.

In view of the pathophysiology and biomechanics of severe closed head injury (CHI) in children, we postulated that the frontal lobes sustain diffuse injury, even in the absence of focal brain lesions detected by magnetic resonance imaging (MRI). This study quantitated the morphological effects of CHI on the frontal lobes in children who sustained head trauma of varying severity. The MRI findings of 14 children who had sustained severe CHIs (Glasgow Coma Scale score of < or = 8) were compared with the findings in a matched group of 14 children having sustained mild head injuries (Glasgow Coma Scale score of 13-15). The patients ranged in age from 5 to 15 years at the time of their MRIs, which were acquired at least 3 months postinjury. MRI findings revealed no focal areas of abnormal signal in the frontal lobes. Volumetric analysis disclosed that the total prefrontal cerebrospinal fluid increased and the gray matter volume decreased in the patients with severe CHI, relative to the mildly injured comparison group. Gray matter volume was also reduced in the orbitofrontal and dorsolateral regions of the brains of children with severe CHI, relative to the children who sustained mild head trauma. These volumetric findings indicate that prefrontal tissue loss occurs after severe CHI in children, even in the absence of focal brain lesions in this area. Nearly two-thirds of the children who sustained severe CHIs were moderately disabled after an average postinjury interval of 3 years or more, whereas 12 of the 14 patients with mild CHIs attained a good recovery (2 were moderately disabled) by the time of study.(ABSTRACT TRUNCATED AT 250 WORDS)

Involvement of sarcoplasmic reticulum 'Ca2+ release channels' in excitation-contraction coupling in vertebrate skeletal muscle.

1. Pharmacological blockers of calcium-induced calcium release from isolated skeletal sarcoplasmic reticulum (SR) vesicles have been introduced into frog skeletal muscle fibres to determine their effects on excitation-contraction coupling. 2. Among the blockers tested, Ruthenium Red, neomycin, gentamicin and 9-aminoacridine inhibited the SR Ca2+ release associated with excitation-contraction (E-C) coupling as much as they inhibited caffeine potentiation of that release. Protamine, certain of its derivatives, and spermine were ineffective in both in situ tests. 3. Alternative sites of polyamine action on the contractile proteins, SR Ca2+ uptake or charge movements were ruled out. 4. All polyamines tested required considerably higher concentrations to inhibit excitation-contraction coupling than to block Ca2+ release from isolated SR vesicles. 5. The quantitative pharmacological difference in sensitivity between isolated and intact systems serves as a reminder that results on isolated systems cannot generally be used to predict results of the same substances on more physiological systems. 6. Since caffeine is known to open the SR 'Ca2+ release channels' (the ryanodine receptors that mediate Ca(2+)-induced Ca2+ release), the equal effectiveness of these blockers at inhibiting excitation-contraction (E-C) coupling and its potentiation by caffeine suggests that the SR 'Ca2+ release channels' are indeed involved in excitation-concentration coupling in skeletal muscle, although the results do not indicate how the channel is gated open during E-C coupling.

Measurement of brain compartment volumes in MR using voxel composition calculations.

A computer method was developed for brain compartment volume measurement in MR images. The method is a statistical averaging technique, in which each voxel is viewed as a mixture of adjacent tissues in a measurable proportion. This method is based on sampling representative tissue intensities and then interpolating intermediate intensities. It can automatically correct for volume averaging artifacts occurring in voxels that contain heterogeneous tissues.

Heavy metal-induced Ca2+ release from sarcoplasmic reticulum.

Two distinct forms of Ca2+ release from isolated sarcoplasmic reticulum vesicles in response to additions of heavy metals (silver and mercurials) are described. One form of heavy metal-induced Ca2+ release involves the ruthenium red-sensitive Ca2+ release channel localized in terminal cisternae. The other form of heavy metal-induced Ca2+ release appears to involve all portions of the sarcoplasmic reticulum and is insensitive to ruthenium red. This latter form of Ca2+ release occurs over a similar range of heavy metal concentrations as inhibition of the sarcoplasmic reticulum Ca2+ pump but does not appear to be a result solely of such pump inhibition. Both forms of Ca2+ release are inhibited by glutathione, an endogenous constituent of muscle fibers, and by dithiothreitol, agents which prevent sulfhydryl oxidation. To assess the role of any sulfhydryl oxidation in sarcoplasmic reticulum Ca2+ release physiologically, dithiothreitol and glutathione were introduced inside muscle fibers and effects on excitation-contraction coupling examined. The results strongly suggest that sulfhydryl oxidation plays no essential role in skeletal muscle excitation-contraction coupling.

Studies of axon-glial cell interactions and periaxonal K- homeostasis--I. The influence of Na+, K+, Cl- and cholinergic agents on the membrane potential of the adaxonal glia of the crayfish medial giant axon.

The ionic basis for the low (-40 mV) resting membrane potential of glial cells surrounding the giant axons of the crayfish and their hyperpolarization by cholinergic agents (to -55 mV) was studied using standard electrophysiological techniques, ionic substitutions and pharmacological agents. The resting membrane potential of the glial cell was depolarized by increasing [K+]o, but the response was not Nernstian. Na+ depletion caused a small depolarization of the glial resting membrane potential, whereas Cl- depletion resulted in a hyperpolarization comparable to that seen with carbachol at various [K+]o. Both furosemide (1 mM) and bumetanide (0.1 mM) produced an 8-10 mV hyperpolarization as compared to 15-17 mV seen with Cl- depletion or carbachol. Carbachol has no further effect on the potential following furosemide treatment or Cl- depletion. After carbachol administration or Cl- depletion the resting membrane potential of the glial cell responded to [K+]o in a more Nernstian manner. The data indicate that the low resting membrane potential of glial cells is due to a combination of a low [K+]i and an outwardly-directed (depolarizing) Cl- electrochemical gradient. Carbachol acts to decrease Cl- conductance, resulting in the hyperpolarization of the glial cell membrane and a decrease in the outwardly-directed K+ electrochemical gradient by approximately two-thirds. We hypothesize that this mechanism for modulation of the glial cell membrane potential and the K+ electrochemical gradient serves to enhance the uptake of K+ by the glial cell transport system.

Habituation and sensitization in an aneural cell: some comparative and theoretical considerations.

Several shorter- and longer-term non-associative modifications in behavior are known to occur in neural as well as aneural systems. Thus neural investment is not essential for these phenomena to occur. Cellular studies of these behaviors in Protozoa, where a single cell is also a whole organism, may be useful in investigating the evolution of mechanisms underlying these plastic behavioral changes.