Correlation between scalp-recorded electroencephalographic and electrocorticographic activities during ictal period.

OBJECTIVE: To investigate the correlation between scalp-recorded electroencephalographic (EEG) and electrocorticographic (ECoG) activities during ictal periods. METHODS: Simultaneous EEG and ECoG recordings with chronic subdural electrodes were performed in eight patients with partial epilepsy. RESULTS: In two cases where the ictal ECoG discharges originated in deep brain structures such as the hippocampus and interhemispheric surface of the frontal lobe, ictal discharges could not be detected on EEG until they expanded to the cortex of convexity. In four cases, the ictal onset zones were located in the lateral convexity. When synchronous or near synchronous ictal ECoG discharges with amplitudes of 200-2000muV were recorded on more than 8-15cm(2) of cortex, corresponding discharges were recorded on EEG in these four cases. However, in a case of frontal lobe epilepsy, asynchronous ictal ECoG discharges were recorded on 10 electrodes of convexity but no ictal EEG activity was recorded. Furthermore, in two frontal lobe epilepsy cases, ictal EEG discharges did not always reflect the ictal ECoG spike, but occasionally reflected slow background ECoG activity around the ictal discharges. CONCLUSIONS: Multiple factors such as the width of the cortical area involved, amplitude of ictal discharges and degree of synchronization of electrical potentials play important roles in the appearance of ictal EEG recordings, and the relationship between ictal EEG and ECoG is not straightforward.     

Veno-arterial ECLA (extracorporeal lung assist) for severe respiratory failure due to meconium aspiration

A full term newborn female, 3262g, aspirated meconium at birth and began to suffer from severe hypoxia and acidosis due to progressing pneumonitis, pneumothorax and pneumomediastinum. She also had severe hypotension and anuria. Venoarterial ECLA with a Kolobow membrane lung via the right internal jugular vein and the right common carotid artery was initiated. Blood gas parameters and blood pressure improved, and urine output increased to normal. ECLA permitted a reduction in FIO2 and airway pressure of mechanical ventilation, as well as frequent lavage of the lung. As the physical condition improved, the bypass flow was gradually decreased from 200 ml.kg-1.min-1 at the start to 130 ml.kg-1.min-1 for maintenance, then to 25 ml.kg-1.min-1 at the end. Bleeding throughout the ECLA for 69 hours could be minimized by a meticulous control of the activated coagulation time with a minimum dose of heparin and the transfusion of fresh frozen and platelet rich plasma. After ECLA, the carotid artery was simply ligated, and mechanical ventilatory support was carried out for 5 days. Her condition improved and she left the hospital without any neurological sequelae. ECLA will become an effective means of life support for a baby with severe MAS irresponsive to conventional ventilatory support.     

An Autopsied Case of Interferon Encephalopathy

Abstract: A 78-year-old male with renal carcinoma was treated with a high dose infusion of interferon-alpha (IFN-alpha) for eight months. The patient had evidence of organlc brain syndrome such 88 : dysfunction of memory, slowing of behavior, and development of mental confusion that appeared eight months after the treatment. MRI at the time of mental confusion revealed difise white matter lesions. Neuropathologic findings were compatible to Binswanger's disease and Senile Dementia of Alzheimer Type (SDAT), Preexisting neurologic abnormalities including intracerebral arteriosclerosis and cerebral atrophy may increase susceptibility to unacceptably severe IFN neurotoxicity.     

Whole-Blood Assay to Measure Oxidative Burst and Degranulation of Neutrophils for Monitoring Trauma Patients

AbstractBackground and Purpose: Polymorphonuclear neutrophils (PMNs) protect the host from invading microorganisms, but excessive PMN activation after trauma causes tissue injury. Rapid monitoring of PMN function is critical for the assessment of the inflammatory state of trauma patients. Here, the authors adapted two simple and rapid methods to measure oxidative burst and degranulation of human PMNs in whole blood to avoid potential interference of cell isolation procedures with the assessment of PMN function.Material and Methods: Heparinized blood was drawn from healthy volunteers or trauma patients, preincubated at 37 °C for 5 min, and stimulated with N-formyl-methionyl-leucyl-phenylalanine (fMLP). Four assays for oxidative burst were tested: (1) cytochrome C; (2) homovanillic acid (HVA); (3) Amplex^® Red; and (4) flow cytometry with dihydrorhodamine 123 (DHR). PMN degranulation was assessed with flow cytometry using antibodies to: (1) CD11b/Mac-1 (CD18); (2) CD63; and (3) CD66b (CD67).Results: With the exception of the DHR method, all methods to measure oxidative burst were found to be unsuitable in whole blood due to interference of plasma proteins and hemoglobin with the fluorimetric or photometric readouts. By contrast, all degranulation methods were suitable for whole-blood studies. However, for the assessment of formyl peptide-induced degranulation, anti-antibodies to CD11b/Mac-1 and CD66b were up to five times more sensitive than antibodies to CD63. Thus, the degranulation and DHR methods were optimized for increased sensitivity, speed, and specificity and their usefulness to measure PMN function in trauma patients was tested.Conclusion: The whole-blood methods based on flow cytometry with DHR, anti-CD11b/Mac-1, and anti- CD66b are rapid, simple, and reliable techniques to assess PMN function for trauma research.     

Morphine-3-glucuronide: hyperglycemic and neuroendocrine potentiating effects

The greater potency of morphine-6-glucuronide (M6G) as well as the inactivity of morphine-3-glucuronide (M3G) with respect to the antinociceptive effects of the parent molecule, morphine (MOR), have been well established. It has been suggested that M3G is an antagonist of MOR's antinociceptive and respiratory depressive effects. The present study addressed the central nervous system (CNS) interaction of these opiate metabolites on their metabolic and hormonal effects. Whole body glucose kinetics were assessed on conscious, chronically catheterized, unrestrained rats. M3G (5 μg) or H₂O (5 μl) was injected intracerebroventricularly (i.c.v.) 15 min prior to the bolus administration of H₂O (5 μl), M6G (1 μg), or MOR (80 μg). i.c.v. M3G (5 μg) resulted in behavioral excitation, hyperglycemia (+50%), stimulation of glucose rate of appearance (R_a; +100%), glucose rate of disappeaance (R_d; +70%), and metabolic clearance rate (MCR; +33%) within 30 min after injection with no alterations in hormone concentrations. i.c.v. M6G and MOR produced progressive hyperglycemia with significantly high catecholamine and corticosterone levels. M3G pretreatment resulted in enhanced elevations in plasma glucose levels (+52% and +18%), plasma lactate (+138% and +108%), norepinephrine (+96% and +30%), and epinephrine (+62% and +67%) in response to both i.c.v. MOR and M6G administration. These findings suggest a non-opiate and non-hormonal mechanism for M3G-induced hyperglycemia. In contrast, the metabolic and hormonal responses to i.c.v. M6G and MOR are associated with elevations in catecholamine and corticosterone levels, which are remarkably enhanced by M3G pretreatment, most likely through accelerated catecholamine release. Our findings suggest a modulatory role for MOR glucuronidation, not only by rendering it inactive, as in the case of M3G, but by an interplay of the metabolic effects of the parent molecule and its metabolite     

Impaired protective immunity and T helper 2 responses in alymphoplasia (aly) mutant mice infected with Trichinella spiralis

The alymphoplasia (aly) mutation of mice prevents the development of systemic lymph nodes and Peyer's patches. The mutant homozygotes (aly/aly) are partially deficient in both humoral and cell-mediated immune functions. In the present study, we show that adult worm expulsion was slightly delayed and that T helper 2 (Th2)-type responses were partially defective in aly/aly mice after infection with Trichinella spiralis. Male aly/aly and aly/+ mice (8-weeks old) were infected with 400 muscle larvae. There was no difference in worm recovery between the two groups on day 5. However, worm recovery in aly/aly mice was significantly higher than that in aly/+ mice on day 14. Mucosal mast cells increased in number and peaked 14 days after infection in aly/+ mice. aly/aly mice were deficient in their mucosal mast cell response through out the primary infection. To examine the existence of mast cell precursors, aly/aly mice were treated with recombinant interleukin-3 (rIL-3) before infection. The mast cell response was poorly induced in aly/aly mice treated with rIL-3. An immunoglobulin E (IgE) response was not detected in aly/aly mice during the course of infection. Serum IgG1 levels in aly/aly mice were significantly lower than that of aly/+. The serum IgG2a levels increased in both strains of mice. However, IgG2a production in aly/aly mice on day 14 was half as much as that in aly/+mice. Stimulation of splenic T cells in vitro with anti-CD3 monoclonal antibody (mAb) showed that spleen cells from aly/+ mice on day 5 produced more IL-4 than spleen cells from aly/aly mice. IL-4 production from aly/aly mice on day 14 was half that from aly/+ mice. Interferon-gamma (IFN-gamma) was produced in both aly/aly and aly/+ mice on day 14. Proliferation assay showed that T cells of aly/aly mice responded poorly when cultured with antigen-presenting cells. These results suggest that aly gene is needed for the induction of protective immunity and Th2 responses in mice infected with T. spiralis.     

Effects of cocaine on a hypogastric nerve-vas deferens preparation of the guinea pig

Effects of cocaine on a hypogastric nerve-vas deferens preparation of the guinea pig, in vitro, were investigated with the microelectrode and the double sucrose gap methods. 1) Cocaine, at a concentration of more than 3 X 10 minus-5 M, depolarized the membrane and enhanced the electrical activity of the postjunctional membrane. These effects were, however, not due to accumulated noradrenaline near the postjunctional membrane. 2) The electrical resistance of the postjunctional membrane was slightly increased by treatment with cocaine (3 X 10 minus-5M) but the length constant of the tissue was almost unaffected. The electrical threshold to evoke a spike from the postjunctional membrane was lowered. 3) Cocaine (3 X 10 minus-5M) did not change the amplitude and frequency of the miniature excitatory junction potentials but it markedly suppressed the amplitude of the excitatory junction potentials evoked by hypogastric nerve stimulation. Cocaine prolonged the falling phase of the excitatory junction potentials. 4) The inhibitory action of cocaine on the junction potential evoked by nerve stimulation was not specific for the adrenergic fiber. Cocaine also suppressed the amplitude of the non-adrenergic inhibitory junction potential evoked in the taenia coli by field stimulation. 5) Exogeneously applied noradrenaline enhanced the electrical and mechanical activities of the postjunctional organ but suppressed the amplitude of the excitatory junction potential. This effect of noradrenaline was still observed on pretreatment with cocaine. 6) In the presence of cocaine, the dose-response curves plotted from the mechanical activity induced by excess [K]o or by noradrenaline shifted to the left and the maximum responses evoked by either treatment were enhanced. 7) From the present experiments, it was concluded that supersensitivity induced by cocaine or cocaine potentiation of the mechanical response may be mainly due to direct action on the smooth muscle tissue rather than to inhibition of noradrenaline re-uptake into the nerve terminals.