Paramedic and emergency department care of stroke: baseline data from a citywide performance improvement study.

BACKGROUND: Rapid diagnosis and transport by paramedics and efficient, effective emergency management are essential to improving care of acute stroke patients. OBJECTIVES: To measure the performance of paramedics and emergency departments providing care for patients with suspected acute stroke. METHODS: Two stroke centers and 4 other hospitals where most patients with acute stroke in Houston, Tex, are admitted participated. Hospital and paramedic performance data were collected prospectively on 446 patients with suspected acute stroke transported by paramedics between September 1999 and February 2000. RESULTS: Paramedics had a sensitivity of 66%, specificity of 98%, and overall accuracy of 72% in diagnosing stroke. For patients with suspected stroke, 58.5% arrived in the emergency department within 120 minutes of symptom onset; in confirmed cases, that percentage was 67%. Mean total transport time was 42.2 minutes and was significantly longer (P < .001) to inner-city hospitals (44 minutes) than to suburban, community-based centers (39 minutes). Door to computed tomography times were significantly (P < .001) shorter for the 2 stroke centers than the other hospitals. Overall thrombolysis treatment rate among patients with confirmed ischemic stroke was 7.4% (range, 0-19.4%); treatment rates at the 2 stroke centers were 5.9% and 19.4%. CONCLUSIONS: More than half of patients with suspected stroke arrive at hospitals while thrombolytic treatment is still feasible. Although the current rate for thrombolytic treatment in Houston exceeds the national rate, performance of paramedics and hospitals in treating acute stroke can be improved by increasing efficiency and standardizing medical practices.     

Residual Flow Signals Predict Complete Recanalization in Stroke Patients Treated With TPA

BACKGROUND: Residual blood flow around thrombus prior to treatment predicts success of coronary thrombolysis. The authors aimed to correlate the presence of residual flow signals in the middle cerebral artery (MCA) with completeness of recanalization after intravenous tissue plasminogen activator (TPA). METHODS: The authors studied consecutive patients treated with intravenous TPA therapy who had a proximal MCA occlusion on pretreatment transcranial Doppler (TCD). Patients were continuously monitored for 2 hours after TPA bolus. Absent residual flow signals correspond to the thrombolysis in brain ischemia (TIBI) 0 grade, and the presence of residual flow signals was determined as TIBI 1-3 flow grades. Complete recanalization was defined as flow improvement to TIBI grades 4-5. RESULTS: Seventy-five patients with a proximal MCA occlusion had median pre-bolus NIHSS 16 (85% with > or = 10 points). TPA bolus was given at 141 +/- 56 minutes (median 120 minutes). Complete recanalization was observed in 25 (33%), partial in 23 (31%), and no early recanalization was seen in 27 (36%) patients within 2 hours after TPA bolus. Only 19% with absent residual flow signals (TIBI grade 0, n = 26) on pretreatment TCD had complete early recanalization. If pretreatment TCD showed the presence of any residual flow (TIBI 1-3, n = 49), 41% had complete recanalization within 2 hours of TPA bolus (P = .03). CONCLUSIONS: Patients with detectable residual flow signals before IV TPA bolus are twice as likely to have early complete recanalization. Those with no detectable residual flow signals have less than 20% chance for complete early recanalization with intravenous TPA and may be candidates for intra-arterial therapies.     

Kasuistischer Beitrag zur operativen Behandlung der Trigeminusneuralge nach Krause

Ohne Zusammenfassung (Mit 4 Abbildungen.) Nach einer klinischen Demonstration der Schweiz. neurolog. Gesellschaft zu Basel, 12. Nov. 1910.     

Variationsstatistische Untersuchungen über Refraktion

Ohne Zusammenfassung     

Hysterische Gesichtsfeldveränderungen und der hysterische Mechanismus

Ohne Zusammenfassung     

Ueber die chemische Natur der vegetabilischen Diastase

Ohne Zusammenfassung     

NMDA receptors regulate developmental gap junction uncoupling via CREB signaling

Signaling through gap junctions (electrical synapses) is important in the development of the mammalian central nervous system. Abundant between neurons during postnatal development, gap junction coupling subsequently decreases and remains low in the adult, confined to specific subsets of neurons. Here we report that developmental uncoupling of gap junctions in the rat hypothalamus in vivo and in vitro is associated with a decrease in connexin 36 (Cx36) protein expression. Both developmental gap junction uncoupling and Cx36 downregulation are prevented by the blockade of NMDA glutamate receptors, action potentials and the calcium-cyclic AMP response element binding protein (CREB), and are accelerated by CREB overexpression. Developmental gap junction uncoupling and Cx36 downregulation are not affected by blockade of non-NMDA glutamate receptors, and do not occur in hypothalamic neurons from NMDA receptor subunit 1 (NMDAR1) knockout mice. These results demonstrate that NMDA receptor activity contributes to the developmental uncoupling of gap junctions via CREB-dependent downregulation of Cx36.     

Zinc is a voltage-dependent blocker of native and heterologously expressed epithelial Na+ channels

Zn(2+) (1-1,000 microM) applied to the apical side of polarized A6 epithelia inhibits Na(+) transport, as reflected in short-circuit current and conductance measurements. The Menten equilibrium constant for Zn(2+) inhibition was 45 microM. Varying the apical Na(+) concentration, we determined the equilibrium constant of the short-circuit current saturation (34.9 mM) and showed that Zn(2+) inhibition is non-competitive. A similar effect was observed in Xenopus oocytes expressing alphabetagammarENaC (alpha-, beta-, and gamma-subunits of the rat epithelial Na(+) channel) in the concentration range of 1-10 microM Zn(2+), while at 100 microM Zn(2+) exerted a stimulatory effect. The analysis of the voltage dependence of the steady-state conductance revealed that the inhibitory effect of Zn(2+) was due mainly to a direct pore block and not to a change in surface potential. The equivalent gating charge of ENaC, emerging from these data, was 0.79 elementary charges, and was not influenced by Zn(2+). The stimulatory effect of high Zn(2+) concentrations could be reproduced by intra-oocyte injection of Zn(2+) (approximately 10 microM), which had no direct effect on the amiloride-sensitive conductance, but switched the effect of extracellular Zn(2+) from inhibition to activation.