Painless aortic dissection presenting as a progressive myelopathy.

We report a patient with a painless aortic dissection whose neurologic symptoms progressed over 5 days to a complete transverse myelopathy. She did not experience pain as her neurologic deficits evolved. Magnetic resonance imaging revealed a thoracic aortic dissection extending from the arch to the level of the 12th thoracic vertebra and demonstrated ischemic changes in the spinal cord and one thoracic vertebral body. Aortic dissection must be included in the differential diagnosis of spinal cord syndromes even in the absence of pain. Early recognition of aortic dissection as a cause of progressive myelopathy may become increasingly important as new therapies for central nervous system ischemia are developed.

Kinetic properties of single sodium channels modified by fenvalerate in mouse neuroblastoma cells.

(1) The kinetic properties of single sodium channels modified by the pyrethroid fenvalerate have been analyzed by patch clamp techniques using the cultured mouse neuroblastoma cells. (2) Fenvalerate drastically prolonged the open time of single sodium channels from the normal value of 5 ms to several hundred milliseconds during a depolarizing pulse. The channels remained open after termination of a depolarizing pulse for as long as several seconds. (3) The channel lifetime varied with the membrane potential, attained a maximum at -70 mV, and decreased with hyperpolarization and depolarization from -70 mV. (4) Prolonged openings of the modified channels allowed a current-voltage curve for a single channel to be plotted by sweeping a ramp pulse. The single channel conductance had a value of 11 pS and was linear over potentials ranging from 0 to -100 mV. (5) Power density spectral analysis of the open channel current noise indicated a single Lorentzian curve with a cut-off frequency at 90 Hz, indicating that the increase in noise during channel opening resulted from a relatively slow kinetic process. (6) The probability of the channel being modified by fenvalerate was independent of the length of time during which the channel was opened. This observation suggests that channel modification had taken place before the channel opened. This study of the prolonged opening at the single channel level provides a new insight into open channel properties and the kinetics of channel modification.

Post-tetanic hyperpolarization evoked by depolarizing pulses in crayfish stretch receptor neurones in tetrodotoxin.

A post-tetanic hyperpolarization (p.t.h.) that is quantitatively identical to that evoked by a train of action potentials in stretch receptor neurones of crayfish Procambarus clarki and Pacifastacus leniculus is evoked when the normal Na+ influx is blocked with tetrodotoxin (TTX) and a train of depolarizing pulses is used to simulate a train of action potentials. The p.t.h. evoked by depolarizing pulses in the presence of TTX is attributable to an electrogenic Na-K pump, because it (a) is abolished by strophanthidin, (b) is abolished by removal of external K+, (c) depends in magnitude on internal Na+ concentration, (d) is not associated with a change in membrane conductance and (e) does not exhibit a reversal potential. When each action potential in the stimulus train is followed by a hyperpolarizing pulse, generation of the p.t.h. is prevented even though the action potentials are unchanged. The time constant for build-up of the p.t.h. is longer than the time constant of decay. Increasing the magnitude of depolarizing pulses increases the magnitude of the p.t.h. response in the presence of TTX and also increases the time constant for its build-up. The suppression of the p.t.h. occurring in low external Na+ appears to represent a response to a change in internal Na+ concentration, characterized by a time constant much longer than the decay of the p.t.h. The activity of the pump appears to be regulated by two mechanisms: a Na+-sensitive mechanism with a time constant of the order of a minute and an apparently voltage-sensitive mechanism with a time constant of about 5 s. The hypothesis is proposed that changes in the transmembrane electric field influence the enzymatic systems of the pump and disrupt the steady-state distribution of conformation states. The decay of the p.t.h. represents a relaxation back to the resting distribution.