Deficiencies in anti-acetylcholine receptor antibody measurement in myasthenia gravis.

In a retrospective case note study of 86 patients with myasthenia gravis, 60 had an anti-acetylcholine receptor antibody assay performed by the regional immunology laboratory. Antibody was detected in 38% which compares with 66-93% in other series. Whilst the use of staphylococcal protein A to precipitate the antibody-receptor complex, rather than anti-human immunoglobulin, may be partly responsible for this low sensitivity, other methodological problems are likely to exist. It is suggested that this potentially critical assay becomes a subject for regular audit.

Depth sense aesthesiometry: an advance in the clinical assessment of sensation in the hands.

Fingertip depth sense threshold has been examined in fifty normal subjects using the simple pocket aesthesiometer invented by Renfrew. Index fingers possessed the lowest thresholds and little fingers the highest, whilst there were no significant differences between the same fingers of either hand. Sex and age (at least up to 70 years) had no significant influence on depth sense threshold, but thickened skin and low intelligence tended to raise thresholds. Fingertip depth sense thresholds were then compared with the results of conventional sensory testing in fifty patients with sensory symptoms in the hands. The depth sense threshold of affected fingers was more often abnormal than were the results of clinical tests for light touch appreciation, joint position sense and two-point discrimination. Depth sense aesthesiometry is recommended as a simple, sensitive and quantifiable routine technique for the evaluation of sensory disturbance in the hands.

General anaesthetics and the acetylcholine-sensitivity of cortical neurons.

1The effects of general anaesthetics on neuronal responses to iontophoretically-applied acetylcholine have been examined in slices of guinea-pig olfactory cortex maintained in vitro. 2 Acetylcholine excited 61% of the prepiriform neurones tested. The excitation was blocked by atropine, but not by dihydro-beta-erythroidine or gallamine. 3 Alphaxalone reversibly depressed the acetylcholine-sensitivity of prepiriform neurones. Pentobarbitone did not consistently depress the acetylcholine sensitivity of these cells. 4 Ether, methoxyflurane, trichloroethylene and halothane caused a dose-related augmentation of acetylcholine-induced firing. 5 These results show that general anaesthetics do not necessarily depress the sensitivity of nerve cells to all excitatory substances and that different anaesthetics may affect a particular excitatory process in various ways.

Anaesthetics depress the sensitivity of cortical neurones to L-glutamate.

1 The effects of general anaesthetics on the responses of neurones to iontophoretically applied L-glutamate have been examined in slices of the guinea-pig olfactory cortex in vitro. 2 Concentrations of pentobarbitone, ether, methoxyflurance, trichloroethylene and alphaxalone that are known to depress synaptic transmission in the prepiriform cortex also depressed the sensitivity of prepiriform neurones to L-glutamate. 3 Halothane, in concentrations that depress synaptic transmission (less than 1%) did not alter sensitivity of neurones to glutamate. Higher concentrations (greater than 1% produced a dose-related depression of the glutamate sensitivity of neurones. 4 All four volatile anaesthetics tested caused some cells to alter their glutamate-evoked firing pattern to one in which the spike discharges were more closely grouped. Pentobarbitone and alphaxalone had no such effect. 5 If the sensitivity of the neurones to the endogenous excitatory transmitter is affected by anaesthetics in the same way as the glutamate-sensitivity, these results suggest that halothane depresses synaptic transmission by decreasing the amount of transmitter released from the nerve terminals, whereas the other anaesthetics depress the sensitivity of the post-synaptic membrane to the released transmitter.

The action of ether and methoxyflurane on synaptic transmission in isolated preparations of the mammalian cortex.

1. The actions of ether and methoxyflurane on the evoked potentials of in vitro preparations of the guinea-pig olfactory cortex were studied. Following stimulation of the lateral olfactory tract (l.o.t.) evoked potentials could be recorded from the cortical surface; these potentials consisted of an initial wave (the compound action potential of the l.o.t.) followed by a negative field potential which was associated with the synchronous excitation of many superficial excitatory synapses (population e.p.s.p.). Superimposed on the population e.p.s.p. was a number of positive peaks. These positive peaks reflect the synchronous discharge of many neurones and so have been called population spikes. 2. When ether or methoxyflurane was added to the gas stream that superfused the surface of the preparations, the population e.p.s.p.s. and population spikes were depressed at lower concentrations than those required to depress the compound action potential of the afferent fibres. 3. The evoked activity of individual cells in the cortex was depressed by ether and methoxyflurane. However, five of the twelve cells tested in ether showed an increase in their evoked activity at concentrations below 4-5%, but at higher concentrations these cells also became depressed. 4. Both ether and methoxyflurane depressed the sensitivity of cortical neurones to iontophoretically applied L-glutamate and may similarly depress the sensitivity of the post-synaptic membrane to the released transmitter substance. 5. Neither anaesthetic appeared to increase the threshold depolarization required for nerve impulse generation. Thus, the decrease of the discharge of the post-synaptic cells was primarily caused by a depression of chemical transmission. 6. Ether caused some cells in the cortex to alter their normal pattern of synaptically evoked discharge and both anaesthetics induced similar changes during excitation by glutamate.