Tremor retrainment as therapeutic strategy in psychogenic (functional) tremor.

BACKGROUND: Entrainment, the change or elimination of tremor as patients perform a voluntary rhythmical movement by the unaffected limb, is a key diagnostic hallmark of psychogenic tremor. OBJECTIVE: To evaluate the feasibility of using entrainment as a bedside therapeutic strategy ('retrainment') in patients with psychogenic tremor. METHODS: Ten patients with psychogenic tremor (5 women, mean age, 53.6 ± 12.8 years; mean disease duration 4.3 ± 2.7 years) were asked to participate in a pilot proof-of-concept study aimed at "retraining" their tremor frequency. Retrainment was facilitated by tactile and auditory external cueing and real-time visual feedback on a computer screen. The primary outcome measure was the Tremor subscale of the Rating Scale for Psychogenic Movement Disorders. RESULTS: Tremor improved from 22.2 ± 13.39 to 4.3 ± 5.51 (p = 0.0019) at the end of retrainment. The benefits were maintained for at least 1 week and up to 6 months in 6 patients, with relapses occurring in 4 patients between 2 weeks and 6 months. Three subjects achieved tremor freedom. CONCLUSIONS: Tremor retrainment may be an effective short-term treatment strategy in psychogenic tremor. Although blinded evaluations are not feasible, future studies should examine the long-term benefits of tremor retrainment as adjunctive to psychotherapy or specialized physical therapy.

Mechanism of ouabain-induced contractions in guinea-pig tracheal rings.

The aim of the present study was to analyse the mechanism that underlies the force development induced by ouabain (ED(100) = 100 micromol/L) in guinea-pig tracheal rings. The dose-response curve showed that concentrations of ouabain above 100 micromol/L evoked smaller contractions. Ouabain, at 100 micromol/L, produced two long-lasting consecutive transient contractions. The peak of the first contraction was 750 +/- 75 mg, whereas the peak of the second contraction was 280 +/- 46 mg. Both contractions induced by ouabain were dependent on extracellular Ca(2+). Consistent with this, verapamil (10 micromol/L) inhibited the first and second contractions by 77 and 59%, respectively. 3,4-Dichlorobenzamil (20 micromol/L) inhibited the first and second contractions by 68 and 97%, respectively. Simultaneous exposure to 15 mmol/L sodium solution and 100 micromol/L ouabain evoked only one transient contraction, larger (987 +/- 135 mg) than either of the ouabain-induced contractions. Inhibition of the sarcoendoplasmic reticulum Ca-ATPase with cyclopiazonic acid potentiated the first and second ouabain-induced contractions by 47 and 300%, respectively. Atropine (1 micromol/L) inhibited the first and second contractions by 44 and 76%, respectively. In conclusion, the results of the present study are relevant to the understanding of the mechanisms by which ouabain (100 micromol/L) contracts guinea-pig tracheal rings. At the muscular level, oubain induces Ca(2+) influx through L-type Ca(2+) channels and the reverse mode of the sodium-calcium exchanger. At the nerve terminals, ouabain promotes the release of acetylcholine secondary to the increase in Ca(2+) influx mediated by the reverse mode of the sodium-calcium exchanger.