SUMMARY1. The effects of different forms of brain stimulation on the discharge pattern of single motor units were examined using the post-stimulus time histogram (PSTH) technique and by recording the compound surface clectromyographic (EMG) responses in the first dorsal interosseous (FDI) muscle. Electrical and magnetic methods were used to stimulate the brain through the intact scalp of seven normal subjects. Electrical stimuli were applied either with the anode over the lateral central scalp and the cathode at the vertex (anodal stimulation) or with the anode at the vertex and the cathode lateral (cathodal stimnulation). Magnetic stiinulation used a 9 cm diameter coil centred at the vertex; current in the coil flowed either clockwise or anticlockwise when viewed from above.2. Supramotor threshold stimuli produced one or more narrow (< 2 ms) peaks of increased firing in the PSTH of all thirty-two units studied. Anodal stimulation always produced an early peak. The latencies of the peaks produced by other forms of stimulation, or by high intensities of anodal stimulation, were grouped into four time bands relative to this early peak, at intervals of -0 5 to 0U5, 1-2, 2-5-3-5 and 4-5-5 ms later. Peaks occurring within these intervals are referred to as P0 (the earliest an6dal), P1, P2 and P3 respectively.3. At threshold, anodal stimulation evoked only the P0 peak; at higher intensities, the P2 or more commonly the P3 peak also was recruited. The size of the P0 peak appeared to saturate at high intensities.4. In five of six subjects, cathodal stimulation behaved like anodal stimulation, except that there was a lower threshold for recruitment of the P2 or P3 peak relative to that of the P0 peak. In the other subject, the P3 peak was recruited before the PO peak.5. Clockwise magnetic stimulation, at threshold, often produced several peaks. These always included a PI peak, and usually a P3 peak. A P0 peak in the PSTH was never produced by a clockwise stimulation at intensities which we could explore with the technique.6. Anticlockwise magnetic stimulation never recruited a P1 peak; in most subjects a P3 peak was recruited first and at higher intensities was accompanied by P0 or P2 peaks. 15PHY 412 B. L. DA ' AND) OTHERS 7. On most occasions when more than one peak was observed in a PSTH, the uniit fired in only one of the preferred intervals after each shock. However, double firing was seen in five units when high intensities of stimulation were used. The intervals between the two discharges was the same as the intervals between peaks in the PSTH.8. Surface EMG responses in the FDI muscle behaved in a way predietable from the behaviour of the single motor units which had been studied.9. These results are discussed in terms of the D and I wave hypothesis proposed for responses of pyramidal tract neurones to surface anodal stimulation of the exposed motor cortex in primates.

BackgroundHuntington's disease (HD) is a fatal inherited neurodegenerative disease, caused by a

Botulinum toxin (BT) has been perceived as a lethal threat for many centuries. In the early 1980s, this perception completely changed when BT’s therapeutic potential suddenly became apparent. We wish to give an overview over BT’s mechanisms of action relevant for understanding its therapeutic use. BT’s molecular mode of action includes extracellular binding to glycoprotein structures on cholinergic nerve terminals and intracellular blockade of the acetylcholine secretion. BT affects the spinal stretch reflex by blockade of intrafusal muscle fibres with consecutive reduction of Ia/II afferent signals and muscle tone without affecting muscle strength (reflex inhibition). This mechanism allows for antidystonic effects not only caused by target muscle paresis. BT also blocks efferent autonomic fibres to smooth muscles and to exocrine glands. Direct central nervous system effects are not observed, since BT does not cross the blood-brain barrier and since it is inactivated during its retrograde axonal transport. Indirect central nervous system effects include reflex inhibition, normalisation of reciprocal inhibition, intracortical inhibition and somatosensory evoked potentials. Reduction of formalin-induced pain suggests direct analgesic BT effects possibly mediated by blockade of substance P, glutamate and calcitonin gene-related peptide.

BPS is a novel and noninvasive method to differentiate highly specifically between IPD and APS. Therefore, BPS might become a standard investigation in parkinsonian disorders.

Positive effects on mood have been observed in subjects who underwent treatment of glabellar frown lines with botulinum toxin and, in an open case series, depression remitted or improved after such treatment. Using a randomized double-blind placebo-controlled trial design we assessed botulinum toxin injection to the glabellar region as an adjunctive treatment of major depression. Thirty patients were randomly assigned to a verum (onabotulinumtoxinA, n = 15) or placebo (saline, n = 15) group. The primary end point was change in the 17-item version of the Hamilton Depression Rating Scale six weeks after treatment compared to baseline. The verum and the placebo groups did not differ significantly in any of the collected baseline characteristics. Throughout the sixteen-week follow-up period there was a significant improvement in depressive symptoms in the verum group compared to the placebo group as measured by the Hamilton Depression Rating Scale (F((6,168)) = 5.76, p < 0.001, η(2) = 0.17). Six weeks after a single treatment scores of onabotulinumtoxinA recipients were reduced on average by 47.1% and by 9.2% in placebo-treated participants (F((1,28)) = 12.30, p = 0.002, η(2) = 0.31, d = 1.28). The effect size was even larger at the end of the study (d = 1.80). Treatment-dependent clinical improvement was also reflected in the Beck Depression Inventory, and in the Clinical Global Impressions Scale. This study shows that a single treatment of the glabellar region with botulinum toxin may shortly accomplish a strong and sustained alleviation of depression in patients, who did not improve sufficiently on previous medication. It supports the concept, that the facial musculature not only expresses, but also regulates mood states.