We tested 24 normal subjects, 24 patients with idiopathic Parkinson's disease (PD), and eight patients with bilateral absence of vestibular function (labyrinthine defective [LD] subjects) in their ability to set a straight line to the perceived gravitational vertical (visual vertical). Measurements were taken in static conditions, sitting upright, and lying down on the right side, and during visual background motion at constant angular velocities around the line of sight (roll-motion) in both sitting upright and sideways position. Aims of the study were to determine if the reported increased "visual dependence" in PD was present in a psychophysical task that is independent of motor performance, and to examine the interaction between visual motion and proprioceptive cues in the perception of verticality, in the absence of vestibular function. LD patients showed abnormally large deviations of the visual vertical induced both by lateral body tilt and by visual roll-motion. This suggests that vestibular cues play a significant part in counterbalancing visually and proprioceptive mediated biases on the perception of verticality. In contrast, PD patients were normal in all these tasks indicating that visual dependence in PD is not present at an afferent/perceptual level.

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Botulinum toxin type A therapy for cervical dystonia.

Cannabis may have medicinal uses in a variety of diseases. The neural mechanisms underlying dystonia involve abnormalities within the basal ganglia-in particular, overactivity of the lateral globus pallidus (GPl). Cannabinoid receptors are located presynaptically on GABA terminals within the GPi, where their activation reduces GABA reuptake. Cannabinoid receptor stimulation may thus reduce overactivity of the GPl and thereby reduce dystonia. A double-blind, randomised, placebo-controlled, crossover study using the synthetic cannabinoid receptor agonist nabilone in patients with generalised and segmental primary dystonia showed no significant reduction in dystonia following treatment with nabilone.

SUMMARY In a bimanual slow matching task patients with asymmetric bradykinesia overestimated the movement of the more bradykinetic limb. Patients with drug induced or idiopathic asymmetric dyskinesia or dystonia, and patients with unilateral arm weakness underestimated movement of the abnormal limb. Bradykinesia may be caused by reduction, and dyskinesia and dystonia by exaggeration of corollary discharges.The movement disorder in Parkinson's disease encompasses a variety of phenomena including abnormalities of initiation, maintenance, accuracy, velocity and extent of active movement, and resistance to passive movement. We lack a unifying explanation of these disparate factors and experiments exploring one feature often ignore others, although concepts derived from such investigation may advance a general theory; in this paper the reduced extent of active movement (strictly, hypokinesia) is considered, but the more familiar term "bradykinesia" is used for convenience.The role of the basal ganglia in the control of movement is unclear, as is the mechanism by which basal ganglia hypofunction results in bradykinesia. Marsden has argued that the basal ganglia are probably not primarily involved in initiating movement or the selection of specific muscles, and suggests that they play a role in scaling the amplitude of movement.1 He proposed that in bradykinesia there is a failure of "automatic execution of learned motor plans", and that although there are abnormalities of proprioceptive feedback, kinaesthetic function is not disturbed and sensory input does not influence the generation of bradykinesia; rather, there is a simple failure to generate an adequate motor signal.1 Hassler, however, points out that there is extensive indirect sensory input to the striatum2 and indeed sensory and other cognitive abnormalities are described in Parkinson's disease.3 Their mere presence is insufficient evidence that sensory abnormalities promote Address for reprint requests: Dr A P Moore,