Intention tremor is related to lesions in the cerebellum or connected pathways. Intention tremor amplitude decreased after peripheral arm cooling in patients with multiple sclerosis (MS), likely caused by a reduction of muscle spindle afferent inflow, while amplitude increased when muscle spindles were artificially stimulated by tendon vibration. This study investigated the contribution of peripheral reflexes to the generation of MS intention tremor. Tendon reflexes of biceps, triceps, and brachioradialis, muscles were measured, using an electromechanical triggered reflex hammer. MS patients with (n = 17) and without (n = 17) upper limb intention and 18 healthy controls were tested. Latency of brachioradialis, biceps, and triceps tendon reflexes was greater in MS patients with tremor than in healthy controls and MS patients without tremor (except for the triceps reflex). Peak and peak-to-peak amplitude were not different between groups. It is concluded that tendon reflexes were delayed but not enlarged in MS patients with tremor. 1. Introduction Tremor in multiple sclerosis (MS) is a low-frequency action tremor with the clinical picture often being a combination of postural and intention tremor [1]. Intention tremor, clinically defined as an increase in tremor amplitude during visually guided movements towards a target at the termination of the movement, is related to lesions in the cerebellum and/or connected pathways in the brain stem and is often synonymously used with cerebellar tremor [1, 2]. Cerebellar tremor is suspected to be related to unstable central motor pathways and a malfunction of feedforward loops within the central nervous system, especially the cerebellum [3–5]. A feedforward system predicts the consequences of a movement, even prior to movement onset. As such, fine-tuning of movements can occur prior and during movement execution, and time delays inherently associated with sensory feedback can be overcome. In contrast, the motor performance is more dependent on feedback information when a malfunction in the feedforward system is present. This may explain the susceptibility of cerebellar tremor to peripheral factors such as mechanical loading. Tremor amplitude and frequency were shown to be modulated by mechanical loads, which indicates the involvement of stretch-elicited peripheral feedback mechanisms in the manifestation of cerebellar tremor [6, 7]. In support of this view, load-compensating tasks, evoking sudden stretch, induced an increase of tremor in cerebellar patients [8]. The tremor increase was suggested to be caused by
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