Movement and electromyographic disorders associated with cerebellar dysmetria

Abstract

The objective of these experiments was to determine whether dysmetric elbow flexions, which occurred during cerebellar dysfunction, had the same kinematic and electromyographic characteristics as movements of the same amplitude and velocity performed under normal conditions. Reversible cerebellar lesions were produced by cooling through two probes implanted on either side of the dentate nucleus in five Cebus albifrons monkeys. Normal, fast, and accurate elbow flexions had single-peaked velocities and a bi- or triphasic EMG pattern in agonist and antagonist muscles. During cerebellar dysfunction movements became ataxic. Ataxic movements were classified into two categories: those with oscillations (tremor) during the movement and those without oscillations. A terminal tremor occurred after both types of movements. Oscillations during movements were more likely to occur when a constant force loaded the antagonist. Addition of mass to the handle attenuated or abolished the oscillations. Movements with oscillations reached the target with increased variability of end position, whereas movements without oscillations were often hypermetric. The movement parameters and EMG patterns associated with flexions without oscillations during the movement were studied in detail. A characteristic of these movements was that the acceleration and deceleration phases were asymmetric. Compared with control movements of the same peak velocity, they had smaller magnitudes of acceleration and larger magnitudes of deceleration. The large deceleration was abnormal because it initiated the terminal tremor. The disorder in acceleration was associated with agonist EMG activity that was less abrupt in onset, smaller in magnitude, and more prolonged in duration. The disorder in deceleration was associated with delayed onset of phasic antagonist EMG activity. The results show that hypermetric arm movements without oscillations have different properties than those of normal movements of similar velocity and amplitude. Thus it is unlikely that dysmetria results from inappropriate selection or triggering of an otherwise normal motor program. We conclude that normal function of the cerebellum is necessary for the generation of agonist and antagonist muscle activity that is both of the appropriate magnitude and timing to control the dynamic phase of arm movements.

Preserved Simple and Impaired Compound Movement After Infarction in the Territory of the Superior Cerebellar Artery

“…33 Yet, upon dentate cooling during movements at the elbow, Flament and Hore reported not only action tremor but in addition, hypermetria. 7 Their inclusion of hypermetria may be a matter of definition. Flament and Hore defined the endpoint of movement as the position at which velocity first reaches zero.…”

Multi-Joint Reaching Movements and Eye-Hand Tracking in Cerebellar Incoordination: Investigation of a Patient with Complete Loss of Purkinje Cells

“…Recordings from the patient showed a number of abnormal features in the temporal profiles for angular velocities at the shoulder and elbow. In experiments involving cooling of cerebellar nuclei in monkeys, Flament and Hore 16 observed that the velocity profile for rapid elbow flexion movements became asymmetric with longer acceleration phases and shorter deceleration phases. In human subjects with a variety of cerebellar disorders, Brown et al 17 found abnormalities of velocity profiles for single joint target -directed movements.…”

Progressive gait ataxia following deep brain stimulation for essential tremor: adverse effect or lack of efficacy?

“…Motor disability in essential tremor results predominantly from the complex interaction of postural-, action-and intention-tremor with goal-directed hand movements, but $10-15% of patients additionally present mild cerebellar symptoms, such as saccadic abnormalities (Helmchen et al, 2003), dysmetria or impaired tandem gait (Flament and Hore, 1986;Hallett et al, 1991;Fasano et al, 2010). There is an ongoing debate on whether a cerebellar dysfunction in essential tremor is caused by disease progression and neurodegeneration (Louis et al, 2007) or a functional disruption of the cerebello-thalamo-cortical network through the interference of tremor-related neuronal oscillations with normal cerebellar timing function (Solomon et al, 1994;Elble, 1998;Deuschl et al, 2000;Blangero et al, 2009;Elble, 2009).…”