Cerebellar reserve compensates for and restores functions lost through cerebellar damage. This is a fundamental property of cerebellar circuitry. Clinical studies suggest (1) the involvement of synaptic plasticity in the cerebellar cortex for functional compensation and restoration, and (2) that the integrity of the cerebellar reserve requires the survival and functioning of cerebellar nuclei. On the other hand, recent physiological studies have shown that the internal forward model, embedded within the cerebellum, controls motor accuracy in a predictive fashion, and that maintaining predictive control to achieve accurate motion ultimately promotes learning and compensatory processes. Furthermore, within the proposed framework of the Kalman filter, the current status is transformed into a predictive state in the cerebellar cortex (prediction step), whereas the predictive state and sensory feedback from the periphery are integrated into a filtered state at the cerebellar nuclei (filtering step). Based on the abovementioned clinical and physiological studies, we propose that the cerebellar reserve consists of two elementary mechanisms which are critical for cerebellar functions: the first is involved in updating predictions in the residual or affected cerebellar cortex, while the second acts by adjusting its updated forecasts with the current status in the cerebellar nuclei. Cerebellar cortical lesions would impair predictive behavior, whereas cerebellar nuclear lesions would impact on adjustments of neuronal commands. We postulate that the multiple forms of distributed plasticity at the cerebellar cortex and cerebellar nuclei are the neuronal events which allow the cerebellar reserve to operate in vivo. This cortico-deep cerebellar nuclei loop model attributes two complementary functions as the underpinnings behind cerebellar reserve.
There are numerous forms of cerebellar disorders from sporadic to genetic diseases. The aim of this chapter is to provide an overview of the advances and emerging techniques during these last 2 decades in the neurophysiological tests useful in cerebellar patients for clinical and research purposes. Clinically, patients exhibit various combinations of a vestibulocerebellar syndrome, a cerebellar cognitive affective syndrome and a cerebellar motor syndrome which will be discussed throughout this chapter. Cerebellar patients show abnormal Bereitschaftpotentials (BPs) and mismatch negativity. Cerebellar EEG is now being applied in cerebellar disorders to unravel impaired electrophysiological patterns associated within disorders of the cerebellar cortex. Eyeblink conditioning is significantly impaired in cerebellar disorders: the ability to acquire conditioned eyeblink responses is reduced in hereditary ataxias, in cerebellar stroke and after tumor surgery of the cerebellum. Furthermore, impaired eyeblink conditioning is an early marker of cerebellar degenerative disease. General rules of motor control suggest that optimal strategies are needed to execute voluntary movements in the complex environment of daily life. A high degree of adaptability is required for learning procedures underlying motor control as sensorimotor adaptation is essential to perform accurate goal-directed movements. Cerebellar patients show impairments during online visuomotor adaptation tasks. Cerebellum-motor cortex inhibition (CBI) is a neurophysiological biomarker showing an inverse association between cerebellothalamocortical tract integrity and ataxia severity. Ataxic gait is characterized by increased step width, reduced ankle joint range of motion, increased gait variability, lack of intra-limb inter-joint and inter-segmental coordination, impaired foot ground placement and loss of trunk control. Taken together, these techniques provide a neurophysiological framework for a better appraisal of cerebellar disorders.
The cerebellum contains more neurons than any other region of the brain and the number of afferent fibers exceeds largely the number of efferences, indicating enormous computational capabilities of the cerebellar circuitry. Thanks to its high connectivity to the other brain areas, the cerebellum is a master-piece for information processing and planning of sensorimotor activities. There is accumulating evidence that cerebellar circuitry holds an internal representation of time to govern timing processes, contributes actively not only to predictions of fast movements but also to the online regulation of slow movements. It has been concluded from clinical observations and experimental studies for more than a century that the cerebellum controls accuracy of movements and coordination of multi-joint movements. Patients exhibit various combinations of oculomotor disturbances, dysarthria, dysmetria, dysdiadochokinesia, tremor, decomposition of movements, loss of check and rebound, disorders of muscle tone, ataxia of stance and gait. Cerebellum is also involved in learning, in particular by tuning the dynamic control of movement. The main mechanisms underlying limb incoordination consist of an inability to recruit the antagonist muscle activities at the appropriate timing, a deficit in the adaptation of muscles to changes of the mechanical state of the hand (namely inertia and damping), errors in the superimposition of motor commands, impaired excitability of the motor cortex, and an inability to update programming based upon sensory events. Cerebellar circuitry contributes also to neural processes beyond the motor domain. In particular, cerebellar patients may present cognitive and behavioral changes, usually not detectable by a conventional neurological examination and therefore often overlooked. The so-called cerebellar cognitive affective syndrome includes impairment of executive functions including planning and working memory, deficits in visuospatial skills, linguistic deficiencies such as agrammatism, and inappropriate behaviour. The constellation of these cognitive/behavioural deficits is suggestive of a disruption of the cerebellar modulation of neural circuits that link prefrontal, posterior parietal, superior temporal and limbic structures including the amygdala, hippocampus and septum. The posterior fossa syndrome can be considered as a very acute form of cerebellar cognitive affective syndrome, affecting mainly children.
Abstract In a prospective study, we repeatedly recorded fast goal‐directed wrist movements of 8 patients who had experienced an acute cerebellar hypermetria due to a stroke and who had subsequently recovered clinically. Movements and the associated agonist and antagonist electromyographic (EMG) activities were recorded before and after addition of inertial loads. Four stages characterized the recovery process. At stage 1, hypermetria was present in the basal state and was not modified by the addition of inertial loads. At stage 2, hypermetria, which was present in the basal state, was enlarged by mass addition. At stage 3, hypermetria was absent in the basal state, but was revealed by an inertial load increase. At stage 4, as in healthy subjects, there was no hypermetria without or with addition of inertial loads. At stage 1, the patients presented several defects. (1) Facing an increased inertia, they could not increase their agonist EMG activity. (2) The onset latency of their antagonist EMG activity was delayed. (3) Facing an increased inertia, they could not increase their antagonist EMG activity. Among these three defects, the first disappeared at stage 2, the second at stage 3, and the third at stage 4.
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We describe a wearable orthosis and an associated algorithm for the simultaneous assessment and treatment of essential tremor, one of the most common movement disorders in humans involving an overactivity of the olivo-cerebellar pathways. A motor providing effective viscosity is fixed on a wearable orthosis in the upper limbs. The motor is controlled by a personal computer with software processing in real time the position and rate of rotation of the joint detected by a chip gyroscope. The orthosis can be used in a monitoring mode and in an active mode. The range of tremor suppression of the signals above the orthosis operational limit ranges from about 3% (percentile 5) to about 79% (percentile 95) in relation to energy in the monitoring mode. Considering both postural and kinetic, the mean tremor energy decreased from 55.49 ± 22.93 rad2 s−3 in the monitoring mode to 15.66 ± 7.29 rad2 s−3 in the active mode. Medians of power reduction were below 60% for the wrist and the elbow. In addition to supplying new information on the interactions between kinematics, dynamics and tremor genesis, this non-invasive technique is an alternative to current therapies. This new approach will provide new insights into the understanding of motor control.
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