## 6 Compensatory Strategies in Cerebellar Dysfunctions
### Neural Plasticity and compensatory Mechanisms  
The idea that intact brain areas may reorganize their activity to compensate for other functionally impaired areas (e.g., because of cerebral lesions or degenerations) is not new. For example, back at the end of the last century, several papers by [PERSON], [PERSON], et al. [100; 101; 102] reported that the posteromedial lateral suprasylvian (PMLS) visual cortical area in the cat showed physiological compensation after damage to hierarchically lower visual areas ([PERSON]'s 17, 18, and 19), provided that the damage occurred early in the animal's life. Even if such compensation could not completely overcome the deficits [101], PMLS neurons could develop the properties they would have had in the absence of brain damage. Moreover, tracing methods revealed an increased projection from the retina through the thalamus to the PMLS after lesion [103], showing that neural pathway reorganization plays a role in the compensatory process. Later, [PERSON] et al. [104] reported such neural pathway reorganization in a blindsight man, who suffered the loss of the left primary visual cortex. In addition to the normal pathways found in healthy subjects, he showed two major features: a pathway from right lateral geniculate nucleus to left MT+ / V5 area and a strong cortico-cortical bilateral connection between MT+ / V5. Figure 2: Role of the cerebellum in the ontogenesis of the APA control. Cerebellar deficits interfere with the correct development of postural control. The later the appearance of the cerebellar deficit, the weaker seems to be the ability of the CNS to develop a compensatory strategy. This is particularly apparent when the disease has a progressive course, since it contrasts with the strategy consolidation. Further evidence supporting a compensatory activation of intact brain areas comes from studies of language production and comprehension deficits, following prefrontal stroke [105] and left temporal lobe damage [106]. In both cases, a specific compensatory pathway involving extra-lesion areas was highlighted. Another study recorded event-related brain potentials in patients with a lesion in the perisylvian area of the language-dominant hemisphere that impaired their ability to apply syntax and grammar rules [107]. Results suggested that these patients overcame their syntactic deficit by relying on another, more semantic processing route. A recent study on patients with cognitive dysfunctions following pontine ischemia [108], probably due to damages in the fronto-cerebellar circuits, reported a hyperactivity of frontal areas and suggested that it could compensate for the cognitive impairments. Another masterpiece of brain compensation regards the recovery of hand motor functions after stroke in the primary motor area (M1). In this condition, multiple structures are called into play, such as the contralateral undamaged M1, the bilateral premotor, and the supplementary and somatosensory areas, as well as the cerebellum and basal ganglia (for a review, see [109]). More recently, a PET study in the monkey [110] showed not only an enhanced activity in the ventral premotor cortex during the early post-recovery period after M1 lesion, but also an increased functional connectivity within the perilesional M1 in the late post-recovery. Another study on macaque [111] provided evidence that fronto-cerebellar circuits may reorganize to sustain functional recovery after M1 lesions. Furthermore, the neural pathway reorganization quoted above has been observed in rats after lesions of the sensorimotor cortices [112]. After neonatal hemidecortification, corticospinal fibers from the intact contralateral sensorimotor cortex send collateral sprouts to the ipsilateral spinal cord, mediating cortical excitation to ipsilateral forelimb, with a different contribution of rostral and caudal forelimb motor areas.