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1 tion of the oculomotor vermis caused saccade dysmetria.
2 lar damage, the same variability resulted in dysmetria.
3 ntaminated by some adaptation to the saccade dysmetria.
4 lities can be reconceptualized as "cognitive dysmetria."
5 ipsilateral dysmetria, and that ipsilateral dysmetria after large pontine stroke represents a discon
7 ty correlated with the degree of dysarthria, dysmetria and dysdiadochokinesia but not with grip stren
10 ontocerebellar fibers to prevent ipsilateral dysmetria, and that ipsilateral dysmetria after large po
11 ny aspects of mental activity, or "cognitive dysmetria." As Bleuler originally proposed, "thought dis
12 h schizophrenia may suffer from a "cognitive dysmetria" due to dysfunctional prefrontal-thalamic-cere
15 nctional integration, and with the cognitive dysmetria hypothesis, which posits a disconnection withi
17 bicuculline produced an amplitude-dependent dysmetria: ipsiversive horizontal saccades elicited by t
18 ate disability with gait ataxia, dysarthria, dysmetria, mild oculomotor abnormalities, and diffuse ce
19 the disorder, as suggested by the cognitive dysmetria model, then cerebellar-targeted treatments may
21 ripheral neuropathy, 53%; cerebellar ataxia, dysmetria, or dysarthria, 38%; and encephalopathy, 27%.
22 fibres destined for the spinal cord, whereas dysmetria results from lesions involving the neurons of
23 creased proprioception leading to ataxia and dysmetria that were markedly worse in the absence of vis
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