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Floating Basilar Artery: An Interesting Clinical Dilemma

596 suggestive of ataxic hemiparesis. In addition, MRI sequences clearly showed that the small deep lesion was restricted to the posterior limb of the internal capsule without involvement of the thalamus. Based on previous observations regarding ataxic hemiparesis and thalamic ataxia together with the 2 previously reported cases of isolated hemiataxia after capsular lacunar infarct, we strongly believe that in our patient, hemiataxia was more likely due to a lesion of the cerebellar pathways, either the ascending dentatorubrothalamocortical tract or the descending corticopontocerebellar pathway at the level of the posterior limb of the internal capsule. Functional MRI, PET or SPECT would have been of great interest in this patient to demonstrate CCD and thus assess our hypothesis. Such investigations were, unfortunately, not performed. To conclude, as previously suggested by Luijckx et al. [1, 2] , as well as discussed in anatomical studies [21–23] , the case reported here provides further clinical evidence of the anatomically segregated passage of the cerebellar fibres through the posterior part of the posterior limb of the internal capsule. Interruption of the cerebellar connections in the internal capsule may therefore cause isolated hemiataxia of the cerebellar type as observed in our patient. The determination of whether the descending or ascending pathway is severed and responsible for the cerebellar symptoms appears difficult. However MR diffusion tensor imaging may provide the answer to this question by studying the development of a descending or ascending wallerian degeneration in a given patient with an infarction in the posterior limb of the internal capsule.