Efferent pathways from the FOR cross immediately to the other side before they enter the brainstem. Accordingly, patients with a lesion to the rostral cerebellum show saccadic contrapulsion [81], i.e. the reverse pattern of a unilateral FOR lesion. It is usually found with lesions in the territory of the superior cerebellar artery. In this case, saccades to the contralateral side are hypermetric and hypometric to the ipsilateral side. However, SPEM show a low gain in both directions [82] occasionally more pronounced to the ipsilateral side [83]. The reason probably is that lesions of the rostral cerebellum do not only affect the FOR pathways but also the pathways to and from the FL.

Lesions of the FL lead to a partial SPEM deficit, more pronounced to the ipsilateral side. In contrast to OV and FOR lesions, the SPEM deficit is usually combined with gaze-evoked nystagmus due to a gaze holding deficit [84].

Medulla

The most common ischemic lesion of the brainstem is the lateral medulla infarction (Wallenberg’s syndrome); in patients, it always (100%) leads to oculomotor deficits [85]. This includes a SPEM deficit to the contralateral side [86]. As pointed out above for OV and FOR lesions, also this deficit corresponds with hypometric saccades to the contralateral side (table 1). It is postulated that this deficit is caused by interruption of olivocerebellar pathways after their crossing in the medulla [87, 88] (fig. 3).

Optokinetic Nystagmus

For patients, there are no good methods available to test the ‘indirect’ component of OKN in isolation. One possible method would be to test their OKAN. However, even in normals OKAN can be missing [19]. On the bedside, usually a handheld optokinetic cylinder is rotated for several seconds in one direction. This however only activates the ‘direct’ (smooth pursuit-related) component, since the time is not sufficient to provide a substantial contribution of the ‘indirect’ component [16]. When optokinetic stimuli are used, a side difference of up to 20 /s for the maximal velocity is still considered normal [89]. Pathological side differences are more obvious with the use of smaller stimuli [90]. For the monkey, it could be shown that mesencephalic lesions in the pretectum lead to a reduction in the ‘indirect’ component to the ipsilateral side. Also the OKAN in this direction is missing or reduced [91]. There is also some evidence that in addition pretectal lesions can affect the ‘direct’ component [92]. Clinical reports on this topic are still missing.