Disorders

Smooth Pursuit Eye Movements

Cortex

Both frontal and parietal lesions in patients lead to SPEM deficits [66]. Lesions of the MT region cause a deficit [67] similar to that seen in monkeys [68]. Moving stimuli within the contralateral visual field defect cannot be adequately tracked independent of the movement direction, whereas saccades to the defective area remain intact. In contrast, lesions of the neighboring MST lead to a directional (ipsiversive) deficit independent of the retinal location. Also lesions of the FEF lead to an ipsiversive SPEM deficit [69]. The MT, MST, FEF and SEF project via the internal capsula to the pons. Accordingly, an ipsiversive deficit is also seen after lesions in the internal capsula [70].

Pontine Structures

Lesions of the pontine nuclei lead to a predominantly ipsiversive SPEM deficit [71, 72]. However, even bilateral lesions of the pontine nuclei do not abolish SPEM. This might reflect that also the NRTP is involved in SPEM generation. Smooth pursuit deficits in ‘progressive supranuclear palsy’ [73] and spinocerebellar ataxia types 1, 2 and 3 [74] have also been related to lesions of the pontine structures.

Cerebellum

In the cerebellar cortex, lesions of the OV and the FL lead to SPEM deficits. Patients with cerebellar ataxia and bilateral vestibulopathy show a reduced SPEM gain [75]. A total loss of SPEM is only seen when both structures are lesioned (total cerebellectomy, monkey). In the OV, SPEMas well as saccade-related neurons are found. Lesions always lead to related deficits [76] (table 1). A bilateral lesion of the OV leads to hypometric saccades and SPEM with a reduced gain. This is also seen in patients [77, 78]. Effects of unilateral lesions have not yet been described in patients.

The Purkinje cells of the OV project to the FOR and have an inhibitory effect. Consequently, a bilateral lesion of the FOR leads to hypermetric saccades. This should be combined with an increased SPEM gain (gain 1). In this case, back up instead of catch up saccades should occur during SPEM. However, this pattern is only rarely seen [79] (fig. 2). Still, a patient with a severe hypermetria due to a bilateral FOR lesion showed highly normal values with a SPEM gain close to 1 [80]. Experimental (monkey) unilateral lesions lead to a SPEM gain reduction and hypometric saccades to the contralateral side and normal SPEM and hypermetric saccades to the ipsilateral side [57] (table 1).

Table 1. The effect of cerebellar midline lesions and lateral medullary infarction on SPEM and saccades

In general, a reduced SPEM gain is combined with hypometric saccades. This is not the case for lesions in the rostral cerebellum since not only FOR efferents but also pathways to and from the FL are affected.

T

RT

10º

H (NORM)

LT

*

Fig. 2. Effect of transient inactivation by local muscimol injection in the right FOR on SPEM. T Target position; H (NORM) horizontal eye position before muscimol injection; H (MUSC) horizontal eye position after muscimol injection; RT right; LT left. During rightward movements, the SPEM gain is 1 and back-up saccades (marked by asterisks) occur. During leftward movements, the smaller gain is corrected by catch-up saccades; from Fuchs et al. [79].