Disjugate ocular bobbing

The clinical spectrum of ocular bobbing and ocular dipping.

“…It was initially postulated that ocular bobbing represented a disturbance in the pathways mediating downward gaze. 23 However, the subsequent demonstration of impaired voluntary upward gaze in this disorder'5 reinforced Fisher's original suggestion that the bobbing may reflect the residual movements of patients who have severe limitations of their horizontal and vertical eye movements.1 I The vertical excursions are usually conjugate but may infrequently be dysconjugate and occupy the full vertical range or only a fraction of it.56 The use of cold calorics have been found to increase the amplitude and frequency of the movements or to have no demonstrable effect. 5 6 In some cases, the bobbing has been found to exist when cold calorics can still induce conjugate horizontal movements and ceases with disease progression.5 The presence of normal pupillary reactivity and respiratory efforts, among other functions, in severely affected patients suggests that major midbrain and medullary centres are intact.5 There is also a monocular form of bobbing which coexists with a contralateral oculomotor nerve palsy.9 Several atypical forms of ocular bobbing have also been described.…”

“…4 A slow conjugate downward movement of the eyes, followed by a rapid return to midposition, has been termed ocular dipping (or inverse ocular bobbing) and has been seen following anoxic coma or after prolonged status epilepticus.2 3 24-26 The generalised electroencephalographic slowing seen with the latter cases suggests that cortical depression may be a necessary concomitant.2 In addition, with anoxic encephalopathy, metabolic suppression or scattered cortical infarcts have been associated with incomplete lenticular nuclear damage and evocation of the dipping with passive eye movements.3 Roving conjugate or dysconjugate horizontal eye movements are prominent findings and normal spontaneous and elicited reflex upgaze are present. 23 No pontine dysfunction is evident and normal recovery is possible.23 The suggestion that ocular dipping may be caused primarily by diffuse dysfunction rather than a single structural locus is supported by the absence of brainstem abnormalities in two necropsy cases and by the tendency of the eye findings to abate as patients regain consciousness. 2 26 The present case report documents a fourth form of abnormal eye movements, termed reverse ocular dipping, which consists of a slow upward deviation of the eyes, a brief tonic phase and then a rapid return to midposition.…”

Ocular Bobbing: Abnormal Eye Movement or Eye Movement’s Abnormality?

“…This hypothesis has been contradicted by the coexistence of a number of cases of ocular bobbing with lesions of the pons as well as with lesions of the medulla oblongata [13]. Newman et al [12] suggested that ocular bobbing results from a pathological func tioning of a specific pathway normally me diating downwards gaze. This pathway would be homolateral and would run from the superior vestibular nucleus to the dorsal column of oculomotor nucleus destined to the inferior rectus.…”

Supranukleäre und internukleäre Augenbewegungsstörungen

“…Bei atypischen Formen können horizontale Augenbewegungen erhalten sein; häufig tritt hier Bobbing auch erst nach kalorischer Stimulation auf. Auch asymmetrische Formen ohne begleitende Paresen der okulomotorischen Hirnnerven gehören zur Gruppe atypischer Bobbing-Formen (227). Meist liegen hier extrapontine Läsionen im Rahmen zerebellärer Blutungen, eines Hydrocephalus obstructivus oder auch metabolischer Enzephalopathien zugrunde, die pontine Strukturen nur sekundär betreffen (35,316).…”