Impairment of vertical motion detection and downgaze palsy due to rostral
midbrain infarction
W. Heide, M. Fahle, E. Koenig, J. Dichgans, and G. Schroth
Summary
We present two cases with acute onset of vertical gaze palsy, mainly consisting
of impaired downgaze and apraxia of downward head movements, together with
neuropsychological deficits (hypersomnia, impaired attention and disorders
of memory and affective control). CT and MRI revealed bilateral post-ischaemic
lesions in the dorsomedial thalamus and the mesodience-phalic junction,
dorsomedial to the red nucleus, thus being restricted to the territory of
the posterior thalamo-subthalamic paramedian artery, which includes the
region of the rostral interstitial nucleus of the medial longitudinal fascicle
as the main premotor nucleus for the generation of vertical saccades. In
our patients, oculo-graphic examination with electro-oculography and magnetic
search coil recording showed severe impairment of downward more than upward
saccades and only minor deficits of vertical pursuit and the vestibulo-ocular
reflex. Visual functions were normal, with one exception: a psychophysical
test of motion perception revealed a significant deficit in the detection
of vertical movements. This could be due to a central adaptive mechanism
which, in order to minimize oscillopsia, might elevate thresholds for vertical
motion perception in cases of vertical gaze palsy. As an alternative explanation,
lesions within the midbrain tegmentum could have damaged subcortical visual
pathways involved in motion perception.
Key words:
Vertical motion detection - Downgaze palsy - Eye-head
coordination - Paramedian mesodiencephalic syndrome - Midbrain infarction