Transcript Horizontal Gaze Palsy

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Horizontal Gaze Palsy
Left esotropia; fascicular sixth nerve
palsy, left horizontal gaze palsy
Full horizontal gaze to the right with
gaze evoked nystagmus
Vergence movements induced the right
eye to cross the midline
Full Downgaze
Impaired eye closure due to left facial
palsy (Bell’s palsy)
Left lower motorneuron facial palsy
(Bell’s palsy)
Figure 1 Axial NECT scan shows a focal hemorrhage in the
posterior pons and fourth ventricle. Patient with known breast
cancer.
Figure 2 Sagittal NECT scan showing the rostral-caudal
extent of the pontine hemorrhage
Ocular Motility
Unilateral horizontal gaze palsy to the left
that impaired saccades and pursuit
Esotropia of the left eye
Fascicular sixth nerve palsy
Horizontal gaze full to the right, gaze
evoked nystagmus
Ocular Motility
Normal convergence, right eye
induced to cross the midline
Horizontal oculocephalic reflex,
absent (Doll’s head maneuver)
Vertical eye movements normal
Signs in Leigh and Zee’s Case
The patient was unable to move her eyes to the right
past the midline using either saccadic or pursuit eye
movements
Head rotation to the left, however, drove the eyes past
the midline, but the right eye abducted incompletely
Vergence movements induced the left eye to cross the
midline
Vertical eye movements were normal
Gaze evoked nystagmus was present on looking to the
left, with slow phases toward the midline
The patient developed a fascicular sixth nerve palsy
Horizontal Gaze Palsy
There are four theoretical possibilities to account
for the ipsilateral horizontal gaze palsy due to a
single unilateral lesion affecting
1. The ipsilateral paramedial pontine reticular
formation (PPRF) only
2. The ipsilateral abducens nucleus (AN) alone
3. Both the ipsilateral PPRF and the AN, or when
two lesions are involved
4. The motoneuron root fibers of the ipsilateral
AN to the lateral rectus and the contralateral
medial longitudinal fasciculus (MLF)
Figure 3 Horizontal section of the lower pons.
1) Basis pontis syndrome. 2) Internuclear ophthalmoplegia 3) Abducens
nucleus syndrome 4) Caudal PPRF syndrome 5) One-and-a-half syndrome 6)
Paramedian midbrain syndrome
Figure 4 Sagittal section of brainstem
Clinical Findings with PPRF Lesion
Loss of horizontal saccades towards the
side of the lesion
Contralateral gaze deviation, in acute
phase
Gaze-evoked nystagmus on looking
contralateral to the lesion
Clinical Findings with PPRF Lesion
Impaired smooth pursuit and vestibular
eye movements may be preserved or
impaired
Bilateral lesions cause total horizontal
gaze palsy and slowing of vertical
saccades
Contralateral gaze deviation in an
acute PPRF lesion
Clinical findings with lesion of the
abducens nuclei
Loss of all conjugate movements towards
the side of the lesion – ipsilateral,
horizontal gaze palsy
Contralateral gaze deviation, in acute
phase
Vergence and vertical movements are
spared
Clinical findings with lesion of the
abducens nuclei
In the intact hemifield of gaze, horizontal
movements may be preserved, but
ipsilaterally directed saccades are slow
Horizontal gaze-evoked nystagmus on
looking contralaterally
Ipsilateral lower motoneuron facial palsy
Clinical signs of a lesion of the
abducens nuclei
Clinical distinction PPRF: AN at the
bedside
PPRF lesions rostral to abducens
paralysis of saccades and pursuit, but the
eyes can be driven to the side of the
ipsilateral gaze palsy with vestibular
stimulation by the oculocephalic reflex
and/or cold calorics
Clinical distinction PPRF: AN at the
bedside
PPRF lesions at the level of abducens
are associated with ipsilateral gaze palsy
and loss of reflex vestibular (and tonic
neck) movements
This presumes that there is a critical
synapse within the caudal PPRF for the
vestibulo-ocular pathways or that the
functional integrity of the PPRF at that
level is necessary for vestibulo-ocular eye
movements
Figure 5 Ocular motor control system. Combination of previous illustrations
indicates saccadic (s), pursuit (P), and vestibular (VIII), inputs to PPRF and its
output to the oculomotor nucleus (III) and the abducens nucleus (VI).
Figure 6 Brainstem ocular motor control system
Figure 7 Brainstem ocular motor control system
The PRF contains three types of saccade – related
neurons
Burst neurons (BN)
Excitatory BN (EBN) create saccadic eye velocity
commands (the pulse)
Inhibitory BN (IBN) permit reciprocal innervation
to occur
Tonic neurons (TN)
Part of the neural integrator that integrates eye
velocity commands and holds position for gaze
Pause neurons (PN)
Exert a normal inhibitory influence upon saccadic
burst neurons during periods of fixation
Figure 8 The motor circuit for horizontal saccades in the brainstem
Conjugate horizontal deviation of the
eyes in coma
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