horizontal gaze palsy
TRANSCRIPT
905-1 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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