Complete bilateral horizontal gaze paralysis disclosing multiple sclerosis

Two women presented with bilateral internuclear ophthalmoplegia evolving in a few days to complete bilateral horizontal gaze paralysis. Convergence and vertical eye movements were normal. Cerebral MRI showed a few small white matter lesions in the lateral ventricle regions, and, at the brainstem level, a single, small, bilateral lesion affecting the posterior part of the medial pontine tegmentum and responsible for the clinical syndrome. The condition gradually improved in both patients, following a similar progression as at the onset: improvement first involved the adduction movements in both eyes, whereas bilateral abduction paresis still persisted for a few weeks, before complete recovery of eye movements. Bilateral damage to the medial longitudinal fasciculus and subsequent lateral extent of damage to the region of the two abducens emerging fibres may explain the clinical findings. In both cases, the cause was probably multiple sclerosis.     

Pontine metastasis with dissociated bilateral horizontal gaze paralysis.

A clinicopathological case of pontine metastatic tumour is reported with an oculomotor syndrome including bilateral horizontal gaze paralysis affecting saccades and foveal pursuit. During full-field pursuit, oculocephalic movement, and after caloric stimulation, the right eye alone was able to move slowly only 30 degrees to the right of the midline. Convergence and vertical eye movements were unaffected in either eye. The lesion lay in the whole left pontine tegmentum and partly in the right pontine tegmentum which was also strongly compressed and displaced to the right. The bilateral horizontal gaze paralysis resulted from damage to both paramedian pontine reticular formations. The unusual combination of an absence of foveal pursuit with the persistence of a rightward full-field pursuit analysed in the light of recent experimental work, suggested a clear separation between the brainstem pathways of these two types of pursuit movement. Lastly, according to our data and other clinicopathological findings previously reported, it appeared also that the paramedian pontine reticular formation role in the triggering of voluntary vertical saccades is less significant in man than in the monkey.     

Bilateral horizontal gaze paralysis due to pontine hemorrhage. A case report

In a case of bilateral horizontal gaze paralysis, vertical gaze was clinically intact but eye movement recordings demonstrated a transient reduction of vertical saccadic velocities. Horizontal caloric vestibulo-ocular responses were absent. CT scanning and NMR imaging showed a hematoma in the median pontine tegmentum. This case provides additional evidence that vertical and horizontal saccade genesis may be independent of caudal paramedian pontine reticular formation lesions.     

Locked-in syndrome with bilateral ptosis: combination of bilateral horizontal pontine gaze paralysis and nuclear oculomotor nerve paralysis

Summary A patient with a classical locked-in syndrome is described, in whom bilateral ptosis was observed on the 2nd day. On the 4th day, ophthalmoplegia was complete with the exception of a voluntary downward movement of the right eye. The syndrome can be explained by the association of bilateral horizontal pontine gaze palsy and a unilateral nuclear oculomotor nerve palsy, and approximates the total locked-in syndrome.     

Midbrain paresis of horizontal gaze

Unilateral paramedian involvement of the midbrain tegmentum causes monocular paralysis of adduction in the ipsilateral eye, paresis of contralateral saccades in the opposite eye, and conjugate paresis of ipsilateral smooth pursuit. The adduction paralysis can be nuclear, or internuclear from a lesion in the medial longitudinal fasciculus. This distinctive midbrain syndrome of horizontal gaze paresis is exemplified by means of quantitative infrared oculographic, radiological, and neuropathological correlation in two patients with predominantly paramedian midbrain tumors involving the mesencephalic reticular formation and the oculomotor nucleus. Binocular paralysis of elevation provided evidence that one human oculomotor nucleus contains axons to both superior rectus muscles, as does the simian oculomotor nucleus. The midbrain tectum was spared. These pathophysiological correlations indicate that the mesencephalic reticular formation contains pathways that control contralateral saccades and ipsilateral smooth pursuit.     

Familial paralysis of horizontal gaze. Associated with pendular nystagmus, progressive scoliosis, and facial contraction with myokymia.

Paralysis of horizontal gaze, pendular nystagmus, and progressive scoliosis were manifestations of an autosomal recessive genetic disease in four siblings. Bilateral facial myokymia with continuous facial contraction developed in the oldest patient. Electromyographic examination of his facial muscles after facial nerve block at the stylomastoid foramen showed absence of all muscle potentials, consistent with a supranuclear origin of the myokymia. Normality of convergence, vertical gaze, and pupillary constrictor reflex activity assured integrity of midbrain ocular motor function. Absence of horizontal vestibulo-ocular reflexes signified involvement of the pontine tegmentum in this distinctive heredofamilial syndrome.     

Bilateral thalamic infarction associated with selective downward gaze paralysis

A 34-year-old man presented with transient downward gaze paralysis and impairment of convergence together with prominent psychic disturbances. Cranial CT and MRI clearly demonstrated a symmetric infarction extending from the bilateral thalamus to the rostral medial midbrain. The existence of downward gaze paralysis following ischemic stroke is contributory to the diagnosis of not only the location of but also the responsible artery for the infarction.     

Vertical and horizontal epileptic gaze deviation and nystagmus

Periods of epileptic nystagmus consisting of rightward eye deviation and right-beating nystagmus, alternating with upward eye deviation and upbeating nystagmus, occurred in a comatose patient with a left hemisphere subdural hematoma and seizures. The periods of upbeating nystagmus were associated with symmetric, low-voltage 3 to 4 Hz bifrontal spikes. Rightward eye deviation and right-beating nystagmus occurred with diffuse, predominantly left hemispheric 4 to 6 Hz sharp waves. No eye movements occurred in the absence of spike and wave activity. These correlations agree with current concepts of the cortical control of saccadic eye movements in monkeys studied by electrical stimulation.     

Pontine tuberculoma presenting with horizontal gaze palsy.

A 38-year-old immunocompetent man presented with a horizontal supranuclear gaze palsy as the only neurologic manifestation of a pontine tuberculoma. Although a biopsy of the brain lesion was not performed, it was attributed to tuberculosis because of chest x-ray evidence. The patient was given empirical anti-tuberculous therapy. After one month, the gaze palsy had fully recovered and repeat MRI showed a decrease in the size of the lesion. This is the first reported case of supranuclear gaze palsy without diplopia as a manifestation of a tuberculous brain stem lesion.     

Eye movements in patients with absent voluntary horizontal gaze

Despite the complete absence of horizontal saccades, two patients with pontine gliomas had horizontal reflex eye movements within a range of +/- 20 degrees. The gain (peak eye velocity/peak stimulus velocity) and phase of the vestibulo-ocular reflex were normal, but the optokinetic gain was decreased. The latency, accuracy, and peak velocity of vertical saccades were normal. Apparently the voluntary gaze centers in the pontine reticular formation are not crucial for generating horizontal vestibular or vertical saccadic eye movements.     

Abducens internuclear neurons and their role in conjugate horizontal gaze

Experimental evidence suggests that brain stem lesions producing paralysis of lateral gaze and dissociation of conjugate horizontal eye movements have certain common features. Both of these disturbances involve abducens internuclear neurons (Abd IN) or their projections. Attempts were made to determine the course and terminal distribution of Abd IN in the monkey by autoradiographic techniques. Tritiated amino acids injected in the abducens nucleus (Abd N) labeled: (1) root fibers ipsilaterally, and (2) fibers that ascended in medial parts of the contralateral medial longitudinal fasciculus (MLF). In the opposite oculomotor complex (OMC) silver grains were profuse over the ventral nucleus (VN, medial rectus muscle) and patchy over caudal parts of the dorsal nucleus (DN, inferior rectus muscle). Labeling of cells in the reticular formation nucleus to Abd N resulted in transport ipsilaterally, outside the MLF, to the rostral interstitial nucleus of the MLF (RiMLF), a cell group considered to be concerned with vertical eye movements. Bilateral labeling of Abd N and cells of the nucleus prepositus (NPP) resulted in bilateral: (1) transport of isotope via root fibers and the MLF, and (2) selective distribution of silver grains in the OMC. Bilateral silver grain distribution in the OMC suggested profuse terminations in VN, patchy terminations in DN and vertical, linear terminations in caudal parts of the medial nucleus (MN, superior rectus muscle). Comparisons with more discrete unilateral labeling of cells in Abd N suggested that cells of the NPP project selectively to terminations in MN, and may be related to upward eye movements. Two conclusions were drawn: (1) The paresis of ocular adduction which occurs in both anterior internuclear ophthalmophlegia and in paralysis of lateral gaze results from involvement of Abd IN or their ascending projections, and (2) the NPP appears to project selectively to parts of MN of the OMC, a cell group said to provide crossed innervation for the superior rectus muscle.