Paresis of contralateral smooth pursuit and normal vestibular smooth eye movements after unilateral brainstem lesions
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Abstract Pursuit and vestibular smooth eye movements were measured in patients with lesions of the caudal brainstem tegmentum identified by magnetic resonance imaging (MRI) and computed tomography (CT), with neuropathological correlation in 1 patient. Contralateral smooth pursuit gain was significantly lower than ipsilateral gain in each patient. Ipsilateral smooth pursuit gain was also subnormal in patients with unilateral pontine damage that caused slowing of ipsilateral saccades. Horizontal vestibulo‐ocular reflex gain and phase were normal. These quantitative correlations indicate that lesions of the pontine tegmentum that paralyze ipsilateral saccades can spare the vestibulo‐ocular reflex, and that smooth pursuit movement and the vestibulo‐ocular reflex can be impaired independently by pontine or medullary lesions. In contrast to lesions at other sites, unilateral lesions of the pontine or medullary tegmentum impair contralateral smooth pursuit more than ipsilateral pursuit movements. These findings provide evidence that a double decussating pathway mediates smooth pursuit; the first decussation is from the pons to the cerebellum, and the second decussation is from the vestibular nucleus to the contralateral abducens nucleus.Keywords:
Decussation
Smooth pursuit
Pons
Medial longitudinal fasciculus
Tegmentum
Internuclear ophthalmoplegia
Electronystagmography
Vestibulo–ocular reflex
Hyperreflexia
Abducens nucleus
One and a half syndrome is an internuclear ophthalmoplegia combined with lateral gaze palsy on the same side. It is caused by ipsilateral lesion of the caudal part of pontine dorsal tegmentum - medial longitudinal fasciculus and paramedian pontine reticular formation or/and abducens nucleus. Usually it is of vascular origin and it can be a sign of lateral pontine haemorrhage. We described a patient with one and a half syndrome caused by spontaneous hypertensive hemorrhage in the lateral pontine legmentum which was visualised by brain CT scanning.
Medial longitudinal fasciculus
Internuclear ophthalmoplegia
Abducens nucleus
Tegmentum
Pons
Abducens nerve
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Lesions that involve the paramedian pontine reticular formation (PPRF) or the sixthnerve nucleus on one side of the brain stem and also interrupt internuclear fibers of the ipsilateral medial longitudinal fasciculus produce an ipsilateral horizontal gaze palsy combined with an internuclear ophthalmoplegia, so that the only preserved horizontal eye movement is abduction of the contralateral eye (1). This syndrome consists of a complete horizontal gaze palsy when the patient looks toward the side of the lesion, combined with half gaze palsy when the patient looks in the opposite direction, and has been termed the “one-and-a-half syndrome” (2–5).
Internuclear ophthalmoplegia
Medial longitudinal fasciculus
Abducens nucleus
Pons
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The site of lesions responsible for horizontal gaze palsy and various types of internuclear ophthalmoplegia (INO) was established by identifying the common areas where the abnormal MRI signals from patients with a given ocular-motor disorder overlapped. Patients with unilateral gaze palsy had lesions in the paramedian area of the pons, including the abducens nucleus, the lateral part of the nucleus reticularis pontis caudalis and the nucleus reticularis pontis oralis. Patients with abducens nucleus lesions showed additional clinical signs of lateral rectus weakness. Lesions responsible for bilateral gaze palsy involved the pontine tegmental raphe. Since this region contains the saccadic omnipause neurons, this finding suggests that damage to omnipause cells produces slowing of saccades rather than opsoclonus, as previously proposed. All INOs, regardless of the presence of impaired abduction or convergence, had similar MRI appearances. Frequently the lesions in patients with INO, were not confined to the medial longitudinal fasciculus (MLF) but also involved neighbouring structures at the pontine and mid-brain levels. There was a statistically significant association between the clinical severity of the INO and the presence of abnormal abduction or convergence. The findings suggest that the lesions outside the MLF, which may affect abducens, gaze or convergence pathways, are responsible for the presence of features additional to INO, depending on the magnitude of functional disruption they produce.
Medial longitudinal fasciculus
Internuclear ophthalmoplegia
Abducens nucleus
Pons
Oculomotor nucleus
Smooth pursuit
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Five patients with "locked-in" syndrome and dysconjugate palsy of horizontal gaze were studied. In all cases internuclear ophthalmoplegia due to dysfunction or destruction of the median longitudinal fasciculus was combined with an ipsilateral gaze palsy, producing the "one-and-a-half" syndrome. Clinical and electro-oculographic examination suggested involvement of the paramedian pontine reticular formation when all ipsilateral saccades were abolished, when exotropia of the contralateral eye was present, and when vestibular stimulation showed full conjugate deviation to the damaged side. Involvement of the abducens nucleus was suggested when the palsy of ipsilateral gaze was not dissociated on vestibular stimulation. In three cases these clinical deductions were confirmed by the pathological study, which showed a corresponding destruction of the median longitudinal fasciculus, paramedian pontine reticular formation and abducens nucleus. In one case the one-and-a-half syndrome evolved into a total horizontal gaze palsy, which corresponded to involvement of the abducens nucleus contralateral to the initially destroyed paramedian pontine reticular formation. Vertical oculocephalic response disappeared, because of destruction of the median longitudinal fasciculus on both sides (bilateral internuclear ophthalmoplegia). Patients with the locked-in syndrome provide a unique situation in which complex pontine oculomotor disturbances may be studied, because consciousness is preserved. In these patients, dissociated and dysconjugate oculomotor palsy may have been underestimated.
Medial longitudinal fasciculus
Abducens nucleus
Internuclear ophthalmoplegia
Oculomotor nucleus
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The one-and-a-half syndrome is a clinical disorder of extraocular movements characterized by a conjugate horizontal gaze palsy in one direction plus an internuclear ophthalmoplegia in the other. The syndrome is usually due to a single unilateral lesion of the paramedian pontine reticular formation or the abducens nucleus on one side (causing the conjugate gaze palsy), with interruption of internuclear fibers of the ipsilateral medial longitudinal fasciculus after it has crossed the midline from its site of origin in the contralateral abducens nucleus (causing failure of adduction of the ipsilateral eye). Twenty cases are reported 14 had multiple sclerosis.
Medial longitudinal fasciculus
Abducens nucleus
Internuclear ophthalmoplegia
Tegmentum
Oculomotor nucleus
Pons
Abducens nerve
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Abducens nucleus
Medial longitudinal fasciculus
Oculomotor nucleus
Abducens nerve
Internuclear ophthalmoplegia
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Citations (3)
To describe the clinical symptoms, anatomical location of the injury and different etiologies of one-and-a-half syndrome and its variants.A small lesion to the brainstem can cause complex syndromes that involve the disfunction of different nuclei and pathways. A 52-year-old man presented with sudden onset of diplopia characterized by horizontal gaze palsy and internuclear ophthalmoplegia (INO). With these clinical characteristics, the patient was diagnosed with the one-and-a-half syndrome. Neuroimaging revealed an acute/subacute ischemic lacunar event in the pontine tegmentum. The one-and-a-half syndrome is described as a horizontal gaze palsy in one direction (damage to the paramedian pontine reticular formation [PPRF] or the VI nerve nucleus) and an internuclear ophthalmoplegia in the other direction (damage to the medial longitudinal fasciculus). Along with the traditional description, the closed anatomical proximity with other nuclei and pathways makes possible the appearance of other more complex syndromes that have been grouped as the one-and-a-half syndrome and its variants.A detailed clinical neuro-ophthalmologic examination, along with a clear understanding of the neuroanatomical pathways, gives clinicians a good diagnostic opportunity to determine the precise location of injuries to the brainstem.
Internuclear ophthalmoplegia
Medial longitudinal fasciculus
Abducens nucleus
Tegmentum
Pons
Ocular Motility Disorders
Abducens nerve
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covers deviations and disorders of horizontal gaze, which are so significantly linked to lesions of the pons that an emphasis on pontine signs is an important focus of this chapter. The pontine syndromes presented include a congenital case of horizontal gaze palsy and progressive scoliosis, and syndromes associated with adjacent tegmental structures, especially the paramedian reticular formation, the facial nerve, and the medial longitudinal fasciculus. A lesion of the medial longitudinal fasciculus causes internuclear ophthalmoplegia Examples are provided of internuclear ophthalmoplegia in childhood, combined unilateral conjugate gaze palsy and internuclear ophthalmoplegia, the one-and-a-half syndrome, and other variants. A case of bilateral horizontal gaze palsy permits discussion of the caloric test, one of the most widely used clinical test of the vestibulo-ocular reflex.
Medial longitudinal fasciculus
Internuclear ophthalmoplegia
Pons
Abducens nucleus
Smooth pursuit
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Abducens nucleus
Internuclear ophthalmoplegia
Medial longitudinal fasciculus
Neuroradiology
Oculomotor nucleus
Pons
Abducens nerve
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Medial longitudinal fasciculus
Abducens nucleus
Pons
Oculomotor nucleus
Decussation
Internuclear ophthalmoplegia
Posterior commissure
Oculomotor nerve
Vestibulo–ocular reflex
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Citations (3)