Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Head movement-dependent oscillopsia (HMDO) with peripheral vestibular, brainstem and cerebellar lesions is reviewed. The differentiation of this kind of oscillopsia is based mainly on clinical grounds. HMDO with bilateral abolition of caloric responses, and in the absence of disease of the central nervous system, is due to bilateral vestibular disease. HMDO in patients with internuclear ophthalmoplegia and other brainstem signs is probably due to a lesion of VOR pathways in or near the medial longitudinal fasciculus. The occurrence of HMDO with ataxia of gait and cerebellar eye movement disorders (rebound nystagmus, flutter-like oscillations), in the absence of brainstem lesions (medial longitudinal fasciculus), is clinical evidence for HMDO due to a cerebellar lesion. An attempt is made to associate the different kinds of oscillopsia with current knowledge of the vestibulo-ocular reflexes.
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PMID:Clinical and theoretical aspects of head movement dependent oscillopsia (HMDO). A review. 8 58

Bilateral transections across the brainstem interrupted the medial longitudinal fasciculus (MLF) in three monkeys trained to make eye movements while subjected to horizontal or vertical angular accelerations. Eye movements measured before and after the lesion revealed deficits in both voluntary and vestibular compensatory eye movements; the deficits differed in the horizontal and vertical directions. Vertical saccades in both directions were normal but eccentric positions of fixation could not be maintained; a drift toward the midline followed by a corrective saccade produced vertical fixation nystagmus. Furthermore, the vertical vestibulo-ocular reflex (VOR) was abolished and vertical smooth pursuit was impaired. Along the horizontal meridian, adduction across the midline could not be achieved during either saccades, smooth pursuit, or the VOR. Temporal saccades were normal whereas nasal saccades were considerably slowed. If the eye was not required to cross the midline, the phase shift during the VOR was within 15 deg of normal in each eye. The gain of the VOR was reduced to about 0.4 immediately after the lesion, but recovered within one month. These findings suggest that the MLF transmits quite different kinds of information to horizontal and vertical oculomotoneurons and that deficits in vertical eye movements may be a sensitive indicator of anterior internuclear ophthalmoplegia.
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PMID:Bilateral lesions of the medial longitudinal fasciculus in monkeys: effects on the horizontal and vertical components of voluntary and vestibular induced eye movements. 40 93

The effect of head position on conjugate horizontal gaze was studied in healthy adults, in patients with multiple sclerosis without eye movement signs, and in patients with downbeat nystagmus indicative of low brain stem lesions. Displacements of gaze from primary position to 30 degrees left and right were recorded using the electro-oculogram, with the head in the primary position, and turned voluntarily to the left and right (in yaw). The quality of eye movements was noted and peak velocities of saccades were measured. The head turning test trebled the incidence of abnormal eye movements found in the multiple sclerosis patients and increased it by tenfold in the patients with downbeat nystagmus. Disorders of eye movement were also found in approximately 20--30% of healthy subjects tested. Weakness of abduction was the most common eye movement defect and appeared to be posterior internuclear ophthalmoplegia. A hypothesis is made which unifies the theoretical explanations of anterior and posterior internuclear ophthalmoplegia. The most likely cause of the disorders of eye movement observed is vertebrobasilar ischaemia induced by stretching and compression of the vertebral arteries during eccentric head posture.
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PMID:Eccentric head positions reveal disorders of conjugate eye movement. 59 79

Multiple sclerosis is a disease of the central nervous system whose clinical manifestations include animportant group of ocular pathologies, e.g., unilateral retrobulbar neuritis, uveitis, decreased visual function, nystagmus, internuclear ophthalmoplegia, diplopia, optic papillitis and Marcus Gunn pupil. Additionally, it is not generally appreciated that bitemporal hemianopia, usually associated with tumors of the optic chiasm, may also result from multiple sclerosis. Since most of a patient's life is spent in the remission phase of the disease, it is important for the practitioner to recognize the ocular findings present during this period. Additionally, studies have shown that such patients lead longer and more productive lives than most practitioners realize, and often have prolonged periods of remission. While the onset of the disease may present with ocular symptoms, such as loss of vision or diplopia, the patients tend to recover and retain relatively good function for many years.
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PMID:The ocular manifestations of multiple sclerosis. 59 46

The eye movements of 25 patients with internuclear ophthalmoplegia were recorded by electrooculography. The velocity of adducting saccades was markedly less than normal. The velocity of abducting saccades was within the normal range, but statistically there was a wider distribution. Recordings were made in 2 patients several months after the onset of internuclear ophthalmoplegia, at which time the adducting eye velocity was greater than the abducting eye velocity. A patient with a unilateral medial fasciculus lesion showed marked overshoot of the abducting eye on contralateral saccades and overshoot of both eyes toward the side of the lesion. Optokinetic and postcaloric nystagmus were recorded, and the slow phase showed increasing velocity exponential waveform for the abducting eye. The recordings also showed decreasing velocity exponential waveform for the abducting eye. Downbeat nystagmus was as common as upbeat nystagmus in our patients. The findings appear to confirm the theoretical analysis of the eye movement disorder in internuclear ophthalmoplegia provided by Pola and Robinson as modified by recent experimental work in primates.
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PMID:An electrooculographic study of internuclear ophthalmoplegia. 61 77

Saccades (horizontal and vertical) and dissociated nystagmus were quantitatively assessed in four patients with internuclear ophthalmoplegia. Two patients had bilateral medial longitudinal fasciculus (MLF) lesions associated with multiple sclerosis and two had unilateral lesions associated with brain stem vascular disease. Adducting saccades made on the side of an MLF lesion were slowed in each patient (P less than .01). At the same time, abducting saccades in the contralateral eye had normal velocity, but consistently overshot the target. After the overshoot, the eye returned to the target with an exponentially decaying course. With large angular deviations (usually more than 15 degrees), the abducting eye developed nystagmus characterized by slow components that moved toward the midposition with an initially high velocity followed by a segment of slower velocity. The adducting eye had either no nystagmus or a low-amplitude nystagmus characterized by a rounded junction between the fast and slow component. The saccade abnormalities and waveform of the dissociated nystagmus can be explained by a pulse-step mismatch at the agonist motoneurons.
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PMID:Internuclear ophthalmoplegia. I. Saccades and dissociated nystagmus. 66 4

Smooth pursuit, optokinetic nystagmus (OKN) and the vestibulo-ocular reflex (VOR) were studied in four patients with internuclear ophthalmoplegia (two with bilateral and two with unilateral lesions). Horizontal smooth pursuit by an adducting eye on the side of a medial longitudinal fasciculus (MLF) lesion was normal in three of four patients; vertical pursuit was abnormal in all four. The horizontal VOR gain of slow components made by an adducting eye on the side of an MLF lesion was normal in all four patients. The vertical VOR gain was decreased in the two patients tested. It is concluded that either there are pathways independent of the MLF for horizontal pursuit and vestibular signals that are not available to vertical signals, or vertical pursuit and vestibular eye movements require a higher rate of oculomotor neuron firing than equal-velocity horizontal eye movements.
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PMID:Internuclear ophthalmoplegia. II. Pursuit, optokinetic nystagmus, and vestibulo-ocular reflex. 66 5

A study is presented of three patients suffering from internuclear ophthalmoplegia without diplopia. The components of the nystagmus and the dysmetry of the oculomotor changes, as well as the difference in the respective speeds during abduction and adduction toward the side opposite to the lesion were recorded. A dysmetric component was found in the saccadic low amplitude movements (reading movements).
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PMID:[So-called internuclear ophthalmoplegias. Electro-oculographic study]. 73 73

In a patient with atypical bilateral internuclear ophthalmoplegia the optokynetic test and the ocular dysmetria test detected an infraclinical bilateral lag of adduction. The optokinetic test showed amplitude asymmetry of nystagmus, which was larger in both eyes when the fast phase was in abduction. The ocular dysmetria test showed in both eyes that saccades were slower in adducting than abducting saccades: the latters overshooted and showed transient nystagmus. Since bilateral internuclear ophthalmoplegia is often indicative of multiple sclerosis, these tests are particularly helpful in those patients who otherwise would require more complex diagnostic investigations.
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PMID:[Optokynetic and ocular dysmetria tests in the diagnosis of atypical internuclear ophthalmoplegia (author's transl)]. 75 5

Recent findings in experiments on monkeys show that a horizontal saccade is made by a pulse-step of neural activity, part of which rises to medial rectus (MR) motoneurons on the fibers of the medial longitudinal fasciculus (MLF). If inhibitory as well as excitatory fibers run in the MLF, then the data show that each MLF must carry both the excitatory and inhibitory activity required for contralateral, horizontal saccades. Therefore, interruption of these fibers removes not only excitation from the ipsilateral MR but inhibition from the contralateral MR. Such a lesion also disturbs the correct relationship between the pulse and the step and creates abnormal saccades. These facts make it possible to explain why, in internuclear ophthalmoplegia, the eye on the side of the lesion adducts slowly and inadequately, while the opposite eye has nystagmus in abduction.
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PMID:An explanation of eye movements seen in internuclear ophthalmoplegia. 82 Mar 13


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