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)

To find out whether the central structures governing conjugate eye movements are affected in ophthalmoplegia plus (OP), we conducted an electro-oculographic study in 6 patients suffering from OP with varying degrees of extraocular involvement and with mitochondrial changes in the skeletal musculature. All the patients presented alterations of the smooth pursuit and saccadic movements, of optokinetic nystagmus as well as of the vestibular reflexes and of visuovestibular interaction, thus confirming impairment of the central oculomotor structures and particularly of those of the archicerebellum and brainstem. These data suggest a supranuclear component in the pathogenesis of ophthalmoplegia and are in accord with the findings of brainstem spongiosis in OP, which in turn seem to express a multisystem pathological state of the mitochondria.
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PMID:Ophthalmoplegia plus, an electro-oculographic study. 387 36

Thirty-two cases of Wernicke's encephalopathy were admitted to hospital for treatment in a period of 33 months; this represented a relatively low incidence in total hospital admissions. Thiamin status was deficient, borderline and normal in 21 (66%), five (16%) and six (19%) patients, respectively, and responded immediately to treatment in those who had abnormal thiamin status. Ophthalmoplegia responded rapidly to treatment. Nystagmus, ataxia, disturbance of mental function and peripheral neuropathy responded incompletely to treatment in both the short-and the long-term. The overall setting for the development of Wernicke's encephalopathy appears to be chronic alcohol abuse, accompanied by cerebral "atrophy" and liver disease, but often without gross evidence of malnutrition.
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PMID:Wernicke's encephalopathy in a metropolitan hospital. A prospective study of incidence, characteristics and outcome. 394 14

A patient with multiple myeloma developed gaze paresis to the left with slowed saccades and gaze-paretic nystagmus, which alternated with abduction palsy in the left eye (with preserved oculocephalic deviation) and dissociated adducting nystagmus in the right eye, suggesting so-called posterior internuclear ophthalmoplegia. At autopsy multiple small infarcts were found with partial destruction of the left paramedian pontine reticula formation (PPRF) extending towards the abducens nucleus, which was involved only in its inferior pole. The medial longitudinal fasciculus and other oculomotor structures were spared. It is suggested that slowing of all ipsilateral saccades with gaze-paretic nystagmus corresponded to partial destruction of the PPRF, and that intermitted abduction palsy in the ipsilateral eye with adduction nystagmus in the fellow eye was due to intermittant dysfunction of the abducens nucleus. Involvement of voluntary saccades, pursuit movements and vestibulo-ocular responses may be dissociated in partial lesions of the abducens nucleus.
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PMID:Paresis of lateral gaze alternating with so-called posterior internuclear ophthalmoplegia. A partial paramedian pontine reticular formation-abducens nucleus syndrome. 399 74

A patient with sporadic pontocerebellar degeneration and downbeat nystagmus limited to the left eye is described. The nystagmus was not modified by head movements, but was associated with a purely tonic upgaze paresis in the same eye. Absence of internuclear ophthalmoplegia indicated sparing of the medial longitudinal fasciculus. It is suggested that the vertical oculomotor abnormalities are due to dysfunction of the ipsilateral brachium conjunctivum.
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PMID:Monocular downbeat nystagmus. 402 Mar 98

The eye movements of 100 patients with multiple sclerosis were examined clinically, including a saccade test. Thirty-four cases of internuclear ophthalmoplegia were found, of which 14 were bilateral and 20 were unilateral. Only three patients had full restriction of adduction, whereas 16 had no restriction at all. A continuous dissociated nystagmus was present in one patient only, while in 15 just a few beats of the abducting eye could be observed. In ten cases both restriction of adduction and dissociated nystagmus were lacking, and the diagnosis could only be made with the saccade test, which in all 34 patients showed a clearly visible disjunction of horizontal saccades. In 15 cases, infrared oculography was performed, which in all cases confirmed the clinical findings, and which in some cases disclosed an additional subclinical internuclear ophthalmoplegia on the opposite side.
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PMID:The clinical spectrum of internuclear ophthalmoplegia in multiple sclerosis. 402 28

Thiamine deficiency in the monkey is the animal counterpart of Wernicke's disease in humans. In the present study, thiamine deficiency was induced in 11 monkeys while three monkeys were given paired feedings supplemented by thiamine hydrochloride and three monkeys were maintained on regular chow. The typical clinical symptoms were apathy, inattention to peripheral stimuli, ataxia, ptosis, mydriasis progressing to pupillary areflexia, nystagmus, and ophthalmoparesis progressing to total ophthalmoplegia. With thiamine treatment, recovery was prompt and complete in mild to moderate cases but delayed and incomplete in severe cases. The animals were killed six or more months after discontinuance of the experiments to determine the chronic effects of treated thiamine deficiency. The significant abnormalities in the brain stem were symmetric gliosis and neuronal loss in the inferior colliculi, the regions of the third and sixth nerve nuclei, and the medial vestibular nuclei. White matter was characteristically spared. With the exception of the inferior colliculi, the target sites for neuropathologic changes were the centers for ocular motor control.
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PMID:Ocular signs in thiamine-deficient monkeys and in Wernicke's disease in humans. 402 52

Four cases of gaze paresis occurred in association with viral disease. In three cases the viral prodrome preceded the oculomotor disturbance. In one, gaze palsy was followed several days later by a viral syndrome. One had isolated bilateral horizontal ophthalmoplegia; another patient had motility disturbance with blepharoptosis and peripheral areflexia. Two patients had clinical evidence of brain-stem involvement: unilateral gaze paresis and gaze-evoked nystagmus in one and Parinaud's syndrome in the other. No accompanying long-tract signs or changes in mental status were present in any case. Recovery was complete in all four patients.
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PMID:Gaze palsy associated with viral syndrome. 403 36

Electrophysiological studies showed that a patient with Aland eye disease had no misrouting of the optic pathways which is always found in all forms of albinism as a consequence of the retino-geniculate anomaly. Also the spontaneous and optokinetic nystagmus did not resemble that of the large majority of human albinos. The marked asymmetry found in this patient seems to be typical for humans with a defective development of foveal binocular vision. These findings are in agreement with clinical, nystagmographic and EM findings that Aland eye disease is distinct from the Nettleship-Falls type of X-linked ocular albinism. Furthermore, Aland eye disease is different from X-chromosomal congenital stationary night blindness with myopia by the fact that the scotopic functions are only moderately affected and there is no restriction of the peripheral photopic visual fields. In addition, there is latent nystagmus of extraocular type that appears also in female carriers. There is no ophthalmoplegia, there is a progression of the myopia and the dyschromatopsia is of secondary type.
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PMID:Aland eye disease: no albino misrouting. 407 63

A 78-year-old hypertensive woman suddenly developed blurred vision, followed shortly by dizziness, difficulty walking with a tendency to veer to the left, and vertical diplopia. Examination 3 weeks later revealed a unique neuro-ophthalmologic motility pattern, which may be described as periodic alternating skew deviation. This previously unreported motility disturbance was associated with downbeat nystagmus in our patient, and a focal lesion at the level of the interstitial nucleus of Cajal was demonstrated on computed tomography. The spectrum of physiologically related motility patterns--including periodic alternating nystagmus, cyclic oculomotor paralysis, see-saw nystagmus, periodic alternating gaze deviation, "ping-pong" gaze, and intermittent aperiodic alternating skew deviation--has been considered and is helpful in topical neuro-ophthalmologic diagnosis.
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PMID:Periodic alternating skew deviation. 621 44

A patient with glioblastoma of the rostral brainstem and hypothalamus exhibited bilateral internuclear ophthalmoplegia and vertical nystagmus; he suffered episodes of cataplexy, narcolepsy, and sleep paralysis. A peculiar fluctuation of posture and tone ("limp man syndrome") proved to be a manifestation of continuous cataplexy, as documented by H-reflex recordings. This is the first report of a remarkable movement disorder caused by continuous, fluctuating, partial cataplexy, and is the second report of an association between cataplexy and a tumor of the rostral brainstem.
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PMID:Continuous cataplexy in a patient with a midbrain tumor: the limp man syndrome. 625 10


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