Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eye movements were quantitatively evaluated in 16 patients with well-documented multiple sclerosis who had minimal or no clinically apparent eye movement disorder. Induced saccade and pursuit eye movements were recorded with electro-oculography and analyzed with newly developed programs on a laboratory digital computer. Thirteen of the 16 patients had significant (p less than 0.05) impairment of saccades and/or smooth pursuit when compared with 25 normal subjects tested in our laboratory. The type and frequency of abnormalities were as follows: saccade dysmetria, eight; delayed saccade reaction time, five; bilateral saccade slowing, four; slowing of adducting saccades only (medial longitudinal fasciculus syndrome), one; and impaired smooth pursuit, both directions, three, and one direction only, three. In addition, four patients had vestibular nystagmus with eyes closed, and one patient had typical rebound nystagmus. These data suggest that quantitative assessment of eye movements in patients with suspected multiple sclerosis can help in identifying the important "second lesion."
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PMID:Subclinical eye movement disorders in patients with multiple sclerosis. 55 65

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

See-saw nystagmus is a unique torsional-vertical eye movement disorder with a characteristic appearance. It is a pendular nystagmus with two distinct components: a conjugate torsional component and a disjunctive vertical component. In those cases of see-saw nystagmus in which a focal lesion has been identified, the lesion is usually a bilateral, symmetric lesion located at the mesodiencephalic junction. We report an unusual case of see-saw nystagmus which was due to a strictly unilateral mesodiencephalic lesion. Furthermore, the see-saw nystagmus had, in this case, a jerk wave-form rather than the usual pendular wave-form, with the torsional component of the jerk see-saw nystagmus beating toward the side of the lesion. These observations have an impact upon the localizing and lateralizing significance of torsional nystagmus in general and of see-saw nystagmus in particular.
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PMID:See-saw nystagmus due to unilateral mesodiencephalic lesion. 183 89

We looked for correlations between otoneurological findings and neurological signs in multiple sclerosis (MS). 41 patients were tested for: spontaneous and caloric nystagmus, horizontal pursuit eye tracking, full-field optokinetic nystagmus and eye movements. The findings were compared with the course of the disease (progressive or remitting), age at onset of MS and disability, in order to test the predictive value of this type of test. The correlation between otoneurological abnormalities and lesion site is very high for brainstem lesions. Subclinical brainstem lesions were detected in 66% of patients with optic neuritis only and in 42% of those with spinal cord involvement only. Eye movement disorders are more frequent (p less than 0.1) in disease of long duration. The vestibular examination was altered in 100% of patients with clinically definite and probable MS, in 91% of those with possible and in 80% of those with suspected MS. No specific otoneurological pattern was identified. No significant correlation with age at onset or with disability was found.
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PMID:Value of otoneurological tests in the staging of multiple sclerosis. 365 69

A 60-year-old black male with a 13-year history of adult onset diabetes mellitus and hypertension with a previous lacunar stroke suddenly developed a periodic head and eye movement disorder characterized by nonalternating skew deviation, rotatory nystagmus, head tilt, and lid retraction. On CT scan, the patient had a lacunar infarct in the right midbrain in the region of the interstitial nucleus of Cajal, an anatomical area involved with head tilt, torsional eye movement, and skew deviation.
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PMID:Periodic nonalternating ocular skew deviation accompanied by head tilt and pathologic lid retraction. 622 16

Duane's retraction syndrome (DRS) is a congenital eye movement disorder characterized by marked limitation or absence of abduction, variable limitation of adduction, and narrowing of the palpebral fissure with retraction of the globe on attempted adduction. We have recently recorded and quantitated ocular motility in five patients with unilateral DRS. In all patients, abduction of the affected eye was greatly limited, whereas adduction was limited, whereas adduction was limited to a lesser degree. Abnormalities in saccadic velocities were found in both the affected eye and the sound eye. Results of testing of the vestibulo-ocular reflex, optokinetic nystagmus, and optokinetic afternystagmus showed notable asymmetry. Our results suggest that DRS is produced by a primary brainstem abnormality involving premotor structures.
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PMID:Central ocular motor abnormalities in Duane's retraction syndrome. 729 31

See-saw nystagmus is an uncommon but highly characteristic eye movement disorder comprising intorsion and elevation of one eye, with synchronous extorsion and depression of the other. It generally has a pendular waveform and is due to a midline, extrinsic, suprasellar mass lesion compressing or invading the brainstem bilaterally at the meso-diencephalic junction. This report deals with the clinical and MRI findings in three patients (and binocular three-dimensional quantitative oculographic findings in one patient) with a jerk waveform see-saw nystagmus due in each case to a unilateral meso-diencephalic lesion. In each patient the torsional component of the nystagmus fast phases rotated the upper poles of the eyes toward the side of the lesion. Jerk see-saw nystagmus can be clinically indistinguishable from pendular see-saw nystagmus and from the torsional-vertical nystagmus which occurs with medullary lesions. We propose that jerk see-saw nystagmus is due to unilateral inactivation of the torsional eye-velocity integrator, thought to be in the interstitial nucleus of Cajal, with sparing of the torsional fast-phase generator, thought to be in the adjacent rostral interstitial nucleus of the medial longitudinal fasciculus.
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PMID:Jerk-waveform see-saw nystagmus due to unilateral meso-diencephalic lesion. 792 66

Congenital ocular motor apraxia (C-OMA) is an infrequently reported eye movement disorder associated with malformation or delayed maturation of the brain. Patients with C-OMA are unable to initiate voluntary horizontal saccades. This results in characteristic head thrusts into the desired field of gaze to compensate for the lack of saccadic ability. Careful examination of an 8-year-old Hispanic male revealed uncoordinated eye movements, lack of voluntary saccades, head thrusts, and gross/fine motor delays all consistent with congenital ocular motor apraxia. Torsional oscillations that resembled rotary nystagmus were also present. These have not been previously reported in association with C-OMA. Because young patients with this condition may appear to have cortical blindness, C-OMA is an important differential to be aware of in making a diagnosis.
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PMID:Congenital ocular motor apraxia with torsional oscillations: a case report. 874 43

Forty-six patients suffering from autosomal dominant cerebellar ataxia type I (ADCA I) underwent to a genotype-phenotype correlation analysis by molecular genetic assignment to the spinocerebellar ataxia type 1, 2, or 3 (SCA1, SCA2, SCA3) genetic locus and electro-oculography. Oculomotor deficits that are attributed to dysfunction of cerebellar structures occurred in all three mutations without major differences between the groups. Gaze-evoked nystagmus, however, was not found to be associated with SCA2. Square wave jerks were exclusively observed in SCA3. The gain in vestibulo-ocular reflex was significantly impaired in SCA3 and SCA1. In SCA3 the severity of vestibular impairment increased with CAG repeat length. Severe saccade slowing was a highly characteristic feature of SCA2. In SCA3 saccade velocity was normal to mildly reduced while SCA1 fell into an intermediate range. The present data show that each mutation is associated with a distinct syndrome of oculomotor deficits. Reduced saccade velocity and the absence of both square-wave jerks and gaze-evoked nystagmus allow one SCA2 to be distinguished from SCA3 patients in almost all cases. The eye movement disorder of SCA1 patients, however, overlaps with both SCA2 and SCA3.
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PMID:Autosomal dominant cerebellar ataxia type I: oculomotor abnormalities in families with SCA1, SCA2, and SCA3. 1052 76

A patient with suspected brain stem glioma involving the area of the left vestibular nuclei and cerebellar peduncle, developed paroxysmal alternating skew deviation and direction changing nystagmus after biopsy of the inferior cerebellar vermis resulting in destruction of the uvula. Between attacks she had right over left skew deviation with asymptomatic right beating horizontal nystagmus. Slow phases of the resting nystagmus showed increasing velocity, similar to congenital nystagmus. At intervals of 40-50 seconds, paroxysmal reversal of her skew deviation occurred, accompanied by violent left beating horizontal torsional nystagmus lasting 10-12 seconds and causing severe oscillopsia. It is proposed that this complex paroxysmal eye movement disorder results from (1) a lesion in the left vestibular nuclei causing right over left skew and right beating resting nystagmus and (2) a disruption of cerebellar inhibition of vestibular nuclei, causing alternating activity in the vestibular system with intermittent reversal of the skew deviation and paroxysmal nystagmus towards the side of the lesion.
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PMID:Paroxysmal alternating skew deviation and nystagmus after partial destruction of the uvula. 1138 16


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