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At least 19 recordsLinked to original sources
PubMed1979

[Dissociated ophthalmoplegia of abduction: so-called posterior internuclear ophthalmoplegia in Fisher's syndrome].

The anterior internuclear ophthalmoplegia, a dissociated ophthalmoplegia of adduction secondary to an ipsilateral supranuclear paresis of the internal rectus, represents a well-know clinical picture. The dissociated ophthalmoplegia of abduction, however, sometimes referred to as posterior internuclear ophthalmoplegia, is debated. Such an oculomotor disturbance emerging from an ophthalmoplegic polyneuropathy (Fisher syndrome) is presented and illustrated by oculographic tracings. A secondary finding was a limited range of accommodation. Oculographically, the dissociated ophthalmoplegia of abduction reflects a true mirror image of the anterior internuclear ophthalmoplegia. Because of anatomical considerations the dissociated ophthalmoplegia of abduction cannot be regarded as internuclear ophthalmoplegia, and the terminology of posterior internuclear ophthalmoplegia is not tenable. Discussing the pathophysiology of the Fisher Syndrome, it is reflected upon an infranuclear lesion causing an ocular motility disorder featuring supranuclear aspects, and avoiding limitations of peripheral nerve damage.

Accommodation, Ocular↗
PubMed2000

[A case of anti-GQ1b-positive atypical Fisher syndrome with internal ophthalmoplegia but without external ophthalmoplegia].

We report a 21-year-old man who developed an atypical form of Fisher syndrome. One week after having a common cold, he was admitted to our hospital because of a gait disturbance. Neurological examination revealed a somnolent state, cerebellar ataxia, areflexia, limb muscle weakness, and numbness in a glove and stocking like distribution. The patient had internal ophthalmoplegia but did not have external ophthalmoplegia. Brain MRI showed no abnormality in the orbital and the pretegmental brain regions. The protein level in the cerebrospinal fluid was 57 mg/dl and the cell count was 5 mononuclear cells/mm3. His serum titer of anti-GQ1b IgG antibody was markedly elevated. There have been only two previous reports of isolated internal ophthalmoplegia with elevated anti-GQ1b antibody. The present case suggests that anti-GQ1b antibody play an important role in the pathogenesis of patients who present with internal ophthalmoplegia but without external ophthalmoplegia.

Adult↗
PubMed2003

Transient impaired vision, external ophthalmoplegia, and internal ophthalmoplegia after blepharoplasty under local anesthesia.

PURPOSE: To report a case of transient bilateral vision impairment with external ophthalmoplegia and internal ophthalmoplegia after blepharoplasty under local anesthesia. DESIGN: Interventional case report. METHODS: A 70-year-old man underwent bilateral upper blepharoplasty under local anesthesia. During orbital fat removal additional anesthetic was injected into both medial fat pads for pain control. RESULTS: Immediate postoperative examination revealed bilateral decreased visual acuity and internal ophthalmoplegia in the right eye. An exotropia was present with marked limitation of right eye adduction. These findings resolved completely 3 hours postoperatively. CONCLUSIONS: Local anesthesia during blepharoplasty can enervate the optic nerve, ciliary ganglion, and extraocular muscle nerves. Local anesthesia should be injected judiciously during orbital fat removal to avoid this reversible but alarming event.

Aged↗
PubMed1988

Internal ophthalmoplegia and cranial neuropathy without external ophthalmoplegia. A report of 2 cases.

Two patients presented with an acute syndrome of internal ophthalmoplegia in the absence of external ophthalmoplegia, bilateral involvement of other cranial nerves, and minimal evidence of peripheral neuropathy. Cerebrospinal fluid protein was slightly raised, and moderate slowing of nerve conduction velocity was observed peripherally. It is suggested that these cases may represent a variant of acute post-infectious polyneuritis.

Adult↗
PubMed1995

Early progression of ophthalmoplegia in patients with ischemic oculomotor nerve palsies.

OBJECTIVE: To describe the frequency and clinical correlates of early progression of ophthalmoplegia in patients with ischemic oculomotor nerve palsies. DESIGN: Cohort survey, case series. SETTING: Multispecialty clinic providing primary, secondary, and tertiary care in central and northern Wisconsin. PATIENTS: Sixteen patients evaluated within 1 week of the reported onset of ischemic oculomotor nerve palsy were identified and followed up prospectively using a standardized ophthalmoplegia grading scheme. All patients were followed up serially until their ophthalmoplegia resolved. MAIN OUTCOME MEASURES: Descriptive analysis of the temporal course of ophthalmoplegia and frequency of progression of deficits. Comparison between the group that had progression of ophthalmoplegia with the group that did not for age, hematocrit, cholesterol level, and adiposity; presence of diabetes, hypertension, hypercholesterolemia, and coronary artery disease; history of stroke; and tobacco use. RESULTS: Eleven (69%) of 16 patients had progression of ophthalmoplegia. The median time between reported onset and peak severity of ophthalmoplegia was 10 days. The only important difference between the progressive and nonprogressive groups was a shorter time to resolution of ophthalmoplegia for the nonprogressive group. CONCLUSIONS: Early progression of ophthalmoplegia occurs often in patients with ischemic oculomotor nerve palsies. The power to find differences between progressive and nonprogressive groups was limited by the small number of patients available for analysis.

Aged↗
PubMed1998

Anti-GQ1b ganglioside antibody and ophthalmoplegia of undetermined cause.

BACKGROUND/AIM: Serum antibody against ganglioside GQ1b is reported to be closely associated with immune mediated ophthalmoplegia in the Fisher and Guillain-Barré syndromes. Its presence against glycolipids, in particular ganglioside GQ1b, was investigated in patients with ophthalmoplegia of unknown origin. METHODS: 16 patients with ophthalmoplegia, the cause of which could not be confirmed from clinical findings or diagnostic testing, were tested. 34 patients who had ophthalmoplegia of definite cause, 16 healthy people, and 23 patients with typical Fisher syndrome served as the controls. The ELISA was used to check for serum antibodies against glycolipids in all study participants. RESULTS: Two of the 16 patients with ophthalmoplegia of unknown cause had serum IgG antibody against GQ1b but not against other glycolipids, and 22 of the 23 patients with typical Fisher syndrome had this antibody. No anti-GQ1b antibodies were found in the patients with ophthalmoplegia of definite cause or in the normal controls. CONCLUSION: A common underlying cause appears to bring about the pathogenesis of palsy in Fisher syndrome and in the ophthalmoplegia with positive anti-GQ1b IgG antibody, called atypical Fisher syndrome. This antibody may prove a useful clinical marker for differentiating Fisher syndrome, typical and atypical, in patients with ophthalmoplegia.

Adult↗
PubMed1980

Orbicularis oculi muscle in chronic progressive external ophthalmoplegia.

Orbicularis oculi muscle biopsies were performed in 38 patients (ten with chronic progressive external ophthalmoplegia and 28 controls) to determine whether ragged red fibers were present and, if so, whether they were specific to progressive external ophthalmoplegia. To our knowledge, the orbicularis muscle has not been previously studied in this regard. Ragged red fibers were seen in the orbicularis oculi in patients with and without ophthalmoplegia, although they were more abundant in patients with ophthalmoplegia. The limb muscles of patients with ophthalmoplegia showed ragged red fibers. Electron microscopy demonstrated that these fibers contain either abnormal or increased numbers of normal mitochondria. Thus, the presence of ragged red fibers in the orbicularis oculi muscle is not limited to patients with chronic progressive external ophthalmoplegia, and the diagnosis of this disorder with ragged red fibers should be based on a combination of clinical and laboratory findings, including those from a limb muscle biopsy.

Adult↗
PubMed1999

Anti-GQ1b IgG antibody is associated with ataxia as well as ophthalmoplegia.

Close association between the increase in anti-GQ1b immunoglobulin G (IgG) antibody and ophthalmoplegia in Miller Fisher syndrome (MFS) and Guillain-Barré syndrome (GBS) has been reported. We investigated whether anti-GQ1b IgG antibody also is associated with ataxia, another of the MFS triad. Of 149 patients who had anti-GQ1b IgG antibody without profound weakness, 144 showed ophthalmoplegia (120 showed both ophthalmoplegia and ataxia; 24, ophthalmoplegia without ataxia). In contrast, five showed ataxia without ophthalmoplegia. Some large neurons of the dorsal root ganglia were immunostained with anti-GQ1b monoclonal antibody. Anti-GQ1b IgG antibody may thus be associated with ataxia as well as ophthalmoplegia. Ataxia may be due to its binding to a subset of primary sensory neurons.

Antibodies↗