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)

We presented a case of probable Bickerstaff's brainstem encephalitis. A 39-year-old woman developed easy falling, progressive consciousness disturbance, total ophthalmoplegia, and bilateral pyramida tract sign. In serum anti-ganglioside antibody assay using enzyme-linked immunosorbent assay, high anti-GQ1b antibody was found. Electroencephalography was dominated by alpha activity, superimposed with occasional theta wave bursts. Brain MRI showed abnormal signal hyperintensities in the tegmentum of the midbrain to the upper pons on T2 weighted images and swelling of the midbrain and pons on T1 weighted images. Five days after the onset of the disease, she had respiratory arrest, which necessitated artificial ventilation for a few days. Then, she began to recover. However, she gained only partial recovery, leaving upward gaze palsy, right abducens nerve palsy, pseudbulbar palsy and quadriplegia.
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PMID:[Probable Bickerstaff's brainstem encephalitis associated with anti-GQ1b antibody]. 819 67

A case is presented of recurrent painful ophthalmoplegia of atypical course, with pain in the orbit, eyelid oedema, and paralysis of external eye muscles. Disease symptoms occurred intermittently in both eyeballs. The performed MRI examination showed the presence of inflammatory focus in the posterior ethmoid.
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PMID:[Recurrent painful ophthalmoplegia (Tolosa-Hunt syndrome)]. 824 86

Since Hunt et al's description (1961) Tolosa-Hunt syndrome has been a matter of controversies about its nosological identity and differential diagnosis. We report 7 cases diagnosed between 1979 and 1990. Four of them had a low-resolution CT and the diagnosis was made after a long follow-up, according to classical criteria of exclusion. The last 3 cases had a modern high-resolution CT or a MRI (2 cases) and the diagnosis was established in a few days. MRI has considerably simplified the differential diagnosis but it has not completely resolved it. Alterations of shape and signal of the cavernous sinus are similar to those of lymphoma, sarcoidosis and meningioma. When MRI is normal diabetic ophthalmoplegia, migrainous ophthalmoplegia and giant-cell arteritis must also be considered. We conclude that the diagnosis of the Tolosa-Hunt syndrome can generally be made in a few days, without a cavernous sinus biopsy. There is no reason to doubt that this syndrome is a specific nosological entity.
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PMID:[Should Tolosa-Hunt syndrome still be an exclusion diagnosis?]. 827 25

MRI using gadolinium contrast material can demonstrate lesions in cranial nerves. Tumors and inflammatory lesions have been described. There is little published information on MRI of cranial nerves in patients with migraine headaches with ophthalmoplegia. We present a case of ophthalmoplegic migraine with a cranial nerve abnormality which was subsequently shown to improve as the patient clinically improved. Implications from this finding are discussed in relation to the pathophysiology of ophthalmoplegic migraine.
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PMID:MRI findings in a case of ophthalmoplegic migraine. 832 96

The so-called Tolosa-Hunt syndrome consists of painful ophthalmoplegia caused by chronic nonspecific inflammation of the cavernous sinus and/or superior orbital fissure, responsive to steroid therapy. We present a case with the unusual feature of sellar erosion, in which angiography. CT and MRI suggested this idiopathic condition.
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PMID:Tolosa-Hunt syndrome with sellar erosion: case report. 837 19

A patient with migraine developed ophthalmoplegia, hemiparesis and cheiro-oral syndrome on the left side. T2-weighted MRI showed infarcts in the tegmentum of bilateral midbrains and right pons but no lesion in the cerebral or cerebellar hemisphere. Infarction in the tegmentum of brainstem secondary to the involvement of perforating arteries has not been reported in basilar artery migraine until now.
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PMID:Ophthalmoplegia, hemiparesis and cheiro-oral syndrome in basilar artery migraine. 846 33

Pure neurologic Whipple's disease (WD) may be suspected by same clinical data (dementia-ophthalmoplegia-myoclonus triad, oculomasticatory myorhythmia) with support of MRI. Diagnosis is confirmed by intestinal and/or brain biopsy. Early recognition is critical in a disease that can lead to irreversible neurologic sequelae and that can potentially be cured. Despite therapy, relapses in patients with WD are common, being neurologic recurrence the most frequent and serious. Antibiotics that do not cross the blood-brain barrier are not adequate initial therapy for WD, because they predispose to neurologic relapse. Patients with WD should be treated for one year with antibiotics that cross the blood-brain barrier (such as parenteral penicillin+streptomycin, followed by oral trimethoprim-sulfamethoxazole). CNS relapse is usually resistant to therapy.
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PMID:[Neurologic manifestations of Whipple disease]. 851 45

We here report a case of Miller Fisher syndrome (MFS) in which serum anti-cerebellar antibody was detected by Western blot analysis. The 32-year-old male studied suffered from diplopia, gait ataxia and sensory disturbance in the distal portion of the upper limbs preceded by cold-like symptoms. Neurological examination on admission revealed that he had external ophthalmoplegia with bilateral ptosis, cerebellar ataxia and areflexia. A cerebrospinal fluid examination showed albuminocytologic dissociation with a protein concentration of 60 mg/dl. Brain CT and MRI showed no significant abnormalities. The patient was diagnosed as MFS, and treated it with two sessions of immunoadsorption plasmapheresis (IAPP). After receiving IAPP therapy, the patient's neurological symptoms and signs were improved. Western blot analysis showed the existence of antibody directed against mouse cerebellum but not against mouse cerebrum, brain stem, and spinal cord in his serum, the level of which was decreased after the IAPP therapy. Serum anti-GQ1b antibody was also elevated. As far as we are aware, there have been no reports showing the existence of anti-cerebellar antibodies detected by Western blot analysis. Though the pathogenesis of MFS remains unclear, our findings suggest that anti-cerebellar antibody detected by Western blot analysis may be caused by cerebellar ataxia in MFS.
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PMID:[The detection of anti-cerebellar antibody western blot analysis in serum from a patient with Miller Fisher syndrome]. 853 14

Tolosa-Hunt syndrome (THS) is characterized by painful ophthalmoplegia due to idiopathic granulomatous inflammation of the cavernous sinus. Steroid therapy dramatically reverses the clinical signs and symptoms of THS. We report a typical case of THS, in which MRI showed a mass lesion in the right cavernous sinus with intermediate signal intensity on T1-weighted images, hypointensity on T2-weighted images and positive gadolinium enhancement. This 24-year-old man had three episodes of painful opthalmoplegia in a period of 9 months. The side of the involved cavernous sinus was different in the first and the second episodes of THS. The symptoms lasted for 1 month and the patient recovered spontaneously from these two episodes. In the third episode, the right pupil was also involved and the light reflex was lost. After steroid therapy, the ocular symptoms improved rapidly within 48 hours and the mass lesion in the right cavernous sinus on MRI was markedly diminished by the 7th day of treatment.
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PMID:Magnetic resonance images of Tolosa-Hunt syndrome before and after steroid therapy. 884 Jul 63

We studied 83 patients from 36 Italian families with autosomal dominant cerebellar ataxia type I. Mean onset age +/- SD was 34.2 +/- 12.8 years with a mean anticipation of 12.8 +/- 15.1 in 52 parent-offspring pairs. Onset age anticipation occurred predominantly through paternal transmission. Mean age at death was at 56.5 +/- 15.5 years. The most common associated features were supranuclear ophthalmoplegia, corticospinal signs, peripheral neuropathy and cognitive impairment. Cerebellar atrophy was constant at MRI and usually associated with shrinkage of the pons and degeneration of the pontine transverse fibres. Direct mutation analysis in 29 families showed two families with SCA1 and none with Machado-Joseph/SCA3 mutation. We performed linkage analysis in the ten largest families. Two of them showed linkage to SCA2 locus and none to SCA4 and SCA5 loci. SCA2 patients showed higher occurrence of peripheral neuropathy and slow saccades, rarer corticospinal signs and a milder course of the disease in comparison with SCA1 patients.
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PMID:Autosomal dominant cerebellar ataxia type I. Clinical and molecular study in 36 Italian families including a comparison between SCA1 and SCA2 phenotypes. 890 34


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