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)

This paper reviews a variety of abnormal eye movements which include abnormal ocular positions, restricted eye motions, impairment of conjugated eye movements, abnormal smooth pursuit, abnormal saccade, gaze-evoked nystagmus, down-beat nystagmus, internuclear ophthalmoplegia, supranuclear ophthalmoplegia, square wave jerks, roving eye movement, ocular bobbing, ocular dipping, reverse ocular bobbing, and ping-pong gaze. Abnormal eye movements occur from stroke, spinocerebellar degeneration, Parkinson disease, multiple system atrophy, progressive supranuclear palsy, multiple sclerosis, Miller Fisher syndrome, myasthenia gravis, opsoclonus-polymyoclonia syndrome, and Creutzfeldt-Jakob disease. In neurological practice, it is important to observe abnormal eye movements accurately and enthusiastically, to make appropriate anatomical and etiological diagnosis.
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PMID:[Clinical aspects of abnormal eye movements]. 1515 59

Pituitary apoplexy is an uncommon syndrome characterised by sudden onset of headache, meningeal signs, visual disturbances, ophthalmoplegia and confusion. Documented recurrent apoplexy or treated apoplexy is even rarer with only few reports in the literature. Between 1994 and 2001, 18 patients were treated for pituitary apoplexy at Bayindir Medical Centre through transsphenoidal route. In all, topical bromocriptine was applied after tumour resection as described by Ozgen. We hereby present the cases of two patients with recurrent apoplexy 3 and 7 years after the initial surgical treatment for pituitary adenoma with apoplexy. The patients were treated non-surgically with success. Additional treatment in the form of radiosurgery was found necessary for the first patient. Surgical excision of the pituitary tumours with apoplexy reduces the risk of recurrent bleedings but eradication is not a rule. These patients need to be followed closely in the postoperative period for possible recurrence of bleeding.
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PMID:Late recurrent bleeding after surgical treatment for pituitary apoplexy. 1517 12

Pituitary tumor apoplexy is an uncommon event heralded by abrupt onset of severe headache, restriction of visual fields, deterioration of visual acuity, and weakness of ocular motility frequently coupled with clinical indications of decreased endocrine function. Hemorrhage into or necrosis of a preexisting sellar mass, usually a pituitary macroadenoma, produces an expansion of sellar contents. Compression of adjacent structures elicits the variable expression of symptoms referable to displacement of the optic nerves and chiasm and impingement of the third, fourth, and sixth cranial nerves. Damage to or destruction of the anterior pituitary leads to multiple acute and/or chronic hormone deficiencies in many patients. Medical management may be used in rare cases in which the signs and symptoms are mild and restricted to meningismus or ophthalmoplegia deemed to be stable. In patients with visual or oculomotor lability or an altered level of consciousness, expeditious surgical decompression, accomplished most commonly through a transsphenoidal approach, should be performed to save life and vision and to optimize the chance of regaining or maintaining pituitary function.
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PMID:Pituitary tumor apoplexy: characteristics, treatment, and outcomes. 1519 35

The 3243A > G mutation is one of the most frequently observed mutations of mitochondrial DNA (mtDNA), and is associated with numerous clinical presentations including mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS), progressive external ophthalmoplegia (PEO) and diabetes and deafness. The routine diagnosis of the 3243A > G mutation in blood is difficult as mutation levels are known to decrease in this tissue over time, while in some patients it may be absent. We have directly compared the levels of the 3243A > G mutation in skeletal muscle, blood and urinary epithelial cells in 18 patients and observed a striking correlation between the mutation load in postmitotic muscle and urinary epithelium, a mitotic tissue. These data strongly support the use of urinary epithelial cells as the tissue of choice in the noninvasive diagnosis of the 3243A > G mutation.
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PMID:Noninvasive diagnosis of the 3243A > G mitochondrial DNA mutation using urinary epithelial cells. 1519 81

A 50-year-old woman developed headache and right-sided ophthalmoplegia upon awakening from general anesthesia after liposuction surgery on her abdomen, hips, and thighs. Neuroimaging showed hemorrhage within a previously undiagnosed pituitary adenoma. The confirmatory surgical specimen contained areas of gross infarction and hemorrhage. The anesthesia record revealed intraoperative reduction of systolic blood pressure to 90 mm Hg for 30 minutes from a baseline of 120 mm Hg. This first reported case of pituitary apoplexy during liposuction surgery probably resulted from intraoperative hypotension attributed to a combination of general anesthesia, the use of subcutaneous lidocaine, sequestration of plasma in injured tissues, and blood loss.
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PMID:Pituitary apoplexy occurring during large volume liposuction surgery. 1520 36

A 29-year-old man presented with lethargy, headache, high fever, and visual disturbance. Neurological examination showed mydriatic pupil, ptosis, diminished light reflex, and ophthalmoplegia on the left. Magnetic resonance (MR) imaging showed the typical findings of pituitary apoplexy, and cerebral angiography disclosed mild narrowing of the A1 segment of the left anterior cerebral artery (ACA). Transsphenoidal tumor resection was performed. Transient severe right hemiparesis occurred directly after the operation. Computed tomography demonstrated cerebral infarction in the territory of the left Heubner's and medial lenticulostriate arteries. Pituitary apoplexy followed by cerebral infarction is very rare. Vasospasm of the perforating arteries of the ACA probably caused the cerebral infarction. Subarachnoid blood or vasoactive agents released from the tumor were the most likely cause of the vasospasm. MR imaging findings of contrast enhancement around the vessels may indicate reactive processes around the vessels.
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PMID:Cerebral infarction following pituitary apoplexy--case report. 1560 Feb 83

Extremely variable clinic and genetic features characterize mitochondrial encephalomyopathy (MEM). Pathogenic mitochondrial DNA (mtDNA) defects can be divided into large-scale rearrangements and single point mutations. Clinical manifestations become evident when a threshold percentage of the total mtDNA is mutated. In some MEM, the "mutant load" in an affected tissue is directly related to the severity of the phenotype. However, the clinical phenotype is not simply a direct consequence of the relative abundance of mutated mtDNA. Other factors, such as nuclear background, can contribute to the disease process, resulting in a wide range of phenotypes caused by the same mutation. Using Affymetrix oligonucleotide cDNA microarrays (HG-U133A), we studied the gene expression profile of muscle tissue biopsies obtained from 12 MEM patients [4 common 4977 bp deleted mtDNA and 8 A3243G: 4 progressive external ophthalmoplegia (PEO) and 4 mitochondrial myopathy, encephalopathy, lactic cidosis, and stroke-like episodes syndrome (MELAS) phenotypes] compared with age-matched healthy individuals. We found several differentially expressed genes: 35 were markedly up-regulated in the mtDNA macro-deletion group (vs. the control group) and 4 decreased; 56 genes were dysregulated in A3243G-related disorders (53 down-regulated in PEO and 3 up-regulated in MELAS). Finally, 12 genes were similarly regulated in the majority of the MEM patients under study. Amongst these, we identified an increased expression of genes related to the metabolism of the amino groups, as well as of several genes involved in genetic information processing. Moreover, few genes were similarly decreased in MEM patients vs. the control group. Real-time PCR demonstrated excellent reproducibility of the microarray-based findings. The observed expression changes are likely to represent a molecular signature for mitochondrial disorders. Furthermore, the differential expression profile of MELAS(A3243G) vs. PEO(A3243G) may support a role of nuclear background in contributing to these different clinical phenotypes. MEM microarray data are available from GEO database (http://www.ncbi.nlm.nih.gov/geo/) with the accession number: GSE1462.
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PMID:Skeletal muscle gene expression profiling in mitochondrial disorders. 1572 62

Brain single photon emission computed tomography (SPECT) studies were conducted in three patients with A3243G mutation of the mitochondrial (mt) DNA tRNA. All were born to mothers suffering from chronic progressive external ophthalmoplegia (CPEO) with the same A3243G point mutation of the mtDNA tRNA. The first case manifested clinically with MELAS, the second case manifested with CPEO, and third case was characterized by recurrent migraine-like headache, tremor, and epilepsy. Brain SPECT of all patients, regardless of whether they had or had not suffered from stroke-like episodes, showed multiple areas of asymmetrical decreased perfusion, particularly in the posterior and lateral head regions, especially the temporal lobes. Crossed-cerebellar diaschisis may occur. Conventional brain magnetic resonance images failed to show some of the lesions. Decreased regional cerebral blood flow, rather than previously proposed hyperemia, is likely to be the cause. We conclude that mitochondrial vasculopathy with regional cerebral hypoperfusion may be seen on brain SPECT in patients with mitochondrial disorders and A3243G mutations, regardless of whether they have or have not suffered from stroke-like episodes.
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PMID:Brain single photon emission computed tomography in patients with A3243G mutation in mitochondrial DNA tRNA. 1596 44

The aim of this study was to describe the clinical characteristics of atypical lacunar syndrome (ALS) based on data collected from a prospective acute stroke registry. In total, 2500 acute stroke patients were included in a hospital based prospective stroke registry over a 12 year period, of whom 39 were identified as having ALS and radiologically proven (by computed tomography or magnetic resonance imaging) lacunes. ALS accounted for 1.8% of all acute stroke patients, 2.1% of acute ischaemic stroke, and 6.8% of lacunar syndromes. ALS included dysarthria facial paresis (n = 12) or isolate dysarthria (n = 9), isolated hemiataxia (n = 4), pure motor hemiparesis with transient internuclear ophthalmoplegia (n = 4), pure motor hemiparesis with transient subcortical aphasia (n = 3), unilateral (n = 2) or bilateral (n = 3) paramedian thalamic infarct syndrome, and hemichorea hemiballismus (n = 2). Atypical lacunar syndromes were due to small vessel disease in 96% of patients. Atherothrombotic infarction occurred in one patient and cardioembolic infarct in another, both presenting pure dysarthria. Outcome was good (in hospital mortality 0%, symptom free at discharge 28.2%). After multivariate analysis, the variables of speech disturbances, nausea/vomiting, ischaemic heart disease, and sensory symptoms were found to be significantly associated with ALS. In conclusion, atypical lacunar syndrome is an infrequent stroke subtype (one of each 14 lacunar strokes). ALS occurred in 6.8% of lacunar strokes. Isolated dysarthria or dysarthria facial paresis were the most frequent presenting forms. The prognosis of this infrequent non-classic lacunar syndrome is good.
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PMID:Clinical study of 39 patients with atypical lacunar syndrome. 1648 49

Wernekink commissure involves the decussation of superior cerebellar peduncle (SCP) in midbrain. We report an elderly hypertensive, diabetic man who developed slurred speech, ataxia, and internuclear ophthalmoplegia. MRI examination revealed an unusual ischemic stroke involving Wernekink commissure. This rare stroke pattern involving decussation of SCP occurs in the setting of small arterial disease. The association between the anatomic location of the stroke and clinical findings is noteworthy.
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PMID:Wernekink comissure syndrome: a rare midbrain syndrome secondary to stroke. 1682 56


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