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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Superior oblique palsy is thought to be the most frequent cause of acquired vertical diplopia. It is often the result of blunt head trauma but may also be caused by brain tumor, meningitis, diabetes, lesions of the cavernous sinus, and superior orbital fissure as well as arteriosclerosis. The characteristics frequently include a small vertical strabismus in primary gaze, ipsilateral inferior oblique overaction with an increased hypertropia to the contralateral side, a "V" pattern, excyclotorsion, and a positive Bielschowsky head tilt test to the ipsilateral side. In a typical case, it is not difficult to make the proper diagnosis. Several patients will be described whose superior oblique palsy was marked by an association with another motility disturbance.
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PMID:Think superior oblique palsy. 374 90

A rare case of juxtasellar mycotic abscess with suprasellar extension is reported. The patient had double vision, only a mild abducens palsy, and no sign of inflammation, history of nasal sinusitis, or diabetes mellitus. Although a histologic examination showed massive fungal mycelia with thin capsules and no tumor cells, the neuroradiologic findings were like those in a clival chordoma or epidermoid tumor.
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PMID:Juxtasellar mycotic abscess. 668 9

Nine cases of mitochondrial myopathy are presented and the literature is reviewed. The clinical picture ranges from virtually pure ophthalmoplegia, through 'ophthalmoplegia plus' to predominantly central nervous system disturbance. Morphological mitochondrial abnormalities are likely to reflect generalised metabolic abnormalities of diverse aetiology, but producing common pathophysiological consequences. The association of mitochondrial myopathy with CNS disorders, which may ante-date muscle weakness, is emphasised. The myopathies constitute a clinical continuum within which the following syndromes may be delineated: (1) Kearns-Sayre syndrome (2) Luft's disease (3) a variant of Ramsay Hunt syndrome (4) relapsing febrile neurological deficits with headache and seizures. These may be specific diseases or artificially separated manifestations of some common metabolic disorder(s). There is a similarity between the CNS pathology, and also some clinical features, of Leigh's disease and the findings in certain of the mitochondrial myopathies. The review suggests that the following should be regarded as associations of mitochondrial myopathy and progressive external ophthalmoplegia (a) diabetes mellitus (b) cataracts, in which calcium deposits may, like basal ganglia calcification, be due to abnormal calcium metabolism. Diplopia, although unusual, does occur in progressive external ophthalmoplegia with mitochondrial myopathy.
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PMID:The mitochondrial myopathies: 9 case reports and a literature review. 734 99

Ocular signs and symptoms provide clinical clues to many of the more common metabolic and nutritional disorders seen in older adults. Diabetes mellitus can affect all parts of the eye and orbit. Complications include refractive visual loss, macular edema, retinopathy, increased risk of fungal infection, and diplopia. In patients with gout, urate crystals may precipitate in the eye and cause conjunctivitis, uveitis, or scleritis. Other problems are seen with Wilson's disease, hyperlipidemia, and albinism. Nutritional disorders usually arise from malabsorption, gastrointestinal surgery, and alcohol abuse. Deficiencies in vitamins A, B1 (thiamine), B12, and C may be manifest in the eye.
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PMID:Clues in the eye: ocular signs of metabolic and nutritional disorders. 760 60

Pituitary adenomas are frequently encountered, benign intracranial tumours. Clinically classified according to their capacity to produce and secrete hormones, pituitary tumours are diagnosed from the clinical manifestations and biochemical findings of specific pituitary hormone overproduction or of impaired pituitary function due to pressure on normal pituitary cells, the pituitary stalk or the hypothalamus. Additionally, the tumour may result in neurological manifestations due to its effect as an intracranial space-occupying lesion. Pituitary adenomas may present acutely with pituitary apoplexy after intrapituitary haemorrhage or infarction. The subsequent hypofunction of the pituitary with concomitant neurological sequelae of an expanding intracranial mass are often associated with excruciating headache, diplopia and visual field defects. Gradually developing neurological deficits or secondary endocrine failure over several years may precede the recognition of non-secretory tumours (30-40% of pituitary adenomas) as well as some of the hormone-producing adenomas, especially when they expand beyond the confines of the sella turcica. Asymptomatic masses occur in the pituitary in 5-27% of unselected autopsy series. About 10-20% of pituitaries imaged as part of a brain study contain lesions 'consistent with a pituitary adenoma', with about half being pituitary adenomas ('incidentalomas'). Many advocate screening such cases for a wide spectrum of pituitary function abnormalities. Clinical judgement should be utilized to determine the extent of the work-up and the frequency of follow-up. Acromegaly, a clinical syndrome caused by excess growth hormone secretion, accounts for one-sixth of resected pituitary tumours. This disorder leads to chronic progressive disability and a shortened life span, with approximately 50% of untreated acromegalic patients experiencing premature death. The prevalence of acromegaly has been estimated to range from 50 to 70 per million, with the age of diagnosis usually between the third and fifth decades. Conditions associated with acromegaly include glucose intolerance, diabetes mellitus, lipid abnormalities, cholelithiasis, goitre, and hyperthyroidism, respiratory complications, hypertension, cardiovascular disease, and calcium metabolism abnormalities. An association between acromegaly and cancer, especially of the colon, is now recognized. Epidemiological series have indicated that cancer of the colon, breast and other types of malignancy are a cause of death with increased frequency in acromegalics compared with expected rates. Hypopituitary symptoms secondary to the mass effect of macroadenomas in acromegalic patients are common. Among premenopausal women, menstrual irregularities and galactorrhoea have been reported in 40-70%, while more than half of the men complain of impotence and decreased libido.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and differential diagnosis of pituitary tumours with emphasis on acromegaly. 762 86

A 49-year-old man who had been suffering from poorly controlled diabetes mellitus for 20 years was admitted to our hospital with the chief complaints of diplopia and right ptosis. The onset of his symptoms was sudden. On admission, he had right palpebral ptosis, upward and left lateral gaze paresis of the right eye. Hess screen chart examination revealed paresis of the right superior rectus, inferior oblique and medial rectus muscles. T2 weighted magnetic resonance imaging (MRI) revealed high intensity area in the medial part of the right midbrain tegmentum where the oculomotor nucleus located, and diffusion weighted MRI demonstrated high intensity area which corresponded to the oculomotor fascicles of the midbrain. The latter represented Wallerian degeneration of the fascicles. The diagnosis of small infarction of the right oculomotor nucleus presenting ipsilateral external ophthalmoplegia was made. The superior rectus muscle is innervated by the neurons in the contralateral oculomotor nucleus, and the other external ocular muscles innervated by the third cranial nerve are conducted by the neurons in the ipsilateral oculomotor nucleus; therefore, unilateral oculomotor nuclear lesion generally causes ipsilateral ophthalmoplegia plus contralateral superior rectus palsy. Our case presented here shows that there may be such a case with oculomotor nuclear disturbance which masquerades with oculomotor fascicular or infranuclear disturbance; therefore, it is important to include these lesions in differential diagnosis.
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PMID:[Unilateral external ophthalmoplegia caused by ipsilateral oculomotor nuclear lesion: analysis with diffusion weighted MRI]. 782 Sep 68

A 62-year-old man with a history of diabetes mellitus, hypertension and liver damage has sudden diplopia on Nov. 4, 1992. Ocular movements of this right eye were normal, but his left eyelid was completely ptotic, and left pupil was dilated and nonreactive to light. In primary position, his left eye deviated outward, and could not move to any direction. He was diagnosed as having total oculomotor nerve palsy of the left side without any other neurological signs or symptoms; his consciousness level was alert and mental state was normal. The present case showed normal facial sensation, no facial palsy and no tongue deviation. Deep tendon reflexes were hypoactive bilaterally. Pyramidal tract sign, cerebellar sign, and gait disturbance were not observed. Superficial sensation of the extremity was normal. Brain CT scan revealed a small mesencephalic hemorrhage extending to the tegmentusm ventral to the cerebral aqueduct of the left side. Brain magnetic resonance imaging demonstrated a high-intensity area in the left oculomotor nucleus and its fascicles in the midbrain on T1- and T2-weighted image. The oculomotor nerve palsy of the left eye gradually improved, but mydriasis, adduction impairment and downward gaze palsy continued, and oculomotor nerve palsy of the left eye was compatible with so-called inferior branch palsy of the oculomotor nerve. Moreover, contralateral eye movements were normal except for mild upward gaze palsy. Oculomotor nerve palsy of this type was consistent with the syndrome of oculomotor nucleus described by Pierrot-Deseillingny in 1981. It was presumed that the superior rectus muscle is innervated by the contralateral oculomotor nerve nucleus in man as well as in animals.
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PMID:[Isolated oculomotor nerve palsy caused by mesencephalic hemorrhage]. 783 46

We report a case of non-insulin-dependent diabetes mellitus (NIDDM) complicated with idiopathic hypoparathyroidism. A 74-year-old male was hospitalized because of diplopia. He was revealed to have NIDDM. The levels of serum Ca and intact-PTH were 6.3 mg/dl and < 5 pg/ml, respectively. Brain computed tomography revealed abnormal calcification in the cerebral basal ganglia and the cerebellum. After recovery from hypocalcemia, the endogenous insulin secretion was normalized. It is suggested that the pathogenesis of NIDDM in this patient may have been related to an insulin secretory defect as a result of hypocalcemia in addition to the hereditary risk.
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PMID:Non-insulin-dependent diabetes mellitus complicated with idiopathic hypoparathyroidism. 858 May 67

A 55-year-old man with diabetes mellitus developed diplopia and experienced difficulty in moving his eyes in the vertical plane, especially downward. Horizontal movement of each eye was normal with exotropia. Magnetic resonance imaging revealed small and high signals on both sides of the midbrain near the interstitial nucleus of Cajal (INC). Based upon the recent experimental evidence, we speculate that bilateral lesions involving the INC may have caused downward gaze palsy in our patient.
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PMID:Downward gaze palsy caused by bilateral lesions of the rostral mesencephalon. 956 2

Anticardiolipin antibodies (aCL) are a risk factor for cerebral ischemia. In migraine, the association is controversial, with widely varying results in different small series. The controversy in part may be due to the inherent difficulty in distinguishing the transient focal neurologic events (TFNE) of migraine from TIA. To assess the frequency of aCL in migraine, we prospectively evaluated consecutive adults under 60 years of age with migraine without aura and with recent TFNE (<24-hour duration) clinically suggestive of either migraine with aura or TIA. We concomitantly enrolled persons with no CNS disease. Each person was interviewed and had blood drawn for solid-phase ELISA with IgG and IgM aCL isotyping. Neuroradiologic studies were reviewed. Patients with TFNE were followed every 6 months for the duration of the 3-year study. The frequency of aCL positivity (IgG >20, IgG >40, IgM >7.5) for the 645 patients with TFNE (8.8, 3.1, 4.2%), the 518 persons in the TFNE subgroup with migraine with aura (8.9, 3.3, 4.1%), the 497 persons with migraine without aura (7.0, 2.0, 3.6%), and the 366 control subjects (9.3, 3.6, 3.9%) did not differ significantly between groups. In TFNE patients with elevated aCL titer, the association was positive with diabetes mellitus, TFNE duration <15 minutes, and diplopia and was negative with hemiparesis, tinnitus, and family history of stroke. Findings on imaging consistent with cerebral ischemia were more frequent in aCL-positive persons. The short-term risk of stroke was uniformly low. In young persons, aCL is not associated with migraine or with TFNE, although diabetes mellitus, negative family history of stroke, and brief duration of symptoms (including diplopia) may predict immunoreactivity. Imaging studies suggest an ischemic etiology of TFNE in this cohort.
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PMID:Role of anticardiolipin antibodies in young persons with migraine and transient focal neurologic events: a prospective study. 1010 49


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