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Stressed and non-stressed antenatal fetal monitoring was carried out 9 520 times in 5 932 high-risk patients. Intra-uterine death occurred in 48 patients. In 19 patients the fetus died within 1 week of monitoring but before the onset of labour; the results of monitoring had been normal in 14 of these. Abruptio placentae was the cause of 6 of these deaths. Many of the other causes of intra-uterine death were also acute complications such as haemorrhage due to placenta praevia, amniotic fluid infection, and cord prolapse. True false-negative test results were rare, and were seen most often in patients with preeclampsia, diabetes and haemolytic disease. Twin pregnancies also caused a problem, as double recording of the heart rate of the normal fetus could create a false sense of security.
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PMID:Intra-uterine deaths after suspicious, uncertain and normal antenatal fetal heart rate monitoring. 740 46

Ophthalmoplegia is common cranial neuropathy of Diabetes. In case of 3rd nerve involvement, usually unilateral extra ocular muscles are affected. However, ptosis is very rare in patients with diabetic neuropathy. In this report, we describe bilateral ptosis with ophthalmoplegia in diabetes. In ophthalmoplegia associated with diabetes, ischemic nerve infarction was reported. We treated this patient with Lipo prostaglandin (PG) E1. Since then, increased platelet aggregation activity was found in this patient. After two months, the symptoms of this patient were improved.
Diabetes Res 1994
PMID:Bilateral ptosis with ophthalmoplegia in a 72-year-old woman with diabetes. 755 29

Grandmultiparity (GMP) has long been considered an obstetric complication for both mother and fetus, although recent studies indicate that, with proper perinatal care, women with high-parity rates are no longer at high risk. The current study examines the outcome of delivery in 1700 women in their fifth or more delivery, as compared with two control groups: 622 primiparas and 735 multiparas (two to three previous deliveries). Excellent prenatal care was available free of charge to all parturients. Our objectives were to evaluate the management of GMP in contemporary obstetrics and to assess whether grand multiparas are still high-risk patients. The age of the grandmultiparas was significantly higher compared with with the control groups, which may explain the higher incidence among them of antenatal medical disorders, such as diabetes mellitus and hypertensive disease. No significant differences were found among the three groups for preterm or post-term births, small-for-gestational-age infants, polyhydramnios, oligohydramnios, perinatal death, fetal distress, multiple births, placenta previa, abruptio placentae or cord prolapse. Macrosomia was markedly higher in the grandmultiparas and multiparas than in nulliparas. Thus, our results indicate that good perinatal care can ensure better results in grandmultiparas, and that grandmultiparity no longer needs to be considered a high-risk obstetric category in our population.
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PMID:The grand multipara. 755 29

We examined the locomotor-enhancing action of mu-opioid receptor agonists, such as morphine and [D-Ala2, N-MePhe4, Gly-ol5]enkephalin (DAMGO), and physical dependence on morphine in diabetic and nondiabetic mice. Morphine (5-20 mg/kg, s.c.) and DAMGO (1-4 nmol, i.c.v.) had a dose-dependent locomotor-enhancing effect in both nondiabetic and diabetic mice. The locomotor-enhancing effects of morphine and DAMGO were significantly less in diabetic mice than in nondiabetic mice, and were significantly reduced after pretreatment with either beta-funaltrexamine (20 mg/kg, s.c.), a selective mu-opioid receptor antagonist, or naloxonazine (35 mg/kg, s.c.), a selective mu1-opioid receptor antagonist. Both diabetic and nondiabetic mice were chronically treated with morphine (8-45 mg/kg, s.c.) for 5 days. During this treatment, neither diabetic nor nondiabetic mice showed any signs of toxicity. After morphine treatment, withdrawal was precipitated by injection of naloxone (0.3-10 mg/kg, s.c.). Several withdrawal signs, such as weight loss, diarrhea, ptosis, jumping and body shakes, were observed after naloxone challenge in morphine-dependent nondiabetic mice. Although morphine-dependent diabetic mice showed greater weight loss than nondiabetic mice, the incidence of jumping and body shakes after naloxone challenge in diabetic mice were lower than that in nondiabetic mice. These results suggest that diabetic mice are selectively hyporesponsive to mu1-opioid receptor-mediated locomotor enhancement. Furthermore, diabetes may affect mu1-opioid receptor-mediated naloxone-precipitated signs of withdrawal from physical dependence on morphine.
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PMID:Modification of mu-opioid agonist-induced locomotor activity and development of morphine dependence by diabetes. 763 31

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

Three cases of ocular myasthenia gravis were observed. The first patient, a 74-year-old man was found to have complete left ophthalmoplegia and ptosis unchanged at examination on month after onset. The second patient, a 42-year-old man, developed incomplete right ophthalmoplegia with pseudoanterior internuclearis ophthalmoplegia, then ptosis two days later. The third patient, a 70-year-old man, presented with sudden onset complete right palsy of the third nerve. Diabetes mellitus or intra-cranial lesions were suspected in all three patients although laboratory tests, tomodensitometry, nuclear magnetic resonance imaging, or arteriography gave no confirmation. Ptosis was relieved and eye movement was improved after the intravenous edrophonium test, but electromyography was negative. The three patients were treated with anticholinesterase agents and showed unequivocal improvement. The second patient underwent thymectomy. Clinicians should inform patients of the contraindications of drugs in this disease. The diagnosis of pure oculomotor forms of myasthenia gravis is sometimes difficult to establish and should be suspected in cases of unexplained oculomotor palsy.
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PMID:[Ocular myasthenia: an etiology to consider in unexplained oculomotor paralysis]. 808 6

We have investigated a 15 year old girl with progressive external ophthalmoplegia, including bilateral ptosis and retinal rod and cone cell dysfunction with atypical retinal pigmentation, complicated by cerebellar ataxia, partial cardiac conduction block, and diabetes mellitus. In infancy she had a severe crisis of bone marrow depression, and as a child she suffered from hypersensitivity to light, increasing fatigue, and vertigo, signs that were initially though to be psychosomatic. Histological examination showed mitochondrial myopathy, and subsequent mitochondrial DNA (mtDNA) analysis showed a deletion of approximately 5500 base pairs in 35 to 40% of her muscle mtDNA. We therefore conclude that this patient has developed the Kearns-Sayre syndrome after a Pearson syndrome-like crisis in her first year of life.
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PMID:Juvenile Kearns-Sayre syndrome initially misdiagnosed as a psychosomatic disorder. 815 37

Recent discoveries in mitochondrial clinical genetics have revealed that a broad spectrum of clinical phenotypes are associated with mutations in mitochondrial DNA. Diseases caused by mutations in mitochondrial DNA are by nature quantitative. Myoclonic epilepsy and ragged-red fiber disease are caused by a mutation in the transfer RNA gene lysine. Although everyone in a maternal lineage will harbor the same mutation, the nature and severity of the symptoms vary markedly among individuals. This variability correlates with the inherited percentage of mutations in the individual's mitochondrial DNA and the individual's age. Age-related expression of mitochondrial disease has also been demonstrated for mitochondrial DNA deletions. Although deletions that retain both origins of replication result in late-onset disease because of the progressive enrichment of the deleted mitochondrial DNA, a 10.4-kb deletion that lacks the light-strand replication origin and maintains a stable mutant percentage in both tissues and cultured cells has been discovered. This deletion is associated with adult-onset diabetes and deafness, but not with ophthalmoplegia, ptosis, or mitochondrial myopathy. Biochemically, it causes a generalized defect in mitochondrial protein synthesis and oxidative phosphorylation. The age-related decline in oxidative phosphorylation could reflect the accumulation of somatic mitochondrial DNA mutations. Inhibition of oxidative phosphorylation stimulates this accumulation. The general paradigm for mitochondrial DNA diseases may be that inherited mutations inhibit the electron transport chain. This damages the mitochondrial DNA, further reducing oxidative phosphorylation. Ultimately, oxidative phosphorylation drops below the expression threshold of cells and tissues, and clinical symptoms appear.
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PMID:Mitochondrial DNA mutations in epilepsy and neurological disease. 829 23

It was the aim of this study to evaluate the obstetric performance of Ethiopian Jewish immigrants in comparison to the general Jewish obstetric population. The study was performed at the Soroka Medical Center, Beer Sheva, which manages the busiest delivery ward in Israel. Between 1988 and 1991 a total of 20,047 non-Ethiopian women (Group N) and 431 parturients of Ethiopian origin (group E) delivered at the Soroka Medical Center. Group E included a significantly higher percentage of grandmultiparous women than group N. Among diseases complicating pregnancy there was a statistically significant higher incidence of severe pregnancy-induced hypertension (PIH) in group E than in group N. Mild PIH and chronic hypertension were of comparable prevalence in both groups. The prevalence of class A diabetes mellitus was significantly lower in group E than in group N; the same trend was also observed for diabetes class B but without reaching statistical significance. There was no significant difference between the groups in the prevalence of polyhydramnios, postdatism and poor obstetric history, or fetal distress, s/p cesarean section, and prolapse of cord. Statistical analysis indicated a tendency towards significance for higher prevalence of premature rupture of membranes in group N. Malpresentations and malpositions were of similar prevalence in both groups. The incidence of premature delivery in group E showed a higher relative risk, suggesting a tendency of significance. The incidence of meconium-stained amniotic fluid in group E was significantly higher than in group N. There was no significant difference in the prevalence rates of placental complications such as placenta previa and abruption of placenta between the groups. The mode of delivery, the prevalence of complications during the third stage of labor, birthweight of infants and perinatal mortality were similar for both groups. In conclusion, the obstetric performance in Ethiopian Jewish immigrants is surprisingly similar to that of Israeli Jewish parturients. The only prominent pathology that does not seem to be related to life-style and nutrition is pregnancy-induced hypertension.
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PMID:Obstetric performance in Ethiopian immigrants compared with Israeli parturients. 834 62

Ophthalmic surgery is one of the most valuable indications for ambulatory anaesthesia (AA). Respecting the usual recommendations for AA and the specificity of ophthalmic surgery, AA has very few problems. In USA it concerns about 90% of ophthalmic surgery. Most of the patients are very young or very old. Adults are often poly-medicamented: diabetes and arterial hypertension are the most frequent pathologies. A lot of multivisceral pathologies are responsible of ocular diseases and can complicate anaesthesia. It is necessary to diagnose them before anaesthesia. Maligna hyperthermia risk is increased during strabismus and ptosis surgery. Some ocular treatments have systemic repercussion and require to be stopped before anaesthesia. Most of ophthalmic surgery can be practiced under any types of local anaesthesia. In postoperative of strabismus and retinal detachment repair, pain, nausea, vomiting are frequently observed. Their prevention is not very well known. The atropine used for cardiac reflex treatment may be responsible of an acute urine retention or a disorientation in elderly patients and delays the home readiness. Paper and pencil tests after general anaesthesia are very difficult to do, because requesting a good vision. The postoperative complications are essentially surgical complications.
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PMID:[Characteristic problems posed to the anesthetist by ambulatory surgery in ophthalmology]. 840 83


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