| 1. |
- Lindén, Thomas, 1962, et al.
(författare)
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Risk of central pontine myelinolysis in the treatment of severe hyponatremia
- 1989
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Ingår i: Läkartidningen. - 0023-7205. ; 86:20, s. 1905-7
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Tidskriftsartikel (refereegranskat)abstract
- Central pontine myelinolysis is a life-threatening condition involving the demyelination of axons in certain areas of the brain. It has been shown almost invariably to occur in connection with hospital care. In recent years, a connection has been noted between the rapid restitution of low serum sodium and the development of the condition. In this review, the most recent scientific information is summarized. It is concluded that the risk should always be considered in treating a hyponatremic patient. The serum sodium level should be raised slowly and the acute treatment ended before normal serum sodium levels are reached, ie when the patient is still slightly hyponatremic.
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| 2. |
- Follér, Maj-Lis, 1946
(författare)
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A new approach to community health
- 1989
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Ingår i: Social Science and Medicine. - 0277-9536. ; 28:8, s. 811-818
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Tidskriftsartikel (refereegranskat)abstract
- This article deals with the local health care among the Shipibo-Conibo in eastern Peru. A project called AMETRA—application of traditional medicine—is functioning in the area. The aim of AMETRA is to give courses and stimulate co-operation between traditional medical practice and Western medicine. The solutions to the health problems are seen in direct relation to the socio-economic structure and to the environmental prerequisites. The aim and purposes of AMETRA are described and analysed. It is proposed that the two medical systems should co-operate in such a manner that their complementary nature is emphasized and fully utilized.
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| 3. |
- Hanner, P, et al.
(författare)
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Clinical observations of effects on central nervous system in patients with acute facial palsy.
- 1987
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Ingår i: Archives of otolaryngology--head & neck surgery. - 0886-4470. ; 113:5, s. 516-20
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Tidskriftsartikel (refereegranskat)abstract
- Twenty-eight consecutive patients with acute unilateral facial palsy were examined with special reference to clinical signs of central nervous system involvement. The clinical investigation in the acute stage of the disease showed that only seven patients had solitary facial nerve dysfunction, while the remaining patients had evidence of more widespread disease involvement. The most frequent finding was a trigeminal dysfunction of the paretic side, as shown by paresthesia and sensibility disturbance corresponding to the sensoritrigeminal area, as well as a dysfunction of the trigeminal component of the corneal reflex of the paretic side. Three patients showed migrating symptoms that were suggestive of a brain-stem disorder. In addition, four patients had an optic neuropathy, while an abnormal brain-stem audiometry response was demonstrated in five patients. The outcome of acute facial palsy one to two years after onset, however, could not be predicted from the clinical central nervous system signs. The degree of the palsy in the acute stage of the disease still seemed to be one of the most important prognostic factors. It is concluded that acute facial palsy is not a single entity, but rather a feature of different neurologic conditions.
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| 4. |
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| 5. |
- Lannering, Birgitta, 1948, et al.
(författare)
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Early onset group B streptococcal disease. Seven year experience and clinical scoring system.
- 1983
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Ingår i: Acta paediatrica Scandinavica. - 0001-656X. ; 72:4, s. 597-602
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Tidskriftsartikel (refereegranskat)abstract
- Early onset group B streptococcal disease was reviewed for the seven year period between 1975 to 1981 at Vanderbilt University Medical Center. One hundred and twenty cases were identified. The disease varied from asymptomatic bacteremia to fatal cardiopulmonary collapse. Factors associated with a poor outcome were prematurity, low Apgar score at 5 min, the presence of shock, leukopenia, rupture of membranes for more than 12 hours, and a delay in treatment after the onset of symptoms. A scoring system for probability of death based on these 6 factors was then developed. Over the seven year period mortality decreased from 50% to 10%. The only factor identified with the decrease in mortality was a significant decrease in the number of hours between the onset of symptoms and the beginning of treatment. Early recognition and prompt treatment seem to be the major causes of the decreasing mortality over the seven years of this report.
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| 6. |
- Lindén, Thomas, 1962, et al.
(författare)
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Protective effect of lesion to the glutamatergic cortico-striatal projections on the hypoglycemic nerve cell injury in rat striatum.
- 1987
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Ingår i: Acta neuropathologica. - 0001-6322. ; 74:4, s. 335-44
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Tidskriftsartikel (refereegranskat)abstract
- In rat striatum severe hypoglycemia causes an irreversible nerve cell injury, which does not become manifest until during the post-insult recovery period. This injury can be ameliorated by lesions of the glutamatergic cortico-striatal pathway, which suggests that an "excitotoxic" effect mediated by the glutamatergic input is the likely cause of the post-hypoglycemic nerve cell destruction. In this paper we further characterize the protective effect of abolishing the glutamatergic innervation to striatum at the ultrastructural level. Two weeks after a unilateral cortical ablation rats were subjected to 30 min of severe hypoglycemia with isoelectric EEG and killed either immediately after the insult or following 60 min of recovery induced by restoring the blood glucose levels. Immediately after the hypoglycemic insult the structure of striatum was similar on both sides (except for the changes attributable to the ablation); i.e., the neurons and their dendrites had pale cytoplasm with condensed mitochondria, sparse RER and pinpoint ribosomes. After 60 min restitution numerous striatal neurons on the non-protected, non-ablated side had turned variably dark and condensed, whereas underneath the ablation they remained similar as immediately after hypoglycemia. This sequence indicates that the most likely cause of nerve cell destruction on the non-protected side is the "excitotoxic" effect mediated by the glutamatergic innervation, which is superimposed on the action of the hypoglycemic insult per se. Furthermore, the primary condensation of neurons and their dendrites indicate existence of another type of acute "excitotoxic" nerve cell injury which differs from the previously described injury characterized by neuronal swelling.
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| 7. |
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| 8. |
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| 9. |
- Wennergren, Göran, 1947, et al.
(författare)
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Neonatal breathing control mediated via the central chemoreceptors.
- 1983
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Ingår i: Acta physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 119:2, s. 139-46
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Tidskriftsartikel (refereegranskat)abstract
- Respiratory changes elicited via the central chemoreceptor system have been studied in anesthetized newborn guinea pigs and newborn rabbits. Periodic breathing was induced by inhibition of the central chemoreceptors by superfusion with alkaline cerebrospinal fluid. The periodic breathing was promptly reversed to steady by increasing the oxygen or carbon dioxide concentration in the inspired air or by intravenous theophylline. Elicitation of periodic breathing simply by exposing the animals to hypoxia succeeded only when very low oxygen concentrations were given. Clearcut respiratory excitation was produced by small amounts of theophylline applied onto the ventral surface of the medulla. Not only theophylline intravenously but also theophylline topically applied on the ventral medullary surface normalized spontaneously developed periodic breathing. Application of meperidine onto the ventral medullary surface gave respiratory inhibition with dosages considerably lower than required when given intravenously. The results emphasize the importance of an adequate respiratory drive from the central chemoreceptors for the maintenance of a regular breathing pattern. The findings support a view that at least part of the respiratory effects seen in the newborn following administration of meperidine or theophylline is due to effect of the drugs on the central chemosensitive system.
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| 10. |
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