| 1. |
- Lindén, Thomas, 1962, et al.
(författare)
-
Risk of central pontine myelinolysis in the treatment of severe hyponatremia
- 1989
-
Ingår i: Läkartidningen. - 0023-7205. ; 86:20, s. 1905-7
-
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.
|
|
| 2. |
- Hanner, P, et al.
(författare)
-
Clinical observations of effects on central nervous system in patients with acute facial palsy.
- 1987
-
Ingår i: Archives of otolaryngology--head & neck surgery. - 0886-4470. ; 113:5, s. 516-20
-
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.
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
- Lindén, Thomas, 1962, et al.
(författare)
-
Protective effect of lesion to the glutamatergic cortico-striatal projections on the hypoglycemic nerve cell injury in rat striatum.
- 1987
-
Ingår i: Acta neuropathologica. - 0001-6322. ; 74:4, s. 335-44
-
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.
|
|
| 6. |
- Lindblom, B, et al.
(författare)
-
Sahlgren's Saturation Test for acquired dyschromatopsia: increased lightness enhances sensitivity.
- 1988
-
Ingår i: Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie. - 0721-832X. ; 226:5, s. 447-8
-
Tidskriftsartikel (refereegranskat)abstract
- Sahlgren's Saturation Test (SST) is a simple sorting test designed for the detection and grading of acquired color vision defects. Like other pigment-based color vision tests, the SST color samples have medium lightness, i.e., they belong to the intermediate part of the gray scale. We tested normal controls and subjects with congenital or acquired dyschromatopsia with five SST versions that differed only in the amount of lightness. The sensitivity of the test increased considerably with increasing lightness. Therefore, the lightness level of SST has now been changed from 30 to 10 Natural Color System units.
|
|
| 7. |
- Frisén, Lars, 1939
(författare)
-
Computerized perimetry: possibilities for individual adaptation and feedback.
- 1988
-
Ingår i: Documenta ophthalmologica. Advances in ophthalmology. - 0012-4486. ; 69:1, s. 3-9
-
Tidskriftsartikel (refereegranskat)abstract
- Computerized perimetry is often poorly accepted by the tested subjects, presumably because of sparse feedback and lack of adaptation to individual capacity. Several remedies are suggested, including visual response feedback, active correction of erroneous responses, various fixation prompts, and continuous adaptation to current reaction time. Intuitively intelligible result displays are also desirable. A novel format representing threshold level by symbol size may meet this need.
|
|
| 8. |
|
|
| 9. |
- Strigård, Karin, et al.
(författare)
-
In vivo monoclonal antibody treatment with Ox19 (anti-rat CD5) causes disease relapse and terminates P2-induced immunospecific tolerance in experimental allergic neuritis.
- 1989
-
Ingår i: Journal of Neuroimmunology. - 0165-5728 .- 1872-8421. ; 23:1, s. 11-18
-
Tidskriftsartikel (refereegranskat)abstract
- The role of CD5+ lymphocytes in the recovery phase and on immunospecific protection against experimental allergic neuritis (EAN) was examined in Lewis rats by in vivo treatment with Ox19, a mouse anti-rat CD5 monoclonal antibody. Animals pretreated with the peripheral nerve basic protein P2 and thereby rendered resistant to the disease showed clinical signs of EAN after intraperitoneal (i.p.) Ox19 injection given at the same time as the rechallenge with neuritogenic doses of myelin in Freund's complete adjuvant. Non-pretreated rats recovered from signs of EAN developed a clinical relapse after i.p. Ox19 injections. Taken together, these data suggest an important regulatory role of the CD5 receptor in the immune response.
|
|
| 10. |
- Strigård, Karin, et al.
(författare)
-
Modulation of experimental allergic neuritis in rats by in vivo treatment with monoclonal anti T cell antibodies.
- 1988
-
Ingår i: Journal of the Neurological Sciences. - 0022-510X .- 1878-5883. ; 83:2-3
-
Tidskriftsartikel (refereegranskat)abstract
- Monoclonal antibodies (MCA) to different T lymphocyte cell surface antigens have been used to treat rats during different phases of the development of experimental allergic neuritis (EAN). The effects of this treatment were followed by clinical evaluation and in some instances by immunohistochemical analysis of lymphoid organs and affected nerves of the antibody-treated rats. Several MCA, W3/13 (pan T cell reactive), W3/25 (anti-rat CD4), Ox 8 (anti-rat CD8) as well as Ox 6 (anti-Ia) partly prevented clinical signs of EAN when given shortly before expected onset of disease, whereas W3/13 and Ox 8 given at the height of disease did not further affect disease development. However, Ox 19 (anti-rat CD5) given at the same time as immunization partly prevented clinical signs of EAN, while Ox 19 given shortly before expected onset of disease or during height of disease drastically exaggerated disease symptoms. Immunohistochemical studies after Ox 8 or Ox 19 treatment showed a complete absence of staining for the respective antibodies, while staining was preserved with the other MCA. It is concluded that: (1) Ox 8 positive "suppressor/cytotoxic" T lymphocytes do not exert any suppressive effects on EAN during the now investigated phases of disease, and that (2) anti T lymphocyte antibodies (here Ox 19) may exert opposite effects on autoimmune disease when given at different phases of disease development. This may have implications for potential therapeutic trials of MCA therapy for putative autoimmune demyelinating diseases in man.
|
|
