| 1. |
- Holtz, A, et al.
(författare)
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Blocking weight-induced spinal cord injury in rats : effects of TRH or naloxone on motor function recovery and spinal cord blood flow.
- 1989
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Ingår i: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 80:3, s. 215-20
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Tidskriftsartikel (refereegranskat)abstract
- The ability of thyrotropin releasing hormone (TRH) or naloxone to reduce the motor function deficit and to improve the spinal cord blood flow (SCBF) was investigated in a rat spinal cord compression injury model. Spinal cord injury was induced by compression for 5 min with a load of 35 g on a 2.2 x 5.0 mm sized compression plate causing a transient paraparesis. One group of animals was given TRH, one group naloxone and one group saline alone. Each drug was administered intravenously as a bolus dose of 2 mg/kg 60 min after injury followed by a continuous infusion of 2 mg/kg/h for 4 h. The motor performance was assessed daily on the inclined plane until Day 4, when SCBF was measured with the 14C-iodoantipyrine autoradiographic method. It was found that neither TRH nor naloxone had promoted motor function recovery or affected SCBF 4 days after spinal cord injury.
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| 2. |
- Holtz, A, et al.
(författare)
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Spinal cord injury in rats : inability of nimodipine or anti-neutrophil serum to improve spinal cord blood flow or neurologic status.
- 1989
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Ingår i: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 79:6, s. 460-7
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Tidskriftsartikel (refereegranskat)abstract
- The role of a calcium-mediated increase in vascular resistance and of vascular damage caused by polymorphonuclear leukocytes (PMNLs) in the development of neurologic deficit and disturbance of spinal cord circulation following spinal cord compression was studied in the rat. Spinal cord injury was induced by 5 min of compression with a load of 35 g on a 2.2 X 5.0 mm compression plate. This caused transient paraparesis. The rats received either the calcium receptor antagonist nimodipine or an anti-rat neutrophil serum (ANS). Nimodipine was infused i.v. for 4 h in an amount of 1.5 micrograms/kg/min starting 60 min after trauma. The number of circulating PMNLs was depleted by intraperitoneal injection of an ANS raised in sheep given 12 h before trauma. This caused a reduction to about 2% of the pre-ANS value. Controls received saline or normal sheep serum. The motor performance was assessed daily on the inclined plane. On day one, the day after injury, the capacity angle had decreased from about 63 degrees preoperatively to close to 32 degrees in the experimental groups. There was then a slow improvement in both the control and experimental groups and on day 4 the capacity angle was close to 43 degrees in all 3 groups. Spinal cord blood flow, as measured with the 14C-iodoantipyrine autoradiography method, was similar in all groups on day 4. As neither the neurologic dysfunction nor the spinal cord blood flow was affected by post-trauma treatment with nimodipine or pretreatment with ANS, the possibility that calcium-mediated vasoconstriction or PMNLs play a role in the development of posttraumatic neurologic disability was not supported by this study.
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| 3. |
- Jensson, O, et al.
(författare)
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Hereditary cystatin C (gamma-trace) amyloid angiopathy of the CNS causing cerebral hemorrhage
- 1987
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Ingår i: Acta Neurologica Scandinavica. - : Hindawi Limited. - 0001-6314 .- 1600-0404. ; 76:2, s. 102-114
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Tidskriftsartikel (refereegranskat)abstract
- Hereditary CNS amyloid angiopathy occurring in Icelanders is the first human disorder known to be caused by deposition of cystatin C amyloid fibrils in the walls of the brain arteries leading to single or or multiple strokes with fatal outcome. One or more affected members have been verified by histological examination in 8 families containing 127 affected. These originated from the same geographic area. Abnormally low value of cystatin C found in the cerebrospinal fluid of those affected can be used to support or make diagnosis of this disease, also in asymptomatic relatives. By amino acid sequence analysis the amyloid fibrils in the patients are found to be a variant of cystatin C (gamma-trace), a major cysteine proteinase inhibitor. The variant protein has an amino acid substitution (glutamine for leucine) at position 58 in the amyloid molecule. It is postulated that a point mutation has occurred leading to production of amyloidogenic protein causing the disorder.
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| 4. |
- Lindvall, O., et al.
(författare)
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Transplantation strategies in the treatment of Parkinson's disease : experimental basis and clinical trials
- 1989
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Ingår i: Acta Neurologica Scandinavica. - : Hindawi Limited. - 0001-6314 .- 1600-0404. ; 80, s. 197-210
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Tidskriftsartikel (refereegranskat)abstract
- Abstract– Neural grafting has over the last decade emerged as a possible tool for the substitution of damaged neurons in the central nervous system and for the promotion of symptomatic recovery after brain damage. Transplantation studies in the 6‐hydroxydopamine lesion rat model of Parkinson's disease were initiated in the late seventies. The first studies were based on the neuronal replacement paradigm, using developing dopamine brain cells obtained from the substantia nigra region of embryonic cadavers. When implanted into the striatum such grafts were found to reinnervate part of the previously denervated striatum and restore dopamine turnover and release to near‐normal levels. In both rats and monkeys the nigral grafts have been shown to normalize some, but not all, Parkinson‐like symptoms in the dopamine deficient recipients. Grafting of adrenal medullary tissue was introduced in the early eighties as an alternative to the use of embryonic cadaver tissue. The adrenal medullary grafts have, however, so far shown poor long‐term survival in both rats and monkeys, and consistent with this no sustained dopamine release have been observed in the brain of long‐term grafted animals. Likewise, no long‐lasting effects of adrenal medullary grafts on spontaneous motor or sensori‐motor behavior have so far been documented in either the rat or the monkey model. The results so far reported from trials using adrenal medullary grafts in patients with Parkinson's disease appear to conform to the available animal experimental data at least in two important respects: significant long‐term graft survival has not been possible to document, and any clear‐cut functional effects consistent with sustained graft‐induced dopamine release have not been demonstrated. Initial results from ongoing trials using grafts of fetal nigral tissue are presented and discussed.
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| 5. |
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| 6. |
- Strigård, Karin, et al.
(författare)
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In vivo treatment of rats with monoclonal antibodies against gamma interferon : effects on experimental allergic neuritis.
- 1989
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Ingår i: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 80:3, s. 201-207
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Tidskriftsartikel (refereegranskat)abstract
- To elucidate the role of gamma interferon in experimental allergic neuritis (EAN) a mouse monoclonal antibody (DB-1) directed against rat gamma interferon was 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 for presence of MHC class II antigens and various T cell subsets. DB-1 treatment given after onset of clinical symptoms (Day 15 after immuniozation with myelin) shortened disease duration, compared with non-treated EAN controls. Affected nerves of DB-1 treated animals showed reduced expression of MHC class II antigens and lower numbers of T lymphocytes within the affected nerves. In contrast, when DB-1 treatment was given on the day of immunization (Day 0), the disease duration increased, and when given before onset of the disease (Day 9) the clinical course was not significantly affected. The results support an important role for gamma interferon in the pathogenesis of EAN.
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| 7. |
- Wester, P, et al.
(författare)
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Monoamine metabolite concentrations and cholinesterase activities in cerebrospinal fluid of progressive dementia patients : relation to clinical parameters.
- 1988
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Ingår i: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 77:1, s. 12-21
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Tidskriftsartikel (refereegranskat)abstract
- Forty-five well clinically characterized patients with progressive dementia were investigated for lumbar cerebrospinal fluid (CSF) monoamine metabolites and cholinesterase activities. Monoamine concentrations were determined by reverse phase liquid chromatography with electrochemical detection and the cholinergic enzymes were measured photometrically. Firstly, all clinical and CSF parameters were studied in statistical cluster analyses to detect groups of variables which demonstrated a high correlation with respect to each other. The CSF transmitter markers were then used in multiple regression models to explain the variance of clinical variables as chosen from the cluster analyses. The degree of dementia, as assessed by global deterioration score (GDS) and activity in daily life (ADL) status, as well as the Alzheimer-related symptoms dyspraxia and dysphasia, were associated with low AChE activities in CSF. A presumed subgroup of dementia patients clinically characterized by asymmetry of neurological signs, increased unilateral tonus, stepwise progression, and high Hachinski score, showed low HVA concentrations in CSF. These data suggest a coupling of clinical/neurological parameters to different CSF transmitter profils and, thus, that CSF biochemical parameters are of use as antemortem markers in dementia conditions.
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