| 321. |
- Hoglund, A., et al.
(author)
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Is excessive daytime sleepiness a separate manifestation in Parkinson's disease?
- 2015
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In: Acta Neurologica Scandinavica. - : Hindawi Limited. - 0001-6314 .- 1600-0404. ; 132:2, s. 97-104
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Journal article (peer-reviewed)abstract
- BackgroundExcessive daytime sleepiness (EDS) is common in Parkinson's disease (PD), but its role and relation to other PD features is less well understood. ObjectiveTo investigate potential predictors of EDS in PD and to explore how EDS relates to other motor and non-motor PD features. Methods118 consecutive persons with PD (54% men; mean age, 64) were assessed regarding EDS using the Epworth Sleepiness Scale (ESS) and a range of motor and non-motor symptoms. Variables significantly associated with ESS scores in bivariate analyses were used in multiple regression analyses with ESS scores as the dependent variable. Principal component analysis (PCA) was conducted to explore the interrelationships between ESS scores and other motor and non-motor PD aspects. ResultsAmong 114 persons with complete ESS data, significant independent associations were found between ESS scores and axial/postural/gait impairment, depressive symptoms, and pain (R-2, 0.199). ESS scores did not load significantly together with any other PD features in the PCA. ConclusionsOnly a limited proportion of the variation in EDS could be accounted for by other symptoms, and EDS did not cluster together with any other PD features in PCAs. This suggests that EDS is a separate manifestation differing from, for example, poor sleep quality and fatigue.
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| 322. |
- Holmegaard, Lukas, et al.
(author)
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Proinflammatory protein signatures in cryptogenic and large artery atherosclerosis stroke
- 2021
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In: Acta neurologica Scandinavica. - : Hindawi Limited. - 1600-0404 .- 0001-6314. ; 143:3, s. 303-312
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Journal article (peer-reviewed)abstract
- The cause of ischemic stroke remains unknown, cryptogenic, in 25% of young and middle-aged patients. We hypothesized that if atherosclerosis is prominent in cryptogenic stroke, it would have a similar proinflammatory protein signature as large artery atherosclerosis (LAA) stroke.Blood was collected in the acute phase and after 3months from cryptogenic (n=162) and LAA (n=73) stroke patients aged 18-69years and once from age-matched controls (n=235). Cryptogenic stroke was divided into Framingham Risk Score (FRS) quartiles to compare low and high risk of atherosclerosis. Plasma concentrations of 25 proteins were analyzed using a Luminex multiplex assay. The discriminating properties were assessed with discriminant analysis and C-statistics.We identified proteins that separated cryptogenic and LAA stroke from controls (area under the curves, AUCs≥0.85). For both subtypes, RANTES, IL-4, and IFN-γ contributed the most at both time points. These associations were independent of risk factors of atherosclerosis. We also identified proteins that separated cryptogenic strokes in the lowest quartile of FRS from those in the highest, and from LAA stroke (AUCs≥0.76), and here eotaxin and MCP-1 contributed the most.The protein signature separating cases from controls was different from the signature separating cryptogenic stroke with low risk of atherosclerosis from those with high risk and from LAA stroke. This suggests that increased RANTES, IL-4, and IFN-γ in stroke may not be primarily related to atherosclerosis, whereas increased eotaxin and MCP-1 in cryptogenic stroke may be markers of occult atherosclerosis as the underlying cause.
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| 323. |
- Holmqvist Andersson, Elisabeth, et al.
(author)
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Epidemiology of traumatic brain injury : a population based study in western Sweden.
- 2003
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In: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 107:4, s. 256-259
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Journal article (peer-reviewed)abstract
- BACKGROUND: This study on traumatic brain injury (TBI) is based on prospective and retrospective population based data from a head injury register in Boras. METHODS: Data was collected from the hospital emergency unit, the discharge register, the regional neurosurgical clinic and the coroner's records during 1 year. This district is mixed urban and rural with a population of 138 000. RESULTS: The 753 cases identified represent an incidence of 546 per 100 000 which includes deaths (0.7%), hospital admissions (67%) and attendance at the emergency department in patients not admitted (32%). Males (644 per 100 000), had 1.46 higher overall rate than females (442 per 100 000). The external causes were dominated by fall from same level (31%) and fall from different level (27%) followed by traffic accidents (16%) and persons hit by objects (15%). CONCLUSIONS: The incidence of TBI found in this study is high but well in accordance with earlier published Swedish studies.
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| 324. |
- Holmøy, Trygve, et al.
(author)
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Vitamin D supplementation and neurofilament light chain in multiple sclerosis.
- 2019
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In: Acta neurologica Scandinavica. - : Hindawi Limited. - 1600-0404 .- 0001-6314. ; 139:2, s. 172-176
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Journal article (peer-reviewed)abstract
- The effect of vitamin D supplementation on the disease course of multiple sclerosis (MS) is not established. Neurofilament light chain (NFL) is a sensitive marker of axonal degeneration. The aim of this study was to establish whether high-dose vitamin D supplementation reduces serum levels of NFL.We have performed a 96weeks placebo-controlled randomized study of weekly supplementation with 20000IU vitamin D3 in 71 patients with relapsing remitting MS (RRMS). Serum levels of NFL were measured at baseline, week 48 and week 96 with a single molecule (Simoa) assay in 69 of these patients.Serum levels of 25-hydroxyvitamin D more than doubled in the vitamin D group. Compared to placebo, vitamin D supplementation had no overall effect on the change in serum levels of NFL from baseline (P=0.93 at week 48 and P=0.56 at week 96). In the subgroup of patients not receiving disease-modifying therapy, NFL decreased by 30.9% to week 48% and 32.6% to week 96 from baseline in the vitamin D group as compared to the placebo group (P=0.06 for both time points).With a possible exception for patients not treated with disease-modifying drugs, weekly supplementation with 20000IU vitamin D3 did not affect NFL levels in these RRMS patients.
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| 325. |
- Holtback, Charlotte, et al.
(author)
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Mid-life extrapyramidal symptoms predict cognitive impairment 23 years later
- 2022
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In: Acta Neurologica Scandinavica. - : Hindawi Limited. - 0001-6314 .- 1600-0404. ; 145:3, s. 305-313
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Journal article (peer-reviewed)abstract
- Objectives The prevalence of dementia is growing rapidly worldwide. The early identification and treatment of cognitive decline could reduce the burden on the health care system. Our objective was to investigate whether factors measured at an examination at age 50 predict cognitive impairment (CI) 23 years later. Materials & Methods In 1993 we enrolled a randomly selected sample of 798 men, 50 years of age, from the general population. They all underwent a physical examination, provided blood samples and filled out questionnaires addressing lifestyle and psychosocial factors. Cognitive testing was offered to all participants still alive in 2016, at age 73. Results A total of 333 men participated in the cognitive study, of which 80 (24.0%) performed at a level corresponding to mild cognitive impairment, and four (1.2%) at a level consistent with severe cognitive impairment. After the first step in the multivariable analysis, hypertension, heavy smoking, high intake of alcohol, financial stress, difficulty falling asleep, and cogwheel rigidity were associated with cognitive impairment. After further adjustment, only wide waist circumference measured in cm (OR 1.04, 95% CI 1.00-1.08, p = .04), leg pendulousness (OR 41.97, 95% CI 3.27-538.62, p = .004) and self-assessed hidden irritability (OR 2.18, 95% CI 1.10-4.32, p = .03) at baseline, remained as being associated with cognitive impairment 23 years later. Conclusions Extrapyramidal symptoms such as leg pendulousness, at the age of 50, may be an indicator for very early identification of future cognitive decline.
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| 326. |
- Holtz, A, et al.
(author)
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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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In: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 80:3, s. 215-20
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Journal article (peer-reviewed)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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| 327. |
- Holtz, A, et al.
(author)
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Effect of methylprednisolone on motor function and spinal cord blood flow after spinal cord compression in rats.
- 1990
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In: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 82:1, s. 68-73
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Journal article (peer-reviewed)abstract
- The effect of methylprednisolone (MP) on neurologic recovery and spinal cord blood flow (SCBF) was investigated up to 4 days after a spinal cord compression injury in rats. The injury was produced at midthoracic level by applying a load of 35 g on a 2.2 x 5.0 mm compression plate for 5 min, which resulted in transient paraparesis. MP was given as a bolus dose of 30 mg/kg i.v. 60 min after injury (n = 20) and controls were given saline (n = 10). The motor performance was assessed daily as the capacity angle on the inclined plane and SCBF was measured by 14C-iodoantipyrine autoradiography on Days 1 or 4. On Day 1 the capacity angle was reduced from about 63 degrees preoperatively to 33 +/- 2 degrees (mean +/- SEM) in the control group and to 50 +/- 1 degrees in the group treated with MP (p less than 0.05). Thereafter there was a slight improvement in both groups, but the difference persisted throughout the observation period. On Day 4 both gray and white matter SCBF was better preserved in MP-treated animals than in the control group (59 +/- 4 versus 49 +/- 3 ml/min/100 g tissue for gray matter and 13.6 +/- 0.6 versus 10.7 +/- 0.8 ml/min/100 g tissue for white matter). Posttraumatic treatment with MP, thus, improved both the neurologic recovery during the first 4 days and SCBF as measured on Day 4. It is speculated that the effect of MP is at least partly exerted on the vascular bed.
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| 328. |
- Holtz, A, et al.
(author)
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MK 801, an OBS N-methyl-D-aspartate channel blocker, does not improve the functional recovery nor spinal cord blood flow after spinal cord compression in rats.
- 1991
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In: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 84:4, s. 334-8
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Journal article (peer-reviewed)abstract
- Damage to the central nervous system is followed by local release of excitatory amino acids, e.g. glutamate. These have been claimed to increase the metabolic need of already hypoxic neurons, and thereby to promote cell death. To investigate whether N-methyl-D-aspartate (NMDA) receptor-mediated mechanisms are involved in the damage consequent to spinal cord injury, 20 rats were exposed to 5-min compression of the thoracic spinal cord produced with a load of 35 g on a 2.2 x 5 mm sized plate. One group of animals was given a noncompetitive NMDA channel blocker, MK-801, in a dose of 10 mg/kg b.w and one group saline alone. The neurologic function was evaluated on the inclined plane for 4 days when spinal cord blood flow (SCBF) was measured with the 14C-iodoantipyrine autoradiographic technique. One day after trauma the animals in both groups were paraparetic and exhibited a significantly decreased capacity angle at the inclined plane test (about 35 degrees compared with about 63 degrees before compression). Thereafter, the motor function improved slightly, but to a similar extent in the two groups. On Day 4, gray and white matter SCBF was similar in the two groups. The results indicate that MK 801 in the dose used does not prevent the development of neurologic dysfunction or the reduction in SCBF after spinal cord compression.
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| 329. |
- Holtz, A, et al.
(author)
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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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In: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 79:6, s. 460-7
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Journal article (peer-reviewed)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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| 330. |
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