| 21. |
- Fredrikson, S, et al.
(författare)
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Elevated suicide risk among patients with multiple sclerosis in Sweden
- 2003
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Ingår i: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 22:2, s. 146-152
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Tidskriftsartikel (refereegranskat)abstract
- Results from previous studies of suicide risk among patients with multiple sclerosis (MS) are inconsistent. This may be explained partly by differences in methodology and study populations. The purpose of our study was to investigate suicide risk among hospital patients with MS in Sweden. During the period 1969–1996, 12,834 cases were recorded in the Swedish Hospital Inpatient Register, with 77,377 hospital admissions, in which MS was a primary or secondary diagnosis at discharge. The mean follow-up time for the whole cohort was 9.9 (SD 7.3) years. When the data for these MS patients were linked to the Swedish Causes of Death Register for the same period, 5,052 (39.4%) were found to have died. Among the 5,052 deaths, suicide was an underlying cause of death in 90 cases (1.8%). The mean period between the initial admission date with an MS diagnosis at discharge and the date of death for the 90 MS suicide cases was 5.8 (SD 5.1) years. This was significantly shorter (p = 0.002) than the mean of 7.9 (SD 6.4) years for MS cases who died due to other causes. Suicide risk, calculated as the standardized mortality ratio (SMR), was significantly elevated (SMR = 2.3) among both male and female MS cases compared with the general population. Suicide risk was particularly high in the first year after initial admission with an MS diagnosis, and among younger male MS cases. The mean age at the time of suicide was 44.5 (SD 12.4) years, and 58% of the suicides were committed within 5 years after the first admission with an MS diagnosis. The crude suicide rate among MS patients during the study period was 71 per 100,000 person-years. The rate was significantly higher (p < 0.001) in males (114) than in females (47), with an odds ratio of 2.4 (95% CI: 1.6–3.8). These findings have implications for suicide preventive measures in neurological practice.
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| 22. |
- Grönberg, Angelina, et al.
(författare)
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Incidence of Aphasia in Ischemic Stroke
- 2022
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Ingår i: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 56:3, s. 174-182
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: A decrease in ischemic stroke (IS) incidence has been observed in high income countries during the last decades. Whether this has influenced the occurrence of aphasia in IS is uncertain. We therefore examined the incidence rate and potentially related determinants of aphasia in IS. Methods: We prospectively examined consecutive patients admitted to hospital with first-ever acute IS between March 1, 2017, and February 28, 2018, as part of the Lund Stroke Register (LSR) Study, comprising patients from the uptake area of Skåne University Hospital, Lund, Sweden. Patients were assessed with National Institutes of Health Stroke Scale (NIHSS) at stroke onset. Presence of aphasia was evaluated with NIHSS item 9 (language). We registered IS subtypes and risk factors. To investigate possible temporal changes in aphasia incidence, we made comparisons with corresponding LSR data from 2005 to 2006. Incidence rates were calculated and adjusted to the European Standard Population (ESP) and to the Swedish population. Results: Among 308 included IS patients, 30% presented with aphasia (n = 91; 95% CI: 25-35), a proportion of aphasia in IS that was similar to 2005-2006. The incidence rate of aphasia was 31 per 100,000 person-years adjusted to the ESP (95% CI: 25-38 per 100,000 person-years) corresponding to a significant decrease of 30% between 2005-2006 and 2017-2018. The decrease was significantly more pronounced in men. The initial severity of aphasia remained unchanged, with the majority of patients having severe to global aphasia. No significant differences between vascular stroke risk factors were noted among stroke patients with or without aphasia. Conclusion: Even though the overall IS incidence rate has decreased during the first decades of the 21st century, the proportion of IS patients with aphasia at stroke onset remains stable at 30%. Aphasia continues to be an important symptom that needs to be considered in stroke care and rehabilitation.
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| 23. |
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| 24. |
- Hafsteinsdottir, Brynhildur, 1986, et al.
(författare)
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Decreased incidence of Guillain-Barre syndrome during the COVID-19 pandemic: a retrospective population-based study
- 2023
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Ingår i: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 57:1, s. 1-6
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Tidskriftsartikel (refereegranskat)abstract
- Background: Guillain-Barre syndrome is an immune-mediated acute inflammatory polyneuropathy that is associated with various triggers, including certain infections and vaccines. It has been suggested that both SARS-CoV2 infection and vaccination may be triggering factors for Guillain-Barre syndrome, but evidence remain equivocal. Here we conducted a population-based incidence study of Guillain-Barre syndrome spanning the three years immediately prior to and the two years during the pandemic. Methods: Cases were identified by searching a regional diagnostic database for the ICD-10 code for Guillain-Barre syndrome. Individuals who fulfilled the Brighton Criteria for Guillain-Barre syndrome were included. Information on clinical presentation, laboratory values, and vaccination status were retrieved from medical records. We calculated the incidence immediately prior to and during the pandemic.Results: The Guillain-Barre syndrome incidence rate was 1.35/100,000 person-years for the pre-pandemic period, and 0.66/100,000 person-years for the pandemic period (incidence rate ratio: 0.49; p = 0.003). Three cases were temporally associated with SARS-CoV2 infection, and one case each to the Astra Zeneca and Pfizer-BioTech COVID-19 vaccines.Conclusions: Our results show that the incidence of Guillain-Barre syndrome decreased during the pandemic. This is most likely due to decreased prevalence of triggering infections, due to social restrictions. Our findings do not support a causal relationship between Guillain-Barre syndrome and COVID-19.
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| 25. |
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| 26. |
- Hardell, Lennart, et al.
(författare)
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Mobile phone use and the risk for malignant brain tumors : A case-control study on deceased cases and controls
- 2010
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Ingår i: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 35:2, s. 109-114
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Tidskriftsartikel (refereegranskat)abstract
- We investigated the use of mobile or cordless phones and the risk for malignant brain tumors in a group of deceased cases. Most previous studies have either left out deceased cases of brain tumors or matched them to living controls and therefore a study matching deceased cases to deceased controls is warranted. Recall error is one issue since it has been claimed that increased risks reported in some studies could be due to cases blaming mobile phones as a cause of the disease. This should be of less importance for deceased cases and if cancer controls are used. In this study brain tumor cases aged 20-80 years diagnosed during 1997-2003 that had died before inclusion in our previous studies on the same topic were included. Two control groups were used: one with controls that had died from another type of cancer than brain tumor and one with controls that had died from other diseases. Exposure was assessed by a questionnaire sent to the next-of-kin for both cases and controls. Replies were obtained for 346 (75%) cases, 343 (74%) cancer controls and 276 (60%) controls with other diseases. Use of mobile phones gave an increased risk, highest in the >10 years' latency group yielding odds ratio (OR) = 2.4, and 95% confidence interval (CI) = 1.4-4.1. The risk increased with cumulative number of lifetime hours for use, and was highest in the >2,000 h group (OR = 3.4, 95% CI = 1.6-7.1). No clear association was found for use of cordless phones, although OR = 1.7, 95% CI = 0.8-3.4 was found in the group with >2,000 h of cumulative use. This investigation confirmed our previous results of an association between mobile phone use and malignant brain tumors.
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| 27. |
- Hardell, L, et al.
(författare)
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Vestibular schwannoma, tinnitus and cellular telephones
- 2003
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Ingår i: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 22:2, s. 124-129
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Tidskriftsartikel (refereegranskat)abstract
- Cases with tinnitus after using analogue cellular telephones are presented. An increased odds ratio of 3.45, 95% confidence interval (CI) 1.77–6.76, was found for vestibular schwannoma (VS) associated with the use of analogue cell phones. During the time period 1960–1998, the age-standardized incidence of VS in Sweden significantly increased yearly by +2.53% (CI 1.71–3.35). A significant increase in the incidence of VS was only found for the latter of the two time periods 1960–1979 and 1980–1998. For all other brain tumors taken together, the incidence significantly increased yearly by +0.80% (CI 0.59–1.02) for the time period 1960–1998, although the increase was only significant for benign tumors other than VS during 1960–1979.
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| 28. |
- Hemminki, K, et al.
(författare)
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A population-based study of familial central nervous system hemangioblastomas
- 2001
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Ingår i: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 20:4, s. 257-261
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Tidskriftsartikel (refereegranskat)abstract
- We used the nationwide Swedish Family-Cancer Database to analyze the risk for central nervous system hemangioblastoma (HB) in offspring (0–61 years) of parents with cancer. Eighty-three offspring were identified, and the age at onset showed a bimodal distribution. The early-onset component peaked at 25–29 years, was associated with von Hippel-Lindau (VHL) disease and presented with HBs, renal cell carcinomas, pheochromocytomas and insulomas in the proband or other family members. Standardized incidence ratios (SIRs) were 600 for offspring HB by parental HB, and they were even high for the other VHL-related tumors. Second tumors were common in this early-onset group, and the types were as expected in VHL. The late-onset component peaked at 40–44 years, and it was twice as prevalent as the early-onset component. Because there was no evidence of familial risks, this is suggested to be a sporadic form of HB.
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| 29. |
- Hemminki, K, et al.
(författare)
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Familial risks for epilepsy among siblings based on hospitalizations in Sweden
- 2006
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Ingår i: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 27:2, s. 67-73
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Tidskriftsartikel (refereegranskat)abstract
- <i>Purpose:</i> Epilepsy is a common disabling condition, with high heritability according to twin studies. Characterization of familial risks for common subtypes of epilepsy will advance the search for the heritable causes of these conditions and their underlying mechanisms. We aim at defining familial risks for siblings to be hospitalized because of epilepsy. <i>Methods:</i> A nationwide ad hoc epilepsy database was constructed by linking the Multigeneration Register on 0- to 69-year-old siblings to the Hospital Discharge Register for data on epilepsies covering the years 1987–2001. Standardized risk ratios (SIRs) were calculated for affected sibling pairs by comparing them to those whose siblings had no epilepsy. <i>Results:</i> Among a total of 26,799 hospitalized cases, 598 affected siblings were identified with a familial SIR of 2.35; the SIR was highest at ages 0–4 years (6.82). Infantile spasms showed the highest risk for any subtype (10.45), when a co-sibling was diagnosed with any epilepsy. When both siblings were diagnosed with a concordant (same) subtype of epilepsy, the SIRs were high, i.e. 8.43 for generalized idiopathic epilepsy, 2.56 for partial epilepsy, 24.72 for status epilepticus and 24.39 for other epilepsies. Generalized idiopathic epilepsy was also associated with grand mal (4.06) and other epilepsies (7.61). The numbers of cases were small but concordant diagnoses always showing higher SIRs compared with discordant diagnoses. <i>Conclusions:</i> Within the limits of the present sample size, our results suggest high familial aggregation for certain subtypes of epilepsy for which distinct genetic mechanisms may underlie.
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| 30. |
- Horstmann, Vibeke, et al.
(författare)
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Occurrence of Depression in Families with Frontotemporal Dementia: A Family History Study.
- 2009
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Ingår i: Neuroepidemiology. - : S. Karger AG. - 1423-0208 .- 0251-5350. ; 33:2, s. 124-130
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Tidskriftsartikel (refereegranskat)abstract
- Background: There are clinical similarities between frontotemporal dementia (FTD) and depression. The aim is to study co-aggregation of depression in families with FTD, indicating the existence of common aetiological factors. Methods: The study included 74 index patients with FTD and their 540 first-degree relatives above the age of 15 years. Occurrence of depression was studied at 3 different levels. Results: The incidence of depression in first-degree relatives of FTD patients was not higher than that of a general population. Occurrence of depression was not higher in families where parents had FTD compared to families with parents having no indications of FTD. Individuals with FTD had not suffered from depression to a greater extent than those without FTD. Conclusions: The hypothesis of a common aetiological factor of FTD and depression was not supported.
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