• Evaluation of small nerve fiber dysfunction in type 2 diabetes.

      Ekman, Linnéa; Thrainsdottir, Soley; Englund, Elisabet; Thomsen, Niels; Rosén, Ingmar; Hazer Rosberg, Derya Burcu; Petersson, Jesper; Eriksson, Karl-Fredrik; Dahlin, Lars B; 1 Department of Hand Surgery, Skåne University Hospital, Malmö, Sweden. 2 Department of Clinical Sciences, Neurology, Lund University, Lund, Sweden. 3 Department of Neurology, Landspitali University Hospital, Reykjavik, Iceland. 4 Department of Clinical Sciences, Oncology and Pathology, Lund University, Lund, Sweden. 5 Department of Translational Medicine - Hand Surgery, Lund University, Malmö, Sweden. 6 Department of Clinical Sciences, Clinical Neurophysiology, Lund University, Lund, Sweden. 7 Department of Neurosurgery, Mugla Sitki Kocman University, Mugla, Turkey. 8 Vascular Department of Angiology, Skåne University Hospital, Malmö, Sweden. (Wiley, 2019-09-24)
      OBJECTIVES: To assess potential correlations between intraepidermal nerve fiber densities (IENFD), graded with light microscopy, and clinical measures of peripheral neuropathy in elderly male subjects with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and type 2 diabetes (T2DM), respectively. MATERIALS AND METHODS: IENFD was assessed in thin sections of skin biopsies from distal leg in 86 men (71-77 years); 24 NGT, 15 IGT, and 47 T2DM. Biopsies were immunohistochemically stained for protein gene product (PGP) 9.5, and intraepidermal nerve fibers (IENF) were quantified manually by light microscopy. IENFD was compared between groups with different glucose tolerance and related to neurophysiological tests, including nerve conduction study (NCS; sural and peroneal nerve), quantitative sensory testing (QST), and clinical examination (Total Neuropathy Score; Neuropathy Symptom Score and Neuropathy Disability Score). RESULTS: Absent IENF was seen in subjects with T2DM (n = 10; 21%) and IGT (n = 1; 7%) but not in NGT. IENFD correlated weakly negatively with HbA1c (r = -.268, P = .013) and Total Neuropathy Score (r = -.219, P = .042). Positive correlations were found between IENFD and sural nerve amplitude (r = .371, P = .001) as well as conduction velocity of both the sural (r = .241, P = .029) and peroneal nerve (r = .258, P = .018). Proportions of abnormal sural nerve amplitude became significantly higher with decreasing IENFD. No correlation was found with QST. Inter-rater reliability of IENFD assessment was good (ICC = 0.887). CONCLUSIONS: Signs of neuropathy are becoming more prevalent with decreasing IENFD. IENFD can be meaningfully evaluated in thin histopathological sections using the presented technique to detect neuropathy.
    • Incidence of osmotic demyelination syndrome in Sweden: A nationwide study.

      Aegisdottir, Hildur; Cooray, Charith; Wirdefeldt, Karin; Piehl, Fredrik; Sveinsson, Olafur; 1 Department of Neurology, The National University Hospital of Iceland, Reykjavik, Iceland. 2 Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. 3 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. 4 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. (Wiley, 2019-07-25)
      OBJECTIVE: To report the incidence rate of osmotic demyelination syndrome (ODS), associated risk factors, treatment, and long-term outcomes in a nationwide cohort. METHODS: We conducted a retrospective study of individuals diagnosed with central pontine myelinolysis (ICD-10 code G37.2) in the Swedish National Patient Register during 1997-2011. RESULTS: During the study period, we identified 83 individuals with ODS, 47 women and 36 men. Median age at diagnosis was 55 years. The incidence rate of ODS for the entire study period was 0.611 (95% CI: 0.490-0.754) per million person-years and increased during the study period from 0.271 (95% CI: 0.147-0.460) in 1997-2001 to 0.945 (95% CI: 0.677-1.234) individuals per million person-years in 2007-2011. Most cases (86.7%) were hyponatremic with a median sodium level at admission of 104 mmol/L. All hyponatremic cases were chronic. The cause of hyponatremia was multifactorial, including drugs (56.9%), polydipsia (31.9%), and vomiting or diarrhea (41.7%). A majority of patients (69.9%) were alcoholics. Hyponatremic patients were predominantly treated with isotonic saline (93.1%) and only 4.2% with hypotonic fluids. The median correction rate was 0.72 mmol/L/h. Only six patients were corrected in accordance with national guidelines (≤8 mmol/L/24/h). At three months, 7.2% had died and 60.2% were functionally independent (modified Rankin Scale 0-2). INTERPRETATION: We found an increasing incidence during the study period, which could partly be explained by increased access to magnetic resonance imaging. ODS occurs predominantly in patients with extreme chronic hyponatremia which is corrected too fast with isotonic saline. Most patients survived and became functionally independent.
    • Post-stroke epilepsy in an ischemic stroke cohort-Incidence and diagnosis.

      Hassani, Mujtaba; Cooray, Gerald; Sveinsson, Olafur; Cooray, Charith; 1) Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. 2) Clinical Neurophysiology, Karolinska University Hospital, Stockholm, Sweden. 3) Department of Neurology, The National University Hospital of Iceland, Reykjavik, Iceland. 4) Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. (Wiley, 2019-10-03)
      OBJECTIVES: Stroke is a common cause of adult-onset epilepsy (post-stroke epilepsy, PSE). Despite an increasing awareness, there is a concern for underdiagnosis of the condition. We aimed to study the adherence to the latest updated epilepsy definition, as well as the incidence and diagnosis of PSE in an ischemic stroke cohort admitted to a tertiary University Hospital. MATERIALS AND METHODS: We retrospectively investigated the occurrence and diagnosis of unprovoked seizures and PSE in all ischemic stroke patients admitted to Karolinska University Hospital in Stockholm during 2015 and registered in the Swedish Stroke Register. Patient records were scrutinized for the presence of post-stroke seizures/epilepsy. RESULTS: A total of 240 patients fulfilling the inclusion criteria were surveyed. Median follow-up time was 1062 days (IQR 589-1195 days). Thirteen patients were diagnosed with PSE according to the study criteria, the incidence of PSE 23/1000 person-years (95% CI 13-38/1000 person-years). Median time to PSE from stroke-onset was 237 days (IQR 33-688). Eleven of 13 PSE patients received an epilepsy diagnosis, eight patients after one unprovoked seizure, and three patients after two. CONCLUSIONS: The majority of PSE patients were given a correct epilepsy diagnosis and treated with antiepileptic drugs. However, this study suggests that there still is potential for improvement in the adherence to the latest updated epilepsy definition. The incidence of PSE in a Swedish ischemic stroke cohort using updated epilepsy definitions is similar to previous studies. Larger studies are needed to confirm our findings on the incidence of PSE.