Alcohol use among NTNU students 2007-19. / Alkoholvaner blant NTNU-studenter 2007­19.

BACKGROUND: Alcohol consumption is widespread in student environments. The objective of the study was to examine alcohol use among students at the Norwegian University of Science and Technology (NTNU) in a twelve-year perspective. MATERIAL AND METHOD: The study is cross-sectional, based on two questionnaire surveys conducted in lecture breaks at NTNU in 2007 and 2019. Participation was voluntary and anonymous. The questionnaire surveyed background variables and alcohol use, and included questions from the Alcohol Use Disorders Identification Test (AUDIT). The respondents were categorised into risk profiles based on their results. An AUDIT score of ≥ 8 was used as the threshold value for risky/potentially harmful alcohol use. RESULTS: The study included 2,247 students: 857 from 2007 and 1,390 from 2019. The proportion of women was 42.3 % in 2007 and 54.9 % in 2019. The average age was 21.5 years (2007) and 22.5 years (2019). The average AUDIT score was 10.7 in 2007 and 8.5 in 2019. A total of 937 students (67.6 %) consumed alcohol two to four times per month or more in 2019, a reduction of 9.8 % from 2007. Altogether 885 students (67.8 %) consumed five or more alcohol units on a typical drinking day in 2019, a reduction of 12.8 % from 2007. INTERPRETATION: A considerable one-fifth reduction in the proportion of students with risky alcohol use occurred from 2007 to 2019. However, the alcohol use of more than half of the students may still pose a long-term risk.

Erratum to "The Assistive Device Situation for ALS Patients in Norway".

[This corrects the article DOI: 10.1155/2021/5563343.].

Sleep restriction alters cortical inhibition in migraine: A transcranial magnetic stimulation study.

OBJECTIVE: Migraine is a primary headache disorder with a well-known association with insufficient sleep. However, both the underlying pathophysiology of the disease and the relationship with sleep is still unexplained. In this study, we apply transcranial magnetic stimulation to investigate possible mechanisms of insufficient sleep in migraine. METHODS: We used a randomised, blinded crossover design to examine 46 subjects with migraine during the interictal period and 29 healthy controls. Each subject underwent recordings of cortical silent period, short- and long-interval intracortical inhibition, intracortical facilitation and short-latency afferent inhibition after both two nights of habitual eight-hour sleep and two nights of restricted four-hour sleep. RESULTS: We found reduced cortical silent period duration after sleep restriction in interictal migraineurs compared to controls (p = 0.046). This effect was more pronounced for non-sleep related migraine (p = 0.002) and migraine with aura (p = 0.017). The sleep restriction effect was associated with ictal symptoms of hypersensitivity such as photophobia (p = 0.017) and overall silent period was associated with premonitory dopaminergic symptoms such as yawning (p = 0.034). CONCLUSIONS: Sleep restriction reduces GABAergic cortical inhibition during the interictal period in individuals with migraine. SIGNIFICANCE: Sleep related mechanisms appear to affect the pathophysiology of migraine and may differentiate between migraine subgroups.

A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer's disease.

Late-onset Alzheimer's disease is a prevalent age-related polygenic disease that accounts for 50-70% of dementia cases. Currently, only a fraction of the genetic variants underlying Alzheimer's disease have been identified. Here we show that increased sample sizes allowed identification of seven previously unidentified genetic loci contributing to Alzheimer's disease. This study highlights microglia, immune cells and protein catabolism as relevant to late-onset Alzheimer's disease, while identifying and prioritizing previously unidentified genes of potential interest. We anticipate that these results can be included in larger meta-analyses of Alzheimer's disease to identify further genetic variants that contribute to Alzheimer's pathology.

The Assistive Device Situation for ALS Patients in Norway.

AIMS: There are limited analytical descriptions of the assistive device situation in Norway for patients with ALS and other motor neuron diseases. This study is aimed at investigating how patients, caregivers, and healthcare professionals (occupational therapists and physiotherapists) experience the assistive device situation. METHODS: Twenty-four interviews were conducted with patients with motor neuron disease, caregivers, and healthcare professionals involved in procurement and adaptation of assistive devices. Systematic text condensation was used to analyse the interviews. RESULTS: The majority of patients and caregivers had positive experiences of follow-up by the specialist healthcare service. Several found follow-up by the primary health service to be deficient owing to inadequate expertise, continuity, and resources. Healthcare professionals reported having a proactive approach to identifying needs for assistive devices, but for various reasons, application processes were often delayed. Several patients indicated a reluctance to use assistive devices and were ambivalent regarding proactivity. The availability of assistive devices for some functional impairments was described as inadequate. Some patients felt there was too little focus on sexuality in the follow-up. The respondents had a number of suggestions for improving the assistive device situation. CONCLUSIONS: Multidisciplinary ALS teams are found to ensure follow-up expertise and continuity. Healthcare professionals wish to take a proactive approach to assistive devices, but a number of bureaucratic obstacles occur. The study findings are preliminary and should be validated through a prospective national quality registry for motor neuron diseases.

A young man with convulsive laughter. / En ung mann med krampaktig latter.

BACKGROUND: Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) can manifest with a wide range of neurological and psychiatric symptoms. CASE PRESENTATION: A previously healthy man in his late twenties was admitted several times over the course of half a year. He had acute episodes of reduced consciousness, involuntary movements and psychotic symptoms (e.g. hallucinations and delusions). Initial examinations were normal except for a positive urine drug screen (tetrahydrocannabinol), and the patient was diagnosed with cannabinoid intoxication. During the next admission cerebrospinal fluid analysis showed mild pleocytosis. Screening for anti-neuronal antibodies was negative, but anti-thyroid peroxidase antibodies were detected in serum and cerebrospinal fluid. He was successfully given steroid treatment on a tentative diagnosis of SREAT, but relapsed when the steroids were discontinued. After receiving a prolonged steroid treatment with gradual dose reduction over a year, he remains symptom-free 18 months after treatment discontinuation. INTERPRETATION: The diagnostic delay might have been mitigated with an earlier inclusion of neuroimmunological disorders in the differential diagnosis. Unexplained pleocytosis in the cerebrospinal fluid in the presence of paroxysmal neuropsychiatric symptoms should trigger an investigation that includes autoimmune encephalopathies.

Region- and age-dependent alterations of glial-neuronal metabolic interactions correlate with CNS pathology in a mouse model of globoid cell leukodystrophy.

Globoid cell leukodystrophy (GLD) or Krabbe disease is a lysosomal storage disorder caused by genetic defects in the expression and activity of galactosylceramidase, a key enzyme in the catabolism of myelin-enriched sphingolipids. While there are several histologic, biochemical, and functional studies on GLD, correlations between morphologic and biochemical alterations in central nervous system (CNS) tissues during disease progression are lacking. Here, we combined immunohistochemistry and metabolic analysis using (1)H and (13)C magnetic resonance (MR) spectra of spinal cord, cerebellum, and forebrain to investigate glial-neuronal metabolic interactions and dysfunction in a GLD murine model that recapitulates the human pathology. In order to assess the temporal- and region-dependent disease progression and the potential metabolic correlates, we investigated CNS tissues at mildly symptomatic and fully symptomatic stages of the disease. When compared with age-matched controls, GLD mice showed glucose hypometabolism, alterations in neurotransmitter content, N-acetylaspartate, N-acetylaspartylglutamate, and osmolytes levels. Notably, age- and region-dependent patterns of metabolic disturbances were in close agreement with the progression of astrogliosis, microglia activation, apoptosis, and neurodegeneration. We suggest that MR spectroscopy could be used in vivo to monitor disease progression, as well as ex vivo and in vivo to provide criteria for the outcome of experimental therapies.

Alteration of glial-neuronal metabolic interactions in a mouse model of Alexander disease.

Alexander disease is a rare and usually fatal neurological disorder characterized by the abundant presence of protein aggregates in astrocytes. Most cases result from dominant missense de novo mutations in the gene encoding glial fibrillary acidic protein (GFAP), but how these mutations lead to aggregate formation and compromise function is not known. A transgenic mouse line (Tg73.7) over-expressing human GFAP produces astrocytic aggregates indistinguishable from those seen in the human disease, making them a model of this disorder. To investigate possible metabolic changes associated with Alexander disease Tg73.7 mice and controls were injected simultaneously with [1-(13)C]glucose to analyze neuronal metabolism and [1,2-(13)C]acetate to monitor astrocytic metabolism. Brain extracts were analyzed by (1)H magnetic resonance spectroscopy (MRS) to quantify amounts of several key metabolites, and by (13)C MRS to analyze amino acid neurotransmitter metabolism. In the cerebral cortex, reduced utilization of [1,2-(13)C]acetate was observed for synthesis of glutamine, glutamate, and GABA, and the concentration of the marker for neuronal mitochondrial metabolism, N-acetylaspartate (NAA) was decreased. This indicates impaired astrocytic and neuronal metabolism and decreased transfer of glutamine from astrocytes to neurons compared with control mice. In the cerebellum, glutamine and GABA content and labeling from [1-(13)C]glucose were increased. Evidence for brain edema was found in the increased amount of water and of the osmoregulators myo-inositol and taurine. It can be concluded that astrocyte-neuronal interactions were altered differently in distinct regions.