1. |
- Bockhop, Fabian, et al.
(author)
-
Measurement invariance of six language versions of the post-traumatic stress disorder checklist for DSM-5 in civilians after traumatic brain injury
- 2022
-
In: Scientific Reports. - : Springer Nature. - 2045-2322. ; 12:1
-
Journal article (peer-reviewed)abstract
- Traumatic brain injury (TBI) is frequently associated with neuropsychiatric impairments such as symptoms of post-traumatic stress disorder (PTSD), which can be screened using self-report instruments such as the Post-Traumatic Stress Disorder Checklist for DSM-5 (PCL-5). The current study aims to inspect the factorial validity and cross-linguistic equivalence of the PCL-5 in individuals after TBI with differential severity. Data for six language groups (n ≥ 200; Dutch, English, Finnish, Italian, Norwegian, Spanish) were extracted from the CENTER-TBI study database. Factorial validity of PTSD was evaluated using confirmatory factor analyses (CFA), and compared between four concurrent structural models. A multi-group CFA approach was utilized to investigate the measurement invariance (MI) of the PCL-5 across languages. All structural models showed satisfactory goodness-of-fit with small between-model variation. The original DSM-5 model for PTSD provided solid evidence of MI across the language groups. The current study underlines the validity of the clinical DSM-5 conceptualization of PTSD and demonstrates the comparability of PCL-5 symptom scores between language versions in individuals after TBI. Future studies should apply MI methods to other sociodemographic (e.g., age, gender) and injury-related (e.g., TBI severity) characteristics to improve the monitoring and clinical care of individuals suffering from PTSD symptoms after TBI.
|
|
2. |
- Kondziella, Daniel, 1976, et al.
(author)
-
B-type natriuretic peptide plasma levels are elevated in subcortical vascular dementia.
- 2009
-
In: Neuroreport. - 1473-558X. ; 20:9, s. 825-7
-
Journal article (peer-reviewed)abstract
- High levels of B-type natriuretic peptide (BNP), a serum marker of congestive heart failure, are associated with an increased risk for cognitive decline. However, no study has yet assessed this marker in different subtypes of dementia. We tested the hypothesis that BNP has a more significant association with vascular dementia than Alzheimer disease. Plasma BNP was measured in 15 patients with subcortical vascular dementia, in 19 Alzheimer patients without evidence of vascular comorbidity, and in age-matched controls. Compared with controls (28+/-7 ng/l), BNP was elevated in subcortical vascular dementia (63+/-17 ng/l; P=0.03), but not in Alzheimer disease (36+/-5 ng/l). In conclusion, subcortical vascular dementia is indeed associated with moderately elevated BNP levels, whereas this could not be shown for Alzheimer disease. This probably reflects the larger cardiovascular burden in patients with subcortical vascular dementia.
|
|
3. |
- Kondziella, Daniel, 1976, et al.
(author)
-
Brain metabolism in adult chronic hydrocephalus.
- 2008
-
In: Journal of neurochemistry. - : Wiley. - 1471-4159 .- 0022-3042. ; 106:4, s. 1515-24
-
Journal article (peer-reviewed)abstract
- Normal pressure hydrocephalus (NPH) is the most frequent form of chronic hydrocephalus in adults. NPH remains underdiagnosed although between 5% and 10% of all demented patients may suffer from this disorder. As dementia is an increasing demographic problem, treatable forms such as in NPH have become a central issue in neurology. Despite the traditional perception of hydrocephalus being a disorder of disturbed CSF dynamics, in NPH metabolic impairment seems at least as important. So far, the only valid animal model of NPH is chronic adult kaolin hydrocephalus. In this model, opening of alternative CSF outflow pathways leads to normal or near-normal intracranial pressure and CSF outflow resistance. Yet, various metabolic disturbances cause ongoing ventricular enlargement and characteristic symptoms including cognitive decline and gait ataxia. Delayed hippocampal neuronal death, accumulation of beta-amyloid and disturbed cholinergic neurotransmission may contribute to memory dysfunction. Compromised periventricular blood flow, decreased dopamine levels in the substantia nigra and damaged striatal GABAergic interneurons may reflect basal ganglia symptoms. At least in human hydrocephalus cerebrovascular co-morbidity of the white matter plays an important role as well. It seems that in hydrocephalus from a certain 'point of no return' metabolic impairment becomes decoupled from CSF dynamics and, at least partly, self-sustained. This is probably the reason why despite restored CSF circulation by shunting many patients with chronic hydrocephalus still suffer from severe neurological deficits. The present paper offers a comprehensive review of the experimental and clinical data suggesting metabolic disturbances in chronic hydrocephalus.
|
|
4. |
- Kondziella, Daniel, 1976, et al.
(author)
-
Choreathetosis due to abuse of levothyroxine.
- 2009
-
In: Journal of neurology. - : Springer Science and Business Media LLC. - 1432-1459 .- 0340-5354. ; 256:12, s. 2106-8
-
Journal article (peer-reviewed)abstract
- Choreathetosis due to thyrotoxicosis is a rare movement disorder of acute onset. Here we present the first report of choreathetosis secondary to abuse of levothyroxine. A 35-year-old woman with autoimmune thyroiditis tripled her daily levothyroxine intake and lost 20 kg of weight during the following 6 months. She soon developed incapacitating choreathetosis. When levothyroxine was reduced to her usual dosage, all symptoms vanished in 7 days. The prompt effect of dose correction points towards a direct influence of levothyroxine on the basal ganglia; alternatively, the effects of levothyroxine might have been indirect and, possibly, autoimmune-mediated. Abuse of levothyroxine and related thyroid-tropic substances should be included into the differential diagnosis of acute choreathetosis.
|
|
5. |
|
|
6. |
|
|
7. |
- Kondziella, Daniel, 1976, et al.
(author)
-
Hyperphosphorylation of tau protein in superficial CNS siderosis.
- 2008
-
In: Journal of the neurological sciences. - : Elsevier BV. - 0022-510X. ; 273:1-2, s. 130-2
-
Journal article (peer-reviewed)abstract
- In superficial CNS siderosis chronic subarachnoidal hemorrhage leads to hemosiderin deposits in the subpial layers of the brain and spinal cord. Many years usually pass between the initial event causing chronic bleedings and the development of cerebellar ataxia, sensory hearing loss and various sensorimotor deficits. The only therapeutic option is to identify and eliminate the bleeding source. Otherwise slow relentless decline to a bedridden state and dementia is usually unavoidable. However, it is not known how precisely leptomeningeal hemosiderin deposits induce progressive neurodegeneration. Here we present the first report of a patient with superficial CNS siderosis in whom cerebrospinal fluid biomarkers of brain damage were assessed. Levels of neurofilament light protein, glial fibrillary acidic protein, total tau protein and, most importantly, hyperphosphorylated tau protein were increased. The results indicate that in superficial CNS siderosis neurodegeneration may be secondary to iron toxicity and oxidative stress. Similar mechanisms have been suggested for other neurodegenerative disorders such as Alzheimer's disease.
|
|
8. |
- Kondziella, Daniel, 1976, et al.
(author)
-
Hypertension in spontaneously hypertensive rats occurs despite low plasma levels of homocysteine
- 2008
-
In: Physiological Research. - 0862-8408. ; 57:3, s. 487-490
-
Journal article (peer-reviewed)abstract
- Hyperhomocysteinemia has been suggested to induce hypertension due to its role in endothelial dysfunction. However, it remains controversial whether homocysteine and hypertension are truly causally related or merely loosely associated. To test the hypothesis that hyperhomocysteinemia occurs in Spontaneously Hypertensive Rats (SHR) we measured plasma levels of homocysteine in 10 male adult SHR and in 10 normotensive controls using Ion Exchange Chromatography. In addition, plasma concentrations of the 22 most common amino acids were measured to explore the relation of homocysteine with amino acid metabolism. Plasma levels of homocysteine were significantly lower in SHR (4.1 micromol/L +/-0.1) than in controls (7.2 micromol/L +/- 0.3; p<0.00001). The amounts of aminobutyric acid (ABU), alanine, citrulline and valine were decreased as well, whereas we found increased levels of aspartate, glutamate, glutamine, histidine and ornithine. Thus, contrary to our hypothesis, hypertension in SHR occurs despite low plasma levels of homocysteine. We provide a new hypothesis whereby reduced conversion of arginine to citrulline is related to increased ornithine levels, but decreased bioavailability of nitric oxide, resulting in impaired blood vessel relaxation and hypertension. In conclusion, our findings do not necessarily exclude that homocysteine and hypertension might be pathophysiologically connected, but corroborate the notion that hypertension can arise due to mechanisms independent of high homocysteine levels.
|
|
9. |
|
|
10. |
|
|
11. |
|
|
12. |
- Strandberg, Joakim, 1978, et al.
(author)
-
Ketogenic diet does not disturb neurogenesis in the dentate gyrus in rats
- 2008
-
In: Neuroreport. - 0959-4965. ; 19:12, s. 1235-1237
-
Journal article (peer-reviewed)abstract
- The ketogenic diet, a high-fat diet, is a therapeutic alternative in the treatment of refractory epilepsy, especially in children. However, there are concerns that a high-fat diet may influence the normal development of the central nervous system and cognition. In this study we investigated the influence of ketogenic diet on adult neurogenesis in the dentate gyrus. Rats were provided with either a high-fat diet (80% fat) or a standard rat diet (5% fat) ad libitum for 4 weeks. In both female and male rats, the amounts of bromodeoxyuridine immunoreactive cells in the dentate gyrus were the same in the different groups. Our results suggest that the ketogenic diet does not disturb the neurogenesis in the rat dentate gyrus.
|
|
13. |
|
|