SwePub - sökning: WFRF:(Killer C)

Numrering	Referens	Omslagsbild	Hitta
1.	Dinklage, A, et al. (författare) Magnetic configuration effects on the Wendelstein 7-X stellarator 2018 Ingår i: NATURE PHYSICS. - 1745-2473. ; 14:8, s. 855- Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
2.	Nogueira, RG, et al. (författare) Global Impact of COVID-19 on Stroke Care and IV Thrombolysis 2021 Ingår i: Neurology. - 1526-632X. ; 96:23, s. E2824-E2838 Tidskriftsartikel (refereegranskat)
3.	Pircher, Achmed, et al. (författare) Elevated perioptic lipocalin-type prostaglandin D synthase concentration in patients with idiopathic intracranial hypertension 2022 Ingår i: Brain Communications. - : Oxford University Press. - 2632-1297. ; 4:5 Tidskriftsartikel (refereegranskat)abstract Pircher et al. report significant higher concentrations of lipocalin-type prostaglandin D synthase in the perioptic subarachnoid space compared with the lumbar subarachnoid space. These findings indicate that next to cerebrospinal fluid pressure gradients, biochemical gradients might play a role in the pathophysiology of optic nerve damage in idiopathic intracranial hypertension. The pathophysiology of vision loss and loss of visual field in patients with idiopathic intracranial hypertension with papilloedema is not fully understood. Although elevated CSF pressure induces damage to the optic nerve due to stasis of axoplasmic flow, there is no clear relationship between the severity of papilloedema and CSF pressure. Furthermore, there are cases of purely unilateral papilloedema and cases without papilloedema despite significantly elevated intracranial pressure as well as papilloedema that can persist despite a successfully lowered intracranial pressure. We hypothesize that at least in some of such cases, in addition to purely pressure-induced damage to the optic nerve, the biochemical composition of the CSF in the subarachnoid space surrounding the orbital optic nerve may play a role in the pathogenesis of vision loss. In this retrospective study, we report on lipocalin-type prostaglandin D synthase concentrations in the CSF within the perioptic and lumbar subarachnoid space in 14 patients with idiopathic intracranial hypertension (13 females, mean age 45 +/- 13 years) with chronic persistent papilloedema resistant to maximum-tolerated medical therapy and visual impairment. CSF was collected from the subarachnoid space of the optic nerve during optic nerve sheath fenestration and from the lumbar subarachnoid space at the time of lumbar puncture. CSF was analysed for lipocalin-type prostaglandin D synthase and the concentrations compared between the two sites using nephelometry. The mean lipocalin-type prostaglandin D synthase concentration in the perioptic subarachnoid space was significantly higher compared with the concentration in the lumbar subarachnoid space (69 +/- 51 mg/l without correction of serum contamination and 89 +/- 67 mg/l after correction of serum contamination versus 23 +/- 8 mg/l; P < 0.0001, Mann-Whitney U-test). These measurements demonstrate a change and imbalance in the biochemical environment of the optic nerve. Its possible effect is discussed.

Pircher, Achmed, et al. (författare)
Elevated perioptic lipocalin-type prostaglandin D synthase concentration in patients with idiopathic intracranial hypertension
2022
Ingår i: Brain Communications. - : Oxford University Press. - 2632-1297. ; 4:5
Tidskriftsartikel (refereegranskat)abstract
- Pircher et al. report significant higher concentrations of lipocalin-type prostaglandin D synthase in the perioptic subarachnoid space compared with the lumbar subarachnoid space. These findings indicate that next to cerebrospinal fluid pressure gradients, biochemical gradients might play a role in the pathophysiology of optic nerve damage in idiopathic intracranial hypertension. The pathophysiology of vision loss and loss of visual field in patients with idiopathic intracranial hypertension with papilloedema is not fully understood. Although elevated CSF pressure induces damage to the optic nerve due to stasis of axoplasmic flow, there is no clear relationship between the severity of papilloedema and CSF pressure. Furthermore, there are cases of purely unilateral papilloedema and cases without papilloedema despite significantly elevated intracranial pressure as well as papilloedema that can persist despite a successfully lowered intracranial pressure. We hypothesize that at least in some of such cases, in addition to purely pressure-induced damage to the optic nerve, the biochemical composition of the CSF in the subarachnoid space surrounding the orbital optic nerve may play a role in the pathogenesis of vision loss. In this retrospective study, we report on lipocalin-type prostaglandin D synthase concentrations in the CSF within the perioptic and lumbar subarachnoid space in 14 patients with idiopathic intracranial hypertension (13 females, mean age 45 +/- 13 years) with chronic persistent papilloedema resistant to maximum-tolerated medical therapy and visual impairment. CSF was collected from the subarachnoid space of the optic nerve during optic nerve sheath fenestration and from the lumbar subarachnoid space at the time of lumbar puncture. CSF was analysed for lipocalin-type prostaglandin D synthase and the concentrations compared between the two sites using nephelometry. The mean lipocalin-type prostaglandin D synthase concentration in the perioptic subarachnoid space was significantly higher compared with the concentration in the lumbar subarachnoid space (69 +/- 51 mg/l without correction of serum contamination and 89 +/- 67 mg/l after correction of serum contamination versus 23 +/- 8 mg/l; P < 0.0001, Mann-Whitney U-test). These measurements demonstrate a change and imbalance in the biochemical environment of the optic nerve. Its possible effect is discussed.

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