JNS.jpgThe May issue of the Journal of the Neurological Sciences Vol 400 is now available online.


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Issue highlights

The multifactorial etiology of stroke-associated pneumonia

The occurrence of hospital-acquired pneumonia is the most common, feared complication after a stroke that impairs outcomes leading to death and disability.

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Evaluation of MS-related central fatigue using MR neuroimaging methods: Scoping review

A systematic literature search and of MRI-based studies assessing the pathophysiological mechanisms of MS-related central fatigue.

Fatigue is a common and debilitating symptom in multiple sclerosis (MS). Over the past decade, a growing body of research has focussed on the pathophysiological mechanisms underlying central (cognitive and physical) fatigue in MS.

The precise mechanisms causing fatigue in MS patients are complex and poorly understood, and may differ between patients. Advanced quantitative magnetic resonance imaging (MRI) techniques allow for objective assessment of disease pathology and have been used to characterise the pathophysiology of central fatigue in MS.

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The progress of neuronal autophagy in cerebral ischemia stroke: Mechanisms, roles and research methods

There is increasing evidence indicating that autophagy may be a new target in the treatment of ischemic stroke. Moderate autophagy can clear damaged organelles, thereby protecting cells against various injuries. However, long-term excessive autophagy brings redundant degradation of cell contents, leading to cell death and eventually serious damage to tissues and organs. A number of different animal models of ischemic brain injury show that autophagy is activated and involved in the regulation of neuronal death during ischemic brain injury.

This article summarizes the role of autophagy, its underlying regulators and mechanisms in ischemic neuronal injury. We briefly introduce the relationship between apoptosis and autophagy and give a summary of research methods and modulators of autophagy.

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Mitochondrial metabolic stroke: Phenotype and genetics of stroke-like episodes

Stroke-like episodes (SLEs) are the hallmark of mitochondrial encephalopathy with lactic acidosis and stroke-like episode (MELAS) syndrome but rarely occur also in other specific or nonspecific mitochondrial disorders. Pathophysiologically, SLLs are most likely due to a regional disruption of the blood-brain barrier triggered by the underlying metabolic defect, epileptic activity, drugs, or other factors.

SLEs manifest clinically with a plethora of cerebral manifestations, which not only include features typically seen in ischemic stroke, but also headache, epilepsy, ataxia, visual impairment, vomiting, and psychiatric abnormalities. The morphological correlate of an SLE is the stroke-like lesion (SLL), best visualised on multimodal MRI.

In the acute stages, an SLL presents as vasogenic edema but may be mixed up with cytotoxic components. Additionally, SLLs are characterized by hyperperfusion on perfusion studies.

In the chronic stage, SLLs present with a colourful picture before they completely disappear, or end up as white matter lesion, cyst, laminar cortical necrosis, focal atrophy, or as toenail sign. Treatment of SLLs is symptomatic and relies on recommendations by experts. Beneficial effects have been reported with nitric-oxide precursors, antiepileptic drugs, antioxidants, the ketogenic diet, and steroids. A lot of research is still needed to uncover the enigma SLE/SLL.