Lancet neurology
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Almost two decades have elapsed since posterior reversible encephalopathy syndrome (PRES) was described in an influential case series. This usually reversible clinical syndrome is becoming increasingly recognised, in large part because of improved and more readily available brain imaging. Although the pathophysiological changes underlying PRES are not fully understood, endothelial dysfunction is a key factor. ⋯ The range of symptoms that can comprise the syndrome might be broader than usually thought. In its mild form, this disorder might cause only one clinical symptom (headache or seizure) and radiographically might show few areas of vasogenic oedema or even normal brain imaging in some rare cases. In severe forms, PRES might cause substantial morbidity and even mortality, most often as a result of acute haemorrhage or massive posterior fossa oedema causing obstructive hydrocephalus or brainstem compression.
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Seizures are often the key manifestation of neurological diseases caused by pathogenic mutations in 169 of the genes that have so far been identified to affect mitochondrial function. Mitochondria are the main producers of ATP needed for normal electrical activities of neurons and synaptic transmission. Additionally, they have a central role in neurotransmitter synthesis, calcium homoeostasis, redox signalling, production and modulation of reactive oxygen species, and neuronal death. ⋯ Seizures, irrespective of their origin, represent an excessive acute energy demand in the brain. Accordingly, secondary mitochondrial dysfunction has been described in various epileptic disorders, including disorders that are mainly of non-mitochondrial origin. An understanding of the reciprocal relation between mitochondrial dysfunction and epilepsy is crucial to select appropriate anticonvulsant treatment and has the potential to open up new therapeutic approaches in the subset of epileptic disorders caused by mitochondrial dysfunction.
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A third of transient ischaemic attacks (TIAs) and ischaemic strokes are of undetermined cause (ie, cryptogenic), potentially undermining secondary prevention. If these events are due to occult atheroma, the risk-factor profile and coronary prognosis should resemble that of overt large artery events. If they have a cardioembolic cause, the risk of future cardioembolic events should be increased. We aimed to assess the burden, outcome, risk factors, and long-term prognosis of cryptogenic TIA and stroke. ⋯ Wellcome Trust, Wolfson Foundation, UK Stroke Association, British Heart Foundation, Dunhill Medical Trust, National Institute for Health Research, Medical Research Council, and the NIHR Oxford Biomedical Research Centre.