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Symptoms and signs of syncope: a review of the link between physiology and clinical clues


Brain. 2009 Oct;132(Pt 10):2630-42. doi: 10.1093/brain/awp179. Epub 2009 Jul 8.

Wieling W, Thijs RD, van Dijk N, Wilde AA, Benditt DG, van Dijk JG (Department of Internal Medicine, Academic Medical Centre/University of Amsterdam, Amsterdam, The Netherlands)


Detailed history taking is of paramount importance to establish a reliable diagnosis in patients with transient loss of consciousness. In this article the clinical symptoms and signs of the successive phases of a syncopal episode are reviewed. A failure of the systemic circulation to perfuse the brain sufficiently results in a stereotyped progression of neurological symptoms and signs culminating in loss of consciousness; when transient, this is syncope. Prior to loss of consciousness the affected individual tends to exhibit unclear thinking, followed by fixation of the eyes in the midline and a ‘frozen’ appearance. Narrowing of the field of vision with loss of colour vision (‘greying’ out) and finally a complete loss of vision (hence ‘blacking’ out) occurs. Hearing loss may occur following loss of vision. This process may take as little as approximately 7 s in cases of sudden complete circulatory arrest (e.g. abrupt asystole), but in other circumstances it may take longer depending on the rate and depth of cerebral hypoperfusion. Complete loss of consciousness occurs with the ‘turning up’ of the eyeballs. Profound cerebral hypoperfusion may be accompanied by myoclonic jerks.

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Neurological Aspects of Syncope and Orthostatic Intolerance


Medical Clinics of North America Volume 93, Issue 2, March 2009, Pages 427–449

Louis H. Weimer, MD, Pezhman Zadeh, MD (The Neurological Institute of New York, 710 West 168th Street, Unit 55, New York, NY 10032, USA)

Sudden falling with loss of consciousness from syncope and symptoms of orthostatic intolerance are common, dramatic clinical problems of diverse cause, but cerebral hypoperfusion is the ultimate mechanism in most. Cardiac, reflex, and orthostatic hypotension are important forms to consider. Syncope must be differentiated from seizures, psychiatric events, drop attacks, and other mimics. However, factors such as syncopal induced movements, ictal bradycardia, and insufficient clinical information can confound accurate diagnosis and hamper appropriate treatment. Progress in the diagnosis, treatment, and understanding of underlying mechanisms is continually advancing.

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Clinical outcome of generalized periodic epileptiform discharges on first EEG in patients with hypoxic encephalopathy postcardiac arrest


Epilepsy and Behavior, August 2015 Volume 49, Pages 268–272

A. Ribeiro, R. Singh, F. Brunnhuber (Department of Clinical Neurophysiology, King’s College Hospital, London, UK)



The EEG, alongside clinical examination, imaging studies, and SSEPs, is used to determine the prognosis following hypoxic encephalopathy postcardiac arrest. Generalized periodic epileptiform discharges (GPEDs) are recognized as a “malignant” EEG pattern associated with very poor outcome with previous studies reporting no or few survivors. We looked at our database of cardiac arrest patients who subsequently developed GPEDs to determine clinical outcome and profile any survivors.


We identified all cardiac arrest patients treated at King’s College Hospital between 2011–2014 who developed hypoxic encephalopathy associated with GPEDs, BiPLEDs (bilateral periodic lateralized epileptiform discharges), and periodic discharges on first EEG. We collected clinical data including age, gender, downtime, EEG reactivity, presence of seizures or myoclonus, and outcome. Survivors were defined as patients who were discharged from the hospital to home or a neurorehabilitation unit.


Thirty-six postcardiac arrest patients with hypoxic encephalopathy were identified, 24/36 with GPEDs, and 12/36 with BiPLEDs on first EEG. The mean age of patients was 62.8 ± 14.5 years old, with 27 males (75%) and 9 females (25%). Ten of thirty-six patients survived, which is slightly higher than previously reported. Statistical tests to compare clinical characteristics between survivors and nonsurvivors demonstrated no significant differences except for trend to significance for the presence of reactivity on first EEG (p = 0.0794). On discharge, one survivor had good functional outcome (and subsequently became independent), but all others were dependent for all ADLs (activities of daily living).


Generalized periodic epileptiform discharges carry a grave clinical prognosis following cardiac arrest. This study did identify a higher number of survivors compared to previous studies, but most were severely disabled at hospital discharge. Reactivity of the first EEG might predict better prognosis and merit further evaluation.

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Altitude and the Nervous System


Arch Neurol. 1998;55(7):1007-1009. doi:10.1001/archneur.55.7.1007.

Otto Appenzeller, MD, PhD

Traditionally, altitude research has been conducted by those who profess themselves to be physiologists, pulmonologists, cardiologists, and other general physicians. There are no eminent neurologists among altitude medicine researchers. This is likely a reflection of the comparatively recent establishment of the specialty of neurology. Nevertheless, the dependence of the brain on oxygen and hypoxia at high altitudes should long ago have attracted the attention of neurologists avowedly concerned with the function of the nervous system.

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The relationship between exercise intensity, cerebral oxygenation and cognitive performance in young adults


European Journal of Applied Physiology October 2015, Volume 115, Issue 10, pp 2189–2197

Saïd Mekari, Sarah Fraser, Laurent Bosquet, Clément Bonnéry, Véronique Labelle, Philippe Pouliot, Frédéric Lesage, Louis Bherer



To assess the relationship between exercise intensity, cerebral HbO2 and cognitive performance (Executive and non-Executive) in young adults.


We measured reaction time (RT) and accuracy, during a computerized Stroop task, in 19 young adults (7 males and 12 females). Their mean ± SD age, height, body mass and body mass index (BMI) were 24 ± 4 years, 1.67 ± 0.07 m, 72 ± 14 kg and 25 ± 3 kg m−2, respectively. Each subject performed the Stroop task at rest and during cycling at exercise of low intensity [40 % of peak power output (PPO)], moderate intensity (60 % of PPO) and high intensity (85 % of PPO). Cerebral oxygenation was monitored during the resting and exercise conditions over the prefrontal cortex (PFC) using near-infrared spectroscopy (NIRS).


High-intensity exercise slowed RT in both the Naming (p = 0.04) and the Executive condition (p = 0.04). The analysis also revealed that high-intensity exercise was associated with a decreased accuracy when compared to low-intensity exercise (p = 0.021). Neuroimaging results confirm a decrease of cerebral oxygenation during high-intensity exercise in comparison to low- (p = 0.004) and moderate-intensity exercise (p = 0.003). Correlations revealed that a lower cerebral HbO2 in the prefrontal cortex was associated with slower RT in the Executive condition only (p = 0.04, g = −0.72).


Results of the present study suggest that low to moderate exercise intensity does not alter Executive functioning, but that exercise impairs cognitive functions (Executive and non-Executive) when the physical workload becomes heavy. The cerebral HbO2 correlation suggests that a lower availability of HbO2 was associated with slower RT in the Executive condition only.

© Springer-Verlag Berlin Heidelberg 2015

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Explanations for coagulation activation after air travel


Journal of Thrombosis and Haemostasis Volume 8, Issue 5, pages 971–978, May 2010


Summary. Background: It is unknown whether venous thrombosis after long haul air travel is exclusively attributable to immobilization. Objectives: We determined whether the following mechanisms were involved: hypoxia, stress, inflammation or viral infection. Patients/Methods: In a case crossover setting in 71 healthy volunteers who were exposed to an 8-h flight, 8-h movie marathon and 8 h of regular activities, we compared markers for several hypothetical pathways: plasminogen activator inhibitor-1 (PAI-1), stress, plasma factor (F)VIII coagulant activity (FVIIIc), soluble P-selectine (sP-selectine), interleukin-8 (IL-8) and neutrophil elastase. We reported earlier an activated clotting system, as evidenced by thrombin generation, in 17% of volunteers after the flight. Results: PAI-1 increased by 4.2 ng mL−1 (CI95:−49.5 to 6.5) in volunteers with an activated clotting system whereas it decreased in those without (−20.0 ng mL−1, CI95:−33.2 to −14.0). FVIIIc levels rose more in individuals with clotting activation (18.0%, CI95:−1.0 to 33.0) than in those without (2.0%, CI95:−2.0 to 5.0). The increases in FVIIIc were not associated with stress, which appeared unrelated to clotting activation. sP-selectin increased in those with clotting activation (3.5 μg L−1, CI95: −3.0 to 10.0), but decreased in those without (−0.5 μg L−1, CI95: −2.0 to 2.0). Changes in levels of neutrophil elastase or IL-8 were not different between the subjects with and without clotting activation. Conclusions: Our results do not support the hypotheses that stress, infection or air pollution are involved in the development of a prothrombotic state in air travellers. After long haul air travel, this state is more pronounced in patients with risk factors and may be caused by hypoxia, triggering systemic inflammation and platelet activation, leading to coagulation induction and degranulation of platelets.

© 2010 International Society on Thrombosis and Haemostasis

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Acute combined central and peripheral nervous system demyelination in children


Pediatr Neurol. 2008 Nov;39(5):307-16. doi: 10.1016/j.pediatrneurol.2008.07.022.

Adamovic T, Riou EM, Bernard G, Vanasse M, Décarie JC, Poulin C, Gauvin F (Department of Paediatrics, Sainte-Justine Hospital, Université de Montréal, Montreal, Quebec, Canada)


Reports of acute combined central and peripheral nervous system acquired inflammatory demyelination are rare in children. This study aimed to (1) define the clinical features and prognoses of patients with this entity; and (2) compare these patients with children presenting isolated acute central or peripheral nervous system demyelination. A retrospective chart review of 523 children with central or peripheral nervous system demyelination hospitalized between 1993-2006 was undertaken. Among these, 93 fulfilled criteria (clinical features and positive magnetic resonance imaging or electromyography/nerve conduction studies) for either acute central (n = 37; 39.8%) or peripheral (n = 43; 46%) nervous system demyelination, or a combination of the two (n = 13; 14%). Significant differences between groups were evident for age (median, 10 versus 7 versus 11 years, respectively; P = 0.047), admission to pediatric intensive care unit (8% versus 30% versus 58%, respectively; P = 0.001), length of hospital stay (median, 8 versus 9 versus 29 days, respectively; P < 0.001), treatment with steroids (52% versus 7% versus 75%, respectively; P < 0.001) and immunoglobulins (11% versus 81% versus 75%, respectively; P < 0.001), and poor evolution (3% versus 12% versus 54%, respectively; P = 0.002). This entity in children is not rare, and has a poorer outcome than isolated central or peripheral nervous system demyelination. Assessment is needed for a better understanding of risk factors, etiologies, management, and prognosis.

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