Livros: "Cerebral ischaemia"

1

Bories, Jacques, ed. Cerebral Ischaemia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2.

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2

Loddick, Sarah Ann. The role of interleukin-1 in cerebral ischaemia. Manchester: University of Manchester, 1996.

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3

Nelson, Rachael M. Cellular effects of cerebral ischaemia in vitro: Cerebroprotective actions of GABAmimetic agents. Leicester: De Montfort University, 2002.

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4

Smith, T. C. G. 1939-, ed. Ischaemia in head injury: 10th European Congress of Neurosurgery, Berlin 1995 ; proceedings of a special symposium. Berlin: Springer, 1996.

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5

Kramer, G., W. Hacke, H. J. Gelmers e M. Hennerici. Cerebral Ischaemia. Springer-Verlag Berlin and Heidelberg GmbH & Co. K, 1991.

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6

Krieglstein, Josef. Pharmacology of Cerebral Ischaemia. Elsevier, 1986.

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7

Cerebral Ischaemia: A Neuroradiological Study. Springer, 2011.

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8

Jacques, Bories, e Aymard A, eds. Cerebral ischaemia: A neuroradiological study. Berlin: Springer-Verlag, 1985.

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9

Alarcón, Gonzalo, Marian Lazaro e Antonio Valentín. Migraine, stroke, and cerebral ischaemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0033.

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This chapter reviews the electroencephalographic changes associated with migraine, stroke and cerebral ischaemia, and their interpretation to aid in their differential diagnosis. The incidence of stroke and cerebral ischaemia is increasing with population aging. They are some of the most common problems faced in emergency medicine, and their diagnosis can be puzzling. This chapter describes and illustrates the patterns seen in such conditions, such as slowing, frontal intermittent delta activity (FIRDA), periodic lateralized epileptiform discharge (PLED), generalized periodic lateralized epileptiform discharge (GPED), and bilateral periodic lateralized epileptiform discharge (BiPED). The chapter reviews their prognostic value in critical care medicine and their differential diagnosis with status epilepticus.

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10

R, Caplan Louis, ed. Cerebrovascular ischaemia investigation and management. London: Med-Orion, 1996.

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11

Nicolaides, Andrew N., Wesley S. Moore, Louis R. Caplan e Edward G. Shifrin. Cerebrovascular Ischaemia: Investigation and Management. Med-Orion Publishing Co Ltd, 1996.

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12

(Editor), Richard C. Green, Alan J. Cross (Editor), Ronald J. Bradley (Series Editor), Robert Adron Harris (Series Editor) e Peter Jenner (Series Editor), eds. Neuroprotective Agents and Cerebral Ischaemia, Volume 40 (International Review of Neurobiology.). Academic Press, 1996.

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13

(Editor), Richard C. Green, Alan J. Cross (Editor), Ronald J. Bradley (Series Editor), Robert Adron Harris (Series Editor) e Peter Jenner (Series Editor), eds. Neuroprotective Agents and Cerebral Ischaemia, Volume 40 (International Review of Neurobiology.). Academic Press, 1996.

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14

Bories, Jacques. Cerebral Ischaemia: A Neuroradiological Study (Neuroradiobiology, Monograph No 6, Vol 27). Springer, 1986.

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15

Gaddam, Samson Sujit Kumar, e Claudia S. Robertson. Cerebral blood flow and perfusion monitoring in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0222.

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Prevention of secondary cerebral ischaemic insults is an important management strategy in acute neurological conditions. Monitoring of cerebral perfusion may aid in early identification of ischaemic insults and help with management. A number of tools are available for this purpose. Cerebral perfusion pressure (CPP) is the simplest assessment of cerebral perfusion, but in some cases ischaemia can be present even with a normal CPP. Cerebral blood flow (CBF) imaging, either with computed tomography or magnetic resonance imaging techniques, can provide quantitative regional CBF measurement, but only at a single instance in time. Such studies are valuable in the diagnosis of ischaemia, but are difficult for the management of critically-ill patients. CBF can also be measured within the intensive care unit (ICU), either directly or indirectly through the measurement of cerebral oxygenation. These monitors provide a more continuous measure of CBF, and are more useful in assessing response to treatment. Some of the ICU tools monitor global perfusion and some assess perfusion only in a local area of brain surrounding the monitor. With local monitors, the location of the probe is important for interpretation of the findings.

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16

(Editor), Richard C. Green, Alan J. Cross (Editor), Ronald J. Bradley (Series Editor), Robert Adron Harris (Series Editor) e Peter Jenner (Series Editor), eds. Intl Reveiw of Neurobiology: Neuroprotective Agents & Cerebral Ischaemia, Volume 40 (International Review of Neurobiology). Academic Press, 1997.

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17

(Editor), Richard C. Green, Alan J. Cross (Editor), Ronald J. Bradley (Series Editor), Robert Adron Harris (Series Editor) e Peter Jenner (Series Editor), eds. Intl Reveiw of Neurobiology: Neuroprotective Agents & Cerebral Ischaemia, Volume 40 (International Review of Neurobiology). Academic Press, 1997.

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18

Rothwell, Peter. Cerebrovascular diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0767.

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This chapter is concerned with those diseases of the cerebral and ocular circulation that cause ischaemia or infarction of the brain and eye or spontaneous haemorrhage into or around the brain. The main clinical manifestations of these diseases are transient ischaemic attack and stroke.

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19

Aisiku, Imoigele, e Claudia S. Robertson. Epidemiology and pathophysiology of traumatic brain injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0341.

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Although medical management of traumatic brain injury (TBI) may have improved in developed countries, TBI is still a major cause of mortality and morbidity. The demographics are skewed towards the younger patient population, and affects males more than females, but in general follow a bimodal distribution with peaks affecting young adults and the elderly. As a result, the loss of functional years is devastating. Pathology due to brain trauma is a complex two-hit phenomenon, frequently divided into ‘primary’ and ‘secondary’ injury. Hypoxia, ischaemia, and inflammation all play a role, and the importance of each component varies between patients and in an individual patient over time. The initial injury may increase intracranial pressure and reduce cerebral perfusion due to the presence of mass lesions or diffuse brain swelling. Further secondary insults, such as hypotension, reduced cerebral perfusion pressure, hypoxia, or fever may exacerbate swelling and inflammation, and further compromise cerebral perfusion. Although there are currently no specific effective treatments for TBI, an improved understanding of the pathophysiology may eventually lead to treatments that will reduce mortality and improve long-term functional outcome.

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20

Vespa, Paul M. Electroencephalogram monitoring in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0221.

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Electroencephalography monitoring provides a method for monitoring brain function, which can complement other forms of monitoring, such as monitoring of intracranial pressure and derived parameters, such as cerebral perfusion pressure. Continuous electroencephalogram (EEG) monitoring can be helpful in seizure detection after brain injury and coma. Seizures can be detected by visual inspection of the raw EEG and/or processed EEG data. Treatment of status epilepticus can be improved by rapid identification and abolition of seizures using continuous EEG. Quantitative EEG can also be used to detect brain ischaemia and seizures, to monitor sedation and aid prognosis.

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21

Leys, Didier, Charlotte Cordonnier e Valeria Caso. Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0067_update_002.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, mechanical thrombectomy in case of proximal occlusion (middle cerebral artery, intracranial internal carotid artery, basilar artery), on top of thrombolysis in the absence of contraindication or alone otherwise, aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, while surgery does not seem effective to reduce death and disability.

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22

Bleck, Thomas P. Pathophysiology and causes of seizures. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0231.

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Seizures result from imbalances between excitation and inhibition, and between neuronal synchrony and dyssynchrony. Current models implicate the cerebral cortex in the genesis of seizures, although thalamic mechanisms (particularly the thalamic reticular formation) are involved in the synchronization of cortical neurons. Often, the precipitants of a seizure in the critical care setting are pharmacological. Several mechanisms linked to critical illness can lead to seizures. Failure to remove glutamate and potassium from the extracellular space, functions performed predominantly by astrocytes, occurs in trauma, hypoxia, ischaemia, and hypoglycaemia. Loss of normal inhibition occurs during withdrawal from alcohol and other hypnosedative agents, or in the presence of GABA. Conditions such as cerebral trauma, haemorrhages, abscesses, and neoplasms all produce physical distortions of the adjacent neurons, astrocytes, and the extracellular space. Deposition of iron in the cortex from the breakdown of haemoglobin appears particularly epileptogenic. Although acute metabolic disturbances can commonly produce seizures in critically-ill patients, an underlying and potentially treatable structural lesion must always be considered and excluded.

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23

Magalhaes, Eric, Angelo Polito, Andréa Polito e Tarek Sharshar. Sepsis-Associated Encephalopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0032.

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Brain dysfunction is a major complication of sepsis and is characterized by alteration of consciousness, ranging from delirium to coma and marked electroencephalographic changes. It reflects a constellation of dynamic biological mechanisms, including neurotransmitter imbalance, macro- and microcirculatory dysfunction resulting in ischaemia, endothelial activation, alteration of the blood-brain barrier impairment with passage of neurotoxic mediators, activation of microglial cells within the central nervous system, cumulatively resulting in a neuroinflammatory state. Sepsis-associated brain dysfunction is associated with increased mortality and long-term cognitive decline, whose mechanisms might include microglial activation, axonopathy, or cerebral microinfarction. There is no specific treatment, other than the management of the underlying septic source, correction of physiological and metabolic abnormalities, and limiting the use of medications with neurotoxic effects.

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24

Markus, Hugh, Anthony Pereira e Geoffrey Cloud. Cerebral haemorrhage. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737889.003.0013.

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This chapter covers the several types of cerebral haemorrhage: extradural, subdural, subarachnoid, and intracerebral. Subarachnoid haemorrhage (SAH) is an important cause of neurological disability and mortality, although only occasionally present with focal stroke symptoms. Intracerebral haemorrhage usually presents with a stroke, which can only be reliably distinguished from ischaemic stroke by brain imaging. The chapter discusses the diagnosis, investigation, and management of both SAH and intracerebral haemorrhage.

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25

Leys, Didier, Charlotte Cordonnier e Valeria Caso. Stroke. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0067.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, otherwise aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, but surgery does not seem effective to reduce death and disability.

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26

Leys, Didier, Charlotte Cordonnier e Valeria Caso. Stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0067_update_001.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, otherwise aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, but surgery does not seem effective to reduce death and disability.

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27

Patarroyo, Sully Xiomara Fuentes, e Craig Anderson. Management of ischaemic stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0236.

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Ischaemic stroke is the most common cause of stroke around the world. It is a complex disease with a range of causes, manifestations, outcomes, and treatments. As the therapeutic time window to rescue or ‘protect’ the brain from ischaemic damage is extremely short, effective treatment requires coordinated systems of care, which commence in the prehospital paramedical setting and continue through the emergency department into the critical care environment, neurology ward, rehabilitation, and re-settlement back home. Successful outcomes from ischaemic stroke can be achieved through the effective use of thrombolytic therapy to re-canalize an occluded vessel and re-perfuse the ‘at risk’ area of the brain. Other aspects of management include the prevention of complications of the neurological (cerebral) disability, timely introduction of rehabilitation, realistic goal-setting towards satisfactory recovery, and secondary prevention measures to reduce the high risk of recurrent stroke and other serious vascular events.

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28

Transient Ischaemic Attacks of the Brain and Eye. W.B. Saunders Company, 1994.

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29

Levine, Steven R., e Seemant Chaturvedi. Transient Ischemic Attacks. Wiley & Sons, Incorporated, John, 2008.

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30

Levine, Steven R., e Seemant Chaturvedi. Transient Ischemic Attacks. Wiley & Sons, Incorporated, John, 2008.

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31

Seemant, Chaturvedi, e Levine Steven R, eds. Transient ischemic attacks. Malden, Mass: Blackwell Futura, 2004.

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32

De Deyne, Cathy, Ward Eertmans e Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0016_update_001.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables—with possible impact on optimal cerebral perfusion/oxygenation—such as invasive arterial blood pressure monitoring or arterial blood gas analysis.

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33

De Deyne, Cathy, e Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0016.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables such as invasive arterial blood pressure monitoring or arterial blood gas analysis.

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34

Ferioli, Simona, e Lori Shutter. Normal anatomy and physiology of the brain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0219.

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An understanding of the normal anatomy of the brain is essential to the diagnosis of a number of conditions that may be encountered in patients in the intensive care unit (ICU). Common structural cerebral conditions causing patients to be admitted to the ICU include cerebral trauma (traumatic brain injury), cerebrovascular accidents (both ischaemic and haemorrhagic), and infections. Cerebral conditions with a structural basis occurring after admission to the ICU are not as common as functional abnormalities, such as delirium, and peripheral complications, such as critical illness neuropathy and myopathy. An understanding of brain physiology, in particular factors that control or influence intracranial pressure (ICP) and cerebral blood flow (CBF) underpin much of the theory behind the management of acute brain injuries and syndromes.

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35

J, Reulen H., Philippon Jacques e European Association of Neurosurgical Societies. Meeting, eds. Prevention and treatment of delayed ischaemic dysfunction in patients with subarachnoid haemorrhage: An update. Wien: Springer-Verlag, 1988.

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36

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson e David Ledingham. Cerebrovascular disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0004.

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This chapter on cerebrovascular disease discusses the evidence-based management of acute stroke, transient ischaemic attacks (TIAs), and secondary stroke prevention (antiplatelet therapy, risk factor modification, atrial fibrillation (AF), carotid and vertebral artery dissection, and symptomatic carotid artery disease). Drug treatment of intracerebral haemorrhage, subarachnoid haemorrhage, and cerebral venous sinus thrombosis are also discussed.

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37

Saeed, Sahrai, e Eva Gerdts. Echocardiography. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0010.

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Current guidelines recommend extensive cardiovascular imaging in patients who experience ischaemic stroke or a transient ischaemic attack to prevent recurrent stroke. High-quality echocardiography is crucial for detection of the wide range of cardiac and proximal aortic conditions that can predispose to cerebral embolism. These conditions may be classified as major, minor, or uncertain risk sources of embolism. Although both transthoracic (TTE) and transoesophageal echocardiography (TOE) have substantial clinical utility in patients with cryptogenic stroke, these methods offer complementary information. TOE is typically used for assessment of defects in the atrial septum or detection of thrombus in the left atrial appendage. In contrast, TTE is the recommended method for assessment of cardiac chamber structure and function, and valvular disease. Furthermore, assessment of aortic stiffness and electrocardiography may offer additional insight to cardiac function. This chapter gives an overview of the use of echocardiography in ischaemic stroke patients.

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38

Haunton, Victoria, Aung Sett, Amit Mistri e Martin Fotherby. Stroke. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0227.

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The World Health Organization defines stroke as ‘a clinical syndrome consisting of rapidly developing clinical signs of focal (at times global) disturbance of cerebral function lasting greater than 24 hours (or leading to death) with no apparent cause other than that of vascular origin’. Transient ischaemic attack (TIA) is defined as a rapid presentation of neurological deficit with complete recovery within 24 hours of the onset of symptoms. However, the 24-hour cut-off is arbitrary, has no biological basis, and is of limited use clinically. A shorter duration is now regarded as more appropriate, although it has yet to be universally accepted. In clinical practice, stroke and TIA are best thought of as comprising a continuum, as they have similar pathological mechanisms, etiologies, and management strategies. While subarachnoid haemorrhage is a type of stroke based on the above definition, it is not covered in this chapter, as its pathophysiology, clinical manifestations, and management are distinct from those for ischaemic stroke and haemorrhagic stroke.

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39

Morrison, Karen. Prevention of cerebrovascular disease. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0348.

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Stroke is the main cause of neurological morbidity in adults and the third most common cause of death worldwide after ischaemic heart disease and cancer (all forms combined). It is more common in older people, with three-quarters of strokes occurring in people over 65 years of age, and estimates are that overall stroke morbidity will double by the early 2020s. The worldwide figure of increasing incidence of stroke detection masks the fact that mortality from stroke has actually been falling in developed countries since the latter half of the twentieth century while the mortality has continued to rise in China, Asia, and eastern Europe. This chapter discusses prevention of cerebrovascular disease, and includes strategies to reduce the risk of thromboembolic stroke and cerebral haemorrhage.

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40

Koutroumanidis, Michalis, e Robin Howard. Encephalopathy, central nervous system infections, and coma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0032.

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This chapter provides an overview of the indications for and the diagnostic and prognostic value of acute video-electroencephalogram (EEG) and continuous video-EEG monitoring in patients with encephalopathies, encephalitides, and coma. Particular emphasis is placed on the detection of non-convulsive seizures and non-convulsive status epilepticus secondary to acute and sub-acute cerebral insults, including post-cardiac arrest hypoxic-ischaemic brain injury, and on the related pitfalls and uncertainties. It also discusses key technical aspects of the EEG recording, including artefact identification and limitation, timing and type of external stimulation and assessment of EEG reactivity, and highlights the main relevant pitfalls. Finally, it explores the role of evoked potentials (EPs) in outcome prediction and the value of Cognitive EPs and quantitative EEG in the assessment of chronic disorders of consciousness.

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41

Henzi, Bettina, e Maja Steinlin. Stroke in children. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0013.

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Stroke in children is a rare, but terrifying disease and its lifelong sequelae weigh heavy on patients and families. It is also increasingly recognized as a socioeconomic burden, ongoing for many years after the acute manifestation. There is a significant delay in diagnosis of childhood stroke. This is caused by several factors: lack of awareness among the public and professionals, childhood-specific manifestations, numerous stroke mimics, and last but not least, limited access to emergency neuroimaging for children. Fast stroke recognition tools need adaption to the special needs in children. Childhood arterial ischaemic stroke differs in aetiology from adult stroke with cerebral vasculopathies being the leading cause and cardioembolic aetiology ranking second. However, treatment guidelines are largely based on adult guidelines and expert consensus. Future research has to put emphasis on understanding pathophysiology, defining specific treatment options, and providing evidence for treatment guidelines in paediatric stroke.

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