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Books on the topic 'Brain metabolic disorders'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Neurochemistry of metabolic diseases: Lysosomal storage diseases, phenylketonuria, and Canavan disease. Nova Science Publishers, 2012.

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2

Philpott, William H. Brain allergies: The psychonutrient connection : including Brain allergies today, an update. Keats Pub., 1987.

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3

A, Horrocks Lloyd, ed. Glycerophospholipids in the brain: Phospholipases A2 in neurological disorders. Springer, 2007.

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4

Kollegger, Harald. Excitatory amino acids and brain damage. Facultas-Universitätsverlag, 1993.

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5

Metal ions and neurodegenerative disorders. World Scientific, 2003.

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6

Nutrient power: Heal your biochemistry and heal your brain. Skyhorse Pub., 2012.

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7

Edvinsson, Lars. Cerebral blood flow and metabolism. Raven Press, 1993.

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8

N, Krause Diana, ed. Cerebral blood flow and metabolism. 2nd ed. Lippincott Williams & Wilkins, 2002.

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9

1924-, Wüllenweber R., Klinger M. 1943-, and Brock M. 1938-, eds. Regulation of cerebral blood flow and metabolism ; Neurosurgical treatment of epilepsy ; Rehabilitation in neurosurgery. Springer-Verlag, 1987.

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10

Biogenic monoamines and their metabolites in the urine, plasma, and cerebrospinal fluid of normal, psychiatric, and neurological subjects. CRC Press, 1990.

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11

International, Workshop on Biomedical Imaging: MR and PET/SPECT (1996 Fukui-shi Japan). Recent advances in biomedical imaging: Proceedings of the International Workshop on Biomedical Imaging: MR and PET/SPECT, Fukui, Japan, 28-30 August 1996. Elsevier, 1997.

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12

1938-, Arieff Allen I., and Griggs Robert C. 1939-, eds. Metabolic brain dysfunction in systemic disorders. Little, Brown, 1992.

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13

1941-, McCandless David W., ed. Cerebral energy metabolism and metabolic encephalopathy. Plenum Press, 1985.

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14

Salvi, Virginio, and Tomas Hajek, eds. Brain-Metabolic Crossroads in Severe Mental Disorders – Focus on Metabolic Syndrome. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88963-079-0.

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15

Uziel, G., S. Di Donato, and R. Parini. Metabolic Encephalopathies, Therapy and Prognosis. John Libbey Eurotext Ltd, 1995.

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16

1941-, McCandless David W., ed. Metabolic encephalopathy. Springer, 2009.

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17

N.R.R. Belton (Editor), N.A.J. Carson (Editor), R. Angus Harkness (Editor), R. J. Pollitt (Editor), and J. Stern (Editor), eds. Brain: Biochemistry and Inherited Metabolic Disease (1982). Springer, 2007.

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18

Stafstrom, Carl E. Dietary Therapy for Neurological Disorders. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0018.

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Dietary and metabolic therapies such as the high-fat, low-carbohydrate ketogenic diet (KD) are best known for the treatment of intractable epilepsy. Yet, dietary and metabolic approaches have also found some efficacy in a wide variety of other neurological diseases, including autism spectrum disorder, brain trauma, Alzheimer’s disease, sleep disorders, brain tumors, pain, and multiple sclerosis, as discussed in other chapters of this volume. This chapter provides an overview of clinical and experimental studies using the KD in an array of other neurologic disorders: amyotrophic lateral scleros

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19

Sutter, Raoul, Trudy Pang, and Peter W. Kaplan. EEG in Metabolic Disorders, Intoxications, and Epileptic Encephalopathies. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0017.

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This chapter provides a systematic overview of the diagnostic and prognostic value of electroencephalography (EEG) in adult patients with different types of encephalopathies in association with metabolic, toxic, and epileptic disorders. Most encephalopathies present with a fluctuating course characterized by typical but not pathognomonic symptoms such as cognitive impairment, altered mental status or confusion, lethargy, decreased or rarely increased motor activity, and disturbed sleep/wake cycles. EEG enables rapid, bedside electrophysiological monitoring, providing dynamic real-time informat

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20

S, Di Donato, Parini Rossella, Uziel Graziella, and Fondazione Pierfranco e Luisa Mariani., eds. Metabolic encephalopathies: Therapy and prognosis : postgraduate course of the Pierfranco e Luisa Mariani Foundation, Milan, Milan State University, 1-3 March 1994. J. Libbey, 1995.

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21

Neurochemistry of metabolic diseases: Lysosomal storage diseases, phenylketonuria and Canavan disease, 2007. Transworld Research Network, 2007.

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22

Maquet, Pierre, and Julien Fanielle. Neuroimaging in normal sleep and sleep disorders. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0011.

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Functional neuroimaging techniques include methods that probe various aspects of brain function and help derive models of brain organization in health and disease. These techniques can be grouped in two categories. Some are mainly based on electromagnetic signals (electroencephalography, magnetoencephalography), recording brain activity using a large number of sensors with exquisite temporal resolution (usually of the order of a kilohertz) but allowing only indirect characterization of three-dimensional brain activity by resorting to mathematical models. The second type includes different tech

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23

Trocello, Jean-Marc, and France Woimant. Disorders of Copper and Iron Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0044.

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Both copper and iron are essential metals that have a critical function in a series of biochemical pathways. This chapter describes the disorders associated with genetic abnormalities in copper and iron metabolic pathways and their manifestations in adult patients. Mutations in the genes of the copper transporting P-type ATPases, ATP7A and ATP7B are associated with Wilson disease, Menkes disease, occipital horn syndrome and ATP7A-related distal motor neuropathy. Neurodegeneration with brain iron accumulation (NBIA) is a group of disorders characterized by excess iron deposition in globus palli

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24

Letendre, Scott, Jennifer Iudicello, Beau Ances, Thomas D. Marcotte, Serena Spudich, and Mary Ann Cohen. HIV-Associated Neurocognitive Disorders. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0016.

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The human immunodeficiency virus (HIV) enters the central nervous system soon after infection; can infect glia and tissue macrophages in the brain; and can injure neurons, resulting in loss of dendrites. These and other processes underpin a syndrome of cognitive and motor impairment termed HIV-associated neurocognitive disorder (HAND). This chapter principally focuses on HAND, although delirium and other neurocognitive disorders are also discussed and should remain in the differential diagnosis of cognitive impairment in persons with HIV. A differential diagnosis of cognitive impairment in HIV

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25

Masino, PHD, Susan A., ed. Ketogenic Diet and Metabolic Therapies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.001.0001.

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Ketogenic diets have been used to treat epilepsy for nearly a century. Alongside enduring clinical success with a ketogenic diet, metabolism’s critical role in health and in diseases in the central nervous system and throughout the body is increasingly appreciated. Furthermore, metabolism-based strategies have been proven equal or even superior to pharmacological treatments in specific cases and for specific diseases. Rather than causing unwanted off-target pharmacological side effects, addressing metabolic dysfunction can improve overall health simultaneously. Enduring interest in the ketogen

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26

McEwen, Bruce S., and Natalie L. Rasgon. The Brain and Body on Stress. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0002.

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Neuroscientists have treated the brain in isolation from the rest of the body, while endocrinology and general medicine have viewed the body largely without regard to the influence of systemic physiology and pathophysiology on higher brain centers outside of the hypothalamus and pituitary gland. But now there is greater recognition of brain–body interactions affecting the limbic and cognitive systems of brain and altering systemic physiology; these are conceptualized as allostasis and allostatic load and overload. These concepts look at both the interactions of brain and body to stressors and

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27

Rho, Jong M. Overview. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0011.

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After nearly a century of clinical use, the ketogenic diet is firmly established as an efficacious treatment for medically intractable epilepsy. Intriguingly, there is growing experimental evidence that the ketogenic diet and its metabolites also render neuroprotective and potentially disease-modifying effects. Hence, dietary and metabolic therapies have been attempted in a variety of neurological disorders other than epilepsy, including brain cancer, cognitive disorders, autism, neurotrauma, pain, and multiple sclerosis. This section, “Ketogenic Diet: Emerging Clinical Applications and Future

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28

Kaye, Walter, and Alice V. Ely. Appetitive Regulation in Anorexia Nervosa and Bulimia Nervosa. Edited by W. Stewart Agras and Athena Robinson. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190620998.013.4.

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Anorexia and bulimia nervosa are complex disorders with dysregulated appetitive behaviors. The underlying causes of disturbed patterns of eating are unknown, but a growing body of research suggests that aberrant functioning of brain or peripheral systems may be responsible. Neuroimaging technologies, such as positron emission tomography (PET) and functional MRI (fMRI), can be used to explore whether there are perturbations of the monoamine systems, the neurocircuitry of gustatory processing in eating disorders, and their relationship to metabolic homeostatic states. Together, PET and fMRI data

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29

Banjara, Manoj, and Damir Janigro. Effects of the Ketogenic Diet on the Blood-Brain Barrier. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0030.

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Ketone bodies (KBs) are always present in the blood, and their levels increase after high-fat diet intake, prolonged exercise, or extended fasting. Thus, one can predict effects on the brain capillary endothelium from high levels of ketones in the blood. Prolonged exposure of blood-brain barrier (BBB) endothelial cells to KBs induces expression of monocarboxylate transporters and enhances brain uptake of KBs. In addition, cell migration and expression of gap junction proteins are up-regulated by KBs. Thus, beneficial effects of the ketogenic diet may depend on increased brain uptake of KBs to

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30

Streijger, Femke, Ward T. Plunet, and Wolfram Tetzlaff. Ketogenic Diet and Ketones for the Treatment of Traumatic Brain and Spinal Cord Injury. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0016.

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Ketogenic diets (KD)—high in fat, adequate in protein, and very low in carbohydrates—were developed almost a century ago and are still used clinically for drug-resistant epilepsy and some rare metabolic disorders. Possible new indications for cancers, diabetes, obesity, and neurodegenerative disorders are being trialed in humans based on a growing body of preclinical data showing efficacy. However the underlying mechanisms of KD remain incompletely understood. This chapter focuses on the neuroprotective effects of KD after spinal cord injury (SCI) and traumatic brain injury (TBI), and discusse

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31

Tuschl, Karin, Peter T. Clayton, and Philippa B. Mills. Disorders of Manganese Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0045.

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Manganese is an essential trace metal for numerous metalloenzymes. Manganese homeostasis requires tight regulation in vivo and disruption of this balance can lead to manganese overload and subsequent accumulation of manganese in brain, liver, and blood. Mutations in SLC30A10, a cell surface-localized manganese efflux transporter, cause an autosomal recessive hypermanganesemia syndrome with two distinct phenotypes: childhood onset dystonia and adult onset Parkinsonism, associated with chronic liver disease, polycythemia and features of iron depletion. MRI brain appearances are characteristic of

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32

Laureno, Robert. Selective Vulnerability. Edited by Robert Laureno. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190607166.003.0006.

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This chapter on “Selective Vulnerability” examines the selective vulnerability of different parts of the brain to particular diseases. In one disease, certain areas of brain are particularly vulnerable. In other diseases, different parts of the brain are more susceptible. The concept of selective vulnerability was originally applied to toxic/metabolic and hereditary disorders, but it is also useful in thinking about other neuropathologic processes including neoplastic, infectious, demyelinative, vascular, and traumatic diseases. Diseases can selectively affect brain systems, brain structures,

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33

Cheillan, David, and Frédéric Sedel. Disorders of Creatine Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0010.

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Creatine is a physiological guanidino compound playing a major role in energy metabolism in muscle and implicated in neurotransmission in brain. The three disorders of creatine metabolism (AGAT and GAMT deficiencies and the X-linked creatine transporter defect) are a group of inborn errors of metabolism characterized by a depletion of creatine that could be easily diagnosed by mesasurement of guanidinoacetate and creatine in body fluid or cranial MRS spectroscopy. The main clinical features of these paediatric disorders are intellectual disability and speech delay and some adult patients have

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34

Klein, Reva B. Aggression and Violence in the Elderly. Edited by Phillip M. Kleespies. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199352722.013.26.

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Aggression and violence are often overlooked in the aging population. Changes in personality, behavior, and mood are well known in psychiatric disorders, but they are also seen in neurologic conditions, often where there is alteration in brain chemistry, as in metabolic disorders; or alteration in brain structure, as in degenerative disorders, strokes, subdural hematomas, and tumors; or with alteration in brain function, as in epileptic and nonconvulsive status. This chapter provides an overview of specific behaviors, the underlying neurochemistry and pathophysiology behind specific disorders,

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35

Beed, Martin, Richard Sherman, and Ravi Mahajan. Neurology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199696277.003.0005.

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Decreased consciousnessSeizures and status epilepticusStroke/thromboembolic strokeIntracerebral haemorrhageSubarachnoid haemorrhageTraumatic brain injuryRaised intracranial pressureMeningitis and encephalitisAgitation/confusion/aggressionAlcohol withdrawalNeuromuscular weakness and paralysisGuillain–Barré syndromeMyasthenia gravis↓consciousness occurs in many diseases requiring admission to intensive care, and is often a cause for admission in its own right. Changes in neurological state may be related to intracranial pathology, or may occur in response to respiratory, circulatory, or metaboli

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36

Roy, Skinner E., ed. Brain lipids and disorders in biological psychiatry. Elsevier, 2002.

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37

Farooqui, Akhlaq, and L. A. Horrocks. Glycerophospholipids in brain: Phospholipase A2 in neurological disorders. Springer, 2006.

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38

Donard, Dwyer, ed. Glucose metabolism in the brain. Academic Press, 2002.

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39

Eyre, Janet. Neurodevelopmental disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0189.

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Remarkable advances in the neurosciences, particularly in the fields of genetics, molecular biology, metabolism, and nutrition, have greatly advanced our understanding of how the brain develops and responds to environmental influences. Neurodevelopmental disorders arise from perturbation of these normal developmental processes, by insults from heterogeneous aetiological factors. These factors trigger a sequence of molecular, biochemical, and morphological alterations of the brain, resulting in a morphologically and/ or functionally abnormal brain. Rapidly advancing understanding of basic neuro

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40

Horrocks, Lloyd A., and Akhlaq A. Farooqui. Glycerophospholipids in the Brain: Phospholipases A2 in Neurological Disorders. Springer, 2014.

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41

A, Nasrallah Henry, and Pettegrew Jay W, eds. NMR spectroscopy in psychiatric brain disorders. American Psychiatric Press, 1995.

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42

Forsyth, Rob, and Richard Newton. Specific conditions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0004.

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This chapter adopts a systematic approach to common diagnoses in paediatric neurology, aetiologies, management to include investigation and treatment, and outcome. For each condition current knowledge on cause and underlying biology is summarized. A rational approach to investigation and treatment is summarized for each topic. These include: acquired brain injury; autoimmune and autoinflammatory disease of the CNS; cerebral palsy and neurodisability which covers feeding, communication, special senses, and respiratory disease; demyelinating disease; epilepsy including its impact on daily life;

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43

Heckers, Stephan, Neil Woodward, and Dost Öngür. Neuroimaging of Psychotic Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0014.

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Neuroimaging of psychotic disorders began in the 1970s with studies of brain structure, followed by studies of blood flow, glucose metabolism, and receptor chemistry. More recently, studies of functional activation, connectivity, and neurotransmission have been added. The widespread availability of MRI has liberated researchers from the constraints of postmortem research and the limitations of inferring brain abnormalities through neurochemical effects in plasma or urine. Neuroimaging researchers aim to establish diagnostic markers, explain abnormal mental states, test anatomical and neurochem

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44

Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.

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Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pat

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45

Poretti, Andrea, and Michael V. Johnston. Genetic Disorders and Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0110.

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A variety of monogenic and polygenic genetic disorders have been linked to stroke, making it important for the clinician to keep up with the new discoveries and the potential to provide new gene-based therapies. Hematologic disorders such as sickle cell disease and thrombophilia due to mutations in prothrombin, factor V Leiden, and homocysteine metabolism are fairly well known, but mutations in mitochondrial metabolism and matrix metalloproteinases are less recognized. In addition, results of genome-wide association studies (GWAS) in stroke populations are revealing mutations that could predis

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46

Gaitanis, John, Phillip L. Pearl, and Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.

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Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted e

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47

Lester, Packer, Hiramatsu Midori, and Yoshikawa Toshikazu, eds. Free radicals in brain physiology and disorders. Academic Press, 1996.

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48

P, Riederer, and Youdim Moussa B. H, eds. Iron in central nervous system disorders. Springer-Verlag, 1993.

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49

(Editor), Peter Riederer, and M.B.H. Youdim (Editor), eds. Iron in Central Nervous System Disorders (Key Topics in Brain Research). Springer, 2001.

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50

M, Platt Frances, and Walkley Steven U, eds. Lysosomal disorders of brain: Recent advances in molecular and cellular pathogenesis and treatment. Oxford University Press, 2004.

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