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The Oxford Textbook of Neurohaematology is a single source of knowledge on the diverse neurological conditions associated with malignant and classical haematological diseases. The book covers the full range of haematological diseases, both malignant and classical, that impact the central, peripheral, and autonomic nervous systems.
The book is divided into three sections. In the first section, neurological conditions associated with malignant haematological diseases are presented. This section begins with chapters on primary haematological malignancies of the nervous system including primary central nervous system lymphomas, vitreoretinal lymphoma, and other rare primary malignancies such as Hodgkin disease and lymphoproliferative disorders. Next, a chapter on histiocytic tumours of the central nervous system presents the neurological conditions associated with the Langerhans and non-Langerhans histiocytoses. This is followed by chapters covering the neurological complications of systemic myeloid and lymphoid malignancies. The second section of the book covers neurological complications of the treatments used in the management of haematological malignancies such as chemotherapy, radiation, and immunotherapy including chimeric antigen receptor T cells. The third and final section of the book features chapters on the neurological complications associated with classical haematological diseases including disorders of red blood cells (e.g., sickle cell anaemia), disorders of platelets and coagulation (e.g., immune thrombocytopenia), and disorders of white blood cells (e.g., hyperviscosity syndrome).
Edited by leading authorities in the field, this book will serve as a useful resource for neurologists, haematologists, and oncologists, as well as for subspecialists and allied health professionals involved in the management of haematological diseases and their neurological manifestations.
Foreword
Preface
Editors
Contributors
Abbreviations
Neurological conditions associated with malignant haematological diseases
Primary CNS diffuse large B-​cell lymphoma
Immunodeficiency-​associated primary CNS diffuse large B-​cell lymphoma
Vitreoretinal lymphoma
Rare primary CNS lymphomas
Histiocytic tumours of the central nervous system
Neurological complications of myeloid malignancies
Neurological complications of lymphoid malignancies
Neurological complications of treatments used in the management of haematological malignancies
Neurological complications of medical therapies in haematological malignancies
Introduction
Direct neurotoxicity
General aspects
Neurological complications of cell therapies in haematological malignancies
Introduction
Clinical approach
Indications for stem cell transplantation (with levels of evidence I, II, and III)
Neurological complications in theconditioning phase
Drugs
Table 9.2 Timeline of neurological complications with haematological stem cell transplantation
Table 9.3 Neurological complications associated with drugs commonly used in haematological stem cell transplantation
Posterior reversible encephalopathy syndrome
Complications during pancytopenia
Neurological complications of radiation therapies in haematological malignancies
Neurological conditions and complications associated with non-​malignant haematological disorders
Neurological complications of red blood cell disorders
Introduction
Hypoproliferative anaemias
Neurological complications of iron deficiency
Restless legs syndrome
Treatment and outcomes
Neurocognitive symptoms
Neurological complications of cobalamin deficiency
Frequency and risk factors
Aetiology and pathogenesis
Neurological complications of folate deficiency
Frequency and risk factors
Diagnostic testing
Treatment and outcomes
Disorders of haemoglobin
Neurological complications of sickle cell disease
Frequency and risk factors
Aetiology and pathogenesis
Neurological complications of platelet disorders and disorders of coagulation
Introduction
Haemophilia
Epidemiology, frequency, and risk factors
Diagnosis
Figure 12.1 Proposed screening and diagnostic algorithm for haemophilias and acquired haemophilia.
Prevention and treatment
Table 12.2 Selected target factor activity levels per injury
Bypassing agents
Thrombocytopenias
Immune thrombocytopenia (formerlyidiopathic thrombocytopenic purpura)
Diagnosis
Prevention and treatment
Table 12.3 First- and second- line treatment for immunethrombocytopenia
Outcome
Thrombotic thrombocytopenic purpura
Table 12.4 Common neurological manifestationsof thrombotic thrombocytopenic purpura
Epidemiology, frequency, and risk factors
Aetiology/ pathogenesis
Clinical presentation
Prevention and treatment
Heparin- induced thrombocytopenia
Epidemiology, frequency, and risk factors
Figure 12.2 The pathogenesis of heparin- induced thrombocytopenia (HIT) is characterized by gaps in our knowledge. Genomic biomarkers havethe potential to answer critical questions at every stage of HIT pathogenesis, including the predisposing immunogen, the cellular source of antibodies,the identification of pathogenic immunoglobin G (IgG) antibodies, and the mechanisms of thrombosis. Similarly, the clinical progression of a patientwho will eventually develop HIT is characterized by various unmet clinical needs. Genomic biomarkers have the potential to meet many of the unmetclinical needs for HIT, including limitations in the clinical utility of platelet count monitoring, PF4/ heparin antibody testing, functional assay testing, andlimited treatment options. APC, antigen- presenting cell; FcγRIIA, platelet FcγRIIa receptor; HIPA, heparin- induced platelet aggregation; HIT, heparininducedthrombocytopenia; IVIG, intravenous immunoglobulin; NOAC, novel oral anticoagulant; PF4, platelet factor 4; SRA, serotonin release assay.
Diagnosis
Figure 12.3 Algorithm for management of heparin- induced thrombocytopenia (HIT).
Table 12.5 The 4T score
Prevention and treatment
Disseminated intravascular coagulation
Neurological complications of white blood cell disorders
Hyperviscosity syndrome and the nervous system
Introduction
Epidemiology
Pathogenesis
Viscosity
Clinical presentation of hyperviscosity
Treatment of hyperviscosity syndrome
Plasmapheresis
Chemotherapy
AL amyloidosis and the nervous system
Aetiology/ pathogenesis
Clinical presentation
CASE STUDY 13.1 Signs for amyloidosis: fatigue,renal dysfunction, and development of neuropathy
CASE STUDY 13.2 Local amyloid can mimiccranial nerve lesions
CASE STUDY 13.3 Amyloidoma of theperipheral nerve
Central nervous system
Giant cell arteritis
Prevention and treatment
Conclusions
Index