Transient Global Amnesia: From Patient Encounter to Clinical Neuroscience

Description

This extensively revised second edition provides a comprehensive overview of transient global amnesia (TGA). First, it deals with the history of TGA before moving on to clinical and diagnostic features and differential diagnosis. Subsequent chapters then discuss the investigation and predisposing and precipitating factors for TGA before attempting to synthesise these many strands in order to formulate ideas about the pathogenesis of TGA. Each of the chapters is devoted to a practical and structured overview of the particular topic, with use of case studies to illustrate the material. Based in part on the author’s experience of TGA cases over 20 years and in part on a review of the published literature, this book will hopefully enlighten clinicians from a broad range of medical backgrounds on the clinical features, investigation, and pathogenesis of TGA. Transient Global Amnesia is aimed at any clinician with an interest in, or who encounters patients with, acute amnesia: neurologists, general physicians, old age psychiatrists, geriatricians, clinical neuropsychologists, and primary care physicians, as well as other professions allied to medicine with similar interests, such as members of memory assessment teams. Foreword to the Second Edition Preface to the First Edition [2017] Preface to the Second Edition [2022] Acknowledgements Contents Chapter 1: History of TGA 1.1 Beginnings: Fisher and Adams’ First Accounts of TGA 1.2 “Prehistory” of TGA 1.3 After Fisher and Adams 1.4 A Note on Nomenclature 1.5 A Note on Methodology 1.6 Summary and Recommendations References Chapter 2: Clinical Features, Diagnostic Criteria and Possible Variants of TGA 2.1 Clinical Features of TGA 2.1.1 TGA Archetype 2.1.2 Accompanying Neurological and Psychological Symptoms 2.1.3 Chronobiology: Diurnal Time of Onset 2.1.4 Attack Duration 2.1.5 Prognosis, Recurrence 2.2 Diagnostic Criteria of TGA 2.2.1 Essential Features and Inclusion/Exclusion Boundaries 2.2.2 Hodges and Warlow’s 1990 Diagnostic Criteria 2.2.3 TGA Subtypes? 2.3 Possible Variant Forms of TGA 2.3.1 Transient Topographical Amnesia (TTA) 2.3.2 Transient Partial Verbal Amnesia (TPVA) 2.3.3 Transient Semantic Amnesia 2.3.4 Transient Procedural Amnesia 2.3.5 Transient Retrograde Amnesia 2.4 Summary and Recommendations References Chapter 3: Differential Diagnosis of TGA 3.1 Cerebrovascular Disease 3.1.1 Transient Ischaemic Attack (TIA) 3.1.2 Stroke: Cerebral Infarction 3.1.3 Stroke: Cerebral Haemorrhage 3.1.4 Cerebral Vasculopathies 3.1.5 Cerebral Angiography 3.1.6 Cardiac Disorders 3.2 Epilepsy 3.2.1 Transient Epileptic Amnesia (TEA) 3.2.2 TGA and TEA: Is there an Interrelation? 3.3 Transient Psychological Amnesia (TPA) 3.4 Other Symptomatic Causes of Transient Amnesia 3.4.1 Migraine 3.4.2 Adverse Drug Effect 3.4.3 Hypoglycaemia 3.4.4 Traumatic Brain (Closed Head) Injury 3.4.5 Alcohol-Induced Amnesia; Korsakoff Syndrome 3.4.6 Fatigue Amnesia 3.5 Other Causes of Acute Cerebral Disorder 3.5.1 Acute Confusional State/Delirium/Toxic-Metabolic Encephalopathy 3.5.2 Acute Brain Infections, Including COVID-19 3.6 Misdiagnosis 3.7 Summary and Recommendations References Chapter 4: Investigation of TGA (1): Neuropsychology, Neurophysiology and Other Investigations 4.1 Neuropsychology 4.1.1 Neuropsychological Deficits during TGA: Memory 4.1.1.1 “Working Memory” 4.1.1.2 Anterograde Memory 4.1.1.3 Retrograde Memory 4.1.1.4 Semantic Memory 4.1.1.5 Implicit Memory 4.1.1.6 Spatial Memory 4.1.1.7 Metamemory 4.1.2 Neuropsychological Deficits during TGA: Other Cognitive Domains 4.1.2.1 Language 4.1.2.2 Visuoperceptual and Visuospatial Skills 4.1.2.3 Executive Function 4.1.3 Neuropsychological Deficits after TGA 4.2 Neurophysiology 4.2.1 Electroencephalography (EEG) 4.2.2 EEG during TGA 4.2.3 Magnetoencephalography (MEG) 4.2.4 Transcranial Magnetic Stimulation (TMS) 4.3 Other Investigations 4.3.1 Blood Tests 4.3.2 Cerebrospinal Fluid (CSF) 4.3.3 Sonography 4.3.3.1 Arterial 4.3.3.2 Venous; Internal Jugular Vein Valve Incompetence 4.4 Summary and Recommendations References Chapter 5: Investigation of TGA (2): Neuroimaging 5.1 Structural Neuroimaging 5.1.1 Computed Tomography (CT) 5.1.2 Magnetic Resonance (MR) Imaging 5.1.2.1 Clinical Phenotype Vs. MR-DWI Changes 5.1.2.2 Lesion Location, Number and Size 5.1.2.3 Timing of MR-DWI Changes 5.1.2.4 MR Field Strength, Slice Thickness and T2-Weighting 5.1.2.5 Diagnostic Value of MR-DWI Changes 5.1.2.6 Pathogenesis of MR-DWI Changes 5.1.2.7 Other MR Findings 5.1.3 Voxel-Based Morphometry (VBM) and Diffusion Tensor Imaging (DTI) 5.2 Functional Neuroimaging 5.2.1 Single-Photon Emission Computed Tomography (SPECT) 5.2.2 Positron Emission Tomography (PET) 5.2.3 CT Perfusion (CTP) Imaging 5.2.4 MR Spectroscopy (MRS) 5.2.5 Perfusion-Weighted MR Imaging 5.2.6 Functional MRI (fMRI) 5.3 Summary and Recommendations References Chapter 6: Prognosis and Management of TGA 6.1 Recovery and Persisting Cognitive Deficit 6.2 Recurrence 6.2.1 Annual Recurrence Rate 6.2.2 Recurrent TGA 6.2.3 Possible Risk Factors for Recurrent TGA 6.2.4 Is Family History of TGA a Risk Factor for Recurrent TGA? 6.3 Future Risk 6.3.1 Cognitive Decline: Dementia and Mild Cognitive Impairment (MCI) 6.3.2 Cognitive Decline: Progressive Aphasia 6.3.3 Stroke 6.3.4 Epilepsy 6.3.5 Depression 6.4 Management 6.4.1 Driving 6.4.2 Pharmacotherapy 6.5 Summary and Recommendations References Chapter 7: Epidemiology of TGA (1): Possible Predisposing Factors 7.1 Incidence 7.2 Chronobiology: Time of Onset by Day, Month and Season 7.3 Place of Onset: Geographical Distribution 7.4 Patient Age 7.5 Patient Gender 7.6 Patient Ethnicity 7.7 Patient Social Class 7.8 Family History of TGA 7.9 Migraine 7.10 Patient Personality Traits and Psychological Factors 7.11 Vascular Risk Factors and Stroke 7.12 Structural Brain Lesions 7.13 Summary and Recommendations References Chapter 8: Epidemiology of TGA (2): Possible Precipitating Factors 8.1 Emotional Stress 8.2 Physical Effort 8.3 Water Contact or Temperature Change 8.4 Sexual Activity 8.5 Pain 8.6 Migraine 8.7 Brain Infections 8.8 Medical Procedures and Therapies 8.9 Valsalva Manoeuvre 8.10 Other Possible Precipitating Factors 8.11 Summary and Recommendations References Chapter 9: Pathogenesis of TGA 9.1 What Is the Cause of TGA? 9.2 Cerebrovascular Disease 9.2.1 Arterial 9.2.2 Venous 9.3 Epilepsy 9.4 Migraine 9.5 Genetics 9.6 Psychiatry 9.7 Formulation: Towards a Neural Network Hypothesis 9.7.1 Existing Models of TGA: Experimental and Theoretical 9.7.2 State-Transition Models 9.7.3 Feedback Loop Model 9.7.4 CA3 Autoassociative Attractor Model 9.7.5 Spreading Depolarisation 9.7.6 Hypothesis: Proposal, Evidence, Predictions and Shortcomings 9.8 The Future? 9.9 Closing Summary References Index