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Unique in approach and authority and illustrated with informative case histories, Behavior and Mood Disorders in Focal Brain Lesions, first published in 2000, makes a major contribution to understanding the relationship between focal brain disorders and emotional and behavioural symptoms, summarising the current state of research and providing the basis for improved patient care. This is the first clinical reference work to address specifically the relationship of focal brain dysfunction to behavioral and emotional disorders, giving the most comprehensive account available of these manifestations of brain lesions including stroke, trauma, epilepsy, multiple sclerosis, and even neurosurgery. A worldwide team of neuroscientists and clinicians examines the links between regional brain dysfunction and disorders of mood, thought and affect processing, and behaviour. Chapters are devoted to methodological issues, to lesions of specific sites, such as the frontal lobes, basal ganglia and thalamus, and to symptoms such as mood disorder, violent behaviour and anosognosia.
One third of people after stroke, having survived the first few weeks, return home with significant residual disability, and can therefore benefit from an active, multidisciplinary rehabilitation programme. This is a comprehensive guide to rehabilitation after stroke, in which leading international authorities set out the basic neuroscientific principles that underlie brain recovery, including chapters on neural plasticity and neural imaging, and describe appropriate rehabilitation strategies for the many different functional problems that can arise after stroke. These include movement disorders, sensory loss, dysphagia and dysarthria, problems with continence and secual difficulties, and cognitive disorders. Also covered are measurement of disability and quality of life, assistive technology and vocational rehabilitation. It is therefore an essential handbook and reference for all members of the multidisciplinary stroke rehabilitation team, including medical personnel, therapists, clinical neuropsychologists and rehabilitation nurses.
Prospective studies of mood changes after stroke in large samples of patients may permit the delineation of the acute emotional behavioral changes that are markers for the delayed development of emotional disturbances. Mood disorders can be quantified using specifically designed scales, such as the Center for Epidemiological Studies-Depression (CES-D) or the Hospital Anxiety and Depression Scale (HADS), and may be predictors of the later development of depression. The standardized diagnostic criteria of the DSM-IV for mood disorders are appropriate for stroke, as poststroke depression has a similar symptomatic profile to primary depression. Fear and anxiety are common following stroke. Anxiety is the second most prevalent mood disorder following stroke, being found in 3.5%-24% of patients. Careful monitoring of stroke and measurement of monoamine metabolites and neuroexcitatory amino acids, may give a better understanding of the biological mechanism underlining poststroke emotional disturbances.
The first edition of Stroke Syndromes was widely welcomed as a new and authoritative reference in the assessment and diagnosis of stroke. This revised and updated edition remains the definitive guide to patterns and syndromes in stroke. A comprehensive survey of all types of neurological, neurophysiological and other clinical dysfunction due to stroke, the book is organised to make pattern recognition easier. It contains descriptions of clinical problems encountered in stroke patients and their differential diagnosis, and will enable clinicians to differentiate between possible locations on the basis of symptoms and signs. A companion volume Uncommon Causes of Stroke completes this highly authoritative reference work which clinicians in neurology will find essential to the understanding and diagnosis of stroke.
Most strokes are attributed to atherosclerosis of neck and intracranial arteries, brain embolism from the heart, and penetrating artery disease; these are discussed in detail in many other books. This compendium fills an important niche by providing authoritative discussions on the other, less common causes of stroke, including various forms of angiitis, coagulation disorders, infective, paraneoplastic and metabolic disorders that may be associated with stroke, and a number of rare syndromes such as Eales disease and Fabry's disease. This new edition contains detailed, up-to-date information about the nature, diagnosis, and treatment of those relatively uncommon types of cerebrovascular disease that cause strokes. It is therefore a unique scientific and clinical resource that provides a useful reference to help physicians diagnose and treat stroke patients who do not fit well into the usual clinical categories. New chapters include stroke in patients with Lyme disease, scleroderma, Cogan's syndrome, Chagas' disease, and HIV.
The care of stroke patients has changed dramatically. As well as improvements in the emergency care of the condition, there have been marked advances in our understanding, management and rehabilitation of residual deficits. This book is about the care of stroke patients, focusing on behavioural and cognitive problems. It provides a comprehensive review of the field covering the diagnostic value of these conditions, in the acute and later phases, their requirements in terms of treatment and management and the likelihood and significance of long-term disability. This book will appeal to all clinicians involved in the care of stroke patients, as well as to neuropsychologists, other rehabilitation therapists and research scientists investigating the underlying neuroscience.
Intravascular lymphoma is a rare, extranodal, large B-cell lymphoma in which neoplastic, lymphoid cells proliferate within the lumina of small to medium-sized vessels. Neurological findings develop in about two-thirds of patients and usually present as multifocal cerebrovascular events, subacute encephalopathy, spinal cord or nerve root vascular syndromes, or peripheral and cranial neuropathies. In the brain, intravascular lymphoma manifests primarily as multiple infarcts. The strokes may involve any area of the brain, although supratentorial infarcts are more prevalent than cerebellar or brainstem infarction. Encephalopathy is observed in intravascular lymphoma patients and may be accompanied by focal neurological signs or seizures. The peripheral neuropathy observed in intravascular lymphoma is a predominantly axonal neuropathy. Computed tomography (CT) and cerebral angiography may show characteristics of stroke and vessel occlusion, in many instances, these studies are normal. Systemic chemotherapy with anthracycline-based regimens has been the most commonly pursued treatment in the literature.
This chapter explores the complex relationship of stroke with polyarteritis nodosa (PAN) and microscopic polyangiitis (MPA). MPA is a systemic necrotizing vasculitis that clinically and histologically involves capillaries, venules, or arterioles without granulomata, and is associated with necrotizing crescentic glomerulonephritis and hemorrhagic pulmonary capillaritis, which are the main causes of mortality and morbidity. Hemorrhagic strokes occur more frequently than ischemic infarction in MPA. Immunohistochemical studies from muscle and nerve biopsies showed that macrophages and T cells, mostly CD8+, are involved in the pathogenesis of PAN. Neurological symptoms and signs are a major and common feature of PAN, occurring in nearly three-quarters of patients. A close relationship between the use of corticosteroids and stroke exists in PAN. From a therapeutic point of view, antiplatelet drugs, which inhibit platelet thromboxane production, might reduce the risk of corticosteroid-induced, antiplatelet drugs in PAN. The use of aspirin and corticosteroids prospectively prevents stroke recurrence.
Cerebral venous sinus thrombosis (CVST), although a relatively rare cause of stroke, is important to diagnose and treat early because of the significant morbidity and mortality associated with it. CVST tends to affect younger patients, who have fewer traditional risk factors, than do arterial infarcts. CVST can also follow traumatic injury to the venous sinuses or jugular veins after neurosurgical or other procedures. Bilateral basal ganglionic and thalamic infarcts or hemorrhages are pathognomic of deep venous involvement. Magnetic resonance imaging (MRI) and computed tomography (CT) scanning are essential in confirming the diagnosis of CVST. The major pathology in CVST is thrombosis of cerebral veins or dural sinuses leading to impaired drainage, venous hypertension with subsequent edema formation, venous infarction, and hemorrhage. Anticoagulation plays a central role in management of intracranial venous occlusive disease. Anticoagulants are likely to prevent further thrombus growth and propagation, helping to arrest the thrombotic process.
Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) is an ophthalmologic syndrome rather than a specific entity, characterized by multiple cream-colored placoid lesions located in the posterior pole "lying at the level of the pigment epithelium and choroids". The ophthalmoscopic hallmarks of APMPPE consist of creamcolored, flat, and discrete placoid, without clear-cut marginal lesions at the level of the retinal pigment epithelium, masking the fundus view of the underlying choroids, which typically involve the macula but are never seen anterior to the equator. The fact that cardiovascular diseases (CVDs) occur in patients with APMPPE strongly supports the thesis that it represents a particular "uveo-cerebral vasculitic syndrome". Various etiologies have been found (infectious/postinfectious; vaccinations; inflammations; autoimmune diseases; vasculitis; paraneoplastic syndrome). The neurological complications of APMPPE are headache, aseptic meningitis, encephalitis, multiple sclerosis-like disease, and pseudo tumor cerebri. CVDs associated with APMPPE consist of ischemic cortical strokes and deep infarcts with striatocapsular infarctions.
The term cervico-cephalic arterial dissection (CAD) encompasses a group of arteriopathies not necessarily with an identical pathogenesis but that have in common an intramural hemorrhage. This most frequently affects the extracranial arterial segments, predominantly the internal carotid artery (ICA), the vertebral artery (VA), or multiple arteries in typical locations. Spontaneous cervico-cephalic arterial dissections (sCAD) have typical predilection sites in the different arteries affected, which in part may be explained by mechanical influences: high cervical segment of extracranial ICA or V2 and V3 segments of VA. In the case of a severe head and/or neck trauma, the pathogenesis is straightforward. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) have replaced angiography as the gold standard, at least in the extracranial segments of ICA and VA. The risk of having a stroke or transient ischemic attack (TIA) after having suffered a CAD in general is very low.
This chapter deals with isolated angiitis of the central nervous system (CNS), and begins with an overview of the pathology and pathogenesis of the condition. The nonspecific pathological pattern of isolated CNS angiitis is characterized by infiltrations of the vascular walls with mononuclear cells including lymphocytes, macrophages, and histiocytes. The pathogenesis of isolated CNS angiitis is unknown and progress is slow because of the rarity of tissue samples acquired from carefully documented cases. Brain imaging, angiography, and brain biopsy are the diagnostic options investigated in the chapter. In patients with a unique focal presentation such as stroke, and with isolated CNS angiitis suspected on the basis of angiography alone, a course of several-weeks of high-dose corticosteroids associated with a calcium channel blocker and no immunosuppressor can be proposed. The diagnosis of reversible cerebral angiopathy should be carefully considered in these patients.
Eales retinopathy associates peripheral retinal changes often described as "vasculitis", peripheral capillary nonperfusion (retinal ischemia), and retinal or optic nerve neovascularization (secondary to chronic retinal ischemia) resulting in vitreous hemorrhage and retinal detachment. Some of the syndromes are associated with lesions of the central nervous system, explaining why Eales retinopathy is considered an uncommon cause of stroke. It should be interpreted with caution because other entities may be the cause of the retinopathy and the central nervous system lesions. Various neurologic findings have been reported, including meningitis, encephalitis, cerebral vasculitis, brain infarctions and hemorrhages, cerebral venous thrombosis, and white matter diseases. The treatment of the retinopathy is limited to stimulating regression of neovascularization by applying laser photocoagulation to the nonperfused retina. Vitrectomy is indicated for nonclearing vitreous hemorrhage, extensive retinal neovascularization, epiretinal membrane, and traction retinal detachment.