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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.
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.
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.
Rupture of an aneurysm is associated with a very high degree of morbidity and mortality. Stroke-like apoplectic clinical syndromes occur with aneurysmal intra cerebral hemorrhage and correspond to the affected area. Lateralized focal neurologic deficits are most common with intra parenchymal hemorrhages due to middle cerebral aneurysms. Intracranial aneurysms are not a rare cause of both hemorrhagic and ischemic stroke. Although the initial and most serious manifestation of an intracranial aneurysm, subarachnoid hemorrhage (SAH), does not typically result in focal neurologic deficits, several complications of ruptured or unruptured aneurysms can lead to focal neurologic deficits, which may develop suddenly in a stroke-like fashion. This is most often seen as a result of intracerebral hemorrhage from the initial rupture of the aneurysm. Cerebral vasospasm after SAH is another common cause of stroke-like, focal deficits. Thromboembolism from the dislodgement of an intra-aneurysmal clot is a less frequent cause of ischemic stroke.