Handbook of clinical neurology
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The diagnosis of brain death should be based on a simple premise. If every possible confounder has been excluded and all possible treatments have been tried or considered, irreversible loss of brain function is clinically recognized as the absence of brainstem reflexes, verified apnea, loss of vascular tone, invariant heart rate, and, eventually, cardiac standstill. This condition cannot be reversed - not even partly - by medical or surgical intervention, and thus is final. ⋯ Generally, the concept of brain death has been accepted by all major religions. But patients' families may have different ideas and are mostly influenced by cultural attitudes, traditional customs, and personal beliefs. Suggestions are offered to support these families.
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This chapter describes the clinical presentation, diagnosis, and treatment of patients with both aseptic meningitis and encephalitis. It also addresses the major causes of aseptic meningitis. ⋯ Aseptic meningitis, on the other hand, is typically a benign childhood infection requiring supportive care alone. It also reviews available clinical decision rules that may assist the clinician in distinguishing which children with aseptic meningitis are at very low risk of bacterial meningitis using predictors available at the time of clinical presentation.
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To most doctors, brachial and lumbosacral plexopathies are known as difficult disorders, because of their complicated anatomy and relatively rare occurrence. Both the brachial, lumbar, and sacral plexuses are extensive PNS structures stretching from the neck to axillary region and running in the paraspinal lumbar and pelvic region, containing 100000-200000 axons with 12-15 major terminal branches supplying almost 50 muscles in each limb. The most difficult part in diagnosing a plexopathy is probably that it requires an adequate amount of clinical suspicion combined with a thorough anatomical knowledge of the PNS and a meticulous clinical examination. ⋯ The most common cause of brachial plexopathy is probably neuralgic amyotrophy and the most common cause of lumbosacral plexopathy is diabetic amyotrophy. Traumatic and malignant lesions are fortunately rarer but just as devastating. This chapter provides an overview of both common and rarer brachial and lumbosacral plexus disorders, focusing on clinical examination, the use of additional investigative techniques, prognosis, and treatment.
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Tinnitus is a common disorder and traditional treatment approaches such as medication, active or passive sound enhancement, and cognitive behavioral therapy have limited efficacy. Thus, there is an urgent need for more effective treatment approaches. Functional imaging studies in patients with tinnitus have revealed alterations in neuronal activity of central auditory pathways, probably resulting as a consequence of sensory deafferentation. ⋯ Transcranial direct current stimulation (tDCS) has also shown potential for the treatment of tinnitus. Both auditory and frontal tDCS have shown tinnitus reduction in a subgroup of patients. In spite of the promising results of the different brain stimulation approaches, further research is needed before these techniques can be recommended for routine clinical use.
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Neurorehabilitation is based on the assumption that motor learning contributes to motor recovery after injury. However, little is known about how learning itself is affected by brain injury, how learning mechanisms interact with spontaneous biological recovery, and how best to incorporate learning principles into rehabilitation training protocols. Here we distinguish between two types of motor learning, adaptation and skill acquisition, and discuss how they relate to neurorehabilitation. ⋯ The emphasis in current neurorehabilitation practice is on the rapid establishment of independence in activities of daily living through compensatory strategies, rather than on the reduction of impairment. Animal models, however, show that after focal ischemic damage there is a brief, approximately 3-4-week, window of heightened plasticity, which in combination with training protocols leads to large gains in motor function. Analogously, almost all recovery from impairment in humans occurs in the first 3 months after stroke, which suggests that targeting impairment in this time-window with intense motor learning protocols could lead to gains in function that are comparable in terms of effect size to those seen in animal models.