Handbook of clinical neurology
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Painful diabetic neuropathy (PDN) is one of several clinical syndromes in patients with diabetic peripheral neuropathy (DPN) and presents a major challenge for optimal management. The epidemiology of PDN has not been extensively studied. On the basis of available data, the prevalence of pain ranges from 10% to 20% in patients with diabetes and from 40% to 50% in those with diabetic neuropathy. ⋯ Quantifying neuropathic pain is difficult, especially in clinical practice, but has improved recently in clinical trials with the development of neuropathic pain-specific tools, such as the Neuropathic Pain Questionnaire and the Neuropathic Pain Symptom Inventory. Hyperglycemia-induced pathways result in nerve dysfunction and damage, which lead to hyperexcitable peripheral and central pathways of pain. Glycemic control may prevent or partially reverse DPN and modulate PDN.
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Posterior reversible encephalopathy syndrome (PRES) is a recently proposed cliniconeuroradiologic entity with several well-known causes, such as hypertensive encephalopathy, eclampsia, and the use of cytotoxic and immunosuppressive drugs, as well as some causes more recently described. PRES is characterized by neuroimaging findings of reversible vasogenic subcortical edema without infarction. The pathogenesis is incompletely understood. ⋯ The clinical syndrome of PRES typically involves headache, encephalopathy, visual symptoms, and seizures. The clinical presentation is often nonspecific, and therefore the diagnosis of PRES has come to increasingly rely on magnetic resonance imaging (MRI) abnormalities consistent with PRES with documented recovery clinically and on repeated neuroimaging. The diagnosis has important therapeutic and prognostic implications because the reversibility of the clinical and radiologic abnormalities is contingent on the prompt control of blood pressure and/or discontinuing the offending drug.
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There is an increasing incidence and prevalence of patients with chronic kidney disease (CKD) in Western industrialized countries and currently is estimated at approximately 10% of adults aged over 20 years. Renal failure causes an excessively increased risk of cerebrovascular and cardiovascular complications. Moreover, renal failure leads to a number of the neurologic symptoms neurologists are often confronted with. ⋯ Complications of the central nervous system (e.g., uremic encephalopathy, disequilibrium syndrome, and drug induced disorders) are reviewed. It has long been known that uremia leads to peripheral nerve injury. Frequent neurological diseases such as uremic polyneuropathy, autonomic neuropathy, and a range of mononeuropathies are discussed.
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Electrical burns are classified as either high voltage (1000 volts and higher) or low voltage (<1000 volts). The typical injury with a high-voltage electrical contact is one where subcutaneous fat, muscles, and even bones are injured. Lower voltages may have lesser injuries. ⋯ A full neurologic examination must be performed on admission, documenting initial presentation and at any change in symptoms. Electrical injuries can have devastating consequences. Prevention of electrical injuries is clearly the preferable strategy for treatment.
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Increased survival of critically ill patients has focused the attention on secondary complications of intensive care unit (ICU) stay, mainly ICU-acquired weakness (ICUAW). ICUAW is relatively common with significant impact on recovery. Prolonging mechanical ventilation and overall hospitalization time, increased mortality, and persistent disability are the main problems associated with ICUAW. ⋯ The approach to the diagnosis and the yield of various techniques (mainly electrophysiological and histological) is discussed. Possible therapeutic interventions of this condition that modify the course of this deleterious situation and lead to better rehabilitation are discussed. The current postulated mechanisms associated with ICUAW (mainly the more frequent critical illness neuropathy and myopathy) are reviewed.