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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The cerebrospinal fluid (CSF) is a bodily fluid, which is both easily accessible and the most proximate to the pathological alterations of multiple sclerosis (MS). Consequently, the analysis of this fluid provides an important window into the pathological underpinnings of this disease. For example, for years, it has been known that the CSF of MS patients contains oligoclonal gamma immunoglobulins (IgG), which are synthesized within the central nervous system and presumably relate to the immune dysfunction, which is characteristically found in MS. ⋯ Thus, patients without a definite diagnosis who have CSF IgG bands are significantly more likely to develop definite MS compared to those patients without such a banding pattern. Other biological molecules can also be found in the CSF including neurofiliment, myelin basic protein (MBP), glial fibrillary acidic protein (GFAP), tau, neuronal cell adhesion molecule (NCAM), and the growth associated protein (GAP-43). However, the value of measuring these (and other) CSF constituents for both diagnostic and prognostic purposes and for following response to therapy is still to be determined.
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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.
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Carbon monoxide poisoning remains a common neurologic problem as it causes more than one-half of fatal poisonings in many countries leading frequently to acute and delayed brain injury. Mild carbon monoxide intoxication is difficult to diagnose as symptoms can be nonspecific and therefore can be easily misdiagnosed. Common acute and delayed clinical presentations and their associated neuropathology and neuroimaging findings are discussed. Treatment remains limited and outcome is highly variable.