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Our knowledge of EDX in tick paralysis is limited Sensory nerve conduction parameters have been reported to fall within population-based norms but often demonstrate faster speeds and higher amplitudes when studied again following recovery240,241,403 407 The implication is that tick paralysis may produce a mild sensory neuropathy The EDX detection of this neuropathy may well be obscured by the wide range of population-based norms Normal premorbid values for sensory nerve action potential (SNAP) amplitudes in these typically otherwise healthy young people may be considerably higher than population norms, thereby precluding the detection of mild sensory axon loss or dysfunction The recovery of electrical parameters appears to follow the physical resolution of paralysis, implicating channel dysfunction or

Step 7 While the computer is turned off, pretend you lost power and must remove the disc from the optical drive without power Use a paper clip as noted in the accompanying Lab Hint to remove the disc Step 8 As a technician, you need to understand the keyboard, because it is still one of the most important human interfaces on a PC Look at the way your keyboard is laid out: it basically has three main sections, with some extra keys thrown in for good measure (see Figure 2-3)

There is a limited evidence basis from which to determine a sensitive, speci c, and cost-effective laboratory evaluation for most neuromuscular syndromes Laboratory evaluations for speci c neuromuscular syndromes

Figure 7-8

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will be addressed in detail in subsequent chapters of this book and will be mentioned here only in summary terms An ideal test would be cost effective, noninvasive, and accurate in identifying or excluding a speci c disorder in a large percentage of the tested population There are few tests that resemble this description, anti-ACH receptor binding antibodies (ACHRBA) being arguably the best example Peripheral neuropathy is the most common neuromuscular syndrome with an extensive differential diagnosis Numerous publications and clinical experience indicate that a signi cant number of these individuals will go undiagnosed despite extensive evaluation Understandably, there is an incentive to extensively test in an attempt to ll in this gap There have been a number of attempts to clarify which tests come closest to meeting the criteria outlined in the rst paragraph17,36,60,61 This includes a practice parameter being currently constructed by the American Academy of Neurology In summary, there is a low diagnostic yield for any routine blood test in the detection of an abnormality that is causally related to a patient s neuropathic symptoms De ciency of vitamin B1, B6, B12, and E are potentially causally related to peripheral neuropathy In addition, a sensory neuropathy/neuronopathy may occur with vitamin B6 toxicity in daily doses that are estimated to exceed 200 mg62 Testing for vitamin de ciency is generally not recommended on a routine basis61 and is generally reserved for those patients perceived to be at higher risk This group would include patients with a sensory predominant neuropathy who are at risk of nutritional de ciency due to alcoholism, dietary anomalies, isoniazid exposure, and malabsorption from bariatric surgery or enteral disease such as celiac sprue The onset of symptoms in the hands may indicate a myeloneuropathy, which is a common presentation of vitamin B12 de ciency Measurements of serum levels of methylmalonic acid and/or homocysteine may improve detection of this latter disorder An increased incidence of serum monoclonal proteins (MCPs) in patients with polyneuropathy has been recognized for decades Most MCPs associated with peripheral neuropathy will initially be designated as being of unknown signi cance (MGUS) The neuropathy associated with MGUS may vary depending on MCP type but is typically a nonspeci c, sensory > motor, and length dependent phenotype with primarily EDX axonal features63,64 The association between the neuropathy and MGUS in these cases is strictly statistical, a causal relationship being dif cult if not currently impossible to prove The MGUS that is most likely to have a causal relationship to peripheral neuropathy and has the most homogenous phenotype is that associated with an IgM kappa MCP This is in turn often associated with antibodies directed toward myelin-associated glycoprotein in a signi cant percentage of cases These antibodies will be discussed further in the following section.

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