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“Tut, man, one fire burns out while another's burning. One pain is lessen'd by another's anguish; turn giddy and behold by backward turning; one's desperate grief is cured by another's languish: take thou to some new infection of thine eye and the rank of poison of.”
—William Shakespeare (1564–1616)
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On completion of this chapter, the student/practitioner will be able to:
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Define the common infection diagnoses that may lead to peripheral neuropathy.
Develop a clinical understanding of the typical neurological signs and symptoms associated with specific infections that may lead to peripheral neuropathy.
Apply knowledge of the common infection diagnoses into “clinical scripts” used in the development of the differential diagnoses list.
Choose the appropriate assessment tools that will “map back” to the potential diagnosis.
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Hepatitis
Infection
Lyme disease
Parasite
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When comparing the prevalence of etiologies of suspected peripheral nerve disease, infectious causes are much less frequent than traumatic, overuse, metabolic, environmental, and degenerative etiologies. However, many of the infectious etiologies described in this chapter, such as tuberculosis (TB), hepatitis, HIV, Lyme disease, and leprosy, have prevalence rates in the United States and worldwide that are either staying consistent or increasing. One would expect peripheral nerve injuries resulting from the aforementioned infectious diseases to, at best, remain at their current levels or, at worst, increase in prevalence. HIV-related neuropathy is discussed in detail in Chapter 27.
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The clinician attempting to identify the etiology of suspected peripheral nerve injury must be aware of the potential of infection to cause neuropathy. This statement is true for several reasons. Correct diagnosis is a requirement for correct intervention. With many infectious etiologies, time from onset to treatment may have a great impact on potential recovery. Lastly, many of the diseases described in this chapter are contagious. Early diagnosis may prevent further dissemination of the offending agent. As with all peripheral nerve injury etiologies, exhaustive history taking, review of the clinical data set, and performance of valid and reliable tests and measures are required for the diagnostician to reach the correct diagnosis.
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A large amount of knowledge has been acquired since the original descriptions of Lyme borreliosis (LB) and of its causative agent, Borrelia burgdorferi. The complexity of the organism, the variations in the clinical manifestations of LB caused by the different B. burgdorferi species, and the difficulty in obtaining an evidence-based treatment regimen were not originally anticipated. Considerable improvement in reliability and validity of the detection of B. burgdorferi by laboratory and physical assessment as well as in the effectiveness of therapy has occurred since the early stage of disease presentation.1–3
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The etiologic agent, B. burgdorferi, was recovered in 1982 from the vector tick Ixodes dammini (now Ixodes ...