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CHAPTER 10 177 Davis MD, Weenig RH, Genebriera J, WendelschaferCrabb G, Kennedy WR, Sandroni P Histopathologic ndings in primary erythromelalgia are nonspeci c: Special studies show a decrease in small nerve ber density J Am Acad Dermatol 2006;55(3):519 522 178 Yang Y, Wang Y, Li S, et al Mutations in SCN9 A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia J Med Genet 2004;41(3):171 174 179 Michiels JJ, te Morsche RH, Jansen JB, Drenth JP Autosomal dominant erythermalgia associated with a novel mutation in the voltage-gated sodium channel alpha subunit Nav17 Arch Neurol 2005;62(10):1587 1590 180 Lampert A, Dib-Hajj SD, Tyrrell L, Waxman SG Size matters: Erythromelalgia mutation S241 T in Nav17 alters channel gating J Biol Chem 2006;281(47):36029 36035
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OTHER HEREDITARY NEUROPATHIES
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181 Sheets PL, Jackson Ii JO, Waxman SG, Dib-Hajj S, Cummins TR A Nav17 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity J Physiol 2007 Apr 12 [Epub ahead of print] 182 Cohen JS Erythromelalgia New theories and new therapies J Am Acad Dermatol 2000;43:841 847 183 McGraw T, Kosek P Erythromelalgia pain managed with gabapentin J Anesthesiol 1997;86(4):988 990 184 Dawkins JL, Hulme DJ, Brambhatt SB, Auer-Grumbach M, Nicholson GA Mutations in SPTLC1, encoding serine palmitoyl transferase long chain base subunit-1, cause hereditary sensory neuropathy type 1 Nat Genet 2001;27:309 312
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11
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Guillain Barr Syndrome e and Related Disorders
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Landry described a neuropathy characterized by acute ascending paralysis in 1859 Later, Guillain, Barr , and e Strohl noted the are exia and the albuminocytological dissociation in the cerebral spinal uid (CSF) associated with this neuropathy1 The contributions of Landry and Strohl have been neglected, and the neuropathy has been most commonly referred to as Guillain Barr e syndrome (GBS) In 1949, Haymaker and Kernohan detailed the histopathological features seen in 50 fatal cases of GBS The earliest features noted were edema of the proximal nerves and the subsequent degeneration of the myelin sheaths within the rst week of the illness They did not appreciate in ammatory cells in ltrate until later in the course of the illness2 However, another group reported prominent perivascular in ammation in the spinal roots, dorsal root ganglia, cranial nerves, and randomly along the whole length of peripheral nerves, along with segmental demyelination adjacent to the areas of in ammation, in 19 autopsy cases of GBS3 Thus, the term acute in ammatory demyelinating polyradiculoneuropathy (AIDP), which is quite descriptive of the disease process, has been used synonymously with GBS4 7 It is now appreciated that GBS is not a single disorder but again a syndrome of several types of acute immune-mediated polyneuropathies (Table 11 1)8,9 In addition to AIDP, there are two axonal forms of GBS: acute motor sensory axonal neuropathy (AMSAN) and acute motor axonal neuropathy (AMAN) Further, some disorders that appear clinically different from AIDP (eg, the Miller Fisher syndrome [MFS] and acute autonomic neuropathy) may share similar pathogenesis and can be considered a variant of GBS mately 38 40 years There may be a slight male predominance Approximately 60 70% of patients with AIDP have a history of a recent infection a few weeks prior to the onset of the neuropathy7,11 A control study of 154 patients with GBS revealed serological evidence of recent infections with Campylobacter jejuni (32%), cytomegalovirus (13%), Epstein Barr virus (10%), and Mycoplasma pneumoniae (5%)12 These were more frequent than that seen in the control population Other studies have also reported that 15 45% of patients with AIDP have serologic evidence of recent Campylobacter enteritis13 20 The relationship between C jejuni infection and the different variants of GBS (AIDP, AMSAN, and AMAN) has been the subject of many reports and is discussed in detail in the pathogenesis sections of these disorders Other infectious agents associated with GBS include cytomegalovirus, Epstein Barr virus, in uenza, hepatitis A, hepatitis B, hepatitis C, and human immunode ciency virus (HIV)7,11,18 In HIV infection, AIDP usually occurs at the time of seroconversion or early in the course of the disease Vaccinations, most notably to swine u, have been associated with GBS Further, other disorders have been linked to GBS, including other autoimmune disorders (ie, systemic lupus erythematosus), lymphoma, organ rejection or graft vs host disease following solid organ and bone marrow transplantation, and perhaps recent surgery11 Certain immunomodulating agents, such as tumor-necrosis alpha blockers, may increase the risk of developing GBS
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Clinical Features ACUTE INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY Epidemiology and Antecedent Illness
AIDP is the most common cause of acute generalized weakness, with an annual incidence ranging from 1 to 4 per 100,000 population7,10,11 The neuropathy can occur at any age, with a peak age of onset of approxiAIDP usually presents with numbness and tingling in the feet that gradually progresses up the legs and then into the arms (Table 11 2)7,11 Numbness and paresthesia can also involve the face Severe, aching, prickly, or burning neuritic pain sensations in the back and limbs are present in at least half of patients Large ber modalities (touch, vibration, and position sense) are more severely affected than small ber functions (pain and temperature perception) Progressive weakness typically accompanies the sensory disturbance The severity can
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