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worse in the legs1,3,4,6 10,13 Sensory NCV are normal or only mildly slow Quantitative sensory testing (QST) demonstrates abnormal thermal and vibratory perception in as many as 85% of patients7,10 In addition, autonomic testing (eg, quantitative sudomotor axon re ex and heart rate testing with deep breathing or Valsalva) is abnormal in some patients Despite the fact that sensory symptoms predominate, motor NCS are often abnormal Wolfe and colleagues reported that 60% of their patients with idiopathic polyneuropathy had abnormal motor NCS10 The most common motor abnormalities are reduced peroneal and posterior tibialis compound muscle action potentials (CMAP) amplitudes, while distal latencies and conduction velocities of the peroneal and posterior tibial CMAPs are normal or only slightly impaired Abnormalities of median and ulnar CMAPs are much less common In patients with pure small ber neuropathies, motor and sensory NCS are, by de nition, normal2,3,7,33 The peripheral autonomic nervous system is often affected in small ber neuropathies; thus, autonomic testing can be useful30,34 36 The quantitative sudomotor axon re ex test (QSART) can be performed in the distal and proximal aspects of the legs and arms (Fig 20 1) Sweat glands are innervated by small nerve bers, and impaired QSART is highly speci c and sensitive for small ber damage, with 59 80% of patients having an abnormal study (Table 20 2)30,34 36,39 Other autonomic tests (eg, heart rate (HR) variability with deep breathing (DB) or Valsalva maneuver) may also be abnormal in individuals7,39,40 In this regard, assessments can included variability of HR to DB (Fig 20 2) and response of the HR and blood pressure to Valsalva maneuvers and positional changes (eg, response to tilt table or supine to standing position) Abnormal thermal and vibratory perception thresholds may be demonstrated using QST3,7,41,42 Unlike NCS that only assess the physiology of large-diameter sensory bers, QST of heat and cold perception can.

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This rare neuropathy is caused by mutations in LITAF gene (lipopolysaccharide-induced tumor necrosis factor-alpha factor) located on chromosome 16p131 p12316,41,42 In a large study of 968 unrelated cases of CMT1, the percentage of patients with LITAF mutations was only 06%42 LITAF, also known as SIMPLE (small integral membrane protein of the lysosome/late endosome), is expressed on Schwann cells and may play a role in protein degradation pathways43

Figure 9 6 HNPP nerve biopsy Transverse section of toluidine blue-stained epon-embedded sural nerve from a patient with HNPP reveals scattered thinly myelinated nerve bers and bers with redundant myelin swellings (A) Teased Fiber preparation demonstrates a sausage-shaped myelin swelling or tomacula (B)

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affected manifest with a progressive or relapsing, generalized, and symmetric sensorimotor peripheral neuropathy that resembles CMT or even chronic in ammatory demyelinating polyneuropathy19,47,50 On examination, there is decreased sensation to all modalities, particularly large ber functions Muscle stretch re exes are usually reduced throughout, but these can be normal Pes cavus deformities and hammertoes are often evident as seen in CMT

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ber preparations47,52,58,61 The thickened myelin resembles as a sausage, hence the name tomaculous neuropathy (Latin: sausage) (Fig 9 6) These tomaculae represent redundant loops of myelin In addition, nerve biopsies reveal a reduction in large myelinated bers, segmental demyelination and remyelination, and axonal atrophy and degeneration similar to but not as severe as that seen in CMT1

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Although the clinical symptoms and signs are typically focal, NCS often reveal diffuse abnormalities19,47 51,53 55, 58,59,60 Sensory and motor NCS usually demonstrate moderately prolonged distal latencies and slightly slow NCV with normal or reduced amplitudes Slowing of NCVs, conduction block, and temporal dispersion are accentuated across typical sites of entrapment or compression (ie, the carpal and cubital tunnel, Guyon s canal, and across the bular head) and can also be demonstrated across sites of compression In addition, there also appears to be a distal accentuation of nerve conduction slowing, irrespective of possible compression47,48,55 However, this length-dependent slowing has not been appreciated by all56,57 NCS may also be abnormal in asymptomatic family members who carry the mutation

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