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Erratum

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Several figures were published out of focus and the histological sections were difficult to evaluate in the review ‘Nerve conduction studies in selected peripheral nerve disorders’ by Christian Krarup which appeared on pp 579-593 of Current Opinion in Neurology, Volume 15, issue 5 [1]. The figures are reproduced below.

Figure 1. Distal segment conduction abnormalities
Figure 1. Distal segment conduction abnormalities:
From a 61-year-old woman with diabetes mellitus for 4 years and symptoms of mild polyneuropathy with numbness and paresthesia in the toes gradually spreading to the lower legs. Decreased touch and vibration sense in the toes, absent ankle and knee jerks. Conduction studies in the right sural nerve (a) showed amplitude and conduction velocity of the CSAP at the lower limit of normal (LLN) from lateral malleolus (LM) to midcalf (MC) (b), whereas the amplitude was 78% reduced from dorsum pedis (DP) to the LM (c). Stim, stimulation; R, site of recording; S, site of stimulation.
Figure 2. The influence of conduction distance on the amplitudes and durations of compound motor and sensory action potentials
Figure 2. The influence of conduction distance on the amplitudes and durations of compound motor and sensory action potentials:
From the median and ulnar nerves of normal subjects. The distances were measured from the wrist (distance, 0). The compound motor action potential (CMAP) was recorded through surface electrodes over the abductor pollicis brevis or the abductor digiti minimi muscles, and the compound sensory action potential CSAP through near-nerve needle electrodes at wrist, elbow, axilla, and Erb's point. (a) The percentage amplitudes of the CMAPs and CSAPs were fitted with exponential functions and the 95% lower limits indicate the lower limits of normal reduction, which were markedly different for motor and sensory responses. (b) Sensory conduction velocities were about 10% greater than motor conduction velocities. (c) The duration of the CSAPs increased markedly with conduction distance as compared with CMAPs. (d) The amplitude reductions were related to increases in duration. Adapted with permission [58]
Figure 3. Erroneous diagnosis of spinal muscular atrophy in patient with presumed chronic inflammatory demyelinating neuropathy
Figure 3. Erroneous diagnosis of spinal muscular atrophy in patient with presumed chronic inflammatory demyelinating neuropathy:
A 53-year-old woman with progressive weakness of the arms and legs since the age of 30 years was diagnosed as having spinal muscular atrophy due to marked atrophy of the hands (a) and legs, and electromyography (EMG) changes suggesting anterior horn cell involvement. Four years before the latest study (June 1998) she was referred for repeat studies due to rapidly evolving weakness of right elbow flexion. EMG of the right brachial biceps (BicBR) showed chronic partial denervation and (b) discrete recruitment at maximal effort Vmax. Motor conduction studies (c) showed 95% conduction block and reduced conduction velocity between axilla and Erb's point. Sensory conduction studies (d) also showed conduction block and reduced conduction velocity across the brachial plexus. She was treated repeatedly with intravenous immunoglobulin, which had a dramatic effect on the elbow weakness but no effect on the weakness in the hands and legs probably due to severe denervation of these muscles. In January 2002 the repeat study showed full recruitment (b), no definite motor (c) or sensory (d) conduction blocks and improved motor and sensory conduction velocities. The sural nerve conduction (e) showed normal velocity and amplitude but dispersed shape of the compound sensory action potential. Cerebrospinal fluid was normal (36 mg%), definitely increased anti-GM1 antibodies, absent anti-MAG, and no evidence of spinal muscular atrophy I, II or III at survival motor neuron gene testing. The study indicated that the patient had chronic inflammatory demyelinating neuropathy rather than motor neuron disease.
Figure 4. Motor and sensory conduction block in chronic inflammatory demyelinating neuropathy
Figure 4. Motor and sensory conduction block in chronic inflammatory demyelinating neuropathy:
A 46-year-old man presented with numbness of the right hand in digits I and II 5 years previously. The symptoms progressed to the other fingers and the left hand, and he also developed weakness of the hands and the legs, which also became numb. He was treated with intravenous immunoglobulin with good effect on the numbness and weakness. Nerve conduction studies of the right ulnar nerve (a) showed marked reduction of the compound sensory action potential (CSAP) (b) (and also shown in (c) with high gain) evoked at digit V and recorded at wrist, forearm, below elbow and above elbow with near-nerve needle electrodes. This reduction indicated conduction block and temporal dispersion of sensory fibers which were localized to the distal forearm and much more pronounced than in normal nerve (d). Motor conduction studies showed conduction block of the abductor digiti minimi (ADQ) compound motor action potential (CMAP) localized to the forearm (e), and the graph in (f) shows the reduction compared with controls. The control graphs originated from values presented in Fig. 2. DV, digit 5; ADQ, adductor digiti minimi; Wr, wrist; Fo, forearm; BE, below elbow; AE, above elbow.
Figure 5. Anti-myelin-associated glycoprotein polyneuropathy treated with cyclophosphamide
Figure 5. Anti-myelin-associated glycoprotein polyneuropathy treated with cyclophosphamide:
A 65-year-old man with rapidly progressive gait ataxia and distal weakness with markedly positive Romberg's test and absent tendon reflexes was found to have an immunoglobulin M κ M-component without evidence of malignancy, and immunoglobulin M anti-myelin-associated glycoprotein antibodies (twice repeated in different laboratories). No other abnormalities, in particular no evidence of diabetes mellitus. Treated with cyclophosphamide with pronounced effect on both gait, strength and reflexes. Conduction studies before treatment in December 1999 showed severe reduction of the sural compound sensory action potential (CSAP) amplitude and moderate slowing (a), and markedly reduced compound motor action potential (CMAP) and CSAP amplitudes, slowed motor and sensory conduction and prolonged distal motor latency in the peroneal nerve (b). The sural nerve biopsy showed both light and electron microscopy (c) evidence of severe fiber and capillary changes (lower right), and the morphometry showed severe depletion of large myelinated fibers (d), which accounted for the slowing in conduction. After treatment in November 2001, the amplitude of the sural nerve CSAP had increased by 500% (a), by 100% in the peroneal nerve and the distal motor latency and motor conduction velocity showed 60% improvement (b). LM, lateral malleolus; MC, midcalf; FH, fibular head; EDB, extensor digitorum brevis. Histology reproduced by courtesy of H. Schmalbruch, University of Copenhagen, Copenhagen, Denmark.
Figure 6. Critical illness polyneuropathy
Figure 6. Critical illness polyneuropathy:
A multitraumatized 46-year-old man with sepsis, treated with steroids, antibiotics and on mechanical ventilation became tetraparetic with absent tendon reflexes. Reduced level of consciousness. Electromyography showed profuse denervation activity and absent voluntary activity in the anterior tibial muscle. (a) Median nerve conduction studies showed marked reduction of compound motor action potential amplitude and mild reduction of motor conduction velocity. The compound sensory action potentials (CSAPs) from digit (Dig) I and digit III showed mildly reduced amplitudes and conduction velocities. (b) The sural nerve CSAP showed markedly reduced amplitude and moderately reduced conduction velocity. Percentage deviations indicated in (a) and (b) are from the lower limits of normal in age-matched controls. Biopsy of the sural nerve (c) showed a large number of fibers with Wallerian degeneration (arrows); the fiber distribution (d) was normal and the number of fibers was slightly reduced. The discrepancy between the conduction studies of the sural nerve and the number and distribution of fibers was due to maintained myelin of degenerated fibers at light microscopy at this early time point. R, right; Elb, elbow; Wr, wrist; APB, abductor pollicis brevis; LM, lateral malleolus; MC, midcalf. Histology reproduced by courtesy of H. Schmalbruch, University of Copenhagen, Copenhagen, Denmark.

Reference

1 Krarup C. Nerve conduction studies in selected peripheral nerve disorders. Curr Opin Neurol 2002; 15:579-593.
© 2003 Lippincott Williams & Wilkins, Inc.