LETTER TO THE EDITOR
LONG-TERM RECOVERY IN CRITICAL ILLNESS MYOPATHY IS COMPLETE, CONTRARY TO POLYNEUROPATHY We read the article by Koch et al. with great interest.1 They found that, 1 year after discharge from the intensive care unit, patients diagnosed initially solely with critical illness myopathy (CIM) had a better prognosis than patients with either critical illness polyneuropathy (CIP) or CIM/CIP. The authors diagnosed CIM if the amplitude of compound muscle action potentials after direct muscle stimulation (dmCMAPs) or the duration of motor unit action potentials on electromyographic (EMG) examination were reduced. The sole indicator for CIP was reduced sensory nerve action potential (SNAP) amplitudes. dmCMAP amplitudes are reduced in both myopathy and motor neuropathy.2 On the other hand, quantitative needle EMG can only be done in conscious patients who are able to cooperate. Therefore, CIM will be overdiagnosed in all sedated patients, in whom quantitative EMG is unavailable. Similarly, motor neuropathy will be underdiagnosed if reduced SNAP amplitudes are the sole criterion for CIP. As a result, it seems likely that several patients were misclassified as CIM-only in the study by Koch et al.1 Based on these considerations and our own observations3 we disagree with their conclusion that CIM patients enjoy complete recovery, and we offer an alternative explanation for the findings. We previously studied the pattern of electrophysiological abnormalities prospectively in 30 patients with sepsis/systemic inflammatory response syndrome.3 Motor (median and ulnar unilaterally, and common fibular and tibial bilaterally) and sensory (median and ulnar unilaterally, and sural bilaterally) nerve conduction studies were performed weekly from admission until discharge, and after 6 months. Differences from reference values of compound muscle action potentials (CMAPs), SNAPs, and motor and sensory nerve conduction velocities (NCVs) were subject to cluster analysis. We were able to delineate 4 different topographical patterns of neuromuscular injury (Table 1), which reflect different levels of severity and
were associated with clinical outcome.3 Although cluster 1 contained patients and controls with normal electrophysiological values, cluster 2 included only patients with abnormal CMAPs in the lower extremities. Cluster 3 contained patients with moderately abnormal CMAPs, SNAPs, and sensory NCVs in the extremities and motor NCVs in the lower extremities. Finally, cluster 4 was comprised of patients with severely abnormal CMAPs, SNAPs, and NCVs in all extremities. Thus, decreased CMAP amplitude was the most benign abnormality, whereas SNAP and sensory NCV were affected only in more severe patterns.3 Importantly, because the abnormalities in cluster 2 were restricted to the lower extremities, a length-dependent pathophysiology was suggested, implicating the (co-)presence of CIP. Therefore, although the electrophysiological signature of cluster 2 was broadly similar to that of patients classified as CIM by Koch et al.,1 a more parsimonious explanation is less severe neuromuscular injury, rather than an exclusive myopathic pathology. From these observations we conclude that, if electrophysiological investigation is employed for prognostication in critically ill patients, it may be more favorable to assess the load of neuromuscular injury rather than attempt to differentiate CIM from CIP. Petra Baum, MD Joseph Classen, MD Department of Neurology, University Hospital Leipzig, Leipzig, Germany 1. Koch S, Wollersheim T, Bierbrauer J, Haas K, Morgeli R, Deja M, et al. Long-term recovery in critical illness myopathy is complete, contrary to polyneuropathy. Muscle Nerve 2014;50:431–436. 2. Lefaucheur J, Nordine T, Rodriguez P, Brochard L. Origin of ICU acquired paresis determined by direct muscle stimulation. J Neurol Neurosurg Psychiatry 2006;77:500–506. 3. Baum P, Bercker S, Villmann T, Classen J, Hermann W. Critical illness myopathy and neuropathy (CRIMYN). Electroneurographic classification. Nervenarzt 2011;82:468–474.
Published online 00 Month 2014 in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/mus.24532
---------------------------------------------------------
C 2014 Wiley Periodicals, Inc. V
Letter to the Editor
MUSCLE & NERVE
Month 2014
1
Table 1. Patterns of electrophysiological disturbances by cluster analysis in 30 patients with sepsis/SIRS and 63 healthy subjects. Pattern clusters
SNAP
SNCV
UE: normal LE: normal UE: normal/borderline LE: normal/borderline
UE: normal LE: normal UE: normal/borderline LE: normal/borderline
3 (12 pts.)
UE: pathological LE: pathological
UE: pathological LE: pathological
4 (10 pts.)
UE: pathological LE: pathological (same as cluster 3)
UE: pathological LE: pathological (same as cluster 3)
1 (3 pts.) 2 (5 pts.)
CMAP UE: normal LE: normal UE: normal LE: fibular nerve pathological, tibial nerve normal > pathological UE: pathological; LE: pathological (better than 4)
UE: pathological LE: pathological
MNCV UE: normal LE: normal UE: normal LE: normal/borderline
UE: normal LE: fibular nerve pathological > normal tibial nerve normal > pathological UE: pathological LE: pathological
SIRS, systemic inflammatory response syndrome; UE, upper extremity; LE, lower extremity; SNAP, amplitude sensory nerve action potential; SNCV, sensory nerve conduction velocity; CMAP, compound muscle action potential; MNCV, motor nerve conduction velocity.
LONG-TERM RECOVERY IN CRITICAL ILLNESS MYOPATHY IS COMPLETE, CONTRARY TO POLYNEUROPATHY We read the article by Koch et al. with great interest.1 They found that, 1 year after discharge from the intensive care unit, patients diagnosed initially solely with critical illness myopathy (CIM) had a better prognosis than patients with either critical illness polyneuropathy (CIP) or CIM/CIP. The authors diagnosed CIM if the amplitude of compound muscle action potentials after direct muscle stimulation (dmCMAPs) or the duration of motor unit action potentials on electromyographic (EMG) examination were reduced. The sole indicator for CIP was reduced sensory nerve action potential (SNAP) amplitudes. dmCMAP amplitudes are reduced in both myopathy and motor neuropathy.2 On the other hand, quantitative needle EMG can only be done in conscious patients who are able to cooperate. Therefore, CIM will be overdiagnosed in all sedated patients, in whom quantitative EMG is unavailable. Similarly, motor neuropathy will be underdiagnosed if reduced SNAP amplitudes are the sole criterion for CIP. As a result, it seems likely that several patients were misclassified as CIM-only in the study by Koch et al.1 Based on these considerations and our own observations3 we disagree with their conclusion that CIM patients enjoy complete recovery, and we offer an alternative explanation for the findings. We previously studied the pattern of electrophysiological abnormalities prospectively in 30 patients with sepsis/systemic inflammatory response syndrome.3 Motor (median and ulnar unilaterally, and common fibular and tibial bilaterally) and sensory (median and ulnar unilaterally, and sural bilaterally) nerve conduction studies were performed weekly from admission until discharge, and after 6 months. Differences from reference values of compound muscle action potentials (CMAPs), SNAPs, and motor and sensory nerve conduction velocities (NCVs) were subject to cluster analysis. We were able to delineate 4 different topographical patterns of neuromuscular injury (Table 1), which reflect different levels of severity and
were associated with clinical outcome.3 Although cluster 1 contained patients and controls with normal electrophysiological values, cluster 2 included only patients with abnormal CMAPs in the lower extremities. Cluster 3 contained patients with moderately abnormal CMAPs, SNAPs, and sensory NCVs in the extremities and motor NCVs in the lower extremities. Finally, cluster 4 was comprised of patients with severely abnormal CMAPs, SNAPs, and NCVs in all extremities. Thus, decreased CMAP amplitude was the most benign abnormality, whereas SNAP and sensory NCV were affected only in more severe patterns.3 Importantly, because the abnormalities in cluster 2 were restricted to the lower extremities, a length-dependent pathophysiology was suggested, implicating the (co-)presence of CIP. Therefore, although the electrophysiological signature of cluster 2 was broadly similar to that of patients classified as CIM by Koch et al.,1 a more parsimonious explanation is less severe neuromuscular injury, rather than an exclusive myopathic pathology. From these observations we conclude that, if electrophysiological investigation is employed for prognostication in critically ill patients, it may be more favorable to assess the load of neuromuscular injury rather than attempt to differentiate CIM from CIP. Petra Baum, MD Joseph Classen, MD Department of Neurology, University Hospital Leipzig, Leipzig, Germany 1. Koch S, Wollersheim T, Bierbrauer J, Haas K, Morgeli R, Deja M, et al. Long-term recovery in critical illness myopathy is complete, contrary to polyneuropathy. Muscle Nerve 2014;50:431–436. 2. Lefaucheur J, Nordine T, Rodriguez P, Brochard L. Origin of ICU acquired paresis determined by direct muscle stimulation. J Neurol Neurosurg Psychiatry 2006;77:500–506. 3. Baum P, Bercker S, Villmann T, Classen J, Hermann W. Critical illness myopathy and neuropathy (CRIMYN). Electroneurographic classification. Nervenarzt 2011;82:468–474.
Published online 00 Month 2014 in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/mus.24532
---------------------------------------------------------
C 2014 Wiley Periodicals, Inc. V
Letter to the Editor
MUSCLE & NERVE
Month 2014
1
Table 1. Patterns of electrophysiological disturbances by cluster analysis in 30 patients with sepsis/SIRS and 63 healthy subjects. Pattern clusters
SNAP
SNCV
UE: normal LE: normal UE: normal/borderline LE: normal/borderline
UE: normal LE: normal UE: normal/borderline LE: normal/borderline
3 (12 pts.)
UE: pathological LE: pathological
UE: pathological LE: pathological
4 (10 pts.)
UE: pathological LE: pathological (same as cluster 3)
UE: pathological LE: pathological (same as cluster 3)
1 (3 pts.) 2 (5 pts.)
CMAP UE: normal LE: normal UE: normal LE: fibular nerve pathological, tibial nerve normal > pathological UE: pathological; LE: pathological (better than 4)
UE: pathological LE: pathological
MNCV UE: normal LE: normal UE: normal LE: normal/borderline
UE: normal LE: fibular nerve pathological > normal tibial nerve normal > pathological UE: pathological LE: pathological
SIRS, systemic inflammatory response syndrome; UE, upper extremity; LE, lower extremity; SNAP, amplitude sensory nerve action potential; SNCV, sensory nerve conduction velocity; CMAP, compound muscle action potential; MNCV, motor nerve conduction velocity.
