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P156 How does hydroquinine prevent frequent ordinary muscle cramp? New insights from surface-electromyography
Poster Session: Electromyography and Neurography
312 ~P-~
SERIAL SINGLE FIBER EMG STUDIES OF HUMAN ORBICULARIS OCULI MUSCLE AFTER ADMINISTRATION OF BOTULINUM TOXIN
A. Bogucki. EMG Laboratory, Department of Neurology, Dr K. Jonscher Hospital, 93-113 L6d£, Poland Botulinum toxin (BoTx) blocks the acetylcholine release from presynaptic motor nerve terminals. This chemical denervation leads to sprouting of motor axons and formation of new neuromuscular junctions. SF EMG was used to follow the changes of innervation in orbicularis oculi muscle after administration of BoTx. Seven patients, 4 with blepharospasm and 3 with hemifacial spasm, were studied. SF EMG examinations were performed (1) before the first injection of BoTx, at the time of (2) early and (3) stabilized clinical improvement, (4) when the dystonic movements recurred and (5) during remission produced by the second injection. Five to 8 SF EMG records were made in every patient and fiber density, jitter and frequency of blocking were always evaluated. The clinical improvement was related to severe elevation of jitter, more profound in later phase of improvement. After return of muscle function and recurrence of dystonic movements increased fiber density and tendency to lower jitter, although it remained still elevated, was observed. The second drug injection produced an elevation of jitter again. Our results suggest that terminal motor axon sprouting induced by BoTx leads to formation of new, functionally active, neuromuscular junctions, which are, at least partially, responsible for muscle function recovery.
F WAVE CHANGES AFTER TREATMENT WITH BOTULINUM TOXIN A
K. Wohlfarth, M. Schubert, B. Rothe, R. Dengler. Medical University
Hannover, Germany The clinical effects of botulinum toxin A can be explained by actions at the neuromuscular junction. Further effects on the alpha motoneurone are supposed. Therefore we performed an electrophysiological study on ten patients with torticollis spasmodicus and three patients with graphospasm before, one and five weeks after the first treatment with botulinum toxin A. We measured compound muscle action potentials (CMAPs), nerve conduction velocities (NCVs), minimal F wave latencies (Fmin) and F wave persistence of not treated muscles for each side (ulnar nerve-abductor digiti minimi muscle, peroneal nerve-tibialis anterior muscle). CMAPs and NCVs showed no significant changes after treatment. Fmin of ulnar and peroneal nerves increased significantly one week and decreased five weeks after treatment (p < 0.05). F wave persistence of ulnar nerve on the right side was reduced significantly one week after treatment (p < 0.05) whereas reduction of the values on the left side did not reach statistical significance. F wave persistence of peroneal nerve was reduced on both sides significantly one week after treatment (p < 0.05). Decreased excitability of alpha motoneurones, possibly caused by impairment of Renshaw inhibition or muscle spindle input may be the reason for the delay of F waves and the reduced F wave persistence. Endplate effects may also be discussed.
-] THE NEUROPHYSIOLOGICAL EFFECT OF THE BOTULINUM TOXIN TYPE A, F AND C ON THE HUMAN MOTOR UNITS: A COMPARISON STUDY
R. Eleopra, V. Tugnoli, O. Rossetto ~, C. Montecucco ~, R. Bombardi, D. De Grandis. Neurological Department of St. Anna Hospital of Ferrara,
Italy; I Dept. of Biological Science of the University of Padua, Italy Recently, the molecular action of the seven Botulinum Toxin (BoNT) serotypes have been unravelled. BoNT type B, D, F and G cleave at single points VAMP/synaptobrevin. BoNT A (BoNT/A) and E act specifically on SNAP-25, whereas BoNT C (BoNT/C) cleaves both SNAP-25 and syntaxin. In humans B botulism, the neuromuscular block was well studied. Nevertheless, the neurophysiological effect of other different neurotoxins was not completely clarify in humans. In order to study the electrophysiological pattern of the various neurotoxins on the Motor Units (MUs) in humans, we injected BoNT/A, BoNT/F and BoNT/C at low dosage in EDB muscle of the feet. In 8 voluntary subjects, 3 I.U. of BoNT/C in one EDB muscle and 3 I.U. of BoNT/A in the contralateral one. Similarly, in other 5 subjects we injected
3 I.U. of BoNT/F in one side and 3 I.U. of BoNT/A in the contralateral one. Before and after the injections (until 3 months), we analysed in both muscles of each subject various neurophysiological parameters: the "maximal CMAP percentage" variation after single electrical shock and after the electrical repetitive nerve stimulation (RNS), the "concentric EMG needle" examination and the "Motor Unit Number Estimation" (by multiple nerve point stimulation technique). Our data revealed no statistical differences before and after the injections of the electrophysiological parameters considered, when the CMAP amplitude was completely recovered. Nevertheless, in the side where the CMAP was less than the basal value the electrophysiological parameters revealed a decrease in the number of the active MUs, with a electrophysiological pattern of the CMAP and RNS different for the various BoNTs.
•]
ACUTE EFFECTS OF INTRAVENOUS INJECTION OF BETA-ADRENORECEPTOR- AND CALCIUM CHANNEL ANTAGONISTS AND AGONISTS IN MYASTHENIA GRAVIS
C. Swemp, I. Jonkers, R. Pirskanen. Dept of Clinical Neurophysiology, S6der Hospital, Stockholm, Sweden; University of Leiden, Leiden, The Netherlands; Dept of Neurology, S6der Hospital, Stockholm, Sweden The effect of intravenous injection of therapeutic doses of propranolol, verapamil, terbutaline, calcium and edrophonium on neuromuscular transmission has been studied with clinical tests and repetitive nerve stimulation in 10 patients with moderate myasthenia gravis (MG). The mean decrement of the deltoid muscle was not significantly changed after injection of propranolol or verapamil. Terbutaline applied after propranolol and calcium applied after verapamil improved the decrement substantially. Edrophonium applied after propranolol or verapamil also greatly improved the decrement. We conclude that there is no rapid deterioration of neuromuscular transmission in patients with moderately severe MG after injection with therapeutic doses of propranolol and verapamil. However, we do not know if the most severely disabled MG patient could have reacted otherwise. We consider that in cardiovascular emergencies propranolol and verapamil may be used even in severe MG but with resuscitation equipment as well as specific antidotes available.
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HOW DOES HYDROQUININE PREVENT FREQUENT ORDINARY MUSCLE CRAMP? NEW INSIGHTS FROM SU RFACE-ELECTROMYOGRAPHY
K. Roeleveld 1, P.H.P. Jansen 2, D.F. Stegeman 1. i Dept of Clinical Neurophysiology, University Hospital Nijmegen, The Netherlands; 2 Dept of Neurology, Hospital Gelderse Vallei, Ede. The Netherlands Hydroquinine and its derivatives are effective in preventing frequent ordinary muscle cramp (1). Their exact mechanism of action however is still unknown. We studied the effects of hydroquinine on voluntarily induced muscle cramp and maximal voluntary contraction of calf muscles by 64 channel surface-EMG-topography. As expected hydroquinine reduced the number of voluntarily induced cramps; their electro-physiological properties were not influenced. Only parts of calf musculature were involved in the cramps, that could start anywhere, often at several places simultaneously, and spread slowly and erratically over the muscle. During cramps the EMG spectrum showed higher frequencies. Hydroquinine reduced the muscle fibre conduction velocities during maximal voluntary contraction to values below normal but did not influence the nerve conduction velocities. We conclude that hydroquinine raises the threshold for frequent ordinary muscle cramp by acting on the sarcolemma and possibly also on the unmyelinated terminal nerve branches. Reference
[l] Jansen PHP et al J Neurol Sci 1994; 122:157-61 ~ - ~
ACUTE STEROID MYOPATHY IN PATIENTS UNDER SEDATION WITHOUT NDMBA
Ph. Hanson, Th. Deltombe, A. Dive, J.M. Brucher. Mont-Godinne
University Hospital & Saint-Luc University Hospital, B-5530 Yvoir, Belgium Several recent papers have attributed the occurrence of acute myopathy in
312 ~P-~
SERIAL SINGLE FIBER EMG STUDIES OF HUMAN ORBICULARIS OCULI MUSCLE AFTER ADMINISTRATION OF BOTULINUM TOXIN
A. Bogucki. EMG Laboratory, Department of Neurology, Dr K. Jonscher Hospital, 93-113 L6d£, Poland Botulinum toxin (BoTx) blocks the acetylcholine release from presynaptic motor nerve terminals. This chemical denervation leads to sprouting of motor axons and formation of new neuromuscular junctions. SF EMG was used to follow the changes of innervation in orbicularis oculi muscle after administration of BoTx. Seven patients, 4 with blepharospasm and 3 with hemifacial spasm, were studied. SF EMG examinations were performed (1) before the first injection of BoTx, at the time of (2) early and (3) stabilized clinical improvement, (4) when the dystonic movements recurred and (5) during remission produced by the second injection. Five to 8 SF EMG records were made in every patient and fiber density, jitter and frequency of blocking were always evaluated. The clinical improvement was related to severe elevation of jitter, more profound in later phase of improvement. After return of muscle function and recurrence of dystonic movements increased fiber density and tendency to lower jitter, although it remained still elevated, was observed. The second drug injection produced an elevation of jitter again. Our results suggest that terminal motor axon sprouting induced by BoTx leads to formation of new, functionally active, neuromuscular junctions, which are, at least partially, responsible for muscle function recovery.
F WAVE CHANGES AFTER TREATMENT WITH BOTULINUM TOXIN A
K. Wohlfarth, M. Schubert, B. Rothe, R. Dengler. Medical University
Hannover, Germany The clinical effects of botulinum toxin A can be explained by actions at the neuromuscular junction. Further effects on the alpha motoneurone are supposed. Therefore we performed an electrophysiological study on ten patients with torticollis spasmodicus and three patients with graphospasm before, one and five weeks after the first treatment with botulinum toxin A. We measured compound muscle action potentials (CMAPs), nerve conduction velocities (NCVs), minimal F wave latencies (Fmin) and F wave persistence of not treated muscles for each side (ulnar nerve-abductor digiti minimi muscle, peroneal nerve-tibialis anterior muscle). CMAPs and NCVs showed no significant changes after treatment. Fmin of ulnar and peroneal nerves increased significantly one week and decreased five weeks after treatment (p < 0.05). F wave persistence of ulnar nerve on the right side was reduced significantly one week after treatment (p < 0.05) whereas reduction of the values on the left side did not reach statistical significance. F wave persistence of peroneal nerve was reduced on both sides significantly one week after treatment (p < 0.05). Decreased excitability of alpha motoneurones, possibly caused by impairment of Renshaw inhibition or muscle spindle input may be the reason for the delay of F waves and the reduced F wave persistence. Endplate effects may also be discussed.
-] THE NEUROPHYSIOLOGICAL EFFECT OF THE BOTULINUM TOXIN TYPE A, F AND C ON THE HUMAN MOTOR UNITS: A COMPARISON STUDY
R. Eleopra, V. Tugnoli, O. Rossetto ~, C. Montecucco ~, R. Bombardi, D. De Grandis. Neurological Department of St. Anna Hospital of Ferrara,
Italy; I Dept. of Biological Science of the University of Padua, Italy Recently, the molecular action of the seven Botulinum Toxin (BoNT) serotypes have been unravelled. BoNT type B, D, F and G cleave at single points VAMP/synaptobrevin. BoNT A (BoNT/A) and E act specifically on SNAP-25, whereas BoNT C (BoNT/C) cleaves both SNAP-25 and syntaxin. In humans B botulism, the neuromuscular block was well studied. Nevertheless, the neurophysiological effect of other different neurotoxins was not completely clarify in humans. In order to study the electrophysiological pattern of the various neurotoxins on the Motor Units (MUs) in humans, we injected BoNT/A, BoNT/F and BoNT/C at low dosage in EDB muscle of the feet. In 8 voluntary subjects, 3 I.U. of BoNT/C in one EDB muscle and 3 I.U. of BoNT/A in the contralateral one. Similarly, in other 5 subjects we injected
3 I.U. of BoNT/F in one side and 3 I.U. of BoNT/A in the contralateral one. Before and after the injections (until 3 months), we analysed in both muscles of each subject various neurophysiological parameters: the "maximal CMAP percentage" variation after single electrical shock and after the electrical repetitive nerve stimulation (RNS), the "concentric EMG needle" examination and the "Motor Unit Number Estimation" (by multiple nerve point stimulation technique). Our data revealed no statistical differences before and after the injections of the electrophysiological parameters considered, when the CMAP amplitude was completely recovered. Nevertheless, in the side where the CMAP was less than the basal value the electrophysiological parameters revealed a decrease in the number of the active MUs, with a electrophysiological pattern of the CMAP and RNS different for the various BoNTs.
•]
ACUTE EFFECTS OF INTRAVENOUS INJECTION OF BETA-ADRENORECEPTOR- AND CALCIUM CHANNEL ANTAGONISTS AND AGONISTS IN MYASTHENIA GRAVIS
C. Swemp, I. Jonkers, R. Pirskanen. Dept of Clinical Neurophysiology, S6der Hospital, Stockholm, Sweden; University of Leiden, Leiden, The Netherlands; Dept of Neurology, S6der Hospital, Stockholm, Sweden The effect of intravenous injection of therapeutic doses of propranolol, verapamil, terbutaline, calcium and edrophonium on neuromuscular transmission has been studied with clinical tests and repetitive nerve stimulation in 10 patients with moderate myasthenia gravis (MG). The mean decrement of the deltoid muscle was not significantly changed after injection of propranolol or verapamil. Terbutaline applied after propranolol and calcium applied after verapamil improved the decrement substantially. Edrophonium applied after propranolol or verapamil also greatly improved the decrement. We conclude that there is no rapid deterioration of neuromuscular transmission in patients with moderately severe MG after injection with therapeutic doses of propranolol and verapamil. However, we do not know if the most severely disabled MG patient could have reacted otherwise. We consider that in cardiovascular emergencies propranolol and verapamil may be used even in severe MG but with resuscitation equipment as well as specific antidotes available.
~
HOW DOES HYDROQUININE PREVENT FREQUENT ORDINARY MUSCLE CRAMP? NEW INSIGHTS FROM SU RFACE-ELECTROMYOGRAPHY
K. Roeleveld 1, P.H.P. Jansen 2, D.F. Stegeman 1. i Dept of Clinical Neurophysiology, University Hospital Nijmegen, The Netherlands; 2 Dept of Neurology, Hospital Gelderse Vallei, Ede. The Netherlands Hydroquinine and its derivatives are effective in preventing frequent ordinary muscle cramp (1). Their exact mechanism of action however is still unknown. We studied the effects of hydroquinine on voluntarily induced muscle cramp and maximal voluntary contraction of calf muscles by 64 channel surface-EMG-topography. As expected hydroquinine reduced the number of voluntarily induced cramps; their electro-physiological properties were not influenced. Only parts of calf musculature were involved in the cramps, that could start anywhere, often at several places simultaneously, and spread slowly and erratically over the muscle. During cramps the EMG spectrum showed higher frequencies. Hydroquinine reduced the muscle fibre conduction velocities during maximal voluntary contraction to values below normal but did not influence the nerve conduction velocities. We conclude that hydroquinine raises the threshold for frequent ordinary muscle cramp by acting on the sarcolemma and possibly also on the unmyelinated terminal nerve branches. Reference
[l] Jansen PHP et al J Neurol Sci 1994; 122:157-61 ~ - ~
ACUTE STEROID MYOPATHY IN PATIENTS UNDER SEDATION WITHOUT NDMBA
Ph. Hanson, Th. Deltombe, A. Dive, J.M. Brucher. Mont-Godinne
University Hospital & Saint-Luc University Hospital, B-5530 Yvoir, Belgium Several recent papers have attributed the occurrence of acute myopathy in