Journal of

rqeurao

J. Neurol. 221, 151--162 (1979)

~) by Springer-Verlag 1979

Influence of Temperature on Isometric Contraction and Passive Muscular Tension in Paramyotonia Congenita (Eulenburg) A. Haass Z, K. Ricker l*, G. Hertel ~, and R. Heene 2 ~Neurologische Universit~itsklinik, Josef-Schneider-Stral3e 11, D-8700 Wiirzburg, and 2Universitiitsnervenklinik, D-3500 Marburg/Lahn, Federal Republic of Germany

Summary. Four patients without symptoms of episodic hyperkalemic weakness from two families with paramyotonia congenita (Eulenburg) are described. 1. Maximum voluntary muscle contraction of the upper and lower arm was studied under isometric conditions at different temperatures. If the temperature was lowered stepwise, distinct paresis occured at 32--3 I°C which increased with the amount of muscular effort. The upper arm muscles, however, developed weakness gradually after cooling. 2. During cooling of the resting muscle, the E M G showed dense spontaneous activity of the fibrillary type, which decreased again at about 30 ° C. It can be assumed that in paramyotonia congenita cooling produces muscle cell membrane depolarization which at a critical level causes the firing of action potentials and finally muscular paresis. 3. Increasing muscular stiffness can be interpreted as abnormally slow muscular relaxation after isometric contraction. In the forearm muscles the time to 3/4 relaxation after cooling was about six times normal, in the upper arm muscles only two times normal. As an additional parameter the mechanical resistance to passive stretching of a muscle has been studied. This passive muscular tension increased simultaneously with the onset of weakness. 4. The close relation between weakness and stiffness suggests that both symptoms are caused by the same basic defect which is probably located in the sarcolemma. It is suggested that a defect of the sodium channel causes a coolingdependent increase in sodium conductance. Raised intracellular sodium causes in the first place membrane depolarization, and in the second place depression of calcium reuptake through competition by sodium for calcium binding sites. This would explain muscle stiffness and delayed relaxation as well. Key words: Paramyotonia congenita - Muscle cooling - Isometric muscle contraction - Muscular tension passive - Muscle fiber discharges - Membrane depolarization. * Corresponding author

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Zusammenfassung. Es werden 4 Patienten aus zwei neuentdeckten Familien mit Paramyotonia congenita (Eulenburg) beschrieben. 1. Untersucht wurde die maximale willkürliche Muskelkontraktion unter isometrischen Bedingungen bei unterschiedlichen Temperaturen. Wurde die Muskelarbeit konstant gehalten und die Temperatur schrittweise gesenkt, so trat an den Flexormuskeln des Unterarms bei 32--31°C eine ausgeprägte Parese auf. An den Oberarmmuskeln entwickelte sich dagegen die Schwäche nach Kühlung allmählich. 2. Während der Abkühlung des ruhenden Muskels wurde dichte spontane, fibrillationsartige Aktivität im E M G registriert, die bei etwa 30°C wieder abnahm. Daraus läßt sich folgern, daß durch Abkühlung bei Paramyotonie die Muskelzellmembran depolarisiert, wodurch bei einem kritischen Potentialniveau das Feuern der Aktionspotentiale verursacht wird und schließlich die Lähmung. 3. Die zunehmende Muskelsteife (,paradoxe Myotonie") läßt sich als verzögerte Muskelerschlaffung nach einer isometrischen Kontraktion registrieren. An den Flexoren des Unterarms war die Zeit bis zur 3/4-Erschlaffung nach Kühlung auf das Sechsfache verlängert, an den Oberarmmuskeln nur auf das Zweifache. Als ein weiterer Parameter wurde der mechanische Muskelwiderstand bei passiver Dehnung gemessen. Dieser passive Widerstand steigt zur selben Zeit erheblich an, in der die Muskelschwäche beginnt. 4. Die enge Verbindung von Schwäche und Muskelsteifigkeit legt den Gedanken nahe, daß beide Symptome durch ein und denselben Defekt hervorgerufen werden, welcher wahrscheinlich im Sarcolemm liegt. Als Hypothese wird vorgeschlagen, daß sich die Natriumleitfähigkeit der Membran unter Abkühlung erhöht. Vermehrung des intracellulären Natriums würde erstens eine Membrandepolarisierung hervorrufen, und zweitens könnte durch Verdrängung an den Calciumbindungsstellen die Calciumrückresorption in das sarkoplasmatische Retikulum behindert werden. Dadurch wäre die paramyotone Muskelsteifigkeit zu erklären.

Introduetion Muscle stiffness and weakness are the essential signs of paramyotonia congenita (Eulenburg). The disturbance develops always after cooling the muscle during repeated and strong muscle contractions. Sometimes stiffness occurs even at normal temperature (Magee, 1963, 1966). The influence of muscle temperature as weil as of the force of contraction on stiffness and paresis have rarely been studied in detail. Burke et al. (1974) investigated the adductor digiti mimimi muscle and stressed that the paramyotonic disturbance is essentially produced by muscle effort: "Although cooling accentuates the defect, it does not appear to introduce any new factor not seen at normal or elevated temperature". LaJoie (1960), however, pointed out that with the application of cold for a sufficient length of time all electrical activity can be obliterated producing a temporary paralysis of the muscles. Ricker et al. (1974) found that the abductor pollicis brevis is almost completely paralyzed after cooling the resting muscle for about half an hour.

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Similar paresis due to cooling has not been observed in a n y other m u s c u l a r disease. P a r a m y o t o n i a congenita does not show the same s y m p t o m s in all muscles. Paralysis develops rapidly in the small muscles of the h a n d as weil as the long extensors of the fingers after cooling. The first s y m p t o m of the long flexors of the fingers is muscle stiffness, which then progresses to weakness. The f u n c t i o n of the p r o x i m a l a r m muscles is disturbed only after long lasting a n d u n u s u a l l y deep cooling. This holds at least true for most patients with p a r a m y o t o n i a in West G e r m a n y (Becker, 1970). It seemed a p p r o p r i a t e to study other muscles besides the small h a n d muscles. The present investigation aims at answering the following questions: 1. W h a t influence has t e m p e r a t u r e o n the force of isometric c o n t r a c t i o n ? 2. W h a t is the relation between t e m p e r a t u r e a n d m u s c u l a r stiffness? The latter is defined in terms of relaxation time after m a x i m u m c o n t r a c t i o n , a n d mechanical resistance to stretching of the cooled muscle (=passive m u s c u l a r tension).

Case Reports 1. F.R., a man aged 37, had, since childhood, experienced stiffness and subsequent weakness of his fingers after exposure to cold and sudden temperature changes. He could not open his eyes immediately after forced lid closure. Symptoms of adynamia episodica never occured. The muscles are strikingly hypertrophic. Slight percussion myotonia was demonstrated on the forearm muscles. The EMG showed series of typical myotonic discharges. The motor unit pattern was normal. Several times the CPK was increased to 200mU/ml (normal: 50mU/ml). After ingestion of 120mval potassium the plasma potassium concentration increased from 4.9 to 6.8 mval/1. The patient experienced a slight transient stiffness in his legs. Muscle weakness did not occur. A biopsy from the left biceps brachii displayed increased internal nuclei, moderate hypertrophy of the muscle fibers with mean diameters of about 80 lam for type 1 (ATPase) and 95 lam for type 2 fibers. ATPase type 2B fibers were completely absent. He suffered from occasional psychomotor and generalized epileptic seizures since the age of 12. His daily medication is 0.3g phenytoin and 0.6g carbamazepine. A daughter, aged 10, also has paramyotonia. The patient's mother was healthy. His father died early and it is uncertain whether he had paramyotonia, although he might have had since his brother (the uncle of the patient) definitely had paramyotonic symptoms. 2. G.R., a girl aged 10 (daughter of F.R.), had been troubled by muscle stiffness since the age of 6 when playing outdoors during cold weather. Her muscular system was weil developed. The EMG demonstrated series of myotonic discharges. The motor unit pattern was normal. The CPK was 50mU/ml. A biopsy taken from the right rectus femoris muscle displayed normal histological and histochemical findings. 3. E.R., a man aged 29, had symptoms of paramyotonia since early childhood. His face and fingers become stift when he exposed to slight cold. The ensueing weakness can last for 1-2 h. He experiences stiffness of the fingers even in his warm office after having written for some time. Symptoms of adynamia episodica have never been observed. When falling down during soccer games, his legs may become stift for some seconds and he cannot get up immediately, His mother (F.R.) has paramyotonia and his grandmother is said to have had the same symptoms. The muscles are hypertrophic. Slight percussion myotonia was elicited in the extensor digitorum longus. Lid lag occurred after sudden downward gaze. After having clenched his rist firmly, the patient opened it without difficulty. Slight cooling induced paradoxical myotonia, and stronger cooling and physical activity caused complete immobility. Typical myotonic

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discharges were observed in the EMG at normal temperature. The motor unit pattern was normal. Two determinations of CPK showed increased values: 340 and 820mU/ml. 4. F.R., a woman aged 57 (mother of E.R.), had symptoms of paramyotonia since childhood. But it was only during strong cooling as in winter or in cold water that the fingers became stift and weak. She never noticed this at warm temperatures. Therefore she was worried about her son, because sometimes he suffered from stiffness of bis hands at room temperature. The muscles were weil developed but not hypertrophic. No percussion myotonia and no lid lag were found. She could open her fingers immediately after forceful fist closure. The EMG demonstrated typical myotonic discharges. The motor unit pattern was normal. The CPK was 37 mU/ml. After the muscles of the hand and forearm had been cooled to 32°C the movements of the fingers were distinctly slower and after some contractions, weakness appeared which vanished within 2h.

Methods 1. Muscles of the upper arm: The strength of the muscles which flex the forearm (biceps, brachialis, brachioradialis) was recorded under isometric conditions. The upper arm was fixed in a horizontal position, the lower arm held up vertically (the angle between the upper and lower arm thus being 90°). The force developed was measured at the wrist, which was connected to a force transducer by a metal cuff and rod (Vredenbregt and Rau, 1973). The patient was instructed to develop maximum force and then relax the muscle immediately. The maneuver was repeated several times. The patient could observe the registration on an oscilloscope. The intramuscular temperature was measured by a needle electrode which was also used for EMG recording. The electrode was inserted approximately 2cm into the belly of the biceps muscle. The arm was cooled in water at about 10°C. 2. Muscles of the forearm: The EMG was recorded with two platinum wires with 1 mm of the tip exposed. These were inserted into the flexor digitorum muscle at a distance of 10 mm from each other in the longitudinal direction of the fibers. The force when clenching the fist was measured under isometric conditions. The patient pressed the fingers on a metal plate which was connected to a force transducer. The forearm and the hand were placed in a tube which could be filled with warm or cold water. The temperature was measured with a needle electrode from inside the flexor digitorum communis muscle. A marked slowing of the finger movements occurs in patients with paramyotonia after cooling when they open and close the rist repeatedly (paradoxical myotonia). When the movement is stopped after several muscle contractions, the fingers remain in a flexed position (paramyotonic stiffness) and there was strong resistance to passive stretching of the flexed fingers. This muscular resistance (passive muscular tension) was measured as follows. A metal

Fig. 1. Method of recording isometric contraction and the mechanical resistance to stretching (=passive muscular tension) of flexor digitorum muscle

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plate at the flexor side of the fingers was connected to an electromotor by a cord (Fig. 1). The motor was started by a special switch immediately after the full relaxation of the isometric contraction. It opened the hand with a constant velocity of 8cm/s to an almost stretched position of 135° (180°=complete stretching). This velocity was greater than the speed with which the patient was able to open his hand voluntarily under conditions of paramyotonic stiffness. The passive tension was measured by a force transducer between the electromotor and the fingers.

Results

1. Force of Contraction and Relaxation Time of the Muscles of the Upper Arm. Figure 2 shows the force of isometric c o n t r a c t i o n of patient F.R. At an intram u s c u l a r t e m p e r a t u r e of 36°C the force was n o r m a l . After cooling to 29°C the force of the first c o n t r a c t i o n was a b o u t 40% less t h a n at 36°C. D u r i n g the following c o n t r a c t i o n s the force a n d the E M G activity gradually decreased. The force of the 30th c o n t r a c t i o n was a b o u t 85% smaller than the initial one. This paresis persisted after rewarming. Only during the following 4 h did the force

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Fig.2. Patient F.R. Force of isometric contraction of muscles which flex forearm (biceps, brachialis, brachioradialis). Repetitive maximum voluntary contraction at 36°C and 29°C, and after rewarming to 39°C. Between the two registrations at 29°C the muscle was rested for 5 min. Time in seconds (s); force in Newton (N)

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slowly return to normal values. Similar results were obtained from the daughter G.R. (Fig. 3). Muscle relaxation was not essentially p r o l o n g e d (Fig. 2). The time to 3/4 relaxation was measured on a high speed recording similar to Figure 5. After cooling, this time increased twofold. 2. EMG, Force, Relaxation and Passive Tension of the Forearm Muscles. With patient F.R., the temperature in the flexor digitorum muscle was lowered from 36 ° to 32°C within 15 min. When the temperature was about 3 4 ° - 3 3 ° C (Fig. 4) increasingly dense spontaneous activity was registered in the EMG. This activity occurred in the resting muscle without any mechanical irritation, obviously caused only by the temperature decrease. In spite of the E M G activity the patient experienced no stiffness when moving his fingers slightly. The spontaneous activity consisted of spikes resembling fibrillation potentials. At about 32°C the activity was strongly reduced and disappeared at about 28°C. It did not reappear during the following rewarming. The activity also disappeared after voluntary contractions. At 32°C the relaxation after voluntary contraction was distinctly prolonged. However, the E M G revealed no "afteractivity" (Fig. 5). In some recordings at 3 2 ° - 3 0 ° C the spontaneous activity gradually reappeared several seconds after the last voluntary muscular contraction. The intramuscular temperature was lowered stepwise in further investigations. At each temperature level the patient delivered the same amount of muscular effort consisting of ten short maximal contractions. The passive muscle tension was measured immediately after the full relaxation of the last contraction as described above. During the following 15 min of muscle rest, the temperature was furtherlowered by about I°C. Then 10 contractions were recorded again. Figure 6 gives the original recordings of the last contractions at 36 °, 32 °, 30°C. In Figure 7 the values of the maximum force, the time to 3/4 relaxation and the passive muscular tension at the different temperatures are registered. A marked decrease of the force occurred at about 30°C. At this temperature, the force of the first contraction was already low. During the following nine contractions no further reduction occurred. At 29°C the force had decreased further. The

Influence of Temperature on Isometric Contraction

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muscle relaxation was considerably delayed at about 33°-32°C. At 30°C the time to ~4 relaxation was six times longer as compared to the time at 36°C (Fig. 7). At normal temperature and after slight cooling no passive tension could be measured. The patient still was able to open his rist voluntarily with a higher speed than the pull of the electromotor. At 32°C, the voluntary opening was distinctly delayed, and at 30°C was nearly impossible. Increased passive muscular tension was recorded between 32 ° and 30°C. This passive tension reached its peak value (about 12Newton) at the same time when the force of voluntary contraction weakened, and it decreased again below 29°C.

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Fig.5. Patient F. R. Repetitive maximum voluntary contraction of flexor digitorum muscle after cooling to 32°C. Upper line: force of isometric contraction. Lower line: EMG recorded by wire electrodes. Above: 3rd contraction. Below: 8th contraction. Muscle relaxation is delayed without after-activity in EMG (only one short myotonic discharge of a single muscle fiber)

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Fig. 6. Patient F. R. Original recordings of repetitive voluntary closing and opening of fingers at different temperatures (Fig. 1). Only last of 10 repetitive contractions performed at 36 °, 32 °, and 30°C are shown. Above: force of maximum isometric contraction of flexor digitorum muscle (N = Newton). Middle: finger position (closed or opened). Below: passive muscle tension (Newton) at 32 ° and 30°C. (Fist is opened by pull of electromotor; Figure 1 and Methods). At 32°C force of isometric contraction is only slightly reduced. Muscle relaxation is delayed and voluntary opening of fingers is slow. Passive muscular tension is only slightly increased. At 30°C force is definitely decreased, voluntary opening of fingers is almost impossible, and passive muscular tension is high. (Complete data at each temperature are shown in Figure 7)

Influence of Temperature on Isometric Contraction

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Fig. 7. Patient F.R. Repetitive closing and opening of fingers at different temperatures (original recordings of this study are given in Figure 6), Above: time to 3/4 relaxation after maximum isometric contraction of flexor digitorum muscle; thin line: 1st contraction at each temperature; broken line: 10th contraction; thick line: mean time to 3/4relaxation of nine contractions at each temperature. Middle: each column represents maximum force of ten repetitive isometric contractions at each temperature. Below: passive muscular tension recorded at end of 10th contraction. (Finger position as recorded in Figure 6 is not shown.) At about 30°C muscular paresis develops and, simultaneously, time to 3/4relaxation is prolonged maximally, and passive muscular tension reaches its highest value. At 28°C, muscle is no longer able to produce force or passive tension (-- state of complete flaccid paresis)

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Fig. 8. Patient E.R. Recording of finger position. Repetitive closing and opening of fingers. At normal intramuscular temperature (35,6°C) in flexor digitorum muscle an increasing slowness of finger opening develops (= paradoxical myotonia). After warming to 38.5°C, no paradoxical myotonia occurs

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3. Paramyotonic Stiffness at Normal Temperature. In patient E.R., only finger positions were recorded (Fig. 8). He closed the fingers and clenched his fist forcibly and then opened his fingers again. In this investigation the isometric force could not be measured. The muscle was rested for 20 min at room temperature; the temperature in the flexor digitorum muscle was then 35.6°C. After six contractions "paradoxical myotonia" developed with delayed opening of the fingers. Within 20min the rested muscles were warmed up to 38.5°C; then fast closing and opening of the fingers was possible without any slowness of movement. Both times the patient exerted himself as much as he could. So it appears highly probable that the amount of muscle work has been about equal in both studies.

Comment Investigations have shown that in paramyotonia congenita the defect is located in the muscle itself (Buchthal et al., 1958; Lajoie, 1960; Magee, 1963, 1966; Caraceni et al., 1970; Burke et al., 1974; Ricker et al., 1972, 1974). Cooling and muscle effort play an important part in the development of the paresis which has been recorded in the hand and forearm muscles as well as in the upper arm muscles. The decisive influence of low intramuscular temperature became evident in our studies of the forearm muscles. With the stepwise lowering of the temperature, paresis developed as soon as a certain temperature (of about 32°-31°C) was reached. Because only one patient could be studied with this particular method we do not know to what extent the critical temperature level may vary in other patients. Considering the behavior of the forearm muscles observed, we do not agree with Burke et al. (1974) who believed that muscle temperature is of only minor importance. Because of the larger volume of the upper arm muscles, the cooling turned out to be more difficult. Therefore stepwise lowering of the temperature was not attempted. Weakness developed only gradually in these muscles after cooling, and severe weakness occurred only after prolonged muscular effort. This might demonstrate a different behavior of the proximal muscles compared to the distal ones or it might just be a result of the different cooling methods applied. Increasing muscular stiffness (paradoxical myotonia) is another major symptom in paramyotonia congenita. Corresponding with clinical observations, paradoxical myotonia is most obvious in the hands. In the present investigations, the delay in relaxation of the forearm muscles after cooling and under isometric conditions was about six times normal, that, of the upper arm muscles only two times normal. Magee (1963) observed paradoxical myotonia occurring at normal temperature in a patient who stayed for 2h in a room at 37°C air temperature. However, in some cases a warming up to 3 8 ° - 3 9 ° C intramuscularly seems necessary in order to prevent the paramyotonic stiffness, which therefore clearly proves to be dependent on low muscular temperature. Any speculation about the underlying defect in paramyotonia congenita has to consider the relation between muscular weakness and stiffness. We have there-

Influence of Temperature on Isometric Contraction

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fore studied another parameter of paramyotonic stiffness, i.e. the mechanical resistance to passive stretching of a cooled muscle. It turned out that this passive muscular tension increased at the moment the weakness developed. At a still lower temperature, the passive tension decreased again while the muscular weakness developed further. This relation of weakness to stiffness favors the idea that both symptoms are caused by the same basic defect located in the sarcolemma and probably also in the membrane of the tubular system. Another observation gives some information of the way low temperatures effect muscular weakness. During cooling of the nonexercised muscle dense fibrillation-like spontaneous activity occurs, which differs markedly from the myotonic discharges after needle movement or percussion at normal temperatures. Caraceni and Negri (1970) also observed intense spontaneous activity during cooling in paramyotonia. With dominant or recessive myotonia congenita cooling did not induce this type of activity (Ricker et al., 1977). It has been recorded, however, in adynamia episodica hereditaria during the development of hyperkalemic weakness (Buchthal et al., 1958). This is due to a decrease in the resting membrane potential which leads to the muscular paresis (Creutzfeld et al., 1963). It can be assumed that in paramyotonia congenita, too, cooling produces muscle cell membrane depolarization which at a critical level causes the firing of action potentials and finally muscular paresis. A temperature dependent disturbance of the ion fluxes through the membrane might lead to a fall of the resting membrane potential. Muscular effort might also contribute to this assumed disturbance. To our knowledge useful recordings of the resting membrane potential and membrane resistance do not exist for paramyotonia congenita. Studies of Hayn and Trush (1972) were carried out on motor point biopsies of the forearm muscle and not on intact muscle cells. We would like to suggest the following hypothesis: cooling alone and in combination with muscle effort causes depolarization of the sarcolemma. This membrane depolarization leads to spontaneous activity and then to inexcitability and paresis. The underlying mechanism could well be an increased sodium membrane conductance initiated by cooling. The raised intracellular sodium is thought to release bound calcium and to depress the reuptake of calcium into subcellular structures. The competition between sodium and calcium for intracellular binding sites is well established (Lee and Klaus, 1971). In this way the supposed alteration in the sodium channel could also explain the stiffness and delayed muscle relaxation (paradoxical myotonia). In this model the ,,defect" would be located at sarcolemmar level influencing only secondarily the function of sarcoplasmatic reticulum and the myofilaments. On the other hand one might also assume that another distinct defect located at the sarcoplasmic reticulum and interfering with the mechanisms of calcium release, binding or uptake exists (Blinks, Rfidel and Taylor, 1978). At a certain temperature, the myofilaments seem to have lost their ability to separate after contraction, or they separate only with delay. Unfortunately, nothing is known about the function of the calcium dependent mechanism in paramyotonia congenita.

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References Becker, P. E.: Paramyotonia congenita (Eulenburg). Stuttgart: Thieme 1970 Blinks, J. R., Rüdel, R., Taylor, S. R.: Calcium transient in isolated amphibian skeletal muscle fibres: detection with aequorin. J. Physiol. 277, 291--323 (1978) Buchthal, F., Engbaek, L., Gamstorp, J.: Paresis and hyperexcitability in adynamia episodica hereditaria. Neurology 8, 347--351 (1958) Burke, D., Skuse, N. F., Lethlean, D. K.: Contractile properties of the abductor digiti minimi muscle in paramyotonia congenita. J. Neurol. Neurosurg. Psychiat. 37, 894--899 (1974) Burke, D., Skuse, N. F., Lethlean, A. K.: An analysis of myotonia in paramyotonia congenita. J. Neurol. Neurosurg. Psychiat. 37, 900--906 (1974) Caraceni, T., Negri, S.: Electromyographic study of congenital paramyotonia. In: Muscle diseases, pp. 181--185, J. N. Walton, N. Canal, G. Scarlato (eds.). Amsterdam: Excerpta Medica 1970 Creutzfeld, O. A., Abbot, B. C., Fowler, W. M., Pearson, C. M.: Muscle membrane potentials in episodic adynamia. EEG clin. Neurophysiol. 15, 508--519 (1963) Haynes, J., Trush, D. C.: Paramyotonia congenita: an electrophysiological study. Brain 95, 553--558 (1972) La Joie, W. J.: Paramyotonia congenita, clinical features and electromyographic findings. Arch. phys. Med. 42, 507--512 (1961) Lee, K. S., Klaus, W.: The subcellular basis for the mechanism of inotropic action of cardiac glycosides. Pharmacol. Rev. 23, 193--261 (1971) Magee, K. R.: A study of paramyotonia congenita. Arch. Neurol. (Chic.) 8, 461--470 (1963) Magee, K. R.: Paramyotonia congenita. Arch. Neurol. (Chic.) 14, 590--594 (1966) Ricker, K., Meinck, H.-M.: Paramyotonia congenita (Eulenburg). Neurophysiologic studies of a case. Z. Neurol. 203, 13--22 (1972) Ricker, K., Samland, O., Peter, A.: Elektrische und mechanische Muskelreaktion bei Adynamia episodica und Paramyotonia congenita nach Kälteeinwirkung und Kaliumgabe. J. Neurol. 208, 95--108 (1974) Ricker, K., Hertel, G., Langscheid, K., Stodieck, S.: Myotonia not aggravated by cooling. Force and relaxation of the adductor pollicis in normal subjects and in myotonia as compared to paramyotonia. J. Neurol. 216, 9--20 (1977) Vredenbregt, J., Rau, G.: Surface electromyography in relation to force, muscle length and endurance. In: New developments in electromyography and clinical neurophysiology, J. E. Desmedt (ed.), Vol. 1, pp. 607--622. Basel: Karger 1973

Received September 19, 1978

Influence of temperature on isometric contraction and passive muscular tension in paramyotonia congenita (Eulenburg).

Journal of rqeurao J. Neurol. 221, 151--162 (1979) ~) by Springer-Verlag 1979 Influence of Temperature on Isometric Contraction and Passive Muscul...
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