Fritz Buchthal

Electrophysiological findings in entrapment of the median nerve at wrist and elbow

In 117 consecutive patients with carpal tunnel syndrome and 11 patients with a compression syndrome of the median nerve at elbow, motor and sensory conduction along the median and ulnar nerves and quantitative electromyography were compared with findings in 190 normal controls of the same age. In 25% of patients with carpal tunnel syndrome in whom motor conduction and EMG were normal, the lesion was located from abnormalities in sensory conduction. The fact that conduction along the same fibres was moderately slowed from digit to palm, severely slowed across the flexor retinaculum, and normal from wrist to elbow indicates that slowing was due to demyelination at the site of compression. Fifteen per cent of the patients with carpal tunnel syndrome had clinical and electrophysiological signs of ulnar involvement. In the other patients conduction along the ulnar nerve was as in 100 normal controls. Compression at the elbow was located by electromyographical findings rather than by abnormalities in conduction.

Spontaneous electrical activity of human muscle

Abstract The spontaneous electrical activity of human muscle was studied in 197 normals, 67 patients with peripheral nerve involvement and 29 patients with progressive muscular dystrophy. “Noise” was observed in the end-plate zones of normal muscle; after minute displacements of the electrode the noise could be seen to consist of randomly occurring purely negative discharges 0.5–2 msec in duration and up to 100 μV in amplitude. This activity probably represents extracellularly recorded miniature end-plate potentials. Outside the end-plate zones of normal muscle a single site was rarely encountered yielding a spontaneous discharge similar to the fibrillation potentials of denervated muscle. In normal muscle such a discharge may correspond to the propagated disphasic potentials superimposed on the “end-plate noise”. The fibrillation potentials in patients with lower motor neurone disease were found to have longer durations than usually stated (1–5 msec as compared with 0.5–2 msec), a significant proportion of triphasic potentials (30%) and voltages half of which were of the same order (100–300 μV) as those of motor unit potentials. The fibrillations found in 29 of 76 patients with progressive muscular dystrophy had the same average duration, amplitude and shape as in denervated muscles. The fibrillation potentials were initiated in the end-plate zone as evidenced by the initial negative deflection of the potential recorded there and the initial positive deflection outside the end-plate zone. The initiation of the fibrillation potentials cannot be ascribed to mechanical stimulation by the intramuscular needle electrode since fibrillation potentials could also be recorded subcutaneously. With the 50 μ diameter leads of a multi-electrode fibrillation potentials were recorded with peak-to-peak amplitudes as high as 8.5 mV. The decline in amplitude along the multi-lead electrode was the same for fibrillation potentials 1 mV or more in amplitude as for the spike components of motor unit potentials, the voltage falling to less than one-tenth of maximum within 0.45 mm. This suggests that “high voltage” fibrillation potentials represent the spontaneous discharge of a sub-unit. The amplitudes of 100–600 μV fibrillation potentials declined relatively less with distance, suggesting that they were recorded farther away from the generators (about 0.5 mm) than the high voltage potentials. The small amplitude and rapid attenuation of positive sharp waves suggest that they are derived from a single muscle fibre. Cross talk in our multi-lead electrodes was insignificant and cannot explain the discrepancy between our findings and those of other investigators with regard to the voltage decline of spike potentials. The cause of fibrillation potentials is discussed in the light of the present knowledge of the properties of the membrane of denervated muscle fibres.

Sensory conduction from digit to palm and from palm to wrist in the carpal tunnel syndrome

In normal subjects the maximum and minimum conduction velocity along sensory nerve was the same from digit to palm and from palm to wrist. Severe slowing from palm to wrist in patients with the carpal tunnel syndrome was often associated with only slight slowing from digit to palm. The distal slowing is attributed to a reversible constriction of nerve fibres, an assumption supported by the recovery in distal conduction velocity as early as two and a half months after decompression. The sensory velocity from wrist to elbow was normal or supernormal, whereas the motor velocity was often slightly decreased. The exclusion of the normal segment of the median nerve distal to the flexor retinaculum made it possible to demonstrate abnormalities across the flexor retinaculum in patients with clinical signs of carpal tunnel syndrome in whom distal motor latency and sensory conduction from digit to wrist were normal.

ACTION POTENTIAL PARAMETERS IN DIFFERENT HUMAN MUSCLES

Clianges i i i duration, :iinl)litude, and shape of muscle action poteutials are used as signs of the degree and the localisation of involvement in neuroinuscular diseases. Normative values of these parameters are necessary. Previous papers dealing with the influence of soine physical and physiological factors on the action potential parameters concerned the brachial biceps only (Buchthal et al. 1954, b and c) . There are, however, differences in different muscles (PefersCn and Iiugelberg 1949 ; Jasper and Hallein 1949 ; Buchtlial and Pinelli 1951 : Feinstein et nl. 1954, a and h ) , and i t is the aim of the present study to provide data on different muscles for comparison with findings i n clinical electromyography.

Motor and Sensory Conduction in Infancy and Childhood: Reappraisal

Maximum motor and sensory conduction along peripheral nerve increased with age, from 20 m/sec at a conceptional age of 33 weeks to 33 m/sec at one month after term. From one month to four years of age the increase was 20 m/sec, the velocity along adult nerve being reached at three to four years of age. Therefore abnormalities in motor and sensory conduction velocity must always be compared with findings in normal nerves matched for age. Data obtained on the nerves of infants are less uniform than in adults. Some of the scatter may be unavoidable because of the difficulty of establishing the precise age of the newborn; some of the scatter is due to inadequate control of temperature and other parameters.

ON THE DIFFERENTIATION OF MUSCLE ATROPHY BY ELECTROMYOGRAPHY

Loss of function of a spinal motor cell or interruption of the conduction through a motor nerve fibre is accompanied by a cessation of the functions -and a later atrophy of the corresponding 30-300 niiiscle fibres. On a transverse section of the muscle the atrophy appears as larger or smaller degenerated fields surrounded by normal tissue. After loss of iiumwous motor units, the picture becomes almost of the opposite character since we find scattered islands of normal tissue on a background of degenerated muscle tissue. I n the case of myogenic atrophy, however, these changes are of ZL more diffuse distribution, with the innervation intact. It is the purpose of the present investigations to look for a differentiation of these various types of atrophy by means of a registration of the electrical phenomena in the muscles, i.e. the potential differences which, in general, accompany the innervation processes and are an essential indicator for these phenomena. In a case of severe neurogenic atrophy and partial lesion of the peripheral nerve, we can succeed in registering a few fibres which belong to a single motor unit and the potential variations may be followed under a number of different conditions and states without disturbing interferences from neighbouring fibres.

Aspects of the Pharmacology of Phenytoin (Dilantin®) and Phenobarbital Relevant to their Dosage in the Treatment of Epilepsy

Findings are reviewed concerning the distribution and fate of phenytoin and pheno‐barbital in animals and in man. The serum concentration of these drugs can be considered an adequate expression of their concentration in the brain and hence of their anticonvulsant effect.

Muscle Action Potentials in Polymyositis

THE recent description of virus infections similar in symptomatology to poliomyelit i~,~,**~ but characterized by extensive lesions in skeletal muscle, has aroused new interest in the study of inflammatory reactions of skeletal muscle. Primary inflammatory processes have been described in polymyositis and dermatomyositis (the literature on this subject has recently been reviewed) In a number of myopathies, inflammation may occur secondarily, e. g. in progressive muscular dystrophy and myasthenia. It is well known that the clinical diagnosis of the subacute and chronic phases of polymyositis can be extremely difficult since symptoms are nonspecific, and in a number of cases there is not the characteristic involvement of the skin. Therefore, the diagnosis must be based on muscle biopsy. Microscopic examination reveals the presence of lymphocytes, histiocytes, in severe cases of polynucleocytes, and sometimes eosinophilic cells infiltrating the interstitial tissue of the muscle and surrounding the individual muscle fibers. The degree of atrophy varies according to the duration and severity of the disease. In most cases, inflammation is patchy, with localized foci of atrophic tissue (nodular polymyositis5 ) . The inflammatory process can either persist for several years or, unless regeneration occurs, result in dystrophic changes histologically indistinguishable from progressive muscular dy~trophy.~ The mean duration of muscle action potentials has been used to differentiate between atrophies of neurogenic and of myogenic origin. In atrophies caused by affection of the lower motor neuron, the mean duration of the muscle action potentials was found to be considerably increased,6 while in muscular dystrophies a decrease has been de~cribed.~ It is the aim of the present study to investigate muscle action potentials in polymyositis with respect to mean duration, shape and amplitude. It was thought possible that such a study might contribute to our knowledge of the etiology of dystrophic changes in muscle in view of the fact that, in our experience,s patients with genuine muscular dystrophy do not always show the changes in mean duration of action potentials described as t y p i ~ a l . ~

Muscle Action Potentials in Myopathies With Special Regard to Progressive Muscular Dystrophy

IN PREVIOUS INVESTIGATIONS it has been demonstrated that the electromyogram can contribute to the differential diagnosis between muscular atrophies of myogenic and of neurogenic origin.’ Histologically, myogenic atrophies are characterized by involvement of many muscle fibers from different motor units, and contraction tension is correspondingly reduced. Moderate and strong effort are, therefore, accompanied by the simultaneous recruitment of many fibers to produce an electromyographic pattern essentially like that of normal muscle. In atrophy of neurogenic origin, characterized histologically by the total loss of entire motor units with corresponding “mute areas” on electromyography, a similar moderate or strong voluntary effort brings about an entirely different pattern of discharge. Individual action potentials of motor units near the electrode can be led off without interference from the responses of neighboring units, as occurs only with slight effort in normal muscle (table 1). Apart from this general electromyographic pattern recorded during maximum effort at low speed, the duration, amplitude and shape of the individual action potentials recorded at high speed during weak voluntary contraction reveal differences of diagnostic significance. In muscular atrophies of neurogenic origin, there is an increase in action potentials of long duration1 A reduction in mean duration has been described as characteristic of progressive muscular dystrophy and other myopathies.2 However, the finding of action potentials of long or short duration is not in itself specific for any pathologic condition, since a wide range of action potentials, both extremely short and long, is recorded from normal muscle during voluntary activity. This has been found to be the case independent of the type, shape and dimensions of the electrode used for leading off. Therefore, comparisons between action potential duration in normal and atrophic

The Ineffectiveness of Diphenylhydantoin in Preventing Febrile Convulsions in the Age of Greatest Risk, under Three Years

1 A well‐controlled trial of prophylactic medication with diphenylhydantoin showed it to be ineffective in preventing febrile convulsions in children under 3 years of age. Twenty‐three children were followed for 6 to 30 months. The serum concentration of diphenylhydantoin was determined every 2–3 months and was consistently above 10 μg/ml. The recurrence rate was slightly higher in them than to be expected in untreated children. Consideration was taken of the relation of age, sex and family history to the rate of recurrence. The serum concentration of the drug at the time of 5 febrile convulsions was in and above the therapeutic range in adults. 2 It is possible that diphenylhydantoin (<10 μg/ml in the serum) prevented severe convulsions. In children under 2 years 21% of the convulsions before medication and on inadequate medication (<10 μg/ml) were severe; 8% of convulsions at age 2–3 years were severe. None of 14 febrile convulsions on adequate diphenylhydantoin was severe. 3 In 3 adequately treated children 3 years old and older, diphenylhydantoin probably prevented febrile convulsions. Two of them were having frequent episodes, which ceased when adequate medication was begun, and another child developed a convulsion a week after medication was withdrawn. 4 Acute toxic symptoms–lethargy, ataxia and vomiting–were rare though the serum concentration was transiently above 30 μg/ml in 9 children. Nystagmus was not reported. Chronic toxic signs–gingival hypertrophy, hirsutism and ataxia–did not occur. Two children may have had petit mal seizures when the serum concentration of diphenylhydantoin was high.