Biomedical subjects
Publications and source records attributed to H P Ludin.
In the course of long-term treatment of Parkinson's disease many problems, which cannot yet be satisfactorily solved, arise with time in a large number of patients. This overview describes some strategies which are used nowadays to tackle these problems. Special attention is drawn to the treatment of painful dystonias and off-periods with apomorphine.
Surgical interventions can give rise to peripheral nerve lesions by various mechanisms. The neurologist is asked to define which nerve has been lesioned at which site. We also have to define the type of lesion and its severity. The electrophysiological investigation is a very important diagnostic tool in this particular situation. Together with the clinical examination it will allow to plan an optimal treatment for the patient.
Among nine monozygotic (MZ) and 12 dizygotic (DZ) twin pairs in which an index case had typical Parkinson's disease (PD) or PD with associated dementia, three MZ and three DZ pairs were concordant. Three of the six affected co-twins were first diagnosed during the study. Occurrence of PD in families of MZ and DZ index cases was more frequent than expected from population rates. The study underlines the need for personal examination using defined criteria in a cross-sectional twin study on PD. Although the study did not establish a major genetic impact in the etiology of PD, a genetic predisposition for the disease cannot be ruled out for some individuals.
Migraine patients suffering from frequent and severe attacks may need prophylactic treatment. Propranolol, a beta-receptor blocker, and flunarizine, a calcium antagonist, are considered to be the most effective compounds for the prophylaxis of migraine. In a number of controlled studies, flunarizine has been shown to reduce the number of migraine attacks significantly. In migraine studies, sedation and weight gain are the most frequent side effects of flunarizine.
Clinical, electrophysiological, and the nerve and muscle biopsy findings from a case treated with amiodarone are reported. Marked distal motor and sensory impairment and distal muscular atrophy were observed clinically. The electrophysiological examination revealed normal motor and sensory conduction velocities in the median nerve; the sensory action potentials were polyphasic and reduced in amplitude. Electromyography revealed denervation potentials and severe loss of motor units in the M. extensor digitorum brevis and in the M. tibialis anterior. The light and electronmicroscopical study of a N. suralis biopsy displayed total loss of large myelinated fibers and an almost total reduction of small myelinated fibers. The number of unmyelinated axons was markedly reduced. Fibrocytes and degenerative axons polymorphous inclusion bodies were present in Schwann cells. The muscle biopsy revealed both neurogenic and myopathic changes. Lipid storage was also present in the muscle fibers. Physical and chemical analysis of the nerve and muscle biopsy revealed the content of iodine to be more than 40 times increased. The findings indicate damage of axons, schwann cells and muscle fibers. It is suggested that the lipid storage in nerve and muscle tissue might be related to the accumulation of the drug or its metabolites.
The present paper describes the clinical, electrophysiological and histological findings made in 12 patients belonging to 2 genealogical lineages in Switzerland, suffering from paramyotonia congenita. This is the first report of this disease in Switzerland. The myopathy, transmitted by autosomal dominant inheritance, is characterized by a typical past medical history and by the persistent contraction of the muscles of the face, arms and legs provoked by exposure to cold. Also of diagnostic importance are the myotonic reactions inducible at room temperature, such as percussion myotonia, active myotonia and paradoxical myotonia. During paramyotonic episodes provoked by exposure of the subjects in a refrigeration chamber, serum potassium concentrations remained within normal limits. Potassium loading producing serum levels above 6 mEq/1 in 2 patients gave rise to stiffness and weakness of the arms and legs, but no signs of paralysis. Induced hypokalemia in 3 cases caused no paramyotonic symptoms. Electromyographic recordings in 5 patients showed myotonic discharges, which disappeared upon cooling of the limb, giving way to progressive muscular stiffness. Histological, histochemical and electronmicroscopical examination of the muscle tissue revealed only diagnostically unspecific myopathological changes.
Using a commercially available television set for stimulation of 78 healthy subjects, the upper limit of normal for the latency of the major positive wave (p 100) of checkerboard pattern reversal evoked potentials is practically the same as that obtained by employing slide projector combined with a rotating mirror. Potentials evoked by a small pattern, for purely foveal stimulation, were often difficult to evaluate exactly. Fixation of a large pattern at the upper border of the stimulus field brought no advantages as compared to the usual fixation in the center. Continuous prolonged recordings, with successive averaging of 64 pattern reversals, confirmed statements that only the major positive wave and its latency are constantly reproducible without being influenced by fatigue or inattention. Repeated examinations in the same subjects at intervals of 2 weeks showed a considerable spread of the latencies from one session to the other but the absolute values always ranged within the normal. More or less large latency differences (up to 12ms with large pattern stimulation) were found in every subject at least once. A longer latency found at a control examination, or a newly appearing latency difference, therefore do not prove a fresh optic nerve lesion as long as the absolute values are still within the limits of normal. From repeated examinations it could also be seen that foveal stimulation with a small pattern is not suitable for routine examinations because of high variation in the results.
The purpose of the following contribution is to give a survey about the basic conditions of electromyographic examination. The necessary apparatus will be described as well as the course of examination. Moreover the parameter for the evaluation will be explained together with exogenous falsifying influences. This contribution is thought to be a guide for orientation to improve electromyographic recording and evaluation.
In the first part of this study 17 patients with a clinically clear-cut carpal tunnel syndrome but with normal electrophysiological findings have been controlled after 1 to 3 years. In 12 of these patients an other cause of the complaints could be found. In 2 patients no definite diagnosis could be made and in 3 the previous diagnosis was considered to be corrected. Control electromyography was pathological in 2 of them and 1 patient was symptom-free after the operation. In the second part 133 hands with clinical symptoms of a carpal tunnel syndrome were examined clinically and electrophysiologically. In the group of patients with pathological electrophysiological findings there were significantly more objective signs than in those with normal EMG findings. In 13 of these patients which could be followed an other diagnosis could be made. It was not possible to establish a clinical index for the carpal tunnel syndorme. For a definite diagnosis, positive clinical and electrophysiological findings are required.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A 7-year-old boy who suffered from increasing stiffness and contractures of the extremities had distally pronounced atrophy and absent tendon reflexes. Electromyography showed continuous electrical activity during rest, sleep, after intravenous injection of diazepam, and after peripheral nerve block. The H reflex was elicitable; the silent period after the reflex was absent. Histopathological examination of the peroneus muscle disclosed a marked preponderance of type I fibers and slight atrophy of the type II fibers. Electron microscopic examination of the endplates demonstrated a marked atrophy of the postsynaptic regions and widened synaptic clefts. After one year's treatment with phenytoin, 200 mg daily, the patient showed an almost normal muscle tone. As not all of these electrophysiological phenomena can be fully explained by disturbances of the nerve terminals or the endplates, a further anomaly proximal from the peripheral nerve block seems to have been present.
Sensory conduction velocities of normal subjects are increasing linearly with rising temperature. The duration of the compound sensory action potentials recorded from the median nerve at the wrist and elbow shows a negative temperature coefficient. The peak-to-peak amplitude of these potentials increases from 22 degrees to approximately 26 degrees C and then decreases progressively again up to 36 degrees C. It is believed that this behavior is due to a combination of decreasing temporal dispersion, height and duration of the individual spike potentials.
In a case of cephalic tetanus the amplitudes and the latencies of the compound action potentials recorded from the facial muscles after stimulation of the facial nerve at the mastoid were not significantly different on the two sides. With repetitive stimulation at 30/sec a pathological facilitation was observed on both sides. The blink reflex bilaterally had normal latencies but the amplitudes of the reflex potentials were always significantly lower on the paretic side. It is concluded that facial palsy in cephalic tetanus is mainly due to a functional block of conduction in the course of the peripheral nerve whereas the disturbance of neuromuscular transmission probably has little importance in these cases.
One hundred and twenty-three patients, 68 males and 55 females in whom acute polyradiculitis Guillain-Barré appeared at an age of between 1,6 and 76 years were re-examined after 0.9 to 12.3 years. The initial symptoms, the signs during the acute phase, in particular the cranial nerve signs and central nervous signs, as well as findings in the cerebrospinal fluid and complications are described. Three patients died during the acute phase. At follow-up only 57% of the patients were completely cured. In 22% motor signs, mainly distal in the lower extremities were found. Only 6 of these patients however were handicapped. Twenty-two patients had loss of one or more tendon reflexes, in general the ankle jerk. Only 6 showed very slight central nervous system signs. Eleven of 55 follow-up cases had pathological findings in needle electromyography. A disturbance of conduction velocity or distal latency was also found in several adults and children without residual clinical signs. The time span between the maximum of the initial signs and the beginning of recovery seemed to be particularly long in patients who showed residual signs on follow-up. These patients also seemed frequently to have had a severe tetraparesis in the initial phase. We could not confirm the therapeutic effect of cortisone or ACTH in our patients: amongst the 30 adults treated with cortisone 6 (20%) had residual signs at follow-up, whilst 5 (25%) of the 22 untreated ones had similar findings.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In 32 healthy volunteers aged between 10 and 72 years the orthodromic and the antidromic sensory nerve conduction in the median nerve have been studied. Normal values for conduction velocities and for the configuration of the orthodromic nerve action potentials are described in detail. 26 patients suffering from a carpal tunnel syndrome have been examined both with the orthodromic and the antidromic method. It could be shown that the diagnostic yield of both methods is about the same for this special problem.