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Biomedical subjects

A Struppler

Publications and source records attributed to A Struppler.

At least 91 records · Page 5Linked to original sources
PubMed1979

[Basic conditions for electromyographic examination. Part I: EMG, nerve conduction velocity and test of motor end-plate function (author's transl)].

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.

Electric Stimulation↗
PubMed1978

[Pathophysiology of facial neuralgia (authors' transl)].

Facial neuralgia appears in a variety of forms which have different fundamental pathophysiological mechanisms. Of decisive importance are neuralgias with sensitive trigeminal, intermediate (sensory root), glossopharyngeal and vagus nerves which are caused by functional disturbances or damage to the nerve. In addition, projected or referred pain occurs in intracranial and cervical affections. A vascular origin may be assumed for Horton's neuralgia. This periodic paroxysmal and unilateral facial neuralgia is related to migraine. Serotonin, histamine and plasma kinin may be important eliciting factors; the concomitant symptoms of lachyrmation and rhinorrhea, reddening of the eyes and the face and a transitory Horner's syndrome suggest participation of the sympathetic and parasympathetic systems. Consideration of the previously known pathophysiological mechanisms permits a differentiated therapy for the various facial neuralgias.

Cluster Headache↗
PubMed1978

Myasthenia gravis: further electrophysiological and ultrastructural analysis of transmission failure in the mouse passive transfer model.

Using the mouse passive transfer model the mean amplitude of miniature endplate potentials and endplate potentials of mice treated with myasthenic immunoglobulins was markedly decreased. Miniature endplate potential frequency and quantum content of endplate potentials were normal, arguing against a major presynaptic disarrangement. Under electron-microscopy no gross structural alterations of endplates were demonstrated. It is concluded that the mouse passive transfer model closely resembles human myasthenia gravis of recent onset.

Acetylcholine↗
PubMed1977

[Functional anatomy of low back pain and ischialgia (author's transl)].

The neuronal systems involved in low back pain are first described in a functional anatomical review and then an attempt is made to work out the special functional structure data which seem to be decisive for the origin and localization of low back pain and ischialgia. Low back pain may arise as a deep pain through stimulation of the nociceptive afferents in the musculature and supporting tissues and as a neural pain through irritation of nociceptive nerve fibers within the innervation area of the lumbosacral plexus. The nociceptive influx from the viscera only elicits pain in the rarest cases, however, it often has a conductive influence. Skeletal muscle plays a special role here, along with the sensory supply to the vertebral motor segment through the spinal nerve and the particular innervation scheme of the lumbosacral plexus caused by the limb budding.

Back Pain↗
PubMed1976

[Therapy of myasthenia (author's transl)].

The types of symptoms of myasthenia (Ossermann), specific problems of myasthenia therapy and the fundamental principles of treatment with cholinesterase inhibitors are discussed. In addition to the improved techniques in the observation room, the consistent performance of an immunosuppressive therapy usually leads to improvement of the prognosis of severe myasthenia. The principles of cortisone and Imurek therapy are commented on and the indication for thymectomy are discussed.

Adrenocorticotropic Hormone↗
PubMed1976

[Treatment of organic brain psychosyndrom in the old age. A double blind study with Hydergin (author's transl)].

The efficacy of Hydergin was compared against placebo in a 15 weeks cross-over trial in 51 patients with cerebral insufficiency. The daily dosage was 3 mg of Hydergin. Criteria of evaluation consisted of clinical rating and electroencephalographic registrations, which were evaluated visually and partly automatically. The clinical symptoms as well as the electroencephalographic criteria (base line activity, theta- and delta activity) were both positively influenced by Hydergin. The base-line activity was stabilised and the alpha activity of the power spectrum increased. The most impressive result was the carryover effect of Hydergin, which could still be demonstrated in the post trial period. In case of "dizziness" the good results were limited to the period of active treatment. The relations between symptomatic and more basic therapy of cerebral insufficiency will be discussed.

Aged↗
PubMed1975

Clinical and electrophysiological observations in patients with myotonic muscle disease and the therapeutic effect of N-propyl-ajmalin.

Six patients with congenital myotonia and 4 patients with myotonic dystrophy have been examined clinically before and after the administration of N-propyl-ajmalin, an alkaloid frequently used as a cardiac antiarrhythmic drug. All patients but one reported a good to moderate improvement of their myotonic muscle stiffness. This was verified by measuring the time the patients needed to ascend a flight of stairs and by recording the speed of opening the hand. The amplitude of the compound muscle action potential decreased during repetitive nerve stimulation in myotonic patients. This decrease was not influenced by N-propyl-ajmalin. It seems to be due to the increased after-depolarization observed in myotonic fibres which causes partial inactivation of the Na-carrying system. From one patient a muscle biopsy was taken and intracellular potentials were measured with a microelectrode. Almost all muscle cells investigated showed myotonic activity which was completely abolished by addition of 10(-5) g/ml N-propyl-ajmalin to the bathing fluid. The development and duration of "warm-up" is illustrated and a possible electrophysiological basis is discussed.

Action Potentials↗