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J Lütschg

Publications and source records attributed to J Lütschg.

42 records · Page 3Linked to original sources
PubMed1976

[Pseudoparalytic myasthenia gravis. Diagnostic and therapeutic aspects in 60 separate cases].

Based on 60 of our own cases and on the medical literature the authors discuss the diagnostic, pathophysiological and therapeutic aspects of myasthenia gravis. Myasthenia is suspected in cases of motor weakness of changing intensity, diminishing by rest. The weak muscles are innervated by different peripheral nerves. At the beginning a weakness of upperlid-muscles, external eye muscles and bulbar muscles is particularly frequent. There is no sensory loss or other neurological symptoms. A transitory disappearance of motor weakness after an intravenous dose of Edrophonium (Tensilon) is a typical diagnostic sign. The effect is less evident with eye-muscle weakness. A typical appearance of potentials after repetitive stimulation of peripheral nerves as well as other characteristics in electrophysiological testing of muscles are of high diagnostic value. This allows differentiation from other types of muscle weakness. In the pathogenesis of myasthenia an autoimmune process related to a persistent thymus gland plays an important part. This leads to an ultrastructural change in the postsynaptic membrane of the muscle fibre. The postsynaptic membrane no longer reacts in a normal way to acetylcholine as a transmitter substance at the level of the motor endplate. Therefore the first step in the treatment of myasthenia consists of cholinesterase-inhibitors, specially Neostigmin (Prostigmin) and Pyridostigmin (Mestinon). Thymectomy is advised in all cases of myasthenia with the exception of the pure ocular form and of myasthenia in patients older than 60 years. The thymus gland is practically always persistent or hypertrophic in myasthenia. The suprasternal access is recommended. A thymoma should always be operated upon because of the danger of malignancy. In cases where thymectomy is not performed or not successful and if cholinesterase-inhibitors are not sufficiently efficient, treatment with corticosteroids or ACTH is recommended.

Adolescent↗
PubMed1976

Guillain-Barré syndrome in children with special reference to the natural history of 38 personal cases.

38 children which had had an episode of Guillain-Barré syndrome were studied after a period between 2 and 12 years. The age of the children at the follow-up varied between 7 years 9 months and 27 years. 11 of the children were not completely cured from the point of view of the peripheral nervous system. 9 showed slight signs of motor weakness, 2 of which also had a slight distal atrophy of some leg muscles. None of these 9 patients however had any subjective symptoms of diminished capacity in every-day life. 2 of these and 2 other patients without any muscle weakness had loss of one or more tendon reflexes. 4 other patients apart from the 9 mentioned above had a very slight intention tremor. All of these had had some cerebellar ataxia during the acute phase. A sweat test done in 19 of the 38 controls never showed any asymmetry. 36 patients were examined electrophysiologically during the follow-up: EMG was done in only 35 and in one only conduction velocities were measured. In 16 patients a pathological EMG and (or) an anomalous conduction velocity was found. The only correlations which seemed to exist between the amount of residual findings and some elements during the acute phase of the illness were a positive correlation with the importance of maximum motor deficiency and with the time between the beginning of maximum motor weakness and the beginning of recovery.

Adolescent↗
PubMed1975

[Polyneuropathy in vitamin B 12 and folic acid deficiency. Clinical and histopathological study with electron-microscopy analysis of the sural nerve].

One case each of pernicious anemia and folic acid deficiency with chronic malabsorption with disease of the cord and histologically demonstrated concomitant disease of the peripheral nerve system in the sense of a polyneuropathy are described. The histological findings of nerve obtained by biopsy show, in both cases, the loss of individual nerve fibers as an expression of a chronic axonal degeneration. The pathogenetic basis to be considered in these cases is presented.

Aged↗
PubMed1975

Progressive neural muscular atrophy in a case of phenylketonuria.

Clinical, neurophysiological and nerve-biopsy findings are described in a 13-1/2-year-old boy with classical phenylketonuria who developed progressive muscular atrophy. Clinical examination revealed atrophy of the calf muscles and pes varus. Tendon jerks were brisk in the upper extremities but were absent in the right leg and weak in the left leg. Nerve conduction velocities of the median and peroneal nerve were strongly reduced. Light- and electronmicroscopic investigation of sural nerve biopsy revealed axonal dystrophy and 'onion-bulb' formation of the Schwann cells. It is assumed that the combination of phenylketonuria and progressive muscular atrophy in this patient is an accidental occurrence.

Adolescent↗