[Classification of electromyography findings in Parkinson syndrome compared with clinical assessment scales].
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Biomedical subjects
Publications and source records attributed to K Fasshauer.
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Neurological complications resulting from pronounced cerebrovascular changes were observed in a 59-year-old female suffering from Grönblad-Strandberg syndrome. In addition to typical skin changes of the pseudoxanthoma elasticum and ocular alterations (exudative macular degeneration and angioid streaks) there were an unusual number of disturbed endocrinological functions. The ophthalmological findings revealed characteristic breaks in Bruch's membrane, proliferation of chorioidal vessels into the subretinal space, hyperplasia of retinal pigment epithelium and disciform macular degeneration. Postmortem examination of the brain showed multiple cerebral infarcts due to recurrent disturbances in cerebral blood supply and particularly pronounced changes in the elastica interna of many cerebral arteries. Although the observed neurological signs in our patient were not characteristic of Grönblad-Strandberg syndrome, the histopathological findings led to the assumption that the same basic mechanisms result in alterations of elastic fibres and collagen, mainly in the ocular-cerebral system.
Communications on posttraumatic syringomyelia, a late sequel of complete or incomplete paraplegia or even tetraplegia, are rather infrequently in German literature. The problems of this well known complication occurring several months, years or even decades after a severe spinal cord trauma are discussed by two own cases. Both patients suffering from paraplegia developed signs and symptoms of posttraumatic syringomyelia 6 months and 3 years respectively after the accident. Case history and clinical findings correspond with reports in literature. Cystic degeneration in the cervical spinal cord could only be demonstrated in one patient by metrizamid -T-myelography combined with computerized tomography. The value of radiological and other technical investigations, pathogenesis, morphological findings and treatment are discussed.
Between 1968 and 1981 52 patients with syringomyelia were investigated clinically and with several additional procedures. The introduction of computerized axial tomography (CAT) has led to a change in diagnostic measurements in this disease. Therefore it has become necessary to evaluate the usefulness of additional investigations made in recent past. From own experiences the following measurements are indicated in patients with presumed syringomyelia: X-rays of the cervical and thoracal spinal column and the skull have to be complemented by automatic computerized transverse axial tomography (ACTA) of the spinal canal. CSF should be investigated before metrizamide myelography combined with computerized tomography--the so called computed assisted myelography--is done. These methods both the automatic computerized transverse axial tomography of the spinal canal and the computed assisted myelography allow a differentiation between communicating and non communicating syringomyelia. Computerized axial tomography of the skull is indicated to detect interval hydrocephalus that may be associated with communicating syringomyelia. The other methods evaluated in this study cannot be used to ascertain diagnosis. These measurements combined with clinical and radiological findings may only support diagnosis. Their significance lies in the critical examination of lost functions in the individual case. Especially electrodiagnostic test--as electromyelography and measurement of nerve conduction velocity--show the extension and distribution of the involved peripheral nervous system. These methods are necessary for the critical evaluation of both the spontaneous clinical course and the results of therapeutic procedures. The electromyography findings show the process of denervation already occurred and the degree of motor activity yet available. The measurement of nerve conduction velocity indicates the localization of involved peripheral nerves. The determination of evoked potentials yields informative findings. But at present the value of this method cannot yet be estimated finally. The indication of the discussed investigations depends on the clinical findings in the individual case with the exception of the radiological procedures.
32 patients with a disturbed function of the cricothyroid muscle were examined electromyographically and some also electroneurographically. Thyroid surgery had preceded in 22 patients and a traumatic lesion in 10 patients. Clinical observation showed that all patients suffered from an instability and lowering of the speaking voice as well as a reduction of vocal range. This was caused by a deficient tension of the vocal cords due to an insufficiently innervated cricothyroid muscle. In healthy subjects a continuous muscle activity of the cricothyroid muscle can be noted even in a resting position. During phonation the density and amplitude of this activity increases, showing a spindle-shaped pattern. In our strumectomised patients the resting activity of the impaired side was either greatly diminished when compared with the healthy side, or showed signs of denervation including the recording of fibrillations and positive sharp waves. The activity during phonation was reduced or completely missing. Electrical stimulation of the superior laryngeal nerve produced a delayed indirect muscle response. In those patients with traumatic lesions, the resting activity was reduced while a regular activity increase during phonation was completely missing. However, no signs of denervation were found in these patients. Our findings show evidence of neurogenic damage during thyroid surgery and an impairment of structures of the muscle itself following traumatic lesions.
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Telemetrical electromyographical investigations were performed in 23 healthy subjects and 33 patients with various diseases of the extrapyramidal system. The comparison of our findings leads to electromyographic criteria in the differential diagnosis of these disorders. As the majority of previous investigations with this method centered on questions concerning functional anatomy, a number of modifications were introduced to apply telemetrical methods to neurological problems. The following pathological findings were elicited by comparison of normal subjects and patients with extrapyramidal diseases: activity of hyperkinesias, coinnervation of antagonists, exceeding activity, altered patterns of single bursts of activity, retarding of activity, changes of the temporal proportions of alternating activity in the tibial muscles while walking. The latter finding was interpreted as sign of disturbed temporal coordination of automatic movement patterns in distinct diseases of the extrapyramidal system.
Standardized patterns of examination were developed in order to differentiate the disorders of the extrapyramidal system by means of electromyography. Pathological muscle activity was registered by stationary electromyography during rest, maintained posture, directed movements and passive extremity-excursions. Telemetric electromyography using eight-channel-biotelemetry-equipment showed pathological patterns of innervation in movements which are connected with migration such as walking. Characteristic findings were acquired in parkinsonism, choreatic, torsion dystonic and athetotic syndromes, ballism, Wilson's disease and drug induced dyskinesia as well as other hyperkinetic syndromes. The electromyographic findings proved to be useful in objectifying and differentiating the insufficient clinical data.
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Electrodiagnostical studies were carried out on three patients with Wilson's disease. The motor nerve conduction velocity was low but not markedly decreased. Some values of the sensory conduction velocity were decreased; the sensory action potentials showed low amplitudes and contained large amounts of late phases. Also, the electromyogram of one female patient showed denervation in the begin of treatment. There are no indications of polyneuropathy in Wilson's disease in the literature. There have been histological reports, however, which indicated lesions of the peripheral nerves in Wilson's disease as our own electrodiagnostical findings do.
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In ten patients with para- or tetraspastic syndromes of various etiology 5 different spastic phenomena demonstrating pathologically raised excitability of muscle regulation functions were registered electromyographically before and 1 h after i.v. administration of N-(hydroxy-2-ethyl)-cinnamamide (LCB-29). In the majority of cases a marked decrease of spasticity was registered. The rapid onset of this effect of LCB-29 allowed constant test conditions and therefore eliminated other influences on spasticity. The decrease of raised polysynaptic excitability at spinal level led, at least in part, to the assumption of a spinal site of action of LCB-29. The absence of a sedative effect with oral medication makes a strong central effect seem less probable.