Biomedical subjects
V Schrader
Publications and source records attributed to V Schrader.
[Reliability of magnetic stimulation in the diagnosis of peripheral facial paralysis of idiopathic origin].
To evaluate the transcranial magnetic stimulation in the early diagnosis of traumatic facial palsy 7 patients with an incomplete Bell's palsy were examined. The clinical examination, electric stimulation and magnetic stimulation were performed daily from the 2nd day until the 6th day, at the 12th day and three months after onset of the disease. The mean latency of the surface potential of the orbicularis oculi muscle after electrical stimulation was 2.7 msec. On the healthy side the answer following transcranial ipsilateral cisternal magnetic stimulation was detectable after 6.8 msec. From the beginning no response could be recorded on the affected side. After clinical restitution of the Bell's palsy after three months there was still no response. On the other hand, the controlateral, cortical transcranial magnetic stimulation was not significantly reduced. In conclusion, the cisternal transcranial magnetic stimulation gives no further information beyond the clinical examination. The cisternal stimulation is useful, if a clinical examination is impossible e.g. in an unconscious patient after head injury.
Spinal arteriovenous malformations and fistulae: clinical, neuroradiological and neurophysiological findings.
Twenty-six patients with myelographic signs suggestive of a spinal arteriovenous malformation (AVM) were examined neurologically and neurophysiologically. By selective spinal angiography it was possible to differentiate between dural arteriovenous fistulae (dAVF 20 patients) and intradural AVMs (iAVM, 6 patients). Initial complaints were nonspecific and variable, mainly consisting of sensory disorders and muscle weakness. Later, patients suffered involvement of both the upper and lower motor neurons. There was a high percentage of lower motor neuron lesions (95%), especially in dAVF patients, which were mostly of widespread distribution and included several myotomes. Electrophysiological examination regularly revealed lower neuron involvement, frequently with pathological spontaneous activity in several myotomes, pathological sensory-evoked potentials after tibial nerve stimulation, but normal sensory conduction velocities of the sural nerve, indicating sparing of the sensory ganglion. Frequently there was a discrepancy between the localization of the dural fistula or angioma and the spinal level responsible for clinical symptoms. This suggests that it may be the inadequacy of the venous drainage system to cope with the blood volume rather than the AV-shunt that is responsible for the symptoms. An early diagnosis is essential, as removal of the shunt before there has been progression to severe neurological deficits (paraplegia) is the only way to ensure a satisfactory outcome.
Neurophysiological characteristics of spinal arteriovenous malformations.
The aim of the study was to identify the clinical and neurophysiological pattern of deficits in spinal arteriovenous malformations (AVM) to allow an early diagnosis which is the prerequisite for effective treatment by early surgery or embolization. Among 26 patients with myelographic signs of a spinal AVM, selective spinal angiography disclosed 20 cases with a dural AV-fistula (dAVF) and 6 patients with an intradural AV-malformation (iAVM). Although the main pathogenetic factor in both disorders may be different, clinical and neurophysiological findings proved to be of limited value in differential diagnosis. Clinical symptoms presented by the patients were a variable combination of lower motor neuron lesion, sphincter disturbance, sensory transverse lesion and partly additional signs of upper motor neuron involvement. Electromyography invariably showed an increased rate of polyphasia and frequently pathological spontaneous activity usually in several myotomes. Normal sensory conduction velocity of the sural nerve contrasted with almost regularly pathological SEP's after tibial nerve stimulation. The distribution if clinical and neurophysiological findings suggests rather widespread lesions of the lower cord and/or cauda equina, frequently at a lower level than the angiographically localized shunt. This suggests a vascular myelopathy on the basis of insufficient venous drainage at least for the frequent dural AV-anomaly.
Impaired discharge of the eye velocity storage mechanism in patients with lesions of the vestibulo-cerebellum.
Explore the source record for details and available documents.
[Mechanism of the antagonistic catecholamine effect on depot lipid mobilization in humans].
Explore the source record for details and available documents.
Inhibition of human fat cell adenylate cyclase mediated via alpha-adrenoceptors.
Human adipose tissue contains alpha- as well as beta-adrenoceptor sites mediating antagonistic catecholamine effects on lipolysis. To characterize the mechanisms of catecholamine action in biochemical terms we have studied the effects of the almost pure beta-adrenoceptor agonist isoproterenol and of the mixed adrenergic agonist adrenaline on human fat cell adenylate cyclase in the presence of alpha- and beta-adrenoceptor blocking drugs. In contrast to the almost pure beta-adrenergic agent isoproterenol, the mixed agonist adrenaline, besides its stimulatory action, also had inhibitory effects which became apparent upon complete beta-adrenoceptor blockade using 0.05 mmol/l propranolol. Under these conditions adrenaline caused a dose-dependent inhibition of basal and parathyroid hormone-activated enzymic activity with a maximum of 30-50%, which was dependent on GTP and could be reversed by simultaneous alpha-adrenergic blockade using 5 mumol/l dihydroergotamine or 10 mumol/l phentolamine. These results support the concept of antogonistic alpha- and beta-adrenoceptor sites coexisting as regulatory subunits of the human fat cell adenylate cyclase.
alpha-adrenoceptor mediated inhibition of human fat cell adenylate cyclase.
Explore the source record for details and available documents.
The effect of lateral head tilt on horizontal postrotatory nystagmus I and II and the Purkinje effect.
The influence of an active lateral head tilt on postrotatory nystagmus I and II (PI, PII) was explored in normal humans. During postrotatory nystagmus the head was tilted laterally either towards the direction of the previous rotation (ipsilateral tilt) or towards the opposite direction (contralateral tilt) or the head was kept erect. Both ipsi- and contralateral head tilts led to a substantially weaker and shorter PI and PII as compared with the trial without head tilt. The time constants of the decline of PI were shortened to the ones observed in the peripheral nerve of animals. The reduction of PI and PII suggests a position-dependent tonic inhibition of the vestibular storage mechanism in the vestibular nuclei probably by the otoliths. The stronger reduction of time constant and cumulative amplitude of PI after contralateral as compared with ipsilateral head tilt may be explained by different combinations of asymmetric responses in canal and otolith afferents.
Direction and angle of active head tilts influencing the Purkinje effect and the inhibition of postrotatory nystagmus I and II.
Postrotatory nystagmus I and II (P I, P II) were evoked in four normal humans by velocity steps (prior velocity of rotating chair 90 degrees/s). 4 s after the stop the head was actively tilted by the subject 90 degrees forwards, backwards, to the shoulder of the previous direction of rotation -'ipsilaterally', or to the other shoulder-'contralaterally'. In control trials, the head was kept in the previous erect position. Compared with the control experiments, P I was significantly reduced by all head tilts. Inhibition of P I was strongest with forward and weakest with backward tilts. This difference is explained by the inclination of the utricular base by 30 degrees backward with respect to the horizontal of the skull and by the elastic properties of the sensory matrix. A smaller amplitude (45 degrees) of head tilt about the roll axis leads to a weaker inhibition (28.5%) than a 90 degree tilt, which corresponds to the difference of the sine of the tilt angle and thereby reflects the mechanical force acting on the receptor layer.