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Biomedical subjects

M Strupp

Publications and source records attributed to M Strupp.

At least 73 records · Page 4Linked to original sources
PubMed1998

Perceptual and oculomotor effects of neck muscle vibration in vestibular neuritis. Ipsilateral somatosensory substitution of vestibular function.

Afferent cervical somatosensory input may substitute for absent vestibular information as part of central vestibular compensation after unilateral peripheral vestibular deficit. In order to determine the particular contribution of neck muscle spindles to the perception of body orientation and to the oculomotor system, we measured (i) the subjective visual straight ahead (SVA) by psychophysical tests and (ii) the changes in eye position by video-nystagmography during unilateral stimulation of the posterior neck muscles by vibration (100 Hz). Twenty-five patients with subacute unilateral vestibular lesion (vestibular neuritis) and 25 controls participated in the study. Vibration elicited a horizontal displacement of SVA towards the side of stimulation in all subjects. Mean displacement (+/- SD) was 3.28 +/- 2.96 degrees for right-side and 3.45 +/- 2.93 degrees for left-side stimulation in controls. Muscle stimulation on the patients' lesion side induced a significantly higher displacement (11.51 +/- 6.63 degrees) than contralateral stimulation (3.04 +/- 2.95 degrees, P < 0.01, paired Student's t test). The mean difference during stimulation between the two sides in the patients was 8.02 +/- 5.52 degrees; in the controls, however, it was only 0.74 +/- 0.47 degree (P < 0.001, Student's t test). This asymmetry increased gradually in patients over a period of weeks, reaching a maximum at days 60-80 and declining thereafter. Videonystagmography revealed that ipsilateral stimulation in patients induced large horizontal eye deviations of up to 25 degrees towards the side of the lesion (9.1 +/- 7.6 degrees, n = 18). Contralateral stimulation induced only small shifts, which were within the range of controls. The correlation coefficient between displacement of the SVA and change in eye position was high (r = 0.94, P < 0.0001), indicating that the shift of SVA is the perceptual correlate of the directional change of gaze in space. This interpretation was supported by two control experiments in which the subject was required to (i) indicate the subjective straight ahead by finger-pointing with the eyes closed and (ii) adjust SVA when looking through horizontally reversing prisms. Vibration of neck muscles caused almost no displacement of the SVA when it was indicated by pointing with the eyes closed, but reversed the direction of the displacement if the subject wore reversing prisms. In summary, our data showed: (i) an increase in muscle spindle input following unilateral vestibular lesion; (ii) this increase is asymmetrical, restricted to the affected side, and gradually builds up over weeks; and (iii) the perceived effects during vibration are secondary to changes in eye position rather than changes in cortical representation of body orientation. This is the first study to demonstrate a unilateral increase in somatosensory weight, which substitutes for missing vestibular input.

Adolescent↗
PubMed1998

Common variable immunodeficiency leading to spinal subacute combined degeneration monitored by MRI.

A patient is reported on with a common variable immunodeficiency syndrome (CVID), in whom chronic gastritis with antibodies against parietal cells and a cytomegalovirus associated enteritis led to vitamin B12 deficiency with consecutive subacute combined degeneration of the spinal cord. The resulting medullary changes, most probably representing demyelination, were visualised with MRI. The effects of treatment were also monitored over three years by MRI and clinical examination. The resolution of the MRI changes correlated with clinical improvement of the patient's signs. In the medical literature only five cases of vitamin B12 related spinal cord changes have been identified by MRI; none was caused by a CVID syndrome.

Autoimmune Diseases↗
PubMed1998

Vestibular exercises improve central vestibulospinal compensation after vestibular neuritis.

OBJECTIVE AND BACKGROUND: Animal experiments have shown that central vestibular compensation of unilateral peripheral vestibular lesions can be improved by vestibular exercises. There are, however, no equivalent clinical studies on the efficacy of such specific physiotherapy on acute unilateral peripheral vestibular lesions in humans. DESIGN AND METHODS: To quantify the differential effects of specific vestibular exercises on central compensation in patients with an acute/subacute unilateral vestibular lesion (vestibular neuritis), we determined the time course of recovery of 1) the ocular torsion (OT) for the vestibulo-ocular system, 2) the subjective visual vertical (SVV) for perception, and 3) the total sway path (SP) values for postural control in 19 patients with and 20 patients without vestibular exercises. All patients had a persisting peripheral vestibular deficit for at least 30 days (statistical end point). RESULTS: Although normalization of OT and SVV was similar in the control and physiotherapy groups, the total SP values on day 30 after symptom onset differed significantly: 3.2 +/- 1.9 m/min in the physiotherapy group and 16.9 +/- 6.1 m/min in the control group (ANOVA, p < 0.001). CONCLUSIONS: This prospective clinical study suggests that specific vestibular exercises improve vestibulospinal compensation in patients with acute peripheral vestibular lesions.

Adult↗
PubMed1998

Alternating episodes of vestibular nerve excitation and failure.

Recurrent episodes of oscillopsia, rotational vertigo, and postural imbalance were elicited and modulated by changing the horizontal head positions of a patient with an arachnoid cyst in the right cerebellopontine angle that distorted the vestibulocochlear nerve. Oculomotor analysis revealed two different types of attacks depending on the particular head position: 1) episodes of vestibular hypofunction (minutes to several hours) with normal head position and 2) paroxysmal vestibular excitation (seconds) with head rotation to the left. The most likely cause is a transition from conduction block to ectopic discharges, which occurs when various peripheral nerves are compressed. One week after resection of the cyst and decompression of the eighth cranial nerve the patient was symptom free, and the electronystagmogram was normal.

Arachnoid Cysts↗
PubMed1997

Cyclic GMP inhibits and shifts the activation curve of the delayed-rectifier (I[K1]) of type I mammalian vestibular hair cells.

NITRIC oxide (NO) plays a role in the modulation of the predominant potassium current of type I vestibular hair cells, a low-voltage activated current called I(K1). Since many effects of NO are mediated via cGMP, patch-clamp recordings were made to evaluate the effects of cGMP on I(K1). In whole-cell recordings 1 mM cGMP shifted Vhalf of I(K1) by 15.0 +/- 2.4 mV (n = 6) to more positive. In cell-attached 'multichannel' recordings 1 mM 8-bromo-cGMP caused a reversible shift of Vhalf by 13.8 +/- 2.6 mV (n = 12) and in single channel recordings in the cell-attached configuration the open probability was reduced at -60 mV from 0.39 +/- 0.14 to 0.08 +/- 0.01. cGMP had no effect on excised inside-out patches, indicating that an intact cytosolic milieu with functioning phosphorylation cascades is necessary. cGMP seems to be an important second messenger which reduces the potassium conductance of vestibular hair cells.

Animals↗
PubMed1997

[Imaging of the labyrinth and vestibular nerve. Clinical significance for differential diagnosis of vestibular diseases].

High resolution magnetic resonance imaging (HR-MRI) and computed tomography (HR-CT) of the inner ear are becoming more important for the diagnosis of peripheral vestibular lesions. Modern HR-MRI techniques allow visualization of detailed anatomic features of the vestibulo-cochlear regions as well as pathologic findings in the inner ear such as, neoplastic lesions (e.g., small intracanalicular acoustic neuromas), anomalies causing vertigo and hearing loss (e.g. Mondini's-malformation, perilymph fistula, vestibular paroxysmia), and inflammatory diseases (e.g., Cogan's syndrome, labyrinthitis, zoster neuritis). HR-CT is still the first examination that should be performed in patients with middle ear diseases (e.g., tumor, infection), trauma (e.g. temporal bone fractures), or fibro-osseous diseases. Although the imaging of the vestibulo-cochlear system has dramatically improved, there are still several peripheral vestibular disorders that cannot be visualized so far, e.g., benign paroxysmal positioning vertigo, idopathic vestibular neuritis or Menière's disease.

Diagnosis, Differential↗
PubMed1995

Horizontal canal benign paroxysmal positioning vertigo: reversible ipsilateral caloric hypoexcitability caused by canalolithiasis?

Bithermal caloric stimulation in a patient with a benign paroxysmal positioning vertigo of the horizontal (lateral) semicircular canal (HC-BPPV) revealed a significant hypoexcitability of the affected ear that was reversible when treated by liberatory maneuvers. Both the positional vertigo and caloric hypoexcitability in HC-BPPV are caused by canalolithiasis, a concept strongly supported by the intensity of the positioning nystagmus being maximal when the patient turned his head around the longitudinal z-axis from the left lateral to right lateral position while recumbent (maximum slow-phase velocity [SPV] 176 deg/sec) and being much lower (maximum SPV 55 deg/sec) when he turned his head to the right lateral position while in a supine position (nose up). The dependence of this difference in nystagmus intensity on the initial head position and direction of rotation indirectly proves that the clot moves freely (to and fro) within the segment of the HC diametrically opposite to the ampulla. The reversibility of ipsilateral caloric hypoexcitability is attributed to the clot's (functional) plugging of the HC, which agrees with studies in squirrel monkeys. These data support the view that physiologic caloric responses consist of a major convective and minor nonconvective component.

Aged↗
PubMed1993

A Ca(2+)- and pH-dependent K+ channel of rat C6 glioma cells and its possible role in acidosis-induced cell swelling.

The aim of the present study was to explore whether a change in membrane K+ conductance contributes to acidosis-induced swelling of cultured rat C6 glioma cells. Electrophysiological studies were performed using whole-cell and single-channel recordings in combination with cell volume measurements in cell suspension by flow cytometry. Whole-cell recordings revealed a voltage-dependent K+ conductance. The predominant K+ channel in single-channel recordings with symmetrical high K+ concentrations was inwardly rectifying and had conductances of 35 and 15 pS, respectively. A raised internal free Ca2+ concentration and membrane depolarization increased the open probability of this channel. Internal acidosis (pH 6.4-5.4), on the other hand, reduced open probability and single-channel conductance. Both whole-cell and single-channel K+ currents were blocked by quinidine (0.1-1 mM), which was therefore used to analyze the functional consequences of an inhibition of this conductance for cell volume. Thereby, quinidine (1 mM) produced a small (5%) and transient cell swelling of C6 glioma cells. In contrast, acidosis (pH 5.6) caused a much larger (about 20%) and maintained swelling. Since quinidine produced only a minor swelling of C6 cells, it is unlikely that inhibition of the K+ conductance caused acidosis-induced cell swelling. Other mechanisms, such as activation of ion transporters, must therefore be responsible.

Acidosis↗
PubMed1993

Interstitial lactate and glucose concentrations of the isolated perfused rat heart before, during and after anoxia.

In isolated rat hearts perfused according to the Langendorff technique lactate and glucose concentrations were determined in the interstitial transudate and the venous effluent before, during and after periods of 15 or 30 min anoxia. The interstitial transudate emerged at the surface of the heart as a result of albumin-free perfusion. During normoxic perfusion the interstitial lactate concentration was 0.144 +/- 0.025 mmol/l (n = 6); the venous lactate concentration was 0.033 +/- 0.005 mmol/l. From the interstitial and the mean vascular concentration, together with the lactate release and the glucose uptake, the apparent permeability surface area products (P.S product) were calculated using Fick's law. The apparent P.S products for lactate and glucose were 4.6 and 3.9 ml/(min x g), respectively. During anoxia we measured a four- to sixfold increase of the interstitial lactate concentration. At the end of the anoxic periods the apparent P.S product was two- to threefold higher than during normoxia; the apparent glucose P.S product increased about fourfold. After 15 min anoxia the increases of permeability were completely reversed in the reoxygenation period. However, after a period of 30 min anoxia the apparent P.S products for lactate and glucose remained raised, which means that there was a prolonged or even irreversible increase of capillary permeability. Besides the marked transcapillary concentration difference for lactate, these data show prolonged functional alteration of the capillary wall after 30 min anoxia.

Animals↗
PubMed1993

[Neurogenic intermittent claudication of the femoral nerve caused by occlusion of the common iliac artery].

A 52 year old heavy smoker complained of paresthesiae and pain at the ventral side of the right thigh and the antero-medial side of the right lower leg as well as weakness of the right quadriceps femoris during exercise. Clinical examination revealed a paresis of the right quadriceps, hypesthesia and hypalgesia in the area of the femoral nerve and a reduced right patellar reflex after 10 min walking. An occlusion of the right common iliac artery was diagnosed by angiography. Following transluminal angioplasty and implantation of an intravascular stent, the patient was free of symptoms. On the basis of the clinical observations following recanalisation of the common iliac artery, the symptoms can best be explained by a reduced perfusion of the iliolumbar artery supplying the upper part of the femoral nerve, causing ischemia of the femoral nerve during exercise. In conclusion, stenosis/occlusion of the common iliac artery should be considered as a differential diagnosis of quadriceps weakness and paresthesia in the area of the femoral nerve associated with exercise.

Angiography, Digital Subtraction↗
PubMed1992

High conductance anion channel in Schwann cell vesicles from rat spinal roots.

Potassium uptake, possibly together with chloride, is one of the presumed functions of Schwann cells in the peripheral nervous system. However, the presence of chloride channels has not been demonstrated in adult Schwann cells. We present here a new method which allows single channel recordings to be made from Schwann cells in situ without enzymatic treatment. Isolated rat spinal roots were split mechanically into several bundles. Within about 30 min after this procedure small bleb-like vesicles (approximately 20-30 microns in diameter) with a clean surface appeared at the edges of the fibre bundles. Immunofluorescence microscopy with a surface marker for Schwann cell membranes (monoclonal antibody O4) revealed that the vesicles originate from Schwann cells. In standard patch clamp recordings with symmetrical bath and pipette solutions (excised inside-out configuration) an anion channel with the following characteristics was mainly observed: 1) single channel slope conductance of 337 +/- 5 pS in 125 mM KCl and 209 +/- 6 pS in 125 mM K+ methylsulphate; 2) ion permeability ratio: PCl/PK/Pgluconate = 1/0.12/0.06; 3) linear current-voltage relationship (range +/- 60 mV); and 4) voltage- and time-dependent inactivation (the channel was most active at potentials +/- 20 mV). Pharmacologically, the channel was completely blocked with zinc (1 mM) and barium (10 mM). A similar anion channel, showing characteristics 1-4), has been described in cultured Schwann cells of newborn rats (Gray et al., 1984). We now demonstrate that this channel is also present in adult Schwann cells in situ.

Action Potentials↗
PubMed1992

Glutathione accelerates sodium channel inactivation in excised rat axonal membrane patches.

The effects of glutathione were studied on the gating behaviour of sodium channels in membrane patches of rat axons. Depolarizing pulses from -120 to -40 mV elicited sodium currents of up to 500 pA, indicating the simultaneous activation of up to 250 sodium channels. Inactivation of these channels in the excised, inside-out configuration was fitted by two time constants (tau h1 = 0.81 ms; tau h2 = 5.03 ms) and open time histograms at 0 mV revealed a biexponential distribution of channel openings (tau short = 0.28 ms; tau long = 3.68 ms). Both, the slow time constant of inactivation and the long lasting single channel openings disappeared after addition of the reducing agent glutathione (2-5 mM) to the bathing solution. Sodium channels of excised patches with glutathione present on the cytoplasmatic face of the membrane had inactivation kinetics similar to channels recorded in the cell-attached configuration. These observations indicate that redox processes may contribute to the gating of axonal sodium channels.

Animals↗
PubMed1992

Otoneurology.

This review on progress in otoneurology focuses on peripheral and central vestibular disorders rather than auditory dysfunction. Recent literature reflects an imbalance between quantity and quality. For instance, several of the numerous papers on Menière's disease contribute little to furthering our knowledge of pathophysiology and treatment. The comparatively few papers on neurotransmitters, otolith function, and central vestibular pathway syndromes illustrate a promising area for scientific and clinical research in the future. Identification of vestibular pathway lesions as the cause of many oculomotor syndromes, such as downbeat and upbeat nystagmus or ocular tilt reaction lesions, will broaden the scope of otoneurology and the clinical responsibility of the neurologist.

Humans↗