Search PubMed⌕ Search

Biomedical subjects

S Zierz

Publications and source records attributed to S Zierz.

At least 73 records · Page 4Linked to original sources
PubMed2000

Automated identification of Doppler microembolic signals: comparison of two techniques.

An alternative technique for identification of Doppler microemboli signals (MES), based on intensity measurements in the vessel and in an arbitrary sample volume was recently reported. We evaluated the applicability of this approach as stand alone system, and compared it to the standard bigate method (TCD 8, version 8T). Bilateral TCD monitoring was performed in 11 patients with prosthetic heart valves and 15 patients during elective cardiac surgery, using three sample volumes (29 mm, 50 mm and 55 mm). All data was saved on digital audio tapes and evaluated by two experienced observers. Only signals unanimously identified as MES or artifacts by both observers were evaluated. A total of 6189 MES and 11,241 artifacts were further analysed. Sensitivity and specificity of the bigate approach and the technique utilising the arbitrary sample volume were 90.7%, 91.3% and 88%, 91.9% respectively. Simultaneous monitoring over three sample volumes and combination of the two detection algorithms could potentially provide an adequate stand-alone system for MES detection.

Aged↗
PubMed2000

New insights into the metabolic consequences of large-scale mtDNA deletions: a quantitative analysis of biochemical, morphological, and genetic findings in human skeletal muscle.

In order to study putative genotype phenotype correlations in mitochondrial disorders due to large-scale mtDNA deletions we performed a quantitative analysis of biochemical, morphological, and genetic findings in 20 patients. The size of the mtDNA deletions varied from 2 to 7.5 kb with a degree of heteroplasmy ranging from 16% to 78%. Applying improved methods for measuring respiratory chain enzyme activities, we found highly significant inverse correlations between the percentage of cytochrome c oxidase (COX)- negative fibers and citrate synthase (CS) normalized COX ratios. Significant correlations were also established between CS normalized complex I and complex IV ratios as well as between the degree of heteroplasmy of mtDNA deletions and the percentage of ragged red fibers, COX-negative fibers, and CS normalized complex I and complex IV ratios. Our results indicate that the degree of heteroplasmy of mtDNA deletions is mirrored on the histological as well as the biochemical level. Furthermore, our findings suggest that single large-scale deletions equally influence the activities of all mitochondrially encoded respiratory chain enzymes. Even low degrees of heteroplasmy of mtDNA deletions were found to result in biochemical abnormalities indicating the absence of any well-defined mtDNA deletion threshold in skeletal muscle.

Adolescent↗
PubMed1999

Transcranial magnetic stimulation compared with upper motor neuron signs in patients with amyotrophic lateral sclerosis.

If patients with amyotrophic lateral sclerosis (ALS) present without upper motor neuron signs (UMNS) they do not meet current ALS research criteria. To compare how sensitively degeneration of upper motor neurons is detected clinically and by transcranial magnetic stimulation, 35 patients with ALS were studied. Nineteen patients had definite UMNS, nine patients had probable UMNS, and seven patients had no UMNS. Cortex, cervical nerve roots, and lumbar plexus were stimulated with a magnetic stimulator. Compound muscle action potentials from abductor digiti minimi and from anterior tibial muscles were recorded with surface electrodes. Responses to transcranial magnetic stimulation were considered abnormal if central motor conduction time was above the 99% upper limits or if there was no response to cortical but to peripheral stimulation. In all patients with definite UMNS central motor conduction was abnormal. In patients with probable UMNS it was abnormal in 67%, and in patients without UMNS it was abnormal in 71%. Abnormality of central motor conduction was neither correlated with the duration nor with the severity of the disease. The high rate of abnormalities of central motor conduction found in patients with ALS but without definite UMNS suggests that, in these patients, the diagnosis of ALS can be made more reliably if transcranial magnetic stimulation studies are performed.

Action Potentials↗
PubMed1999

Treatment of tension-type headache with botulinum toxin: a pilot study.

We studied if injections of botulinum toxin into multiple pericranial muscles reduce pain of patients with tension-type headache. Nine patients with tension-type headache not sufficiently responding to physical therapy or to amitriptyline were studied. Patients kept a headache diary that was used to calculate the area under the headache curve (AUC) of 4 weeks before and after treatment. After a run-in phase of 4 weeks equal doses of 25 units (0.25ml) of botulinum toxin type A (Dysport) were injected into both frontal, temporal, occipital, and sternocleidomastoid muscles. Mean AUC of the 8 patients who completed the study was significantly reduced from 404 to 196 (p = 0.039). No major side effects were reported by the patients. These results justify further studies of botulinum toxin therapy in patients with tension type headache. The presented scheme for injections of botulinum toxin into multiple pericranial muscles is a rational basis for the design of such studies.

Adult↗
PubMed1999

Focal sensory nerve abnormalities in patients with amyotrophic lateral sclerosis.

Slowing of sensory nerve conduction is an unexplained finding in patients with sporadic amyotrophic lateral sclerosis (ALS). To study the frequency of these abnormalities and to study if a predisposition to the development of entrapment neuropathies is causal, 23 patients with definite ALS and 23 age-matched healthy volunteers were investigated prospectively. Antidromic sensory and motor nerve conduction velocities (NCVs) were measured in ulnar and median nerves. Median sensory NCV was abnormally low in three patients if compared with the lower limit of the control group; and median sensory NCV was abnormally low in nine patients (six right, eight left hands) if compared with ipsilateral ulnar sensory NCV. Sensory nerve conduction data did not correlate with clinical findings, such as forearm weakness or usage of canes. Motor nerve conduction data did not correlate with sensory nerve conduction data, with the exception of distal motor latency of right median nerves, which correlated with right median sensory NCV. Our findings show how affection of sensory fibers of distal segments of median nerves can be detected in individual patients with ALS. Nerve entrapment may contribute to this affection, but it is not the only cause. This should be considered in discussions about diagnostic criteria for ALS.

Adult↗
PubMed1999

Recurrent orbital myositis: report of a familial incidence.

BACKGROUND: In orbital myositis, painful diplopia develops owing to an enlargement of the extraocular muscles. Diagnosis is established based on history, clinical manifestations, and therapeutic response to steroids, with the findings of magnetic resonance imaging providing additional information. OBSERVATION: We observed a family in which 4 members had an ophthalmopathy suggestive of orbital myositis. The affected members are a sibling pair (female and male) and 2 children of the brothers of their father's father. CONCLUSION: The familial incidence suggests a potential genetic predisposition in the development of orbital myositis.

Adolescent↗
PubMed1999

Mitochondrial 3243 A-->G mutation (MELAS mutation) associated with painful muscle stiffness.

The mitochondrial mutation A-->G at nucleotide position 3243 is associated with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and other mitochondrial encephalomyopathies. We found this mutation in a 61-year-old patient who developed at the age of 54 a myopathy with painful muscle stiffness as the predominant symptom. Additionally hypacusis, a mild hemisensory syndrome and impaired glucose tolerance were present. Muscle histopathology showed few ragged red fibers. The mutation was detected heteroplasmatically in DNA from muscle and blood. So far painful muscle stiffness has not been a known phenotype of the 3243 mutation.

DNA, Mitochondrial↗
PubMed1999

Assessment of temporal dispersion in motor nerves with normal conduction velocity.

Demyelinated nerves attenuate high-frequency components of propagating action potentials. In order to study if there is diagnostic use of this in motor nerves, the spectral energy above 49 Hz, amplitude, area, and duration of the compound muscle action potentials were measured; values after distal and proximal stimulation of posterior tibial nerves were compared. Normative data were collected in 48 control subjects. The same measurements were made in 20 patients with polyneuropathy and reduced motor nerve conduction velocity, in 21 patients with mild polyneuropathy but normal motor nerve conduction velocity, and in 8 patients with myasthenia gravis. Overall, high-frequency attenuation was closely correlated with amplitude decay (r = 0.63, P<10(-19)) and with increase of action potential duration (r = 0.34, P = 10(-5)). In the group of patients with normal NCV, high-frequency attenuation was abnormal in 9 (43%), amplitude decay was abnormal in two (10%), and area decay was abnormal in one (5%) patient. The action potential duration was normal in all of these patients. High-frequency attenuation was not influenced by stimulus intensity, thus it is not changed by conduction block, and it was not influenced by impaired neuromuscular transmission. Hence, high-frequency attenuation, both sensitively and specifically does indicate abnormal temporal dispersion. In conclusion, the simple measurement of high-frequency attenuation markedly improves detection and characterization of demyelination of human motor fibers.

Action Potentials↗
PubMed1999

Impaired energy metabolism in hearts of septic baboons: diminished activities of Complex I and Complex II of the mitochondrial respiratory chain.

Recent findings support the view that the bioenergetic part of septic organ failure is not caused by insufficient supply of oxygen but by disturbances of the mitochondrial function. Therefore, the aim of the present study was to investigate key enzymes of energy metabolism in septic hearts to answer the question whether or not impairment of mitochondrial or glycolytic enzymes occur under these conditions. For this purpose the well established model of septic baboons was used. Baboons under general anesthesia were made septic by infusion of Escherichia coli. Single challenge with infusion of high amounts of bacteria was compared with a multiple challenge protocol (less bacteria infused). Some animals obtained no E. coli (sham). The hearts of the baboons were removed after 72 h (survival: yes) or after death (survival: no) of the animals, frozen in liquid nitrogen, and stored at -80 degrees C until spectrophotometrical measurement of nine mitochondrial and glycolytic enzymes. A reduction of the activity of NADH:cytochrome-c-reductase (Complex I + III) to 67% and succinate:cytochrome-c-reductase (Complex II + III) to 45% was found in the hearts of surviving animals after infusion of high amounts of bacteria. After multiple challenge with lesser amounts of bacteria, no significant changes in enzyme activity were detectable. After lethal septic shock, activities of Complex I + III (12%) and Complex II + III (13%) as well as of phosphofructokinase (16%) were found to be strongly diminished. Decylubiquinol:cytochrome-c-reductase (Complex III, 59%), cytochrome-c-oxidase (51%), succinate dehydrogenase (60%), glucosephosphate isomerase (61%), lactate dehydrogenase (61%), and citrate synthase (120%) were less or unaffected. Similar but less pronounced effects were found after infusion of lesser amounts of bacteria. By means of inhibitor titrations of succinate: cytochrome-c-reductase, it was shown that the loss of activity is not caused by Complex III but by disturbances in Complex II. It is concluded that E. coli-induced sepsis causes decreased activities of Complex I and Complex II in baboon heart mitochondria in a dose-dependent manner.

Animals↗
PubMed1998

Dextran strongly increases the Michaelis constants of oxidative phosphorylation and of mitochondrial creatine kinase in heart mitochondria.

Macromolecules restore the morphological changes which occur upon isolation of mitochondria in normally used isolation media. It was shown that in the presence of dextrans the permeability of mitochondrial outer membrane for adenine nucleotides decreases which may have considerable implications for the transport of ADP into the mitochondria. In this study the effect of dextran on the apparent Michaelis constants of oxidative phosphorylation and mitochondrial creatine kinase (mi-CK) of rat heart mitochondria was investigated. Mitochondria were isolated either in normally used isolation media or in the additional presence of 15% dextran 20 in order to avoid changes in the oncotic conditions on the mitochondria during preparation and investigation. Except for an increased contamination with extramitochondrial ATPases the basic functional properties of these mitochondria were normal. With oxygraphic measurements it was found that Km(ADP) of oxidative phosphorylation increased from 16 +/- 4 microM ADP (without dextran) to 50 +/- 15 microM (15% dextran 20) and to 122 +/- 62 microM (25% dextran 20) irrespective of the mode of preparation of the mitochondria. Using spectrophotometric measurements the effect of dextran on the Km(ATP) of mi-CK was investigated in three systems (a) as soluble enzyme, (b) bound to mitoplasts, (c) and in intact rat heart mitochondria. The addition of 10% dextran had no effect on kinetic properties of solubilized mi-CK. In intact heart mitochondria, however, the addition of dextran caused an augmentation of Km(ATP) from 332 +/- 91 microM (control) to 525 +/- 150 microM ATP (10% dextran) and 641 +/- 160 microM ATP (30% dextran). In mitoplasts the effect of dextran disappeared (control, 230 +/- 19 microM ATP; 10% dextran, 238 +/- 28 microM ATP) indicating that the outer mitochondrial membrane is a prerequisite for the modulation of the transport of adenine nucleotides into the intermembrane space by macromolecules. To investigate the effects of viscosity of dextran solutions on the diffusion of adenine nucleotides across the outer membrane, dextrans with different molecular size (20, 40 70 and 500 kDa) were used. The viscosity of the 10% solutions drastically increased with the molecular size of the dextrans used, but the effects of different dextran solutions on the kinetic constants were the same. From these results it was concluded that neither the viscosity nor the molar concentration but the content of macromolecules (mass/vol.) correlates with restrictions of diffusion into the intermembrane space of mitochondria with intact outer membranes. Assuming that a dextran concentration of 15% mimicks the intracellular oncotic pressure on mitochondria in vivo, the apparent Km(ATP) of oxidative phosphorylation within the intact cell seems to be about 50 microM ADP which is somewhat higher than the cytoplasmic free ADP concentration as reported for the intact heart.

Adenine Nucleotides↗
PubMed1998

Intracranial microembolic signals in patients with artificial heart valves: drowning in numbers.

Five years after the first description of Doppler microembolic signals, both their clinical significance and underlying material remain a matter of debate. It appears certain that MES depend on valve type and position, while their relation to other clinical parameters, including neurological complications, is still unclear. A number of clinical and experimental studies are reviewed, most of which argue towards gaseous embolic material.

Embolism, Air↗
PubMed1998

The forgotten condyle: Delayed hypoglossal nerve palsy caused by fracture of the occipital condyle.

Fracture of the occipital condyle is a rare injury that can be easily overlooked. Palsies of lower cranial nerves can be the only symptom of the fracture. We report a patient with isolated post-traumatic hypoglossal nerve palsy who developed hypoglossal nerve palsy within 2 months after a car accident, indicating that the acute trauma itself did not damage the hypoglossal nerve. Most likely the palsy is caused by pressure to the nerve prior to the entry or within the hypoglossal canal. Since, in the present case, the fracture was stable and the patient showed only moderate neurological deficits, the operation was deferred.

Cranial Nerve Diseases↗
PubMed1998

Influence of transducer frequency on Doppler microemboli signals in an in vivo model.

The purpose of this study was the comparison between 1 MHz and 2 MHz transducers in the detection of Doppler microembolic signals (MES). Intraoperative monitoring was performed over the arterial tubing of the extracorporal circulation circuit in 10 patients undergoing coronary artery bypass surgery, using a pulsed ultrasound machine (DWL X-4). 1 MHz and 2 MHz probes were mounted to insonate sequential tubing segments and all monitoring sessions saved on digital audio tapes (DAT). MES counts and intensity as detected by each probe were subsequently evaluated. Specific interobserver agreement was assessed using Cohen's kappa-statistic. Time delay in the appearance of MES between the transducers was minimal (0-0.1 msec). A total of 5293 (64%) MES were detected by both probes, 2796 (33.8%) only with the 1 MHz and 181 (2.2%) only with the 2 MHz probe. Significant differences in MES intensity were evident when comparing the 1 MHz to the 2 MHz transducer (16.4 +/- 0.1 and 11 +/- 0.1 dB with the 1 MHz and 2 MHz transducers respectively, p < 0.0001). Specific interobserver agreement was satisfactory (k = 0.78). Use of 1 MHz instead of 2 MHz transducers increases the yield of embolus detection in vitro. Evaluation of the applicability and performance of this transducer in clinical settings is warranted.

Catheters, Indwelling↗