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Biomedical subjects

D Sander

Publications and source records attributed to D Sander.

At least 55 records · Page 3Linked to original sources
PubMed1996

Sleep apnea syndrome and cerebral hemodynamics.

The dynamics of cerebral blood flow velocity (CBFV) during sleep were investigated in the right middle cerebral artery of 10 patients with sleep apnea syndrome (SAS) (mean age, 37 years) and 10 healthy control subjects (mean age, 32 years) throughout the entire sleep period. A computer-assisted pulsed (2 MHz) transcranial Doppler ultrasonography system was modified for continuous long-term and on-line recording of cerebral hemodynamics. Concurrently, simultaneous polysomnography, continuous BP recordings, and measurement of the end-expiratory carbon dioxide were undertaken. CBFV showed comparable nocturnal profiles in both groups with decreases during non-rapid eye movement (NREM) sleep and increases during rapid eye movement (REM) sleep, indicating that the general pattern of brain perfusion during normal sleep is maintained in SAS. Sleep stage changes were not regularly accompanied by corresponding changes in CBFV. This reflected a quantitative uncoupling between cerebral electrical activity and cerebral perfusion during sleep and indicated a dissociation in the activity of central regulatory mechanisms. Sleep stage-related analysis showed slightly reduced CBFV in patients with SAS compared with healthy control subjects during wakefulness and the first NREM sleep period, suggesting depressed brain activity in the patient group. The higher CBFV values observed in patients with SAS compared with control subjects during REM sleep and sleep stage 2, both preceding and following REM sleep, underline the influence of dynamically changing sleep patterns on cerebral perfusion in these patients. Reproducible rapid decreases in CBFV were related to EEG arousals. Since apneas are terminated by arousals, these results showed that direct neuronal influences on brain perfusion during apnea are evident.

Adult↗
PubMed1996

[Intracranial blood flow parameters in cerebral functional changes and cognitive cerebral performance].

Extensive studies have revealed a close relationship between neuronal activity and regional cerebral blood flow. However, SPECT and PET, the technologies most commonly used in these studies, are of limited value for assessment of the dynamics of cerebral blood flow changes at different states of functional brain activity. The introduction of transcranial Doppler sonography and the extended application of stimuli presentation and perception have now been added to the investigator's armamentarium. Simple sensory stimulation (visual, acoustic and tactile) and complex mental tasks (viewing of complex pictures, tactile differentiation of objects) changed the blood flow velocity in the basal intracranial arteries. These changes corresponded to the current concepts of functional cortical organization. The magnitude of the flow velocity increases upon visual stimulation was dependent on the complexity of the stimuli used, and was up to 38% in our studies. The introduction of continuous and bilateral simultaneous Doppler recordings, the calculation of mean flow velocity from cardiac cycle to cardiac cycle and a specially designed averaging method for data analysis allowed effective elimination of non-specific influences and made it possible to demonstrate rapid changes of perfusion in both middle cerebral artery territories in direct response to hemisphere-specific tasks. These changes were correlated with known functional cerebral asymmetries. A language task, for instance, was associated with a significantly larger flow velocity increase in the middle cerebral artery of the dominant hemisphere than in the corresponding artery of the non-dominant hemisphere (5.2 +/- 1,8% vs 3.0 +/- 1.8%, p < 0.001). The excellent time resolution of this technology made it possible to record hemodynamic changes taking place in response to modifications of neuronal activity within less than 1 s. The shortest time interval between stimulus presentation and the first significant increase in flow velocity was on average 717 +/- 191 ms. The latency of less than 1 s suggest that the coupling between alterations of neuronal activity and the regional cerebral blood flow response is mediated by an remarkably rapid mechanism.

Arousal↗
PubMed1995

Changes of circadian blood pressure patterns and cardiovascular parameters indicate lateralization of sympathetic activation following hemispheric brain infarction.

The effects of left- and right-sided hemispheric brain infarction on variability in circadian blood pressure and cardiovascular measures were investigated in 35 patients to test for asymmetry of the sympathetic consequences of stroke. No significant differences regarding age, size of infarction or extent and frequency of damage to the insular cortex could be detected between the two groups. Patients with right-sided infarction showed a significantly reduced circadian blood pressure variability [diastolic: -1% (95% CI -4 to 1) vs -6% (-9 to -2); P < 0.05] and a higher frequency of nocturnal blood pressure increase (47% vs 35%; P < 0.05) as compared with patients with left-sided infarction. Right-sided infarction was also associated with higher serum noradrenaline concentrations [546 pg/ml (95% CI 415-677) vs 405 pg/ml (266-544); P < 0.05], and ECG more frequently showed QT prolongation (53% vs 35%; P < 0.05) and cardiac arrhythmias (67% vs 20%; P < 0.005). However, irrespective of the hemisphere damaged, patients with insular infarction showed the most pronounced changes of these parameters. In addition, two patients with right-sided strokes (13%) involving the insula, but none with a left-sided infarction, developed myocardial infarction. These findings suggest lateralization of sympathetic activation with right-sided dominance for sympathetic effects following hemispheric stroke.

Aged↗
PubMed1995

Dynamics of cerebral blood flow velocities during normal human sleep.

Bilateral flow patterns of the middle cerebral artery (MCA) were recorded continuously throughout the night in 18 healthy male subjects (mean age 27.4 years) by a computer-assisted pulsed Doppler (2 MHz) system together with simultaneous polysomnography. After inception of sleep, mean flow velocity (MFV) decreased steadily during deepening sleep stages reaching -15.0 +/- 3.6% (p < 0.001) in the right MCA and -16.2 +/- 3.4% in the left MCA (p < 0.001) in stage 4 of the first sleep cycle compared to the waking state. Lowest MFV values were found in stage 2 preceding the last REM period (right MCA: -19.2 +/- 4.1%: left MCA: -19.7 +/- 5.1%). Changing from non-REM into REM sleep, a sudden rise of MFV, which varied from 8.9% (first sleep cycle, left MCA) to 18% (last sleep cycle, right MCA), could be consistently detected indicating a coupling of cerebral electrical activity and cerebral perfusion in REM sleep. During non-REM sleep this concomitant change of MFV and EEG activity was only found in the first sleep cycle, whereas no parallel changes could be observed in later sleep cycles. These results indicate a decoupling of EEG measured cerebral electrical activity and perfusion and suggest that factors other than metabolic mechanisms contribute to the regulation of cerebral perfusion during human non-REM sleep.

Adult↗
PubMed1995

Effect of hemisphere-selective repetitive magnetic brain stimulation on middle cerebral artery blood flow velocity.

The changes of cerebral hemodynamics following repetitive hemisphere-selective magnetic stimulation over the motor cortex were investigated in 8 healthy volunteers. Bilateral simultaneous monitoring of middle cerebral artery blood flow velocity was done using transcranial Doppler ultrasonography during magnetic stimulation with single, double and triple stimuli with interstimulus intervals of 100 msec. Magnetic cortex stimulation was followed by a significant increase of ipsilateral flow velocity ranging from 5.3% +/- 2.7% for single stimuli up to 8.5% +/- 4.1% for triple stimuli and by a smaller increase of contralateral flow velocity. The ipsilateral increases are comparable to those measured previously during voluntary finger movements and indicate a physiological cortex stimulation. In parallel, the average sum of the baseline to peak hand motor response amplitudes increased from 1.5 +/- 0.7 mV (single stimuli) to 4.5 +/- 3.2 mV (triple stimuli). The increase of flow velocity in the non-stimulated hemisphere occurred during the absence of motor responses and might reflect a transcallosal activation of inhibitory neuronal structures. The occurrence of maximum velocity responses within 2-3 heartbeats following the first cortex stimulus points to a fast adjustment of cerebral perfusion in response to transcranial brain stimulation. No significant change of flow velocity was observed following motor responses evoked by unilateral magnetic stimulation of the brachial plexus or following acoustic artifacts of the coil discharge.

Adult↗
PubMed1995

Plexus neuropathy following vaccination against tick-borne encephalitis and tetanus due to a sports related altered immune state.

A 45-year-old female patient who was practising sports on a competition level, developed a plexus neuropathy subsequent to a vaccination against tick-borne encephalitis (TBE) followed by an inoculation of tetanus toxoid six days later. After the TBE vaccination she continued to exercise intensely until symptoms of a neuritis were noticed. Pronounced endurance exercise has been described to alter the composition and function of the immune system. In our patient a decrease of T-helper cells and a significant lowered CD4/CD8 ratio could be detected. The possible link between an altered immune state and post-vaccinal neuropathy is discussed.

CD4-CD8 Ratio↗
PubMed1995

Cerebral perfusion during sleep-disordered breathing.

Snoring, a leading symptom of the sleep apnoea syndrome (SAS), has been reported to be one of the risk factors for sleep-related cerebral strokes. Episodes of apnoea are accompanied by hypoxaemia as well as hypercapnia. As CO2 constitute a major regulatory factor controlling cerebral blood flow, it is likely that changes in cerebral perfusion are to be found in patients with SAS, which may be related to nocturnal stroke. A computer-assisted pulsed (2 mHz) Doppler ultrasonography system has been modified for continuous long-term and on-line recording of cerebral haemodynamics together with simultaneous polysomnography, continuous blood pressure recordings, and measurement of the end-expiratory CO2. The dynamics of cerebral blood flow velocity (CBFV) during sleep were measured in the right middle cerebral artery in 10 SAS patients. CBFV showed a characteristic nocturnal pattern with decreases during non-rapid eye movement (NREM) sleep and increases during REM sleep. Changes in sleep stage patterns as well as awakenings from NREM sleep were not regularly accompanied by corresponding changes in CBFV. Dramatic increases in CBFV could be observed during apnoeic episodes, with maximum increases during REM sleep. CO2 reactivity and changes in CBFV related to apnoea duration were markedly increased during sleep compared with the waking state in SAS patients. The dynamic feature of CBFV in relation to sleep patterns reflects quantitative uncoupling between cerebral electrical activity and cerebral perfusion during sleep in SAS patients as has been previously reported for normal subjects (Hajak et al. 1994). It supports a dissociation in the activity of central regulatory mechanisms during human sleep which might cause abnormal cerebral perfusion under certain circumstances. The increased CO2 reactivity during sleep in SAS suggests a 'hypersensitivity' of intracranial vasoactive receptors and/or disturbances in the central autonomic control of cerebrovascular functions. It may be concluded that, under certain conditions, the interaction of decreased cerebral perfusion in SAS patients with sleep-related cerebral perfusion patterns and haemodynamic changes during apnoeic episodes might lead to a critical reduction in cerebral perfusion.

Journal Article↗
PubMed1995

An anti-alpha v-integrin antibody that blocks integrin function inhibits the development of a human melanoma in nude mice.

A series of murine monoclonal antibodies were raised against purified human alpha v beta 3 integrin and against M21 human melanoma cells. Five notable hybridomas were identified by ELISA on purified integrins, and the isolated antibodies bound the alpha v-chain. These antibodies, 17E6, 20A9, 23G5, 14D9.F8 and 10G2, recognised the extracellular domains of the integrin, and were shown to be reactive in FACS, immunoprecipitation, ELISA, and ELISA on fixed cells with M21, M21-L4, and UCLA-P3, but not with the alpha v-deficient M21-L or M21-L-IIb (M21-L transfected with GpIIb integrin). One antibody, 17E6, strongly perturbed cell attachment mediated by alpha v integrins, reacting at least with alpha v beta 3, alpha v beta 5, and alpha v beta 1, and strongly inhibiting cell attachment to alpha v-ligands vitronectin and fibronectin with an IC50 of approximately 0.1 microgram ml-1. Furthermore, 17E6 at this concentration could induce cell retraction from the substrate, while LM609 (anti-alpha v beta 3) and control antibody 14E2 (anti-200 kDa melanoma surface protein) at 1,000-fold higher concentrations had minimal effects on cell morphology. The action of 17E6 was reversible and was not due to toxic effects: in vitro 17E6 at 0.1 mg ml-1 did not affect either cell proliferation or DNA synthesis. In two nude-mouse tumour models, subcutaneous tumour development and a lung colonisation ('experimental metastasis') assay, injection of 17E6 strongly inhibited tumour development, while isotype-matched controls had no effect. There was no obvious mechanism of cell or of complement-mediated tumour cytotoxicity; the antibody did not mediate ADCC or AECDC, or complement fixation. The data strongly support previous studies which have indicated the importance of alpha v-integrins, and especially alpha v beta 3, in the tumour progression of human melanoma.

Animals↗
PubMed1994

Relationship between cerebral blood flow velocities and cerebral electrical activity in sleep.

The dynamics of cerebral blood flow velocity during sleep were measured in the right and left middle cerebral artery of 12 and 10 healthy male volunteers, respectively. A computer-assisted pulsed (2-MHz) Doppler ultrasonography system was modified for continuous long-term and on-line recording of cerebral hemodynamics in combination with polysomnography. Mean flow velocity (MFV) decreased steadily during deepening nonrapid eye movement (NREM) sleep and increased suddenly during rapid eye movement sleep, corresponding to changes in brain function. However, spontaneous or provoked changes in sleep stage patterns as well as awakenings from NREM sleep were not regularly accompanied by corresponding changes in MFV. Differing values for MFV in subsequent sleep cycles could be shown for several sleep stages. Furthermore, MFV values in sleep stage II at the end of an NREM-sleep period were lower than in preceding slow-wave sleep. After application of short acoustic signals the electroencephalogram frequency rose, indicating an arousal, whereas MFV rapidly decreased for several seconds and then gradually returned to the prior level. These results imply an uncoupling between cerebral electrical activity and cerebral perfusion during sleep and support a dissociation in the activity of central regulatory mechanisms. In light of the proposal that cortical energy consumption can be accounted for by cerebral electrical activity, the concept that cerebral perfusion during sleep is regulated solely by the metabolic rate must be reconsidered.

Adult↗
PubMed1994

Changes of circadian blood pressure patterns after hemodynamic and thromboembolic brain infarction.

BACKGROUND AND PURPOSE: We investigated the changes of circadian blood pressure patterns after thromboembolic and hemodynamic brain infarction and evaluated the relation between circadian blood pressure variation, infarct location, and activation of the autonomic nervous system after thromboembolic stroke. METHODS: Repeated 24-hour blood pressure measurements were performed in 45 patients with proven first-ever brain infarctions of different origins. Evaluation of serum norepinephrine concentration, prolongation of the QT interval, and degree of cardiac arrhythmias were used to determine the extent of sympathetic activation after thromboembolic stroke. RESULTS: Whereas circadian blood pressure variation was significantly increased after hemodynamic infarction compared with a control group (diastolic, -25.2 +/- 4.5% versus -13.8 +/- 6.5%; p < .005), a clearly reduced variation was observed after thromboembolic infarction (diastolic, -5.2 +/- 6.9%). Blood pressure variation was positively related to serum norepinephrine concentration (r = .79; P < .01) after thromboembolic infarction. Patients with involvement of the insular cortex showed a nocturnal rise of blood pressure significantly more frequently (66.7% versus 11.8%; P < .005) and had higher norepinephrine levels (66.7 +/- 110 pg/mL versus 290 +/- 178 pg/mL; P < .01) than patients without insular cortex infarction, indicating increased sympathetic activity. This was associated with a significantly more frequent occurrence of QT prolongation and cardiac arrhythmias. CONCLUSIONS: The observed differences in circadian blood pressure patterns may (1) help to distinguish the pathophysiological basis of the stroke, (2) help to explain worsening in some cases of hemodynamic stroke, (3) confirm the importance of the insular cortex for sympathetic activation, and (4) identify subgroups of patients with increased risk of myocardial infarction and arrhythmia.

Aged↗
PubMed1994

[The importance of 24-hour-blood pressure monitoring in hemodynamic and thromboembolism-induced cerebral infarcts].

Night and day blood pressure profiles of 45 patients with cerebral infarction of hemodynamic or thromboembolic origin were assessed to detect subsequent changes of circadian blood pressure variability. The data were also analysed for a possible relationship between variability of circadian blood pressure, site of cerebral infarction and activation of the autonomic nervous system. Patients with a stroke of hemodynamic origin, when compared to a control group, manifested significantly greater variability of circadian blood pressure (diastolic: -25.2 +/- 4.5% vs. -13.8 +/- 6.5%; p < 0.005). Patients who showed the greatest decrease in vasomotor reactivity (< 40%) developed a prolonged disturbance of the blood-brain barrier. This disturbance regressed slowly only after the pathological 24-hour blood pressure profile had normalized. By way of contrast, patients with cerebral infarctions due to thromboembolic events, when compared to normal individuals, showed a distinctly decreased circadian blood pressure variability (diastolic: -5.2 +/- 6.9%). Initially 40% of these patients presented a pathological increase of nocturnal blood pressure. Circadian blood pressure variability was positively correlated with serum concentration of norepinephrine (r = 0.79; p < 0.01). Patients with a stroke affecting the insular cortex manifested an increase of nocturnal blood pressure significantly more often (66.7% vs. 11.8%; p < 0.005), indicating increased sympathetic activation. They had higher serum levels of norepinephrine (540 +/- 110 pg/ml vs. 290 +/- 178 pg/ml) as compared to patients without damage to the insula and also a significantly higher incidence of prolonged QT intervals and cardiac arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Interactions between the bone matrix proteins osteopontin and bone sialoprotein and the osteoclast integrin alpha v beta 3 potentiate bone resorption.

We have investigated the mechanism by which osteoclasts adhere to and resorb bone. We show that these cells express beta 1 and beta 3 integrins which are involved in attachment to purified bone matrix proteins. Binding to osteopontin and bone sialoprotein is mediated by alpha v beta 3, while a beta 1 integrin is responsible for attachment to fibronectin. Both the rapid attachment by osteoclasts to intact bone particles and their subsequent resorption are blocked by a monoclonal antibody directed to the alpha v beta 3 complex but not by an antibody against beta 1 integrins. Attachment of osteoclasts to bone is also inhibited with soluble osteopontin, Arg-Gly-Asp-containing peptides derived from both osteopontin and bone sialoprotein, or a monospecific polyclonal antibody against osteopontin. We conclude that both osteoclast adherence to bone and subsequent resorption of its matrix are dependent on interactions between the bone matrix proteins osteopontin and/or bone sialoprotein and the integrin alpha v beta 3. Moreover, collagen, which constitutes 90% of its organic matrix, is minimally involved in binding of chicken osteoclasts to bone.

Amino Acid Sequence↗
PubMed1993

Cerebral vasospasm following post-traumatic subarachnoid hemorrhage evaluated by transcranial Doppler ultrasonography.

We studied the incidence and time course of flow velocity changes suggesting a vasospasm following post-traumatic subarachnoid hemorrhage (SAH) considering the intracranial pressure (ICP) in 38 SAH patients as compared to 30 patients with spontaneous SAH. The first investigation was done within 24 h after onset of hemorrhage and regularly followed up during the clinical course. Additionally, the index of cerebral circulatory resistance was calculated and the ICP was measured using an epidural transducer. A significant correlation between middle cerebral artery maximum mean flow velocity and the quantity of blood seen on a computed tomographic scan in patients with post-traumatic SAH indicates a similar pathogenetic mechanism of the development of vasospasm to that after spontaneous SAH. In contrast, there was a significantly earlier occurrence of mean flow velocities over 120 cm/s following post-traumatic SAH irrespective of the ICP. Therefore, additional factors must be considered in the evaluation of these pathologically raised flow velocities after posttraumatic SAH. In both SAH groups there was a highly significant correlation between clinical outcome and clinical grade on admission, ICP and resistance index. The weak correlation between maximum mean flow velocity and clinical outcome following post-traumatic SAH supports the notion that final clinical outcome of these patients is of multifactorial origin.

Adolescent↗
PubMed1993

Circadian blood pressure patterns in four cases with hemodynamic brain infarction and prolonged blood-brain barrier disturbance.

We report on four patients with hemodynamic brain infarction and pathological circadian blood pressure patterns with nocturnal hypotension which gave rise to a prolonged disturbance of the blood-brain barrier. Besides at least one severe stenosis of the internal carotid artery, there was an untreated chronic arterial hypertension and a pathologically reduced vasomotor reactivity after CO2 stimulation in all patients. The 24-h blood pressure monitoring then carried out showed a distinctly pathological circadian profile with hypertensive day values and nocturnal hypotension with minimum values of 95/50 mm Hg. The range of variation between day and night values was significantly raised (systolic: 20% +/- 2.15%; diastolic: 22.9% +/- 2.58%) compared to patients with essential hypertension as well as normotensive subjects (P < 0.01), and was in excess of 40% in the individual case. There was a slow recovery of the blood-brain barrier after drug-induced normalization of the pathological circadian blood pressure profile. We conclude that the registration of circadian blood pressure patterns may be of prognostic and therapeutic relevance. It may also contribute to further clarification of the pathophysiological significance of blood pressure variability for the development of brain infarction.

Aged↗
PubMed1993

[Importance of antiphospholipid antibodies in cerebral ischemia].

The association between cerebrovascular complications and detection of antiphospholipid antibodies (aPA) has been under clinical and immunological investigation during the last ten years. The occurrence of aPA in coincidence with recurrent thrombosis, miscarriages and thrombocytopenia is termed "primary antiphospholipid syndrome". The most important neurological symptoms are recurrent cerebral arterial and venous ischemias. Especially in the case of young patients with a history of recurrent infarcts, migraine-like headaches and the absence of classical risk factors should lead to a determination of these antibodies. Although the pathogenetic importance of these antibodies is still unclear, patients positive for them seem to carry a higher cerebrovascular risk and should be observed more cautiously. More studies are necessary to define the origin of these antibodies and their role in thrombogenesis. To develop standards for therapeutic management a multicenter study is desirable.

Adult↗
PubMed1992

Results of four technical investigations in fifty clinically brain dead patients.

Fifty consecutive patients (aged 19-77 years, median 56 years) with primary cerebral diseases and the clinical signs of absent cortical and brainstem function were subjected to electroencephalography (EEG), brainstem acoustic evoked potentials (BAEP), extracranial Doppler ultrasonography (ECD) and arterial digital subtraction angiography (DSA). In the majority of cases the results of the technical tests agreed with the clinical signs and were suggestive of brain death. However, in one patient EEG revealed clear bioelectrical activity. In 6 cases, doubts existed about whether the EEG was isoelectric; in 3 of the 6 cases biological activity might have been present. In 31 of 42 patients ECD showed a typical pattern of intracranial circulatory arrest, in 9 of 42 ECD revealed a pattern suggestive of the cessation of cerebral blood flow. In four patients BAEP recordings compatible with brain death were recorded 2-3 days before intracranial circulatory arrest. In 2 patients with isoelectric EEG and absent BAEP arterial DSA demonstrated residual perfusion. The findings are discussed in view of the conceptional differences concerning brain death. It is concluded that the strict application of the concept of death of the whole brain requires angiographic demonstration of absent intracerebral blood flow.

Adult↗
PubMed1992

Relationships between dopamine infusions and intracranial hemodynamics in patients with raised intracranial pressure.

Dopamine, 1-10 micrograms/kg body weight/min was infused in 6 patients suffering from cerebrovascular diseases with elevated intracranial pressure and a critical cerebral perfusion pressure. Dopamine decreased intracranial pressure in 3 and increased it moderately in the other 3 patients. In all patients, the dopamine-induced rise of mean arterial pressure led to an increase of cerebral perfusion pressure. Transcranial Doppler ultrasonographic recordings of the middle cerebral artery in patients whose intracranial pressure declined revealed a decrease of the pathologically elevated cerebrovascular resistance, and an augmentation of cerebral blood supply. In conclusion, dopamine infusions may improve cerebral hemodynamics in some patients with severe brain edema. Such patients can be identified by intracranial pressure and Doppler monitoring.

Blood Flow Velocity↗