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Biomedical subjects

G F Hamann

Publications and source records attributed to G F Hamann.

At least 55 records · Page 3Linked to original sources
PubMed1999

[Acute therapy of stroke].

In recent years, organized basic care and the use of thrombolysis have been significantly effective in improving the acute stroke therapy especially for the ischemic stroke subtype. Combining the efforts for the basic care of stroke patients in the setting of the so-called stroke-units is the goal for a qualified therapy. Main parts in the basic care algorhythm are: optimization of the cerebral perfusion, maintenance of an initial high blood pressure, best oxygen supply, reduction of an increased body temperature and antiinfectious treatment, reduction in the rate of complications (like deep vein thrombosis, pneumonia, falls etc.) and the early physiotherapeutic therapy. Thrombolysis is restricted to selected patients with infarctions of the middle cerebral artery with symptoms starting not longer than three hours before treatment, without hemorrhage in CCT and fulfilling the strict in- and exclusion criteriae established by the recent multicenter trials. The use of rt-PA (0.9 mg/kg body weight) is recommended. Local fibrinolysis is used in patients suffering from basilar artery thrombosis. The use of other recanalizing techniques like PTA or stenting is yet still experimental in acute stroke patients. Neuroprotective agents which were proven in clinical trials are still not available. In recent years therapy with hemodilution was widely used, nowadays the intravenous application of fluids with hemodilutive properties is restricted to patients with reduced cardiac output and macroangiopathy to maintain or to improve cerebral perfusion. Early intravenous anticoagulation with heparin is defined as secondary prevention and not as therapeutical intervention.

Acute Disease↗
PubMed1999

Hemorrhagic transformation of cerebral infarction--possible mechanisms.

To analyse the risk/benefit of cerebral thrombolysis the role of hemorrhagic transformation, either as clinically silent hemorrhagic infarction or disastrous parenchymal hemorrhage, is crucial. Thrombolysis in acute ischemic stroke increases the risk of severe, life-threatening hemorrhagic complications by up to 10 times compared to controls. In this paper, previous proposed concepts for the development of intracerebral hemorrhage and hemorrhagic transformation are presented. The role of the cerebral microvasculature will be emphasized. In experimental focal cerebral ischemia a significant loss of basal lamina components of the cerebral microvessels has been demonstrated. This loss in vessel wall integrity is associated with the development of petechial hemorrhage. The mechanisms for this microvascular damage may include plasmin-generated laminin degradation, matrix metalloproteinases activation, transmigration of leukocytes through the vessel wall, and other processes. We propose that attenuation of the microvascular integrity loss with subsequent reduction in hemorrhage is theoretically possible 1) by an improvement in the definition of an individual time window of therapy (by means of imaging techniques), 2) by a biochemical quantification of the basal lamina damage to avoid dangerous interventions, and 3) by pharmacological strategies to protect the basal lamina during thrombolysis.

Animals↗
PubMed1998

[Value of magnetic stimulation and F-wave determination in diagnosis of proximal demyelinating lesions. Follow-up of acute Guillain-Barré polyradiculitis].

A 47-year-old woman developed acute Guillain-Barré-syndrome (GBS) within one day, presenting tetraparesis (muscle strength 1/5 for the upper and 2/5 for the lower extremities) and respiratory failure. On day 5 a cardiac pacemaker was necessary due to severe bradycardia. Electrophysiological studies were performed on days 2, 3, 5, 6, 8, 12, 15, 30 and 40. Our initial findings revealed normal motor conduction velocities and normal spinal motor evoked potentials. However, neither F-waves nor cortical motor evoked potentials could be registered from the upper or lower extremities. The motor conduction of the median nerve remained normal until day 6. The compound motor action potential declined thereafter and disappeared by day 12, indicating axonal degeneration. No axonal degeneration occurred in the lower extremities. The cervical or lumbar magnetic stimulation excites nerve roots at the level of the foramen intervertebrale. Thus, our findings suggest a conduction block between the foramen intervertebrale and the point where the nerve roots enter the spinal cord.

Afferent Pathways↗
PubMed1998

Hand gripping and acetazolamide effect in normal persons and patients with carotid artery disease.

Transcranial Doppler measurement (TCD) of cerebrovascular reserve (CVR) is usually performed by the CO2 test, the acetazolamide test, or the breath-holding test. Since these tests are time-consuming and labor-intensive, alternative methods such as the hand-gripping test are of interest. Twenty-one normal persons and 25 patients with unilateral carotid artery disease were studied. Flow velocity changes in both middle cerebral arteries (MCAs) during bilateral hand gripping were measured by TCD and compared with acetazolamide test results. The increase in MCA mean flow velocity (FVmean) during hand gripping was 18.0 +/- 6.3% in normal persons; the increases in the post-stenotic MCA were 15.8 +/- 9.7% in all patients and 9.4 +/- 5.4% in patients with impaired CVR as determined by the acetazolamide test. Only in the group with impaired acetazolamide reactivity was the increase in the poststenotic MCA significantly lower compared to that in controls (p < 0.01) and to the contralateral, nonstenotic side (p < 0.01). Nevertheless the FVmean increases in both tests showed a weak, but significant correlation (r = 0.59, p < 0.01). All FVmean increases during hand gripping were significantly (p < 0.01) lower than those during the acetazolamide test. The test appears as a weaker stimulus for MCA blood flow velocity increase than the acetazolamide test. Thus, only a substantial reduction of acetazolamide reactivity leads to a reduced MCA FVmean increase using hand gripping. Although it is highly specific but less sensitive, hand gripping does not appear to be suitable as a screening measure of CVR, but might be useful in addition to standard tests.

Acetazolamide↗
PubMed1998

Femoral injection of echo contrast medium may increase the sensitivity of testing for a patent foramen ovale.

OBJECTIVE: The diagnosis of a patent foramen ovale (PFO) as a cause of stroke is of increasing interest especially in young (<45 years) patients. METHODS: We studied potential right-to-left shunting using transesophageal echocardiography (TEE) and bilateral transcranial Doppler sonography (TCD) of the middle cerebral artery (MCA) simultaneously in 44 patients. All patients were younger than age 45 years and suffered from an acute ischemic stroke or transient ischemic attack. Other possible etiologies were excluded. Echo contrast medium was injected in an alternating mode via antecubital or femoral veins. Tests were performed with and without the Valsalva maneuver. The criteria for a PFO were that the contrast pass from the right to the left atrium (TEE) and early detection (<10 seconds) of more than 10 micro air bubbles in at least one MCA by TCD. RESULTS: A PFO was diagnosed in 22 patients (50%). The detection rate with TEE/TCD was 11.4%/4.5% via antecubital injection, 18%/13.6% via antecubital injection plus the Valsalva maneuver, 38.6%/36% via femoral injection alone, and 50%/50% via femoral injection plus the Valsalva maneuver. The difference between femoral and antecubital injections was significant with and without the Valsalva maneuver (p < 0.01, chi2 test). There were no differences between TEE and TCD after femoral injection with the Valsalva maneuver. The brain transit time was 4.6 +/- 2.1 seconds for femoral injection and 6.3 +/- 4.1 seconds for antecubital injection. CONCLUSIONS: The sensitivity in detecting a PFO was markedly increased by femoral injection. This may be caused by different inflow patterns to the right atrium: inferior vena caval flow is directed to the right atrial septum, whereas superior vena caval flow is directed to the tricuspid valve. Thus, femoral injection may help to improve the detection of PFO and may explain the differences between TEE and TCD findings in previous studies.

Adolescent↗
PubMed1997

[Acute cerebral infarct: physiopathology and modern therapeutic concepts].

This review focuses on the pathophysiological changes in acute cerebral ischemia, with special emphasis on disturbances of the cerebral blood flow (CBF) and the associated penumbra concept. Alternatively, the model of peri-infarct depolarization is demonstrated. Metabolic and molecular changes caused by cerebral ischemia and reperfusion are discussed, namely energy failure, release of glutamate with an excitatoric burst, calcium influx in neurons, generation of free radicals, activation of different proteases, disturbances of protein synthesis, induction of gene expression and apoptosis, loss of membrane integrity, edema formation and microvascular disturbances. In summary, the pathophysiological changes after focal cerebral ischemia and reperfusion are most adequately described by a network of interacting different mechanisms of tissue alterations. The simple concept of a cascade of ischemic effects which would be easy to block seems to be less applicable. A time window of approximately 6 h for the acute stroke therapy is postulated on the base of the above mentioned pathophysiological changes. The recently introduced treatment regimen with optimized basic treatment, recanalization using thrombolysis and neuroprotection by different agents is presented. Different modes of a possible intervention are discussed. Modern concepts of stroke therapy including stroke-unit care and thrombolysis with add-on neuroprotection seem to have potential for improving the outcome of acute stroke patients.

Acute Disease↗
PubMed1996

[Reduced sympathetic nervous system activity during the cluster period of cluster-headache].

Cluster headache is a rare, very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. Alterations of the hypothalamic-pituitary axis due to chronobiological changes, such as typical temporal pattern of both cluster periods and attacks, point to a central etiopathogenesis. Multiple local and systemic autonomic symptoms are compatible with an altered balance of the sympathetic and parasympathetic nervous system. In this connection, too, a central etiology is postulated. To evaluate the activation of the sympathetic nervous system, in 12 cluster headache patients we investigated the plasma catecholamines norepinephrine and epinephrine four times a day (7.00, 12.00, 17.00, 23.00) in the cluster period. In the cerebrospinal fluid we determined the transmitters norepinephrine, epinephrine, dopamine and the metabolites homovanillic acid (HVA), vanillymandelic acid (VMA) and 5-hydroxyindoleacetic acid (5-HIAA). Values of plasma norepinephrine in the morning (p < 0.01), in the evening (p < 0.01) and the daily mean value (223.8 = 58.3 nmol/ml) were significantly decreased in the cluster headache group in comparison to the control group (328.8 = 53.0 nmol/ml, p < 0.01). The plasma epinephrine showed no significant changes. In the CSF of cluster headache patients norepinephrine (p < 0.05), HVA (p < 0.01), and 5-HIAA (p < 0.01) were significantly decreased. Plasma norepinephrine was correlated with CSF values of HVA and 5-HIAA. The longer the duration of the disease, the lower the values of HVA and 5-HIAA in the CSF of cluster headache patients. Moreover, plasma norepinephrine showed a significant correlation with the duration, the intensity and the frequency of the attacks. The results of this study implicate decreased activity of the sympathetic nervous system with alteration of circadian rhythmicity during the cluster period. The decreased CSF transmitter values may support the hypothesis of a central etiopathogenesis of cluster headache. Moreover, plasma norepinephrine seems to be involved in triggering and continuing the attacks. The anatomical region in which this interface of sympathetic and neurogenic inflammatory processes might be located is the trigemino-vascular system.

Adult↗
PubMed1996

Altered activity of the sympathetic nervous system and changes in the balance of hypophyseal, pituitary and adrenal hormones in patients with cluster headache.

Twelve patients (age 43.4 +/- 6.3 years) with episodic cluster headache (CH) were examined during the cluster period. Plasma norepinephrine levels in patients suffering from CH were significantly decreased compared with the control group (p < 0.01). There were also statistically significant correlations between norepinephrine levels and clinical features of the pain attacks including duration (r = 0.75, p < 0.05), intensity (r = 0.64, p < 0.05) and frequency (r = 0.68, p < 0.06), thereby suggesting a pathophysiological involvement of the sympathetic nervous system in CH. Increased plasma levels of plasmacortisol and ACTH in patients with CH, especially in the morning and in the evening, suggest an alteration of the feedback circuit involving the hypothalamus, the pituitary and the adrenal gland, an imbalance in the hormones related to these structures, as well as an alteration of the circadian rhythm. In addition, CH patients demonstrated significantly decreased levels of norepinephrine (p < 0.05), HVA (p < 0.01) and 5-HIAA (p < 0.01) in the cerebrospinal fluid (CSF) consistent with a central genesis of CH. These significant relationships between neurochemical parameters and the clinical patterns suggest a complex interplay between the hypothalamus, neuroendocrinological parameters, activity of the autonomic nervous system and the pain of CH.

Adrenal Cortex Hormones↗
PubMed1996

Somatostatin, its molecular forms and monoaminergic transmitter metabolites in Binswanger's disease. Neurochemical-neuropathological considerations.

Cerebrospinal fluid (CSF) concentrations of somatostatin-like immunoreactivity (SLI), high molecular weight form somatostatin (HMV-SST), somatostatin-25/28 (SST-25/28), somatostatin-14 (SST-14), Des-ala-somatostatin (Des-ala-SST), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were measured in 21 patients with Binswanger's dementia (BD). Patients were classed into three stages of intellectual deterioration according to the Global deterioration scale (GDS). Levels of SLI were significantly decreased in patients suffering from BD, compared to a control group (19.7 +/- 11.6 fmol/ml vs. 30.5 +/- 8.6 fmol/ml, P < 0.01). There was no correlation with dementia scores (r = 0.34, P = 0.51). The observed qualitative and quantitative changes in the molecular pattern of SLI suggest that occurrence of a dysregulated posttranslational processing in patients with BD. Whereas 5-HIAA levels were not significantly changed in patients with BD, HVA was significantly increased in mild to moderate dementia (GDS 2-4) and significantly decreased in severe cases (GDS 7) (224.3 +/- 69.9 nmol/ml vs. 364.9 +/- 103.8 nmol/ml, P < 0.01); this correlated with dementia scores (r = -0.59, P < 0.01). The existence of significant correlations between SLI, 5-HIAA and HVA in BD point to a heterogeneous and generalized neurochemical process affecting several transmitter systems and functions.

Aged↗
PubMed1996

Somatostatin-like immunoreactivity, its molecular forms and monoaminergic metabolites in aged and demented patients with Parkinson's disease--effect of L-Dopa.

There is some evidence that Parkinson's disease (PD) seems to be a heterogenous and generalized brain disorder reflecting a degeneration of multiple neuronal networks, including somatostatinergic neurons. Somatostatin-like immunoreactivity (SLI) and its molecular forms, high molecular weight form (HMV-SST), somatostatin-14 (SST-14), somatostatin-25/28 (SST-25/28) and Des-ala-somatostatin (Des-ala-SST), as well as homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were estimated using HPLC and radioimmunoassay in the cerebrospinal fluid (CSF) of 35 aged parkinsonian patients with different stages of intellectual deterioration. The influence of L-dopa-treatment on these neurochemical parameters was evaluated. Without a correlation with dementia scores (p = 0.11), SLI was significantly reduced in PD in comparison to the control group (p < 0.05). The reduction was related to the progression of the disease. Correlations between SLI, HVA and 5-HIAA indicate a heterogenous brain disorder in PD with alterations of several transmitter systems and functions. Complex qualitative and quantitative changes in the molecular pattern of SLI are compatible with a dysregulated synthesis and/or posttranslational processing. L-dopa-treatment was associated with a significant increase of HVA (p < 0.05) and HMV-SST (p < 0.05) and a slight, but insignificant increase of SLI (p = 0.11).

Aged↗
PubMed1996

[Involvement of the central nervous system in hemolytic uremic syndrome/thrombotic thrombocytopenic purpura].

Cerebral involvement is typical for thrombotic microangiopathies like haemolytic uremic syndrome (HUS) and thrombotic-thrombopenic purpura (Moschcowitz disease or TTP). Symptoms are irritation, restless behaviour, disorientation, disturbance of consciousness, seizures, and focal neurological deficits. The lack of typical imaging changes or pathological observations may explain the unknown pathophysiological cascade leading to the neurological symptoms. We describe the development of HUS/ TTP in a 52-year-old woman after acute pneumonia caused by Diplococcus pneumoniae. The patient showed an increasing psycho-organic syndrome with disorientation, followed by severe loss of consciousness and coma. Initially, computed tomography showed slight diffuse brain oedema, which was not found in later follow-up images. Magnetic resonance imaging was normal. The TCD examination revealed general velocity increases and vasospasms (especially MCA, ACA and PCA bilateral and BA). The reduction in blood flow velocities in the basal arteries was accompanied by a marked clinical improvement. The development of vasospasms may be an explanation for the neurological deficits in HUS/TTP. The origin of the vasospasms may be found in disturbed prostacyclin production, increased serotonin or platelet factor IV release, and leucocyte activation with consecutive endothelial damage.

Blood Flow Velocity↗
PubMed1996

Hemorrhagic transformation and microvascular integrity during focal cerebral ischemia/reperfusion.

Hemorrhagic transformation after cerebral ischemia is a well known clinical concern. The frequency of intact basal lamina (BL), identified by laminin antigen, in hemorrhagic and nonhemorrhagic zones after middle cerebral artery occlusion (MCA:O) and 3-h MCA:O with reperfusion in adolescent male baboons was assessed. Parenchymal hemoglobin was not detected prior to 24-h reperfusion. A significant decrease in the density of laminin (BL) in hemorrhagic zones (6.2 +/- 2.4) compared with nonhemorrhagic ischemic zones (10.5 +/- 2.4) (p < 0.05) and nonischemic basal ganglia (17.0 +/- 2.7) (p < 0.01) was observed. Time-dependent changes in BL integrity appear linked to the extravasation of blood components.

Animals↗
PubMed1996

Time course of acetazolamide effect in normal persons.

The intravenous injection of the carbonic anhydrase inhibitor acetazolamide causes a sustained increase of blood flow velocity in the middle cerebral artery. This effect is used in the acetazolamide test of the so-called cerebrovascular reserve capacity. The acetazolamide test is performed routinely as a two-point measurement of the blood flow velocity by transcranial Doppler before and 15 to 20 minutes after drug injection. Based on the assumption that evaluation of the time course will more sensitively detect an impaired cerebrovascular reserve capacity, suitable parameters for description of the time course were developed and normal values were established from 18 healthy persons (31 hemispheres). The mean value for the maximal increase of the mean flow velocity (MFV) was 29.7 +/- 8.3 cm/sec (as percentage of increase, 62.0 +/- 17.3%) and the time of the maximal increase was 15.35 +/- 8.46 seconds. Also calculated were the velocity of the MFV rise to the maximal value (3.0 +/- 3.2 cm/sec/min), the mean of the changes of the continuously measured MFV to the baseline value (21.0 +/- 7.4 cm/sec), and the integral of MFV represented by the plane under the MFV curve (967.8 +/- 350.0 cm). The best parameter for the description of the time dependency of the acetazolamide effect is the integral of MFV.

Acetazolamide↗