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Biomedical subjects

G F Hamann

Publications and source records attributed to G F Hamann.

At least 37 records · Page 2Linked to original sources
PubMed2001

Detection of hyperacute parenchymal hemorrhage of the brain using echo-planar T2*-weighted and diffusion-weighted MRI.

We investigated the usefulness of echo-planar imaging (EPI) as well as T2*-weighted and diffusion-weighted MRI (DWI) to identify hyperacute hemorrhage (within 24 h after ictus) in the brain. Seven patients were examined 3.5 to 24 h after onset of symptoms using a whole-body 1.5-T MR system. Two diffusion-weighted sequences were run to obtain isotropic and anisotropic diffusion images. Apparent diffusion coefficients (ADC) were calculated from the isotropic diffusion images. All DWI images as well as the T2*-weighted EPI images showed the hematomas as either discrete, deeply hypointense homogeneous lesions, or as lesions of mixed signal intensity containing hypointense areas. We conclude that even in the early phase after hemorrhage, sufficient amounts of paramagnetic deoxyhemoglobin are present in intracerebral hemorrhages to cause hypointensity on EPI T2*-weighted and DWI images; thus, use of ultrafast EPI allows identification of intracerebral hemorrhage.

Acute Disease↗
PubMed2001

Reduced cerebrovascular CO(2) reactivity in CADASIL: A transcranial Doppler sonography study.

BACKGROUND AND PURPOSE: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukencephalopathy (CADASIL) is a hereditary angiopathy caused by mutations in Notch3. Cerebral microvessels show an accumulation of granular osmiophilic material in the vicinity of degenerating vascular smooth muscle cells. To study cerebrovascular function in CADASIL, we performed measurements on cerebral hemodynamics by using transcranial Doppler sonography. METHODS: Middle cerebral artery (MCA) mean blood flow velocity (MFV), cerebrovascular CO(2) reactivity, and the resistance index were measured by bilateral transcranial Doppler sonography in 29 CADASIL individuals (mean age, 49.0+/-2.4 years) and an equal number of age- and sex-matched control subjects. RESULTS: Compared with control subjects, CO(2) reactivity was reduced in CADASIL (33.4+/-2.7% versus 45.3+/-3.0%; P:<0.01). This difference remained significant when only nondisabled CADASIL individuals (Rankin=0, n=21) were included in the analysis (P:<0.05). CO(2) reactivity was significantly lower in disabled than in nondisabled CADASIL individuals (24.5+/-2.7% versus 36.8+/-3.4%; P:<0.05). MCA MFV was reduced in CADASIL (45.6+/-2.2 cm/s versus 54.2+/-2.4 cm/s; P:<0.05) and correlated negatively with age both in affected individuals (r=-0.314; P:<0.05) and control subjects (r=-0.339; P:<0.05). Resistance index was not significantly altered (59.0+/-1.0% versus 57.7+/-1.2%; P:=0.42). CONCLUSIONS: In CADASIL, there is a reduction of both CO(2) reactivity and basal MCA MFV. The reduced CO(2) reactivity suggests functional impairment of cerebral vasoreactivity probably related to vascular smooth muscle cell dysfunction. The reduction of CO(2) reactivity in nondisabled CADASIL individuals suggests an early role of impaired cerebral vasoreactivity in the evolution of the disease.

Adult↗
PubMed2000

Plasminogen activation in experimental permanent focal cerebral ischemia.

BACKGROUND: Previous experimental work using in situ zymography has shown very early increased plasminogen activation in ischemic regions after 3 h of ischemia with and without reperfusion. The objective of the present study was to evaluate the time course and extent of plasminogen activation in long-term permanent focal cerebral ischemia. MATERIAL AND METHODS: The middle cerebral artery in male Fisher rats was irreversibly occluded by electrocoagulation. Duration of ischemia was 48, 72, and 168 h. Occlusion was controlled in vivo by MRI at day 2. Plasminogen activation was detected by in situ zymography of 10 microm cryosections with an overlay containing plasminogen and the plasmin substrate caseine. Areas of plasminogen activation were compared to structural lesions (immunohistochemical loss of microtubule-associated protein 2; MAP 2). RESULTS: Compared to controls, increased plasminogen activation was observed in the basal ganglia and the cortex of the ischemic hemisphere after 48, 72, and 168 h (affected area of basal ganglia: 44.5+/-21.9, 70.1+/-2.3 and 66.6+/-2.8%, respectively; affected area of cortex: 63.4+/-9.8, 67.7+/-0.7 and 64.0+/-3.7%, respectively). The duration of ischemia had no significant influence on the extent of plasminogen activation. Areas of increased plasminogen activation significantly overlapped with and exceeded areas of MAP 2 loss (P<0.005). DISCUSSION: Permanent focal cerebral ischemia leads to increased plasminogen activation in ischemic regions. This plasminogen activation remains elevated at persistent levels over days. It may contribute to extracellular matrix (ECM) disruption, secondary hemorrhage, and brain edema in subacute stages of ischemic stroke.

Animals↗
PubMed2000

Plasminogen activation in focal cerebral ischemia and reperfusion.

In focal cerebral ischemia the plasminogen-plasmin system plays a role in the fibrinolysis of vessel-occluding clots and also in the proteolysis of extracellular matrix components, which potentially contributes to brain edema and bleeding complications. The authors investigated the plasminogen activation after middle cerebral artery occlusion with and without reperfusion (reperfusion intervals 9 and 24 hours) in rats by histologic zymography and compared areas of increased plasminogen activation to areas of structural injury, which were detected immunohistochemically. After 3 hours of ischemia, increased plasminogen activation was observed in the ischemic hemisphere. The affected area measured 5.2%+/-8.5% and 19.4%+/-30.1% of the total basal ganglia and cortex area, respectively. Reperfusion for 9 hours after 3 hours of ischemia led to a significant expansion of plasminogen activation in the basal ganglia (68.8%+/-42.2%, P < 0.05) but not in the cortex (43.0%+/-34.6%, P = 0.394). In the basal ganglia, areas of increased plasminogen activation were related to areas of structural injury (r = 0.873, P < 0.001). No such correlation was found in the cortex (r = 0.299, P = 0.228). In this study, increased plasminogen activation was demonstrated early in focal cerebral ischemia. This activation may promote early secondary edema formation and also secondary hemorrhage after ischemic stroke.

Animals↗
PubMed2000

Dynamic CT perfusion imaging of acute stroke.

BACKGROUND AND PURPOSE: Because cerebral perfusion imaging for acute stroke is unavailable in most hospitals, we investigated the feasibility of a method of perfusion scanning that can be performed rapidly during standard cranial CT. Our aim was to identify the scanning parameters best suited to indicate tissue at risk and to measure a perfusion limit to predict infarction. METHODS: Seventy patients who had suffered stroke and had undergone cranial CT 0.5 to 12 hours (median, 3.75 hr) after the onset of symptoms participated in the study. While undergoing conventional CT, each patient received a bolus of iodinated contrast medium. Maps of time to peak (TTP), cerebral blood volume (CBV), and CBF were calculated from the resulting dynamically enhanced scans. These perfusion images were compared with follow-up CT scans or MR images showing the final infarctions. RESULTS: CBF maps predicted the extent of cerebral infarction with a sensitivity of 93% and a specificity of 98%. In contrast, CBV maps were less sensitive and TTP maps were less specific and also showed areas of collateral flow. Infarction occurred in all of the patients with CBF reduction of more than 70% and in half of the patients with CBF reduction of 40% to 70%. CONCLUSION: Dynamic CT perfusion imaging safely detects tissue at risk in cases of acute stroke and is a feasible method for any clinic with a third-generation CT scanner.

Acute Disease↗
PubMed1999

Increased intracellular calpain detection in experimental focal cerebral ischemia.

Calpains are intracellular proteinases whose proteolytic activity is directed mainly against the cytoskeleton and regulatory proteins. We studied the presence of calpain by immunohistochemistry in a rat model of reversible focal cerebral ischemia (3 h) at various times of reperfusion. The numbers of calpain-positive cells on the ischemic side were compared with the non-ischemic side. In controls only 2 +/- 1% cells were positive, whereas the cortex of the ischemic vs the non-ischemic side showed 88 +/- 3% vs 13 +/- 4% calpain-positive cells (p < 0.001), and the basal ganglia 47 +/- 3% vs 13 +/- 4% (p < 0.01) after 3 h ischemia and 24 h reperfusion. This is the first demonstration of elevated intracellular levels of calpains in areas of cerebral ischemia. Longer reperfusion resulted in an increase in calpain positivity.

Animals↗
PubMed1999

[Mechanisms for the development of intracranial hemorrhage. Possible implications for thrombolysis in cerebral infarct].

The role of cerebral hemorrhagic transformation, either as clinically silent hemorrhagic infarction or disastrous parenchymal hemorrhage, is crucial for any risk/benefit analysis of thrombolysis. Especially, thrombolysis in acute ischemic stroke increases the risk of severe, life-threatening hemorrhagic complications up to 10 times compared to untreated 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 the plasmin-generated laminin degradation, matrix metalloproteinases activation, and the transmigration of leukocytes through the vessel wall. The 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↗
PubMed1999

Emotionally evoked changes in cerebral hemodynamics measured by transcranial Doppler sonography.

The cerebral representation of emotions has previously been investigated by the study of patients with local brain damage, experiments with selective stimulation of only one hemisphere, and more recently by imaging techniques such as positron-emission tomography or magnetic resonance imaging measuring local cerebral blood flow. We investigated the mean flow velocity (FVmean) in the middle cerebral artery (MCA) by transcranial Doppler sonography during emotional stimulation with video scenes in 24 healthy test persons. The videos consisted of an erotic scene and a violent scene shown in contrast to a calming scene. Blood pressure, heart rate, and breathing frequency were monitored continuously by noninvasive measurement. FVmean increased during the erotic scene to 108.5+/-11.9% (P < 0.05) of the baseline value in the right MCA and to 109.0+/-10.6% (n.s.) in the left MCA. During the violent scene FVmean reached 109.0+/-8.7% (P < 0.05) on the right side and 108.1+/-13.0% (n.s.) on the left side. The FVmean time course showed a close relationship to the video sequence. During scenes involving great tension FVmean showed a plateaulike state and peaked during sudden actions. Blood pressure, heart rate, and respiratory rate showed no significant changes. However, we observed a tendency towards lower heart rates (lowest value 94.5+/-13.6%) during the erotic scene and two peaks (103.2+/-13.3%, 104.8+/-16.8%) coinciding with sudden violent actions. The significant increase in FVmean in the right MCA supports the theory of a right hemisphere dominance for the processing of emotions.

Adult↗
PubMed1999

Intravenous immunoglobulins in the therapy of paraneoplastic neurological disorders.

The treatment of paraneoplastic neurological syndromes (e.g., tumor therapy, immunosuppressive therapy, plasmapheresis) rarely leads to an improvement in the neurological symptoms. We treated four patients suffering from paraneoplastic neurological syndromes with intravenous immunoglobulins. All four had high titers of antineuronal antibodies in serum and CSF. Two of the patients, one suffering from paraneoplastic cerebellar degeneration and the other from paraneoplastic brain stem encephalitis and polyneuropathy, received intravenous immunoglobulin treatment within 3 weeks of the onset of neurological symptoms. Both patients showed clinical improvement within 2 weeks after the initiation of therapy. They also showed a decline in the intrathecal antibody synthesis of the antineuronal antibody. Two other patients, who had suffered from paraneoplastic neuropathy for 3 and 6 months showed no improvement with the intravenous immunoglobulin therapy. In these cases there was no effect on intrathecal antibody synthesis. When started early, intravenous immunoglobulins may be of therapeutical value in treating paraneoplastic neurological syndromes. Specific intrathecal antibody synthesis may be a better measure of clinical course that autoantibody serum titers.

Adult↗
PubMed1999

Cerebral microemboli during left heart catheterization.

BACKGROUND: The aim of this study was to describe the rate of microemboli signals (MES) during left heart catheterization (LHC). METHODS: A monitoring of both middle cerebral arteries using transcranial Doppler ultrasonography was performed to investigate cerebral microemboli during LHC. Seventy-two patients undergoing LHC and 29 patients with LHC followed by coronary intervention were studied. RESULTS: During a standardized LHC (n = 52), 95 +/- 45 MES were detected of which 67.5% occurred during injection of contrast media or saline solution, 30% during movements of wire and catheter, and 2% during catheter manipulation. During coronary interventions only, rotablation (n = 2) was followed by a massive increase in MES. The use of injection fluids prepared with minor gas content reduced the MES rate by 67% (P <.05). All MES were clinically silent. CONCLUSIONS: Cerebral microembolism is a current finding during LHC. The dependence of the MES rate during diagnostic LHC on the gas content of the injection fluids provides evidence that most of the MES are caused by microbubbles and not by solid emboli. The high rate of MES during coronary rotablation may be explained by the formation of cavitation bubbles. The clinical results of the MES during LHC appear to be benign.

Adult↗
PubMed1999

[Intima media thickness in patients with vertebrobasilar and carotid stenosis/occlusions].

AIM: The purpose of this study was to investigate the degree of atherosclerosis in patients with stenoses or occlusions in the vertebrobasilar system (VBS) and the carotid system (CS). METHOD: The Intima-Media-Thickness (IMT) and the diameter of the common carotid artery (CCA) (as parameters of the proliferative and dilatative form of atherosclerosis) were measured on both sides on areas of vessel wall without stenoses and plaques. We examined of the neck 134 people, including 32 normal healthy counds, 57 patients with stenoses or occlusions in the CS and 16 patients with macroangiopathy exclusively in the VBS (following doppler- and duplex sonographical criteria). RESULTS: In control persons, a IMT of 0.67 +/- 0.2 mm and a CCA-diameter of 5.8 +/- 1.2 mm was found. Patients with CS-macroangiopathy exhibited a statistically significant increase in IMT with 0.97 +/- 0.2 mm (p < 0.001) and dilatation of the CCA (6.6 +/- 1.2 mm, p < 0.01). In comparison to the controls we also found a significant increase in IMT (0.86 +/- 0.2 mm, p < 0.001) and in diameter (6.8 +/- 0.9 mm, p < 0.01) in patients with VBS-macroangiopathy. There was no significant difference between both groups, despite a tendency of less severe changes in patients suffering from VBS-macroangiopathy. Patients with diabetes (1.1 +/- 0.2 mm, p < 0.001), with hypertension (0.99 +/- 0.2 mm, p < 0.05) and with coronary heart disease (0.96 +/- 0.2 mm, p < 0.05) showed a significant increase in IMT. CONCLUSION: Parameters of generalized atherosclerosis do not significantly differ between patients with stenoses or occlusions in the VBS and patients with changes in the CS and are correlated to the classical risk factors.

Aged↗
PubMed1999

Orthostasis as a test for cerebral autoregulation in normal persons and patients with carotid artery disease.

Orthostasis reduces mean flow velocity (FVmean) in cerebral arteries. This might be used as an alternative provocation test for cerebral hemodynamics in patients with carotid artery disease (CAD). In 21 unilateral CAD patients and 21 controls, FVmean in both middle cerebral arteries (MCA) was measured by transcranial Doppler, together with blood pressure (BP) and heart rate (HR) during a tilt table test. Cerebrovascular reserve (CVR) was measured by an acetazolamide test. In all cases, FVmean dropped to a lower level (controls: 81.9 +/- 9.4% of baseline; patients: 84.3 +/- 7.9% symptomatic side, 85.6 +/- 9.0% contralateral). Impaired CVR patients showed a smaller (p < 0.01) decrease (90.6 +/- 3.3%) compared to contralateral (84.9 +/- 6.0%), to normal CVR patients (81.1 +/- 7.8%) and to controls. Heart rate increased in both groups (controls: +16.6 +/- 9.9%, patients +10.3 +/- 9.9%; p < 0.01); BP showed no change. Orthostasis induces a decrease of MCA FVmean as already previously described. This decrease is significantly smaller in patients with impaired CVR. Since BP does not change, some authors explain the lower MCA Fvmean during orthostasis as caused by sympathetic induced vasoconstriction of cerebral resistance vessels. The authors speculate that in impaired CVR-patients autoregulative protection against ischemia might limit vasoconstriction. In combination with standard tests for measurement of CVR, this test might be useful for evaluation of cerebral autoregulation.

Acetazolamide↗
PubMed1999

Increased cerebral CO(2) reactivity after heparin-mediated extracorporal LDL precipitation (HELP) in patients with coronary heart disease and hyperlipidemia.

BACKGROUND AND PURPOSE: There is experimental and clinical evidence that hypercholesterolemia leads to an impairment of endothelial function in coronary and cerebral arteries. Using transcranial Doppler sonography, we examined CO(2) reactivity as a marker of cerebral vasoreactivity in patients with coronary heart disease and hyperlipidemia before and after drastic lowering of LDL cholesterol, lipoprotein(a) [Lp(a)], and fibrinogen levels by heparin-mediated extracorporal LDL precipitation (HELP). METHODS: CO(2) reactivity was determined in 13 patients with coronary artery disease and hyperlipidemia undergoing regular HELP therapy. Middle cerebral artery mean blood flow velocity (MFV) was detected by transcranial Doppler. CO(2) reactivity was calculated as the percent change of MFV during hypercapnia, induced by ventilation of carbogene (5% CO(2), 95% O(2)), to normocapnia. Patients with extracranial or intracranial stenoses were excluded. Other parameters such as blood viscosity, heart rate, and blood pressure were measured to control hemorheologic and systemic influences on CO(2) reactivity. RESULTS: A single HELP treatment reduced total cholesterol, LDL cholesterol, Lp(a), triglycerides, and fibrinogen levels by >50% (P<0.001). Blood viscosity significantly decreased from 1.24+/-0.04 to 1.07+/-0.02 mPa (P<0.001). Blood pressure, heart rate, and MFV did not change significantly. CO(2) reactivity increased from 22% +/- 21% to 36% +/- 18% (P<0.05). CONCLUSIONS: Fast and drastic removal of LDL cholesterol, Lp(a), and fibrinogen from plasma results in an improvement of cerebrovascular reactivity in patients with coronary heart disease and hyperlipidemia. The clinical use of HELP in patients with impaired cerebrovascular reactivity might be promising.

Aged↗