Long-term follow-up of aneurysms developed during extracranial internal carotid artery dissection.
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Carotid Artery, Internal, Dissection↗
Biomedical subjects
M Hennerici
Publications and source records attributed to M Hennerici.
Temporal profile of release of interleukin-1beta in neurotrauma.
Timing and extent of trauma-induced release of interleukin-1beta (IL-1beta) in extracellular fluid of the CNS were analyzed. In brain tissue perfusates obtained by in vivo microdialysis a marked release of IL-1beta was unexpectedly detected within less than 60 min. At such an early stage of neurotrauma, mRNA expression of IL-1beta was detected whereas immunoreactivity for the IL-1beta protein was negative. Concentrations of extracellularly secreted IL-1beta protein gradually increased, peaked at day 2 and decreased thereafter. Drugs acting on mononuclear phagocytes significantly modulated IL-1beta secretion. This so far unrecognized acuity of IL-1beta release demonstrated here, may represent a precondition for the orchestrating role of this mediator in the cascade of inflammatory host response.
Animals↗
Pulse-inversion contrast harmonic imaging: ultrasonographic assessment of cerebral perfusion.
Pulse-inversion contrast harmonic imaging is a new ultrasonographic technique that can assess brain perfusion. In an adult with moyamoya disease and multiple recurrent strokes, this method detected subtle hemispheric differences in temporal-lobe perfusion, presumably due to neovascularisation, which were not shown by xenon-computed tomography or magnetic resonance perfusion imaging.
Adult↗
Multifocal cerebral demyelination after magic mushroom abuse.
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Adult↗
Assessment of gait in subcortical vascular encephalopathy by computerized analysis: a cross-sectional and longitudinal study.
In subcortical vascular encephalopathy (SVE) gait disturbance is a common and early clinical sign which might be used to monitor disease progression. In the absence of reliable scales and with regard to the equivocal results of highly complex gait imaging devices we assessed the natural course of SVE in a prospective study, using a new straight forward technique to quantify and compare sequential gait studies. We report the results of 300 computerized gait analyses in 119 patients with SVE and 63 age-matched controls. Thirty-nine SVE patients were re-evaluated to monitor the natural course of the disease and to study the correlation of gait disturbances with MRI changes and neuropsychological findings. The system consists of a set of shoes containing 16 load sensors and a measuring-unit reading each sensor at 20-ms intervals. By off-line analysis we graded each recording on a Gait Disorder Score (GDS) with six variables indicating gait steadiness: step frequency, length of gait lines (which represent the movement of the centre of gravity during heel to toe movement), length of single support lines, variability of single and of double support lines, and double support time. In cross-sectional analysis, patients with SVE showed cadence (steps/min) to be reduced at 87.3 +/- 19.5 (96.4 +/- 7.8 in controls, P < 0.05). Length of gait lines was significantly less: 0.70 +/- 0.13 vs. 0.80 +/- 0.05 in controls, with length of single support gait lines reduced at 0.42 +/- 0.14 in SVE (0.58 +/- 0.06 in controls, P < 0.05). Variability of both single support lines (5.69 +/- 1.90%; 4.24 +/- 1.07% in controls, P < 0.05) and double support lines was elevated (3.59 +/- 1.62% vs. 2.54 +/- 0.59%), while duration of double support phases was increased (0.19 +/- 0.10 s vs. 0.13 +/- 0.02 s in controls, P < 0.05). The progressive character of the disease was demonstrated by increasing GDS values in 39 SVE patients with a frontal gait disorder who were re-investigated after a mean interval of 26 months (5.4 +/- 4.5 vs. 8.4 +/- 5.5, P < 0.05). This study shows the value of a new and practicable gait analysis system for the evaluation of gait disorders and it quantifies the deterioration of gait in SVE patients.
Aged↗
Acceleration of thrombolysis with ultrasound through the cranium in a flow model.
Thrombolysis is an efficient therapy for hyperacute stroke within a limited time window. Neurological outcome depends on the recanalization time of the occluded vessel. Nonthermal effects of low-frequency ultrasound (US) accelerate enzymatic fibrinolysis in vitro. We examined the effects of transcranially applied US on recombinant tissue plasminogen activator (rt-PA)-mediated thrombolysis in a flow model in vitro. Pure fibrin clots were placed in a continuous-pressure flow model and treated with rt-PA during 1-MHz US exposure (0.5 W/cm(2); spatial peak, temporal peak intensity). Transcranial and direct US application in combination with rt-PA significantly (p<0.001) shortened recanalization time, increased perfusion flow and reperfusion rate in comparison with rt-PA-mediated thrombolysis alone. Recanalization rate within 30 min was 90-100% in the US-exposed clots vs. 30% in the clots treated only with rt-PA. Our results suggest that transcranial application of 1-MHz US may accelerate reperfusion and recanalization rate of occluded intracerebral vessels by enhancing rt-PA-mediated thrombolysis. Shortening of recanalization time could contribute to optimizing effects of acute thrombolytic stroke therapy.
Blood Flow Velocity↗
Reconstruction and visualization of irregularly sampled three- and four-dimensional ultrasound data for cerebrovascular applications.
Although recent studies have demonstrated the potential value of compounded data for improvement in signal-to-noise ratio and speckle contrast for three-dimensional (3-D) ultrasonography, clinical applications are lacking. We investigated the potential of six degrees-of-freedom (6-DOF) scanhead position and orientation measurement (POM) devices for registration of in vivo multiplanar, irregularly sampled ultrasound (US) images to a regular 3-D volume space. The results demonstrate that accurate spatial and temporal registration of four-dimensional (4-D) US data can be achieved using a 6-DOF scanhead tracking system. For reconstruction of arbitrary, irregularly sampled US data, we introduce a technique based upon a weighted, ellipsoid Gaussian convolution kernel. Volume renderings of 3-D and 4-D compounded in vivo US data are presented. The results, although restricted to the field of cerebrovascular disease, will be of value to other applications of 3-D sonography, particularly those in which compounding of data through irregular sampling may provide superior information on tissue or vessel structure.
Blood Flow Velocity↗
Subacute NO generation induced by Alzheimer's beta-amyloid in the living brain: reversal by inhibition of the inducible NO synthase.
Glial activation contiguous to deposits of amyloid peptide (Abeta) is a characteristic feature in Alzheimer's disease. We performed complementary in vitro and in vivo experiments to study the extent, kinetics, and mechanisms of microglial generation of nitric oxide (NO) induced by challenge with Abeta. We showed that Abeta fibrils dose-dependently induced a marked release of stable metabolites of NO in vivo that was strikingly similar regarding extent and temporal profile to the one in the parallel designed microglial cell culture experiments. However, costimulation with interferon gamma, which was a prerequisite for Abeta-induced NO generation in vitro, was not required in vivo, demonstrating that factors are present in the living brain that activate glial cells synergistically with Abeta. Therefore, in Alzheimer's disease, deposits of Abeta fibrils alone may be sufficient to induce a chronic release of neurotoxic microglial products, explaining the progressive neurodegeneration associated with this disease. Our observation that systemic administration of selective iNOS inhibitors abolishes Abeta-induced NO generation in vivo may have implications for therapy of Alzheimer's disease.
Amyloid beta-Peptides↗
Simultaneous assessment of brain tissue oxygenation and cerebral perfusion during orthostatic stress.
Simultaneous registration of cerebral tissue oxygenation parameters obtained by near infrared spectroscopy (NIRS), intracranial blood flow velocity (CBFV) measured by transcranial Doppler sonography (TCD) and basic cardiovascular parameters was carried out during a passive 80 degrees head-up tilt table test in 15 patients with a history of orthostatic syncope and 20 control subjects. In normals, the cardiovascular parameters showed a specific course after changing to a vertical position: the heart rate increased, the mean arterial blood pressure remained unchanged, and the CBFV decreased. The NIRS measurements showed an increase in deoxyhemoglobin (HHb) and a decline in oxyhemoglobin (O(2)Hb) and the regional oxygen saturation (RSAT). Patients had a significantly more prominent decline in arterial blood pressure (p < 0.001), CBFV (p < 0.001) and RSAT (p = 0.04). Five patients experienced symptoms of (pre)syncope during the experiment, which were associated with a further sudden and marked (>10%) drop of O(2)Hb. The results indicate that the combination of TCD and NIRS increases the understanding of hemodynamic and metabolic changes during orthostatic stress, which may lead to individually suited therapeutic procedures.
Blood Flow Velocity↗
Imaging arterial wall disease.
Ultrasonographic imaging of the carotid arteries allows assessment of both early and advanced atherosclerotic disease. This noninvasive technique has played a central role in many recent epidemiological studies and is being used increasingly for evaluating the efficacy of atherosclerosis prevention trials. New developments in ultrasound equipment, the use of echocontrast agents, novel applications of three- and four-dimensional sonography and in vivo characterization of plaque constituents with high-resolution MRI have broadened the scope of imaging of arterial walls, providing both enhanced information on disease progression as well as new insights into pathomechanisms of carotid plaque embolization. This article highlights pertinent issues of imaging of arterial wall disease and discusses important areas of current and future research in this field.
Arteries↗
Endothelin-1 in subarachnoid hemorrhage: An acute-phase reactant produced by cerebrospinal fluid leukocytes.
BACKGROUND AND PURPOSE: The most potent vasoconstrictor known, endothelin-1, is currently considered to mediate cerebral vasospasm in subarachnoid hemorrhage (SAH), which can cause delayed cerebral ischemia. In our study, we performed clinical and in vitro experiments to investigate the origin and the mechanisms of the secretion of endothelin-1 in SAH. METHODS: Endothelin-1 and markers of inflammatory host response (interleukin [IL]-1ss, IL-6, and tumor necrosis factor-alpha) were comparatively quantified in the cerebrospinal fluid (CSF) of SAH patients and control subjects, and concentrations were related to clinical characteristics. Furthermore, mononuclear leukocytes isolated from the CSF of SAH patients and control subjects were analyzed regarding their mRNA expression of endothelin-1 and inflammatory cytokines. Finally, complementary in vitro experiments were performed to investigate whether coincubation of blood and CSF can trigger leukocytic mRNA expression and release of these factors. RESULTS: Activated mononuclear leukocytes in the CSF of SAH patients synthesize and release endothelin-1 in parallel with known acute-phase reactants (IL-1ss, IL-6, and tumor necrosis factor-alpha). Complementary in vitro experiments not only further confirmed this leukocytic origin of endothelin-1 but also showed that aging and subsequent hemolysis of blood is sufficient to induce such endothelin-1 production. CONCLUSIONS: The demonstration that endothelin-1 is produced by activated CSF mononuclear leukocytes suggests that subarachnoid inflammation may represent a therapeutic target to prevent vasospasm and delayed cerebral ischemia after SAH.
Acute-Phase Proteins↗
Subacute but not acute generation of nitric oxide in focal cerebral ischemia.
BACKGROUND AND PURPOSE: Excessive release of nitric oxide (NO) has been implicated in the pathophysiology of neurodegeneration in ischemic stroke. We compared intracerebral release of indicators of NO generation at the acute and subacute stages of transient focal cerebral ischemia. METHODS: In vivo microdialysis in the rat striatum was performed at the acute (first hours) and subacute (after 24 or 48 hours) stages of cerebral ischemia or sham operation to monitor intracerebral release of the stable NO metabolites nitrite and nitrate. RESULTS: Whereas only a nonsignificant trend toward increased release of these NO metabolites was evidenced in acute cerebral ischemia, a significant NO generation was observed subacutely, 48 hours after induction of cerebral ischemia. Aminoguanidine, a selective inhibitor of inducible NO synthase, suppressed this delayed release of nitrite and nitrate. CONCLUSIONS: Whereas these observations do not support a major NO generation in acute cerebral ischemia, they indicate an inducible NO synthase-dependent NO generation predominantly at the subacute phase of ischemic neurodegeneration. Therefore, NO generation may play a pathophysiological role in delayed ischemic neurodegeneration.
Animals↗
Bilateral diabetic infarction of the anterior tibial muscle.
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Aged↗
Inverse association between endogenous glucocorticoid secretion and L-selectin (CD62L) expression in trauma patients.
Exogenously administered glucocorticoids downregulate inflammatory host response, i.e. by inhibition of adhesion molecule expression on leukocyte surfaces. Here, possible associations between the trauma-induced endogenous secretion of cortisol and the expression of neutrophil adhesion molecules (L-selectin/CD62L, CD 11b, CD54) were studied in humans. Standardized elective hip arthroplasty was investigated as an exemplary condition of acute inflammation. In 20 patients, blood for quantification of cortisol and adrenocorticotropic hormone was obtained at minutes 10, 20, 30, 60, hours 1, 2, 4 and 10 and days 1,3 and 7. Expression of L-selectin/CD62L, CD11b and CD54 on neutrophil surfaces was determined preoperatively, and postoperatively at hours 1, 2, 3, 4, and 10 and at days 1 and 3. Secretion of both, adrenocorticotropic hormone and cortisol was significantly increased between 1-10 hours after onset of tissue injury. Compared to baseline values, CD11b expression was increased at hour 1 and normalized after day 1, whereas L-selectin/CD62L expression, mirroring this pattern was decreased until day 1. Patients with high endogenous glucocorticoid secretion exhibited significantly decreased expression selectively of L-selectin/CD62L. However, we also observed that glucocorticoids do not directly induce L-selectin shedding from neutrophil surfaces in vitro, arguing for more indirect glucocorticoid action on adhesion molecule expression. Together, this study showed that increased endogenous cortisol secretion is associated with lower expression of L-selectin on neutrophil surfaces in humans that is consistent with a downmodulating role of this neuroendocrine stress response in inflammatory leukocyte recruitment.
Adrenocorticotropic Hormone↗
Interferon-gamma-inducing factor (IL-18) and interferon-gamma in inflammatory CNS diseases.
OBJECTIVE: To examine the intrathecal production of a newly identified cytokine, interferon-gamma-inducing factor (IL-18), together with interferon-gamma itself, in inflammatory diseases of the CNS (i.e., bacterial meningitis, viral meningoencephalitis, and MS). RESULTS: IL-18 concentrations in CSF were significantly increased in bacterial meningitis and tended toward increased levels in viral meningoencephalitis. In contrast, IL-18 was detectable only in a few patients with MS and healthy controls. Interestingly, interferon-gamma was significantly increased selectively in CSF of patients with viral meningoencephalitis. CONCLUSION: The observation of an intrathecal release of IL-18 in patients with meningitis argues for a pathophysiologic role of this novel cytokine in immunity against invading microorganisms the CNS.
Adult↗
Vasoneuronal coupling in migraineurs after subcutaneous sumatriptan: a TCD study.
According to the trigeminovascular model of pain in migraine, sterile neurogenic inflammation of dural vessels stimulates nociceptive fibres of the trigeminal nerve. Sumatriptan, a 5-HT1 receptor agonist, blocks this reaction and mediates vasoconstriction of meningeal arteries. However, it is uncertain, whether sumatriptan also has a vasoconstrictive effect on cerebral arteries, which may influence vasoneuronal coupling and induce secondary cerebral blood flow changes. We studied changes of cerebral blood flow velocity (CBFV) and the pulsatility index (PI) in the posterior cerebral artery (PCA) after stimulus activation before, 10 min and 30 min after subcutaneous application of 6 mg sumatriptan, in order to assess potential vasoactive effects on cerebral circulation. CBFV was recorded from both PCAs simultaneously in 27 migraineurs (twenty women, seven men, mean age 29 years), and arterial blood pressure (BP), heart rate (HR) and respiration rate (RR) were monitored. Although the mean diastolic blood pressure rose significantly from 75 mm Hg to 81 mm Hg (P<0.05) and systolic blood pressure and respiration rates remained constant, average CBFV values remained constant. Similarly, the relative increase of CBFV by visual stimulation, which is clearly higher compared to controls in other studies (55.0% before, 52.6% after 10 min, and 52.4% after 30 min), and absolute mean values for CBFV and PI did not change after visual stimulation. These results provide evidence against the hypothesis that sumatriptan produces vasoconstriction in the intracranial human arterial circulation as a potential risk of cerebral ischemia.
Adult↗
Homocysteine in cerebral macroangiography and microangiopathy.
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Aged↗
Arterial gas embolism after decompression: correlation with right-to-left shunting.
Paradoxical gas embolism is a possible cause of neurologic sequelae after decompression in divers. The authors detected arterial bubbles after decompression from chamber dives in two of six divers using transcranial Doppler sonography (TCD). Arterial bubbles correlated with the size of right-to-left shunting as diagnosed by contrast TCD. The pathway of spontaneous paradoxical embolism was tracked for the first time, supporting the concept of paradoxical gas embolism as a cause of early neurologic sequelae after decompression in at-risk divers.
Adult↗