Search PubMed⌕ Search

Biomedical subjects

G Hagemann

Publications and source records attributed to G Hagemann.

At least 19 recordsLinked to original sources
PubMed2006

Multiple reversible MR signal changes caused by Epstein-Barr virus encephalitis.

This report presents the imaging findings of an unusual case of Epstein-Barr virus (EBV) encephalitis. A young man presented with a short-lasting history of febrile infection, neuropsychologic deficits, ataxia, and seizures. MR imaging revealed fully reversible signal intensities (T2, diffusion-weighted imaging with a decreased apparent diffusion coefficient) in the splenium of the corpus callosum and both posterior hemispheres. EBV infection must be added to the list of differential diagnoses of (reversible) splenial lesions.

Adult↗
PubMed2005

Outcome after decompressive craniectomy in patients with severe ischemic stroke.

Decompressive craniectomy after space occupying infarction of the middle cerebral artery (MCA) tends to decrease mortality and increase functional outcome. The aim of this retrospective study was to evaluate mortality rates and functional outcome in our centre and to identify predictors of prognosis. The charts of 30 consecutive patients (6 women, 24 men, mean age 59.3 +/- 11.0 years) who underwent craniectomy after space occupying MCA-infarction from 1996 to 2002 were analyzed. Functional outcome was assessed by semistructured telephone interview as Barthel-Index, modified Rankin scale and extended Barthel-Index. Five patients (mean age 67.2 +/- 6.1 years) died within 5.2 +/- 2.4 days (range 2-8 days) after the first symptoms due to herniation. Nine patients (mean age 63.1 +/- 7.1 years) died 141.0 +/- 92.5 days (range 40-343) after stroke onset due to internal complications. 16 patients survived (mean surviving time 2.1 +/- 1.5 years, mean age 54.1 +/- 11.4 years). Mortality was related to age and the number of risk factors/comorbidity, and functional outcome was dependent on the number of risk factors/comorbidity. Our small observational, retrospective study suggests that hemicraniectomy in patients with space occupying MCA-infarction decreases mortality rate and increases functional outcome. Further randomized trials may prove useful to better define the indications, timing and prognosis for this procedure.

Adult↗
PubMed2005

Localized reversible reduction of apparent diffusion coefficient in transient hypoglycemia-induced hemiparesis.

BACKGROUND AND PURPOSE: The pathophysiology of hypoglycemia shares a common mechanism with cerebral ischemia, but so far, little is known regarding MRI of humans with hypoglycemia. METHODS: We report a patient with left hemiparesis and dysarthria associated with a blood glucose level of 1.7 mmol/L. The patient recovered completely after glucose infusion. RESULTS: The initial diffusion-weighted imaging (DWI) showed increased signal intensities and a reduction of apparent diffusion coefficient (ADC) values localized in the corpus callosum (splenium) and asymmetrically in the corona radiata. After 48 hours, follow-up revealed complete recovery of DWI and ADC signal abnormalities. CONCLUSIONS: To our knowledge, this is the first presentation of a case with transient hypoglycemia-induced focal neurological deficits revealing completely reversible MRI changes in terms of disturbed DWI and ADC with a peculiar as yet undescribed topography.

Aged↗
PubMed2004

Recurrent posterior reversible encephalopathy syndrome (PRES).

Posterior reversible encephalopathy syndrome is a proposed cliniconeuroradiological entity characterized by headache, altered mental status, cortical blindness, seizures, and other focal neurological signs, and a diagnostic magnetic resonance imaging picture. A variety of different etiologies have been reported like hypertension, pre-eclampsia/eclampsia, cyclosporin A or tacrolimus neurotoxicity, uraemia and porphyria. With early diagnosis and prompt treatment, the syndrome is usually fully reversible. We report a case of recurrent PRES of unknown aetiology following intensive care unit treatment and only moderately elevated blood pressure. Clinicians as well as radiologists must be familiar with this clinically frightening, underdiagnosed condition to assure timely diagnosis and treatment to prevent persistent deficits.

Adult↗
PubMed2004

Shoulder pathoanatomy in marathon kayakers.

OBJECTIVES: To determine the prevalence of soft and hard tissue abnormalities and their interrelations in the shoulders of marathon kayakers and to examine the pathoanatomical factors that predispose these athletes to injury. METHODS: Fifty two long distance kayakers completed a questionnaire. Their shoulders were examined for range of motion, pain, and stability using a standard set of 10 clinical tests. The shoulder was subsequently scanned by magnetic resonance imaging (MRI) in three planes and evaluated for evidence of injury or other abnormality. The relation of clinical symptoms and MRI findings was investigated with respect to kayaker's age, number of years kayaking, and number of marathon races completed. RESULTS: Thirty subjects were asymptomatic at the time of scanning, and twenty two showed symptoms of pain and/or instability. MRI showed acromioclavicular hypertrophy, acromial or clavicular spur, supraspinatus tendinitis, and partial tear of the supraspinatus as the most common abnormalities. Kayaker's age, number of years kayaking, and number of races completed did not relate significantly to symptoms or to the presence of an abnormality on MRI scan. Of all the pathoanatomical findings that are reported to predispose to rotator cuff injury, only acromial and clavicular spurs were found to correlate highly with supraspinatus muscle pathology. CONCLUSIONS: Rotator cuff injuries make up a large portion of the injuries seen in marathon kayakers, about twice the number reported for sprint kayakers. These injuries are the result of secondary impingement factors associated with overuse, possibly specific to kayakers, and not the result of bony restrictions around the shoulder joint. Acromioclavicular hypertrophy is a common finding in marathon kayakers, but is possibly the result of portaging or a previous injury.

Adult↗
PubMed2003

Differential sensitivity to induction of spreading depression by partial disinhibition in chronically epileptic human and rat as compared to native rat neocortical tissue.

Spreading depression (SD) is characterized by a transient breakdown of neuronal function concomitant with a massive failure of ion homeostasis. It is a phenomenon that can be induced in neocortical tissue by raising excitability, e.g. injection of K(+), application of glutamatergic agonists, or blocking Na(+)/K(+) ATPase. Here we report a novel method of SD induction using minimal disinhibition with application of low concentrations (5 microM) of the GABA(A) receptor blocker bicuculline. This procedure-while subthreshold for epileptiform activity-readily induced spontaneous SDs in native rat neocortical slices, accompanied by typical depolarizations of neurons and glial cells. In contrast, in human neocortical preparations obtained from epilepsy surgery, in approximately 20% of the slices spontaneous epileptiform activity appeared with this bicuculline dosage without SDs. Raising the concentration of bicuculline to an epileptogenic dose (10 microM) in human tissue also resulted in the generation of epileptiform activity only. Likewise, in slices from pilocarpine-treated, chronically epileptic rats, bicuculline also only induced epileptiform activity without eliciting SDs. The experiments indicate that chronic epilepsy causes a differential sensitivity to partial GABA(A) receptor blockade with regard to induction of SD.

2-Amino-5-phosphonovalerate↗
PubMed2003

Distribution of glutamate receptor subunits in experimentally induced cortical malformations.

Electrophysiological studies in humans and animal models have revealed an intrinsic epileptogenicity of cortical dysplasias which are a frequent cause of drug-resistant epilepsy. An imbalance of inhibition and excitation has been causative related. Receptor-binding studies in rodents demonstrated reduced binding to GABA and increased binding to glutamate receptors within cortical dysplasias and increments of AMPA- and kainate-receptor binding in its surround. Immunohistochemically a differential downregulation of GABA(A) receptor subunits could be demonstrated in widespread areas within and around dysplasias. As receptor binding critically depends on receptor subunit composition the observed changes in binding properties might be related to this. Here, we immunohistochemically analyzed the regional expression of four NMDA receptor subunits and two major AMPA- and kainate-receptor complexes in adult rats after neonatal freeze lesions. These lesions are characterized by a three- to four-layered cortex and a microsulcus which mimic human polymicrogyria. Using antibodies against NR1, NR2A, NR2B, NR2D, GluR2,3, and GluR5,6,7 receptor subunits we demonstrated a pronounced disturbance of cortical immunostaining pattern in the cortical malformation. These changes reflected the structural disorganization of the microgyrus with some distortion of the apical dendrites of paramicrogyral pyramidal cells, a decrease and disorganization of cells at the bottom of the microsulcus, and an inflection of apical dendrites toward the microsulcus. The neuronal staining pattern of large pyramidal cells in the neighborhood of the dysplasia did not differ for any subunit investigated. No remote or widespread changes of glutamate-receptor subunit distribution could be detected. The lack of gross and/or widespread alterations of glutamate-receptor subunit distribution in the surround of focal cortical dysplasia suggests the presence of other or additional mechanisms underlying the increased excitatory neurotransmitter binding and excitability in cortical malformations.

Action Potentials↗
PubMed2002

(68)(28)Ni(40): Magicity versus superfluidity.

The neutron-rich (66,68)Ni have been produced at GANIL via interactions of a 65.9A MeV 70Zn beam with a 58Ni target. Their reduced transition probability B(E2;0(+)(1)-->2+) has been measured for the first time by Coulomb excitation in a (208)Pb target at intermediate energy. The B(E2) value for (68)Ni(40) is unexpectedly small. An analysis in terms of large scale shell model calculations stresses the importance of proton core excitations to reproduce the B(E2) values and indicates the erosion of the N = 40 harmonic-oscillator subshell by neutron-pair scattering.

Journal Article↗
PubMed2002

[Problems of differential diagnosis in tick-borne encephalitis-induced polyradiculitis].

In about 10% of cases, tick-borne encephalitis (TBE) presents with additional myeloradiculitic features mimicking acute poliomyelitis, which can rarely appear as the sole symptom. We report on a 59-year-old man infected with TBE in Thuringia,Germany, who developed polyradiculitis with rapidly progressive, predominantly proximal tetraparesis and respiratory failure. We discuss the differential diagnosis and the epidemiological relevance in conjunction with a second typical case of TBE acquired in the same region and time period.

Antibodies, Viral↗
PubMed2002

Cerebellar volumes in newly diagnosed and chronic epilepsy.

Cerebellar atrophy is assumed to be a common finding in patients suffering from epilepsy. Anticonvulsants as well as seizure activity itself have been considered to be responsible for it but many studies have addressed these questions in specialised centres for epilepsy thus having a referral bias towards patients with severe epileptic syndromes. The purpose of this study was: 1. To develop a quantitative method on 3D-MRI data to achieve volume or planimetric measurements (of cerebrum, cerebellum and cerebellar substructures). 2. To investigate the prevalence of cerebellar atrophy (and substructure atrophy) in a prospectively investigated population-based cohort of patients with newly diagnosed and chronic epilepsy. 3. To quantify cerebellar atrophy in clinic-based patients, who had had atrophy previously diagnosed on routine visual MRI assessment. 4. To correlate the measures of atrophy with clinical features in both patient groups. A total of 57 patients with either newly diagnosed or chronic active epilepsy and 36 control subjects were investigated with a newly developed semiautomated method for cerebral as well as cerebellar volume measurements and substructure planimetry, corrected for intracranial volume. We did not find any significant atrophy in the population-based cohort of patients with newly diagnosed epilepsy or with chronic epilepsy. Visually diagnosed cerebellar atrophy was mostly confirmed and quantified by volumetric analysis. The clinical data suggested a correlation between cerebellar atrophy and the duration of the seizure disorder and also the total number of lifetime seizures experienced and the frequency of generalised tonic-clonic seizures per year. Volumetry on 3D-MRI yields reliable quantitative data which shows that cerebellar atrophy might be common in severe and/or longstanding epilepsy but not necessarily in unselected patient groups. The results do not support the proposition that cerebellar atrophy is a predisposing factor for epilepsy but rather are consistent with the view that cerebellar atrophy is the aftermath of epileptic seizures or anticonvulsant medication.

Adolescent↗
PubMed2001

Differentiation of GABA(A) receptors in subcortical heterotopias: subunit distribution of displaced cortex reflects original commitment.

Recent evidence suggests that the expression of GABA(A) receptor subunits is determined by an early innate program which can be further modified by thalamic input and local factors. We analyzed the GABA(A) subunit distribution in experimentally induced subcortical heterotopia which are a subgroup of neuronal migration disorders. Heterotopias consist of clusters of neurons which have stopped migration early, before they have reached their final commitment and well before thalamic afferents have reached their targets. Immuno- histochemical analyses of five important GABA(A) receptor subunits revealed an expression pattern typical for upper cortical layers reflecting the original commitment of the heterotopic neurons. These results point towards detailed innate determinants of cell fate which even contain information on receptor subunit distribution and are not affected by ectopic positioning.

Animals↗
PubMed2001

[Radiation sensitivity for delayed reproductive death (DRD) following single or split-dose irradiation].

BACKGROUND: The growth kinetics of tumors after irradiation (Figure 1) is defined by cells surviving with delayed reproductive death (DRD). The prediction of radiation sensitivity of locally recurrent tumor growth is among other factors dependent on the knowledge of the impact of fractionated irradiation on these surviving cells with DRD. Short recovery effects can be estimated in vitro by comparing the difference of the medians of the distributions of clone sizes, the median clone sizes difference (MCD) after single and split exposure irradiation of the progenitor cells. MATERIALS AND METHODS: CHO-cells of a sub clone of the line T71 have a spontaneous cell loss rate of < 5%. The cells were irradiated a) by a single exposure 3 hours after synchronization and b) by a fractionated irradiation of half the exposure of a 200-kVp radiation exposure 3 hours and 6 hours after synchronization, respectively. Clone survival was determined (Figure 2). As function of dose and incubation time the distributions of clone sizes and the MCD were determined by tapping the clone cells in microscopic projections. RESULTS: The radiation sensitivity El of the DRD can be defined as the proportional factor of the linear relationship between the MCD on one side and the dose K x the cell division factor m on the other side. EI is dependent on the age of the cells during irradiation (Figure 3) and the cell line (Table 1). The slope of the dually logarithmic growth curve of the cell population is: s = 1 - El.K. Experimentally El was found to be equal for single and split dose irradiation (Figures 4 and 5) and amounted to El = 0.065 with Sd = +/- 0.004.--Literature analysis for the mathematical estimation of El.K (Figure 6) was based on reports of measurements of the local tumor recurrence growth of carcinomas and sarcomas of rodents and pulmonary metastases of sarcomas in humans, respectively, after fractional irradiation. We obtained values of 0 < or = El.K < or = 0.77 (Table 2). Values for El are independent of the dose and lie considerably below data derived from in-vitro measurements of different cell cultures. CONCLUSIONS: Since recurrence kinetics of tumors are determined by the radiation sensitivity El of the DRD, El can be used for estimating the kinetics of tumor recurrence. As lately described, MCD is linearly proportional to the micro-nucleus frequency [12]. Determinations of the micro-nucleus frequencies in tumor cell biopsies pre and post radiation onset offer the option for developing a fast predictive assay. Organ malformations of embryos after exposition to ionizing radiation can be mathematically deduced by DRD to the partial cell mortality.

Abnormalities, Radiation-Induced↗
PubMed2000

Differential downregulation of GABAA receptor subunits in widespread brain regions in the freeze-lesion model of focal cortical malformations.

Focal cortical malformations comprise a heterogeneous group of disturbances of brain development, commonly associated with drug-resistant epilepsy and/or neuropsychological deficits. Electrophysiological studies on rodent models of cortical malformations demonstrated intrinsic hyperexcitability in the lesion and the structurally intact surround, indicating widespread imbalances of excitation and inhibition. Here, alterations in regional expression of GABA(A) receptor subunits were investigated immunohistochemically in adult rats with focal cortical malformations attributable to neonatal freeze-lesions. These lesions are morphologically characterized by a three- to four-layered cortex with microsulcus formation. Widespread regionally differential reduction of GABA(A) receptor subunits alpha1, alpha2, alpha3, alpha5, and gamma2 was observed. Within the cortical malformation, this downregulation was most prominent for subunits alpha5 and gamma2, whereas medial to the lesion, a significant and even stronger decrease of all subunits was detected. Lateral to the dysplastic cortex, the decrease was most prominent for subunit gamma2 and moderate for subunits alpha1, alpha2, and alpha5, whereas subunit alpha3 was not consistently altered. Interestingly, the downregulation of GABA(A) receptor subunits also involved the ipsilateral hippocampal formation, as well as restricted contralateral neocortical areas, indicating widespread disturbances in the neocortical and hippocampal network. The described pattern of downregulation of GABA(A) receptor subunits allows the conclusion that there is a considerable modulation of subunit composition. Because alterations in subunit composition critically influence the electrophysiological and pharmacological properties of GABA(A) receptors, these alterations might contribute to the widespread hyperexcitability and help to explain pharmacotherapeutic characteristics in epileptic patients.

Animals↗
PubMed2000

[Cortical dysgenesis. Current views on pathogenesis and pathophysiology].

Cortical dysgenesia are a heterogenous group of genetic or acquired disturbances of cortical development which, due to the enormous progress in modern neuroimaging techniques, are increasingly recognized in association with a variety of clinical disorders. The spectrum of clinical manifestations, depending on type and extent of the alterations, includes severe mental retardation and epilepsy as well as neuropsychological deficits and some psychiatric disorders. Although pathogenesis and pathophysiology of cortical dysgenesis are still not fully understood, the recent discovery of responsible genes, growth factors, neurotransmitters, and exogenous factors sheds light on elementary mechanisms. The development of animal models mimicking different types of human cortical malformations helped to increase further the understanding of functional consequences of focal cortical dysgenesis. Several studies on these models reveal widespread alterations of cortical connectivity and excitability which are probably of crucial importance in different clinical disorders.

Animals↗
PubMed2000

[Cortical dysgenesis: current classification, MRI diagnosis, and clinical review].

Cortical dysgenesis comprises a heterogenous group of genetic or acquired disturbances of cortical development which, due to progress in modern neuroimaging techniques, are increasingly recognized in association with a variety of clinical disorders. The spectrum of clinical manifestations, depending on type and extent of the alterations, includes severe mental retardation and epilepsy as well as neuropsychological deficits and psychiatric disorders. Up to now, the nomenclature of cortical malformations has been difficult and ambiguous. Recently, the understanding and terminology of these disorders has been facilitated by the proposal of a new classification scheme based on pathophysiological as well as pathogenetic mechanisms. This proposal has been elaborated by a group of experts and is not yet well-known in the German literature. Magnetic resonance imaging (MRI) allows diagnosis and classification in many cases of cortical dysgenesis during lifetime, thereby helping to identify prognostic and therapeutic options. Early diagnosis of cortical malformations is of particular importance in patients with drug-resistant epilepsy, as they can either be cured or benefit from epilepsy surgery. This review gives examples of the most relevant cortical malformations using the new classification scheme and summarizes their clinical as well as MRI characteristics. Besides routine MRI applications, some experimental techniques are discussed which may help to identify even subtle alterations.

Brain Diseases↗
PubMed2000

Frequency of and interaction between polymorphisms in the beta3-adrenergic receptor and in uncoupling proteins 1 and 2 and obesity in Germans.

OBJECTIVE: To determine the role of polymorphisms in the genes for beta3-adrenergic receptor (beta3-AR) and in uncoupling proteins 1 and 2 (UCP-1, UCP-2) in obesity. DESIGN: Association study with three polymorphisms and obesity. SUBJECTS: Two hundred and thirty-six morbidly obese patients who underwent gastric banding surgery, 381 patients from the medical clinic and 198 healthy blood donors. MEASUREMENTS: The frequencies of the W64R in beta3-AR, the 3826A-->G in UCP-1 and the 45bp insertion in the 3 untranslated region of exon 8 in UCP-2 polymorphisms were determined. RESULTS: There were no significant differences in the frequencies of the beta3-AR and UCP-1 polymorphisms between obese (body mass index, BMI > 30 kg/m2) and lean subjects. Lean, but not obese, carriers of the R allele of beta3-AR had a significantly higher BMI. The mean age of obese subjects (excluding diabetics) who were carriers of the G allele of the UCP-1 polymorphism, 36y, was significantly younger than wild-type, 40y (P= 0.007). This effect was not seen in lean subjects. The effect of the G allele on the mean age of obese subjects was more apparent in subjects who were also carriers of the R allele of the beta3-AR polymorphism. The frequency of the ins allele of UCP-2 was significantly higher in obese subjects, 0.31, than in lean, 0.24 (P= 0.002) and carriers of the ins allele had a significantly higher BMI, 38 vs 35 (P= 0.005). There was no association between any of the polymorphisms and type II diabetes. CONCLUSION: In a German population, there was no association between the W64R in beta3-AR or the 3826A-->G in UCP-1 polymorphisms and obesity. However, they act synergistically to accelerate the development of obesity. The 45bp insertion in the 3 untranslated region of exon 8 in UCP-2 polymorphism is associated with obesity.

Adult↗
PubMed2000

Functional differentiation of multiple perilesional zones after focal cerebral ischemia.

Transient and permanent focal cerebral ischemia results in a series of typical pathophysiologic events. These consequences evolve in time and space and are not limited to the lesion itself, but they can be observed in perilesional (penumbra) and widespread ipsi- and sometimes contralateral remote areas (diaschisis). The extent of these areas is variable depending on factors such as the type of ischemia, the model, and the functional modality investigated. This review describes some typical alterations attributable to focal cerebral ischemia using the following classification scheme to separate different lesioned and perilesional areas: (1) The lesion core is the brain area with irreversible ischemic damage. (2) The penumbra is a brain region that suffers from ischemia, but in which the ischemic damage is potentially, or at least partially, reversible. (3) Remote brain areas are brain areas that are not directly affected by ischemia. With respect to the etiology, several broad categories of remote changes may be differentiated: (3a) remote changes caused by brain edema; (3b) remote changes caused by waves of spreading depression; (3c) remote changes in projection areas; and (3d) remote changes because of reactive plasticity and systemic effects. The various perilesional areas are not necessarily homogeneous; but a broad differentiation of separate topographic perilesional areas according to their functional state and sequelae allows segregation into several signaling cascades, and may help to understand the functional consequences and adaptive processes after focal brain ischemia.

Brain↗