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C Rossberg

Publications and source records attributed to C Rossberg.

At least 19 recordsLinked to original sources
PubMed1997

Primary malignant ectomesenchymoma of the orbit.

Malignant ectomesenchymoma is a rare soft tissue tumor of the childhood believed to arise from a remnant of pluripotential migratory neural crest cell (ectomesenchym) and composed of both a mesenchymal element (most often embryonal rhabdomyosarcoma) and a neuroectodermal element (ganglioneuroma, schwanomma neuroblastoma or melanocytic cells). Reported sites of origin are the abdomen, perineum or scrotum, the extremities, the middle ear, nasopharynx, face, and neck. Herein we report a new case of an orbital ectomesenchymoma studied by means of histochemistry and immunohistochemistry in order to increase the morphologic and histogenetic knowledge of this peculiar tumor and its significance concerning the differential diagnosis.

Child, Preschool↗
PubMed1994

"Stereology" of intracranial lesions.

Endoscopy of the intracranial space requires a new understanding of the anatomy and pathology of pertinent structures. This meets with the new development of imaging methods which equally require three dimensional interpretation of intracranial pathology. The stereological arrangement of intracranial lesions is examplified on three neuropathological conditions: brain tumours, territorial infarction and mass displacement.

Brain↗
PubMed1993

[Primary cerebral lymphoma. Current status of diagnosis and therapy].

Primary cerebral lymphomas are rare tumors. In the last years the frequency of these space occupying lesions is increasing. Diagnosis by image-generating methods is often difficult. Stereotactic biopsy is a reliable diagnostic tool. Explorative craniotomy with tumor resection should be avoided if possible. An effective multimodal therapeutic regimen is the combination of radiotherapy and chemotherapy. Epidemiologic data, diagnostic methods and therapeutic proceedings are presented and discussed on a series of 7 patients with primary cerebral lymphomas treated in our department.

Aged↗
PubMed1991

Neuroprotective properties of 5-HT1A receptor agonists in rodent models of focal and global cerebral ischemia.

5-Hydroxytryptamine1A (5-HT1A) receptor agonists have been shown to inhibit the activity of hippocampal, cortical, and dorsal raphé neurons. We tested urapidil and a new 5-HT1A agonist, CM 57493 [4-(3-trifluoromethylphenyl)-1-(2-cyanoethyl)-1,2,3,6-tetrahydropyridine ], for their neuroprotective activity in models of focal and global cerebral ischemia in rodents. After middle cerebral artery-occlusion (MCA-0) in mice, the infarct size was reduced dose dependently by both urapidil and CM 57493. In MCA-occluded rats, CM 57493 (1 and 5 mg/kg) reduced the cortical infarct volume by 30% and application of 10 mg/kg CM 57493 led to a 40% reduction in the cortical infarct volume. The striatal damage could not be influenced by CM 57493 treatment. Furthermore, 1 and 5 mg/kg CM 57493 significantly reduced the neuronal damage within the CA1 sector of the rat hippocampus after 10 min of forebrain ischemia followed by 7 days of recovery. Measurement of cerebral and rectal temperature revealed that the neuroprotective effect of CM 57493 was not caused by a hypothermic effect. We assume that the neuroprotective activity of 5-HT1A agonists is mediated by an inhibitory action on neurons.

Animals↗
PubMed1991

[Stereotactic intervention as a contribution to diagnosis and therapy of paramedian processes].

In open brain surgery, access to processes in the midline region is difficult. Exact diagnosis of the tumour type is crucial to the choice of therapeutic modality. In many cases, modern imaging procedures such as CT and MRI are useful diagnostic tools. The diagnosis is confirmed by direct biopsy and histological examination. Selected cases of tumours close to the midline (germinoma, pilocytic astrocytoma, primary cerebral malignant lymphoma) are presented. CT and MRI are helpful in demonstrating space-occupying processes. The tumour's histological type is determined by CT-stereotactic biopsy. The histopathological diagnosis is established by means of a crush preparation. Appropriate forms of therapy are proposed on the basis of the diagnosis of tumour type. The results are impressive, due to the efficacy of stereotactic procedures as an additional means of diagnosing and treating space-occupying processes of the midline region.

Astrocytoma↗
PubMed1991

[Epithelial cyst of the central nervous system. A rare abnormality].

A cystic process in the right frontal lobe of the brain in a man of 35 years of age, and an intramedullary cyst in the upper cervical spinal cord in a 29-year old woman, are described. In both cases, the wall of the cyst consisted of mucosal cells and cells having cilia pointing to the inside, located on a thin tissue layer, the structure of which resembled that of a meningioma. Central nervous cysts of this kind are usefully classified together with other, similar cysts (bronchogenic, ependymal and others) as "epithelial cysts". They must be differentiated from neoplastic tumours. Analysis of the cystic contents can prove helpful.

Adult↗
PubMed1990

Neuroprotective effect of memantine demonstrated in vivo and in vitro.

The purpose of the present study was to test whether the anticonvulsant, memantine (1-amino-3,5-dimethyladamantane), can protect neurons against hypoxic or ischemic damage. To this end, we used a rat model of transient forebrain ischemia and cultured neurons from chick embryo cerebral hemispheres. Ischemia was induced for 10 min by clamping both carotid arteries and lowering the mean arterial blood pressure to 40 mm Hg; the rats were allowed to recover for 7 days. Cultured neurons were made hypoxic with 1 mmol/l NaCN added to the incubation medium for 30 min followed by a recovery period of 3 days. The possible effects of memantine were compared with those produced by a typical non-competitive NMDA antagonist, dizocilpine. Similar effects were obtained with both drugs. The drugs reduced the damage caused by transient ischemia to neurons of the hippocampal CA1 subfield. Memantine (10 and 20 mg/kg) had a dose-dependent effect when administered intraperitoneally to the rats 1 h before ischemia. Dizocilpine was active in this model at a dosage of 1 mg/kg. When administered after ischemia, 10 mg/kg memantine significantly protected CA1 neurons against ischemic damage. Furthermore, the drugs protected cultured neurons against hypoxic damage. The lowest effective concentration was 0.1 mumol/l for dizocilpine and 1 mumol/l for memantine. Thus, memantine possesses neuroprotective activity but is less potent than dizocilpine.

Adenosine Triphosphate↗
PubMed1990

Protective effect of nimodipine against ischemic neuronal damage in rat hippocampus without changing postischemic cerebral blood flow.

The purpose of the present study was to investigate the neuroprotective action of nimodipine. Furthermore, the influence of nimodipine on postischemic local CBF (LCBF) was examined. Forebrain ischemia of the rat was performed for 10 min by bilateral carotid clamping, administration of trimethaphan, and blood withdrawal to obtain an MABP of 40 mm Hg. LCBF was measured after 10 min of postischemic recirculation by injecting [14C]iodoantipyrine in saline solution. Nimodipine (0.1, 0.3, and 1.0 mg/kg) was suspended in miglyol oil and applied orally 60 min prior to ischemia. Histological evaluation was performed 7 days after ischemia. Hippocampal neuronal damage was determined as the percentage of necrotic neurons. After preischemic application of nimodipine, neuronal damage was significantly reduced in the hippocampal CA1 subfield. Postischemic LCBF was not affected by treatment with nimodipine. These findings show that nimodipine is able to protect neurons against ischemic damage. The neuroprotective effect of nimodipine was not mediated by a postischemic cerebral vasodilation, but by a direct action on the neurons.

Animals↗
PubMed1990

PAF antagonist ginkgolide B reduces postischemic neuronal damage in rat brain hippocampus.

We investigated the effect of the known antagonist of platelet-activating factor (PAF), ginkgolide B, on postischemic neuronal damage in the rat. Neuronal necroses were evaluated in the hippocampus 7 days after a 10-min forebrain ischemia. Preischemic application of ginkgolide B (50 mg/kg p.o.) significantly reduced neuronal damage. It is suggested that the antagonism of PAF is responsible for this beneficial effect of ginkgolide B.

Animals↗
PubMed1990

Effects of ipsapirone on spatial and temporal changes in somatosensory evoked potentials after middle cerebral artery occlusion in the rat.

The present study investigates the effects of the 5-hydroxytryptamine1A agonist ipsapirone on electroencephalography and somatosensory evoked potentials after middle cerebral artery occlusion in the rat. We implanted 17 silver ball electrodes symmetrically distributed over the skull in 14 rats and registered electroencephalography activity and somatosensory evoked potentials before, 1 hour, and 1 week after permanent occlusion of the left middle cerebral artery. Before vessel occlusion, a symmetric distribution of electroencephalography power was seen over both hemispheres. Middle cerebral artery occlusion caused a complete abolishment of electroencephalography power in the frontolateral aspects of the affected hemisphere. When electroencephalographic recordings 7 days after the insult were superimposed with three-dimensional-reconstructed pictures of the infarct, a close correspondence of the extention and spatial orientation was noted. Two negative and two positive peaks were consistently recorded before middle cerebral artery occlusion. In both control and ipsapirone-treated (30 mg/kg i.p. 30 minutes after induction of ischemia) animals, the vessel occlusion caused a severe reduction in amplitudes of somatosensory evoked potentials in all areas under record (p less than 0.05). One week after middle cerebral artery occlusion, amplitudes of somatosensory potentials over the lesioned hemisphere were still significantly (p less than 0.05) lower than preischemic values in the control group. When compared with the corresponding values 1 hour after middle cerebral artery occlusion, an albeit insignificant tendency toward increased amplitudes was observed in most areas under record. By contrast, in ipsapirone-treated animals, significant differences compared with preischemic values were no longer present 1 week after the vessel occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Spinal angiomatous malformation: clinical course and limits of technical diagnosis].

The sensitivity of the diagnostic procedures in space occupying lesions of the spine have been markedly improved in the recent past, mainly due to the application of CT and MRI--technology and the introduction of superselective angiography. Despite these 'high-tech'-investigations, neurological examination still provides the sole in neurological diagnosis. To show the discrepancies between the techniques mentioned, we present a case of a vascular malformation of the spine with secondary myelopathy (so-called "Foix-Alajouanine-syndrome").

Adult↗
PubMed1989

Reliability of simple cytological methods in brain tumour biopsy diagnosis.

Stereotactic procedures in brain tumour diagnosis and therapy are used increasingly because small lesions are more frequently detected and methods of interstitial irradiation are gaining wide acceptance among neurosurgeons. The diagnosis of underlying pathological processes has to be performed from very small tissue samples. The method of smear and/or squash preparations therefore has long been used by neurosurgeons. Neuropathologists, formerly reluctant, are becoming more and more enthusiastic over this simple and elegant method. Since the diagnostic reliability in such small samples is questioned, we have undertaken to analyse 200 open tumour biopsies in a comparative investigation: the diagnosis from smear preparation on the one hand has been performed without knowledge of the lesion, and on the other hand the remaining material was submitted to the whole pattern of diagnostic methods including frozen sections, paraffin sections with special staining, immunohistochemistry, electron microscopy and tissue culture. Diagnostic reliability was estimated in a four step procedure: Is there tumour or not--is there neuroepithelial newgrowth or metastasis--what kind of tumour is it--has the degree of malignancy--according to the criteria of the WHO--been estimated correctly? The overall diagnostic reliability in our material is about 75%. This is less than the diagnostic reliability of other methods, mostly due to the lack of histologic "architecture" criteria in evaluating the cytological biopsies.

Adolescent↗
PubMed1989

Naftidrofuryl protects neurons against ischemic damage.

The effects of naftidrofuryl on postischemic neuronal damage and on local cerebral blood flow (LCBF) were examined in a rat model of forebrain ischemia (occlusion of carotid arteries and hypotension). Ischemia was induced for 10 min. LCBF was measured after 2 and 10 min of recirculation. A histological evaluation of cell loss in the hippocampal areas was performed 7 days after ischemia. Naftidrofuryl (10 mg/kg) was administered intraperitoneally 15 min before ischemia. The drug reduced the percentage of necrotic neurons in the CA1 and CA4 sector of the hippocampus, while the LCBF of these hippocampal sections was not significantly altered. Thus, naftidrofuryl is suggested to protect hippocampal neurons against ischemic damage mainly by a direct effect on brain parenchyma.

Animals↗
PubMed1988

Effects of flunarizine on postischemic blood flow, energy metabolism and neuronal damage in the rat brain.

The effects of flunarizine on local cerebral blood flow, cortical energy metabolism and neuronal necrosis were evaluated in a rat model of forebrain ischemia. The application of flunarizine (2 X 40 mg/kg p.o.) at 24 and 4 h before ischemia accelerated the restoration of cortical high-energy phosphates during early post-ischemic recirculation and also increased the flow in cortical but not in hippocampal areas. Neuronal necrosis was reduced in the hippocampal CA 1 sector but unchanged in the cortex. It is concluded that flunarizine reduces ischemic damage mainly via a direct effect on brain tissue.

Animals↗
PubMed1988

Phencyclidine reduces postischemic neuronal necrosis in rat hippocampus without changing blood flow.

In this report the effects of phencyclidine (PCP) on physiologic variables, local cerebral blood flow (LCBF), and on hippocampal cell damage were measured in a rat model of forebrain ischemia (2-vessel occlusion and hypotension). Ischemia was induced for 10 min. LCBF was determined after 2 min of recirculation, using the [14C]iodoantipyrine technique. Hippocampal cell loss was quantified histologically 7 days postischemia as the percentage of acidic stainable neurons. Intravenous application of PCP (2 mg/kg) at 15 min prior to ischemia left postischemic LCBF unchanged, but neuronal damage was significantly reduced in hippocampal CA1 sector from 46 to 15.7%. PCP is concluded to reduce ischemic damage of neurons mainly via a direct effect on brain tissue.

Animals↗
PubMed1988

Vinpocetine prevents ischemic cell damage in rat hippocampus.

The effects of vinpocetine on hippocampal cell damage and local cerebral blood flow (LCBF) were measured in a rat model of forebrain ischemia (2-vessel occlusion and hypotension). Duration of ischemia was 10 min. LCBF was determined after 2 min of recirculation using the 14C-iodoantipyrine technique. Hippocampal cell loss was quantified histologically 7 days post-ischemia. Intraperitoneal application of vinpocetine (10 mg/kg) 15 min prior to ischemia significantly reduced neuronal cell loss in hippocampal CA 1 sector from 60% to 28%. The drug led to a marked increase in blood flow in cortical areas, whereas LCBF remained unchanged in hippocampus and all other structures measured. It is suggested that the protective effect of vinpocetine does not depend on increased postischemic blood flow.

Animals↗
PubMed1988

Morphology of tissue damage due to experimental cerebral ischemia in rats.

Two models of experimental cerebral ischemia in rats were developed and used. The first model was permanent occlusion of both carotids up to 3 weeks, the second model the temporal occlusion of both carotids and systemic hypotension for 10 min. Rats treated by the first experimental set were investigated after one, 2 and 3 weeks. In all groups, about 40% of so treated animals had territorial infarcts, often more than one in the animal in question. These infarcts developed from necrotic, pale areas to ischemic cysts and this copied the evolution of human territorial infarction. Astroglial reaction was only seen in the border zone. In the second model, rats preferentially developed, as known, the so called delayed ganglion cell necrosis in the field CA 1 of the hippocampus. Cells were not altered on the second, but damaged on the sixth day after experimental ischemia. In both models the hippocampus was damaged, however in the first the damages were morphologically distinct from the damage in carotid occlusion in systemic hypotension. The first experimental model suits better for human territorial infarction, the second is highly reproducible and thus provides a much better experimental tool.

Animals↗