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Biomedical subjects

C Rossberg

Publications and source records attributed to C Rossberg.

29 records · Page 2Linked to original sources
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↗
PubMed1986

[Xanthofibrogranulomatosis with meningocortical involvement].

The history of a 52-year old female with xanthofibrogranulomatosis (X.) is presented. Clinical and pathologic-anatomical findings of this rare disease are described. We report the case, because of the unusual intracranial spread of the X.

Brain Stem↗
PubMed1984

Neurological complications of Grönblad-Strandberg syndrome.

Neurological complications resulting from pronounced cerebrovascular changes were observed in a 59-year-old female suffering from Grönblad-Strandberg syndrome. In addition to typical skin changes of the pseudoxanthoma elasticum and ocular alterations (exudative macular degeneration and angioid streaks) there were an unusual number of disturbed endocrinological functions. The ophthalmological findings revealed characteristic breaks in Bruch's membrane, proliferation of chorioidal vessels into the subretinal space, hyperplasia of retinal pigment epithelium and disciform macular degeneration. Postmortem examination of the brain showed multiple cerebral infarcts due to recurrent disturbances in cerebral blood supply and particularly pronounced changes in the elastica interna of many cerebral arteries. Although the observed neurological signs in our patient were not characteristic of Grönblad-Strandberg syndrome, the histopathological findings led to the assumption that the same basic mechanisms result in alterations of elastic fibres and collagen, mainly in the ocular-cerebral system.

Cerebral Infarction↗
PubMed1982

[CT differential diagnosis and findings in intracerebral haemorrhage (author's transl)].

The CT findings of 73 patients with spontaneous and traumatic intracerebral haematomas are described. The course and pattern of resorption of the bleeding is evaluated. It is shown that the resorption of all haematomas is terminated by the end of week 7 independent of their maximum diameter. Only smaller haemorrhage of less than 2 cm can be resorbed in a shorter time. Moreover, the underlying pathophysiologic mechanisms of faster resorption of bleeding located in the basal ganglia and the neighbouring white matter are discussed. The CT findings revealed no clear-cut characteristics for differential diagnosis of the etiology of haematomas, but proved very helpful in defining the prognosis.

Adolescent↗
PubMedDate not supplied

Effects of emopamil on postischemic blood flow and neuronal damage in rat brain.

The effects of the calcium entry blocker emopamil on physiological variables, local cerebral blood flow (LCBF) and on hippocampal cell damage were evaluated after 10 min of forebrain ischemia in the rat. LCBF was determined with the 14C-iodoantipyrine technique after 2, 10, and 60 min of postischemic recirculation. Histological evaluation was performed 7 days after ischemia in cortical and hippocampal tissue by determination of the percentage of necrotic neurons. Preischemic application of emopamil [4 mg/kg racemate or 2 mg/kg (S)-emopamil; i.v.] caused increased in LCBF in cortical areas but did not alter blood flow in the hippocampus at 2 min of recirculation. After 10 and 30 min of flow resumption no differences in LCBF between drug-treated and control animals were observed. In the histological series (S)-emopamil was applied at doses of 2, 4 or 6 mg/kg before the induction of ischemia. After 7 days of postischemic recovery, neuronal damage was significantly reduced by the calcium antagonist in hippocampal CA1 sector at all doses tested, the most prominent effects being observed with the lowest dose. At this dose cell loss in the CA3 sector was also reduced. In cortical tissue the number of necrotic cells remained unchanged by emopamil treatment. It is concluded that the calcium antagonist emopamil can reduce ischemia-induced neuronal cell damage. The compound improves circulation in cortical tissue only during early recovery but not at later phases of reflow, i.e. the period of delayed hypoperfusion. These increases in blood flow are not of crucial importance for ultimate neuronal death in this area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Infarct of the basal ganglia in childhood--clinico-neuroradiologic findings and differential diagnosis].

Basal ganglionic infarctions during childhood are comparable in size and favourable prognosis with lacunary infarctions in adults. Considering their etiology they are comparable with capsular infarctions in adults. In four children with basal ganglionic infarctions and acute motoric hemiparesis, a quick and complete regression of clinical signs and CT-findings was observed. With regard to the differential diagnosis of basal ganglionic infarction we additionally report of a female patient with initially unilateral lesion who had silently developed the hemiparesis. In this case the clinical course and the neuroradiological follow-up findings suggested Leigh disease.

Adolescent↗