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  • 1
    Electronic Resource
    Electronic Resource
    Cerebellomedullary compression in recessive craniometaphyseal dysplasia (1996)
    Springer
    Neuroradiology 38 (1996), S. S193 
    Details
    ISSN: 1432-1920
    Keywords: Key words Craniometaphyseal dysplasia ; Skeletal dysplasia ; Basilar invagination ; Magnetic resonance imaging ; Posterior cranial fossa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Craniometaphyseal dysplasia (CMD) is a very rare disorder of bone remodelling characterised by sclerosis of the skull base, vault and facial bones and metaphyseal splaying of tubular bones. The recessive form appears to be more severe than the dominant. Cranial nerve deficits have been reported in infancy and early childhood in a few patients, but the long-term history of recessive CMD is not well documented. We report cerebellomedullary compression in a girl with recessive CMD recognised at 14 years because of progressive truncal ataxia. MRI revealed backward angulation of the thickened clivus, narrowing of the foramen magnum and upward deviation of the cerebellum by a markedly thickened occipital squama, tonsillar herniation and obliteration of the infratentorial cerebrospinal fluid spaces. Posterior cranial fossa decompression resulted in marked improvement of the ataxia. Compression of posterior cranial fossa structures has to be considered in the natural history and management of CMD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002340050952
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Cerebellomedullary compression in recessive craniometaphyseal dysplasia (1996)
    Springer
    Neuroradiology 38 (1996), S. S193 
    Details
    ISSN: 1432-1920
    Keywords: Craniometaphyseal dysplasia ; Skeletal dysplasia ; Basilar invagination ; Magnetic resonance imaging ; Posterior cranial fossa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Craniometaphyseal dysplasia (CMD) is a very rare disorder of bone remodelling characterised by sclerosis of the skull base, vault and facial bones and metaphyseal splaying of tubular bones. The recessive form appears to be more severe than the dominant. Cranial nerve deficits have been reported in infancy and early childhood in a few patients, but the long-term history of recessive CMD is not well documented. We report cerebellomedullary compression in a girl with recessive CMD recognised at 14 years because of progressive truncal ataxia. MRI revealed backward angulation of the thickened clivus, narrowing of the foramen magnum and upward deviation of the cerebellum by a markedly thickened occipital squama, tonsillar herniation and obliteration of the infratentorial cerebrospinal fluid spaces. Posterior cranial fossa decompression resulted in marked improvement of the ataxia. Compression of posterior cranial fossa structures has to be considered in the natural history and management of CMD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02278158
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Effect of nerve growth factor on delayed neuronal death after cerebral ischaemia (1994)
    Springer
    Acta neurochirurgica 129 (1994), S. 64-71 
    Details
    ISSN: 0942-0940
    Keywords: Cytoskeleton ; delayed neuronal death ; nerve growth factor (NGF) ; neurofilament (NF)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the protective action of nerve growth factor (NGF) on delayed neuronal death, and we also studied the involvement of the 200 kDa neurofilament (NF 200) cytoskeletal proteins. Wistar rats were divided into three groups: Group I, in which transient forebrain ischaemia was produced; Group II, ischaemic group which received intraventricular administration of artificial cerebrospinal fluid (CSF); and Group III, ischaemic group which received intraventricular administration of 2 Μg of 2.5 S NGF. Forebrain ischaemia in these rats was produced by causing transient bilateral occlusion of the common carotid arteries and lowering the mean blood pressure to 50 mmHg for 8 minutes. On the 1st and 7th day after ischaemia we histologically examined neuronal death in the hippocampal CA1 sector. On the 7th day after ischaemia, mean cell death (degenerative cell number/total cell number) was 87±9% in group I (n=7), 51±36% in group II (n=7), and 14±16% in group III (n=8) (p〈0.05 vs. group II). The concentration of NF 200 in the hippocampal homogenate was measured by the Western blotting method on the 1st and 7th day after ischaemia. On the 1st day it was found to be 67±11% of that in the control group in group I (n=6), 73±21% in group II (n=6), and 84±7% in group III (n=6) (p〈0.05 vs. group II). The concentration of NF 200 in all groups remained at the same level until the 7th day after ischaemia (each group, n=6). These results suggest that 1) intraventricular NGF has a protective effect on delayed neuronal death, 2) these protective actions occur within one day after ischaemia, and 3) these effects may be mediated by the suppressed degradation and/or promoted restoration of neuronal cytoskeletal proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01400875
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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