Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Pelizaeus-Merzbacher disease in a brother and sister (1986)
    Springer
    Acta neuropathologica 69 (1986), S. 343-346 
    Details
    ISSN: 1432-0533
    Keywords: Leukodystrophy ; Demyelination ; Pelizaeus-Merzbacher disease ; Genetics ; Neurochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A brother and sister developed a slowly progressive neurological disorder with cerebellar and pyramidal signs and mild dementia. The brother developed symptoms at 6 months and died aged 11 years; the sister developed symptoms at 3 years and died aged 18 years. At post-mortem both had severe widespread central nervous system demyelination with islands of preserved myelin, and small amounts of sudanophilic lipid products. Metachromatic material, globoid cells, and adrenal abnormalities were not seen. The features were those of Pelizaeus-Merzbacher disease (PMD). It has been proposed, on the basis of only a few family studies, that PMD is an X-linked recessive disorder. These cases suggest that autosomal recessive inheritance may occur.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688316
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Infective endocarditis with inflammatory lesions in the peripheral nervous system (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 101-104 
    Details
    ISSN: 1432-0533
    Keywords: Infective endocarditis ; Peripheral neuropathy ; Intensive care unit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A 64-year-old woman developed septicemia and a generalized peripheral neuropathy while being ventilated postoperatively. No cause for the neuropathy could be found during life. At autopsy she was found to have infective endocarditis and multifocal inflammatory lesions in the central and peripheral nervous systems, consistent with damage due to septic emboli. Infective endocarditis may be a cause of a generalized polyradiculoneuropathy and could be responsible for a proportion of cases of “critical illness polyneuropathy”.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687409
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Brain stem serotonin-synthesizing neurons in Alzheimer's disease: a clinicopathological correlation (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 638-650 
    Details
    ISSN: 1432-0533
    Keywords: Raphe ; Immunohistochemistry ; Neuritic plaques ; Neurofibrillary tangles ; Alzheimer's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The location and number of brain stem serotonin-synthesizing neurons were analyzed in 11 patients with Alzheimer's disease (AD) and 5 agematched controls using immunohistochemical techniques. In addition, the number of neuritic plaques and neurofibrillary tangles in the cortex and brain stem raphe was evaluated, as was the number of Nissl-stained raphe neurons. AD patients could be classified into two groups based on their raphe pathology; patients with such pathology (AD+) and those without (AD−). The number of large raphe neurons correlated significantly with the number of serotonin-synthesizing neurons in control material, indicating that all large neurons were serotonergic. This relationship was not apparent in AD+ patients, in whom the number of serotonin-synthesizing neurons correlated with the number of neurofibrillary tangles in the raphe of these patients. This indicates that in AD+ patients the serotonin-synthesizing neurons were selectively affected. There was no correlation between raphe and cortical pathology or raphe pathology and patient sex, age, mini-mental score or depression score, even when such scores were weighted for the interval between testing and death. There was a trend for the raphe pathology to correlate with the age of onset and duration of dementia and the Blessed dementia score in AD+ patients. Most AD+ patients with severe raphe lesions had clinical dementia only, while AD− patients had additional clinical features. The raphe lesions were more dramatic in AD+ patients with a rapid progression of symptoms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227741
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Ubiquitin-positive achromatic neurons in corticobasal degeneration (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 68-75 
    Details
    ISSN: 1432-0533
    Keywords: Key words Neuropathology ; Ballooned neurons ; Ubiquitin ; Quantitation ; Alien limb
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 66-year-old woman presented with an alien limb syndrome without dementia. The course of her illness was unremitting and at autopsy 6 years later her diagnosis was confirmed as corticobasal degeneration without Alzheimer-type pathology. Although the presence of ballooned achromatic cortical neurons and cell loss from the substantia nigra distinguishes such patients, the site and density of achromatic neurons has not previously been quantified. We show that immunohistochemistry for the cell stress protein ubiquitin selectively stains these achromatic neurons, whereas they do not stain for abnormally phosphorylated tau protein. Phosphorylated neurofilament antibodies recognise both ballooned and non-ballooned neurons. In this case, high densities of ubiquitin-positive ballooned neurons were found in frontal cortical regions with the highest densities in layers V and VI of the anterior cingulate cortex. In addition, high densities of ubiquitin-positive ballooned neurons were found in the insular cortex, claustrum and amygdala. These results confirm past reports of frontal pathology, but show that there is also considerable pathology in insular and parahippocampal cortical regions and some subcortical regions. Our findings suggest that the distribution and staining characteristics of ballooned neurons in corticobasal degeneration may help to differentiate these cases pathologically, while the absence of dementia appears to be an important clinical criterion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294461
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Ubiquitin-positive achromatic neurons in corticobasal degeneration (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 68-75 
    Details
    ISSN: 1432-0533
    Keywords: Neuropathology ; Ballooned neurons ; Ubiquitin ; Quantitation ; Alien limb
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 66-year-old woman presented with an alien limb syndrome without dementia. The course of her illness was unremitting and at autopsy 6 years later her diagnosis was confirmed as corticobasal degeneration without Alzheimer-type pathology. Although the presence of ballooned achromatic cortical neurons and cell loss from the substantia nigra distinguishes such patients, the site and density of achromatic neurons has not previously been quantified. We show that immunohistochemistry for the cell stress protein ubiquitin selectively stains these achromatic neurons, whereas they do not stain for abnormally phosphorylated tau protein. Phosphorylated neurofilament antibodies recognise both ballooned and non-ballooned neurons. In this case, high densities of ubiquitin-positive ballooned neurons were found in frontal cortical regions with the highest densities in layers V and VI of the anterior cingulate cortex. In addition, high densities of ubiquitin-positive ballooned neurons were found in the insular cortex, claustrum and amygdala. These results confirm past reports of frontal pathology, but show that there is also considerable pathology in insular and parahippocampal cortical regions and some subcortical regions. Our findings suggest that the distribution and staining characteristics of ballooned neurons in corticobasal degeneration may help to differentiate these cases pathologically, while the absence of dementia appears to be an important clinical criterion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294461
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Phrenic nerve maturation in the sudden infant death syndrome (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 422-426 
    Details
    ISSN: 1432-0533
    Keywords: Key words Sudden infant death syndrome ; Phrenic ; nerve ; Axon ; Diaphragm ; Quantitation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been suggested that delayed development in either the peripheral or central nervous system could underlie the sudden infant death syndrome (SIDS). We studied the phrenic nerve in an attempt to find if maturation in this nerve was delayed in SIDS, and to see if fiber size differences could explain the paucity of type I muscle fibers described in SIDS diaphragms. Samples of phrenic nerves were taken at post mortem from 11 SIDS and 10 control infants. Myelinated fibers were quantitated in 1-μm silver-stained resin sections using a semi-automatic image analysis system. The numbers and sizes of all myelinated fibers in the right phrenic nerve were compared between SIDS and control groups. The proportion of small (less than 6-μm diameter) phrenic nerve fibers was similar in SIDS (53.1%, SD 12.8%) and control (53.6%, SD 14.0%) cases. The proportion of small fibers decreased with increasing age at an equivalent rate in both SIDS and control groups. Total numbers of myelinated fibers were similar in the right phrenic nerves of SIDS (3429, SD 440) and control (3457, SD 507) infants, but varied widely between cases and were not correlated with age. Maturation of the phrenic nerve, as judged by increasing size of myelinated fibers, is therefore similar in SIDS and control infants. This argues against a widespread developmental delay in SIDS. No changes in phrenic nerve fiber sizes were found to account for the finding of fewer type I fibers in SIDS diaphragms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050445
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Uptake of inorganic mercury by the human brain (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 525-527 
    Details
    ISSN: 1432-0533
    Keywords: Key words Mercury ; Human ; Neurotoxicity ; Cortical ; motor neuron ; Amyotrophic lateral sclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 24-year-old man injected himself intravenously with metallic mercury in a suicide attempt, and died 5 months later after cutting his wrists. The brain was removed at postmortem and 7-μm paraffin sections were cut from representative blocks. Dense deposits of mercury were found on autometallography in large cortical motor neurons, but in no other cerebral neurons. Smaller mercury deposits were found in the brain stem (in the mesencephalic trigeminal nucleus, noradrenergic neurons, and in neurons for extraocular muscles), the cerebellum (in the dentate nucleus) and in lateral motor neurons in the C2/3 spinal cord. Mercury deposits were found in glial cells in all regions. The finding that elemental mercury enters human cortical motor neurons in preference to other cerebral neurons raises the possibility that this neurotoxin may play a part in the pathogenesis of some human motor neuron diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050556
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Mercury in human spinal motor neurons (1998)
    Springer
    Acta neuropathologica 96 (1998), S. 515-519 
    Details
    ISSN: 1432-0533
    Keywords: Key words Amyotrophic lateral sclerosis ; Mercury ; Motor neuron disease ; Neurotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inorganic mercury has been proposed as a neurotoxin that could cause sporadic motor neuron disease (SMND). We were therefore interested to see if mercury could be detected in the upper and lower motor neurons of SMND patients, and if mercury accumulated within motor neurons during life. Paraffin sections of formalin-fixed spinal cord (22 control adults, 20 SMND adults, 25 infants) and frontal primary motor cortex (9 control adults, 18 SMND adults, 20 infants) were stained with silver nitrate autometallography to detect ionic mercury. Mercury was found in the spinal motor neurons of 36% of adult control cases and 45% of adult SMND cases, with no significant difference between groups. No mercury was seen in infant spinal motor neurons, or in any adult or infant corticomotoneurons. In conclusion, many humans appear to accumulate mercury in their spinal motor neurons by the time they are adults, but mercury does not appear to play a major role in the loss of upper or lower motor neurons in SMND.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050927
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...