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  • Amyotrophic lateral sclerosis  (2)
  • Spinal cord  (2)
  • Acute autonomic and sensory neuropathy  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Phosphorylated high molecular weight neurofilament protein in the peripheral motor, sensory and sympathetic neuronal perikarya: system-dependent normal variations and changes in amyotrophic lateral sclerosis and multiple system atrophy (1992)
    Springer
    Acta neuropathologica 83 (1992), S. 240-245 
    Details
    ISSN: 1432-0533
    Keywords: High molecular weight neurofilament ; Phosphorylation ; Peripheral nervous system ; Amyotrophic lateral sclerosis ; Multiple system atrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Using monoclonal antibody (Ta-51) that specifically binds phosphorylated high molecular weight neurofilament (pNFH) proteins, we investigated the occurrence of perikaryal pNFH in the spinal ventral horn motoneurons, intermediolateral column (ILC) neurons, sympathetic ganglion neurons and dorsal root ganglion (DRG) neurons obtained from patients with amyotrophic lateral sclerosis (ALS) and multiple system atrophy (MSA) and from control cases. In the controls, a system-dependent variation in perikaryal Ta-51 immunoreactivity was observed. Very few ventral horn cells and ILC neurons were stained with Ta-51, while large population of DRG neurons and sympathetic neurons were Ta-51 positive. The incidence of perikaryal immunoreactivity in the ventral horn cells was significantly increased in ALS and MSA. Some ILC neurons in ALS were Ta-51 positive and their incidence was significantly higher than that of the controls. These data suggest that both ILC neurons and ventral horn cells are affected with respect to pNFH metabolism in ALS and MSA. No significant difference was, however, detected in the Ta-51 immunoreactivity of both DRG and sympathetic ganglion neurons in ALS and MSA as compared with the controls.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296785
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  • 2
    Electronic Resource
    Electronic Resource
    Spinal and cranial motor nerve roots in amyotrophic lateral sclerosis and X-linked recessive bulbospinal muscular atrophy: Morphometric and teased-fiber study (1981)
    Springer
    Acta neuropathologica 55 (1981), S. 227-235 
    Details
    ISSN: 1432-0533
    Keywords: Nerve roots ; Amyotrophic lateral sclerosis ; X-linked recessive bulbospinal muscular atrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Amyotrophic lateral sclerosis (ALS) and adult onset X-linked recessive bulbospinal muscular atrophy (SPMA), constituting the category of adult onset form of motor neuron disease, were analyzed on motor nerve roots. The results of morphometric analysis on ventral spinal roots (VSR) of all spinal segments from ALS and SPMA revealed the following three findings: (1) the large-myelinated α-motoneuron fibers were markedly decreased in number throughout all segments; (2) thin-myelinated autonomic preganglionic fibers were almost completely preserved; (3) small-intermediate-myelinated fibers which are considered to correspond to γ-motoneuron fibers were generally well preserved in ALS, but decreased by one-half to one-third in SPMA. However, all the components of the nerve roots of the oculomotor, trochlear, and abducent nerves were completely preserved in both ALS and SPMA. Moreover, the teasedfiber study showed that the regenerating-sprouting process rarely occurred in the VSR of ALS and SPMA. The present study suggested that the site of the primary lesion seems to be in the α-motoneuron fibers in motor neuron diseases, such as ALS or SPMA. However, the marked discrepancy in the pathologic change in the α-motoneuron fibers in the VSR and the nerve roots innervating the external ocular muscles was noteworthy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691322
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Expression of low-affinity neurotrophin receptor p75NTR in the peripheral nervous system of human neuropathies (1998)
    Springer
    Acta neuropathologica 95 (1998), S. 597-604 
    Details
    ISSN: 1432-0533
    Keywords: Key words p75NTR ; Nerve regeneration ; Spinal cord ; Dorsal root ganglia ; Sympathetic ganglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Expression of low-affinity neurotrophin receptor (p75NTR) was immunohistochemically examined in the peripheral nerve trunks, dorsal root ganglia, sympathetic nerve ganglia and spinal cords in various human neurological diseases manifesting peripheral neuropathies. p75NTR was expressed in the nerves with axonal degeneration, and was also prominent in the nerves with newly regenerating axons. In contrast, axonal pathology tended to reduce the expression of p75NTR in the neuronal perikarya of the dorsal root genglion and sympathetic nerve ganglion neurons. In the ventral and lateral horn cells, the p75NTR immunoreactivity was not detected in the normal and diseased nerves except for amyloid polyneuropathy. These p75NTR expressions in the diseased human peripheral nervous tissues would be regulated by an underlying pathology-related process, and could play a role in peripheral nerve repair.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050846
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Age-related morphologic changes of the central canal of the human spinal cord (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 253-259 
    Details
    ISSN: 1432-0533
    Keywords: Key words Aging ; Spinal canal ; Histology ; Spinal cord ; Syringomyelia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To elucidate the role of the human central canal on the physiology and pathogenesis of acquired syringomyelia, we analyzed the age-related morphologic changes in the normal human central canal of the spinal cord. The subjects included 158 autopsy cases ranging in age from 1 week postnatally to 116 years of age. Each segment of the whole spinal cords was investigated from the C3 to S3 levels. The microscopic pictures of the central canal were classified as patent or occluded at each level for each age decade. The patency rate under 1 year of age was 100% in almost all the segments, which markedly decreased in the second decade, and the canals were occluded in all the segments with advancing age. According to the longitudinal pattern of the central canal occlusion, 19 of 20 cases where the canals were patent in all segment levels were less than 10 years of age. Cases in which the canals were occluded in all segment levels appeared in the second decade, and their number increased gradually with advancing age. The occlusion of the central canal started at the T6 and L5 to S2 levels. We suggest that the central canal does not function after infancy because of its occlusion, and that it is not involved in the development of syringomyelia in adult patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050982
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  • 5
    Electronic Resource
    Electronic Resource
    Clinico-pathophysiological features of acute autonomic and sensory neuropathy: A long-term follow-up study (1995)
    Springer
    Journal of neurology 242 (1995), S. 623-628 
    Details
    ISSN: 1432-1459
    Keywords: Acute autonomic and sensory neuropathy ; Sensory ataxia ; Ganglioneuronopathy ; Neuron-specific enolase ; S-100b protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We evaluated the clinicopathophysiological features of three patients with acute autonomic and sensory neuropathy (AASN) who were followed for over 3 years. Signs of an autonomic disturbance including vomiting, anhidrosis, urinary disturbances, orthostatic hypotension and reduced coefficient of variation of the R-R interval on electrocardiography gradually improved about 1 year after onset. However, all three exhibited severe generalized sensory impairment for all modalities with the development of persistent sensory ataxia. No sensory nerve action potentials could be elicited and no somatosensory evoked potentials could be obtained. Sural nerve biopsy revealed severe axonopathy. In two patients, a high-intensity area was observed in the posterior column of the spinal cord on T2*-weighted axial magnetic resonance images. The level of neuron-specific enolase in cerebrospinal fluid was markedly elevated in two patients, indicating spinal nerve root or sensory neuron damage. Motor nerve function was well preserved in all patients. Our findings suggests that the major lesion in patients with AASN, particularly those with a sensory deficit, is present in the dorsal root ganglion neurons, that is there is a ganglioneuronopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00866911
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