Spinal cord pathology in pediatric acquired immunodeficiency syndrome

D. W. Dickson, A. L. Belman, T. S. Kim, D. S. Horoupian, Arye Rubinstein

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

We examined the spinal cords from 15 consecutive autopsies of infants and chil$en with AIDS using a battery of histochemical and immunocytochemical stains, and in four cases, electron microscopy. Corticospinal tract (CST) signs were a notable clinical finding in 14; however, the age of onset, rate of progression, severity of dysfunction, and duration varied among patients. Ten cases had pathologic changes in the CST. In four of the ten cases, the changes were consistent with an “axonopathy” since axons and myelin were both diminished in the CST. These cases may represent CST wallerian degeneration, since they had marked injury to cerebral white matter in the form of chronic inflammation with multinucleated cells, gliosis, and myelin pallor. In five cases, with an average age at death of 31 months, the CST showed poor myelination with relative preservation of axons. These cases may represent delayed myelination or possibly cytokine-mediated injury to newly formed myelin since the CST is one of the last tracts to myelinate in the spinal cord. One child with primary CNS lymphoma had a complicated pattern of spinal injury due to unilateral CST wallerian degeneration possibly superimposed upon delayed myelination, in addition to patchy areas of demyelination associated with perivascular lymphomatous infiltrates. Four children with mild CST signs, ranging in age from 5 to 6 months, had CST myelin pallor that was consistent with the degree of myelination expected for age. We did not find vacuolar myelopathy similar to that seen in adult AIDS, but did note focal vacuolar changes in the thoracic posterior columns in the oldest child.

Original languageEnglish (US)
Pages (from-to)227-235
Number of pages9
JournalNeurology
Volume39
Issue number2
StatePublished - 1989

Fingerprint

Pyramidal Tracts
Spinal Cord
Acquired Immunodeficiency Syndrome
Pediatrics
Pathology
Myelin Sheath
Wallerian Degeneration
Pallor
Axons
Cord
Syndrome
Spinal Injuries
Gliosis
Spinal Cord Diseases
Wounds and Injuries
Demyelinating Diseases
Age of Onset
AIDS/HIV
Degeneration
Autopsy

ASJC Scopus subject areas

  • Arts and Humanities (miscellaneous)
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Dickson, D. W., Belman, A. L., Kim, T. S., Horoupian, D. S., & Rubinstein, A. (1989). Spinal cord pathology in pediatric acquired immunodeficiency syndrome. Neurology, 39(2), 227-235.

Spinal cord pathology in pediatric acquired immunodeficiency syndrome. / Dickson, D. W.; Belman, A. L.; Kim, T. S.; Horoupian, D. S.; Rubinstein, Arye.

In: Neurology, Vol. 39, No. 2, 1989, p. 227-235.

Research output: Contribution to journalArticle

Dickson, DW, Belman, AL, Kim, TS, Horoupian, DS & Rubinstein, A 1989, 'Spinal cord pathology in pediatric acquired immunodeficiency syndrome', Neurology, vol. 39, no. 2, pp. 227-235.
Dickson DW, Belman AL, Kim TS, Horoupian DS, Rubinstein A. Spinal cord pathology in pediatric acquired immunodeficiency syndrome. Neurology. 1989;39(2):227-235.
Dickson, D. W. ; Belman, A. L. ; Kim, T. S. ; Horoupian, D. S. ; Rubinstein, Arye. / Spinal cord pathology in pediatric acquired immunodeficiency syndrome. In: Neurology. 1989 ; Vol. 39, No. 2. pp. 227-235.
@article{dfc484997e8f4ba784367027ecf38d5b,
title = "Spinal cord pathology in pediatric acquired immunodeficiency syndrome",
abstract = "We examined the spinal cords from 15 consecutive autopsies of infants and chil$en with AIDS using a battery of histochemical and immunocytochemical stains, and in four cases, electron microscopy. Corticospinal tract (CST) signs were a notable clinical finding in 14; however, the age of onset, rate of progression, severity of dysfunction, and duration varied among patients. Ten cases had pathologic changes in the CST. In four of the ten cases, the changes were consistent with an “axonopathy” since axons and myelin were both diminished in the CST. These cases may represent CST wallerian degeneration, since they had marked injury to cerebral white matter in the form of chronic inflammation with multinucleated cells, gliosis, and myelin pallor. In five cases, with an average age at death of 31 months, the CST showed poor myelination with relative preservation of axons. These cases may represent delayed myelination or possibly cytokine-mediated injury to newly formed myelin since the CST is one of the last tracts to myelinate in the spinal cord. One child with primary CNS lymphoma had a complicated pattern of spinal injury due to unilateral CST wallerian degeneration possibly superimposed upon delayed myelination, in addition to patchy areas of demyelination associated with perivascular lymphomatous infiltrates. Four children with mild CST signs, ranging in age from 5 to 6 months, had CST myelin pallor that was consistent with the degree of myelination expected for age. We did not find vacuolar myelopathy similar to that seen in adult AIDS, but did note focal vacuolar changes in the thoracic posterior columns in the oldest child.",
author = "Dickson, {D. W.} and Belman, {A. L.} and Kim, {T. S.} and Horoupian, {D. S.} and Arye Rubinstein",
year = "1989",
language = "English (US)",
volume = "39",
pages = "227--235",
journal = "Neurology",
issn = "0028-3878",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Spinal cord pathology in pediatric acquired immunodeficiency syndrome

AU - Dickson, D. W.

AU - Belman, A. L.

AU - Kim, T. S.

AU - Horoupian, D. S.

AU - Rubinstein, Arye

PY - 1989

Y1 - 1989

N2 - We examined the spinal cords from 15 consecutive autopsies of infants and chil$en with AIDS using a battery of histochemical and immunocytochemical stains, and in four cases, electron microscopy. Corticospinal tract (CST) signs were a notable clinical finding in 14; however, the age of onset, rate of progression, severity of dysfunction, and duration varied among patients. Ten cases had pathologic changes in the CST. In four of the ten cases, the changes were consistent with an “axonopathy” since axons and myelin were both diminished in the CST. These cases may represent CST wallerian degeneration, since they had marked injury to cerebral white matter in the form of chronic inflammation with multinucleated cells, gliosis, and myelin pallor. In five cases, with an average age at death of 31 months, the CST showed poor myelination with relative preservation of axons. These cases may represent delayed myelination or possibly cytokine-mediated injury to newly formed myelin since the CST is one of the last tracts to myelinate in the spinal cord. One child with primary CNS lymphoma had a complicated pattern of spinal injury due to unilateral CST wallerian degeneration possibly superimposed upon delayed myelination, in addition to patchy areas of demyelination associated with perivascular lymphomatous infiltrates. Four children with mild CST signs, ranging in age from 5 to 6 months, had CST myelin pallor that was consistent with the degree of myelination expected for age. We did not find vacuolar myelopathy similar to that seen in adult AIDS, but did note focal vacuolar changes in the thoracic posterior columns in the oldest child.

AB - We examined the spinal cords from 15 consecutive autopsies of infants and chil$en with AIDS using a battery of histochemical and immunocytochemical stains, and in four cases, electron microscopy. Corticospinal tract (CST) signs were a notable clinical finding in 14; however, the age of onset, rate of progression, severity of dysfunction, and duration varied among patients. Ten cases had pathologic changes in the CST. In four of the ten cases, the changes were consistent with an “axonopathy” since axons and myelin were both diminished in the CST. These cases may represent CST wallerian degeneration, since they had marked injury to cerebral white matter in the form of chronic inflammation with multinucleated cells, gliosis, and myelin pallor. In five cases, with an average age at death of 31 months, the CST showed poor myelination with relative preservation of axons. These cases may represent delayed myelination or possibly cytokine-mediated injury to newly formed myelin since the CST is one of the last tracts to myelinate in the spinal cord. One child with primary CNS lymphoma had a complicated pattern of spinal injury due to unilateral CST wallerian degeneration possibly superimposed upon delayed myelination, in addition to patchy areas of demyelination associated with perivascular lymphomatous infiltrates. Four children with mild CST signs, ranging in age from 5 to 6 months, had CST myelin pallor that was consistent with the degree of myelination expected for age. We did not find vacuolar myelopathy similar to that seen in adult AIDS, but did note focal vacuolar changes in the thoracic posterior columns in the oldest child.

UR - http://www.scopus.com/inward/record.url?scp=0024583664&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024583664&partnerID=8YFLogxK

M3 - Article

VL - 39

SP - 227

EP - 235

JO - Neurology

JF - Neurology

SN - 0028-3878

IS - 2

ER -