Abstract
The unusual occurrence of spasticity at birth with symmetrical thalamic damage was found in a male infant delivered at 36 weeks' gestation following an episode of traumatically induced premature labor at 32 weeks. The infant was found to be spastic in flexion with increased stretch reflexes, depressed primitive reflexes, and moderate flexion contractures. Computerized tomographic scans showed bilateral nonenhancing thalamic densities. Neuropathologically, the lateral thalamic nuclei and the red nucleus showed neuron loss, astrocytosis, and, as confirmed by electron microprobe analysis, calcified neurons. The striatum was uninvolved. These findings closely resemble those reported as 'symmetrical thalamic degeneration in infancy' and are strongly reminiscent of the pattern of thalamic involvement frequently seen in status marmoratus. It would appear that there is a period during perinatal life in which the lateral thalamus can be rendered vulnerable to hypoxic-ischemic injury, and that the thirty-second week of gestation must be included within this period.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 94-97 |
| Number of pages | 4 |
| Journal | Annals of Neurology |
| Volume | 13 |
| Issue number | 1 |
| State | Published - 1983 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Neuroscience(all)
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Prenatal symmetrical thalamic degeneration with flexion spasticity at birth. / Parisi, Joseph E; Collins, G. H.; Kim, R. C.; Crosly, C. J.
In: Annals of Neurology, Vol. 13, No. 1, 1983, p. 94-97.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Prenatal symmetrical thalamic degeneration with flexion spasticity at birth
AU - Parisi, Joseph E
AU - Collins, G. H.
AU - Kim, R. C.
AU - Crosly, C. J.
PY - 1983
Y1 - 1983
N2 - The unusual occurrence of spasticity at birth with symmetrical thalamic damage was found in a male infant delivered at 36 weeks' gestation following an episode of traumatically induced premature labor at 32 weeks. The infant was found to be spastic in flexion with increased stretch reflexes, depressed primitive reflexes, and moderate flexion contractures. Computerized tomographic scans showed bilateral nonenhancing thalamic densities. Neuropathologically, the lateral thalamic nuclei and the red nucleus showed neuron loss, astrocytosis, and, as confirmed by electron microprobe analysis, calcified neurons. The striatum was uninvolved. These findings closely resemble those reported as 'symmetrical thalamic degeneration in infancy' and are strongly reminiscent of the pattern of thalamic involvement frequently seen in status marmoratus. It would appear that there is a period during perinatal life in which the lateral thalamus can be rendered vulnerable to hypoxic-ischemic injury, and that the thirty-second week of gestation must be included within this period.
AB - The unusual occurrence of spasticity at birth with symmetrical thalamic damage was found in a male infant delivered at 36 weeks' gestation following an episode of traumatically induced premature labor at 32 weeks. The infant was found to be spastic in flexion with increased stretch reflexes, depressed primitive reflexes, and moderate flexion contractures. Computerized tomographic scans showed bilateral nonenhancing thalamic densities. Neuropathologically, the lateral thalamic nuclei and the red nucleus showed neuron loss, astrocytosis, and, as confirmed by electron microprobe analysis, calcified neurons. The striatum was uninvolved. These findings closely resemble those reported as 'symmetrical thalamic degeneration in infancy' and are strongly reminiscent of the pattern of thalamic involvement frequently seen in status marmoratus. It would appear that there is a period during perinatal life in which the lateral thalamus can be rendered vulnerable to hypoxic-ischemic injury, and that the thirty-second week of gestation must be included within this period.
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UR - http://www.scopus.com/inward/citedby.url?scp=0020689479&partnerID=8YFLogxK
M3 - Article
C2 - 6830171
AN - SCOPUS:0020689479
VL - 13
SP - 94
EP - 97
JO - Annals of Neurology
JF - Annals of Neurology
SN - 0364-5134
IS - 1
ER -