Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unilateral atrophy of a cerebellar hemisphere occurring as a sequela of ischemic or destructive injury of the contralateral cerebral hemisphere is uncommon in children. We reviewed our experience with this phenomenon and found an unexpected association with extreme prematurity and a complicated perinatal course with a poor subsequent neurologic outcome. We retrospectively identified eight children, aged 8 months to 13 years, in whom cerebellar atrophy associated with cerebral injury was diagnosed on MR or CT, and reviewed their past medical history, neurologic findings, and neuroimaging studies. Seven patients were born extremely premature, EGA 25-28 weeks, and had severe perinatal intracranial hemorrhage. Neurologic problems include severe developmental delay in seven, spastic paresis in six, and seizures in five. Neuroimaging showed severe unilateral holohemispheric atrophy in four, bilateral asymmetric holohemispheric atrophy in two, and left temporoparietal atrophy in one. Cerebellar atrophy was unilateral in five and bilateral but asymmetric in two. Gliosis of the atrophic cerebellum occurred in one patient. Sequential neuroimaging in one patient showed evolution of crossed cerebellar atrophy at 8 months of age. The final patient, a term infant, had an idiopathic perinatal left cerebral infarct. In our experience, crossed cerebellar atrophy was an uncommon manifestation of extreme prematurity complicated by severe intracranial hemorrhage and/or ischemic necrosis of white matter. The cerebellar atrophy is most often a secondary degenerative phenomenon rather than a result of direct cerebellar injury.
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PMID:Crossed cerebellar atrophy in children: a neurologic sequela of extreme prematurity. 857 28

The hemodynamically relevant persistent ductus arteriosus (PDA) impairs pulmonary and cardiac function. Frequently, PDA can be closed only via surgery. In this retrospective study, early and long-term results in very low birth weight newborns are evaluated. Eighty-seven of 634 very low weight newborns presented with PDA All patients (pts; age: +/-14 days; weight: +/-1064 g) were ventilator-dependent. Surgical closure (after 29+/-5 days) was indicated if echocardiography and prolonged ventilation (>20+/-2 days) evidenced a hemodynamically relevant PDA. Sixteen pts, in which indomethacin therapy failed preoperatively are included in the 36 surgically treated pts; no pt died intra- or early postoperatively (<3 day). Overall mortality 30 days after delivery was n=9. Early plus late mortality was n=19. Long-term follow-up (3-12 years) in 46 (68%) pts: 15 were solely physically, 11 were mentally and neurologically, and 4 were physically, mentally and neurologically retarded. From these 30 pts, 15 were severely (e.g. tetraspasm; severe cerebral paresis) and 15 were slightly (e.g. psychosomatic and language development prolongation) retarded. Sixteen pts exhibited no disability; no long-term complications owing to surgery. The relatively large number of neurological injuries was not owing to chromosomal syndromes or pre-existing abnormalities but can be explained by severe and frequent prematurity, hypoxia, and intracerebral bleeding. Indomethacin was successful only in a few patients. Early surgery (after frustran early indomethacin therapy) of a hemodynamically relevant PDA is recommended. In the long-term, severe disabilities develop.
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PMID:Management of the persistent ductus arteriosus in infants of very low birth weight: early and long-term results. 1767 Feb 87