Bilateral basal ganglia-thalamic lesions subsequent to prolonged fetal bradycardia.
We report two infants with bilateral basal ganglia-thalamic lesions subsequent to prolonged fetal bradycardia. Cardiotocogram revealed severe bradycardia lasting for more than 20 min in both. They demonstrated a significant encephalopathy, abnormal muscle tones and signs of brainstem injury. Clinical or electrical seizures were not observed in either of them. CT during early neonatal period demonstrated decreased tissue attenuation in basal ganglia and thalami in the absence of extensive cortical changes. Both of them developed severe mental retardation and quadriplegia. MRI in late infancy demonstrated abnormal high intensity areas in bilateral basal ganglia, thalami and around central sulci on T2-weighted image. Close correlation between prolonged fetal bradycardia and basal ganglia-thalamic lesion was suggested.
Okumura
A
A
Department of Pediatrics, Anjo Kosei Hospital, Anjo, Aichi, Japan.
Hayakawa
F
F
Kato
T
T
Kuno
K
K
Watanabe
K
K
D000328:Adult; D001480:Basal Ganglia Diseases / Q000209:etiology*; D001919:Bradycardia / Q000150:complications* / Q000175:diagnosis; D015148:Cardiotocography; D004569:Electroencephalography; D016057:Evoked Potentials, Auditory, Brain Stem; D005260:Female; D005315:Fetal Diseases / Q000175:diagnosis*; D006801:Humans; D007231:Infant, Newborn; D008607:Intellectual Disability / Q000209:etiology; D008279:Magnetic Resonance Imaging; D008297:Male; D011247:Pregnancy; D011782:Quadriplegia / Q000209:etiology; D013786:Thalamic Diseases / Q000209:etiology*