Table 2 Summary of the postnatal follow-up of 10 fetuses with an abnormal corpus callosum (CC)
From: Retrospective analysis of the prognostic factors of fetal corpus callosum dysplasia
case | diagnostic GA | Diagnosis of CC | other abnormalities | CMA | WES | Follow-up duration(months after birth) | Postnatal outcomes |
|---|---|---|---|---|---|---|---|
1 | 33 | thin CC | NO | NO | NO | 16 | normal |
2 | 21 | thin CC | NO | normal | NO | 8 | gross movements were more sluggish |
3 | 23 | thin CC | NO | normal | NO | 18 | normal |
4 | 37 | the rostral absent | NO | NO | NO | 3 | normal |
5 | 25 | the splenium absent | NO | normal | NO | 5 | normal |
6 | 36 | short CC | Cerebral hemorrhage | NO | normal | 12 | continuous excessive dorsiflexion of both ankle joints |
7 | 34 | thin CC | lateral ventriculomegalyand the ventricular wall was irregular | normal | NO | 12 | epilepsy and delayed motor development |
8 | 25 | thick CC | MCD | normal | NO | 9 | ambiguous articulation and delayed motor development |
9 | 38 | short CC | microcephaly | A possible pathogenic CNV of 29.76 Mb was identified at del(5)(p15.33p13.3)(chr5:24 261-2978284 6) in seq [GRCH37] | died 10 days after birth | ||
10 | 32 | short CC | Severe ventriculomeg-aly | normal | A variant in the ADNP gene was identified and associated with the following diseases: HELSMOORTEL-VAN DER AA syndrome | 24 | ambiguous articulation and delayed motor development, poor rehabilitation treatment |
11 | 37 | thin CC | pericallosal lipoma | normal | normal | 8 | normal |
12 | 34 | thin CC | NO | normal | normal | 4 | normal |
13 | 26 | thin CC | NO | normal | normal | 8 | normal |