A series of 15 monochorionic twins with a great variety of cerebral lesions is reported. Seven cases illustrate the classical situation: the recipient twin was affected and his co-twin, the donor was macerated. In 5 cases, the lesions were described in the donor twin as well and once, as early as 22 weeks. The lesions were usually hypoxic-ischemic, in 2 they were hemorrhagic. In 1 case there was a malformation. Fetal US were performed in 11 cases and the diagnosis of either IUGR, death of a fetus and/or brain lesions in the survivor could be made in 10 cases and once as early as 21 weeks. In fetuses born alive, transfontanellar US or CT scan have confirmed the diagnosis made on fetal US. The pathogenesis of the lesions is not fully understood. Lesions in the recipient twin may result from emboli or thromboplastic material originating from the macerated co-twin. We suggest that blood pressure instability or episodes of severe hypotension might as well lead to brain and/or visceral lesions in the recipient twin. In the donor, the lesions result from hypotension and/or anemia. With improvement and generalization of imaging techniques, the vitality of the fetuses as well as biometric parameters and anatomical structures will be better controlled. However, in case of a fetal death, occurrence of lesions in the survivor is unpredictable and no uniform policy has been proposed yet. Studies with Doppler and continuous monitoring of funicular circulation should improve our knowledge on feto-fetal transfusion and permit to detect hemodynamic fluctuation or impairment.
We report 5 cases of abnormal cortical plate (polymicrogyria or microgyric-like pattern) and heterotopias associated with hypoxic-ischemic brain injuries in monochorionic diamniotic twin fetuses of respectively 22, 26, 28, 31, 32 weeks gestation. These fetuses belonged to a series of 5 pairs of patients (10 cases) presenting with the characteristic features of the twin-to-twin transfusion syndrome. Three of them (2 donors and 1 recipient) were macerated and the brains were not available for study. Two (most likely recipient twins) survived. In the remaining 5 fetuses (3 donors and 2 recipients) with neuropathological study there were cortical plate abnormalities. In 2 cases, the cortex was dysmorphic and consisted of focal nodular distribution or vertical stripes of neurons. True polymicrogyria was focal in 2 cases and involved almost the entire surface of the hemispheres in another one. Heterotopias of immature cells were found in 4 cases, either in the white matter or in the cortex or in both sites. There was a focal laminar necrosis only in 2 cases. The morphological pattern of the anomalies depends on the time of occurrence of the insult and on its severity. These abnormalities, although similar to those already described in singleton fetuses, illustrate the variety of cortical dysmorphia which may be associated with fetal hypoxic-ischemic injuries and emphasize the particular vulnerability of the brain in monozygotic twins, whether it belongs to the donor or the recipient.
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