[Postpartum cerebral angiopathy of iatrogenic origin]
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Published on: June 18, 2021
J P Chartier1, J Y Bousigue, A Teisseyre
1Service de Neurologie, Centre Hospitalier Combarel, Rodez.
A 30 year old women, beginning her 19th day postpartum, was admitted for lowering of alertness. The day before she complained of cephalalagia. Neurologic examination showed pyramidal tract signs on the right part of the body, a bilateral Babinski sign, and central oculomotor palsy. She started a treatment by nasal pulverization of phenylephrine, a sympathomimetic vasoconstrictor, one week before, and took bromocriptine (5 mg per day) from childbirth to second week postpartum. CT scan was normal. Lumbar puncture showed a high level of proteins, from transsudative origin. Cerebral angiography showed a beading aspect of arterial branches, especially in the left middle cerebral artery territory. Two days after drug withdrawal, the patient recovered. This angiographic pattern has already been described in cases of cerebral angiopathy due to sympathomimetic drug abuse, and in cases of postpartum cerebral angiopathy. The chronology, in our case, makes the responsibility of the phenylephrine very likely. Nonetheless, ergot derivatives (i.e. ergonovine, bromocriptine) have also been accused of giving cerebral postpartum angiopathy. In our case, we think that bromocriptine may have triggered the cerebral angiopathy due to phenylephrine.
A 30 year old women, beginning her 19th day postpartum, was admitted for lowering of alertness. The day before she complained of cephalalagia. Neurologic examination showed pyramidal tract signs on the right part of the body, a bilateral Babinski sign, and central oculomotor palsy. She started a treatment by nasal pulverization of phenylephrine, a sympathomimetic vasoconstrictor, one week before, and took bromocriptine (5 mg per day) from childbirth to second week postpartum. CT scan was normal. Lumbar puncture showed a high level of proteins, from transsudative origin. Cerebral angiography showed a beading aspect of arterial branches, especially in the left middle cerebral artery territory. Two days after drug withdrawal, the patient recovered. This angiographic pattern has already been described in cases of cerebral angiopathy due to sympathomimetic drug abuse, and in cases of postpartum cerebral angiopathy. The chronology, in our case, makes the responsibility of the phenylephrine very likely. Nonetheless, ergot derivatives (i.e. ergonovine, bromocriptine) have also been accused of giving cerebral postpartum angiopathy. In our case, we think that bromocriptine may have triggered the cerebral angiopathy due to phenylephrine.
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