Background: Postpartum cerebral angiopathy is associated with the use of ergot alkaloids. The exact mechanism is unclear but may be related to their sympathomimetic properties, as evidenced in patients already on other ergot derivatives who deteriorated only after taking additional sympathomimetic drugs. We postulate that sympathomimetic agents, independent of ergot alkaloids, may produce the same complication.Case Description: A postpartum patient, initially presenting with headaches, subsequently manifested rapid neurological deterioration after ingesting isometheptene, a sympathomimetic drug. She was not on any ergot derivative but presented similar clinical and radiological manifestations. She experienced increased headache severity, visual disturbance, and seizures associated with multiple segmental cerebral vasoconstriction on angiography and increased T2-weighted signal in the occipital areas on magnetic resonance imaging.Conclusions: This case is additional evidence that sympathomimetic actions of some drugs, such as ergot derivatives and isometheptene, may lead to postpartum cerebral angiopathy. Documentation of medication used by postpartum women suffering similar complications is needed to verify these findings. (Stroke. 1993;24:2108-2110

Three women presenting with toxemia of pregnancy revealed reversible increased signal intensity on T2-weighted images by MRI. Overall, neuroradiologic techniques, with MRI the most sensitive, help elucidate the pathophysiology and facilitate the diagnosis in this condition.

We analyzed the results of neuroimaging studies in patients with periodic lateralized epileptiform discharges (PLEDs) or bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) for localization of lesions in gray or white matter to determine if "cortical isolation" is a critical mechanism in the pathogenesis of this phenomena. We assessed 32 patients who had undergone computed tomography (CT) exclusively and 8 patients who had undergone magnetic resonance imaging (MRI) with or without CT. The superior resolution necessary for adequate lesion localization allowed use of only the MRI scans from the 8 patients. Six patients had scans with cortical and subcortical gray and white matter lesions, and 1 patient had a cortical gray matter lesion only. One patient had an indeterminate scan. No patient had white matter lesions only. Our findings in patients with PLEDs and BIPLEDs correlate with postmortem data in patients with generalized periodic EEG patterns that show consistent localization of lesions in the gray matter. These findings do not support cortical isolation as the critical or sole mechanism in PLEDs or BIPLEDs.

We reviewed the EEG, clinical manifestations, computed tomography (CT) and magnetic resonance imaging (MRI) scans of 39 patients with periodic lateralized epileptiform discharges (PLEDs) or bilateral periodic lateralized epileptiform discharges (BIPLEDs) to determine the role of structural lesions (SL) and metabolic abnormalities (MA) in their pathogenesis. Thirty-eight patients had CT and 7 had MRI scans. Thirty-eight had lesions on CT or MRI. All those with PLEDs consistently had lesions on the side of the discharges, and 5 of 6 with BIPLEDs had lesions on both hemispheres. A subgroup of 23 patients with metabolic determination within 24 h of EEG all showed mild to moderate MA. They all also had SL. These findings support a primary role for SL but cannot exclude an additional role for MA.

A case of Möbius syndrome was associated with transposition of the aorta and pulmonary artery, as well as acheiria. This combination of anomalies supports the hypothesis that Möbius syndrome is caused by an intrapartum insult during the fourth to seventh week of gestation and is consistent with the vascular theory of embryopathogenesis.