Cerebral vasospasm and eclampsia.

Abstract

We describe a patient who experienced focal cerebral and brainstem ischemia in the setting of postpartum eclampsia. Cerebral angiography showed spasm of large-and medium-caliber arteries. This case provides rare documentation that vasospasm may account for cerebral ischemia in eclamptic women with focal signs. This observation suggests that in such patients cerebral angiography may be informative and useful. (Stroke 1988; 19:326-329) T he neurologic manifestations of preeclampsiaeclampsia include headache, visual disturbances including cortical blindness, generalized seizures, depressed alertness, and coma.12 Focal neurologic abnormalities are rare and, in the absence of parenchymal hemorrhage, their mechanism is uncertain. 3 We describe a patient with focal deficits in the context of eclampsia in whom we documented spasm of large-and medium-caliber cerebral vessels. This angiographic finding provides rare documentation that in such eclamptic patients vasospasm may be a mechanism of ischemic injury.Case Report A 27-year-old woman, gravida one (Gl), para zero (PO) in the 42nd week of gestation by dates, was admitted shortly after the onset of irregular contractions. Her blood pressure on admission was 120/70 mm Hg. She had 2 + pitting edema, mild hyperrefiexia, and 2 + proteinuria and was without complaint of headache, visual disturbance, or epigastric pain. Pitocin was administered because of minimal progress of labor. She had a normal spontaneous vaginal delivery 12 hours after admission. Fifteen minutes postpartum, she complained of headache, nausea, and epigastric pain. Blood pressure was 172/88 mm Hg. Magnesium sulfate was begun promptly with a loading dose of 4 mg i.v. followed by an infusion of 1.5 mg/hr, which was later increased to 2 mg/hr. Blood pressure initially rose to 190/102 mm Hg and then remained in the range of 160-170/85-90 mm Hg. The following morning, she was found stuporous. Blood pressure was 140/80 mm Hg; respirations were regular. She made no response to verbal stimuli but had purposeful spontaneous movements. No papilledema was evident. The pupils were 2 mm bilaterally and reacted to light. Left lateral gaze paralysis was noted with the oculocephalic (doll's head) maneuver and persisted after ice water calorics. Muscle stretch reflexes were slightly brisk and symmetric. The plantar responses were flexor. Magnesium sulfate was discontinued. A magnesium level was 5 (therapeutic range 3-6) meq/1. A cranial computedFrom the

Rituximab-related posterior reversible encephalopathy syndrome in HUS patient post kidney transplant

“…In some clinical settings, renal failure, sepsis, hypomagnesemia, and other metabolic disturbances may be responsible for the associated symptoms and radiologic findings [26][27][28].…”

Late Occurrence of Diffuse Cerebral Swelling After Intracerebral Hemorrhage in a Patient With the HELLP Syndrome. Case Report.

“…Symptomatic cerebral vasospasm may occur at up to 11 days after the onset of HELLP syndrome and preeclampsia. 6,8,19,24) Hypothermia, which systemically suppresses metabolism, may have delayed the onset of vasomotor dysfunction in our patient.…”

“…HELLP syndrome and preeclampsia are frequently associated with cerebral vasospasm, and the severe subarachnoid hemorrhage occurring with the intracerebral hemorrhage at onset could also have induced diffuse cerebral vasospasm. 6,8,12,15,19,24) Alternatively, cerebral venous or venous sinus thrombosis or embolism could have occurred because platelet count exceeded 800000/ml following her recovery from HELLP syndrome. Deep venous thrombosis has complicated another case of resolving HELLP syndrome.…”

“…2,7,10,14,17,21) Stroke involving cerebral vasospasm frequently complicates HELLP syndrome and severe eclampsia. 3,6,8,12,19) We report a patient with intracerebral hemorrhage associated with HELLP syndrome in whom hematoma evacuation was unexpectedly followed by late diffuse cerebral swelling.…”

Encefalopatia hipertensiva associada a estado de mal epiléptico de repetição: relato de caso

“…Existem duas hipóteses que visam explicar a fisiopatologia do edema. A teoria da "overregulation" consiste na hipótese de que um aumento brusco da pressão arterial promove vasoespasmo compensatório que, em situações especiais, é de intensidade suficiente para determinar isquemia e edema citotóxico 2,14 . A teoria mais provável indica como fator determinante para a formação do edema a quebra ("breakthrough") da auto-regulação da dinâmica vascular pela elevação intensa e súbita da pressão arterial, levando, portanto, à ultrapassagem dos limites pressóricos em que esta pode ocorrer.…”