Cases reported "intracranial hemorrhages"

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1/234. Cerebral arteriovenous malformations and movement disorders.

    A series of six patients with movement disorders associated with cerebral arteriovenous malformations (AVM) is reported. The AVMs were classified according to the Spetzler-Martin classification as grade V (one patient), grade IV (four patients), and as grade III (one patient). One patient had action-induced hemidystonia caused by a contralateral frontoparietal AVM which compressed the putamen and was supplied partially by enlarged lenticulostriate arteries. Two patients presented with unilateral cortical tremor associated with contralateral high-frontal cortical/subcortical AVMs sparing the basal ganglia. Another patient developed hemidystonia and hemichorea-hemiballism after bleeding of a contralateral temporooccipital AVM and subsequent ischemia. Two patients had focal dystonia after thalamic and basal ganglia hemorrhage from AVMs. Five patients were operated on. The movement disorder was abolished in one patient postoperatively. Different mechanisms were identified that are relevant for the development of AVM-related movement disorders: mass effect, diaschisis, local parenchymal altered cerebral blood flow, and hemorrhagic or ischemic structural lesions. ( info)

2/234. Alpha1-antitrypsin deficiency with fatal intracranial hemorrhage in a newborn.

    A 4-week-old boy had a fatal intracranial hemorrhage resulting from vitamin k deficiency. The infant had received no vitamin K prophylaxis and was exclusively breastfed. At autopsy, examination of the liver showed cholestasis and fibrosis. dna was isolated from a blood spot on a Gutherie sample card obtained from the infant for routine metabolic screening. This dna was used for alpha1-antitrypsin genotyping studies. Genotyping studies identified homozygosity for the point mutation 9989G-->A, confirming a diagnosis of alpha1-antitrypsin deficiency (ZZ phenotype), and resulted in appropriate screening of siblings born after this child's death. Alpha1-antitrypsin deficiency should be considered in the differential diagnosis of infants with late hemorrhagic disease of the newborn. Use of blood from the metabolic screening card as a source of dna allowed confirmation of this diagnosis after the infant's death. ( info)

3/234. Antepartum diagnosis of fetal intracranial hemorrhage due to maternal bernard-soulier syndrome.

    BACKGROUND: bernard-soulier syndrome, a lack of glycoprotein IB/IX, is a rare autosomal recessive bleeding disorder characterized by platelet dysfunction. women with bernard-soulier syndrome are at risk of being immunized against glycoprotein IB/IX, leading to severe isoimmune neonatal thrombocytopenia. CASE: A 26-year-old Japanese woman, gravida 1, para 0, with bernard-soulier syndrome presented at 35 weeks' gestation with changes in fetal heart rate patterns and ultrasonographic findings that strongly suggested fetal intracranial hemorrhage. Management was by cesarean hysterectomy and bilateral salpingo-oophorectomy at 36 weeks, but the neonate died 6 hours after birth. CONCLUSION: Maternal immunization to glycoprotein IB/IX during pregnancy can cause severe fetal thrombocytopenia and massive intracranial bleeding. ( info)

4/234. Naming people ignoring semantics in a patient with left frontal damage.

    Studies about proper name anomia generally assume that persons' names are harder to recall than other semantic information one knows about them and that name retrieval is not possible without biographical knowledge. We describe a patient, SB, who, after a left frontal haemorrhage, was unable to recall any biographical information about people she could name. Moreover, she had a normal score in an Object Picture Naming Test, but gave confabulatory answers in a Semantic Questionnaire involving the same items. The role of frontal function in producing this pattern of impairment is discussed, together with the possible existence of a direct route from visual perception to proper name retrieval. ( info)

5/234. Late primary unilateral thalamic hemorrhage in infancy: report of two cases.

    We report on two infants with primary unilateral thalamic hemorrhage which occurred at two months of age. Both infants were normal prior to the onset of hemorrhage. Both children presented with seizures and subsequently developed epilepsy. These cases suggest that primary unilateral thalamic hemorrhage can occur in seemingly well infants outside the neonatal period. ( info)

6/234. Spontaneous intracranial hemorrhage as the presenting sign of hemophilia b in a 3-month-old infant.

    Intracranial hemorrhage (ICH) is an uncommon complication of hemophilia in the 1st year of life and most often is reported after head trauma or birth trauma. Spontaneous ICH unrelated to birth or head trauma is rare at any age, especially in the 1st year of life. We describe a 3-month-old infant who presented to the emergency department (ED) with a spontaneous ICH as the presenting sign of hemophilia b. We review the literature and discuss the ED evaluation and management of hemophiliacs with ICH. ( info)

7/234. Clinical manifestations of bacillus cereus meningitis in newborn infants.

    bacillus cereus (B. cereus) meningitis sometimes occurs in patients with risk factors, which are associated with central nervous system (CNS) anomalies, surgical or anaesthetic access to CNS. We observed two cases of B. cereus meningitis in neonates without such risk factors. The clinical courses of both neonates were fulminant, and routine antibiotic therapy failed. Intracranial haemorrhage was evident at autopsy. According to the previous neonatal case reports and our experience, we found that six of seven neonates were premature babies admitted to the neonatal intensive care unit, five died within a week of onset of the disease, and six had intracranial haemorrhage. We speculate that B. cereus meningitis may occur in neonates, even without any of the risk factors previously described in adult case reports, and that the clinical manifestations of the meningitis might be characterized by the high incidence of intracranial haemorrhage and poor mortality. ( info)

8/234. Neurogenic pulmonary edema induced by primary medullary hemorrhage: a case report.

    We report a case of neurogenic pulmonary edema occurring in association with primary medullary hemorrhage. A pervious healthy 28-year-old man suddenly developed severe dyspnea without cardiac failure. Radiographs and computed tomography of the chest showed pulmonary edema. A diagnosis of primary medullary hemorrhage was made some weeks later by cranial magnetic resonance imaging showing an area of low signal intensity in both T1- and T2-weighted images in the right ventrolateral, medial, and dorsal medulla, extending from low to mid levels. We suspect that edema surrounding the lesion had superimposed an element of left dorsal medullary dysfunction and that bilateral dorsal medullary involvement had induced neurogenic pulmonary edema. ( info)

9/234. Severe factor v deficiency and neonatal intracranial haemorrhage: a case report.

    We report a case of severe factor V (FV) deficiency (<1%) associated with multiple episodes of intracranial bleeding which presented at birth. The clinical course was further complicated by the development of an inhibitor, episodes of sepsis and cardiac failure. The management using virally inactivated FFP and platelets is discussed. ( info)

10/234. Clinical efficacy and recovery levels of recombinant FVIIa (NovoSeven) in the treatment of intracranial haemorrhage in severe neonatal FVII deficiency.

    The use of replacement FVII is critical to the successful treatment of life-threatening bleeds in newborns and infants with severe FVII deficiency (<1%). However, the clinical efficacy, optimum dosage and pharmacologic recovery of rFVIIa in such children has not been studied systematically. This report is a case of an infant with severe FVII deficiency (FVII:C at 0%) and massive intracranial haemorrhage in which successful use of rFVIIa (NovoSeven) was carefully monitored. The drug was administered by intravenous bolus through a central line every 4 h at each of three dose levels: 15 microg kg-1, 22 microg kg-1 and 30 microg kg-1. FVII:C was >100% between 30 and 180 min after each infusion with mean trough levels above 25% for all three dose levels. There was no evidence of hyper-coagulation as indicated by measurements of the platelet count, D-dimer, plasma protamine paracoagulant and fibrinogen levels in spite of high FVII:C concentration. In this infant, rFVIIa was well-tolerated, maintained effective haemostasis with good clinical outcome, and produced consistent therapeutic mean trough levels above 25% FVII:C even at 15 microg kg-1 every 4 h. ( info)
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