Surgical treatment of internal carotid artery anterior wall aneurysm with extravasation during angiography--case report. (1/558)

A 54-year-old female presented subarachnoid hemorrhage from an aneurysm arising from the anterior (dorsal) wall of the internal carotid artery (ICA). During four-vessel angiography, an extravasated saccular pooling of contrast medium emerged in the suprasellar area unrelated to any arterial branch. The saccular pooling was visualized in the arterial phase and cleared in the venophase during every contrast medium injection. We suspected that the extravasated pooling was surrounded by hard clot but communicated with the artery. Direct surgery was performed but major premature bleeding occurred during the microsurgical procedure. After temporary clipping, an opening of the anterior (dorsal) wall of the ICA was found without apparent aneurysm wall. The vessel wall was sutured with nylon thread. The total occlusion time of the ICA was about 50 minutes. Follow-up angiography demonstrated good patency of the ICA. About 2 years after the operation, the patient was able to walk with a stick and to communicate freely through speech, although left hemiparesis and left homonymous hemianopsia persisted. The outcome suggests our treatment strategy was not optimal, but suture of the ICA wall is one of the therapeutic choices when premature rupture occurs in the operation.  (+info)

Aphasic disorder in patients with closed head injury. (2/558)

Quantitative assessment of 50 patients with closed head injury disclosed that anomic errors and word finding difficulty were prominent sequelae as nearly half of the series had defective scores on tests of naming and/or word association. Aphasic disturbance was associated with severity of brain injury as reflected by prolonged coma and injury of the brain stem.  (+info)

Acute hemorrhagic leukoencephalitis in patients with acute myeloid leukemia in hematologic complete remission. (3/558)

The authors describe the cases of three patients affected by acute myeloid leukemia, in complete remission, who rapidly developed neurologic symptoms leading to death. Neither clinical characteristics, nor radiological or microbiological procedures, allowed an etiological diagnosis of the neurologic syndrome. Post-mortem examination of the brain showed both macroscopic and microscopic findings compatible with acute hemorrhagic leukoencephalitis. The difficulty in distinguishing this entity from other CNS disease-related complications (e.g. leukemia infiltration, drug toxicity, hemorrhages) should not lead to an underestimation of the true incidence of this complication. We believe that with more attention to the possibility of this complication there would probably be both a greater possibility of collecting clinical informations about the real impact of this dramatic disease and a stronger hope of finding the right treatment for it.  (+info)

Delayed ischemic hyperintensity on T1-weighted MRI in the caudoputamen and cerebral cortex of humans after spectacular shrinking deficit. (4/558)

BACKGROUND AND PURPOSE: Transient internal carotid artery (ICA)-middle cerebral artery (MCA) occlusion caused by cardiogenic embolus can lead to spectacular shrinking deficit (SSD): sudden hemispheric stroke syndrome followed by rapid improvement. The aim of this study was to investigate sequential neuroradiological changes in the brains of patients after SSD compared with those after brief cardiac arrest and hypoglycemia, which we previously studied with the same methods. METHODS: We serially studied CT scans and MR images obtained at 1.5 T in 4 patients with SSD. All 4 patients suffered from transient neurological deficits due to cardiogenic embolus in ICA-MCA. The symptoms began to disappear from 25 to 50 minutes after onset. RESULTS: Repeated CT scans demonstrated no abnormal findings in the affected cerebral hemisphere in 3 of the 4 patients and a small cortical infarct in the remaining 1. In each patient, repeated MRI between day 7 and month 23 after stroke showed basal ganglionic and cortical lesions. These lesions were hyperintense on T1-weighted and relatively hypointense on T2-weighted imaging. These ischemic lesions of hyperintensity on T1-weighted MRI subsided with time. CONCLUSIONS: Transient ICA-MCA occlusion leading to SSD produces a specific ischemic change with delayed onset in the basal ganglia and cerebral cortex in humans on MRI but not CT scans. We speculate that the lesions represent incomplete ischemic injury, including selective neuronal death, proliferation of glial cells, paramagnetic substance deposition, and/or lipid accumulation. Unlike brief cardiac arrest or hypoglycemia, the localized lesions on MRI of patients after SSD seem to be incomplete and to differ from infarction or hemorrhage.  (+info)

Application of a rheolytic thrombectomy device in the treatment of dural sinus thrombosis: a new technique. (5/558)

We present a novel application of a transvascular rheolytic thrombectomy system in the treatment of symptomatic dural sinus thrombosis in a 54-year-old woman with somnolence and left-sided weakness. The diagnosis of bilateral transverse and superior sagittal sinus thrombosis was made and the patient was treated with anticoagulant therapy. After an initial period of improvement, she became comatose and hemiplegic 8 days after presentation. After excluding intracerebral hemorrhage by MR imaging, we performed angiography and transfemoral venous thrombolysis with a hydrodynamic thrombectomy catheter, followed by intrasinus urokinase thrombolytic therapy over the course of 2 days. This technique resulted in dramatic sinus thrombolysis and near total neurologic recovery. Six months after treatment, the patient showed mild cognitive impairment and no focal neurologic deficit. Our preliminary experience suggests that this technique may play a significant role in the endovascular treatment of this potentially devastating disease.  (+info)

Cerebral malaria versus bacterial meningitis in children with impaired consciousness. (6/558)

Cerebral malaria (CM) and acute bacterial meningitis (ABM) are the two common causes of impaired consciousness in children presenting to hospital in sub-Sahara Africa. Since the clinical features of the two diseases may be very similar, treatment is often guided by the initial laboratory findings. However, no detailed studies have examined the extent to which the laboratory findings in these two diseases may overlap. We reviewed data from 555 children with impaired consciousness admitted to Kilifi District Hospital, Kenya. Strictly defined groups were established based on the malaria slide, cerebrospinal fluid (CSF) leucocyte count and the results of blood and CSF culture and CSF bacterial antigen testing. Our data suggests significant overlap in the initial CSF findings between CM and ABM. The absolute minimum proportions of children with impaired consciousness and malaria parasitaemia who also had definite bacterial meningitis were 4% of all children and 14% of children under 1 year of age. The estimated maximum proportion of all children with impaired consciousness and malaria parasitaemia in whom the diagnosis was dual or unclear was at least 13%. The finding of malaria parasites in the blood of an unconscious child in sub-Saharan Africa is not sufficient to establish a diagnosis of cerebral malaria, and acute bacterial meningitis must be actively excluded in all cases.  (+info)

Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitive. (7/558)

Hypoglycemic injury in the mature brain is mediated by excitotoxicity, which is worsened by disordered cellular energy metabolism. The role of excitotoxicity in relation to brain energy metabolism during hypoglycemia has not been studied in the immature brain. Brain oxygen consumption (CMRO2) increases during hypoglycemia in piglets, whereas CMRO2 decreases in adult pig models. We tested the hypothesis that increased CMRO2 during hypoglycemic coma is temperature dependent and coincides with increased excitatory amino acids (EAA). We measured cerebral blood flow (CBF), CMRO2, and cortical microdiaysate EAA in pentobarbital-anesthetized piglets during hypoglycemic coma and during 2 h of recovery and in normoglycemic controls. In warmed animals brain temperature was kept normothermic (38.5 degrees C). In unwarmed animals brain temperature was allowed to fall (37.6 degrees C). During hypoglycemia CBF increased similarly in warmed animals and unwarmed animals; CMRO2 increased in warmed animals but not unwarmed animals. Glutamate increased during coma and increased more in warmed animals than unwarmed animals but normalized quickly during recovery. EEG recovered earlier in unwarmed animals. We conclude that during a hypoglycemic coma in the immature brain, CMRO2 and glutamate are increased in a temperature-dependent manner.  (+info)

Prevention of cerebral malaria in children in Papua New Guinea by southeast Asian ovalocytosis band 3. (8/558)

Southeast Asian ovalocytosis (SAO) occurs at high frequency in malarious regions of the western Pacific and may afford a survival advantage against malaria. It is caused by a deletion of the erythrocyte membrane band 3 gene and the band 3 protein mediates the cytoadherence of parasitized erythrocytes in vitro. The SAO band 3 variant may prevent cerebral malaria but it exacerbates malaria anemia and may also increase acidosis, a major determinant of mortality in malaria. We undertook a case-control study of children admitted to hospital in a malarious region of Papua New Guinea. The SAO band 3, detected by the polymerase chain reaction, was present in 0 of 68 children with cerebral malaria compared with six (8.8%) of 68 matched community controls (odds ratio = 0, 95% confidence interval = 0-0.85). Median hemoglobin levels were 1.2 g/dl lower in malaria cases with SAO than in controls (P = 0.035) but acidosis was not affected. The remarkable protection that SAO band 3 affords against cerebral malaria may offer a valuable approach to a better understanding of the mechanisms of adherence of parasitized erythrocytes to vascular endothelium, and thus of the pathogenesis of cerebral malaria.  (+info)

• 1
• 2
• 3
• 4
• 5
• 6
• 7
• 8
• 9
• 10