Cerebral Computed Tomography (cerebral + computed_tomography)

Distribution by Scientific Domains


Selected Abstracts


rFVIIa, for acute rebleeding of a cerebral cavernous malformation

EUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2007
K. Engelhardt
Recurrent bleeding episodes of cavernomas especially in the brainstem can cause progressive neurological deficits. Therefore brainstem cavernomas are still a therapeutic dilemma and a treatment challenge for the neuro critical care community. We report a 39-year-old woman with spontaneous ataxia diplopia and vomiting, who has been treated for multiple intracerebral cavernomas during the last 10 years. A cerebral computed tomography (cCT) revealed a re-bleeding cavernoma in the left cerebral peduncle with consecutive obstructive hydrocephalus. As a result of the difficult anatomical location, no surgical approach was possible. As an off-label treatment, recombinant activated factor VII (rFVIIa) was administered to prevent possible further bleeding and especially further sequelae. The patient recovered well and no adverse events and especially no further bleeding of the cavernoma were observed. To our knowledge, this is the first report of the safe and successful use of rFVIIa to treat re-bleeding episodes in cavernomas. Further clinical studies are needed to specify the future potential of rFVIIa. [source]


Cerebral vasospasm and ischaemic infarction in clipped and coiled intracranial aneurysm patients

EUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2002
M. Hohlrieder
The influence of the treatment modalities (clipping/coiling) on the incidence of vasospasm and ischaemic infarction in aneurysm patients is still judged controversially. The purpose of this study was to analyse and compare retrospectively cerebral vasospasm and ischaemic infarction, as well as neurological deficits and outcome within a large population of clipped and coiled patients with ruptured and unruptured aneurysms. Within a 2-year period, a total of 144 interventions (53 clipping/91 coiling) entered the study. Daily bilateral transcranial Doppler sonographic monitoring was performed to observe vasospasm development. All cerebral computed tomography (cCT) and magnetic resonance imaging (MRI) scans were reviewed with respect to occurrence and localization of ischaemic infarctions. Focal neurological deficits were recorded and clinical outcome was evaluated using the Glasgow Outcome Scale. Statistical analysis included the use of multivariate logistic regression models to find determinants of vasospasm, ischaemic infarction and neurological deficits. Altogether, vasospasm was detected after 77 (53.5%) interventions, 61.8% in females (P < 0.01). Clipped patients significantly more often exhibited vasospasms (69.8 vs. 44.0%, P < 0.005) and were treated 1 week longer at the intensive care unit (P < 0.005). Seventy-seven patients (53.5%) developed ischaemic infarctions, 62.3% after clipping and 48.4% after coiling (P > 0.05). In the multivariate analysis, aneurysm-rupture was the strongest predictor for vasospasm and vasospasm was the strongest predictor for infarction. Neurological deficits at discharge (46.5%) were independent of treatment modality, the same applied for the mean Glasgow Outcome Scores. There was no significant difference in mortality between surgical and endovascular treatment (9.4 vs. 12.1%). Whilst the vasospasm incidence was significantly higher after surgical treatment, ischaemic infarctions were only slightly more frequent. The incidence of neurological deficits and clinical outcome was similar in both treatment groups. [source]


Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency

EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2001
S. Gabsi
Ataxia with vitamin E (Vit E) defciency (AVED) is an autosomal recessive disorder caused by mutations of the , tocopherol transfer protein gene. The Friedreich ataxia phenotype is the most frequent clinical presentation. In AVED patients, serum Vit E levels are very low in the absence of intestinal malabsorption. As Vit E is a major antioxidant agent, Vit E deficiency is supposed to be responsible for the pathological process. Twenty-four AVED patients were fully investigated (electromyography, nerve conduction velocity (NVC) studies, somatosensory evoked potentials, cerebral computed tomography scan, sural nerve biopsy, genetic studies) and supplemented with Vit E (800 mg daily) during a 1-year period. Clinical evaluation was mainly based on the Ataxia Rating Scale (ARS) for cerebellar ataxia assessment and serum Vit E levels were monitored. Serum Vit E levels normalized and ARS scores decreased moderately but significantly suggesting clinical improvement. Better results were noted with mean disease duration , 15 years. Reflexes remained abolished and posterior column disturbances unchanged. Vitamin E supplementation in AVED patients stabilizes the neurological signs and can lead to mild improvement of cerebellar ataxia, especially in early stages of the disease. [source]


Neuroimaging Determinants of Cognitive Performances in Stroke Associated With Small Vessel Disease

JOURNAL OF NEUROIMAGING, Issue 2 2005
V. Mok MD
ABSTRACT Background and Purpose. Controversies still exist as to the neuroimaging determinants of cognitive impairment in cerebral small vessel disease (SVD). The authors studied the neuroimaging correlates of cognitive performances among patients with stroke associated with SVD. Methods. The authors per formed cerebral computed tomography, magnetic resonance imaging, and diffusion-weighted imaging among 74 consecu tive patients admitted to the acute stroke unit because of stroke associated with SVD. They examined the association between cognitive performances and the following neuroimaging features: volume of white matter changes (WMC), multiplicity of lacunae, location of lacunae, total cerebral atrophy, and frontal and medial temporal lobe atrophy. Results. Apart from age and education, univariate linear regression analyses revealed that WMC volume, presence of thalamic lacunae, cerebral atrophy, and left frontal lobe atrophy predicted performance on the Mini-Mental State Examination while WMC volume, presence of thalamic infarcts, cerebral atrophy, and frontal lobe atrophy of both sides predicted performance on the Mattis Dementia Rat ing Scale-Initiation/Preservation subscale. In the multivariate analyses, education (R2= 0.22, P < .001), left frontal lobe atrophy (R2= 0.10, P= .004), and presence of thalamic lacunae (R2= 0.04, P= .049) were found to predict performance on the Mini-Mental State Examination while age (R2= 0.23, P < .001) and presence of thalamic lacunae (R2= 0.08, P= .011) were found to predict performance on the Mattis Dementia Rating Scale-Initiation/Preservation. Conclusions. Among patients with stroke associated with SVD, thalamic lacunae and frontal lobe atrophy are key determinants of cognitive performances. [source]