Brain CT (brain + ct)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Cerebral Embolism of Iodized Oil (Lipiodol) after Transcatheter Arterial Chemoembolization for Hepatocellular Carcinoma

JOURNAL OF NEUROIMAGING, Issue 4 2009
Joon-Tae Kim MD
ABSTRACT Cerebral lipiodol embolism is a rare complication of transcatheter arterial chemoembolization (TACE). Its pathological mechanism remains ambiguous despite several investigations. In Case 1, a 67-year-old man with hepatocellular carcinoma (HCC) experienced neurological deficits soon after undergoing a fourth session of TACE. Computed tomography (CT) scan showed multiple hyperdense lesions along the gyrus of frontal lobes and in the subcortical white matter. Transcranial Doppler (TCD) and transesophageal echocardiogram performed during the intravenous injection of agitated saline documented the presence of a right-to-left shunt (RLS) by demonstrating microbubbles in the left middle cerebral artery and left atrium. In Case 2, a 63-year-old woman underwent a third TACE due to a large HCC. After the procedure, her mental status deteriorated. Brain CT showed multiple hyperdense lesions on the cerebral and cerebellar cortex. TCD with agitated saline showed multiple microembolic signals shortly after the injection of agitated saline. The risk of cerebral lipiodol embolism may increase with recurrence and progression of HCC in patients who have a pre-existing RLS in the heart or lung. A test for the detection of an RLS may be necessary to identify patients with a heightened risk of cerebral embolism when multiple TACE procedures are required. TACE for HCC can cause pulmonary embolism or infarction.1,2 However, cerebral lipiodol embolism is rare after TACE. There have been several reports of cerebral embolism after TACE, but their exact mechanism has not yet been fully elucidated. We report herein 2 patients who developed cerebral lipiodol embolism after undergoing multiple TACE procedures for remnant HCC through a pre-existing RLS. [source]

Correlation of a high D-dimer level with poor outcome in traumatic intracranial hemorrhage

EUROPEAN JOURNAL OF NEUROLOGY, Issue 10 2007
J.-R. Kuo
The correlations between D-dimer and Glasgow Coma Scale (GCS), pupillary light reflex, distance of midline shift on brain computed tomography (CT), and Glasgow Outcome Score (GOS) in patients with trauma/non-trauma intracranial hemorrhage (ICH) are not consistent in studies. Ninety-eight traumatic and 59 non-traumatic ICH patients were studied. Pre-existing venous thrombosis, recent surgery, drug use (aspirin or coumadin), or malignancy, were excluded. D-dimer level was estimated within hours after acute insult, and statistical analyses were used for comparisons between groups. Traumatic ICH patients had higher D-dimer levels than controls (2984 vs. 256 ,g/l; P = 0.001). The GCS, midline shift on brain CT, pupillary reflex, and GOS at 3 months were significantly correlated with high D-dimer value in traumatic patients (individual P < 0.001), but not in the non-traumatic group. Using receiver-operating characteristic curve (ROC), the cutoff point was 1496 ,g/l, with sensitivity and specificity of 100% and 83%, respectively. D-dimer ,1496 ,g/l predicted a poor outcome [adjusted odds ratio (OR) 14.44, 95% CI 1.16,179.27; P = 0.038]. A high D-dimer level is associated with a poor outcome in patients with traumatic ICH. It can be used in addition to neurological assessment to predict the outcome. [source]

Bilateral common carotid occlusion without neurological deficit

JOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 4 2002
Serdar Karaköse
Summary A 40-year-old man presented with pain and numbness in his right arm. On his clinical examination, no neurological deficit was found. Bilateral common carotid artery duplex sonography scan demonstrated no flow in either lumen. No abnormality was recognized on brain CT. On cerebral digital substraction angiogram, total occlusion of the brachiocephalic trunk and left carotid artery were shown. There was a modest stenosis in the left vertebral artery. Collateral circulation feeding the intracranial carotid system mainly originated from the left vertebrobasilar system. Previous cases of bilateral carotid occlusion are reviewed and discussed. [source]

An immunohistochemical study on a tetanus fatal case using toxin fragment C (TTC).

NEUROPATHOLOGY, Issue 1 2009
Should it be a useful diagnostic tool?
A 65-year-old man fell in his garden and sustained a right pre-radial cutaneous laceration associated with a Colles' fracture. His status for tetanus immunization was uncertain; so a course of antitetanus treatment was immediately started. Two days after admission the man suddenly developed severe nucal pain, rigidity and dysphagia. A brain CT scan was negative. His condition progressively worsened and then he developed trismus. Cultures from the wound were negative for Clostridium tetani; the CSF analysis was negative. On the 9th day after admission, the man died. A presumptive clinical diagnosis of tetanus was made. Autopsy was performed 24 h after death. An immunohistochemical study was conducted with an antibody directed against tetanus toxin fragment C (TTC). By immunohistochemical evaluation, large motor neurons in the ventral horn were immunopositive for TTC. High power magnification of the ventral horn of spinal cord gray matter samples showed TTC immunoreactivity in motor neuron axons and cell bodies, using a confocal laser scanning microscope. The correct diagnosis could be established on the basis of pathological examination with TTC immunostaining. [source]

Peculiar venous lesions in fatal hyponatremic brain edema

NEUROPATHOLOGY, Issue 1 2005
Makoto Nishie
A 19-year-old woman with a 3-year history of schizophrenia suddenly began to vomit, and rapidly developed a coma an hour after the onset of vomiting. A brain CT scan showed diffuse brain edema with compression of the ventricles. Laboratory tests showed a low serum sodium concentration of 117 mmol/L. She died 67 h after the onset of the first symptom. A postmortem examination showed diffuse swelling of the brain with bilateral uncal and tonsillar herniations. Histologically, no necrotic, hemorrhagic or encephalitic changes were seen. However, microvacuolar changes with lymphocytic infiltration were found in the venous walls (media and adventitia) mainly in the basal ganglia, thalamus and brainstem. To our knowledge, this is the first demonstration of venous alterations in fatal hyponatremic brain edema. These changes may have participated in the exacerbation of the brain edema due to functional disturbance of venous drainage. [source]