Biomedical subjects

I A Awad

Publications and source records attributed to I A Awad.

114 records · Page 7Linked to original sources

PubMedDate not supplied

Incidental subcortical lesions identified on magnetic resonance imaging in the elderly. II. Postmortem pathological correlations.

The pathological correlates of subcortical lesions noted on magnetic resonance imaging (MRI) in the elderly are not known. Postmortem in vitro proton MRI was performed on the brains of seven consecutive elderly patients dying of nonneurologic causes. Scans were done in the fresh and fixed states with the specimen immersed in saline and formaldehyde respectively. A 1.5 Tesla superconductive system was used with a multiple spin-echo protocol generating T2 weighted images. Subcortical MRI lesions were localized in three dimensions and identified at brain cutting. In addition, pathological correlations were obtained from an eighth patient who underwent MRI eleven days before death. Histological examinations were performed in a blinded fashion, including control areas from the same brains. Subcortical MRI lesions were found to be associated with arteriosclerosis, dilated perivascular spaces, and vascular ectasia (p less than 0.05). These histological changes were characteristic of "état criblé" which, like subcortical MRI lesions, is associated with age and hypertension. Shrinkage (or atrophy) of the brain parenchyma around ectatic blood vessels would result in an extensive network of tunnels filled with extracellular water. The proton MRI signal from such areas of the brain would be increased. Gliosis and small areas of infarction occasionally coexisted with "état criblé," but these were not present in all areas with MRI lesions and could not be distinguished by MRI signal alone. In conclusion, clinical and pathological correlations lend support to the uniform hypothesis that MRI provides a nonspecific index of brain parenchymal alterations caused by aging and chronic cerebrovascular disease.

Age Factors↗

PubMedDate not supplied

Clinical vasospasm after subarachnoid hemorrhage: response to hypervolemic hemodilution and arterial hypertension.

Delayed neurologic deterioration from vasospasm remains the greatest cause of morbidity and mortality following subarachnoid hemorrhage. The authors assess the incidence and clinical course of symptomatic vasospasm following subarachnoid hemorrhage using a uniform management protocol over a 24-month period. One hundred eighteen consecutive patients were admitted to the neurovascular surgery service within 2 weeks of subarachnoid hemorrhage not attributed to trauma, tumor, or vascular malformation (113 patients had aneurysms). Early surgery was performed whenever possible, and hypertensive hypervolemic hemodilution therapy was instituted at the first sign of clinical vasospasm. Forty-two patients (35.6%) developed characteristic signs and symptoms of clinical vasospasm with angiographic verification of spasm in 39 cases. All patients with clinical vasospasm received hypervolemic hemodilution therapy aiming for a hematocrit of 33-38%, a central venous pressure of 10-12 mm Hg (or a pulmonary wedge pressure of 15-18 mm Hg), and a systolic arterial pressure of 160-200 mm Hg (120-150 mm Hg for unclipped aneurysms) for the duration of clinical vasospasm. Over the course of treatment, 60% of patients with clinical vasospasm had sustained improvement by at least 1 neurologic grade, 24% maintained a stable neurologic status, and 16% continued to worsen. At the end of hypervolemic hemodilution therapy, 47.6% had become neurologically normal, 33.3% had a minor neurologic deficit, and 19% had a major neurologic deficit or were dead. There were 3 instances of cardiopulmonary deterioration (7%), all of which were in patients without Swan-Ganz catheters, and all resolved with appropriate diuresis. One patient rebled and died while on hypervolemic hemodilution therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Quantification of temporal lobe resections: a new approach.

Extent of resection in temporal lobectomy has been traditionally based on intraoperative linear measurements. The complex geometrical contour of the temporal lobe limits the precision and accuracy of such measurements, and it is often difficult to verify the extent of actual resection after surgery. The authors propose a new method of evaluating extent of resection based on a 20-compartment model of the temporal lobe. The temporal lobe is divided into five anteroposterior coronal sections in relation to the anterior and posterior borders of the mesencephalon. Each section is then divided into superior lateral, inferior lateral, basal, and medial quadrants. The resulting compartments are easily identified on postoperative magnetic resonance images obtained along the coronal plane. Resection within each compartment is noted as none (0), partial (1), or complete (2). An index of resection can then be computed for superior lateral, inferior lateral, basal, and medial quadrants and for the whole temporal lobe. Potentially, this technique can be used to evaluate surgical failures and correlate extent of resection with surgical outcome and neurologic complications. It also allows objective and semiquantitative comparison of surgical approaches practiced at different institutions.

Anthropometry↗

PubMedDate not supplied

Experimental limbic epilepsy: models, pathophysiologic concepts, and clinical relevance.

Complex partial seizures originating in the temporal lobe are one of the most common types of seizures in patients with epilepsy. They are frequently intractable to medical treatment and are increasingly considered for surgical therapy. These seizures are often associated with focal epileptogenicity in limbic structures (amygdala and hippocampus) or with rapid spread of seizure activity to these areas. Much research is being undertaken to better understand this disorder and to develop more effective approaches to diagnosis and treatment. Experimental work in animals has contributed to the understanding of epileptogenesis, the interictal state, and the homeostatic mechanisms that limit seizure activity.

Aluminum Oxide↗

PubMedDate not supplied

Gardner's hydrodynamic theory of syringomyelia revisited.

Several theories have been put forth to explain the pathogenesis of syringomyelia, the formation of longitudinal, fluid-filled cavities within the spinal cord. Chief among them is Gardner's hydrodynamic theory, widely accepted for more than two decades. Gardner attributed the genesis of syringomyelia to craniospinal pressure differentials in the setting of fourth ventricular outlet obstruction; these differentials favor cerebrospinal fluid shifts from the fourth ventricle of the brain through the central canal of the spinal cord. Gardner's theory has been questioned, and several alternative theories of syringomyelia have been proposed. Physiological data and new information from magnetic resonance imaging support many of Gardner's concepts; however, a more comprehensive elucidation of the pathophysiologic mechanisms of syringomyelia requires incorporating facets of the other theories. We propose a unified theory of the pathogenesis of syringomyelia based on recent experience with magnetic resonance imaging, and on elements of other current theories.

Cerebrospinal Fluid Pressure↗

PubMedDate not supplied

Intensive care management of acute hemorrhagic leukoencephalitis with favorable neurologic outcome.

A 36-year-old woman who presented with acute hemorrhagic leukoencephalitis survived with favorable neurologic outcome. The patient underwent evacuation of a right temporal hematoma, with aggressive postoperative management in the neurosurgical intensive care unit. Aggressive surgical and medical therapy, including high-dose corticosteroid therapy and continuous intracranial pressure monitoring may yield favorable outcomes in an entity previously associated with dismal neurologic prognosis.

Acute Disease↗