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Biomedical subjects

L L Sternau

Publications and source records attributed to L L Sternau.

8 recordsLinked to original sources
PubMed1997

Microvascular surgical anatomy of the vertebrobasilar junction.

OBJECTIVE: We examined the pertinent microvascular anatomy of 28 formalin-fixed brains to develop anatomic guidelines for aneurysm surgery in the region of the vertebrobasilar junction. METHODS: Using a surgical microscope, the outer diameters were observed for the following main arteries: vertebral, basilar, posteroinferior cerebellar, and anteroinferior cerebellar. The number of lower brain stem perforating arteries was examined in relation to their course. The distance between the arteries and their perforators was measured with respect to anatomic landmarks. RESULTS: The anatomy of the main arteries was characteristically variable, whereas the anatomy of the perforators was constant, particularly in terms of their numbers and points of penetration into the brain substance. The four major points of entry were the lateral medullary area just caudal to the posterior olivary sulcus, the posterior olivary sulcus, the small lateral fossa at the superior olivary groove, and the foramen cecum. Each of these areas coincides with the origin of common vertebrobasilar aneurysms. CONCLUSION: The anatomy of the main arteries was variable. In contrast, the perforators penetrated the adjoining brain stem at specific locations, regardless of the caliber of the main artery. Despite a small vertebral artery or its major branches, perforators penetrating the brain are significant and may effect the outcome of aneurysm surgery or endovascular procedures.

Adult↗
PubMed1995

CT-assisted percutaneous anterior cordotomy: technical note.

Percutaneous radiofrequency cordotomy remains a useful modality for managing selected patients with unremitting pain due to malignancy. Although the lateral C1-C2 method is widely used, certain clinical situations may call for a low anterior cervical approach via the disc space. The anterior method can be technically exacting due to the need for precision in the angle of approach at the point of disc space entry. Here we describe how CT-imaging can be used to simplify target localization during percutaneous anterior cervical cordotomy.

Cordotomy↗
PubMed1992

Therapeutic modulation of brain temperature: relevance to ischemic brain injury.

Hypothermia was first applied therapeutically as a local anesthetic and later was used to achieve organ protection during procedures necessitating circulatory interruption. Profound whole-body hypothermia, typically carried out in conjunction with extracorporeal bypass, has long been employed during cardiac and neurosurgical operative procedures. More recently, studies in small-animal experimental models of cerebral ischemia have provided persuasive evidence that even small decreases in brain temperature confer striking protection against ischemic neuronal injury. By contrast, small elevations of brain temperature during ischemia accelerate and extend pathologic changes in the brain and promote early disruption of the blood-brain barrier. Hypothermia retards the rate of high-energy phosphate depletion during ischemia and promotes postischemic metabolic recovery. More importantly, mild intraischemic hypothermia markedly attenuates the release of glutamate into the brain's extracellular space and significantly diminishes the release of dopamine. Similarly, the inhibition of calcium-calmodulin-dependent protein kinase II triggered by normothermic ischemia is prevented by hypothermia, as is the ischemia-induced translocation and inhibition of the key regulatory enzyme protein kinase C. Hypothermia also appears to facilitate the resynthesis of ubiquitin following ischemia. Studies of potential clinical importance have shown that moderate hypothermia is capable of attenuating ischemic damage even if instituted early in the postischemic period. In the setting of focal cerebral ischemia, moderate brain hypothermia reduces the infarct size (particularly in the setting of reversible middle cerebral artery occlusion); conversely, hyperthermia markedly increases the infarct volume. These studies underscore the importance of monitoring and regulating the brain temperature during experimental studies of cerebral ischemia to insure a consistent pathologic outcome and to avoid the false attribution of "pharmacoprotection" to drugs that reduce the body temperature. The measurement of brain temperature is now practicable in neurosurgical patients requiring invasive monitoring, and human studies have shown that cortical and cerebroventricular temperatures may exceed systemic temperatures. Mild to moderate decreases in brain temperature are neuroprotective in cerebral ischemia, while mild elevations of brain temperature are markedly deleterious in the setting of ischemia or injury. It is anticipated that controlled clinical trials of therapeutic brain temperature modulation will be undertaken over the next several years.

Body Temperature↗
PubMed1989

Role for gamma-aminobutyric acid in selective vulnerability in gerbils.

We tested the efficacy of various putative neuroprotective agents in the gerbil model of delayed neuronal death. The selective loss of anterior CA1 neurons of the hippocampus 4 days after 5 minutes of bilateral ischemia was complete in greater than 90% of the gerbils examined. We tested 11 agents for their ability to protect against neuronal loss. Only those agents that were associated with the GABAergic system exhibited protection and only when administered before the ischemic insult. The possibility that delayed neuronal death is the result of a primary defect in inhibitory neurotransmission is considered.

Animals↗
PubMed1988

A role for gamma-aminobutyric acid (GABA) in the evolution of delayed neuronal death following ischemia.

A series of putative neuroprotective agents was tested to determine their efficacy in preventing the loss of the CA 1 neurons of the hippocampus at 4 days following 5 min of bilateral ischemia in the gerbil. Agents associated with the GABAergic system were determined to be the most effective, but only when given prior to the ischemic episode, suggesting that there was a gamma-aminobutyric acid (GABA)-related event during ischemia which triggers the delayed neuronal death of these cells. In this report, the unidirectional release of GABA and glutamate from gerbil hippocampal slices was determined under conditions mimicking anoxia and/or ischemia. Pentobarbital, the most effective of the GABAergic agents, had little or no effect on the time-dependent release of glutamate. In contrast, pentobarbital reduced in release of GABA in both anoxia and ischemia, but only after 25 to 30 min of incubation.

Animals↗