✓ The AANS was founded in 1931 as an educational and scientific organization whose principal purpose was to foster optimum neurosurgical care. Because socioeconomic and political pressures on medicine generally and neurosurgery specifically have escalated in recent years, the American Association of Neurological Surgeons (AANS) has been required to respond effectively to matters beyond its traditional role. However, the AANS has lacked an effective, focused policymaking process to deal with socioeconomic concerns despite existing expertise within the specialty. The AANS now needs to develop a comprehensive socioeconomic effort that is consistent with its more traditional educational and scientific activities. A Task Force on Governance has been appointed to address how the Association's governance structure can reflect all the needs of our specialty in times of economic uncertainty and health care reform.
The 1994 presidential address
Julian T. Hoff
Julian T. Hoff
Julian T. Hoff
✓ Cerebral protection from an ischemic/hypoxic insult implies that tissue injury can be controlled or even prevented by certain therapeutic maneuvers. For example, physiological thresholds may be altered so that tissue vulnerability to the insult is reduced, or the intensity of an insult may be blunted by enhancing brain homeostasis. Such a therapeutic maneuver is carotid endarterectomy to improve blood flow in the disordered hemisphere. Alternatively, drugs with protective properties can be used before or even after the insult to “stabilize” injured tissue and prevent the harmful secondary effects that often follow.
Various past and present approaches to cerebral protection employing physiological, pharmacological, and surgical intervention are reviewed. The mechanisms by which each allegedly protects the brain from ischemia and hypoxia are discussed briefly. Promising, but not always successful, approaches used in the past have pointed the way for new and more rational therapies. Truly effective protection of the brain from ischemia and hypoxia depends directly upon our capability to explore basic mechanisms of injury and our willingness to measure accurately and objectively the outcome of newly developed protective measures.
Julian T. Hoff
Julian T. Hoff and D. Gordon Potts
Julian T. Hoff and Bronson S. Ray
Julian T. Hoff and Merry Nishimura
✓ Hemorrhagic pulmonary edema was produced consistently in 19 of 20 anesthetized, paralyzed, ventilated cats when intracranial pressure (ICP) was raised for 30 minutes by intraventricular infusion of mock CSF to 150 mm Hg in 14, or 200 mm Hg in six. However, under identical conditions, except that ICP was raised to only 100 mm Hg, three of seven animals did not develop hemorrhagic edema of the lungs and the remaining four had spotty hemorrhage. Thirteen control animals with normal ICP had normal lungs. Gravimetric lung water analysis by Pearce's method confirmed gross and microscopic appearance of hemorrhagic pulmonary edema. Extravascular lung water (p < 0.05) and lung blood (p < 0.05) were significantly greater than control values when ICP was raised to or exceeded 150 mm Hg. Despite hemorrhagic edema, pulmonary gas exchange (O2, CO2) remained unaffected.
This animal model allows quantitative measurement of neurogenically-mediated hemorrhagic edema of the lungs before gas exchange is impaired. The model may facilitate clarification of the pathogenesis of neurogenic pulmonary edema and, consequently, refine evaluation of therapy.
Shizuo Hatashita and Julian T. Hoff
✓ Does an open skull alter the fundamental biomechanical properties of normal brain tissue? This question was studied in 32 anesthetized cats, 16 of which underwent a standard craniectomy (2.5 × 2.0 cm) in the left frontoparietal region. Brain tissue pressure, regional cerebral blood flow (rCBF), and brain water content were measured from the same area of cortical gray and white matter, and intracranial pressure (ICP) was recorded from the cisterna magna. Brain tissue resistance, tissue compliance, and the pressure-volume index were analyzed in response to a bolus injection of saline into brain tissue or the cisterna magna. Cerebrovascular resistance was also calculated.
In craniectomized animals 2 hours after surgery, ICP had fallen to 3.75 ± 0.39 mm Hg, and cortical gray and white matter tissue pressure had fallen to 3.19 ± 0.47 and 4.69 ± 0.54 mm Hg, respectively (mean ± standard error of the mean); these variables did not fall further over 4 hours. The pressure-volume index in the same animals increased significantly from 0.67 ± 0.01 to 0.86 ± 0.04 ml. Tissue compliance rose in the cortical gray matter but tissue resistance fell, approximating that found in subjacent white matter. There was no significant difference between animals with and without craniectomy in rCBF, cerebrovascular resistance, or brain water content in either gray or white matter.
These findings indicate that in the cat craniectomy causes an increase in the compensatory capacity of the intracranial cavity to increased volume. The data also indicate that cortical tissue has high hydraulic conductivity and compliance when the skull is opened.