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Biomedical subjects

J T Hoff

Publications and source records attributed to J T Hoff.

At least 73 records · Page 4Linked to original sources

Intracerebral infusion of thrombin as a cause of brain edema.

Purified thrombin from an exogenous source is a hemostatic agent commonly used in neurosurgical procedures. The toxicity of thrombin in the brain, however, has not been examined. This study was performed to assess the effect of thrombin on brain parenchyma, using the formation of brain edema as an indicator of injury. Ten microliters of test solution was infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later, and the extent of brain edema and ion content were measured. Concentrations of human thrombin as low as 1 U/microliter resulted in a significant increase in brain water content. Rats receiving 10 U/microliters had a mortality rate of 33% compared to no mortality in the groups receiving smaller doses. Thrombin-induced brain edema was inhibited by a specific and potent thrombin inhibitor, hirudin. A medical grade of bovine thrombin commonly used in surgery also caused brain edema when injected at a concentration of 2 U/microliters. Edema formation was prevented by another highly specific thrombin inhibitor, N alpha-(2-Naphthalenesulfonylglycyl)-4-DL-phenylalaninepiperidid e (alpha-NAPAP). Thrombin-induced brain edema was accompanied by increases in brain sodium and chloride contents and a decrease in brain potassium content. Changes in brain ions were inhibited by both hirudin and alpha-NAPAP, corresponding to the inhibition of brain water accumulation. This study shows that thrombin causes brain edema when infused into the brain at concentrations as low as 1 U/microliter, an amount within the range of concentrations used for topical hemostasis in neurosurgery.

Animals↗

The effects of blood or plasma clot on brain edema in the rat with intracerebral hemorrhage.

The causes and characteristics of the brain edema which forms adjacent to an acute intracerebral hemorrhage (ICH) have not been explored thoroughly. This study was designed to examine the edema process in rat brain provoked by two different blood clot components. An intracerebral clot was produced by stereotactic injection of 100 microl of either blood (bICH) or cryoprecipitate/thrombin (pICH) into the right caudate nucleus. Water, Na+, K+, and Cl- contents were measured at 0, 4.24, 48, and 72 h after instillation of the clot. During the first 24 h, the water content of the ipsilateral caudate nucleus and cortex gradually increased in both groups. By 48 h brain edema was more severe in the bICH compared to that with pICH in the ipsilateral basal ganglia and cortex. The edema formation was accompanied by significant increase in sodium and chloride, as well as a decrease in potassium content by 48 h and sustained to 72 h. These results suggest that both blood and plasma clots can cause brain edema, but a plasma clot is less damaging than a blood clot in the immediate vicinity of the mass.

Animals↗

Experimental intracerebral hemorrhage: relationship between brain edema, blood flow, and blood-brain barrier permeability in rats.

There have been few investigations of brain edema formation after intracerebral hemorrhage (ICH), despite the fact that mass effect and edema are important clinical complications. The present study was designed to investigate the time course for the formation and resolution of brain edema and to determine how changes in cerebral blood flow (CBF) and blood-brain barrier (BBB) permeability are temporally related to edema formation following ICH. Anesthetized adult rats received a sterile injection of 100 microliters of autologous blood into the caudate nucleus. Water and ion contents were measured immediately, at 4 and 12 hours, and daily to Day 7 (10 time points, six rats at each time) after experimental ICH. The water content of the ipsilateral basal ganglia increased progressively (p < 0.002) over the first 24 hours, then remained constant until after Day 5, when the edema began to resolve. Edema was most severe in the tissue immediately surrounding the hemorrhage; however, it was also present in the ipsilateral cortex, the contralateral cortex, and the basal ganglia. Measurements of local CBF (using [14C]-iodoantipyrine) and BBB permeability (using [3H]-alpha-aminoisobutyric acid) were obtained in separate groups of six to eight rats at various time intervals between 1 and 48 hours after ICH. Cerebral blood flow was reduced to 50% of control at 1 hour, returned to control values by 4 hours, but then decreased to less than 50% of control between 24 and 48 hours after ICH. The BBB permeability increased significantly prior to the occurrence of significant edema in the tissue surrounding the clot. However, BBB permeability in the more distant structures remained normal despite the development of edema. These results demonstrate a time course for the formation and resolution of brain edema following ICH similar to that observed during focal ischemia. Brain edema forms in the immediate vicinity of the clot as a result of both BBB disruption and the local generation of osmotically active substances and then spreads to adjacent structures. While local ischemia, due to the mass effect of the hemorrhage, may play a role in producing cytotoxic and vasogenic edema, the release of toxic substances from the clot should also be considered. Since edema is nearly maximal by 24 hours after ICH, therapy directed at reducing edema formation must be instituted within the 1st day.

Aminoisobutyric Acids↗

Toward better balance.

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.

Communication↗

Spinal epidural lipomatosis: two new idiopathic cases and a review of the literature.

Thoracic spinal epidural lipomatosis, a rare cause of myelopathy, is most commonly associated with exogenous corticosteroid use. The authors present the clinical, magnetic resonance imaging, computed tomography, and surgical findings for two patients with idiopathic epidural lipomatosis, successfully treated with decompressive laminectomy accompanied by fatty debulking, followed for > 3 postoperative years. They review the literature on idiopathic spinal epidural lipomatosis as well as cases associated with exogenous steroid use.

Aged↗

Stability of hearing preservation following acoustic neuroma surgery.

Identification of small acoustic neuromas has become commonplace. Frequently, affected individuals are identified prior to the development of significant hearing loss. Whereas many studies have focused on hearing preservation surgery, few have reported on stability of hearing results after resection of acoustic neuroma. Between 1985 and 1991, 36 patients underwent resection of an acoustic neuroma via a retrosigmoid, internal auditory canal approach with attempted hearing preservation. Hearing was preserved in 24 patients; 17 were available for testing for the present study. Follow-up ranged from 1.5 to 8 years. All patients underwent complete audiologic assessment; most patients also underwent auditory brainstem response testing. There was an average 6 dB increase in pure-tone average between early (1 month) postoperative and long-term postoperative test results. A binomial single subject statistic was used to assess for significant changes in speech recognition scores over time. In two subjects there was a significant decrease; however, speech recognition also improved significantly in two subjects. Five of the 17 subjects demonstrated either a significant (at least 15 dB) increase in pure-tone average or a significant decrease in speech recognition over the time-course of the study. All patients maintained usable hearing. We conclude that long-term hearing preservation is a realistic goal in selected acoustic neuroma operations.

Audiometry, Pure-Tone↗

Contributions of ions and albumin to the formation and resolution of ischemic brain edema.

Changes in brain water, sodium, potassium, and albumin contents and blood-brain barrier (BBB) permeability were determined at various times between 1 hour and 6 weeks following occlusion of the middle cerebral artery (MCA) in rats. In the center of the infarct, brain edema increased to a maximum level by 12 hours, remained elevated for 7 days, and then returned to normal. The change in water content was accompanied by a parallel increase in sodium and decrease in potassium contents; however, the increase in sodium always exceeded the decrease in potassium, resulting in a net gain in brain cations during edema formation which returned to normal with edema resolution. The BBB permeability to 3H-alpha-aminoisobutyric acid was increased by 24 hours after MCA occlusion and returned to normal by 1 week after the edema had resolved. The time course for changes in brain albumin content was different than that for brain edema formation. Large increases in brain albumin content were not apparent until 6 hours after the onset of ischemia, rose to a peak at 3 days after occlusion of the MCA, and returned to normal several weeks after the edema had resolved. Albumin appeared to spread from the central infarct zone to surrounding, less ischemic areas. The relative contributions of the osmotic force produced by the increase in brain cations and the oncotic force produced by the increase in brain albumin to the observed change in water content were calculated. At all time points, the increase in brain cations accounted for nearly all of the observed brain edema, while the increase in albumin played essentially no role in edema development.

Albumins↗

Neurogenic hypertension related to basilar impression. Case report.

The authors report the resolution of essential hypertension following transoral odontoidectomy and medullary decompression in a 39-year-old woman with basilar invagination. Current understanding of central regulation of the cardiovascular system is discussed and the pertinent neuroanatomy illustrated. Experimental and clinical evidence supporting the role of neurogenic mechanisms in the pathogenesis of hypertension is reviewed.

Adult↗

Middle cerebral artery occlusion in rats: a neurological and pathological evaluation of a reproducible model.

Middle cerebral artery occlusion (MCAO) in rats produces an infarct of varying size. We examined three factors that may influence this variability: animal weight, vascular anatomy, and extent of occlusion in rats undergoing MCAO. We also developed a four-point neurological evaluation scale and validated its usefulness by comparing it with a four-grade pathological determination of the size of the infarct. Of 82 animals subjected to a standard MCAO, 34 developed small cortical infarcts (pathological grades I-II; infarct size less than 25 mm2, 6-17% of the ipsilateral cortex surface area), and 48 large infarcts (pathological grades III-IV, infarct size greater than 25 mm2, 20-56% of surface area). We were able to predict the size of infarction from the neurological evaluation in 83% of the animals, and this accuracy reached 91% when grades I and II and III and IV were considered together (P less than 0.001). In 41 animals subjected to a more extensive vascular occlusion, 89% exhibited large infarcts. Four vascular patterns were identified but none played a significant role in the incidence or size of the cortical stroke. However, rats weighing less than 300 g showed a smaller lesion size than did rats greater than 300 g. Our proposed new MCAO technique appears useful in reproducing large-sized infarcts of the frontoparietal cortex.

Animals↗

Development of neurosurgery at the University of Michigan.

The University of Michigan Medical School was founded in 1847, 30 years after the university itself. The first hospital in Ann Arbor was a 20-bed unit converted from a private house, that admitted only charity patients. The second University Hospital was built in 1925. The Section of Neurosurgery was founded by Dr. Max Peet, who was followed by Drs. Kahn and Schneider as section heads.

History, 19th Century↗

Glossopharyngeal schwannoma: review of five cases and the literature.

Glossopharyngeal schwannomas are rare tumors in spite of the fact that acoustic schwannomas account for 8%-10% of intracranial tumors. There have been 23 reported cases in the literature. This report of five cases is the largest series of these tumors. The presentation, radiological workup, operation, and long-term postoperative results will be presented, along with a review of the literature.

Adult↗

Extravasation of albumin in ischaemic brain oedema.

Changes in brain water, sodium, potassium, and albumin contents and blood-brain barrier (BBB) permeability were determined between 1 hr and 42 days following occlusion of the middle cerebral artery in rats. Brain oedema was maximal 24 hrs, remained high for 3 days, and was resolved by 4 weeks. These changes in water content were accompanied by a parallel increase in sodium and decrease in potassium, however, the increase in sodium always exceeded the decrease in potassium so that there was a net gain in brain cations. BBB permeability to 3H-alpha-aminoisobutyric acid was normal for the first 4 hrs, but increased by 24 hr and returned to normal at 3 weeks. The time course for changes in brain albumin content was the same as that for BBB permeability and, at its greatest (3 days), the brain albumin was approximately 20% of the plasma albumin concentration. The relative contributions of the osmotic force produced by the increase in brain cations and the oncotic force produced by the increase in brain albumin to the observed change in water content were calculated. At all time points, the increase in brain cations accounted for nearly all of the observed brain oedema, while the increase in albumin played essentially no role in oedema development.

Aminoisobutyric Acids↗

Arachidonic acid metabolite production following focal cerebral ischemia: time course and effect of meclofenamate.

Arachidonic acid metabolites have been implicated in the development of cerebral edema following ischemia. To define the time course of metabolite production, subtemporal craniectomies were performed on 60 male Sprague-Dawley rats (350-400 g). Thirty rats underwent middle cerebral artery occlusion while 30 rats underwent craniectomy alone. Five rats in each of two groups (middle cerebral artery occlusion and sham) were sacrificed at 15 minutes, 1 hour, 4 hours, 1 day, 3 days, and 6 days. The cerebral hemispheres were removed and divided in the midsagittal plane. Each hemisphere was immediately frozen in isopentane cooled in dry ice and stored at -70 degrees C. Tissue prostaglandins E2 and 6-keto F1 alpha, and leukotrienes (LT) B4 and C4 were measured by radioimmunoassay. Prostaglandin E2 and 6-keto prostaglandin F1 alpha were significantly elevated at 15 minutes in the middle cerebral artery occlusion hemispheres (p less than 0.05). Prostaglandins were not significantly elevated after 15 minutes. LT B4 and C4 were never significantly elevated. Meclofenamate, a nonsteroidal anti-inflammatory agent, was administered to 21 additional rats. Seven controls underwent middle cerebral artery occlusion alone, 7 were given intraperitoneal meclofenamate (20 mg/kg) 30 minutes prior to middle cerebral artery occlusion, and 7 underwent middle cerebral artery occlusion followed immediately by intraperitoneal meclofenamate (20 mg/kg). The animals were sacrificed at 15 minutes and similarly studied. There was a significant reduction of prostaglandin E2 and 6-keto prostaglandin F1 alpha following pretreatment with meclofenamate (p less than 0.01 and p less than 0.05). In pretreated rats, leukotrienes were not affected by meclofenamate. Similarly, prostaglandins and leukotrienes did not change when meclofenamate was administered after middle cerebral artery occlusion. We conclude that cyclo-oxygenase metabolite production begins within 15 minutes of middle cerebral artery occlusion. Treatment with meclofenamate prior to middle cerebral artery occlusion significantly reduced cyclooxygenase metabolite production, suggesting a protective effect of meclofenamate against ischemia-induced elevations of vasoactive prostaglandins implicated in the development of cerebral edema. Lipoxygenase metabolite production was not affected by middle cerebral artery occlusion or pharmacological intervention.

6-Ketoprostaglandin F1 alpha↗

Management of anteriorly located C1-C2 neurofibromata.

The authors discuss their recent experience with anteriorly located C1-C2 neurofibromata in five patients with cervical myelopathy and magnetic resonance scans consistent with intradural extramedullary masses in this region. Surgery was performed using a posterolateral approach with microscopic intradural exploration. Gross total intradural tumor removal was achieved in all cases. Improvement in cervical myelopathy occurred in all patients. This report concludes that C1-C2 neurofibromata located anterior to the spinal cord can be totally and safely removed using a posterolateral approach. Improvement in neurologic dysfunction accompanies posterior decompression and gross total intradural tumor removal.

Adult↗