Hemorrhage following mandibular osteotomies: a report of 21 cases

Hemorrhage associated with mandibular osteotomies, especially to the extent that it becomes life threatening, is a rare occurrence and its risk is less than that following maxillary orthognathic surgery. Twenty-one cases of significant bleeding following mandibular sagittal split ramus osteotomies, vertical and oblique ramus osteotomies, and genioplasties are presented. Life-threatening hemorrhage associated with mandibular osteotomies is primarily an intraoperative problem and the incidence of major postoperative and recurrent hemorrhage is not as great as following maxillary osteotomies. Suggestions for the avoidance and treatment of these bleeding complications are discussed.     

Spontaneous regression of a temporal arachnoid cyst

Surgery is considered to be the standard therapy for arachnoid cysts (ACs). We report the case of a 13-year-old boy in whom a right temporal AC disappeared spontaneously over a period of 10 years. Bulging of the right temporal skull led to the detection of the cyst by computed tomography (CT) scan at the age of 3 years. There were no other clinical symptoms. Subsequent CT scans showed spontaneous regression of the cyst without surgical intervention. The question as to how ACs should be treated is discussed.     

Variations in an assertive outreach model.

The author reviews recent research findings examining variations in an assertive outreach model. Mental health system and client characteristics that have influenced program implementation are discussed.     

Regulation of NGF gene expression in CNS glia by cell-cell contact.

Nerve growth factor (NGF) gene expression in central nervous system (CNS) glia appears to be associated with active glial growth. To study the underlying molecular mechanisms, we examined the effects of a number of growth-related factors on NGF mRNA expression in glial cultures. Our results suggest that glial membrane interaction, as a consequence of growth, actively inhibits NGF gene expression in CNS glia.     

Spatial restriction of light adaptation and mutation-induced inactivation in fly photoreceptors

The spatial spread within fly photoreceptors of 2 forms of desensitization by bright light have been investigated: the natural process of light adaptation in normal Musca photoreceptors and a receptor-potential inactivation in the no-steady-state (nss) mutant of the sheep blowfly Lucilia. The suction-electrode method used for recording from vertebrate rods was applied to fly ommatidia. A single ommatidium in vitro was partially sucked into a recording pipette. Illumination of the portion of the ommatidium within the pipette resulted in a flow of current having a wave form similar to that of the receptor potential and polarity consistent with current flow into the illuminated region of the photoreceptors. Two 5-microns slits of light, positioned at right angles to the ommatidial axis, were employed to determine the spread of light adaptation or inactivation along the ommatidium. The intensity of a flash of light delivered to one (adapting) slit was adjusted until it produced a criterion fractional reduction in the response to the other (test) slit. The reciprocal of this intensity of the adapting slit was taken as a measure of the effectiveness of the slit in causing light adaptation or inactivation. The effectiveness of the slit in causing light adaptation in normal Musca ommatidia fell as the adapting and test slits were moved farther apart along the ommatidial axis, declining to half its maximal value at a distance of 13 +/- 2 microns. Similar measurements of the effectiveness of a slit in causing light-induced inactivation in the nss mutant of Lucilia also demonstrated localization, declining to half its maximal value at a distance between the slits of 9 +/- 1 microns. Neither light adaptation nor inactivation by the nss mutation, therefore, appear to be mediated by voltage or by a highly diffusible agent. The results are consistent with the idea that inactivation by the nss mutation replaces adaptation in the mutant photoreceptors.     

A new method for producing temporary complete cerebral ischemia in rats

A new model of temporary complete cerebral ischemia was developed and tested in 64 rats. With use of microsurgical techniques, both pterygopalatine and external carotid arteries were occluded and the basilar artery was coagulated to reduce potential collateral CBF during ischemia. After this preliminary five-vessel occlusion, temporary global ischemia was induced by occluding the common carotid arteries (CCAs) with microclips. To validate the method, CBF was measured autoradiographically in 24 anatomical regions at death after 5 min of ischemia or after 15 min of ischemia followed by 5 min of reperfusion. Mean arterial blood pressure and arterial blood gases remained stable under controlled endotracheal ventilation and anesthesia (halothane, 70% N2O, and 30% O2) throughout the CBF experiments, except for a 10-15% increase in mean arterial blood pressure for 1-5 min after bilateral CCA occlusion. After the initial five-vessel occlusion, the EEG did not change, and local CBF levels were comparable to those in anesthetized non-surgical controls. When the CCAs were occluded, the EEG flattened rapidly; after 5 min of ischemia, autoradiography showed no detectable blood flow in the forebrain and cerebellum. The local CBF levels measured after 15 min of temporary global ischemia and 5 min of reperfusion demonstrated relatively homogeneous postischemic hyperperfusion; only two of eight rats had several 1- to 3-mm areas of no-reflow. Survival studies showed increasing motor impairment after 10, 15, 30, and 60 min of temporary CCA occlusion. Ischemic neuronal damage was observed histologically in the hippocampus and basal ganglia 24 h after 10 min of temporary ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ganglioside or sialic acid attenuates ethanol-induced decrements in locomotion, nose-poke exploration, and anxiety, but not body temperature.

1. This laboratory has previously reported that pretreatment with ganglioside, or even with its constituent, sialic acid (SA), can attenuate certain intoxicating effects of ethanol. It was important to see if these findings could be replicated, particularly by using other measures of ethanol effects. Herein we report that pretreatment with either gangliosides or SA attenuated ethanol-induced decrements in locomotion, nose-poke exploration, and anxiety, but not body temperature. 2. An ethanol dose of 4 gm/kg caused a temperature drop of about 3 degrees C, which was unaffected by any pretreatment. The onset to sleep, however, was delayed an average of 18 or 36 secs in mice pretreated with ganglioside or SA, respectively. Ethanol-only (4 gm/kg) depressed mean cumulative locomotor activity to 31% of normal, whereas the depression was 83% of normal with beef brain ganglioside pretreatment. At 2 gm/kg ethanol alone decreased nose poking in a hole-board test to 29% of normal, but the depression was only 55-63% of normal with SA or ganglioside pretreatment. In a staircase climbing anxiety test, this dose of ethanol had no effect by itself, but both ganglioside and SA pre-treatment increased climbing by 22%. Ethanol did depress rearing to only 11% of normal, whereas rearing was 51 and 99% of normal with SA and ganglioside pretreatment, respectively. In a dark-preference test, ethanol-only caused mice to spend 64% of the time in the light, compared to 31% for controls. Time in the light was only 39 and 46% with ganglioside and SA pretreatment, respectively. 3. Blood levels of ethanol were not significantly affected by pretreatment. 4. When given alone, gangliosides significantly stimulated locomotion and staircase climbing. SA significantly decreased rearing in the staircase test. Both gangliosides and SA tended to increase nose poking, number of crossings in the dark-preference test, and time in a lighted compartment. Thus, it is possible that some of the attenuation of intoxication is attributable to non-specific stimulant properties of gangliosides and SA.     

Critical illness polyneuromyopathy after artificial respiration.

Up to now, 71 critically ill patients have been reported with neuromuscular complications after artificial respiration. The authors review the literature and present data of a personal series of 22 patients all suffering from severe flaccid tetraparesis and muscle atrophy, which developed after an average of two weeks artificial respiration. The prognosis was relatively good in those surviving the primary disease. The multiconditional causes are discussed with emphasis on the combination of polyneuropathy and myopathy. Tumor necrosis factor (TNF), a key mediator of sepsis, which also has an influence on muscle and nerves, is mentioned as a possible cause of this illness.     

Widespread serum amyloid P immunoreactivity in cortical amyloid deposits and the neurofibrillary pathology of Alzheimer's disease and other degenerative disorders

Amyloid P (AP) component is present in all types of systemic amyloid deposits. Recently, it has been shown to be also present in cerebral amyloid lesions of Alzheimer's disease (AD). In this study, we used immunocytochemical methods to extend these findings at the electron microscope level and characterize the spectrum of AP immunoreactivity in neurofibrillary pathology (NFP) of AD and other neurodegenerative disorders including Down's syndrome (DS), Creutzfeldt-Jakob, Parkinson's, Pick's and diffuse Lewy body diseases and progressive supranuclear palsy. In AD and DS, AP immunoreaction product was evident in all the classical amyloid lesions and NFP in a large sample of all cortical areas examined. The distribution and relative intensity of immunostaining was similar to that of thioflavin S staining in serial sections. In many cases, however, plaques and vessels stained by anti-AP serum were not apparent with thioflavin S. Serial sections immunostained with antiserum to amyloid A, C-reactive protein or to other proteins involved in systemic amyloidoses and the acute phase response showed no evidence of staining in any of the cerebral lesions. Electron microscopy confirmed that AP immunoreactivity was associated with the abnormal filaments characteristic of NFP as well as amyloid fibrils found in plaques and vessels showing congophilic amyloid angiopathy. Plaques of Creutzfeldt-Jakob disease, Pick bodies of Pick's disease, tangles and Lewy bodies in Parkinson's disease and a subpopulation of Lewy bodies in the diffuse Lewy body disease coexistent with AD were also stained. With the exception of vessels in two of the five cases, AP was not detected in age-matched controls. Our observations indicate AP to be a consistent feature of cerebral NFP and amyloid deposits.