Sodium metasilicate affects growth of Salmonella Typhimurium in fresh, boneless, uncooked chicken breast fillets stored at 4°C for 7 days.

The objectives of this study were to determine the antimicrobial effects of sodium metasilicate (SMS) against Salmonella and psychrotrophic organisms in fresh, boneless, uncooked chicken breast fillets and to ascertain the effects of SMS treatments on pH. Chicken breast fillets were inoculated with Salmonella enterica serovar Typhimurium treated with 0% SMS and no inoculum (negative control), 0% SMS and inoculum (positive control), 1% SMS, or 2% SMS solutions and stored at 4 ± 1°C. All samples were analyzed after 0, 1, 3, 5, and 7 d for Salmonella, psychrotrophic organisms, and pH. The fillets that were treated with 1 or 2% SMS had lower (P < 0.05) Salmonella counts as compared with those of the positive control at 3 through 7 d. Reductions in Salmonella Typhimurium were 0.83 to 0.91 log cfu/g and 1.04 to 1.16 log cfu/g for 1 and 2% SMS treatments, respectively. The psychrotrophic counts were similar (P > 0.05) for all treatments. The pH values for samples treated with 1 or 2% SMS were higher (P < 0.05) when compared with those of the negative and positive controls. This study revealed that SMS could restrict the growth of pathogenic Salmonella Typhimurium in fresh poultry.

Sodium metasilicate affects growth of Campylobacter jejuni in fresh, boneless, uncooked chicken breast fillets stored at 4 degrees Celsius for 7 days.

The objectives of this study were to determine the antimicrobial effects of sodium metasilicate (SMS) treatments against Campylobacter jejuni in fresh, boneless, uncooked chicken breast fillets and to ascertain the effects of SMS treatments on pH. The fillets were inoculated with C. jejuni, treated with 0% SMS and no inoculum (negative control), 0% SMS and inoculum (positive control), 1 and 2% SMS solutions, and stored at 4 ± 1°C. All samples were analyzed after 0, 1, 3, 5, and 7 d storage for C. jejuni, psychrotrophic organisms, and pH. Campylobacter jejuni and psychrotrophic counts for samples treated with 1 and 2% SMS solutions were similar (P > 0.05) to the positive control on all storage days. The pH values for 2% SMS marinade treatments were higher (P < 0.05) when compared with the negative and positive controls through 7 d of storage. Based on the findings in this study, a second study was conducted to determine the level of SMS necessary to reduce C. jejuni by at least 1 log cfu/g. The treatments were the same as previously discussed, except SMS was used at levels of 1 and 2% of the weight of the meat instead of percentage of the solution. Chicken fillets treated with 1 and 2% SMS (by weight of meat) resulted in 1.12 to 1.26 and 3.27 to 3.79 log cfu/g reductions in C. jejuni, respectively, when compared with the positive control. Except for d 0, psychrotrophic counts for samples treated with 2% SMS were lower (P < 0.05) than negative and positive controls on all storage days. The pH values were higher (P < 0.05) for all SMS treatments when compared with the negative and positive controls. This study revealed that SMS, when used at elevated levels in excess of the USDA Food Safety and Inspection Service 2% approved level, could function to control Campylobacter jejuni and extend the shelf life of raw poultry by retarding the growth of psychrotrophic bacteria.

Regional patterns of blood-brain barrier breakdown following central and lateral fluid percussion injury in rodents.

In order to determine how fluid percussion injury (FPI) effect is distributed throughout the brain, and to assess the extent to which individual brain nuclei and regions are affected, the pattern of blood-brain barrier (BBB) breakdown was determined in groups with different injury cannula locations. Injury cannulas were placed either at midline, or 2 or 4 mm to the side. One hour following FPI, animals were given horseradish peroxidase (HRP) and the brains were stained using the TMB method. The distribution of HRP leakage varied considerably depending upon the location of the injury cannula, however, there were also common sites of leakage among these groups. Locally the cortex and hippocampus under and adjacent to the injury cannula were heavily affected, with a clear asymmetric effect in the lateral cannula groups. Common sites of leakage included the dorsal thalamus, septal area, pontine tegmentum, periaqueductal gray, substantia nigra, and narrow zones adjacent to ventricular or cisternal surfaces. The hippocampus tended to be involved at greater distances than the cerebral cortex. The cervicomedullary junction proved to be especially vulnerable to FPI with extensive HRP leakage, and petechial hemorrhage ranging from minor to fatal coalescent hemorrhage. A very narrow threshold separated these outcomes. Neurologic impairment of the animals correlated most directly with the extent of cervico-medullary junction injury. Thus FPI produces a mix of local and diffuse effects on the BBB. Injury at the cervicomedullary junction is a prominent effect and is the limiting factor in trying to establish more severe diffuse injury.

Time course for recovery of water maze performance and central cholinergic innervation after fluid percussion injury.

This study further investigates the possible connection between postconcussive cognitive impairment and damage to forebrain cholinergic innervation. Moderate parasagittal fluid percussion injury was delivered to adult male rats. Water maze performance and synaptosomal choline uptake was measured at various times following injury. Water maze learning was severely impaired between 1 and 5 weeks, but recovered to normal by 10 weeks. Synaptosomal choline uptake was significantly decreased by 15-27% in the ipsilateral hippocampus and parietal cortex 3 and 7 days following injury, but not by 3 weeks or thereafter. Choline acetyltransferase was also significantly decreased in the ipsilateral cortex at 3 and 7 days with subsequent recovery. This study shows that parasagittal fluid percussion injury causes significant impairment in water maze learning and ipsilateral forebrain cholinergic innervation. Both of these parameters recover spontaneously, but with different time courses.

Cognitive impairment and synaptosomal choline uptake in rats following impact acceleration injury.

Traumatic brain injury is well known to cause deficits in learning and memory, which typically improve with time. Animal studies with fluid percussion or controlled cortical impact injury have identified transient disturbances in forebrain cholinergic innervation which may contribute to such cognitive problems. This study examines the extent to which water maze performance and forebrain synaptosomal choline uptake are affected one week after injury using the newly developed impact acceleration injury model. Injury or sham injury was delivered to adult male Sprague-Dawley rats under halothane anesthesia using a 500-g 2.1-m weight drop. Based on righting reflex, injured rats were divided into moderate (< or = 12 min) or severe (>12 min) groups. Water maze testing was performed on days 5-7 postinjury. On day 7, choline uptake was determined in synaptosomes from hippocampus, a parietal cortex, and entorhinal cortex. Maze learning was severely impaired in the severe injury group but not in the moderate injury group. Learning retention was slightly impaired in the moderate injury group and severely affected in the severe injury group. There was a very strong correlation between the severity of injury as determined by prolongation of righting times and disruption of maze learning at 1 week postinjury. There was no change in synaptosomal choline uptake in any of the forebrain regions in the severe injury group, but a slight (14%) decrease in the hippocampus and parietal cortex of the moderate injury group. Correlation analysis showed no relationship between synaptosomal choline uptake in any brain region and performance in either water maze learning or retention. This study shows that the impact acceleration model produces cognitive impairments equivalent to those seen with fluid percussion injury and controlled cortical impact. Compared with those models, the impact acceleration model does not produce a similar disruption of forebrain cholinergic nerve terminals.

Recovery of water maze performance in aged versus young rats after brain injury with the impact acceleration model.

Clinically, elderly patients have a higher cognitive morbidity from head trauma than young patients. We have modeled injury in aged rats in an effort to elucidate the pathophysiology of this enhanced sensitivity and, in particular, to determine if there are susceptibility differences in forebrain cholinergic innervation in young versus aged rats. Aged (20-23 months) and young (2-3 months) rats were subjected to injury under halothane anesthesia using the Marmarou impact acceleration model. Injury parameters required adjustment downward for the aged rats (323 g at 1.61 m versus 494 g at 2.06 m) to provide equivalent mortality (30% versus 20%) and loss of righting-reflex times (10-12 min average). At 1 week following injury, the aged animals were markedly more impaired in water maze performance than were young rats, and this difference persisted at least up to 5 weeks following injury. The extent of improvement in performance from 1 to 5 weeks was markedly worse for aged animals compared to young animals. Forebrain synaptosomal choline uptake was decreased in aged injured rats by 8-14% at 1, 3, and 5 weeks postinjury, but not decreased in young injured rats. No differences were noted in entorhinal cortex or hippocampal choline uptake. This model effectively demonstrates the markedly increased susceptibility of older animals to head injury and their decreased capacity for recovery. The neurophysiological basis for this difference is presently unknown, but the differences in cognitive dysfunction between young and aged rats appears to be much greater than would seem to be explained by the small differences in forebrain cholinergic innervation.

A computer-based rotation and activity monitor for non-human primates and other animals.

Because a unilateral lesion of the dopaminergic nigrostriatal system has been found to induce rotational behavior in primates, as well as in rodents, we have designed and constructed a rotation monitoring device suitable for non-human primates. Animals are connected via a tether to a continuous-rotation potentiometer which provides a position-dependent output voltage. This voltage is interfaced via an analog-to-digital converter to an IBM PC. The rotation program then calculates the direction and amount of any turning, as well as total activity, and this data is recorded on diskfile for later analysis. Because the system can operate around the clock unattended, data can be collected over long experimental periods, and detailed circadian analysis of rotation and total activity can be made. The design is also applicable to smaller animals, including rodents, and has many advantages over previously available rotometer designs.

Regional development of norepinephrine, dopamine-beta-hydroxylase and tyrosine hydroxylase in the rat brain subsequent to neonatal treatment with subcutaneous 6-hydroxydopamine.

Neonatal rats were injected subcutaneously with 100 mg/kg 6-hydroxydopamine (6-OHDA), or vehicle, on postnatal days 1, 2 and 3. At several times thereafter, determinations of tyrosine hydroxylase (TOH) and dopamine-beta-hydroxylase (DBH) activities, and norepinephrine (NE) concentration were made in the parietal cortex, cerebellum and pons-medulla in order to assess the extent of initial noradrenergic degeneration induced, and the rate of any ensuing regeneration. By the day following completion of the treatment (postnatal day 4), degeneration of noradrenergic terminals in the parietal cortex and cerebellum was very extensive, with NE levels and DBH activities reduced by more than 80%, and TOH activities reduced by 50%. In the parietal cortex noradrenergic degeneration remained virtually complete; and 9 and 70 days postnatal NE concentration and DBH and TOH activities were all decreased by more than 90--95%. In the cerebellum a progressive regeneration and apparent sprouting of NE fibers was observed. By postnatal day 9, NE, DBH and TOH in this tissue had all recovered to near control levels, and by day 70 these measures exceeded control levels by 95%, 115% and 50% respectively. In the pons-medulla, the initial effect of 6-OHDA on any of the measured parameters was negligible. By postnatal day 9 an increase in NE concentration was apparent, which increased further by day 70 to surpass the control level by 70%. At this same time DBH activity was increased by only 15% and TOH activity was unchanged. Separate analysis of the rostral half of the pons, which contains the locus coeruleus, revealed that on day 70 NE and DBH levels were increased much more substantially than in the whole pons-medulla, and TOH activity was also significantly elevated. This data indicates that the initial amount of degeneration induced by the 6-OHDA treatment is similar in both the parietal cortex and cerebellum, but regeneration proceeds only in the cerebellum. This suggests that noradrenergic fiber growth and regeneration in each target tissue is under independent regulation, possibly by the individual target neurons themselves.

Assessment of the effects of neonatal subcutaneous 6-hydroxydopamine on noradrenergic and dopaminergic innervation of the cerebral cortex.

Female rats, treated at birth with 6-hydroxydopamine (3 x 100 mg/kg s.c. at 24 h intervals) or vehicle, were subjected at 112 days of age to unilateral electrolytic lesions of the locus coeruleus. Two weeks later regions of the telencephalon, both ipsi- and contralateral to the lesion, were simultaneously assayed for norepinephrine (NE) and dopamine (DA) content, and for tyrosine hydroxylase (TOH) and dopamine-beta-hydroxylase (DBH) activities. In the vehicle-treated rats the lesion resulted in at least an 80% reduction of NE and DBH on the ipsilateral side, relative to the contralateral side. TOH was reduced to a similar extent only in the parietal cortex and hippocampus. In the prefrontal cortex and cingulate gyrus TOH was decreased by only 31% and 64% respectively; the remainder was interpreted to be associated with projections of the mesocortical dopamine system. From this data it was possible to calculate that the ratio of TOH to DA in dopaminergic terminals is about 10-fold greater than the ratio of TOH to NE in noradrenergic terminals. Neonatal 6-hydroxydopamine treatment resulted in practically total elimination of noradrenergic terminals throughout the telencephalon, and the locus coeruleus lesion had no additional effect. The drug treatment produced no significant change in DA content or in the TOH to DA ratio in the prefrontal cortex and cingulate gyrus, indicating complete sparing of the mesocortical DA projections.

Distribution of hypertrophied locus coeruleus projection to adult cerebellum after neonatal 6-hydroxydopamine.

Following treatment as neonates with a high subcutaneous dose of 6-hydroxydopamine (6-OHDA), the projections of the locus coeruleus were mapped in the brains of adult rats. This was done using the technique of unilateral lesions in the nucleus followed by simultaneous determinations of norepinephrine (NE) levels, dopamine-beta-hydroxylase (DBH) activity and synaptosomal [3H]NE uptake in various terminal areas. In particular the cerebellum was subdivided into 3 areas in order to assess any changes from normal in the distribution of the hypertrophied noradrenergic projections here. In vehicle-control rats the lesions resulted in an 80--85% loss of NE in the parietal cortex ipsilateral to the lesion and a 15--20% loss contralaterally. In the control cerebellum the locus coeruleus projection, based upon changes in all 3 markers, is distributed 2/3 ipsilaterally and 1/3 contralaterally with the same pattern present in all 3 subregions. The neonatal 6-OHDA treatment resulted in virtually complete loss of noradrenergic terminals in the cerebral cortex. Following neonatal 6-OHDA treatment cerebellar levels of NE, DBH and [3H]NE uptake increased by between 20--60%, with the smallest increases occurring in [3H]NE uptake. In these rats the locus coeruleus accounted for at least 75--80% of the cerebellar noradrenergic parameters. Unlike control rats however, the lesions in these rats produced only ipsilateral decreases in NE and DBH. On the other hand changes in [3H]NE uptake indicated a normal 2/3 ipsilateral, 1/3 contralateral pattern. It is suggested that two separable events occur in the noradrenergic projection to the cerebellum. The first is the regeneration of an increased number of nerve terminals, or sprouting, and the second is a build-up of synaptic vesicles, or collateral accumulation. The sprouting, judging from the [3H]NE uptake data, occurs with apparently normal distribution, but the accumulation of NE and DBH is confined predominantly to the ipsilaterally projecting axon terminals. This may be the consequence of collateral accumulation resulting from the degeneration of the largely ipsilateral coeruleocortical projection.

Intracerebral grafting of dissociated CNS tissue suspensions: a new approach for neuronal transplantation to deep brain sites.

Suspensions of central nervous tissue, prepared by dissociation of selected embryonic brain regions, may be viably transplanted by intraparenchymal injection into a variety of sites in the depth of adult rat host brains. Such grafted neurons can mediate considerable reinnervation of a previously denervated brain region, and they can replace neurons intrinsic to a particular target, such as the caudate-putamen, previously damaged by the neurotoxin kainic acid. The present technique should open entirely new possibilities for experiments on neuronal reconstruction following brain lesions.

Prefrontal cortex: dense dopaminergic input in the newborn rat.

Using a recently introduced modification of the aluminum-formaldehyde histofluorescence method, in combination with exogeneous administration of alpha-methylnoradrenaline and biochemical analyses, a remarkably advanced development of the dopaminergic and noradrenergic afferent to the frontal lobe has been demonstrated in neonatal rat. At birth, the density and general distributional pattern of the catecholamine innervation was similar to that found in the fully developed prefrontal cortex. The previously not recognized, early and extensive maturation of the mesocortical dopamine projection suggests a functional role of dopamine already in the early postnatal period.

Effects of morphine on sprouting of locus coeruleus fibers in the neonatal rat.

Acutely (by 48 h), as well as after one month survival, morphine (20 mg/kg) significantly potentiated the extent of noradrenergic degeneration in the forebrain of newborn rats caused by 50 mg/kg of 6-hydroxydopamine (6-OHDA) s.c. This was associated with increased regenerative sprouting in the cerebellum and pons-medulla as determined by measurements of norepinephrine (NE) concentration and [3H]NE uptake. This potentiating effect of morphine was not seen in either forebrain, brainstem, or cerebellum if it was administered to newborn rats with a 24-h delay following 6-OHDA. Clonidine (0.1 mg/kg) which, like morphine, decreases locus coeruleus activity, acutely tended to enhance the acute degenerative effects of 6-OHDA, whereas yohimbine (5 mg/kg), an alpha 2-antagonist which increases locus coeruleus activity, significantly attenuated the acute effect of 6-OHDA in the forebrain. In order to determine whether morphine directly alters the regenerative growth of neurons independently of its acute interaction with 6-OHDA, we explored its effect on the collateral sprouting of locus coeruleus projections induced by midcollicular hemisection. Unilateral midcollicular hemisection in neonates resulted, at 2 months of age, in a 91% reduction of NE concentration in the ipsilateral forebrain and an increase in the ipsilateral cerebellar hemisphere to over 200% of control. Significant increases of a slightly smaller magnitude were found in the cerebellar vermis, pons-medulla and the colliculi. Morphine given simultaneously with the lesion significantly attenuated this collateral sprouting in the cerebellar hemisphere and colliculi. These results indicate that morphine potentiates the initial toxicity of 6-OHDA, perhaps by altering activity of locus coeruleus neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Regenerative critical periods for locus coeruleus in postnatal rat pups following intracisternal 6-hydroxydopamine: a model of noradrenergic development.

Rat pups were injected intracisternally with 20, 40 or 80 microgram of 6-hydroxydopamine (6-OHDA) at various ages over the first 12 postnatal days in order to determine the critical period of the noradrenergic regenerative-sprouting response in the cerebellum. Twenty-four hours after the treatment NE fibers in the cerebellum had become extensively degenerated. NE levels were reduced by greater than 90-95% and histofluorescence microscopy revealed an absence of innervation except for lesioned axon stumps in the basal white matter and peduncles. The 80 microgram dose produced considerable cellular degeneration in the locus coeruleus and no regenerative growth was seen to follow this treatment. Following the two lower doses, however, regenerative growth did occur. This was maximal in those rats treated closest to birth and declined progressively to become insignificant in rats which were treated on postnatal days 5-12, depending upon the cerebellar subregion. This decline in regenerative potential paralleled the time course for development of NE levels in control cerebella. For this reason the mechanism(s) controlling noradrenergic developmental and regenerative growth in the cerebellum appear to be similar. Such regenerative growth may thus be a useful model for the study of developmental growth of locus coeruleus axons. Contrary to the cerebellar projection, regenerative growth of the forebrain noradrenergic projection was not detected until the rats were between 7 and 12 days old at the time of treatment. This regeneration in the cerebral cortex was preceded by incomplete initial destruction of NE fibers there, in apparent similarity to regenerative growth described to occur in the adult rat forebrain.

Improved catecholamine histofluorescence in the developing brain based on the magnesium and aluminum (ALFA) perfusion techniques: methodology and anatomical observations.

Detailed protocols for the application of two different metal salt perfusion procedures are described for the production of superior catecholamine histofluorescence in the brains of immature rats up to 2 weeks of age. As in the adult, both magnesium and aluminum salts are highly advantageous for catecholamine histofluorescence in developing animals, and yield marked increases in sensitivity. In the magnesium-perfusion technique, animals are perfused in a simple one-step process using a hand-held syringe with cold buffer containing magnesium sulphate, formaldehyde and glyoxylic acid. The aluminum-perfusion (ALFA) technique provides even greater sensitivity and richness of detail, but requires a controlled-pressure perfusion system and a two-step perfusion process. Animals are first perfused with a room-temperature buffer containing magnesium sulphate and procain (to prevent vasoconstriction) followed by cold buffer containing aluminum sulphate and formaldehyde. In both methods, tissue pieces are subsequently freeze-dried, reacted with formaldehyde vapour and paraffin-sectioned according to the standard Falck-Hillarp procedure. Tissue pieces can also be taken from aluminum-perfused brains for simultaneous catecholamine assay using radioenzymatic methods, thereby permitting correlated histochemical and neurochemical analyses on the same brains. Many catecholamine terminal systems can be visualized in the rat brain even at birth with the ALFA procedure following pargyline pretreatment. However, the endogenous intraaxonal catecholamine concentration is so low in immature brains that the full anatomical extent of these systems cannot be reliably seen without recourse to pre-loading with an exogenously administered amine. For this purpose systemic injections of alpha-methyl-noradrenaline were extensively investigated. In combination with the ALFA procedure, such pretreatment was found to cause a dramatic increase in both the intensity and number of terminal and preterminal fibers throughout the brain. Control experiments with 6-hydroxydopamine and the catecholamine uptake blocker, nomifensine, indicate that this loading is specific for catecholamine systems. This approach has indicated that certain of the forebrain noradrenergic and dopaminergic systems are very extensive at birth, and in some regions an intermediate stage of hyperinnervation is a normal feature of ontogeny. Some of these findings are illustrated here and will also be presented in greater detail in further reports.

Origin and termination of the diencephalo-spinal dopamine system in the rat.

Using a combination of neonatal 6-hydroxydopamine and adult 5,7-dihydroxytryptamine treatment we have been able to achieve a 94-99% depletion of noradrenaline in the spinal cord. In such animals the dopamine levels are only marginally affected in the dorsal horn (at all levels) and in the intermediate zone at thoraco-lumbar levels. This combined treatment thus offers new possibilities for selective studies of the spinal dopamine projection. In agreement with the biochemical data the fluorescence histochemistry shows that the spinal dopamine innervation is mainly confined to the dorsal horn, the intermediolateral cell column and associated parts of the intermediate and central gray. Injections of fluorescent retrograde tracer combined with monoamine fluorescence histochemistry reveal that the diencephalic A11 cell group is the principal, and perhaps exclusive, source of this innervation. The area of termination, as well as the organizational similarities with certain diencephalic peptide-containing projections to the spinal cord, suggest that the diencephalo-spinal dopamine system may be importantly involved in autonomic regulatory processes.

Use of a microvascular Doppler probe to avoid basilar artery injury during endoscopic third ventriculostomy. Technical note.

Basilar artery (BA) injury has been reported in a number of cases as a major complication of third ventriculostomy for hydrocephalus. This report describes the deployment of a pulsed-wave microvascular Doppler probe through the endoscope to locate the BA complex and subsequently to select a safe zone for perforation of the third ventricular floor. This procedure is quick and easily learned, and it is hoped that it can decrease the risk of vascular injury during third ventriculostomy.

Loss of forebrain cholinergic neurons following fluid-percussion injury: implications for cognitive impairment in closed head injury.

Disturbances in memory, concentration, and problem solving are common after even mild to moderate traumatic brain injury. Because these functions are mediated in part by forebrain cholinergic and catecholaminergic innervation, in this study the authors sought to determine if experimental concussive injury produces detectable morphological damage to these systems. Fluid-percussion head injury, sufficient to cause a 13- to 14-minute loss of righting reflex, was produced in rats that had been anesthetized with halothane. Injury was delivered either at midline or 2 mm off midline and compared with appropriate sham-injured controls. After 11 to 15 days, the rat brains were stained in serial sections for choline acetyltransferase, tyrosine hydroxylase, dopamine beta-hydroxylase, acetylcholinesterase, and nicotinamide adenine dinucleotide phosphate diaphorase. Cell counts were determined for the entire population of ventrobasal forebrain cholinergic cells. Midline injury produced a bilateral loss of cholinergic neurons averaging 36% in area Ch1 (medial septal nucleus), 45% in Ch2 (nucleus of the diagonal band of Broca), and 41% in Ch4 (nucleus basalis of Meynart), (p < or = 0.05). Lateralized injury resulted in cholinergic neuron loss of similar magnitude ipsilaterally (p < or = 0.05), but a smaller contralateral loss of between 11% and 28%. No loss of neurons was detected in the pontomesencephalic cholinergic groups Ch5 and Ch6. There was no visible effect of head injury on forebrain dopamine or noradrenergic innervation. A significant and apparently selective loss of ventrobasal forebrain cholinergic neurons following brief concussive injury in rats is demonstrated in this study. This type of injury is known to produce significant disturbance in cognitive tasks linked to neocortical and hippocampal cholinergic function. It remains to be determined how this neuron loss occurs, whether it can be prevented with neuroprotective agents, how it affects innervation in target tissues, and whether it occurs in human victims of traumatic brain injury.

Acute cauda equina syndrome from a ruptured aneurysm in the sacral canal. Case report.

The case is presented of a young woman with acute cauda equina syndrome from a ruptured aneurysm in the sacral canal. The lesion was associated with pathological enlargement of the lateral sacral arteries bilaterally, which presumably occurred to provide cross-pelvic collateral flow in response to the diversion of the right internal iliac artery for renal transplantation. The patient presented with signs and symptoms of spontaneous spinal epidural hemorrhage. The radiographic features of this lesion are described. In addition to angiography and partial embolization of the vascular supply, contrast-enhanced high-resolution computerized tomography was essential in the diagnosis and treatment of this unique aneurysm.

Compressive optic neuropathy caused by renal osteodystrophy. Case report.

Compressive optic neuropathy with acute or chronic vision loss has been associated with various skull base tumors, aneurysms, Graves disease, trauma, and, less commonly, fibrous dysplasia and osteopetrosis. The authors present a case of acute visual deterioration in a 25-year-old woman who had massive calvarial hypertrophy with optic canal stenosis secondary to renal osteodystrophy (uremic leontiasis ossea [ULO]: bighead disease). Significant visual field restoration was achieved with high-dose corticosteroids followed by optic nerve decompression. This is the first case report of cranial neuropathy associated with ULO.