Aspergillus parasellar abscess mimicking radiation-induced neuropathy. Case report.

BACKGROUND: Transsphenoidal surgery is a safe procedure for treatment of pituitary adenomas. However, several complications, including post-surgical infection, are known. We describe a case of Aspergillus parasellar abscess that presented with cranial neuropathies following transsphenoidal surgery and radiosurgery. We initially diagnosed the case as radiation-induced neuropathies, which delayed the detection of Aspergillus. CASE DESCRIPTION: A 55-year-old man underwent transsphenoidal surgery for a pituitary adenoma that presented with pituitary apoplexy. Dexamethasone had been continuously administered for hypocortisolism probably caused by pituitary apoplexy. Four years later, radiosurgery was performed for a relapse in the right cavernous sinus. Another 4 years later, he developed painful right ophthalmoplegia, right ptosis, and bilateral visual impairment, successively. We initially suspected that the painful ophthalmoplegia and ptosis were because of radiation-induced cranial neuropathies; however, results of magnetic resonance (MR) imaging and his clinical course were not consistent with those of radiation-induced neuropathies. Therefore, we performed exploratory surgery that revealed a subdural abscess on the planum sphenoidale. Culture of a specimen grew Aspergillus fumigatus. CONCLUSION: Intracranial fungal abscess is a fatal complication unless it is treated early. It is thus important to consider the possibility of parasellar infection and differentiate it from radiation-induced cranial neuropathies when a patient presents with cranial neuropathies after transsphenoidal surgery and radiosurgery.

S-allylcysteine inhibits free radical production, lipid peroxidation and neuronal damage in rat brain ischemia.

The efficacy of S-allylcysteine (SAC) as a free radical scavenger was studied using rat brain ischemia models. In a middle cerebral artery occlusion model, preischemic administration of SAC had the following effects: it improved motor performance and memory impairment and reduced water content and the infarct size. In a transient global ischemia model, the time course of free radical (alkoxyl radical) formation as studied by electron paramagnetic resonance (EPR) spectroscopy and alpha-phenyl-N-tert-butylnitrone (PBN) was biphasic; the first peak occurred at 5 min and the second at 20 min after reperfusion. Although SAC did not attenuate the first peak, it did affect the second peak, which is related to lipid peroxidation. The lipid peroxidation as estimated by thiobarbituric acid reactive substances (TBARS) increased significantly at 20 min after reperfusion. SAC decreased TBARS to the levels found without ischemia. These results suggest that SAC could have beneficial effects in brain ischemia and that the major protective mechanism may be the inhibition of free radical-mediated lipid peroxidation.

Spermine dependent activation of the N-methyl-D-aspartate receptor and the effect of nitric oxide synthase inhibition during hypoxia in the cerebral cortex of newborn piglets.

This study tests the hypothesis that brain tissue hypoxia results in modification of spermine-dependent activation of the cerebral N-methyl-D-aspartate (NMDA) receptor ion-channel in newborn piglet brains and that pretreatment with N(omega)-nitro-L-arginine (NNLA), an inhibitor of nitric oxide synthase, will reduce the hypoxia-induced modification of the spermine-dependent activation of the receptor. Piglets were assigned to one of four groups; normoxia or hypoxia with or without NNLA. The infusion of NNLA or vehicle lasted for 60 min while the animals were ventilated under either hypoxic or normoxic conditions. Cerebral tissue hypoxia was confirmed by measuring ATP and phosphocreatine (PCr) levels. P2 membranes were isolated and 3H-MK-801 binding was measured in the presence of spermine. Steady state 3H-MK-801 binding in the presence of spermine, showed an increase in receptor affinity in both normoxic (47% of control) and hypoxic (42% of control) animals without change in receptor density. During hypoxia, the spermine-dependent increase in the maximal response of the 3H-MK-801 binding correlated inversely with the ATP concentrations. NNLA pretreatment prior to hypoxia, resulted in a decrease in the slope of the regression line describing the relationship between cellular energy state (ATP) and percent change in maximal response to spermine compared with vehicle treated animals indicating attenuation of the response to hypoxia. We conclude that the spermine-dependent modification of the affinity of the NMDA receptor ion-channel as assessed by 3H-MK-801 binding is similar in hypoxic and normoxic cortical tissue. NNLA administration reduces the hypoxia-induced spermine-dependent activation of the receptor indicating that nitric oxide mediates modification of the spermine site activation of the NMDA receptor ion-channel complex.

Pilocytic astrocytoma arising from an area of nodular heterotopia located in the white matter of the temporal lobe: case report.

A 16-year-old girl suffering from intractable temporal lobe epilepsy presented with a pilocytic astrocytoma, which occurred in an area of nodular heterotopia located in the white matter of the temporal lobe. The pilocytic astrocytoma appeared to be covered by an area of gliosis, which contained numerous Rosenthal fibers, while in the lesion the pilocytic astrocytoma occupied a small area. The gliosis eventually became a tumor-like lesion. The white matter around the mass was composed of gliosis with nodular heterotopia. Temporal developmental malformation, which was a basic lesion of the patient, might therefore be a precursor lesion of pilocytic astrocytomas.

NMDA receptor-mediated calcium influx in cerebral cortical synaptosomes of the hypoxic guinea pig fetus.

Calcium influx via the NMDA receptor has been proposed as a mechanism of hypoxia-induced neuronal injury. The present study tests the hypothesis that the increase of [Ca2+]i observed under hypoxic conditions is the result of an NMDA-mediated Ca2+ influx. Changes of [Ca2+]i, measured fluorometrically with Fura-2, were followed after activation of the NMDA receptor with NMDA and glutamate, in the presence of glycine, in cortical synaptosomes prepared from six normoxic and six hypoxic guinea pig fetuses. [Ca2+]i was significantly higher in hypoxic vs normoxic synaptosomes, at baseline and in the presence of glycine as well as following activation of the NMDA receptor. Increase in [Ca2+]i was not observed in a Ca2+ free medium and was significantly decreased by MK-801 and thapsigargin. These results demonstrate that hypoxia-induced modifications of the NMDA receptor ion-channel results in increased [Ca2+]i in hypoxic vs normoxic synaptosomes. This increased accumulation may be due to an initial influx of Ca2+ via the altered NMDA receptor with subsequent release of Ca2+ from intracellular stores. Increase in intracellular calcium may initiate several pathways of free radical generation including cyclooxygenase, lipoxygenase, xanthine oxidase and nitric oxide synthase, and lead to membrane lipid peroxidation resulting in neuronal cell damage.

Oxygen free radical generation during in-utero hypoxia in the fetal guinea pig brain: the effects of maturity and of magnesium sulfate administration.

Previous studies have shown, employing direct measurements with electron spin resonance (ESR) spectroscopy, that hypoxia induces an increased production of oxygen free radicals (OFR) in the brain of the guinea pig fetus. The present study using the same approach, investigated the effects of maturity and Mg2+-pretreatment on hypoxia-induced OFR formation in the guinea pig fetal brain. The normoxic and the hypoxic groups were exposed for 60 min to 21% or 7% oxygen, respectively. The control group consisted of term fetuses exposed to normoxia (n=7) and hypoxia (n=7). The experimental groups consisted of the following: (a) for the investigation on maturity effect, preterm fetuses (40 days) exposed to normoxia (n=6) or hypoxia (n=6); and (b) for the Mg2+-pretreatment investigation, term fetuses (60 days) exposed to normoxia (n=6) or hypoxia (n=6) following maternal pretreatment with Mg2+ which consisted of an initial bolus of MgSO4 (600 mg/kg, i.p.) 1 h prior to hypoxia followed by a second dose (300 mg/kg, i.p.). Oxygen free radicals were measured by ESR spectroscopy in the fetal cerebral cortical tissue utilizing phenyl-N-tert-butylnitrone (PBN) spin trapping. Fetal brain tissue hypoxia was documented biochemically by decreased tissue levels of ATP and phosphocreatine. In the control group of term fetuses, the cortical tissue from hypoxic fetuses showed a significant increase in spin adducts (71% increase, p<0.01). In the preterm group, the cortical tissue from hypoxic fetuses showed a 33% increase in spin adducts (p<0.001). The baseline free radical generation during normoxia was 22.5% higher at preterm than at term (41.4+/-3.5 units/g issue vs. 33.8+/-9.3 units/g tissue, p<0.05). In Mg2+-treated groups, spin adduct levels in cortical tissue from hypoxic fetuses did not significantly differ from those of the normoxic group (30.2+/-9.9 units/g tissue, normoxic-Mg2+ vs. 30. 6+/-8.1 units/g tissue, hypoxic-Mg2+). The results indicate that the fetal brain at term may be more susceptible to hypoxia-induced free radical damage than at preterm and that Mg2+ administration significantly decreased the hypoxia-induced increase in oxygen free radical generation in the term fetal guinea pig brain in comparison with non-treated hypoxic group.

Antegrade recanalization of completely embolized internal carotid artery after treatment of a giant intracavernous aneurysm: a case report.

BACKGROUND: Parent artery occlusion is one of the traditional methods of treatment for unclippable aneurysms. However, parent artery occlusion may not result in permanent exclusion of the aneurysm from the systemic circulation. We present a case of cerebral aneurysm treated by proximal embolization of the parent artery, which recanalized during the follow-up period. CASE DESCRIPTION: A 69-year-old woman presented with a right blepharoptosis and diplopia. A large aneurysm arising from the cavernous portion of the right internal carotid artery was found and endovascularly excluded from the cerebral circulation by proximal internal carotid artery occlusion with balloons. Eleven days after treatment, occlusion of the parent artery and obliteration of the aneurysm were angiographically confirmed. However, the parent artery was found to be recanalized with nearly total obliteration of the aneurysm at the follow-up 6 months after treatment. CONCLUSION: Angiography suggested that recanalization took place through the vaso vasorum. We believe that recanalization was induced by marginal cerebral blood flow in the ipsilateral hemisphere.

In vivo nitric oxide detection in the septic rat brain by electron paramagnetic resonance.

To detect nitric oxide (NO) in the rat brain during lipopolysaccharide (LPS)-induced sepsis, electron paramagnetic resonance (EPR) was employed with the NO trapping technique, using an iron and N,N-diethyldithiocarbamate (DETC) complex. An X-band (about 9.5 GHz) EPR system detected a triplet signal (g = 2.038) derived from an NO-Fe-DETC complex being superimposed on the g(perpendicular) signal of Cu-DETC complex at liquid nitrogen temperature. The height of the triplet signal peaked seven hours after injection of 40 mg/kg of LPS, and over 25 x 10(4) U/kg of IFN-gamma enhanced the LPS-induced NO formation. Pretreatment with N(G)-monomethyl-L-arginine (NMMA), an NO synthase inhibitor, deleted only the triplet signal. A triplet signal (g(iso) = 2.040, aN = 1.28 mT) derived from the NO-Fe-DETC complex was also observed at ambient temperature. Then, a home-built 700 MHz EPR system was used to detect an NO signal in the septic rat brain in vivo. We successfully monitored the NO-Fe-DETC signal in the head region of a living rat under the condition that provided maximum height of the NO-Fe-DETC signal in the X-band EPR study. Pretreatment with NMMA again deleted the NO-Fe-DETC signal. This is the first EPR observation of endogenous NO in the brain of living rats.

Direct measurement of oxygen free radicals during in utero hypoxia in the fetal guinea pig brain.

The present study tested the hypothesis that maternal hypoxia induces oxygen free radical generation in the fetal guinea pig brain utilizing techniques of electron spin resonance spectroscopy and alpha-phenyl-tert-butyl nitrone (PBN) spin trapping. Pregnant guinea pigs of 60 days gestation were divided into normoxic and hypoxic groups and exposed to 21% or 7% oxygen for 60 min. Free radical generation was documented by measuring the signal of PBN spin adducts. Fluorescent compounds were determined as an index of lipid peroxidation and the activity of Na+,K+-ATPase was determined as an index of brain cell membrane function. Hypoxic fetal cerebral cortical tissue showed a significant increase in spin adducts (normoxic: 33.8+/-9.3 units/g tissue vs. hypoxic: 57.9+/-9.2 units/g tissue, p<0.01) and fluorescent compounds (normoxic: 0.639+/-0.054 microg quinine sulfate/g brain vs. 0.810+/-0.102 microg quinine sulfate/g brain, p<0.01) and a decrease in Na+,K+-ATPase activity (normoxic: 43.04+/-2.50 micromol Pi/mg protein/h vs. hypoxic: 33. 80+/-3.51 micromol Pi/mg protein/h, p<0.001). These results demonstrate an increased free radical generation during hypoxia in the fetal guinea pig brain. The spectral characteristics of the radicals were consistent with those of alkoxyl radicals. The increased level of fluorescent compounds and decreased activity of Na+,K+-ATPase indicated hypoxia induced brain cell membrane lipid peroxidation and dysfunction, respectively. These results directly demonstrate an increased oxygen free radical generation during hypoxia and suggest that hypoxia-induced increase in lipid peroxidation and decrease in membrane function, as indicated by a decrease in Na+,K+-ATPase activity, are consequences of increased free radicals. The nature of predominantly present alkoxyl radical indicates ongoing lipid peroxidation during hypoxia. The direct demonstration of oxygen free radical generation during hypoxia is the critical missing link in the mechanism of hypoxia-induced brain cell membrane dysfunction and damage.

Effect of propentofylline on free radical generation during cerebral hypoxia in the newborn piglet.

The present study tests the hypothesis that propentofylline, an adenosine re-uptake inhibitor, will reduce free radical generation during cerebral hypoxia. Ten newborn piglets were pretreated with propentofylline (10 mg/kg), five of which were subjected to hypoxia, while the other five were maintained at normoxia. Five untreated control piglets underwent the same conditions. Hypoxia was induced through a decrease in FiO2 to 0.11 and documented biochemically by a decrease in ATP and phosphocreatine levels. Free radical formation in the cortex was detected directly using electron spin resonance spectroscopy with a spin trap technique. Results demonstrate that free radicals, corresponding to the alkoxyl radical, increased significantly following hypoxia, and that this increase was inhibited by pretreatment with propentofylline. Conjugated dienes, a lipid peroxidation product, also increased following hypoxia and were subsequently inhibited by propentofylline. The administration of propentofylline also significantly limited the hypoxia-induced decrease in tissue levels of ATP and phosphocreatine. These data demonstrate that pretreatment with propentofylline decreased free radical generation and lipid peroxidation as well as preserved high energy phosphates during cerebral hypoxia.

Lipid free radical generation and brain cell membrane alteration following nitric oxide synthase inhibition during cerebral hypoxia in the newborn piglet.

Nitric oxide (NO) is reported to cause neuronal damage through various mechanisms. The present study tests the hypothesis that NO synthase inhibition by N(omega)-nitro-L-arginine (NNLA) will result in decreased oxygen-derived free radical production leading to the preservation of cell membrane structure and function during cerebral hypoxia. Ten newborn piglets were pretreated with NNLA (40 mg/kg); five were subjected to hypoxia, whereas the other five were maintained with normoxia. An additional 10 piglets without NNLA treatment underwent the same conditions. Hypoxia was induced with a lowered FiO2 and documented biochemically by decreased cerebral ATP and phosphocreatine levels. Free radicals were detected by using electron spin resonance spectroscopy with a spin trapping technique. Results demonstrated that free radicals, corresponding to alkoxyl radicals, were induced by hypoxia but were inhibited by pretreatment with NNLA before inducing hypoxia. NNLA also inhibited hypoxia-induced generation of conjugated dienes, products of lipid peroxidation. Na+,K+-ATPase activity, an index of cellular membrane function, decreased following hypoxia but was preserved by pretreatment with NNLA. These data demonstrate that during hypoxia NO generates free radicals via peroxynitrite production, presumably causing lipid peroxidation and membrane dysfunction. These results suggest that NO is a potentially limiting factor in the peroxynitrite-mediated lipid peroxidation resulting in membrane injury.

Attenuation of rat ischemic brain damage by aged garlic extracts: a possible protecting mechanism as antioxidants.

Effects of an aged garlic extract and its thioallyl components on rat brain ischemia were examined using a middle cerebral artery occlusion model and a transient global ischemia model. In focal ischemia, an aged garlic extract, S-allyl cysteine (SAC), Allyl sulfide (AS) or Allyl disulfide (ADS) was administered 30 min prior to ischemic insult. Three days after ischemic insult, water contents of both ischemic and contralateral hemispheres were measured to assess the degree of ischemic damage. The water content of the ischemic control (no drug treatment) group was 81.50 +/- 0.07% (mean +/- SEM). It was significantly reduced with the administration of 300 mg/kg of SAC; the water content was 80.66 +/- 0.11% (P < 0.001). The histological observation using 2,3,5-triphenyltetrazolium chloride staining demonstrated that the administration of SAC reduced infarct volume. Neither AS nor ADS was effective. In global ischemia, the production of reactive oxygen species (ROS) was measured ex vivo using a spin-trapping agent, alpha-phenyl-N-tert-butylnitrone, and electron paramagnetic resonance spectroscopy. The production of ROS had two peaks; first at 5 min and second at 20 min after reperfusion. Both SAC and 7-nitro indazole, a nitric oxide synthase inhibitor, did not attenuate the amount of ROS produced at the first peak, but did the amount of the second peak. A possible involvement of peroxinitrite, which may be formed from superoxide and nitric oxide and is known to be highly toxic in ischemia/reperfusion injury of the brain, was suggested.

Three-dimensional imaging of nitric oxide production in the rat brain subjected to ischemia-hypoxia.

By the systemic administration of diethyldithiocarbamate and iron into the rat, nitric oxide radicals produced in the brain during ischemia-hypoxia were trapped. The right hemisphere of the brain was then removed and frozen with liquid nitrogen. With use of recently developed electron paramagnetic resonance imaging instrumentation and techniques, three-dimensional imaging of the production of the nitric oxide radicals in several brains was performed. The results suggest that nitric oxide radicals were produced and trapped in the areas that are known to have high nitric oxide synthase activity, such as cortex, hippocampus, hypothalamus, amygdala, and substantia nigra. In this ischemia-hypoxia model, which did not interrupt the posterior circulation, the production and trapping of nitric oxide in the cerebellum were approximately 30% of those in the cerebrum.

Local nitric oxide production in viral and autoimmune diseases of the central nervous system.

Because of the short half-life of NO, previous studies implicating NO in central nervous system pathology during infection had to rely on the demonstration of elevated levels of NO synthase mRNA or enzyme expression or NO metabolites such as nitrate and nitrite in the infected brain. To more definitively investigate the potential causative role of NO in lesions of the central nervous system in animals infected with neurotropic viruses or suffering from experimental allergic encephalitis, we have determined directly the levels of NO present in the central nervous system of such animals. Using spin trapping of NO and electron paramagnetic resonance spectroscopy, we confirm here that copious amounts of NO (up to 30-fold more than control) are elaborated in the brains of rats infected with rabies virus or borna disease virus, as well as in the spinal cords of rats that had received myelin basic protein-specific T cells.

[A case of ruptured true posterior communicating artery aneurysm thirteen years after surgical occlusion of the ipsilateral cervical internal carotid artery].

A case is presented of ruptured "true" posterior communicating artery aneurysm thirteen years after surgical occlusion of the ipsilateral cervical internal carotid artery. A 58-year-old female developed the sudden onset of blepharoptosis on the right side. She had had a right superficial temporal artery-middle cerebral artery anastomosis and a surgical occlusion of the right cervical internal carotid artery 13 years earlier for a subarachnoid hemorrhage that occurred as the result of a ruptured aneurysm of the right internal carotid artery. Neurological examination on admission revealed an occulomotor palsy on the right. Cerebral angiograms demonstrated an aneurysm arising from the right posterior communicating artery itself near the right posterior cerebral artery. Also, the right intracranial internal carotid artery was supplied through the right posterior communicating artery. Five days later she experienced the sudden onset of severe headache. CT scan showed subarachnoid hemorrhage in the ambient cistern. Neck clipping of the aneurysm was successfully performed by the contralateral zygomatic approach. The postoperative course was uneventful. It has been well known that internal carotid artery occlusion may be associated with cerebral aneurysm in some cases. However, it seems to be very rare that a "true" posterior communicating artery aneurysm should occur following the ipsilateral carotid artery occlusion. Hemodynamic factors were strongly suggested as the reason for aneurysmal formation in this case.

[Diaschisis in right putaminal hemorrhage: correlation with motor function].

Local cerebral lesions may cause depression of function in remote areas of the brain presumably by a transneural mechanism; it has been called "diaschisis". In the present study, to investigate the relationship between motor function and "diaschisis" regional brain blood flow in hypertensive right putaminal hemorrhage was studied in 33 patients (mean age, 55 years; 22 men, 11 women). The hematoma was treated conservatively in 8 patients, aspirated stereotaxically in 9 patients, and evacuated through a craniotomy in 16 patients. The regional blood flow in the right motor cortex and the left cerebellar hemisphere was measured by a single photon emission CT with N-isopropyl-p- (123 I) iodo-amphetamine intravenous injection method, and was evaluated by the RI count on early image/the decay-corrected RI count on delayed image (E/D) value. The time during which regional brain blood flow was measured ranged from 29 to 35 days from the onset. There was a positive correlation between the grade in the motor function in the subacute stage and the regional blood flow in the right motor cortex and the left cerebellar hemisphere. There was also a positive correlation between the Barthel index in the chronic stage (mean follow-up periods: 40 months) and the regional blood flow in the right motor cortex and the left cerebellar hemisphere. The results of the present study suggest that in right putaminal hemorrhage the flow reduction in areas remote from the primary lesion, i.e., "diaschisis", may reflect not only the degree of functional abnormalities of the internal capsule, but also the possibility of functional recovery.

[Diaschisis in right putaminal hemorrhage: correlation with the degree of the extension to the internal capsule and the volume of hematoma].

Local cerebral lesions may cause depression of function in remote areas of the brain presumably by a transneural mechanism. This has been called "diaschisis". In the present study, regional brain blood flow in hypertensive right putaminal hemorrhage was studied in 33 patients (mean age, 55 year; 22 men, 11 women) to investigate the relationship between the degree in damage of the original lesions and "diaschisis". The hematoma was treated conservatively in 8 patients, aspirated stereotaxically in 9 patients, and evacuated through craniotomy in 16 patients. The regional blood flow in bilateral motor cortices and bilateral cerebellar hemispheres was measured by a single photon emission CT with N-isopropyl-p- [123 I] iodo-amphetamine intravenous injection, and was evaluated by the RI count on early image/the decay-corrected RI count on delayed image (E/D). The regional brain blood flow was measured for 29 to 35 days from the onset. There was a negative correlation between the degree of the extension to the internal capsule and the regional blood flow of the right motor cortex and the bilateral cerebellar hemispheres. There was also a negative correlation between the volume of the hematoma and the regional blood flow of the right motor cortex and the bilateral cerebellar hemispheres. The regional blood flow of the left motor cortex correlated with neither the degree of the extension to the internal capsule nor the volume of the hematoma. On the other hand, there was a positive correlation in the regional blood flow between the bilateral motor cortices.(ABSTRACT TRUNCATED AT 250 WORDS)