Cerebral venous thrombosis: role of CT, MRI and MRA in the emergency setting.

PURPOSE: It is often difficult to diagnose cerebral venous thrombosis (CVT), an uncommon condition that more frequently affects young subjects, is responsible for 1%-2% of strokes in adults and has a subtle clinic onset. The aim of this study was to evaluate the role of computed tomography (CT), magnetic resonance imaging (MRI) and MR venography in the emergency setting and to discuss the risk factors, clinical presentation, outcome and follow-up of this disease. MATERIALS AND METHODS: We retrospectively studied 40 patients with CVT admitted to the emergency department between 1996 and 2006 and examined with unenhanced CT, MRI and MR venography. Fourteen patients also underwent digital subtraction angiography (DSA). RESULTS: Headache was the most common presenting feature (60%). Unenhanced CT showed typical signs (cord or empty delta sign) in 11 cases and nonspecific signs in the other cases. The diagnosis was achieved with MRI and MR venography in 38/40 cases (95%) and with DSA in 2/40 cases. All patients were treated with heparin. Five patients died, and only one of the remaining patients developed serious disability. CONCLUSIONS: Knowledge of the CT, MRI and MR-venography signs of CVT is crucial and enables an early diagnosis and timely treatment with heparin in the majority of cases. DSA should be reserved for doubtful cases only.

Role of diffusion- and perfusion-weighted MR imaging for brain tumour characterisation.

PURPOSE: This study was undertaken to correlate apparent diffusion coefficient (ADC) and relative regional cerebral blood volume (rrCBV) to histological findings in a large series of patients with primary or secondary brain tumours to evaluate diffusion-weighted (DWI) and perfusion-weighted (PWI) imaging in the characterisation of cerebral tumors. MATERIALS AND METHODS: Ninety-eight patients with cerebral tumours, 46 of which were primary (seven grade 0-I, nine low-grade gliomas, two gliomatosis cerebri, nine lymphomas and 19 high-grade gliomas) and 52 secondary, underwent conventional magnetic resonance (MR) imaging completed with DWI and dynamic contrast susceptibility PWI. Both ADC and rrCBV were calculated on a workstation by using Functool 2 software. Student's t test was used to determine any statistically significant differences in the ADC and rrCBV values. RESULTS: Seventeen of 98 tumours were cystic or necrotic (12/17 hypointense and 5/17 hyperintense on DWI); the ADC value of hyperintense cystic areas was 0.97+/-0.23x10(-3) mm2/s. The ADC value of solid tumours varied between 0.64 and 3.5x10(-3) mm2/s. The rrCBV value was 1.4 (sigma 0.66) in low-grade gliomas; 1.22 (sigma 0.25) in lymphomas; 4.5 (sigma 0.85) in grade III gliomas; 3.18 (sigma 1.26) in grade IV gliomas and 2.53 (sigma 1.6) in metastases. CONCLUSIONS: DWI has an important role in the differential diagnosis of cystic cerebral masses but not in tumour characterisation. PWI is helpful in differentiating high-from low-grade gliomas and lymphomas from high-grade gliomas.

Patient dose evaluation by means of DICOM images for a direct radiography system.

PURPOSE: The purpose of this work was to evaluate the statistical distribution of patient dose for different examinations by using the data stored in a DICOM image archive of a direct digital radiography system. MATERIALS AND METHODS: An automatic procedure to extract dose data and exposure parameters from the image archives was implemented. During a 4.5-month period, 8,292 images were collected. Exposure parameters and the air kerma area product (P (KA)) stored in the image DICOM header were examined for each image. The entrance surface air kerma (K (a,e)), a quantity comparable to the current diagnostic reference levels (DRL), was estimated considering the P (KA) and the geometric parameters of each examination. RESULTS: P (KA) and K (a,e ) distributions showed highly variable values. The obtained K (a,e ) values were substantially lower than the DRL. DRL were more than six times the mean value of K (a,e ) distribution for the abdomen anteroposterior (AP) and lumbar spine lateral (LAT) projections, whereas the ratio was equal to 2.7 for posteroanterior (PA) chest examinations. CONCLUSIONS: The method adopted proved to be effective for characterising the dose of each examination by means of the statistical analysis of the dose quantities over extensive samples. The dose values obtained and the comparison with the DRL showed that this radiographic device allows substantial dose savings compared with estimations made for nondigital or for phosphor-based systems.

Diffusion-Weighted Magnetic Resonance Imaging and ADC Maps in the Diagnosis of Intracranial Cystic or Necrotic Lesions. A Retrospective Study on 49 Patients.

This study evaluated the usefulness of diffusion-weighted (DW) magnetic resonance imaging (MRI) and ADC maps in the differential diagnosis of brain abscesses from cystic or necrotic neoplasms. MR images of 49 patients with 54 lesions were examined retrospectively. All patients underwent conventional MRI and DWI, and ADC values were calculated by placing ROIs of 30 mm(2) manually over the cystic part of the lesions. On DWI, all cystic portions of abscesses were hyperintense. Mean ADC values were 0.48×10 mm(2)/s (range 0.41-0.54×10 mm/s) for pyogenic abscesses, 0.73×10 mm(2)/s (range 0.65-0.91×10 mm/s) for mycotic abscesses and 0.6 mm(2)/s for Nocardia abscess. Cystic areas appeared hypointense on DWI in 33/44 tumours (mean value ADC 1.96 mm(2)/s). Eleven tumours (11/44) appeared hyperintense on DWI: eight metastases from lung cancer (mean ADC value 0.86 mm(2)/s, range 0.75-1.2 mm(2)/s), two GBMs (mean 0.7 mm(2)/s, range 0.67-0.76 mm(2)/s) and one anaplastic astrocytoma (ADC value 1.24 mm(2)/s). ADC values may help in differentiating pyogenic abscess from brain tumors or metastatic lesions.

Automated quality control in computed radiography.

PURPOSE: The purpose of this paper is to describe the automation of quality control procedures on photo-stimulable imaging plates by means of an image-processing tool providing automatic reading of the images and automatic calculation of the quality parameters monitored. MATERIALS AND METHODS: Quality-control procedures were performed according to the main available guidelines. The quality assurance programme was applied to several Kodak and Philips devices in four radiological departments. The automatic image-processing tool was developed using public domain software (Java-based ImageJ software) and contains both reading and computation procedures. RESULTS: The quality checks and algorithms described were successfully applied, proving useful for identification of defective plates and for implementation of the quality assurance programme. The use of automation allowed significant savings in the time required for quality checks. CONCLUSIONS: Completely automated image reading allows substantial economic and human resources savings, as it eliminates much of the transfer, reproduction, processing and filing procedures.

Reversible encephalopathy syndrome: report of 12 cases with follow-up.

We report the clinical and neuroradiological features of reversible encephalopathy syndrome and follow-up results in 12 patients. This syndrome seems to be the result of an acute encephalopathy showing with brain edema mainly in the white matter (vasogenic edema). Diffusion-weighted magnetic resonance images are useful to distinguish this entity from acute ischemia. Early recognition and treatment often lead to complete neurological recovery. If unrecognized, the patient's condition can progress to central nervous system failure.

Reversible changes in goldfish brain polyamine concentrations and synthetic enzymes after cold exposure.

Exposure of goldfish to the cold (5 degrees C) caused a sharp increase in brain putrescine level during the first week. Such increase continued at a minor rate for the whole period of exposure (2 months). In contrast, the content of spermidine and spermine remained unchanged. Putrescine increase was concomitant with a remarkable rise in ornithine decarboxylase activity (ODC), which reached a maximum stimulation after 1 week of cold exposure, and declined thereafter, remaining significantly higher than the control for the entire period of study. Cold exposure caused also a reduction of S-adenosylmethionine decarboxylase (AdoMetDC) activity and an increase of ornithine level, whereas methionine content was unchanged. When fish exposed to cold temperature were returned to 20 degrees C, the modifications observed on brain polyamine metabolism were completely reversed. Supported by previous observations, our results suggest that the changes in the polyamine metabolism induced in goldfish brain by cold exposure could represent an homeostatic mechanism carried out by the goldfish to minimize the possible effects of thermal changes.

[Check of compliance with quality criteria for diagnostic radiographic images in quality control]. / Verifica del rispetto dei livelli diagnostici di riferimento nella radiodiagnostica nell'ambito dei controlli programmati della qualità.

PURPOSE: To devise and implement a programme of measurements to assess the entrance surface dose for a standard-sized patient and to check the compliance with diagnostic reference levels. MATERIAL AND METHODS: Dose evaluation was performed on 40 radiographic instruments. The exposure parameters were collected for the main radiographic procedures (chest, skull, spine, pelvis, abdomen) each performed with instrument on a standard-sized patient. The output of each X-ray tube at 70, 80, 90, 100, 110 and 120 kV was measured with a solid state detector during quality controls. Beam quality and geometric characteristics of the equipment were also determined. The entrance surface dose for a standard patient was assessed for each procedure carried out with the 40 instruments, thus obtaining a total of 155 radiographic techniques. Finally, the method was validated by comparing the values obtained with the solid state and an ionization chamber for X-ray beam detector. RESULTS: The comparison between the solid state detector and the ionisation chamber demonstrated a good agreement. Results show that reference diagnostic levels are respected in most examinations (147/155) even if exposure values do not always comply with those indicated by European guidelines. The measurement programme seems to be applicable in hospital practice where the large number of radiographics instruments and procedures requires the acquisition and processing of a large number of data. CONCLUSIONS: The evaluation of patient dose during quality control is feasible and allows a first check of compliance with reference levels in order to identify which procedures can be optimised by means of more specific measurements and assessments.

Pharmacological characterization of adenosine A1 receptors and its functional role in brown trout (Salmo trutta) brain.

The adenosine receptor agonist N(6)-cyclohexyl[(3)H]adenosine ([(3)H]CHA) was used to identify and pharmacologically characterize adenosine A1 receptors in brown trout (Salmo trutta) brain. In membranes prepared from trout whole brain, the A1 receptor agonist [(3)H]CHA bound saturably, reversibly and with high affinity (K(d)=0. 69+/-0.04 nM; B(max)=0.624+/-0.012 pmol/mg protein) to a single class of binding sites. In equilibrium competition experiments, the adenosine agonists and antagonists all displaced [(3)H]CHA from high-affinity binding sites with the rank order of potency characteristic for an adenosine A1 receptors. A1 receptor density appeared not age-related (from 3 months until 4 years), and was similar in different brain areas. The specific binding was inhibited by guanosine 5'-triphosphate (IC(50)=0.778+/-0.067 microM). GTP (5 microM) induced a low affinity state of A1 receptors. In superfused trout cerebral synaptosomes, 30 mM K(+) stimulated the release of glutamate in a calcium dependent manner. Glutamate-evoked release was dose-dependently reduced by CHA, and the inhibition was reversed by the A1 antagonist 8-cyclopentyltheophylline (CPT). In the same synaptosomal preparation, 30 mM K(+) as well as 1 mM glutamate stimulated the release of adenosine in a Ca(2+)-independent manner and tetrodotoxin insensitive. These findings show that in trout brain adenosine A1 receptors are present which are involved in the modulation of glutamate transmitter release. Moreover, the stimulation of adenosine release by K(+) depolarisation or glutamate support the hypothesis that, as in mammalian brain, a cross-talk between adenosine and glutamate systems exists also in trout brain.

Predominant expression of group-II metabotropic glutamate receptors in the goldfish brain.

Group-II metabotropic glutamate (mGlu) receptors (mGlu2/3 receptors) were highly expressed in various regions (telencephalon, optic tectum, and cerebellum, but not vagal lobe) of the goldfish brain. In the goldfish telencephalon, expression of mGlu2/3 receptors was even higher than in the rat cerebral cortex. In contrast, mGlu5 receptors showed low levels of expression in all goldfish brain regions, whereas mGlu1a receptors were only expressed in the goldfish cerebellum. Pharmacological activation of group-II mGlu receptors with the selective agonists, 2R,4R-4-aminopyrrolidine-2, 4-dicarboxylic acid and (2S,2'R,3'R)-2-(2,3-dicarboxycyclopropyl) glycine, reduced the evoked release of glutamate from goldfish brain synaptosomes, whereas agonists of group-I and -III mGlu receptors (3, 5-dihydroxyphenylglycine and L-2-amino-4-phosphonobutanoate) were inactive. The predominance of group-II over group-I mGlu receptors in the goldfish brain may provide a natural defense against excitotoxic neuronal death and contribute to the unusually high resistance of goldfish against hypoxic brain damage.

Effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in goldfish cerebellum: neurochemical and immunocytochemical analysis.

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administered in goldfish for 3 consecutive days (10 mg kg-1 i.p.), caused cerebellar disappearance of dopamine-hydroxylase (DBH) immunoreactive fibres, whereas the noradrenergic cell bodies located in the medulla oblongata appeared intact. This effect was coupled with marked decreases in cerebellar noradrenaline (NA) and dopamine (DA) levels. An increase of immunostaining for glial fibrillary acidic protein (GFAP) was also observed. In the cerebellum of MPTP-treated fish, the contents of glutamate and GABA were significantly reduced, whereas glutamine was strongly increased. These modifications were concomitant with a significant increase of glutamine synthetase (GS) activity, whereas glutamic acid decarboxylase (GAD) activity was decreased. No changes in choline acetyltransferase (ChAT) and ornithine decarboxylase (ODC) activities were observed. High affinity uptake of glutamate and GABA was strongly reduced. Pretreatment of fish with either the monoamine oxidase inhibitor pargyline or the catecholamine (CA) uptake blocker mazindol largely prevented such modifications. The NMDA-sensitive glutamate receptor uncompetitive antagonist, dizocilpine maleate (MK-801), failed to protect against MPTP-induced damage. In conclusion, the neurotoxic effects of MPTP in goldfish cerebellum appear to be not specific against catecholaminergic terminals and could promote astrocytic reactions.

Neuronal nitric oxide synthase is permanently decreased in the cerebellum of rats subjected to chronic neonatal blockade of N-methyl-D-aspartate receptors.

Pharmacological blockade of the (NMDA) receptor at critical stages of brain development may have long-lasting effects on brain chemistry and on animal behavior. We report here experiments in which the competitive NMDA receptor antagonist CGP 39551 was administered to rat pups from postnatal day 7 (P7) to P18. The stage of treatment was selected to primarily target the cerebellum, whose granule cells undergo post-mitotic migration and establishment of synaptic connections during this period. We focused our study on the long-term consequences of CGP 39551 treatment on the neuronal isoform of nitric oxide synthase (nNOS) since nNOS is highly expressed in the cerebellum and it is functionally linked to the NMDA receptor. Treated rats exhibited a long-lasting (up to P70) decrease in the intensity of nNOS immunocytochemical staining in the cerebellar cortex accompanied by a decrement of calcium-dependent NOS catalytic activity. A comparable decrease of enzyme activity was measured in the cerebral cortex, but not in the hippocampus, of adult rats. Other neurochemical markers (glutamatergic, gabaergic, purinergic) and glutamine synthetase were unchanged, while a cholinergic marker was slightly increased in the cerebellum of CGP 39551 treated animals. Taken together these data show that blockade of NMDA receptor during the critical period of formation and stabilization of neuronal circuits preferentially affects long-term nNOS expression and catalytic activity in the cerebellum.

Neurochemical changes in cerebellum of goldfish exposed to various temperatures.

Acclimation of goldfish at 35 degrees C increased the cerebellar content of aspartate, glutamate, and taurine and [3H]glutamate uptake. Acclimation at 4 degrees C increased the levels of glutamine, serine, and alanine and glutamine synthetase (GS) activity. Adenosine content increased in cerebellum of fish acclimated to warm temperature. K+-evoked release of endogenous and exogenous glutamate from cerebellar slices increased in fish acclimated at 35 degrees C compared to 4 degrees C. The basal level of cyclic adenosine 3':5'-monophosphate (cAMP) in perfused cerebellar slices in fish acclimated at 35 degrees C was much higher than in fish acclimated at 5 degrees and 22 degrees C. It is concluded that variations of environmental temperature produces large neurochemical changes in goldfish cerebellum.

Adenosine by activating A1 receptors prevents GABAA-mediated actions during hypoxia in the rat hippocampus.

The relative contribution of adenosine and gamma-aminobutyric acid (GABA) for the hypoxia-induced depression of field excitatory postsynaptic potentials in the CA1 area of rat hippocampal slices, was investigated. It is concluded that both adenosine and GABA, by activating A1 and GABAA receptors, could be responsible for the inhibition of synaptic transmission during hypoxia, but the action of endogenous GABA becomes evident only when the adenosine A1 receptor action is precluded.

Biochemical and pharmacological evidence for the presence of A1 but not A2a adenosine receptors in the brain of the low vertebrate teleost Carassius auratus (goldfish).

In whole brain membranes of goldfish, 3H-chlorocyclopentyladenosine bound to adenosine A1 receptors. The A1 receptors were ubiquitously distributed in the brain with a maximum in the hypothalamus and a minimum in the spinal cord. In superfused goldfish cerebellar slices, cyclohexyladenosine inhibited the cyclic AMP accumulation stimulated by forskolin and the selective adenosine A1 receptor antagonist, 8-cyclopentyltheophylline, reversed this effect. In the same brain preparation, 30 mM K+ stimulated the release of glutamate, glutamine, glycine and GABA in a Ca(2+)-dependent manner, whereas the aspartate and taurine release was Ca(2+)-independent. Cyclohexyladenosine, in a dose-dependent manner, inhibited the 30 mM K(+)-evoked release of glutamate whereas that of aspartate was unaffected. The CHA inhibition of glutamate-evoked release was reversed by 8-cyclopentyltheophylline. The adenosine A2a receptors were not detectable in whole brain membranes of goldfish either using the specific agonist 3H-CGS 21680 or 3H-5'-N-ethylcarboxamidoadenosine. The presence of A2b seems to be suggested by the NECA stimulation of cyclic AMP accumulation, which was reversed by 8-cyclopentyltheophylline. The results, taken together, indicate that adenosine has a neuromodulatory function in the nervous system of lower vertebrates which is comparable to that described in mammalian brain.

Functional adenosine A1 receptors in goldfish brain: regional distribution and inhibition of K(+)-evoked glutamate release from cerebellar slices.

In goldfish brain, [3H]cyclohexyladenosine binding sites are ubiquitously distributed with a maximum in the hypothalamus and a minimum in the spinal cord. The binding parameters measured in cerebellar membranes (Kd = 0.88 +/- 0.08 nM; Bmax = 59.65 +/- 2.62 fmol/mg protein) are not significantly different from those of the whole brain. In perfused goldfish cerebellar slices, stimulation of cyclic AMP accumulation by 10(-5) M forskolin was markedly reduced (58.7%) by treatment with 10(-4) M cyclohexyladenosine, an adenosine A1 receptor agonist, and the reduction was reversed in the presence of 10(-4) M 8-cyclopentyltheophylline, a selective A1 receptor antagonist. In the same brain preparation, 30 mM K+ stimulated the release of glutamate, glutamine, glycine and GABA in a Ca(2+)-dependent manner, whereas the aspartate and taurine release was Ca(2+)-independent. Cyclohexyladenosine inhibited the 30 mM K(+)-evoked release of glutamate in a dose-related manner. This effect was reversed by 8-cyclopentyltheophylline. These results support the hypothesis that adenosine A1 receptors present in goldfish cerebellum are involved in the modulation of glutamate transmitter release.

Adenosine A1 receptor-mediated inhibition of evoked glutamate release is coupled to calcium influx decrease in goldfish brain synaptosomes.

Binding of [3H]cyclohexyladenosine (CHA) to the cellular fractions and P2 subfractions of the goldfish brain was studied. The A1 receptor density was predominantly in synaptosomal membranes. In goldfish brain synaptosomes (P2), 30 mM K+ stimulated glutamate, taurine and GABA release in a Ca(2+)-dependent fashion, whereas the aspartate release was Ca(2+)-independent. Adenosine, R-phenylisopropyladenosine (R-PIA) and CHA (100 microM) inhibited K(+)-stimulated glutamate release (31%, 34% and 45%, respectively). All of these effects were reversed by the selective adenosine A1 receptor antagonist, 8-cyclopentyltheophylline (CPT). In the same synaptosomal preparation, K+ (30 mM) stimulated Ca2+ influx (46.8 +/- 6.8%) and this increase was completely abolished by pretreatment with 100 nM omega-conotoxin. Pretreatment with 100 microM R-PIA or 100 microM CHA, reduced the evoked increase of intra-synaptosomal Ca2+ concentration, respectively by 37.7 +/- 4.3% and 39.7 +/- 9.0%. A possible correlation between presynaptic A1 receptor inhibition of glutamate release and inhibition of calcium influx is discussed.

Spontaneous recovery of MPTP-damaged catecholamine systems in goldfish brain areas.

In goldfish, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administered for 3 consecutive days (10 mg/kg), produced a marked decrease in dopamine (DA) and noradrenaline (NA) levels in telencephalon, diencephalon and medulla oblongata, without affecting the serotonin (5-HT) content. Furthermore the neurotoxin decreased either [3H]DA high affinity uptake or K(+)-stimulated DA release from synaptosomal (P2) preparations, with concomitant up-regulation of D2 postsynaptic receptors as well. No significant changes of choline acetyltransferase and glutamic acid decarboxylase activity or [3H]glutamate uptake were observed. Moreover the pretreatment with deprenyl (1 mg/kg) or mazindol (10 mg/kg) but not with clorgyline (5 mg/kg) prevented catecholamine depletion. Added in vitro to synaptosomal preparations both MPTP and more potently MPP+, in a concentration-dependent manner, inhibited [3H]DA uptake. Time course study revealed that MPTP-induced alteration of neurochemical parameters in goldfish brain areas were almost completely reversed within 6 weeks, suggesting that catecholamine systems in goldfish brain show a remarkable power of recovery after MPTP lesion.