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PubMed1996

[Value of CT-angiography in diagnosis of cerebral sinus and venous thromboses].

Dural sinus thrombosis is not uncommon. Due to the nonspecific symptomatology, as well as the manifold etiology, clinical diagnosis may be difficult. In these cases imaging procedures are frequently crucial in deciding how to proceed and how to treat. The aim of our study was to evaluate the diagnostic utility of helical CT in the detection of dural sinus thrombosis. In 20 patients with clinically suspected thrombosis CT angiography was performed. In 6 patients dural sinus thrombosis was diagnosed. In order to acquire also arterial vessels, a short delay of about 22 s after the onset of the application of contrast medium was selected. By this method we found an occlusion of the MCA in two patients with clinically suspected sinus thrombosis. In all patients the transverse slices and the multiplanar reconstructions showed filling defects or an "empty delta" sign. With irregular outlines the thrombus could be depicted over the complete course of the sinus. The MIP reconstructions were particularly helpful in the evaluation of the vessel anatomy and the pathological collateral venous drainage. In three patients MR angiograms were available for comparison. The smaller veins, such as the v. vermis inferior, were less clearly depicted than in CT angiography. CT angiography is a fast and reliable method to exclude or verify a sinus thrombosis. It can be performed immediately after non-enhanced CT. According to our present experience CT angiography is sufficient for the diagnosis of a sinus thrombosis.

Adolescent↗

PubMed1998

Qualitative versus quantitative assessment of cerebrovascular reserves.

OBJECTIVE: Quantitative studies of cerebral blood flow (CBF) combined with a vasodilatory challenge have defined a subgroup of patients with symptomatic carotid occlusion who have an increased risk for stroke. These are patients whose CBF paradoxically decreases in response to a vasodilatory challenge. Recent reports suggest that qualitative CBF techniques, such as single photon emission tomography with 99m-hexamethylpropyleneamine oxime, can also define the same high-risk subgroup. To determine whether qualitative measures of CBF are sufficient for predicting the risk of stroke, we converted our quantitative CBF data, obtained with xenon-enhanced computed tomography (Xe/CT), to qualitative ratios in a manner similar to that used with single photon emission tomography data. METHODS: We analyzed CBF values within the territory of the middle cerebral artery for 94 patients with symptomatic carotid occlusion. Values obtained using Xe/CT before and after the intravenous administration of 1 g of acetazolamide were used to derive an asymmetry index: (Coccl - Cnon)/Cavg x 100. The difference between the postacetazolamide asymmetry index and the baseline asymmetry index was used to classify the patients into groups according to CBF values. The threshold for abnormal qualitative CBF reactivity was defined as a percent change in the asymmetry index of less than -10%. Quantitative (Xe/CT) CBF was considered abnormal ("steal" response) when the response to acetazolamide (percent change) on the occluded side was a decrease of 5% or greater. RESULTS: Of 34 patients whose cerebrovascular reserves were considered compromised based on qualitative criteria, 17 (50%) did not have a steal response as defined by quantitative Xe/CT CBF (i.e., false positive). Eleven of 62 (18%) who were not considered compromised by qualitative criteria had a steal response (i.e., false negative). Our data indicate that a qualitative approach has a 61% sensitivity and a 75% specificity for detecting patients with compromised reserves. Further, the positive predictive value of this method is only 50%. Therefore, the two methodologies do not predict the same patients as having compromised reserves. CONCLUSION: Previous studies have shown that patients at high risk for stroke can be identified with quantitative CBF methods. This study shows that the important subgroup cannot be accurately defined with qualitative methodology. The implications of using the more reliable methodology are important for individual patient management and for designing clinical trials.

Acetazolamide↗

PubMed2004

Collateral desmitis of the distal interphalangeal joint in 18 horses (2001-2002).

REASONS FOR PERFORMING STUDY: There have been no previously published case series of horses examined using either scintigraphy or MRI to diagnose collateral ligament injuries not detectable using ultrasonography or radiography, nor have other concurrent soft tissue lesions been described. OBJECTIVES: To describe the clinical features of horses with desmitis of the collateral ligaments of the distal interphalangeal (DIP) joint and to evaluate the results of radiographic, ultrasonographic, scintigraphic and magnetic resonance imaging (MRI) examinations. METHODS: Horses were examined between January 2001 and January 2003 and were selected for inclusion in the study if there was unequivocal evidence of collateral desmitis of the DIP joint based on ultrasonography or MRI. Subject details, case history, results of clinical examination and responses to local analgesic techniques were reviewed. The results of radiographic, ultrasonographic, scintigraphic and MRI examinations were assessed. RESULTS: Eighteen horses were identified with desmitis of a collateral ligament of the DIP joint, 3 horses (Group 1) based on ultrasonography alone, 7 (Group II) with positive ultrasonographic and magnetic resonance images and 8 (Group III) with no lesion detectable using ultrasonography, but lesions identified using MRI. Seventeen horses had forelimb injuries and one a hindlimb injury. The medial collateral ligament was injured most frequently (13 horses). In the majority of horses, no localising clinical signs were seen. Lameness was invariably worse in circles compared with straight lines. Lameness was improved by palmar digital analgesia in 16 horses (87%), but only 6 were nonlame. Intra-articular analgesia of the DIP joint produced improvement in lameness in 6/15 horses (40%). In 16 horses, no radiographic abnormality related to the DIP joint or collateral ligament attachments was identified. Eight of 14 horses (57%) had focal, moderately or intensely increased radiopharmaceutical uptake (IRU) at the site of insertion of the injured collateral ligament on the distal phalanx. Alteration in size and signal in the injured collateral ligament was identified using MRI. In addition, 5 horses had abnormal mineralisation and fluid in the distal phalanx at the insertion of the ligament. Eleven horses had concurrent soft tissue injuries involving the deep digital flexor tendon, distal sesamoidean impar ligament, navicular bursa or collateral ligament of the navicular bone. CONCLUSIONS AND POTENTIAL RELEVANCE: Collateral desmitis of the DIP joint should be considered as a cause of foot lameness. Although some injuries are detectable ultrasonographically, false negative results occur. Focal IRU at the ligament insertion on the distal phalanx may be indicative of injury in some horses. MRI is useful for both characterisation of the injury and identification of any concurrent injuries. Further follow-up information is required to determine factors influencing prognosis.

Animals↗

PubMed1993

Protection from ischaemic-reperfusion injury with adenosine pretreatment is reversed by inhibition of ATP sensitive potassium channels.

OBJECTIVE: The aim was to test the hypothesis that the cardioprotective effects against ischaemic-reperfusion injury of pretreatment with adenosine are mediated in part by activation of ATP sensitive potassium channels (K+ATP channels). METHODS: 42 anaesthetised New Zealand White rabbits underwent 30 min coronary occlusion, followed by 2 h reperfusion. Half the animals received a 5 min infusion of 140 micrograms.kg-1.min-1 of adenosine as pretreatment. The remainder of the animals received a 5 min infusion of saline alone as pretreatment. Animals pretreated with adenosine received either a low dose of the K+ATP channel blocker glibenclamide (0.3 mg.kg-1), high dose glibenclamide (3.0 mg.kg-1), or vehicle immediately prior to ischaemia to test whether glibenclamide can reverse the protective effects of adenosine, thus allowing the adenosine effect but antagonising K(+)ATP channel activation during ischaemia. Animals which received saline pretreatment also received low dose glibenclamide, high dose glibenclamide, or vehicle (controls) to evaluate the effect of glibenclamide alone. Infarct size was determined with tetrazolium and Unisperse Blue stains, and transmural blood flow was measured using radioactive microspheres. RESULTS: Although there were no differences in collateral myocardial blood flow during ischaemia or in risk area among the groups, infarct size was reduced by adenosine pretreatment to 8 (SEM 3)% v 36(4)% in controls (p < 0.05). K(+)ATP channel blockade with low dose glibenclamide in saline pretreated animals did not by itself extend the degree of necrosis [33(4)%], whereas low dose glibenclamide prevented the protective effects of adenosine pretreatment [38(3)%]. High dose glibenclamide reversed adenosine protection as well [54(3)%], but at a dose which increased infarct size in saline pretreated animals [52(3)%]. CONCLUSIONS: While adenosine pretreatment protects against necrosis in the rabbit, (1) the expression of this protection depends at least in part upon the actions of K(+)ATP channels during ischaemia, and (2) glibenclamide at higher doses increases infarct size, suggesting either that the K(+)ATP channel is endogenously protective during ischaemia, or that the higher dose has other infarct extending effects.

Adenosine↗

PubMed1992

Blockade of ATP-sensitive potassium channels prevents myocardial preconditioning in dogs.

Single or multiple brief periods of ischemia (preconditioning) have been shown to protect the myocardium from infarction after a subsequent more prolonged ischemic insult. To test the hypothesis that preconditioning is the result of opening ATP-sensitive potassium (KATP) channels, a selective KATP channel antagonist, glibenclamide, was administered before or immediately after preconditioning in barbital-anesthetized open-chest dogs subjected to 60 minutes of left circumflex coronary artery (LCX) occlusion followed by 5 hours of reperfusion. Preconditioning was elicited by 5 minutes of LCX occlusion followed by 10 minutes of reperfusion before the 60-minute occlusion period. Glibenclamide (0.3 mg/kg i.v.) or vehicle was given 10 minutes before the initial ischemic insult in each of four groups. In a fifth group, glibenclamide was administered immediately after preconditioning. In a final series (group 6), a selective potassium channel opener, RP 52891 (10 micrograms/kg bolus and 0.1 micrograms/mg/min i.v.) was started 10 minutes before occlusion and continued throughout reperfusion. Transmural myocardial blood flow was measured at 30 minutes of occlusion, and infarct size was determined by triphenyltetrazolium staining and expressed as a percent of the area at risk. There were no significant differences in hemodynamics, collateral blood flow, or area at risk between groups. The ratio of infarct size to area at risk in the control group (28 +/- 6%) was not different from the group pretreated with glibenclamide in the absence of preconditioning (31 +/- 6%). Preconditioning produced a marked reduction (p less than 0.002) in infarct size (28 +/- 6% to 6 +/- 2%), whereas glibenclamide administered before or immediately after preconditioning completely abolished the protective effect (28 +/- 6% and 30 +/- 8%, respectively). RP 52891 also produced a significant (p less than 0.03) reduction (28 +/- 6% to 13 +/- 3%) in infarct size. These results suggest that myocardial preconditioning in the canine heart is mediated by activation of KATP channels and that these channels may serve an endogenous myocardial protective role.

Adenosine Triphosphate↗

PubMed2003

Lymphoscintigraphic evaluation of chronic lower limb oedema.

Ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), venography, lymphoscinti-graphy (LS) and contrast lymphography are frequently utilized in the evaluation of lower limb oedema but no clinical data from the Caribbean have been published on the role of LS despite its well-recognized clinical application. The successful clinical application of CT, colour doppler sonography and MRI in differentiating the various causes of lower limb oedema is well understood. Lymphoscintigraphy has found less acceptability especially in the Caribbean where nuclear imaging techniques are only now currently being developed. This paper describes the initial experience with this technique in 15 patients over a five-year period and discusses its value when lower limb lymphoedema is suspected. Scintigrams were analyzed for visualization of lymph vessels and lymph nodes, dilatation of lymphatic vessels, collaterals and dermal back flow. Lymphoscintigrams were classified as normal (n = 5) or consistent with lymphoedema (n = 10). Failure to visualize lymphatic vessels occurred in two cases of suspected primary lymphoedema. In the remaining eight cases of secondary lymphoedema, a positive study based on altered lymphatic flow and anatomy was recorded. An alternative explanation was offered in three out of five cases in which a normal lymphoscintigram was obtained.

Adult↗

PubMed2004

Re-evaluating therapeutic neovascularization.

Numerous animal studies have established that neo-vascularization of ischemic tissue can be enhanced with exogenous growth factors and small clinical studies have shown encouraging results. However, the two largest randomized clinical trials to date were negative. Mechanistically, the major stimuli for neo-vascularization are hypoxia and inflammation. Hypoxia-inducible-factor (HIF-1) is a 'master switch' protein that is generated in response to hypoxia and binds to more than 40 hypoxia sensitive genes, inducing a panoply of angiogenic and protective metabolic responses. Inflammatory signals recruit T-lymphocytes and macrophages into areas of neo-vascularization which act as a source of angiogenic and arteriogenic factors. Although hypoxia and inflammation are interdependent in eliciting neo-vascular responses, angiogenesis appears to be hypoxia-dependent, whereas inflammation and hemodynamic factors drive arteriogenesis. The negative outcome of the two largest trials may have many reasons. There are issues relating to patient selection, choice of growth factor therapy, dosing and route administration, concomitant medication, trial design including the efficacy parameters that were selected and a lack of sufficient insight into the mechanisms that are responsible for neo-vascularization. In order to move forward the therapeutic objective should be switched to arteriogenesis although this process is even more poorly understood than angiogenesis. Genetic studies in mice with intrinsically different arteriogenic responses combined with studies in human populations with differences in the extent of collateral development may provide fundamental insight into arteriogenic mechanisms. Attention should also be focused on the way in which arteriogenesis is stimulated and the endpoints of clinical trials should be redefined.

Humans↗

PubMed1999

Multimodal efferent and recurrent neurons in the medial lobes of cockroach mushroom bodies.

Previous electrophysiological studies of cockroach mushroom bodies demonstrated the sensitivity of efferent neurons to multimodal stimuli. The present account describes the morphology and physiology of several types of efferent neurons with dendrites in the medial lobes. In general, efferent neurons respond to a variety of modalities in a context-specific manner, responding to specific combinations or specific sequences of multimodal stimuli. Efferent neurons that show endogenous activity have dendritic specializations that extend to laminae of Kenyon cell axons equipped with many synaptic vesicles, termed "dark" laminae. Efferent neurons that are active only during stimulation have dendritic specializations that branch mainly among Kenyon cell axons having few vesicles and forming the "pale" laminae. A new category of "recurrent" efferent neuron has been identified that provides feedback or feedforward connections between different parts of the mushroom body. Some of these neurons are immunopositive to antibodies raised against the inhibitory transmitter gamma-aminobutyric acid. Feedback pathways to the calyces arise from satellite neuropils adjacent to the medial lobes, which receive axon collaterals of efferent neurons. Efferent neurons are uniquely identifiable. Each morphological type occurs at the same location in the mushroom bodies of different individuals. Medial lobe efferent neurons terminate in the lateral protocerebrum among the endings of antennal lobe projection neurons. It is suggested that information about the sensory context of olfactory (or other) stimuli is relayed by efferent neurons to the lateral protocerebrum where it is integrated with information about odors relayed by antennal lobe projection neurons.

Animals↗

PubMed1988

Projections from upper cervical inspiratory neurons to thoracic and lumbar expiratory motor nuclei in the cat.

Previous studies have demonstrated the existence of axonal projections from propriospinal respiratory neurons in the rostral cervical cord of the cat (upper cervical inspiratory neurons) to the vicinity of the phrenic and rostral thoracic inspiratory (external) intercostal motoneurons. However, no synaptic targets of the upper cervical inspiratory neurons have been identified. This study investigated the axonal projections to the caudal thoracic and upper lumbar cord and the possible existence of inhibitory connections to the expiratory intercostal and abdominal motoneurons. The connections from upper cervical inspiratory neurons to expiratory motoneurons in the lower thoracic cord were examined using the methods of antidromic mapping and the spike-triggered averaging of intracellular potentials. Of the 70 upper cervical inspiratory neurons examined, only four (5.7%) could not be antidromically activated from the T9 segment of the spinal cord. The axons of 66 upper cervical inspiratory antidromic activation at less than 5 microV, and the presence of collaterals was confirmed by antidromic mapping in 30 cases (49.2%). Of 21 axons tested for lumbar projections, 13 (61.9%) projected as far as T12, seven (33.3%) as far as L1, three (14.3%) as far as L2, and one (4.8%) was antidromically activated from L3. Spike-triggered averaging of the synaptic potentials recorded intracellularly from expiratory intercostal motoneurons in T9 and T10 spinal segments was done for 27 upper cervical inspiratory neurons, 17 of these with 4 or more motoneurons, for a total of 111 expiratory motoneurons. In 16 cases the motoneurons were injected with Cl- to reverse IPSPs and the spike-triggered averaging was repeated. No monosynaptic or disynaptic post-synaptic potentials were seen in any of the spike-triggered averages. We concluded that the upper cervical inspiratory neurons may provide inspiratory inhibition to expiratory motoneurons via a di- or oligosynaptic pathway involving segmental inhibitory interneurons and that either the spike-triggered averaging technique was not sensitive enough to detect the ipsilateral connections or the interneuron pathway was to the contralateral side of the spinal cord.

Animals↗

PubMed1994

[Assessment of myocardial viability by thallium-201 reinjection imaging with sublingual nitroglycerin].

Although thallium-201 (201Tl) reinjection imaging improves the detection of myocardial viability compared to standard 3-4-hr redistribution (RD) imaging, it still underestimates the extent of viable myocardium. We examined whether 201Tl reinjection SPECT with sublingual nitroglycerin (NTG) had a higher sensitivity for viability detection than reinjection alone. Eighty patients with coronary artery disease were studied, 38 of them with an old myocardial infarction. At the peak of exercise, 111 MBq 201Tl was injected and the initial and the delayed SPECT images were obtained. Then, all patients were divided randomly into two groups, and in each group, SPECT data were obtained again after the injection of 37 MBq 201Tl with (NTG(+) group) or without 0.6 mg of sublingual NTG (NTG(-) group). Among 50 segments showing fixed defects on the delayed image in the NTG(+) group, 21 (42%) were found to be reversible on the reinjection image, as compared to 16 of 51 (31%) in the NTG(-) group. Twenty-two of 44 (50%) segments showing incomplete RD were found to be reversible in the NTG(+) group, while 17 of 42 (41%) segments in the NTG(-) group. Moreover, the ratio of reversible segments seen in the reinjection images was significantly higher in the collateralized regions of the NTG(+) group than in those of the NTG(-) group (20/26 vs. 14/28, p < 0.05). Thus, 201Tl reinjection SPECT with sublingual NTG improves the detection of ischemic but viable myocardium as compared to SPECT with reinjection alone.

Administration, Sublingual↗

PubMed1998

Alterations in potassium currents may trigger neurodegeneration in murine scrapie.

Conventional electrophysiological intracellular recording techniques were used to test the hypothesis that enhanced calcium entry via voltage-gated calcium channels or the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor-channel complex may be a primary pathological mechanism triggering neurodegeneration in scrapie and related diseases. This study was carried out at a time when cell loss is known to occur and when hippocampal pyramidal cells in area CA1 are rendered hyperexcitable following scrapie infection. There was no change to the NMDA receptor-mediated component of the Schäffer collateral evoked excitatory postsynaptic potential (EPSP) or the level of spontaneous firing activity of CA1 cells following addition of the specific NMDA receptor antagonist, 2-amino-5-phosphonovaleric acid (APV, 20 microM), to the perfusate in scrapie-infected mice, indicating that the NMDA receptor-channel complex is not compromised by scrapie. There was also no change seen in the non-NMDA mediated component of the EPSP. The calcium spike of CA1 pyramidal cells was not significantly altered by scrapie infection, indicating that high threshold voltage-gated Ca2+ channel function is not compromised by scrapie. By contrast, cells from scrapie-infected mice fired calcium spikes repetitively and the long, slow AHP, which in control cells inhibited repetitive firing, was absent. Cells from scrapie-infected mice showed more depolarized membrane potentials than controls but this difference in potential was no longer observed after exposure to TEA. These data indicate a loss of TEA-insensitive and TEA-sensitive potassium conductances. We suggest that altered potassium currents rather than increased calcium entry via voltage-sensitive calcium channels or the NMDA receptor complex may be the primary pathological mechanism triggering neurodegeneration in scrapie and related diseases.

2-Amino-5-phosphonovalerate↗

PubMed1995

Stress-induced behavioral responses and multiple opioid systems in the brain.

Various stressor produce a wide range of behavioral responses such as analgesia, catalepsy and motor suppression, which are sensitive to opioid receptor antagonists. These behavioral responses in stress are accompanied by changes in the contents of opioid peptides, the mRNAs encoding their precursors and opioid receptor binding in the brain. In the present article, experimental data concerning stress-induced analgesia and motor suppression is reviewed and discussed in relation to a possible involvement of different opioid systems in the various observed behavioral responses in stress. Pharmacological studies with subtype-selective antagonists have demonstrated that not only mu- but also delta- and/or kappa-opioid receptors are involved in opioid-mediated stress-induced analgesia. There are two types of stress-induced analgesia referred to as opioid-mediated and non-opioid mediated forms. It has been proposed that the intensity and temporal pattern of stressor may be a critical factor determining the nature of stress-induced analgesia. Accumulated evidence demonstrate that these two forms of pain inhibitory systems interact each other according to a collateral inhibition model. Recent studies show that parallel activation of multiple opioid receptors mediates non-opioid froms of stress-induced analgesia. Dynorphins, by acting at kappa-opioid receptors, may play a pivotal role in the expression of stress-induced motor suppression, whereas enkephalins may act to attenuate this response.

Adaptation, Psychological↗

PubMed2006

Ligament balancing in TKA: evaluation of a force-sensing device and the influence of patellar eversion and ligament release.

Ligament balancing in total knee arthroplasty may have an important influence on joint stability and prosthesis lifetime. In order to provide quantitative information and assistance during ligament balancing, a device that intraoperatively measures knee joint forces and moments was developed. Its performance and surgical advantages were evaluated on six cadaver specimens mounted on a knee joint loading apparatus allowing unconstrained knee motion as well as compression and varus-valgus loading. Four different experiments were performed on each specimen. (1) Knee joints were axially loaded. Comparison between applied and measured compressive forces demonstrated the accuracy and reliability of in situ measurements (1.8N). (2) Assessment of knee stability based on condyle contact forces or varus-valgus moments were compared to the current surgical method (difference of varus-valgus loads causing condyle lift-off). The force-based approach was equivalent to the surgical method while the moment-based, which is considered optimal, showed a tendency of lateral imbalance. (3) To estimate the importance of keeping the patella in its anatomical position during imbalance assessment, the effect of patellar eversion on the mediolateral distribution of tibiofemoral contact forces was measured. One fourth of the contact force induced by the patellar load was shifted to the lateral compartment. (4) The effect of minor and major medial collateral ligament releases was biomechanically quantified. On average, the medial contact force was reduced by 20% and 46%, respectively. Large variation among specimens reflected the difficulty of ligament release and the need for intraoperative force monitoring. This series of experiments thus demonstrated the device's potential to improve ligament balancing and survivorship of total knee arthroplasty.

Aged↗

PubMed2002

NMDA receptor activation mediates hydrogen peroxide-induced pathophysiology in rat hippocampal slices.

Endogenous reactive oxygen species (ROS) can act as modulators of neuronal activity, including synaptic transmission. Inherent in this process, however, is the potential for oxidative damage if the balance between ROS production and regulation becomes disrupted. Here we report that inhibition of synaptic transmission in rat hippocampal slices by H2O2 can be followed by electrical hyperexcitability when transmission returns during H2O2 washout. As in previous studies, H2O2 exposure (15 min) reversibly depressed the extracellular population spike (PS) evoked by Schaffer collateral stimulation. Recovery of PS amplitude, however, was typically accompanied by mild epileptiform activity. Inclusion of ascorbate (400 microM) during H2O2 washout prevented this pathophysiology. No protection was seen with isoascorbate, which is a poor substrate for the stereoselective ascorbate transporter and thus remains primarily extracellular. Epileptiform activity was also prevented by the N-methyl-D-aspartate (NMDA) receptor antagonist, DL-2-amino-5-phosphonopentanoic acid (AP5) during H2O2 washout. Once hyperexcitability was induced, however, AP5 did not reverse it. When present during H2O2 exposure, AP5 did not alter PS depression by H2O2 but did inhibit the recovery of PS amplitude seen during pulse-train stimulation (10 Hz, 5 s) in H2O2. Inhibition of glutamate uptake by l-trans-2,4-pyrrolidine dicarboxylate (PDC; 50 microM) during H2O2 washout markedly enhanced epileptiform activity; coapplication of ascorbate with PDC prevented this. These data indicate that H2O2 exposure can cause activation of normally silent NMDA receptors, possibly via inhibition of redox-sensitive glutamate uptake. When synaptic transmission returns during H2O2 washout, enhanced NMDA receptor activity leads to ROS generation and consequent oxidative damage. These data reveal a pathological cycle that could contribute to progressive degeneration in neurological disorders that involve oxidative stress, including cerebral ischemia.

2-Amino-5-phosphonovalerate↗

PubMed2005

Preoperative evaluation of venous systems with 3-dimensional contrast-enhanced magnetic resonance venography in brain tumors: comparison with time-of-flight magnetic resonance venography and digital subtraction angiography.

BACKGROUND: Recent developments in magnetic resonance (MR) technology now enable the use of MR venography, providing 3-dimensional (3D) images of intracranial venous structures. The purpose of this study was to assess the usefulness of 3D contrast-enhanced MR venography (CE MRV) in the evaluation of intracranial venous system for surgical planning of brain tumors. METHODS: Forty patients underwent 3D CE MRV, as well as 25 patients, 2-dimensional (2D) time-of-flight (TOF) MR venography in axial and sagittal planes; and 10 patients, digital subtraction angiography. We determined the number of visualized sinuses and cortical veins. Degree of visualization of the intracranial venous system on 3D CE MRV was compared with that of 2D TOF MR venography and digital subtraction angiography as a standard. We also assessed the value of 3D CE MRV in the investigation of sinus occlusion or localization of cortical draining veins preoperatively. RESULTS: Superficial cortical veins and the dural sinus were better visualized on 3D CE MRV than on 2D TOF MR venography. Both MR venographic techniques visualized superior sagittal sinus, lateral sinus, sigmoid sinus, straight sinus, and internal cerebral vein and provided more detailed information by showing obstructed sinuses in brain tumors. Only 3D CE MRV showed superficial cortical draining veins. However, it was difficult to accurately evaluate the presence of cortical collateral venous drainage. CONCLUSION: Although we do not yet advocate MR venography to replace conventional angiography as the imaging standard for brain tumors, 3D CE MRV can be regarded as a valuable diagnostic method just in evaluating the status of major sinuses and localization of the cortical draining veins.

Adolescent↗

PubMed1999

GABAergic control of rat substantia nigra dopaminergic neurons: role of globus pallidus and substantia nigra pars reticulata.

Dopaminergic neurons in vivo fire spontaneously in three distinct patterns or modes. It has previously been shown that the firing pattern of substantia nigra dopaminergic neurons can be differentially modulated by local application of GABA(A) and GABA(B) receptor antagonists. The GABA(A) antagonists, bicuculline or picrotoxin, greatly increase burst firing in dopaminergic neurons whereas GABA(B) antagonists cause a modest shift away from burst firing towards pacemaker-like firing. The three principal GABAergic inputs to nigral dopaminergic neurons arise from striatum, globus pallidus and from the axon collaterals of nigral pars reticulata projection neurons, each of which appear to act in vivo primarily on GABA(A) receptors (see preceding paper). In this study we attempted to determine on which afferent pathway(s) GABA(A) antagonists were acting to cause burst firing. Substantia nigra dopaminergic neurons were studied by single unit extracellular recordings in urethane anesthetized rats during pharmacologically induced inhibition and excitation of globus pallidus. Muscimol-induced inhibition of pallidal neurons produced an increase in the regularity of firing of nigral dopaminergic neurons together with a slight decrease in firing rate. Bicuculline-induced excitation of globus pallidus neurons produced a marked increase in burst firing together with a modest increase in firing rate. These changes in firing rate were in the opposite direction to what would be expected for a monosynaptic GABAergic pallidonigral input. Examination of the response of pars reticulata GABAergic neurons to similar manipulations of globus pallidus revealed that the firing rates of these neurons were much more sensitive to changes in globus pallidus neuron firing rate than dopaminergic neurons and that they responded in the opposite direction. Pallidal inhibition produced a dramatic increase in the firing rate of pars reticulata GABAergic neurons while pallidal excitation suppressed the spontaneous activity of pars reticulata GABAergic neurons. These data suggest that globus pallidus exerts significant control over the firing rate and pattern of substantia nigra dopaminergic neurons through a disynaptic pathway involving nigral pars reticulata GABAergic neurons and that at least one important way in which local application of bicuculline induces burst firing of dopaminergic neurons is by disinhibition of this tonic inhibitory input.

Action Potentials↗

PubMed1996

Significance of perfusion of the infarct related coronary artery for susceptibility to ventricular tachyarrhythmias in patients with previous myocardial infarction.

OBJECTIVE: To study the significance of perfusion of the infarct related coronary artery for susceptibility to ventricular tachyarrhythmias in patients with a remote myocardial infarction. SETTING: Tertiary referral cardiac centre. METHODS: Angiographic filling of the infarct related artery was assessed in a consecutive series of 85 patients with different susceptibilities to ventricular tachyarrhythmias after previous (> 3 months) Q wave myocardial infarction: 30 patients had a history of cardiac arrest (n = 16) or sustained ventricular tachycardia (n = 14), and sustained ventricular tachyarrhythmia was inducible in these by programmed electrical stimulation (arrhythmia group); 47 patients had no clinical arrhythmic events and no inducible ventricular tachyarrhythmias during programmed ventricular stimulation (control group). Eight patients without a history of any arrhythmic events were inducible into ventricular tachycardia. RESULTS: The patients in the arrhythmia group were older (63 (SD 8) years) than the control patients (59 (6) years, P < 0.05), and had larger left ventricular volumes in cineangiography (P < 0.01), but ejection fraction, severity of left ventricular wall motion abnormalities, previous thrombolytic therapy, and time from previous infarction did not differ between the groups. Patients with susceptibility to ventricular tachyarrhythmias more often had a totally occluded infarct related artery on angiography (77%) than patients without arrhythmia susceptibility (21%) (P < 0.001), and complete collateral filling of the infarct artery in cases without complete anterograde filling was less common in the arrhythmia group than in the control group (P < 0.001). Patients without a history of malignant arrhythmia but with inducible ventricular tachyarrhythmia also had no or poor perfusion of the infarct artery more often than the patients without inducible arrhythmia (P < 0.001). Logistic multiple regression showed that no or poor anterograde or collateral filling of the infarct related artery was the most powerful predictor of susceptibility to ventricular tachyarrhythmias (P < 0.001). Left ventricular size and function were not independently related to arrhythmic susceptibility. CONCLUSIONS: No or poor angiographic filling of the infarct related artery is closely associated with susceptibility to ventricular tachyarrhythmias late after acute myocardial infarction, suggesting that perfusion of the infarct artery will modify favourably the electrophysiological substrate of the infarct scar independently of the myocardial salvage achieved by early reperfusion.

Coronary Angiography↗

PubMed1998

Requirement of rapid Ca2+ entry and synaptic activation of metabotropic glutamate receptors for the induction of long-term depression in adult rat hippocampus.

1. During block of gamma-aminobutyric acid-A-mediated inhibition, low-frequency stimulation (2 Hz, 900 pulses) to Schaffer collateral-CA1 neuron synapses of adult rat hippocampus induced an N-methyl-D-aspartate receptor-independent, postsynaptic Ca2+-dependent depression of synaptic strength (long-term depression; LTD). 2. Ratio imaging with fura-2 revealed moderate dendritic [Ca2+] increases (approximately 500 nM) during only the initial approximately 30 s of the 7.5 min stimulation period. Conditioning for 30 s was, however, insufficient to induce LTD. 3. The [Ca2+] changes were insensitive to the metabotropic glutamate receptor (mGluR) antagonist (+)-alpha-methyl-4-carboxyphenylglycine (MCPG). MCPG, however, completely blocked LTD when present during conditioning. 4. The [Ca2+] changes were abolished by postsynaptic hyperpolarization (-110 mV at the soma). Hyperpolarizing neurons to -110 mV during conditioning significantly attenuated LTD induction. 5. LTD induction was also blocked by the postsynaptic presence of the protein kinase C inhibitor peptide PKC(19-36). 6. These results suggest that LTD induction in adult hippocampus by prolonged low-frequency stimulation depends on both a rapid Ca2+ influx through voltage-sensitive channels and synaptic stimulation of mGluRs which may be coupled to phospholipase C.

2-Amino-5-phosphonovalerate↗