Interval change in size of venous pouch canine bifurcation aneurysms over a 10-month period.

BACKGROUND AND PURPOSE: The natural history study of experimental aneurysms is important for the evaluation of new endovascular occlusion devices. Our purpose was to evaluate the natural history of experimental venous pouch bifurcation aneurysms in mongrel dogs up to a 10-month period. MATERIALS AND METHODS: Serial digital subtraction angiography was performed in 5 bifurcation aneurysms 1, 4, 7, and 10 months after surgical creation. Aneurysm dimensions, including height, width, and neck diameter, and animal body weights were measured. Comparisons of each parameter were performed using the Friedman test and the paired Wilcoxon signed-rank test. RESULTS: Four of 5 aneurysms were patent during a 10-month follow-up period. One aneurysm was regarded as a partially thrombosed aneurysm at 1 month, though the extent of partial thrombosis lessened at 10 months. Bifurcation aneurysms progressively increased in size (aneurysm height, width, and neck diameter) during the first several months. CONCLUSION: If this experimental model is used to evaluate new endovascular devices for cerebral aneurysm treatment, investigators should be aware of early progressive aneurysm enlargement.

Stenting for Left Subclavian Artery Stenosis before and after Coronary Artery Bypass Grafting Using the Internal Mammary Artery: A Report of Three Cases.

SUMMARY: Stenosis of the subclavian artery proximal to the origin of the internal mammary artery (IMA) used for coronary artery bypass grafting may produce flow reversal (steal syndrome) and cause myocardial ischemia. We present three cases of subclavian artery stenosis proximal to the IMA before and after CABG. The first case developed symptomatic myocardial ischemia resulting from a variant of coronary-subclavian steal syndrome. The second case had asymptomatic subclavian artery stenosis proximal to the IMA used for CABG. In the third case we planned to perform CABG using the left IMA to treat cardiac ischemia. All of the patients were successfully treated by stent placement without the use of a protection device. In the first and second cases, cardiac ischemia did not appear during balloon inflation of the subclavian artery and no embolic complication occurred. In the third case, CABG was performed six months after stenting. Subclavian artery stenting is a valid alternative to surgical treatment to restore the flow to the IMA before or after CABG.

Traumatic bilateral common carotid artery dissection due to strangulation. A case report.

SUMMARY: We report a case of bilateral common carotid artery dissection due to strangulation successfully treated by stent placement, with a review of the literature. A 61-year-old woman was strangled by an apron strap. She was admitted to our hospital with tetraparesis, because of spinal cord injury. On the next day, her left hemiparesis aggravated and left facial palsy newly appeared. Diffusion weighted magnetic resonance imaging (MRI) showed new ischemic lesions in the right cerebral hemisphere. Aortography revealed bilateral common carotid artery dissection. Moreover, thrombus or intimal flap was recognized in the right common carotid artery. The right common carotid dissection was fixed with deployment of self expanding stents to prevent the aggravation of ischemic stroke at that time. The contralateral lesion was also treated ten days later because small ischemic lesions were newly recognized in the left hemisphere on MRI. No new neurological deficit appeared after bilateral carotid artery stenting. Her paraparesis completely improved two months after the spinal cord injury. Carotid artery stenting using self expanding stents was especially effective as the treatment for bilateral carotid artery dissection.

Coil embolization training using a rabbit saccular aneurysm model.

SUMMARY: We developed a rabbit saccular aneurysm model for coil embolization training. Elastaseinduced aneurysms were created successfully in about 80% of the rabbits. The aneurysms were usually broad in the neck and lengthy. At the 28(th) postoperative day, the aneurysms were about 1.5 times larger in both width and height than they had been at the 14(th) day. All aneurysms were successfully embolized with 18-sized electrically detachable (ED) platinum coils. After embolization, almost all aneurysms had a neck remnant. In conclusion, this model is useful not only for learning the technique of coil embolization but also for testing new embolic materials. The rabbit aneurysm model proved to be an efficacious training modality for endovascular coil embolization.

Balloon or Stent-assisted Coil Embolization for Acutely Ruptured Wide-necked Aneurysms.

SUMMARY: In this paper, we report five cases with acutely ruptured wide-necked aneurysms, which were treated with coil embolization using a balloon or stent-assisted technique. Balloon-assisted coil embolization using Equinox balloon, Commodore balloon, and Hyperform balloon were performed for four patients and stent-assisted coil embolization using BX velocity for one patient. We discuss problems of coil embolization for acutely ruptured wide-necked aneurysms with a balloon or stent-assisted technique.

Endovascular coil embolization for cerebral aneurysms solely using ultrasoft coils.

SUMMARY: We report a series of coil embolizations for small aneurysms solely using GDC ultrasoft coils and discuss the advantages of this method. Seven small aneurysms (< 4.0 mm) were embolized solely with ultrasoft coils. Ultrasoft coils were sequentially inserted into aneurysms. Immediately after embolization, five aneurysms were completely occluded, and two exhibited body filling. All cases were treated successfully without any complications. In conclusion, ultrasoft coils were found efficacious for the treatment of small, irregular-shaped, and ruptured aneurysms; their softness and malleability facilitated their compaction into an aneurysm.

Endovascular treatment of unruptured cerebral aneurysms.

76 consecutive patients with 78 unruptured cerebral aneurysms underwent endovascular therapy from July 1999 to May 2004 in our institute. For the wide-necked aneurysms, the remodeling technique, double microcatheter technique, or stent-assisted coil embolization was used, while a parent artery occlusion or covered stent was applied for the giant or fusiform aneurysms. Immediate angiographical results demonstrated 33 complete occlusions, 26 neck remnants, and 14 dome fillings. Four cases were treated with parent occlusion or stenting only, and one case was not treated with embolization but with clipping due to the rupture of the aneurysm during coil embolization. Immediate angiographic findings demonstrated that in aneurysms between 5 to 10 mm, the rate of complete occlusion was 48%, that of neck remnants 33%, and that of dome fillings 27%. In aneurysms between 11 to 25 mm, the rate of complete occlusion was 14%, that of neck remnants 28%, and that of dome fillings was 58%. In the angiographic follow-up results, all aneurysms smaller than 5 mm showed complete occlusion. In aneurysms between 5 to 10 mm, 74% of the aneurysms showed complete occlusion, and 21% showed neck remnants, and 5% showed dome filling. In aneurysms between 10 to 24 mm, 25% showed complete occlusion, while 75% showed dome filling. The overall mortality rate was 0% and the morbidity rate was 3.7% (2 major strokes, 1 minor stroke) at 30-days after embolization. In the clinical follow-up study, one case of a large basilar tip aneurysm caused a fatal rupture 28 months after the initial embolization. Endovascular therapy was performed on the unruptured aneurysms and was found to be an acceptable treatment, except for durability in cases of large aneurysms.

Brain-derived neurotrophic factor increases inhibitory synapses, revealed in solitary neurons cultured from rat visual cortex.

To elucidate chronic actions of brain-derived neurotrophic factor (BDNF) on GABAergic synapses, we examined effects of a long-term application of BDNF for 10-15 days on autapses (synapses) of solitary GABAergic neurons cultured from rat visual cortex. Solitary neuron preparations were used to exclude a possible contamination of BDNF actions on excitatory neurons in dissociated neuron culture or slice preparations. Neurons were confirmed to be GABAergic pharmacologically with bicuculline, a selective antagonist for GABAA receptors and immunocytochemically with antibody against glutamic acid decarboxylase 65, a GABA synthesizing enzyme. To evaluate GABAergic synaptic function, evoked and/or miniature inhibitory postsynaptic currents (IPSCs) were recorded in the whole-cell voltage-clamp mode. The treatment with BDNF at a concentration of 100 ng/ml enhanced the amplitude of evoked IPSCs and the frequency of miniature IPSCs. In contrast, BDNF did not have a detectable effect on the amplitude of miniature IPSCs and the paired pulse ratio of IPSCs evoked by two, successive activations. To evaluate morphological changes, neurons were immunocytochemically stained with antibodies against microtubule-associated protein 2, to visualize somatodendritic region and synapsin I, to visualize presynaptic sites. The quantitative analysis indicated that BDNF increased the area of soma, the numbers of primary dendrites and dendritic branching points, the total length of dendrites and the number of synaptic sites. Such an action of BDNF was seen in both subgroups of GABAergic neurons, parvalbumin-positive and -negative neurons. To visualize functionally active presynaptic sites, neurons were stained with a styryl dye, FM1-43. BDNF increased the number of stained sites that was correlated with the frequency of miniature IPSCs. These results suggest that the chronic treatment with BDNF promotes dendritic and synaptic development of GABAergic neurons in visual cortex.

Clinical results of percutaneous transluminal angioplasty and stenting for intracranial vertebrobasilar atherosclerotic stenoses and occlusions.

SUMMARY: Eighteen patients with intracranial vertebrobasilar stenosis and occlusion were treated by PTA or stenting. In 11 of 18 cases, only PTA was performed and in seven of 18 cases, we used stents. The mean stenosis before and after PTA/stenting was 82.8% and 22.3%, respectively. In 11 cases of PTA only, the stenotic rate decreased from 81.8% to 29.6%, while 85.0% of the stenotic rate remarkably reduced to 6.0% in seven cases of stenting. The 30 days morbidity and 30 days mortality rate were 5.5% and 5.5%, respectively. There was only one haemorrhagic complication (cerebellar haemorrhage) in cases of stenting, and no ischemic events during or after the procedures. Restenosis (more than 50% stenosis) occurred in four of 18 cases(22.2%) during mean followup period of 12 months. Two patients with VA occlusion before treatment, developed restenosis and reocclusion. Complete total occlusion seems to be a high-risk lesion and strict follow-up is required. In this study, PTA/stenting for intracranial vertebrobasilar artery stenosis or occlusion is an effective treatment, but strict indications may be required because procedure-related 30 days morbidity rate was 5.5% in addition to unclear natural history.

Technique and Clinical Results of Carotid Stenting under Distal Protection.

SUMMARY: We perfomed carotid artery stenting(CAS) in 215 patients from August 1997 to October 2003 mainly using the distal protection technique. Our technique and clinical results are described in this paper.

The study on the patency of the perforating arteries after stent placement in atherosclerosis induced rabbits.

SUMMARY: The number of successful case reports with percutaneous transluminal angioplasty (PTA) / stenting for intracranial atherosclerotic stenoses is recently increasing with the advent of flexible coronary stents. However, it is not well known whether the perforating artery is occluded or not after stent placement in the atherosclerotic stenotic vessels. We investigated this issue using five New Zealand white rabbits. We deployed stainless steel stents in the atherosclerosis-induced abdominal aorta across the lumbar artery in which the diameters of the abdominal arteries were similar to those of human intracranial arteries. We evaluated the patency of lumbar artery by angiography and scanning electron microscopy three months after stent placement. The lumbar arteries were patent in four out of five rabbits. However, SEM findings demonstrated stent struts were covered with thick neointima and the ostia between stent struts were partially occluded. It is possible that stent placement in the atherosclerotic arteries can cause the obliteration of the perforating arteries.

Analysis of Complications related to Endovascular Therapy for Dural Arteriovenous Fistulae.

SUMMARY: In this paper, we reviewed our cases of dural arteriovenous fistulae (dural AVFs) and analyzed periprocedural complications. In 157 procedures, we encountered 14 complications. Overall, complication rate of 9% was seen.We divided these complications into five subgroups such as cranial nerve palsy, coil-related trouble, thromboembolic complication, vessel perforation, and radiation-related trouble. There were five transient abducent nerve palsies in cases with cavernous sinus dural AVFs. There were two cases of coil unraveling and two cases of coil migration. In two cases, direct puncture of the internal jugular vein was performed to retrieve the unraveled coil by using dual microcatheter and guidewire snare technique. We encountered two thromboembolic complications. In one case, venous infarction was recognized after polyvinyl alcohol particle embolization. In two cases of vessel perforations, there were no new neurological deficits except one case with transient Gerstmann syndrome. In endovascular treatment of dural AVF, serious complications are rare and can be prevented if maximum attention is paid during the procedure.

Standard Technique of PTA/stenting for Atherosclerotic Intracranial Arterial Stenosis.

SUMMARY: PTA/stenting for the intracranial arteriosclerotic lesion is effective and novel treatment. Our standard technique to avoid serious complications, such as vessel rupture or acute occlusion was introduced in this paper.

Restenosis of the sigmoid sinus after stenting for treatment of intracranial venous hypertension: case report.

We report what we believe to be the first case of restenosis of the sigmoid sinus after stenting, in a 42-year-old man with an arteriovenous malformation with progressive right hemiparesis secondary to venous hypertension. Angiography revealed severe stenosis of the left sigmoid sinus, which was dilated with a self-expandable stent. Six months after the procedure, however, the sinus was again severely stenosed. Intravascular sonography revealed intimal proliferation in the stented sinus. It was dilated percutaneously, and the venous pressure decreased from 51 to 33 mmHg. On sonography, the intimal tissue decreased in thickness and the diameter of the stent enlarged a little.

Low-frequency depression of synaptic responses recorded from rat visual cortex.

To characterize the low-frequency depression (LFD) of synaptic transmission in the visual cortex, we recorded field potentials and minimal excitatory postsynaptic potentials (EPSPs) from layer II/III following intracortical stimulation at various frequencies in cortical slices of rats. Field potentials were stable at 0.017 Hz, but showed an amplitude depression at 0.033-0.1 Hz at stimulus intensity of 1.5 times the threshold for induction of the postsynaptic component and at 0.1-0.2 Hz at intensity of 1.2 times the threshold. The LFD was input-specific and its magnitude correlated with the stimulus frequency. An interruption of stimulation for 15 min yielded a nearly complete recovery from LFD. Minimal EPSPs tested at 0.1-1.7 Hz often showed LFD with similar features. However, some inputs were stable or even facilitated during repeated stimulation. At 0.1 and 0.2 Hz, >50% of inputs were stable, whereas 10% and 25% were depressed, respectively. At 0.5 and 1.7 Hz, LFD was observed in >60% and 80% of inputs, respectively. The magnitude of LFD strongly varied across inputs. In 3 of the 41 inputs analyzed, LFD was so strong that these inputs became virtually silent. Occurrence of responses to the second pulse in the paired-pulse paradigm when the first response was absent and recovery of depressed EPSPs following stimulus interruption or shift to a lower frequency suggest that these synapses were presynaptically silent due to a lowered probability of transmitter release. Altogether, the results indicate that testing intervals of <10 or even < or =30 s cannot be regarded as completely neutral. At the single-cell level, frequency-dependent changes were strongly heterogeneous across different inputs. LFD and its spontaneous recovery may underlie the previously described "post-rest" potentiation, and should be taken into account when considering information processing in cortical networks.

Activity-dependent change in the protein level of brain-derived neurotrophic factor but no change in other neurotrophins in the visual cortex of young and adult ferrets.

Neurotrophins are suggested to play a role in activity-dependent plasticity of visual cortex during the critical period of postnatal development. Thus, the concentration of neurotrophins in the cortex is expected to change with development and/or with alteration in neuronal activities. To test this, we measured protein levels of nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4/5 in visual cortex of young (postnatal day 38-46, at the peak of the critical period) and adult ferrets with two-site enzyme-immunoassay systems. Measurements were carried out also in somatosensory cortex, hippocampus and cerebellum as control. With development the level of brain-derived neurotrophic factor did not significantly change, while those of the other neurotrophins changed in the visual cortex. A blockade of visual inputs for 24 h by an injection of tetrodotoxin into both eyes significantly decreased brain-derived neurotrophic factor protein level in the visual cortex, but not in the other regions in both young and adult ferrets. On the other hand, no significant decrease was seen in the protein level of the other neurotrophins in the visual cortex of young and adult ferrets. A monocular injection of tetrodotoxin in young ferrets resulted in the reduction of brain-derived neurotrophic factor by approximately half that by binocular injection. The degree of the decrease in the contralateral cortex to the injected eye was significantly larger than that in the ipsilateral cortex, reflecting that the contralateral eye is dominantly represented in the cortex in ferrets. Blockade of cortical neuronal activities by a GABA(A) receptor agonist led to a remarkable reduction of brain-derived neurotrophic factor protein in the visual cortex. These results suggest that the level of brain-derived neurotrophic factor protein in visual cortex is regulated by activities of cortical neurons.

Complications associated with stenting for cerebral arteries.

SUMMARY: We have experienced total 116 stenting for 102 of cranio-cephalic arteries and 14 of intracranial arteries including occlusive cerebrovascular diseases, aneurysms, and fistulas.Ten complications were encountered. Three were ischemic complication, four stent migration, two restenosis, and one aneurysmal perforation during coiling across the stent strut. The mechanism and preventive method of these complications were discussed in this paper.

Brain-derived neurotrophic factor induces long-lasting potentiation of synaptic transmission in visual cortex in vivo in young rats, but not in the adult.

Brain-derived neurotrophic factor (BDNF) rapidly enhances excitatory synaptic transmission in cortical slices. To date, however, a question of how long such an action persists remains unanswered as it is hard to record synaptic responses longer than several hours in slice preparations. To address this question and to investigate possible age-dependency of the action, we analysed effects of a brief application of BDNF and nerve growth factor (NGF) on field potentials of visual cortex in rats of postnatal days 13-17 and 19-24 and in the adulthood for 10-24 h. Evoked potentials to stimulation of the lateral geniculate nucleus were recorded simultaneously from two cortical sites into which the neurotrophin and control solution were injected. An application of BDNF induced a slowly developing increase in the field potential amplitude in young rats. The amplitude attained a plateau level 3-4 h after the infusion; 139 +/- 26% (mean +/- SD) and 132 +/- 21% of the baseline in the rats at P13-17 and P19-24, respectively. This potentiation remained stable from 4 to 8 h, then gradually decreased to the baseline 15-16 h after the infusion. NGF applied in the same way did not induce potentiation. An inhibitor of BDNF receptors blocked the potentiation when it was applied immediately after the BDNF application, but was not effective about 2 h later. In the adults, BDNF did not potentiate field potentials. These results indicate that BDNF induces synaptic potentiation lasting for several hours only in the developing cortex through processes downstream of receptor activation.

Activity-dependent transfer of brain-derived neurotrophic factor to postsynaptic neurons.

Neurotrophins such as brain-derived neurotrophic factor (BDNF) are thought to be transferred from post- to presynaptic neurons and to be involved in the formation and plasticity of neural circuits. However, direct evidence for a transneuronal transfer of BDNF and its relation to neuronal activity remains elusive. We simultaneously injected complementary DNAs of green fluorescent protein (GFP)-tagged BDNF and red fluorescence protein into the nucleus of single neurons and visualized expression, localization, and transport of BDNF in living neurons. Fluorescent puncta representing BDNF moved in axons in the anterograde direction, though some moved retrogradely, and transferred to postsynaptic neurons in an activity-dependent manner.

Induction of brain-derived neurotrophic factor by convulsant drugs in the rat brain: involvement of region-specific voltage-dependent calcium channels.

A high level of hippocampal brain-derived neurotrophic factor (BDNF) in normally aged as compared with young rats suggests that it is important to maintain a considerable level of hippocampal BDNF during aging in order to keep normal hippocampal functions. To elucidate possible mechanisms of endogenous BDNF increase, changes in levels of BDNF were studied in the rat brain following systemic administration of various convulsant agents; excitotoxic glutamate agonists, NMDA, kainic acid and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA); GABA receptor antagonists, picrotoxin, pentylenetetrazole (PTZ) and lindane (gamma-hexachlorocyclohexane); and L-type voltage-dependent calcium channel agonist, BAY-K 8644. Kainic acid and AMPA, but not NMDA, caused remarkable increases in BDNF protein in the rat hippocampus and entorhinal cortex. Picrotoxin, PTZ and lindane stimulated BDNF production in the entorhinal cortex and also in the hippocampus of rats showing very severe convulsions. On the other hand, BAY-K 8644 treatment increased BDNF levels in the neocortex and entorhinal cortex. Maximal levels of BDNF protein were observed at 12--24 h, 8--16 h and 6 h following administration of kainic acid, PTZ and BAY-K 8644, respectively. Kainic acid stimulated BDNF synthesis in presynaptic hippocampal granule neurons, but not in postsynaptic neurons with its receptors, while PTZ and BAY-K 8644 produced the same effects in postsynaptic neurons in the entorhinal cortex (in granule neurons in the hippocampus) and in the whole cortex, respectively. Nifedipine inhibited almost completely BAY-K 8644, but not PTZ, effects. omega-Conotoxin GVIA and DCG-IV partially blocked kainic acid-induced enhancement of BDNF, indicating involvement of L-type and N-type voltage-dependent calcium channels, respectively. In addition, BDNF levels in the hippocampus of mice deficient in D-myo-inositol-1,4,5-triphosphate receptor gene were scarcely different from those in the same region of controls, suggesting little involvement of intracellular calcium increase through this receptor. BAY-K 8644, but not kainic acid or PTZ, stimulated the phosphorylation of cyclic AMP responsive element binding protein. Our results indicate convulsant-dependent stimulation of BDNF production and involvement of region-specific voltage-dependent calcium channels.