Shin Nakamura

Comparison of blood-oxygen-level–dependent functional magnetic resonance imaging and near-infrared spectroscopy recording during functional brain activation in patients with stroke and brain tumors

Blood-oxygen-level-dependent contrast functional magnetic resonance imaging (BOLD-fMRI) has been used to perform functional imaging in brain disorders such as stroke and brain tumors. However, recent studies have revealed that BOLD-fMRI does not image activation areas correctly in such patients. To clarify the characteristics of the evoked cerebral blood oxygenation (CBO) changes occurring in stroke and brain tumors, we have been comparing near-infrared spectroscopy (NIRS) and BOLD-fMRI recording during functional brain activation in these patients. We review our recent studies and related functional imaging studies on the brain disorders. In the primary sensorimotor cortex (PSMC) on the nonlesion side, the motor task consistently caused a decrease of deoxyhemoglobin (deoxy-Hb) with increases of oxyhemoglobin (oxy-Hb) and total hemoglobin (t-Hb), which is consistent with the evoked CBO response observed in normal adults. BOLD-fMRI demonstrated robust activation areas on the nonlesion side. In stroke patients, severe cerebral ischemia (i.e., misery perfusion) caused an increase of deoxy-Hb during the task, associated with increases of oxy-Hb and t-Hb, in the PSMC on the lesion side. In addition, the activation volume of BOLD-fMRI was significantly reduced on the lesion side. The BOLD signal did not change in some areas of the PSMC on the lesion side, but it tended to decrease in other areas during the tasks. In brain tumors, BOLD-fMRI clearly demonstrated activation areas in the PSMC on the lesion side in patients who displayed a normal evoked CBO response. However, the activation volume on the lesion side was significantly reduced in patients who exhibited an increase of deoxy-Hb during the task. In both stroke and brain tumors, false-negative activations (i.e., marked reductions of activation volumes) in BOLD imaging were associated with increases of deoxy-Hb, which could cause a reduction in BOLD signal. BOLD-fMRI investigations of patients with brain disorders should be performed while giving consideration to atypical evoked CBO changes.

Effects of Cerebral Ischemia on Evoked Cerebral Blood Oxygenation Responses and BOLD Contrast Functional MRI in Stroke Patients

Background and Purpose— To evaluate the mechanisms of failure of blood oxygenation level–dependent (BOLD) imaging in stroke, we compared the evoked cerebral blood oxygenation (CBO) responses and activation volumes (AVs) of BOLD functional MRI (fMRI) in chronic stroke patients with moderate and severe cerebral ischemia. Methods— We measured the evoked CBO responses in the primary sensorimotor cortex (PSMC) by means of near-infrared spectroscopy during contralateral motor tasks. We compared the AV of BOLD-functional MRI in the PSMC on the nonlesion and lesion sides. Single-photon emission computed tomography was used to classify ischemic status as moderate (slight reduction of regional cerebral blood flow and cerebrovascular reserve capacity [CVRC]) or severe (marked reduction of regional cerebral blood flow and CVRC; ie, misery perfusion). Results— In age-matched controls, deoxyhemoglobin concentration decreased with concomitant increases in oxyhemoglobin and total hemoglobin concentrations during activation. The PSMC on the nonlesion side exhibited a normal CBO response pattern. On the lesion side, moderate cerebral ischemia did not affect the CBO response pattern, but severe cerebral ischemia caused an increase of deoxyhemoglobin during the task, associated with increases of oxyhemoglobin and total hemoglobin. Moderate cerebral ischemia induced only a slight reduction of the AV on the lesion side; however, severe cerebral ischemia markedly reduced the AV on the lesion side. The BOLD signal did not change in some areas of the PSMC on the lesion side in severe cerebral ischemia, whereas it tended to decrease in other areas during the tasks. Conclusions— Misery perfusion caused a marked reduction of the AV on BOLD imaging, associated with an increase of deoxyhemoglobin concentration during activation. BOLD-fMRI investigations of stroke patients should be performed while giving consideration to baseline circulatory status. Functional near-infrared spectroscopy could be an alternative means to assess the CVRC.

SK&F 83959 and non-cyclase-coupled dopamine D1-like receptors in jaw movements via dopamine D1-like/D2-like receptor synergism

This study compared the effects of the dopamine D1-like receptor agents SK&F 83959 (3-methyl-6-chloro-7,8-dihydroxy-1-[3-methyl-phenyl]-2,3,4,5-tetrahydro- 1 H-3-benzazepine), which inhibits the stimulation of adenylyl cyclase, and A 68930 ([1R,3S]-1-aminomethyl-5,6-dihydroxy-3-phenyl-isochroman), a full efficacy agonist, in regulating jaw movements in the rat by synergism with dopamine D2-like receptor agonism. When SK&F 83959 and A 68930 were given in combination with quinpirole, there was a synergistic induction of jaw movements. Responsivity to SK&F 83959 + quinpirole was antagonised by the dopamine D1-like receptor antagonists SCH 23390 ([R]-3-methyl-7-chloro-8-hydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-ben zaz epine) and BW 737C ([S]-6-chloro-1-[2,5-dimethoxy-4-propylbenzyl]-7-hydroxy-2-methyl- 1,2,3,4-tetrahydroisoquinoline); synergism was antagonised also by the dopamine D2-like receptor antagonist YM 09151-2 (cis-N-[1-benzyl-2-methyl-pyrrolidin-3-yl]-5-chloro-2-methoxy-4-++ +methyl-aminobenzamide). Responsivity to A 68930 + quinpirole was enhanced by low doses of SCH 23390, BW 737C and YM 09151-2, and antagonised by higher doses of SCH 23390 and YM 09151-2. These results implicate a novel, dopamine D1-like receptor that is coupled to a transduction system other than/additional to adenylyl cyclase, and suggest that its functional role extends to the regulation of jaw movements by synergistic interactions with dopamine D2-like receptors.

Intraoperative EC-IC Bypass Blood Flow Assessment With Indocyanine Green Angiography in Moyamoya and Non-Moyamoya Ischemic Stroke

OBJECTIVE Superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis has been used in moyamoya disease (MD) and non-moyamoya ischemic stroke (non-MD). It is important to monitor hemodynamic changes caused by bypass surgery for postoperative management. We evaluated the bypass blood flow during STA-MCA anastomosis by using indocyanine green (ICG) fluorescence angiography. METHODS We evaluated the bypass blood flow in 13 MD and 21 non-MD patients during STA-MCA anastomosis by means of ICG angiography with injection of ICG into the anastomosed STA. The ICG perfusion area was calculated when the ICG fluorescence intensity reached maximum. We measured cortical oxygen saturation before anastomosis by means of visual light spectroscopy. RESULTS ICG angiography demonstrated bypass blood flow from the anastomosed STA to the cortical vessels in all patients. The ICG perfusion area in MD (20.7 ± 6.6 cm(2)) was significantly larger than that in non-MD (8.4 ± 9.1 cm(2), P < 0.05). The cortical oxygen saturation (58.9% ± 8.3%) in MD was significantly lower than that in non-MD (73.4% ± 9.5%, P < 0.05). CONCLUSIONS ICG angiography with injection of ICG into the bypass artery allowed quantitative assessment of bypass blood flow. The bypass supplies blood flow to a greater extent in MD than in non-MD during surgery. This might be caused by a larger pressure gradient between the anastomosed STA and recipient vessels in MD. These observations indicate that MD requires careful control of systemic blood pressure after surgery to avoid cerebral hyperperfusion syndrome. ICG angiography is considered useful for facilitating safe and accurate bypass surgery and providing information for postoperative management.

Ventral striatal vs. accumbal (shell) mechanisms and non-cyclase-coupled dopamine D1-like receptors in jaw movements

This study compared the effects of intracerebral injections of the dopamine D(1)-like receptor agents 3-methyl-6-chloro-7,8-dihydroxy-1-[3-methylphenyl]-2,3,4,5-tetrahydro-1H-3-benzazepine (SK&F 83959) and [R]-3-methyl-7-chloro-8-hydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SCH 23390) into the ventrolateral striatum or the shell of the nucleus accumbens on the synergistic induction of jaw movements by intravenous (i.v.) co-administration of [R]-7,8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SK&F 38393) or SK&F 83959 with the dopamine D(2)-like receptor agonist, quinpirole. In the ventrolateral striatum, SCH 23390 and SK&F 83959 each blocked jaw movements induced by i.v. SK&F 38393 with quinpirole, while only SCH 23390 blocked i.v. SK&F 83959 with quinpirole. SCH 23390 was less effective in the accumbens shell than in the ventrolateral striatum, and SK&F 83959 was ineffective to block i.v. SK&F 38393 with quinpirole, while neither SCH 23390 nor SK&F 83959 blocked i.v. SK&F 83959 with quinpirole. As SK&F 83959 inhibits the stimulation of adenylyl cyclase via dopamine D(1A) receptors but acts as an agonist at a putative dopamine D(1)-like receptor site not linked to cyclase, an important role is indicated for non-cyclase-coupled dopamine D(1)-like receptor sites as well as dopamine D(1A) receptors in the regulation of jaw movements via dopamine D(1)-like/D(2)-like receptor synergism, particularly in the ventrolateral striatum.

Jugular bulb venous thrombosis caused by mild head injury: a case report

BACKGROUND We present here the first report of a jugular bulb venous thrombosis after mild head injury, which lacked either a skull fracture or abnormal findings on CT scan. CASE DESCRIPTION An 8-year-old boy was hit on the back of the head and experienced headache and vomiting beginning the next morning. A CT scan and cranial x-ray examination failed to reveal any abnormal findings. The patient was treated conservatively; however, his headache and vomiting persisted. At 13 days after the injury, he began to show double vision due to left VIth nerve palsy and bilateral papilloedemas, suggesting an increased ICP. Although repeated CT scan failed to detect abnormal findings in both the supra- and infra-tentorial regions, MRI clearly visualized a thrombus which was situated within the right jugular bulb. Furthermore, MRV demonstrated disruption of venous flow at the jugular bulb. The patient was administered heparin continuously. His symptoms improved and the CSF pressure on lumbar puncture returned to a normal level at 20 days after admission. Magnetic resonance imaging showed resolution of the clot, and MRV appeared to demonstrate partial recanalization simultaneously. The patient was discharged without any neurologic deficits. The clot in the jugular bulb disappeared completely after 4 months, and he could be followed up for 1 year. CONCLUSION This case underscores the fact that MRI may represent the exclusive screening examination in cases of sinus thrombosis when it occurs within the jugular bulb, as CT scan fails to reveal any findings suggestive of venous thrombosis.

EC-IC bypass function in Moyamoya disease and non-Moyamoya ischemic stroke evaluated by intraoperative indocyanine green fluorescence angiography.

Indocyanine green (ICG) emits near-infrared fluorescence when it is excited by near-infrared light. The near infrared fluorescence of ICG was applied to the imaging of cerebral vessels during neurosurgical operations such as clipping of aneurysms. In this study, ICG angiography was applied to extracranial-intracranial (EC-IC) bypass surgery to evaluate the hemodynamic changes induced by bypass in moyamoya disease (MD) and non-moyamoya ischemic diseases (non-MD). These patients underwent superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis. We compared the cortical areas where the bypass supplied blood flow between MD and non-MD. ICG angiography clearly demonstrated the bypass blood flow from the anastomosed STA to the cortical vessels including arteries, capillaries, and veins in both MD and non-MD. Interestingly, the anastomosed STA supplied blood flow to a larger cortical area in MD than non-MD. The bypass supplied greater extent of blood flow to the ischemic brain in MD than in non-MD. This difference might be caused by the fact that the perfusion pressure was lower in MD than in non-MD.

Optical topography can predict occurrence of watershed infarction during carotid endarterectomy: technical case report.

BACKGROUND The major risk of CEA is perioperative stroke. NIRS can detect ischemic changes during CEA; however, possible watershed-type perfusion defects may not be detected by single-channel NIRS occurring at some distance from the light source. In the present case, we tested the usefulness of optical topography (ie, multichannel NIRS, OT) for this purpose. CASE DESCRIPTION The patient (64-year-old man) exhibited nonsymptomatic 80% stenosis of the right ICA with normal cerebral perfusion. CEA was performed to prevent cerebral infarction. We used single-channel NIRS and OT for monitoring of perfusion changes during CEA. The optodes of OT were placed on the skull to cover the frontal and parietal lobes on the right side, whereas the sensor of the single-channel NIRS was placed on the right forehead. The single-channel NIRS detected no significant perfusion changes during surgery. However, the OT revealed occurrence of watershed-type perfusion defects in the border region between the right middle and posterior cerebral artery supply areas during cross-clamping of the right internal carotid artery. Postoperative MRI showed an ischemic region which corresponded to the area associated with the perfusion defects. CONCLUSION OT could detect watershed-type posterior perfusion defects which the single-channel NIRS failed to detect. OT may represent a useful tool for intraoperative monitoring during CEA.

Effects of Revascularisation on Evoked Cerebral Blood Oxygenation Responses in Stroke Patients

We demonstrated that ischemic strokes exhibit an increase of deoxyhemoglobin during activation. We evaluated the effect of revascu-larization on the abnormal evoked cerebral blood oxygenation (CBO) re-sponses in these patients, employing near-infrared spectroscopy (NIRS). We selected five patients who exhibited an increase of deoxyhemoglobin associated with increases of oxyhemoglobin and total hemoglobin during activation for this study. These patients showed marked reductions of base-line regional cerebral blood flow and cerebrovascular reserve capacity, which were improved 1 week after revascularization. Postoperative NIRS demonstrated that the increase of deoxyhemoglobin during activa-tion was not observed after revascularization. This preliminary study demonstrated that the abnormal evoked-CBO response in ischemic stroke patients could be improved by revascularization.

Endovascular Treatment for Ruptured Vertebral Artery Dissecting Aneurysms at the Acute Stage

OBJECTIVE Ruptured vertebral artery dissecting aneurysms (VADA) should be treated promptly because of the high risk of rebleeding. However, it is difficult to treat dissecting aneurysm during the acute stage using microsurgery because of high intracranial pressure or brain edema. Therefore, endovascular treatment of the ruptured VADA may be a better technique. We retrospectively studied the efficacy and outcome of endovascular treatment of ruptured VADA at the acute stage. METHODS Ten patients with ruptured VADA received endovascular treatment at the acute stage. Eight patients who had dissecting aneurysms were treated by internal trapping of the dissected segment. We performed stent-assisted coiling (SAC) for a case of VADA in contralateral hypoplastic VA and a case of bilateral dissections, ruptured VADA of the right VA and VA dissection of the left VA. RESULTS Four patients had good recovery, 3 patients had moderate disability, 2 patients had severe disability, and 1 patient died from initial severe SAH. There was no rebleeding or procedure-related complication. However, one patient who was treated by SAC had ischemic complications post-treatment. CONCLUSION Endovascular treatment of ruptured VADA in the acute stage appears to be safe and effective.