Effects of a visual search task in a virtual reality space with a moving background on spatial cognition and standing balance in patients with left hemiparetic stroke.

We examined effects of a visual search task (VST) in virtual reality (VR) with a moving background on spatial cognition and standing balance in left hemiparetic strokes. The VST with background deviation was allocated to Case A. In Case B, the VST without the deviation was performed. As a results, in Case A, the reaction time of VST was shortened in the paretic space and ability of weight-shift to the paretic side was improved. In conclusion, the VST in the VR with a spatial manipulation may improve spatial cognition and standing balance in left hemiparetic strokes.

Palliative Care Intervention for End-of-life Patients with Non-cancerous Respiratory Diseases.

While palliative care for patients with cancer is actively performed, it is provided only occasionally for patients with chronic non-cancerous respiratory diseases. This is due to various factors, including the fact that palliative care is not covered by health insurance and the difficulty in determining end-of-life in these patients. This paper presents two case studies to highlight the significance of palliative care team intervention for patients in the terminal stage of chronic non-cancerous respiratory diseases. Palliative care is essential to support physical problems, such as dyspnea, as well as mental disorders, such as depression, and to provide nutrition therapy and rehabilitation. To achieve care at the appropriate time in accordance with the patient's wishes, it is essential for patients to understand and accept the progress and deterioration of their disease and prepare for the end of life at an earlier stage under multidisciplinary involvement (advance care planning).

Edaravone attenuates sustained pial arteriolar vasoconstriction independently of endothelial function after unclamping of the abdominal aorta in rabbits.

BACKGROUND: Cerebral blood flow (CBF) has direct effects on neuronal function and neurocognitive disorders. Oxidative stress from abdominal aortic surgery is important in the pathophysiology of CBF impairment. We investigated the effect of edaravone on the pial arteriolar diameter changes induced by abdominal aortic surgery and the involvement of the endothelium in the changes. METHODS: The closed cranial window technique was used in rabbits to measure changes in pial arteriolar diameter after the unclamping of abdominal aortic cross-clamping with an intravenous free radical scavenger, edaravone (control group [n = 6], edaravone 10 µg/kg/min [n = 6], 100 µg/kg/min [n = 6]). Pial vasodilatory responses to topical application of acetylcholine (ACh) into the cranial window were investigated before abdominal aortic cross-clamping and after unclamping with intravenous administration of edaravone (control group [n = 6], edaravone 100 µg/kg/min [n = 6]). RESULTS: Aortic unclamping-induced vasoconstriction was significantly attenuated by continuous infusion of edaravone at 100 µg/kg/min. Topical ACh after unclamping did not produce any changes in pial arteriolar responses in comparison to before aortic cross-clamping in the control or edaravone groups. The changes in the response to topical ACh after unclamping in the saline and edaravone groups did not differ significantly. CONCLUSIONS: Free radicals during abdominal aortic surgery might have contracted cerebral blood vessels independently of endothelial function in rabbits. Suppression of free radicals attenuated the sustained pial arteriolar vasoconstriction after aortic unclamping. Thus, the free radical scavenger might have some brain protective effect that maintains CBF independently of endothelial function.

Anatomical variants of dorsal scapular nerve in relation to the middle scalene muscle in Japanese population.

Dorsal scapular nerve (DSN) block is often performed in Japanese pain clinics to treat neck pain and katakori (a unique symptom in Japanese population characterized by myofascial pain syndromes such as shoulder girdle pain). However, to the best of our knowledge, there are only a few studies regarding anatomical variations in DSN paths around the middle scalene muscle (MSM) in Japanese population. Thus, we conducted a cadaveric study to examine anatomical variations in DSN paths around the MSM in Japanese population.DSN anatomies of 70 adult Japanese cadavers used for research and gross anatomy practice at the Tokai University School of Medicine between 2015 and 2016 were examined.In all cadavers, DSNs originated from the brachial plexus (BP) and innervated the rhomboid major, rhomboid minor, and levator scapulae muscles via the MSM. Two types of DSN paths were observed: piercing-type (piercing the MSM) and anterior-type (running in front of the MSM). We surveyed all 140 sides in 70 Japanese cadavers; of these, 95 sides had piercing-type and 45 had anterior-type paths. Of the 70 cadavers, 42 had piercing-type and 17 had anterior-type paths on both the sides. In 9 cadavers, the left and right sides had piercing-type and anterior-type paths, respectively. In the other 2 cadavers, the right and left sides had piercing-type and anterior-type paths, respectively.We found 2 distinct anatomical variants for DSN paths around the MSM in this Japanese cohort. Our results suggest that the rate of anterior-type DSN path is higher in Japanese population. Therefore, it is necessary to maintain caution while injecting anesthetic agents during a DSN block and the type of DSN should be considered.

A case of anaphylaxis apparently induced by sugammadex and rocuronium in successive surgeries.

Rocuronium is the agent most frequently involved in perioperative anaphylaxis, and sugammadex has also been known to induce anaphylactic reactions. We describe a case of successive anaphylactic episodes that seemed to be induced by clinical doses of rocuronium and sugammadex. The patient was a 19-year-old woman who had a medical history of asthma, but no history of surgery. She had been injured in a fall, and several surgeries were scheduled for multiple bone fractures. At the first surgery under general anesthesia, she developed anaphylaxis 5 min after sugammadex administration. A second general anesthesia for treatment of calcaneal fracture was induced uneventfully without neuromuscular blockade after 10 days. A third general anesthesia was scheduled to reinforce the spinal column 12 days after the first surgery. She developed anaphylaxis 8 min after rocuronium administration. The level of plasma histamine was elevated, but serum tryptase level remained normal. This surgery was canceled and rescheduled without use of a neuromuscular blockade. Skin tests were performed in a later investigation. The patient showed positive results on intradermal tests for sugammadex and rocuronium, supporting a diagnosis of allergic reactions to both drugs. Clinicians must be aware that anaphylactic reactions can be induced by both sugammadex and rocuronium.

Anaphylactic shock due to intravesical administration of pirarubicin hydrochloride for the fifth time.

We report the first case of anaphylaxis induced by intravesical administration of pirarubicin hydrochloride during spinal anesthesia. The patient was a 64-year-old woman being followed up for transitional cell carcinoma of the bladder. Anaphylaxis occurred the fifth time pirarubicin hydrochloride was administered intravesically. Pirarubicin hydrochloride, an anthracycline antitumor antibiotic that is widely used for intravesical instillation chemotherapy, is administered at the end of surgery. Because this is about the time that the patient is leaving the operating room, attention to patient monitoring tends to be divided. Because anaphylaxis may occur at this time, staff should remain vigilant of the risk of anaphylaxis.

Effect of Postoperative Administration of Pregabalin for Post-thoracotomy Pain: A Randomized Study.

OBJECTIVE: The present study was performed to evaluate the effect of postoperative administration of pregabalin in patients who reported moderate-to-severe pain after epidural analgesia following thoracotomy. DESIGN: An open-label, randomized, controlled, parallel-group study. SETTING: A single center in Japan. PARTICIPANTS: Consecutive patients (aged≥20 years) who reported moderate-to-severe pain after effectual 2-day epidural analgesia post-thoracotomy for lung cancer from February 2012 to March 2013. INTERVENTIONS: Patients were assigned to 2 groups: control (control treatment: acetaminophen, 400 mg, and codeine phosphate powder, 20 mg) or pregabalin (pregabalin, 75 mg, plus control treatment). The 12-week study period included 2-week study treatment and 10-week follow-up. MEASUREMENTS AND MAIN RESULTS: For efficacy, the primary endpoint was the visual analog scale (VAS) scores for pain at rest and with coughing at week 2, and secondary endpoints were the VAS scores for pain and the neuropathic pain questionnaire at week 12. Fifty patients were randomized (25 per group). At week 2, the VAS scores for pain at rest (mean [SD]) were 29.5 (21.9) in the control group and 16.3 (15) in the pregabalin group (p = 0.02); for pain with coughing, the scores were 45.2 (20.9) and 28.8 (25.9), respectively (p = 0.02). VAS scores improved more in the pregabalin group than in the control group over the 12 weeks. Patients free from possible neuropathic pain were 48% of the control group and 88% of the pregabalin group, respectively (p = 0.001). CONCLUSIONS: Postoperative administration of pregabalin effectively reduced post-thoracotomy pain.

Nicorandil protects pial arterioles from endothelial dysfunction induced by smoking in rats.

BACKGROUND: Our aims are to investigate the effect of nicorandil, which is used for angina prevention and treatment, on the endothelial dysfunction induced by acute smoking and to clarify the underlying mechanism. MATERIALS AND METHODS: A closed cranial window preparation was used to measure changes in pial vessel diameters in Sprague-Dawley rats. The responses of arterioles were examined to an endothelium-dependent vasodilator acetylcholine (ACh) before smoking. After intravenous nicorandil (200 µg/kg bolus infusion and then 60 µg/kg/min continuous infusion; n=6) or saline (control; n=6) pretreatment, the pial vasodilator response to topical 10 M ACh infusion was reexamined both before and 1 hour after 1-minute cigarette smoking. Thereafter, either glibenclamide or N-ω-nitro-L-arginine methyl ester (L-NAME) was infused 20 minutes before nicorandil infusion. In the glibenclamide (n=6) or L-NAME; n=6 pretreatment group, the pial vasodilator response to topical ACh was examined before and after smoking. Percentage changes in pial vessel diameters were used for the statistical analysis. RESULTS: Cerebral arterioles were dilated during topical ACh infusion. After smoking, 10 M ACh constricted cerebral arterioles (-7.7±1.8%). After smoking, in the nicorandil-pretreatment group, 10 M ACh dilated cerebral pial arterioles by 10.5±3.0%. When given before nicorandil infusion, glibenclamide, but not L-NAME, abolished the preventive effects of nicorandil against smoking-induced endothelial dysfunction in pial vessels. CONCLUSIONS: Acute cigarette smoking causes dysfunction of endothelium-dependent pial vasodilatation, and nicorandil prevents this effect of smoking. The mechanism underlying this protective effect may depend mainly on adenosine triphosphate-sensitive potassium-channel activation.

Successful treatment by adding duloxetine to pregabalin for peripheral neuropathy induced by paclitaxel.

Although paclitaxel is a commonly used anticancer drug, peripheral neuropathy may develop as a side effect. Worsening of the symptoms with time may cause patients who receive paclitaxel to give up their chemotherapy. Duloxetine, a serotonin- and norepinephrine-reuptake inhibitor, has been used to treat peripheral neuropathic pain. We report the case of a 68-year-old man with gastric cancer, who underwent gastrectomy and then received 8 cycles of chemotherapy involving weekly administrations of paclitaxel. Under this paclitaxel treatment, he complained of severe peripheral neuropathy, leading to a diminished quality of life. Following treatment with a combination of duloxetine and pregabalin, a remission of his symptoms was achieved. Duloxetine plus pregabalin therapy may be useful for the peripheral neuropathy induced by paclitaxel.

Preventive effect of varenicline on impairment of endothelial function in cerebral vessels induced by acute smoking in rats.

Preoperative smoking cessation is important for recovery from surgery without complications. Available evidence suggests nicotine replacement therapy could be safe and effective in the perioperative period. On the other hand, the newly developed selective nicotinic acetylcholine (ACh) receptor partial agonist, varenicline tartrate, is also effective as an aid for smoking cessation and helps people to stop smoking. During the transitional phase between the decision to stop smoking and actual smoking cessation, patients could use varenicline before undertaking smoking cessation. We have previously reported that acute cigarette smoking can cause impairment of endothelium-dependent vasodilation in cerebral vessels; thus, the use of varenicline before surgery in a patient who is still a smoker may not be safe with regard to endothelial function. Therefore, to assess the safety of varenicline in terms of endothelial function, we evaluated its effect on the acute smoking-induced impairment of endothelium-dependent cerebral vasodilation. In anesthetized Sprague-Dawley rats, we applied ACh topically to pial vessels; then, after administering intravenous varenicline or saline injection, we reexamined the ACh-induced vasodilator response both before and after smoking. Under control conditions, cerebral pial arterioles were dose-relatedly dilated by ACh. After smoking, 10(-5) M ACh constricted the arterioles following saline pretreatment (diameter -7.6 ± 1.8 %, n = 6), but induced dilation following varenicline pretreatment (diameter +15.3 ± 3.3 %, n = 6). Thus, varenicline may prevent the smoking-induced impairment of endothelium-dependent vasodilation in cerebral pial arterioles.

Comparative effects of cilostazol and aspirin on the impairment of endothelium-dependent cerebral vasodilation caused by acute cigarette smoking in rats.

We previously reported that acute cigarette smoking can cause a dysfunction of endothelium-dependent vasodilation in cerebral vessels, and that a reduction of oxidative stress by agents such as valsartan, fasudil, or apocynin prevented this impairment. Here, our aim was to investigate the comparative effects of two antiplatelet drugs used for stroke-prevention [a phosphodiesterase-3 inhibitor (cilostazol) and a cyclooxygenase inhibitor (aspirin)] on smoking-induced endothelial dysfunction in cerebral arterioles. In Sprague-Dawley rats, we used a closed cranial window preparation to measure the changes in pial vessel diameters induced by topical application of acetylcholine (ACh) following intraperitoneal injection of 0.5% carboxymethyl cellulose sodium salt (CMC; vehicle control for the antiplatelet drugs). After 1-min smoking (1 mg-nicotine cigarette), the arteriolar responses to ACh were reexamined. Finally, after intraperitoneal cilostazol or aspirin (each in 0.5% CMC) pretreatment, we reexamined the vasodilator responses to topical ACh (before and after cigarette smoking). Under control conditions, cerebral arterioles were dose-relatedly dilated by topical ACh (10(-6) and 10(-5 )M). One hour after 1-min smoking, 10(-5 )M ACh (a) constricted cerebral pial arterioles in the control group and in the aspirin-pretreatment group (responses not significantly different from each other), but (b) dilated cerebral pial arteries in the cilostazol pretreatment groups (responses significantly different from those obtained without cilostazol pretreatment). Thus, cilostazol (but not aspirin) may prevent the smoking-induced impairment of endothelium-dependent vasodilation in cerebral pial arterioles.

Rho-kinase inhibitor and nicotinamide adenine dinucleotide phosphate oxidase inhibitor prevent impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats.

INTRODUCTION: We previously reported that acute cigarette smoking can cause a dysfunction of endothelium-dependent vasodilation in cerebral vessels, and that blocking the angiotensin II (Ang II) type 1 (AT1) receptor with valsartan prevented this impairment. Our aim was to investigate the effects of a Rho-kinase inhibitor (fasudil) and a Nicotinamide Adenine Dinucleotide PHosphate (NADPH) oxidase inhibitor (apocynin) on smoking-induced endothelial dysfunction in cerebral arterioles. METHOD: In Sprague-Dawley rats, we used a closed cranial window preparation to measure changes in pial vessel diameters following topical acetylcholine (ACh) before smoking. After one-minute smoking, we again examined the arteriolar responses to ACh. Finally, after intravenous fasudil or apocynin pre-treatment we re-examined the vasodilator responses to topical ACh (before and after cigarette smoking). RESULTS: Under control conditions, cerebral arterioles were dose-dependently dilated by topical ACh (10(-6) M and 10(-5) M). One hour after a one-minute smoking (1 mg-nicotine cigarette), 10(-5) M ACh constricted cerebral arterioles. However, one hour after a one-minute smoking, 10(-5) M ACh dilated cerebral pial arteries both in the fasudil pre-treatment and the apocynin pre-treatment groups, responses that were significantly different from those obtained without fasudil or apocynin pre-treatment. CONCLUSION: Thus, inhibition of Rho-kinase and NADPH oxidase activities may prevent the above smoking-induced impairment of endothelium-dependent vasodilation.

The effects of transient cerebral ischemia on vasopressin-induced vasoconstriction in rabbit cerebral vessels.

BACKGROUND: Vasopressin is a drug of choice for use during cardiopulmonary resuscitation because several experimental studies have shown that it is better than epinephrine at increasing systemic perfusion pressure and improving cerebral perfusion pressure without increasing myocardial oxygen consumption. We used a pial window preparation to determine the effects of vasopressin when applied topically to pial vessels and whether any effects were altered after cerebral ischemia in rabbits (n = 27). METHODS: We first examined the effects of topical application of arginine-vasopressin (AVP) (10(-11) M, 10(-9) M, 10(-7) M, and 10(-5) M, sequentially). We then examined the effects of topical application of AVP (10(-9) M and 10(-7) M, sequentially) before and after a 5-min intervention consisting of cerebral ischemia produced by inflation of a neck tourniquet plus systemic hypotension or systemic hypotension alone. RESULTS: Pial arteriolar diameters were (a) dilated by 10(-11) M AVP [7% +/- 11% (P = 0.014 versus baseline)], but constricted by 10(-9) M, 10(-7) M, and 10(-5) M AVP [7% +/- 14%, 20% +/- 14%, and 16% +/- 16% (each P < 0.05), respectively], and (b) constricted before hypotension (7% +/- 10% at 10(-9) M, 20% +/- 15% at 10(-7) M) or ischemia (7% +/- 11% at 10(-9) M, 21% +/- 15% at 10(-7) M). However, after the 5-min of ischemia, the decrease in diameter induced by 10(-7) M AVP was significantly reduced but not by hypotension alone [hypotension control group: 7% +/- 10% at 10(-9) M, 19% +/- 14% at 10(-7) M; ischemia group: 5% +/- 11% at 10(-9) M, 10% +/- 13% at 10(-7) M (P = 0.35 versus hypotension control)]. CONCLUSIONS: Topical application of AVP (except at the lowest concentration used here) induced concentration-dependent vasoconstriction of pial arterioles in anesthetized rabbits. The vasoconstrictor effect of 10(-7) M AVP was reduced after transient (5-min) cerebral ischemia.

The comparative effects of intravenous nicardipine and prostaglandin E1 on the cerebral pial arteriolar constriction seen after unclamping of an aortic cross-clamp in rabbits.

BACKGROUND: The potent vasodilators nicardipine and prostaglandin E1 (PGE1) are useful for the treatment of systemic hypertension or pulmonary hypertension during aortic surgery. METHODS: We measured cerebral pial arteriolar diameters, using a rabbit closed cranial window preparation: before (baseline) and 15 min after the start of an IV infusion (preclamp) (0.9% saline [control group], nicardipine [at 0.1, 1.0, or 10 microg x kg(-1) x min(-1)], or PGE1 [at 0.1 or 1.0 microg x kg(-1) x min(-1)]), just after aortic clamping, 20 min after clamping, and at 0-60 min after unclamping. RESULTS: In the control group, a significant decrease in diameter persisted for at least 60 min after unclamping (maximum [at 60 min], -16% for large [> or =75 microm], and -27% for small [<75 microm] arterioles versus baseline). Although the aortic unclamping-induced vasoconstriction was unaffected under the smallest dose of nicardipine, it was significantly attenuated under larger doses in both large and small arterioles (residual vasoconstriction, -10% and -6% for large and -18% and -10% for small arterioles; at 60 min). The pial arteriolar constriction observed at 5 min or more after unclamping in the control group was not altered by PGE1 in either large or small arterioles. CONCLUSIONS: The larger doses of nicardipine, but neither dose of PGE1, attenuated aortic unclamping-induced sustained cerebral pial arteriolar constriction.

Angiotensin II type 1 (AT1)-receptor blocker prevents impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats.

Our aim was to test for smoking-induced endothelial dysfunction in rat cerebral vessels, then to evaluate the effect of valsartan [angiotensin II type I (AT1)-receptor blocker] on that impairment. In pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats, we used a cranial window preparation to measure changes in pial vessel diameters following topical applications of acetylcholine (Ach) (before and after smoking or intravenous nicotine infusion; n = 6 in each group), and adenosine (n = 6 for before and after smoking). Then, after intravenous valsartan pretreatment we reexamined the pial vasodilator response to topical Ach (before and after cigarette smoking). Under control conditions, cerebral arterioles were dilated by 6.9 +/- 4.2% and 13.6 +/- 4.8% by topical Ach (10(-6) M and 10(-5) M, respectively) and by 6.4 +/- 2.5% and 12.2 +/- 3.1% by topical adenosine (10(-5) M and 10(-4) M, respectively). One hour after a 1-min inhalation of mainstream smoke (1-mg nicotine cigarette), 10(-5) M Ach constricted cerebral arterioles (-4.4 +/- 4.1%), while 10(-4) M adenosine dilated them by 13.4 +/- 3.4%. One hour after a 1-min nicotine infusion (0.05 mg), 10(-5) M Ach dilated cerebral arterioles by 9.9 +/- 2.4%. Thus, vasodilator response to topical Ach was impaired after smoking, whereas that to adenosine was unaffected. However, the vasodilator response to Ach was unaffected by intravenous nicotine. Valsartan prevented smoking from impairing Ach-induced vasodilation. In conclusion, acute single-cigarette smoking causes a dysfunction of endothelium-dependent, but not endothelium-independent, vasodilation of rat cerebral vessels in vivo, and the effect was not mimicked by intravenous nicotine. AT1-receptor blockade prevented the above smoking-induced impairment of endothelium-dependent vasodilation.