Inflammatory pseudotumor of the brain following hematopoietic stem cell transplantation.
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Brain↗
Biomedical subjects
N Shimoyama
Publications and source records attributed to N Shimoyama.
Primitive neuroectodermal tumor involving the frontal skull base in an infant.
We report here a case of a primitive neuroectodermal tumor involving the frontal skull base in a 5-month-old male infant. He presented with rapidly progressing exophthalmos on the left side. Preoperative magnetic resonance imaging revealed a well-demarcated, enhanced mass of 6 cm in diameter in the intradural extra-axial frontal region. The tumor was totally removed by surgery. Pathological findings were consistent with a primitive neuroectodermal tumor (PNET). Intradural extra-axial PNET is very rare, and its prognosis is poor.
Cerebral Angiography↗
Report of the Fourteenth International Symposium of the Foundation for Promotion of Cancer Research: Pain Control, Palliative Medicine and Psycho-oncology.
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Anxiety↗
Antinociceptive and respiratory effects of intrathecal H-Tyr-D-Arg-Phe-Lys-NH2 (DALDA) and [Dmt1] DALDA.
DALDA (H-Tyr-D-Arg-Phe-Lys-NH(2)) and [Dmt(1)]DALDA (H-Dmt-D-Arg-Phe-Lys-NH(2)) (Dmt = 2',6'-dimethyltyrosine) are potent and highly selective mu-opioid agonists (K(i)(delta)/K(i)(mu) > 10,000 and K(i)(kappa)/K(i)(mu) > 100). Both peptides carry a 3+ charge at physiological pH. Their antinociceptive and respiratory effects were compared with morphine (MOR) after intrathecal administration in rats. Both DALDA and [Dmt1]DALDA produced dose-dependent and naloxone-reversible antinociceptive effects with relative potencies of 14 and 3000x that of MOR. The antinociceptive potency of [Dmt1]DALDA far exceeded its affinity and potency at the mu-opioid receptor and may be explained by its ability to inhibit norepinephrine (NE) uptake in spinal cord synaptosomes. The antinociceptive response to [Dmt1]DALDA was significantly attenuated by the alpha(2)-adrenergic antagonist yohimbine. Thus, [Dmt1]DALDA may be regarded as a drug with dual actions, and its antinociceptive potency is better described by both its affinity and potency at mu-opioid receptors, and its potency at inhibiting NE uptake. The analgesic duration of an equipotent dose of MOR, DALDA, and [Dmt1]DALDA was 3, 7, and 13 h, respectively, and the long duration may be due to the hydrophilic nature of these peptide analogs. Respiratory effects were determined using whole body plethysmography at 3 and 30x the antinociceptive ED(50). A significant depression in minute ventilation was observed with the higher dose of morphine and both doses of DALDA, but not with either dose of [Dmt1]DALDA. Because of its high antinociceptive potency, long duration of action, and low propensity to induce respiratory depression, [Dmt1]DALDA is of interest as a drug candidate for intrathecal analgesia.
Analgesics↗
[Multidisciplinary support of cancer patients for truth telling].
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Depression↗
[Mechanism-based pharmacotherapy for cancer pain].
Cancer pain is usually treated by 1) pharmacotherapy, 2) nerve block, 3) radiation therapy, 4) cognitive therapy and 5) alternative medicine. Among these methods, pharmacotherapy is the simplest way to relieve cancer pain without special equipment or special settings. WHO cancer treatment guideline shows morphine is effective to most cancer pain. However, 10-20% of the patients' pain is refractory to morphine. A majority of such refractory pain is due to nerve injury caused by cancer itself or by treatment. Recently, many biological processes involved in the mechanism of neuropathic pain have been elucidated. Pharmacological treatment aimed at blocking such processes should produce specific effects on the pain. Such mechanism-based pharmacotherapy is the most effective way to treat difficult pain.
Analgesics, Opioid↗
[A case of granulomatous angiitis of the central nervous system presented with subacute mental deterioration resembling diffuse white matter disease].
We reported a 60-year-old man with granulomatous angiitis of the central nervous system (GACNS) manifesting as subacute mental deterioration. His first symptoms were nausea and vomiting which brought him to a hospital, where no abnormality was found except for gastritis. One month later, he began to feel dizziness and brain tumor was suspected by a neurosurgeon with the MRI findings such as abnormal T2 signal and swelling in his brainstem. While he was followed up, he gradually presented mental change, disorientation and dysmnesia with the abnormal T2 signal spreading over the cerebral white matter bilaterally. Corticosteroid therapy was started based on the suspicion of a lymphoproliferative disease, and his symptoms and the abnormal MRI findings improved. Then he was referred to our department for further evaluation. Because we could not find any evidence of systemic diseases and he had been almost fully recovered, we discontinued the therapy. Soon after that, his mental deterioration as well as the abnormal T2 signal lesions on MRI relapsed. By open brain biopsy, the diagnosis of GACNS was established, and steroid pulse therapy was started. His symptoms and the abnormal T2 signal lesions improved gradually and the steroid was tapered to the maintenance dose without remission. Since the laboratory and imaging findings are not specific for the diagnosis of the angiitis confined to the central nervous system, brain biopsy is recommended for these disorders.
Acute Disease↗
Oral ketamine is antinociceptive in the rat formalin test: role of the metabolite, norketamine.
The present study was designed to evaluate the oral efficacy and bioavailability of ketamine. Antinociceptive efficacy was determined with the rat formalin test and oral bioavailability by the measurement of plasma and brain concentrations of ketamine and its major metabolite, norketamine. Oral ketamine in a dose range from 30 to 180 mg/kg or saline was given prior to intraplantar formalin and the flinching behavior was measured. Oral ketamine dose-dependently reduced the flinching during phase 2, while flinching during phase 1 was reduced only with the highest dose given. Following oral ketamine at 100 mg/kg, blood and brain samples were obtained and plasma and brain ketamine and norketamine levels were measured using high-performance liquid chromatography (HPLC). The average concentration ratio of norketamine/ketamine, as expressed by the area under the curve (AUC) value, was 6.4 for plasma and 2.9 for brain. These results demonstrate that a significant amount of norketamine is formed by first pass biotransformation of ketamine and is distributed to the brain. Competition binding assays for the [3H]MK-801-labeled non-competitive site of the N-methyl-D-aspartate receptor (NMDA) receptor revealed that both norketamine and ketamine displaced [3H]MK-801 at low micromolar concentrations with Ki values of 2.5 and 0.3 mM in the forebrain, and 4.2 and 1.0 mM in the spinal cord, respectively. Spinal norketamine was approximately equipotent to ketamine in producing antinociceptive effects during phase 2 of the formalin test. Thus, norketamine appears to contribute to the antinociceptive effects of oral ketamine through its NMDA receptor antagonist activity.
Administration, Oral↗
Experimental pain augments experimental dyspnea, but not vice versa in human volunteers.
BACKGROUND: Pain and dyspnea frequently coexist in many clinical situations. However, whether the two different symptoms interact with each other has not been elucidated. To elucidate the interaction between pain and dyspneic sensations, the authors investigated separately the effects of pain on dyspnea and the effects of dyspnea on pain in 15 healthy subjects. METHODS: Subjects were asked to rate their sensation of pain or dyspnea using a visual analog scale (VAS) during pain stimulation produced by tourniquet inflation (inflation cuff pressure: 350 mmHg) around the calf, and/or the respiratory loading consisted of a combination of resistive load (77 cm H2O x l(-1) x s(-1)) and hypercapnia induced by extra mechanical dead space (255 ml). In addition to changes in VAS scores, changes in ventilatory airflow and airway pressure were continuously measured. RESULTS: Pain stimulation and loaded breathing increased VAS scores, ventilation, and occlusion pressure (P0.1). The addition of a pain stimulus during loaded breathing increased the dyspneic VAS score (median 56 [interquartile range 50-62] vs. 64 [55-77]: before vs. after addition of pain stimulus, P < 0.05) with concomitant increases in minute ventilation (10.8 [10.1-13.3] vs. 12.4 [11.0-14.8] l/min, P < 0.05) and P0.1 (5.5 [4.9-7.2] vs. 6.8 [5.8-9.0] cm H2O, P < 0.05). The addition of respiratory loading during pain stimulation did not cause a significant change in pain VAS score (40 [33-55] vs. 31 [30-44]: before vs. after addition of respiratory loading), although both additional burdens increased further minute ventilation (10.0 [8.8-10.9] vs. 12.0 [10.6-13.2] l/min, P < 0.05) and P0.1 (2.5 [2.0-3.0] vs. 6.2 [4.9-7.0] cm H2O, P < 0.05). CONCLUSION: The authors' findings suggest that pain intensifies the dyspneic sensation, presumably by increasing the respiratory drive, whereas dyspnea may not intensify the pain sensation.
Adult↗
Spinal gabapentin is antinociceptive in the rat formalin test.
Gabapentin is a novel anticonvulsant that may be of value for the relief of clinical pain. To determine whether gabapentin is antinociceptive after spinal administration, the drug was given via an intrathecal catheter in doses from 6 to 200 micrograms/rat 10 min prior to intraplantar formalin. Five percent formalin injected subcutaneously in the right hind paw produced a biphasic reaction consisting of flinching and licking behaviors (phase 1, 0-10 min; phase 2, 10-60 min). Gabapentin dose-dependently reduced the numbers of flinches and the duration of licking during phase 2 of the formalin test. The highest dose of gabapentin (200 micrograms/rat) did not affect the tail-flick response. These results demonstrate that spinal gabapentin is antinociceptive in the formalin test.
Acetates↗
Oral ketamine produces a dose-dependent CNS depression in the rat.
The oral to parenteral potency of ketamine to produce central nervous system (CNS) depression was estimated in rats using a behavioral scale. As a function of dose, ketamine produces CNS depression that ranges from ataxia to anesthesia by either route of administration. The oral ED50 value for ketamine was 120 mg/kg (82.2-159.2, 95% CI) while the intravenous ED50 value was 3.7 mg/kg (2.4-5.1, 95% CI). Oral ketamine produces CNS effects comparable to intravenous ketamine, although the drug is approximately 32 fold less potent by the oral route.
Administration, Oral↗
Gabapentin enhances the antinociceptive effects of spinal morphine in the rat tail-flick test.
The antinociceptive effects of the combination of spinal morphine and gabapentin were evaluated in the tail-flick test in rats. The intrathecal coadministration of a subantinociceptive dose of morphine at 0.2 microgram and gabapentin at 300 micrograms produced significant antinociception. Pretreatment with spinal gabapentin at 300 micrograms shifted the dose-response curve of spinal morphine to the left with a decrease in morphine ED50 value from 1.06 micrograms to 0.34 microgram. The antinociceptive effects produced by the combination of a subantinociceptive dose of morphine and gabapentin were reversed by spinal naloxone at 30 micrograms but were not reversed by spinal bicuculline at 0.3 microgram. Furthermore, the concurrent administration of spinal naloxone at 30 micrograms with the combination of morphine and gabapentin blocked antinociception, while the concurrent administration of spinal bicuculline at 0.3 microgram failed to prevent antinociception. These results indicate that the combination of spinal gabapentin and morphine produces an enhancement of antinociception that appears to involve the spinal mu opioid receptors. Furthermore, repeated administration of gabapentin for 3 days did not affect the enhancing effect of gabapentin on the antinociceptive effect of morphine, indicating that tolerance did not develop to gabapentin's ability to enhance morphine antinociception.
Acetates↗
d-Methadone is antinociceptive in the rat formalin test.
The l-isomer of methadone possesses opioid activity, whereas the d-isomer is weak or inactive as an opioid. Both d- and l-methadone have been shown to bind to the N-methyl-D-aspartate (NMDA) receptor. To determine whether d-methadone has functional, in vivo NMDA receptor antagonist activity, the antinociceptive effects of d-methadone were evaluated in the rat tail-flick and formalin tests. Cumulative dose-response analysis in the tail-flick test revealed an ED50 value for intrathecal (spinal) l-methadone of 15.6 microg/rat. In contrast, spinal d-methadone produced no antinociception at a cumulative dose of 460 microg/rat. d-Methadone in a dose range from 32 to 320 microg/rat dose-dependently reduced formalin-induced flinching behavior during phase 2 but not during phase 1 of the formalin test. These antinociceptive effects of d-methadone were not blocked by a spinal dose of naloxone that effectively antagonized an antinociceptive (tail-flick test) dose of l-methadone. d-Methadone at an intrathecal dose of 250 microg shifted the ED50 value for NMDA-induced nociceptive behaviors more than 3-fold to the right, which indicates an antagonism of these NMDA receptor-mediated effects. These results indicate that d-methadone is antinociceptive as a result of its NMDA receptor antagonist activity.
Analgesics, Opioid↗
Collective motion in a system of motile elements.
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Journal Article↗
Ketamine attenuates and reverses morphine tolerance in rodents.
BACKGROUND: The development of tolerance complicates the use of morphine to manage persistent pain. N-methyl-D-aspartate receptor antagonists can attenuate or reverse morphine tolerance. The authors studied ketamine's ability to modulate morphine tolerance. METHOD: Tolerance was produced in mice given morphine subcutaneously and was assessed by a cumulative dose-response analysis using the tail-flick test. The ability of ketamine at 0.3, 3, or 10 mg/kg given subcutaneously before and after morphine to attenuate the development of tolerance was assessed. The ability of 10 mg/kg ketamine to reverse tolerance produced by the subcutaneous implantation of morphine pellets to mice was also assessed. Rats were made tolerant to intraspinal morphine and the effects of the coadministration of 12 micrograms intraspinal ketamine were assessed. RESULTS: Morphine given subcutaneously produced a fivefold increase in the median effective (ED50) dose of morphine, which was dose-dependently attenuated by subcutaneously administered ketamine. A tenfold increase in the morphine ED50 produced by morphine pellets was completely reversed by ketamine given subcutaneously. Intraspinal morphine produced a 46-fold increase in its ED50, which was almost completely attenuated by the coadministration of intraspinal ketamine. CONCLUSIONS: Systemically administered ketamine attenuates and reverses systemically induced morphine tolerance in mice, and intraspinal ketamine attenuates tolerance produced by intraspinal morphine in rats.
Analgesia↗
[A case of endodermal cyst in front of the pontomedullary junction].
We reported a rare case of an endodermal cyst on the posterior fossa. The patient was a 51-year-old woman with tinnitus, ear blockage and a mild swallowing disturbance. MR images revealed a cystic mass 5 cm in diameter in front of the pontomedullary junction. Gadolinium-enhanced images showed some spotty lesions in the cystic mass. The brain stem was compressed strongly by the mass. The left vertebral artery was involved in the mass. Total removal of the tumor was performed via the transcondylar approach. During the operation the lower cranial nerves, the bilateral vertebral artery and the vertebral union were recognized. The cystic mass consisted of a yellow colored thin wall and a watery fluid which contained some small hard lesions. Histopathological examination of the cyst wall revealed a single layer of ciliated columnar epithelium, and that of the small lesions showed histiocytes and granulation. Immunohistochemically, the cyst wall was stained by an epithelial membrane antigen and a carcinoembryonic antigen. From these histopathological findings, the final diagnosis of the cystic lesion was an endodermal cyst. Twenty such cases have been reported to date since Afshar reported a case of an endodermal cyst on the posterior fossa in 1981. There are many types of cystic lesions in the intracranial region, and immunohistochemical studies are necessary for diagnosis of these intracranial cysts.
Brain Diseases↗
A case of encapsulated noninvasive thymoma (stage I) with myasthenia gravis showing metastasis after a 2-year dormancy.
We herein describe a case of thymoma in which metastasis to the left lower visceral and parietal pleura was noticed after a 2-year dormancy. A closer examination revealed no evidence that the metastatic tumors were of lymph node origin. The initial thymoma was well encapsulated, and thus it was thought that the development of metastasis might have reflected a sudden rapid growth of the thymoma cells after a 2-year period of inactivity.
Adult↗
OP-1206, a prostaglandin E1 derivative, attenuates the thermal hyperesthesia induced by constriction injury to the sciatic nerve in the rat.
Nerve ischemia induces wallerian degeneration and peripheral neuropathy, the nerve constriction injury induces thermal hyperesthesia. Nerve ischemia is one possible mechanism in the development of thermal hyperesthesia in the nerve constriction injury model. Prostaglandin E1 increases tissue blood flow. In the present study, the authors examine the role of nerve ischemia in the maintenance of the thermal hyperesthesia induced by nerve constriction injury by orally administering OP-1206, a prostaglandin E1 derivative. A nerve constriction injury model was created by making four loose ligations around the rat sciatic nerve, which induces thermal hyperesthesia in the ligated paw in 2-5 days. OP-1206, was administered six times (Day 7, one time; Day 8, two times; Day 9, two times; Day 10, one time). A single administration of OP-1206 had no effect on the thermal hyperesthesia. Six hours after the sixth-administration of OP-1206, the level of the thermal hyperesthesia was attenuated in a dose-dependent manner, and this effect lasted more than 1 day after the last drug administration. These data indicate that nerve ischemia plays an important role in maintaining the thermal hyperesthesia induced by nerve constriction injury in the rat.
Alprostadil↗