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Biomedical subjects

K Kumami

Publications and source records attributed to K Kumami.

12 recordsLinked to original sources
PubMed2001

Primary pineal melanocytic tumor. Case report.

A primary melanocytic lesion arising from the pineal gland is very rare. The authors report a case of primary pineal melanocytic tumor with dissemination to the right hippocampus in a 50-year-old woman who presented with memory disturbance. Magnetic resonance (MR) imaging revealed a mass that was hyperintense on T1-weighted and hypointense on T2-weighted MR images. The pineal tumor was removed subtotally via the occipital transtentorial approach, and the patient underwent whole-brain irradiation. Results of histological examination revealed that the tumor predominantly consisted of atypical cells with scanty melanin pigment and some necrotic foci. The strongly pigmented areas of the tumor contained well-differentiated cells similar to those of melanocytoma. An ultrastructural study demonstrated evidence of a mature type of melanosome. The patient died 11 months after surgery and radiotherapy (1.7 years after the onset of symptoms). The autopsy findings demonstrated tumor invasion into the parenchyma through the leptomeningeal space and the ventricular wall. The tumor was diagnosed as being malignant, and it was finally concluded that the atypical cells in the tumor were probably responsible. This pineal melanocytic tumor exhibited a wide spectrum of differentiation, ranging from highly malignant melanoma to well-differentiated melanocytoma, which may have contributed to the patient's relatively long survival period. The biological behavior and morphological characteristics of this tumor appear to be similar to those of other pineal parenchymal lesions.

Fatal Outcome↗
PubMed2000

Evaluation of regional cerebral blood flow in chronic subdural hematoma.

To clarify the mechanism responsible for neurological impairment associated with chronic subdural hematoma (CSDH), we performed quantitative measurements of cerebral blood flow (CBF) with xenon-enhanced computed tomographic scans in eight patients with unilateral CSDH. Vascular reserve capacity was also evaluated with acetazolamide challenge. CBF was depressed in all regions examined except the corona radiata. There was no statistical difference in hemispheric and regional CBF between the lesion and non-lesion sides. A significant increase in CBF values ranging from 32% to 69% was observed after acetazolamide administration in the whole brain. Postoperatively CBF remained depressed in all regions we analyzed except for the frontal and temporal lobes, despite the fact that all patients had improved clinical symptoms. Amplitude of N20 and central conduction time (N13-20) in SSEP showed no significant change in CSDH patients compared to normal control. So we conclude that preoperative neurological signs in CSDH are related to a reduction of CBF in the whole brain. However, other mechanisms must be involved to explain preoperative focal signs and good postoperative recovery.

Adult↗
PubMed2000

[A case of multiple metastatic brain tumors with repeated intracerebral hemorrhages].

We report a case of multiple metastatic brain tumors with repeated intracerebral hemorrhages. A 73-year-old man suffered from a cerebellar hemorrhage. Subsequent hemorrhages repeatedly occurred in the right temporal lobe, the 4th ventricle, the midbrain, and the septum pellucidum. Three months after admission, CT revealed enhanced masses with surrounding edema in the cerebellar vermis and midbrain, suggesting brain tumors. We eventually diagnosed these masses in an autopsy as metastatic brain tumors of lung adenocarcinoma. Intravascular embolization with tumor cells was a probable cause of the multiple repeated intracerebral hemorrhages.

Adenocarcinoma↗
PubMed1994

Craniosynostosis in the presence of a sinus pericranii: case report.

The case of a 16-month-old baby girl with craniosynostosis associated with venous sinus stenosis and sinus pericranii is reported. Monitoring of intracranial pressure indicated increased cerebrospinal fluid outflow resistance in addition to increased intracranial pressure. Despite intracranial hypertension, however, the pressure-buffering capacity, expressed as pressure-volume index, was remarkably elevated. A similar case has not been reported in the literature. The mechanism of pressure-volume index elevation and the management of this anomaly are discussed.

Angiography, Digital Subtraction↗
PubMed1994

[Protective effects of KC-764 on short-term forebrain ischemia in gerbils].

KC-764, developed as a cyclo-oxygenase inhibitor, was administered to gerbils in a dose of 10 mg/kg, i.p., before subjecting them to 5-minute bilateral forebrain ischemia in order to determine whether it would have any protective effects. No post-ischemic hyperthermia (over 39 degrees C for 120 min) was observed in the KC-764 group. Behavior recovery time after ischemia was 11.4 +/- 2.8 minutes in the KC-764 group versus 87.3 +/- 13.4 minutes in the control group (p < 0.05). Delayed neuronal death (DND) in the CA1 region of the hippocampus was inhibited in the KC-764 group, but when the KC-764-treated animals were exposed to hyperthermia, the degree of DND was the same as in the control group. EEG voltage recovery time in the CA1 region of the hippocampus was almost the same in the control group, the KC-764 group, and the KC-764-plus-hyperthermia (HT) group. Although tissue blood flow measurements in the CA1 region of the hippocampus showed post-ischemic hypoperfusion (81 +/- 18% of the pre-ischemic level at 60 minutes), it was prevented in the KC-764 group (102 +/- 21%) (p < 0.05) and the KC-764-plus-HT group (96 +/- 28%). There was a tremendous increase in PGD2 (1461.4 +/- 863.4 p mol/g) and PGF2 alpha (219.6 +/- 104.2 p mol/g) in the forebrain after 5 minutes of reflow, but this increase in prostaglandin levels was inhibited (p < 0.05) in the KC-764 group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Cefuzonam penetration into cerebrospinal fluid].

We studied the penetration of cefuzonam (CZON) into the cerebrospinal fluid (CSF) in 20 patients with neurosurgical diseases. Influences of the presence of meningeal reaction and the intensity of brain damage on CSF penetration of CZON were also examined. Concentrations of CZON in serum and CSF were determined using the thin-layer cup method before and 1, 2, 4, and 6 hours after 2 g of CZON was administered intravenously. The serum concentration at 1 hour was 60.4 +/- 31.3 (mean +/- S.D.) microgram/ml, then rapidly decreased to 2.1 +/- 2.3 micrograms/ml at 6 hours. In contrast, the CSF concentration gradually increased, reached a peak level of 0.319 +/- 0.313 micrograms/ml at 4 hours and then slowly decreased to 0.273 +/- 0.249 micrograms/ml at 6 hours. The CSF penetration ration: CZON ([CSF]/[serum]) was 5.6% at 4 hours. The peak CSF concentration in patients with meningeal reaction (0.465 +/- 0.364 micrograms/ml at 2 hours) was about 2-fold higher than that in those without the reaction (0.249 +/- 0.223 micrograms/ml at 4 hours). The peak CSF concentrations in patients with slight, moderate, and severe brain damage were 0.231 +/- 0.133 micrograms/ml at 4 hours, 0.270 +/- 0.232 micrograms/ml at 4 hours, and 0.680 +/- 0.467 micrograms/ml at 2 hours, respectively. CSF penetration of CZON was augmented in patients with meningeal reaction or severe brain damage. These findings indicate that the concentration of CZON in CSF after intravenous administration is sufficient for treatment of meningitis or infections after neurosurgical operations caused by such bacteria as Escherichia coli, Klebsiella pneumoniae, Haemophilus influenzae, and Streptococcus pneumoniae.

Adult↗
PubMed1990

Effect of cerebral ischemia on synaptosomal uptake and release of 3H-5-hydroxytryptamine in adult and young Mongolian gerbils.

Cerebral ischemia induced by bilateral common carotid artery occlusion (15 min) with and without release (1 hr) served as a model for comparative regional studies of synaptosomal 3H-5-hydroxytryptamine (3H-5-HT) uptake and release in adult and young gerbils. A decreased uptake and an increased release of 5-HT was observed in the adult after ischemia alone and/or ischemia with reflow. At the same time, 5-HT uptake was not affected except in the cortex and the release was reduced in the young. These findings indicate that the same ischemic insults affect differently the synaptosomal uptake and/or release of 5-HT in adult and young brain.

Aging↗
PubMed1989

Ischemic modification of cerebrocortical membranes: 5-hydroxytryptamine receptors, fluidity, and inducible in vitro lipid peroxidation.

The effect of ischemia on the properties of 5-hydroxytryptamine1A + B (5-HT1A+B) and 5-hydroxytryptamine1B (5-HT1B) binding sites, physical-state "fluidity" of the membrane, and its susceptibility to peroxidation in vitro was investigated in the cerebral cortex of gerbils. Ischemia was induced by bilateral carotid artery occlusion for 15 min alone or with release for 1 h. Ischemia both with and without reflow decreased the number of 5-HT1A + B and 5-HT1B binding sites, whereas ischemia and reflow altered the affinity for 5-HT1B binding sites. Resistance to the temperature-dependent increase in "fluidity" of the membrane was detected (by fluorescence anisotropy using 1,6-diphenyl-1,3,5-hexatriene as a probe) after ischemia and reflow but not in ischemia alone. Susceptibility of the membranes to Fe2+- and ascorbic acid-stimulated lipid peroxidation in vitro was decreased following ischemia and recirculation only. These findings strongly suggest that the composition and the function of the membrane are markedly disturbed during recirculation after ischemia.

Animals↗
PubMed1988

Effect of ischemia on noradrenergic and energy-related metabolites in the cerebral cortex of young and adult gerbils.

Relationships between ischemic changes in the cerebral cortical content of energy and noradrenergic metabolites were evaluated in young and adult gerbils. Groups of 3-week- and 3-month-old gerbils were subjected to 5 or 15 min of bilateral carotid artery occlusion alone or with 1 hr of release. Ischemia of 5 and 15 min depleted energy-related metabolites but did not affect the content of either norepinephrine or homovanillic acid in young and adult gerbils. At 1 h of reflow, after 5 and 15 min of ischemia, the levels of norepinephrine significantly decreased, while those of homovanillic acid increased in the adult but not in the young gerbils. At this time a complete recovery of energy reserves was seen in both the young and the adult gerbils. These results indicate that the ischemic change in homeostasis of energy metabolism is not directly associated with that of the noradrenergic system in young and adult cerebral cortex.

Aging↗
PubMed1987

Cerebrocortical modulation of S2-receptors and turnover rate of 5-hydroxytryptamine in ischemia.

A possible relationship between the changes in the properties of S2-receptor binding sites and the turnover rate of 5-hydroxytryptamine (5-HT) has been investigated in cerebral ischemia associated with either little or marked edema. Bilateral common carotid artery occlusion for 5 or 15 min with 1 hour of reestablished blood flow in gerbils served as a model for the respective studies. An alteration in kinetic characteristics of S2-receptor binding sites labeled with [3H]ketanserin (the potent 5-HT antagonist for postsynaptic receptors) was detected in the synaptosomes separated from brains of gerbils subjected to 1 hour release after 15 but not following 5 min of bilateral ischemia. At the same time, an increased turnover rate of 5-HT was found in the cerebro-cortical homogenate. The duration of ischemic insult which leads to the changes in the properties of S2-binding sites and the increase in turnover rate of 5-HT has been identical with that needed for the marked accumulation of water in the gerbil brain reported previously. Thus, these findings are consistent with the implicated involvement of 5-HT in the formation of ischemic cerebral edema.

Animals↗