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Biomedical subjects

Toru Yamamoto

Publications and source records attributed to Toru Yamamoto.

At least 19 recordsLinked to original sources
PubMed2007

A randomized prospective study on the use of 2 g-IVIG or 1 g-IVIG as therapy for Kawasaki disease.

A single, 2 g/kg dose of immune globulin (IG), denoted 2 g-intravenous (IV)IG, has become a standard regimen for treating Kawasaki disease (KD) because of its highly preventive effect on coronary arterial lesions (CAL). However, IG is obtained from blood specimens, a drawback to many patients, and is also very expensive. This randomized prospective study reported here was carried out with the aim of developing a treatment regimen that would reduce the total dose of IG. The study tested two protocols (A: 2 g-IVIG; B: 1 g-IVIG) that included the strategy of administering additional IVIG to IVIG-resistant patients based on the criteria we described previously. In protocol A, an additional 2 g-IVIG was administered only once; in protocol B, the first additional IVIG was 1 g-IVIG and the second was 2 g-IVIG. One hundred and nine patients who were admitted before the seventh day of illness and had no CAL at the time of admission were enrolled in the study (protocol A: 54 patients; B: 55 patients). In the protocol A group, 7.4% (4/54) of the patients received 4 g/kg IG. In protocol B, 41.8% (23/55) were treated only with 1 g/kg IG, and 10.9% (6/55) received 4 g/kg IG. No significant differences were observed between the patients of the two subgroups receiving 4 g/kg IG in each protocol group. Discriminate analysis also suggested that 52.4% of the patients in the protocol A group could be treated only with 1 g/kg IG. On the other hand, no significant difference was observed in the incidence of aneurysms between patients in the protocol A group (1/54) and those in the protocol B group (4/55). Our protocol based on 1 g-IVIG, including additional IVIG, was assessed to be an effective treatment and to provide a considerably useful means to reduce the total dose of IG.

Child↗
PubMed2005

Central pontine and extrapontine myelinolysis associated with type 2 diabetic patient with hypokalemia.

Central pontine myelinolysis (CPM) is a demyelinating disease of the pons often associated with the demyelination of extrapontine areas of the central nervous system. Although the etiology and pathogenesis are unclear, CPM is usually associated with hyponatremia or its rapid correction, and chronic alcoholism is also a common underlying condition. We observed a 43-year-old man with diabetes mellitus who developed central pontine and extrapontine myelinolysis with no apparent evidence of hyponatremia, serum hyperosmolality or associated rapid correction, or history of alcohol abuse. On admission, the patient was lethargic with dysarthria, dysphagia, and mild tetraparesis and his face and lower extremities were severely edematous. Laboratory examination showed normoglycemia and normonatremia, although hypokalemia, elevated HbA1c, and nephrotic syndrome were also present. Magnetic resonance imaging (MRI) revealed abnormal signal intensity in the pons, the deep layers of the cerebral cortex, and the adjacent white matter consistent with central pontine and extrapontine myelinolysis. Generalized edema was reduced by the use of diuretics and extracorporeal ultrafiltration without significant changes of serum sodium or osmolality. His consciousness level and paresis gradually improved within a few weeks. Our patient is a rare case of CPM associated with diabetes without apparent evidence of sodium or glucose imbalances.

Adult↗
PubMed2004

Significant increase in the number of the SMN2 gene copies in an adult-onset Type III spinal muscular atrophy patient with homozygous deletion of the NAIP gene.

The patient was a 57-year-old Japanese man who gradually developed muscle atrophy and weakness in the trunk and limbs since the age of 20 years and was wheelchair bound at the age of 56 years. The gene copy number assay confirmed the combined homozygous deletion of the survival motor neuron (SMN) 1 and neuronal apoptosis inhibitory protein (NAIP) genes and showed the presence of 4 copies of the SMN2 gene. In this patient, the significant increase in the number of the SMN2 gene copies should compensate for the homozygous deletion of the SMN1 gene and make his disease milder despite the absence of the NAIP gene. Taken together with our previous data, we may reasonably hypothesize that the SMN2 gene copy number is more critical in determining the severity of the disease compared to the NAIP genotype.

Aged↗
PubMed2004

A blood-oxygenation-dependent increase in blood viscosity due to a static magnetic field.

As the magnetic field of widely used MR scanners is one of the strongest magnetic fields to which people are exposed, the biological influence of the static magnetic field of MR scanners is of great concern. One magnetic interaction in biological subjects is the magnetic torque on the magnetic moment induced by biomagnetic substances. The red blood cell is a major biomagnetic substance, and the blood flow may be influenced by the magnetic field. However, the underlying mechanisms have been poorly understood. To examine the mechanisms of the magnetic influence on blood viscosity, we measured the time for blood to fall through a glass capillary inside and outside a 1.5 T MR scanner. Our in vitro results showed that the blood viscosity significantly increased in a 1.5 T MR scanner, and also clarified the mechanism of the interaction between red blood cells and the external magnetic field. Notably, the blood viscosity increased depending on blood oxygenation and the shear rate of the blood flow. Thus, our findings suggest that even a 1.5 T magnetic field may modulate blood flow.

Adult↗
PubMed2004

Efficacy of covered metallic stents in the treatment of unresectable malignant biliary obstruction.

We evaluated the efficacy of covered stents for malignant biliary obstruction. We studied 62 patients with obstruction distal to the hilar confluence who survived longer than 10 weeks and divided them into a covered stent group (group 1, n = 22), a Z stent group (group 2, n = 19), and a mesh stent group (group 3, n = 21), according to their type of the stent. Patency rates of each group were compared. Early stent revision was required after 3 days in 18% (4/22) of group 1, 26% (5/19) of group 2, and 0% (0/21) of group 3. The 10, 20, and 40-week primary patency rates were 77%, 77%, and 59% (group 1), 42%, 25%, and 8% (group 2), and 76%, 71%, and 55% (group 3), respectively. Primary patency rates of groups 1 and 3 were significantly higher than those of group 2 (p < 0.05), and there was no statistically difference between those of group 1 and group 3. The 10, 20, and 40-week assisted primary (secondary) patency rates were 96%, 96%, and 96% (group 1), 68%, 49%, and 39% (group 2), and 86%, 74%, and 58% (group 3), respectively. Assisted primary patency (secondary) rates of group 1 were significantly higher than those of groups 2 and 3 (p < 0.01 and p < 0.05, respectively). Our study suggests that the primary patency rates of the covered stents are equal to those of mesh stents, but these may be improved further if covered stents, which avoid the need for early revision, are used.

Adult↗
PubMed2003

Percutaneous cholecystocholedochostomy for cholecystitis and cystic duct obstruction in gallbladder carcinoma.

Percutaneous cholecystocholedochostomy was performed in a patient with acute cholecystitis caused by cystic duct obstruction by gallbladder carcinoma, but removal of the percutaneous cholecystostomy catheter was unsuccessful because of continuing discharge. After creation of a cholecystocholedochostomy through the cholecystostomy tract with use of a transjugular liver access set and a 21-gauge needle, self-expandable metallic stents were placed in the narrowed common bile duct and the newly created tract between the gallbladder and the common hepatic duct. The external cholecystostomy catheter was successfully removed after the procedure. Jaundice occurred 70 days later as a result of tumor invasion above the segment with the stent, and an additional stent was placed. The patient died of diffuse metastasis 143 days after creation of the cholecystocholedochostomy without recurrence of cholecystitis.

Adenocarcinoma↗
PubMed2003

[Symmetrical necrosis in the gray matter of the brainstem and spinal cord. Two adult cases of anoxic encephalopathy].

We describe distinctive necrosis in the brainstem of two adult patients of anoxic encephalopathy. The patients were a 75-year-old man and an 82-year-old woman, who were resuscitated after cardiac arrest that lasted about 20 minutes and artificially ventilated. The first patient remained comatose without recovery of brainstem reflexes and had persistent hypotension requiring continuous infusion of catecholamine until death that occurred two weeks after the onset of illness. In the second patient, her general circulation recovered on the next day resuscitation, and traces of brainstem reflexes reappeared thereafter, while her consciousness was severely disturbed throughout the three weeks' clinical course. Both of the patients failed to regain spontaneous respiration and required the ventilatory support. On general autopsy, the first patient had small cell carcinoma of the lung with metastasis to the pleura, hilar lymph nodes and liver. In the second patient, an old myocardial infarction and pneumothorax were found. The neuropathological findings in the two patients were similar, varying only in their severity, except for the presence of the degenerative changes compatible with those of progressive supranuclear palsy in the second patient. There were laminar necrosis in the cerebral cortex and severe ischemic changes in the basal ganglia, thalamus and cerebellum. The cerebral white matter, however, exhibited only myelin pallor without apparent destruction. There was no herniation in the brain. In the first patient, fresh hemorrhages were noted in the bilateral globus pallidus. In the brainstem, symmetrical necrosis was present exclusively in the gray matter: the superior and inferior colliculi, periaqueductal gray matter, substantia nigra and the several cranial nuclei including the spinal nucleus of the trigeminal nerve, solitary and vestibular nuclei. In the second patient the symmetrical necrotic foci were also found in the substantia gelatinosa of the lower lumbar and sacral cords which were available for examination. Around these sharply demarcated necrotic lesions of the brainstem and spinal cord were there rarefaction and pronounced astrogliosis. Unlike the cases of neonates or infants, symmetrical necrosis in the brainstem has been reported to be exceptional in adult patients of anoxic encephalopathy. Now that the medical technology of resuscitation is well advanced, the adult patients exhibiting the pathology presented here may be encountered more frequently than previously thought.

Aged↗
PubMed2003

[An autopsy case of encephalopathy associated with small cell carcinoma of the stomach with nonconvulsive status epilepticus resembling Creutzfeldt-Jakob disease].

A 64-year-old man developed progressive dementia and altered consciousness with myoclonus over 2 months. Neurological examination revealed mild dysphagia and negative myoclonus of both hands. Electroencephalography (EEG) showed continuous periodic synchronous discharge (PSD) of 1 Hz, although his EEG abnormality was not similar to that usually observed in Creutzfeldt-Jakob disease (CJD). Magnetic resonance imaging (MRI) of the brain revealed only few lacunes. Laboratory data were also normal. Since his consciousness level fluctuated and the PSD were spiky, we came to a diagnosis of nonconvulsive status epilepticus (NCSE). After administering the valproic acid, his symptoms and EEG finding improved. Nine months after the onset, despite his continued valproic acid, the patient had recurrent NCSE and PSD of 1 Hz. Diffusion-weighted MRI showed a T2-hyperintense lesion in the right parietal lobe, where SPECT scans showed hyperperfusion. After adding zonisamide, he improved slowly. The follow-up MRI and SPECT showed a disappearance of the previous lesion. Now CT scans of the abdomen showed enlarged periaortic lymph node and endoscopic ultrasonography disclosed a submucosal tumor of the stomach. Biopsy of the periaortic lymph node by laparotomy revealed undifferentiated adenocarcinoma with its origin being unclear. Chemotherapy didn't work well for the tumor and the patient underwent a downhill course, although his mental and neurological manifestation were mostly unremarkable. Two years and four months after the onset, he died in emaciation. Autopsy confirmed small cell carcinoma originating in the stomach and metastases in the liver and lungs. Neuropathological examination revealed only mild scattered gliosis. This case was unique in the prolonged CJD-like manifestations, which turned out to be due to NCSE. Despite anti-neuronal antibodies were not detected, we suspect yet another paraneoplastic brain syndrome in this patient.

Aged↗
PubMed2003

[Histopathological features of biopsied peroneus brevis muscle in patients with peripheral neuropathies].

We examined the peroneus brevis (PB) muscles obtained with the sural nerves from 12 consecutively biopsied patients who were clinically and electrophysiologically ascertained to have peripheral neuropathies. Histopathological examinations revealed fiber type grouping in all of the 12 PB muscles and group atrophy associated with hypertrophic fibers in 6. These neuropathic changes were ascribable to denervation and reinnervation, being compatible with the neuropathies. Further, internal nuclei were noted in all PB muscles, and fiber splittings in 10. These myopathic changes tended to be more pronounced in the PB muscles having severe neuropathic changes and regarded as the alteration secondary to the preceding neuropathic changes. Degenerated muscle fibers, consisting of phagocytosis, basophilia and whorled fibers, were sparsely found in 8 PB muscles, while rare necrotic fibers were seen in 2. Type 1 fiber predominance was present in 7 PB muscles, in 4 of which the ratio of type 1 fiber was more than 67%. Overall, the neuropathic changes were milder in the PB muscles of CIDP patients and more marked in those showing definite axonal degeneration in the sural nerve. The severity of the neuropathic changes in the PB muscles, however, did not necessarily correlate with the strength of the leg muscles, prognoses of the diseases or the results of the nerve conduction study in the peroneal nerve. The PB muscle is liable to be affected by trauma or aging, which may modify the histopathological features of the biopsied PB muscle and therefore make the relationship between the clinical findings and the alteration of this muscle seems obscured. The available data of PB muscle have been sparse, particularly in the normal individuals, and we should be cautious in interpretation of the results of PB muscle biopsy.

Adult↗
PubMed2002

Paradoxical correlation between signal in functional magnetic resonance imaging and deoxygenated haemoglobin content in capillaries: a new theoretical explanation.

Signal increases in functional magnetic resonance imaging (fMRI) are believed to be a result of decreased paramagnetic deoxygenated haemoglobin (deoxyHb) content in the neural activation area. However, discrepancies in this canonical blood oxygenation level dependent (BOLD) theory have been pointed out in studies using optical techniques, which directly measure haemoglobin changes. To explain the discrepancies, we developed a new theory bridging magnetic resonance (MR) signal and haemoglobin changes. We focused on capillary influences, which have been neglected in most previous fMRI studies and performed a combined fMRI and near-infrared spectroscopy (NIRS) study using a language task. Paradoxically, both the MR signal and deoxyHb content increased in Broca's area. On the other hand, fMRI activation in the auditory area near large veins correlated with a mirror-image decrease in deoxyHb and increase in oxygenated haemoglobin (oxyHb), in agreement with canonical BOLD theory. All fMRI signal changes correlated consistently with changes in oxyHb, the diamagnetism of which is insensitive to MR. We concluded that the discrepancy with the canonical BOLD theory is caused by the fact that the BOLD theory ignores the effect of the capillaries. Our theory explains the paradoxical phenomena of the oxyHb and deoxyHb contributions to the MR signal and gives a new insight into the precise haemodynamics of activation by analysing fMRI and NIRS data.

Biophysical Phenomena↗
PubMed2002

Neuroaxonal leukoencephalopathy with axonal spheroids.

A 51-year-old woman with no significant family history exhibited progressive presenile dementia followed by right-sided spastic hemiplegia and died 27 months after the onset of her illness. Brain MRI demonstrated a widespread abnormality in the cerebral deep white matter and corpus callosum. Neuropathologically, extensive destruction of axons and myelin and abundant axonal spheroids were found in the deep white matter, preferentially of the frontoparietal areas. The corpus callosum was also severely damaged. The cerebral cortex and subcortical U fibers remained intact. The pathological features were different among the lesions, reflecting the sequential degenerative processes of the white matter. This case is, to our knowledge, the third sporadic case of neuroaxonal leukoencephalopathy with axonal spheroids.

Atrophy↗
PubMed2002

[A case of the persistent vegetative state following symmetrical peduncular infarction].

A 64-year-old woman presented with sudden onset of disequilibrium and dysarthria. Two days later she became lethargic and tetraparetic. An emergency MRI disclosed multiple infarctions in the medulla oblongata and pons. An angiogram revealed severe stenosis of the rostral basilar artery. The patient underwent a rapidly progressive course with impaired consciousness and flaccid tetraplegia. MR images 7 days after the onset disclosed a symmetrical midbrain infarction that was localized mainly in the cerebral peduncles, suggesting a distal basilar artery occlusion as the cause of this pathology. Since 4 weeks after the onset the patient was in the persistent vegetative state, which was essentially unchanged during the 1-year follow-up period. Persistent vegetative state is known to be caused by diffuse supratentorial or bilateral thalamic lesions, but in our case the lesions were restricted to the infratentorial area. We speculate a mechanism to cause the persistent vegetative state by partial impairment of the connection to the thalamic ascending system or extrathalamic ascending system, which leads to the dissociation of arousal(preserved in this case) and awareness(impaired in this case) after the ventral midbrain infarction.

Brain Stem Infarctions↗
PubMed2002

[Horizontal canal benign paroxysmal positional vertigo (HC-BPPV) with direction-changing apogeotropic nystagmus: a case with the more-triggering side altering over a short-term].

We report a 44-year-old man who had apogeotropic nystagmus with the rotation of his head to either side from the supine position. His nystagmus lasted more than 2 minutes and was difficult to treat with. There were no neurological abnormalities except for the nystagmus and no findings suggesting intracranial disease on MRI. The head-position in which more intense nystagmus was evoked changed again and again in a short term. We diagnosed his illness as cupulolithiasis of horizontal canal, however, the affected ear could not be explained by any of the previously supposed mechanisms. In our case, we speculate the following mechanism. Otoliths were located on the right utricular side of the cupula. All of them were attached on the cupula at the beginning(attached phase) and then, some of them were detached from it(detached phase). The extent of the cupular deviation differed in each phase when the otoliths were beneath the cupula with his head turned to the left lateral position. According to Ewald's second law, more intense nystagmus is evoked when the cupula deviates toward the utricle than away from it. The patient's head-position in which more intense nystagmus was evoked changed according to the balance between the effect of Ewald's second law and the amount of otoliths detached from cupula. Our case showed that, in HC-BPPV with direction-changing apogeotropic nystagmus, we could not be certain about which ear was diseased. Therefore, it may be difficult to apply exercise therapy by determining the affected ear based on the head-position in which more intense nystagmus is evoked.

Adult↗
PubMed2002

[Vacuolar myelopathy with symmetrical involvement of the fasciculus cuneatus, in a case of amyotrophic lateral sclerosis with multisystemic degeneration].

We report on vacuolar myelopathy in a case of sporadic amyotrophic lateral sclerosis (ALS) with multisystemic degeneration. The patient was a 75-year-old woman at death, who had been characterized by severe upper and lower motor neuron disturbance and supranuclear ophthalmoplegia. She became dependent on a respirator 14 months and survived 34 months after the onset of her illness. Neuropathologically, severe degeneration of the basal ganglia, substantia nigra, Clark's dorsal nucleus and spinocerebellar tract were noted together with the prominent alteration of the motor neuron system. The unexpected feature in this patient was the prominent vacuolar change in the white matter of the spinal cord. Especially, the fasciculus cuneatus was entirely occupied by various sizes of vacuoles. These vacuoles tended to be rimmed by thin myelin, which was continuous to disintegrated myelin sheaths. Axons were occasionally noted in the vacuoles. Vacuoles were only rarely present in the corticospinal and spinocerebellar tracts where myelin was severely lost due to the primary disease. In the vacuolar lesions lipid-laden macrophages were occasionally found, suggesting that a postmortem artifact was unlikely. Although the etiology of vacuolar myelopathy is unknown, the selective distribution of vacuolar change as seen in our patient has never been described in the past literature of vacuolar myelopathy associated with various diseases.

Aged↗