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Biomedical subjects

K Hamaguchi

Publications and source records attributed to K Hamaguchi.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Idiopathic segmental anhidrosis].

We described two cases of idiopathic segmental anhidrosis. Case 1 was a 47-year-old man, who noticed anhidrosis on the right side of face and chest during body heating. Case 2 was a 54-year-old woman, who complained of anhidrosis on the left side of face and upper chest during exercise. Both cases had neither somatic neurological deficit nor autonomic failure except for anhidrosis pupil size and deep tendon reflexes were normal. Reflex sweating to pilocarpine was exaggerated in the anhidrotic areas in both cases, suggesting lesions in the preganglionic sudomotor nerves. Abnormal laboratory finding was elevated serum rheumatoid factor level in only case 2. Segmental anhidrosis was static for 1.5 year and one year, respectively. The previous literature contains similar four cases. Idiopathic segmental anhidrosis may be an abortive form of Ross' syndrome (tonic pupil, hyporeflexia and segmental anhidrosis).

Female↗
PubMed1996

[A case report of subacute panencephalitis associated with specific T cells sensitized to proteolipid protein (PLP) synthetic peptides identified with rubella virus].

A 37-year-old woman was admitted to the hospital on October 4, 1991 because of fever, headache, and abnormal behavior. Although she was treated with aciclovir, she developed encephalitis, which slowly manifested itself over the next month as meningeal irritation, loss of consciousness, partial seizure, and quadriparesis. Her cerebrospinal fluid showed mild lymphocytic pleocytosis without protein elevation. Serum IgG antibody titer to rubella virus was elevated, but the rubella virus could not be detected in the cerebrospinal fluid by PCR amplification. Her consciousness level improved slowly, and by the end of November she suffered only dystonic posture of her right arm and hand. By the middle of December, there were no abnormal neurological findings except some extrapyramidal tract signs and symptoms, such as tremor and rigidity. The serum rubella virus IgG titer had fallen back into the normal range. Her illness was diagnosed as subacute panencephalitis, and she recovered completely about 5 months after the onset of the disease. The lack of rubella virus in the cerebrospinal fluid suggests that panencephalitis may not be dependent on virus replication within the central nervous system. Specific T cells sensitized to proteolipid protein synthetic peptides (PLP158-166) identified with rubella virus were detected in this case during the active stage. These observations imply that subacute panencephalitis may be dependent on an immune-mediated mechanism and that PLP-specific T cells may play an important role in pathogenesis of the disease.

Adult↗
PubMed1996

[A case of sympathotonic orthostatic hypotension following herpes simplex encephalitis].

The etiology of sympathotonic orthostatic hypotension (SOH) is still unknown. We reported a 50-year-old male case of SOH associated with herpes simplex encephalitis. Eight days before admission to our hospital, he noticed fever, which was followed by intractable hiccup. He was admitted to a local hospital, where nuchal rigidity and mononuclear CSF pleocytosis were noted. On the 9th hospital day, he suddenly developed respiratory arrest, and his consciousness state deteriorated to coma. He was transferred to our hospital with artificial ventilation on the same day. The second CSF examination revealed pleocytosis and positive herpes-simplex-virus antibody. CAT scan showed diffuse high density areas in the bilateral temporal lobes. Intensive anti-herpetic therapy was started. On the 14th hospital day, spontaneous respiration came back and consciousness state was improved from coma to stupor. He gradually recovered to alert state and became ambulatory by the 30th hospital day. Seven weeks after the onset of his illness, he noticed orthostatic dizziness for the first time during his rehabilitation exercises. Blood pressure was 116/78mmHg at supine position and 82/62mmHg at standing position, and the heart rate was 83bpm, and 141bpm, respectively. Plasma noradrenaline concentration was 0.09 ng/ml (within normal range) at supine position, but increased to 0.29ng/ml upon standing. Catecholamine infusion tests revealed hyposensitivity in beta 2-receptors; decrease in blood pressure in response to isoprenaline was blunted, while increase of blood pressure to noradrenaline was not impaired. Nerve conduction studies and sweating tests were normal. When he was discharged from our hospital on the 87th hospital day, he still had orthostatic symptoms. His complete recovery took full one year. Some authors claimed that SOH is an abortive form of acute autonomic neuropathy, while others postulated that it was due to unbalanced cardiovascular alpha- and beta-adrenoceptor functions. SOH of the present case seems to be caused by the central nervous lesions; especially, the brain stem involvement due to herpes simplex encephalitis may well be causing SOH.

Autonomic Nervous System↗
PubMed1996

[Guillain-Barré syndrome and acute disseminated encephalomyelitis (ADEM)].

I would like to report the results of our immunological study on Guillain-Barré syndrome (GBS) and to consider the relationship between GBS and acute disseminated encephalomyelitis (ADEM). First of all, I referred to the historical view of the diagnostic criteria of GBS. Immunological study on GBS started after the report of experimental allergic neuritis (EAN) by Waksman and Adams (1995). We made EAN rabbits by immunization with peripheral myelin and observed the process of motor paralysis. In EAN, humoral and cellular immune responses to P2 protein and its synthetic peptides were obtained in accordance with the motor weakness. In patients with GBS we also investigated the humoral and cellular immune responses to P2 protein. Anti-P2 protein antibody and sensitized lymphocytes against P2 protein and its synthetic peptides were detected in GBS as well as in EAN. We also detected antineural antibodies such as anti-P0, anti-galactocerebroside and anti-GM1 ganglioside antibodies in GBS. And also anti-GQ1b antibody was detected in patients with Fisher syndrome and GBS with ophthalmoplegia. More than 50 years ago, Baker (1943) described 5 forms of GBS including 1) abortive or mononeuritic 2) polyneuritic 3) spinal, 4) bulbar and 5) cerebral forms. Guillain (1953) didn't deny the bulbar and cerebral forms, although he apparently denied the spinal form of GBS with Babinski's sign. According to "Merritt's Textbook of Neurology", lesions of ADEM (postinfectious and postvaccinal encephalomyelitis) involved not only the brain and the spinal cord but also the peripheral nerve. Guillain (1953) objected against "Landry-Guillain-Barré syndrome" proposed by Haymaker and Kernohan (1949). Guillain (1953) described that Landry's ascending paralysis was different from GBS and Landry's paralysis must belong to category of ADEM, as van Bogaert also commented. In our recent study for T cell subsets in GBS and ADEM, significant increase in activated CD4 and helper inducer cells were observed in both GBS and ADEM, which suggested the presence of a common pathogenic mechanism in these diseases. After considering the classification of immunological nervous diseases, we would propose a clinical entity "acute immuno-logical nervous diseases" including GBS, Fisher syndrome and ADEM.

Animals↗
PubMed1995

Regulation of synapse density by 5-HT2A receptor agonist and antagonist in the spinal cord of chicken embryo.

Identification of mechanisms that regulate the number of synapses in the brain has been a key issue for understanding the mechanism of plasticity. Here, we report that the density of synapses can be changed using an antagonist and/or an agonist of serotonin (5-HT) type 2A receptors in the chicken spinal cord. Because of the widespread distribution pattern of 5-HT fibers and 5-HT2A receptors in the central nervous system, 5-HT is thought to play a role in the formation and maintenance of synapses that are involved in normal brain function and mechanism of plasticity.

Amphetamines↗
PubMed1995

Stability of ribonuclease T2 from Aspergillus oryzae.

The stability of ribonuclease T2 (RNase T2) from Aspergillus oryzae against guanidine hydrochloride and heat was studied by using CD and fluorescence. RNase T2 unfolded and refolded reversibly concomitant with activity, but the unfolding and refolding rates were very slow (order of hours). The free energy change for unfolding of RNase T2 in water was estimated to be 5.3 kcal.mol-1 at 25 degrees C by linear extrapolation method. From the thermal unfolding experiment in 20 mM sodium phosphate buffer at pH 7.5, the Tm and the enthalpy change of RNase T2 were found to be 55.3 degrees C and 119.1 kcal.mol-1, respectively. From these equilibrium and kinetic studies, it was found that the stability of RNAse T2 in the native state is predominantly due to the slow rate of unfolding.

Aspergillus oryzae↗
PubMed1995

Cutaneous oxalate deposition in a hemodialysis patient.

We describe calcium oxalate and amyloid arthropathy with cutaneous calcinosis without vitamin C supplement. A 34-year-old woman developed glomerulonephritis requiring chronic hemodialysis. Seven years after beginning hemodialysis, multiple crystal deposits appeared in her skin; she also presented with arthralgia and gait disturbance. A skin biopsy was performed, which disclosed calcium oxalate deposition. In addition, a right femoral neck prosthetic replacement was performed. Pathologic examination of the hip synovia revealed diffuse calcium oxalate, amyloid, and iron deposition. Calcium oxalate and amyloid arthropathy with synovial hemosiderosis was diagnosed, and therapy with desferal and high-flux membrane dialysis was started. Clinical improvement occurred after 6 months.

Adult↗
PubMed1995

Secondary amyloidosis associated with Castleman's disease.

A rare case of secondary amyloidosis associated with Castleman's disease is reported. A 53-year-old woman was referred for investigation of proteinuria. Biopsy specimens from kidney and gastric mucosa revealed numerous amyloid deposits, defined as AA amyloidosis by immunohistological staining. Castleman's disease was found in the abdomen as the primary disease for the amyloidosis. Although the urinary protein was somewhat reduced and the inflammatory findings were improved after removal of the lymphoma, renal insufficiency progressed and hemodialysis was begun.

Amyloidosis↗
PubMed1995

[A case of nephrotic syndrome mimicking membranoproliferative glomerulonephritis (MPGN) and associated with reactive hemophagocytic syndrome after renal death].

We report a case of nephrotic syndrome which mimicked membranoproliferative glomerulonephritis (MPGN) and was associated with hemophagocytic syndrome after renal death. A 41-year-old Japanese man was referred to our hospital because of nephrotic syndrome in February 1979. He had no signs, symptoms nor laboratory data suggestive of liver damage. He was diagnosed as idiopathic MPGN and administered prednisolone and cyclophosphamide (total dose of about 50,000mg). He developed end-stage renal disease, and dialysis therapy was initiated in February 1992. Simultaneously, he was diagnosed as hepatitis C virus (HCV)-positive liver cirrhosis. In August 1994, he died because of reactive homophagocytic syndrome, which occurred in the setting of immunosuppression due to chronic renal failure, liver cirrhosis, and sesecondary diabetes. In this case, we can not deny the possibility that radical therapeutic intervention against "idiopathic MPGN" had a negative effect on the clinical course of chronic HCV infection.

Cyclophosphamide↗
PubMed1995

[Antineuronal autoantibody to a 40-kDa protein in a patient with cerebellar ataxia and breast cancer].

A 49-year-old woman was admitted to Utsunomiya Saiseikai hospital complaining of right breast swelling. There was half a year history of difficulty in walking. A diagnosis of breast cancer was made by biopsy. Neurological examination revealed scanning speech, nystagmus, intention tremor and ataxic gait, but brain CT scan and MRI showed neither metastatic, invasive lesions nor atrophy in the brain. Lumpectomy for breast cancer was performed. For immunocytochemical studies, the cytoplasm of neurons in sections of normal human cerebral cortex, cerebellum, spinal cord and dorsal root ganglia were stained by the patient's serum, but glial cells were not. Upon Western blot, the patient's serum reacted with a 40-kDa protein in extracts of both cerebrum and cerebellum obtained from normal rats. A diagnosis of paraneoplastic cerebellar degeneration (PCD) was made on the basis of clinical manifestations and detection of the antineuronal antibody. The antibody accompanying the breast cancer which stained neuronal cytoplasm and bound to a 40-kDa protein may be a subtype of antibody causing PCD.

Autoantibodies↗
PubMed1995

[A case of metamorphopsia caused by a very localized spotty infarct].

A 51-year-old woman complained that her right side of the face looked blurring and the right margin of all the objects in her visual field looked blurred. Neurological examination on admission showed no abnormalities including higher cortical function and visual fields except the metamorphopsia. In this case, a very localized spotty infarct caused no neurological symptoms other than the metamorphopsia. CT scan and MRI revealed a spotty lesion of infarct between retrosplenium and cingulate gyrus on the left side. This can be a breakthrough case to locate the exact anatomic pathology that causes metamorphopsia.

Cerebral Infarction↗
PubMed1995

[Clinicopathological report of cisplatin encephalopathy].

A 61-year-old woman was treated with cisplatin and etoposide for ovarian carcinoma. After the second course of chemotherapy she developed acute encephalopathy which manifested itself as headache, fever, a partial seizure, confusion, and mild right hemiparesis, although no evidence of a central nervous system infection was found. Ten days after the onset of neurological symptoms, she experienced a sudden loss of vision in both eyes. Neurological findings were compatible with cortical blindness. Neurological symptoms subsided and visual acuity completely returned over the next months. The total cumulative dose of cisplatin was 325 mg/m2. She died of aspiration pneumonia on the 43rd day. Postmortem examination revealed severe nerve cell loss, gliosis and spongy changes in the bilateral occipital cortex including visual field, and slight to moderate demyelination in the subcortical white matter of the occipital cortex, Goll's tract, and dorsal root ganglia. As far as we know this encephalopathy is the second report in which the neuropathological changes associated with cisplatin therapy have been demonstrated by autopsy findings. The first was a case report of leukoencephalopathy, which differed significantly from our case in the primary lesions of the brain. We measured the platinum level in several parts of the cerebrum and cerebellum, optic nerve, spinal cord, and cauda equina by using an atomic absorption spectrophotometric technique. Platinum was detected in the bilateral occipital cortex, spinal cord, and cauda equina. These results were consistent with the distribution of pathological lesions. The mechanism of cisplatin-induced focal encephalopathy remains speculative.(ABSTRACT TRUNCATED AT 250 WORDS)

Blindness↗
PubMed1995

[A study of skin surface temperature in patients with unilateral cerebral infarction--with special reference to central autonomic regulation of skin vasomotor response].

Skin surface temperature was examined using thermography in 26 patients with unilateral ischemic cerebrovascular disease (5 with pontine lesions, 5 with lateral medullary lesions and 16 with hemispheric lesions). Three of the 5 patients with pontine lesions and 4 of the 5 with medullary lesions showed hemihyperthermia on the ipsilateral body surface. However, the face showed no impairment with pontine lesions, whereas it appeared as a hyperthermic area with medullary lesions. Ten of 11 patients with lesions of the internal capsule or putamen had hypothermia on the contralateral body surface except for the face. All the patients with thalamic lesions showed no skin temperature asymmetry. These observations suggest the following: (1) sympathetic skin vasomotor fibers descend through the ipsilateral side of the brainstem; (2) at the level of the medulla, skin vasomotor fibers innervating the body trunk and limbs and those innervating the face descend contiguously, while at the level of the pons the two fiber groups descend separately; (3) hypothermia in patients with cerebral infarction could be explained by interruption of the inhibitory neural pathway that controls vasomotor function on the contralateral side of the body; (4) these inhibitory pathways descend in the vicinity of the pyramidal tract.

Adult↗
PubMed1995

[Cardiovascular alpha-, beta 1- and beta 2-adrenoceptor functions in neurogenic orthostatic hypotension].

It has been believed that patients with neurogenic orthostatic hypotension (NOH) usually develop denervation supersensitivity of cardiovascular alpha-, beta 1- and beta 2-adrenoceptors, because the majority studies have shown augmented cardiovascular responses to intravenously given noradrenaline (NA) or isoprenaline (IP) in these patients. This view, however, leaves room for discussion. First, drugs were administered by means of drip infusion method in most of the previous studies. Since this method necessarily provokes baroreflex, which is buffering fluctuations in blood pressure and heart rate, the results may reflect diminished baroreflex rather than denervation supersensitivity. Second, adrenoceptor functions are modulated by multiple factors, such as ageing, thyroid hormone and chronic inflammation. It is, thus, inappropriate to explain the whole picture of functional change in adrenoceptors by the denervation mechanism only. In order to look over the cardiovascular adrenoceptor functions in NOH, we performed bolus infusion tests of NA and IP on the patients. The subjects comprised 7 cases of NOH with pre-ganglionic sympathetic deficit (NOH-I), 6 cases with post-ganglionic deficit (NOH-II) and 15 healthy controls. NOH-I group included 6 patients with multiple system atrophy and one with Parkinson disease, while NOH-II group consisted of 3 patients with idiopathic orthostatic hypotension (pure autonomic failure) and 3 with diabetic autonomic neuropathy. Both NA and IP infusion tests were carried out under the continuous measurement of blood pressure and heart rate. In NA test, different bolus doses (0.01, 0.02, 0.05 and 0.1 microgram/kg) of NA were intravenously administered, and a degree of subsequent rise in mean blood pressure was used as an index for alpha-adrenoceptor function. IP test was performed in the same manner, and an increase in heart rate and a fall in mean blood pressure in response to the drug (0.001, 0.002 and 0.005 microgram/kg) were measured as indices for beta 1- and beta 2-functions, respectively. A rise in blood pressure following the administration of any dose of NA did not statistically differ among three groups. An increase in heart rate in IP test was generally lower in both NOH groups, and a significant difference was obtained between NOH-I and control when a given dose was 0.005 microgram/kg) (p < 0.02). A fall in blood pressure in IP test was significantly greater in NOH-I compared to control when doses were 0.002 and 0.005 microgram/kg (p < 0.02 and 0.01, respectively). It was also greater in NOH-II than in control when a dose was 0.002 microgram/kg (p < 0.01). In disagreement with most of the previous studies, the present results suggest that alpha-adrenoceptor function is hardly altered, beta 1-function is suppressed, and beta 2-function is augmented in NOH.

Adult↗
PubMed1995

[Chronic recurrent polyneuropathy in a patient with autoimmune hemolytic anemia associated with antibodies to gangliosides GM1, GA1, and GD1b].

We report a case of chronic recurrent polyneuropathy with warm-type autoimmune hemolytic anemia (AIHA) associated with antibodies to gangliosides GM1, GA1 and GD1b. There have been few reports of AIHA associated with polyneuropathy. A 39-year-old man was admitted in May 1991 because of severe hemolytic anemia. Direct Coombs' test was positive of IgG1 and complement type. The treatment was started with prednisolone, the hematological abnormalities disappeared after 6 months, but thereafter, he developed muscle weakness of all limbs and AIHA within 7 weeks. On neurological examination, he was unable to arise from a chair and could not stand, had muscle atrophy and numbness of the distal part of all limbs and areflexia. Cerebrospinal fluid was acellular and protein content was 117 mg/dl. Electrodiagnostic studies showed mild slowing of nerve conduction velocities associated with severe decrease in amplitudes of compound muscle action potential and multifocal conduction block. A sural nerve biopsy specimen showed moderate loss of small myelinated fibers, but not of unmyleinated fibers. AIHA was substantially improved by methylprednisolone (1,000 mg/day) for 3 days, but neurological symptoms remained unchanged. A month later, he was given 2 courses of intravenous gammaglobulin infusion (0.4 g/kg/day) for 5 days. He was able to walk after the second course. In May 1992, the mild motor-sensory polyneuropathy recurred and gammaglobulin infusion was effective for neurological symptoms. We detected the high level of anti-GM1 antibody titer in the patient's serum by ELISA, the level of the antibody titers correlated with neurological manifestation. A thin-layer chromatography with immunostaining showed the presence of anti-GM1, GA1 and GD1b antibodies in his serum. We grouped the reported cases of AIHA into cold and warm types, according to its hemolytic temperature, and characterized the neurological manifestations in each type. We also discussed the pathogenic role of anti-gangliosides antibodies in this case.

Adult↗
PubMed1995

Relationship between the therapeutic effects or side-effects and the serum disopyramide or mono-N-dealkylated disopyramide concentration after repeated oral administration of disopyramide to arrhythmic patients.

After we had developed a method to determine simultaneously the blood concentrations of disopyramide (DP) and its metabolite mono-N-dealkylated disopyramide (MND) by high-performance liquid chromatography, DP was administered repeatedly to arrhythmic patients in order to examine the relationship between the serum DP or MND concentration and the therapeutic effects or side-effects. To 79 arrhythmic patients (57 patients with ventricular premature contraction, 13 with supraventricular arrhythmia and 9 with atrial fibrillation), DP was administered repeatedly at an initial oral dose of 200 to 400 mg/day. Of the 61 patients which were possible to evaluate after reaching a steady state, 32 were evaluated as effective and 29 as non-effective, the effective rate being 52.5%; the mean blood DP concentration (+/- S.D.) was 2.14 +/- 0.65 and 1.74 +/- 0.62 micrograms/ml, respectively, with a significant difference between the two groups (p +/- 0.05). At the final dose, 40 patients were evaluated as effective and 18 as non-effective, the effective rate being 69.0%; the mean blood DP concentration was 2.03 +/- 0.67 and 2.09 +/- 0.68 micrograms/ml, respectively, with no significant difference between the two groups. Among 42 patients with premature contraction, 26 were evaluated as effective and 16 as non-effective, the effective rate being 62%; the mean blood DP concentration was 2.01 +/- 0.62 and 2.20 +/- 0.70 micrograms/ml respectively, with no significant difference between the two groups. The incidence of side-effects was 17.7%, and there were no significant differences in blood DP or MND concentrations between the groups with and without side-effects. A blood DP concentration more than 2 micrograms/ml may be required to achieve the therapeutic effect of DP administered repeatedly.

Adult↗
PubMed1995

[Factors affecting continuation of home medical care--based on the relationship between patient and caregiver status].

In recent years it has gradually become possible to have some control over the medical condition of the end-stage cancer patient. However, there are various problems involved in the continuation of home care. In order to clarify how the mutual relationship between patient and caregiver effects the continuation of home care, we conducted a study on 28 end-stage cancer patients who made the transition from our hospital to home care by means of our HOme Care Service. Using the Kaneda Assessment Score, we obtained information from patients' charts, added reasons for rehospitalizations and analyzed the data. The results showed that the group of patients who remained on home care, despite the fact that their condition was significantly poorer than that of the group who discontinued home care, showed a significantly higher proportion of "wishing to be cared for at home to the last," in the view of the caregiver, a joint commitment of the caregiver together with the family, and a suitable response to changes in the patient. As a direction for forthcoming support in this area, there is a need for sufficient assessment in order to evaluate the balance between caregiver and family. It was suggested that guidance in each case and the use of community resources will be very important.

Activities of Daily Living↗