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Biomedical subjects

N Ohkoshi

Publications and source records attributed to N Ohkoshi.

At least 73 records · Page 4Linked to original sources
PubMed1997

Sympathetic denervation of myocardium demonstrated by 123I-MIBG scintigraphy in pure progressive autonomic failure.

123I-MIBG myocardial scintigrams obtained in 2 cases with pure progressive autonomic failure are presented. In the less advanced case, 123I-MIBG myocardial SPECT disclosed uptake defects of radioisotopes in both the apical region and the inferior wall and a marked decrease in uptake in the lateral wall. However, residual radioactivity was demonstrated in the anterior wall. In the terminal stage, radioactivity over the whole heart was undetectable in planar images, so as to be of no use to obtain SPECT images. These scintigrams might suggest where the sympathetic denervation began and subsequently extended to the whole myocardium in the course of the disease. In addition, 123I-MIBG scintigraphy was recommended in a case with the disease, since an unequal impairment of myocardial sympathetic nervous system has been described to probably induce fatal arrhythmias which were the cause of sudden death in this case.

3-Iodobenzylguanidine↗
PubMed1997

[Ataxic neuropathy in the elderly--clinicopathological study of six cases].

The combination of ataxia with peripheral neuropathy (ataxic neuropathy) is rare. Six elderly patients with peripheral neuropathy who developed ataxia were studied. Of the peripheral neuropathies, ataxic neuropathy was significantly more frequent in patients aged more than 65 years compared with younger patients. Ataxic neuropathy was associated with carcinoma (2 cases), Sjögren's syndrome (1 case), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP, 1 case) and chronic idiopathic ataxic neuropathy (2 cases). The two cases of carcinomatous neuropathy initially showed ataxia, which preceded detection of the carcinomatous lesions in the lung by approximately 1 year. The study cases had many clinical features in common. In the nerve conduction study, sural nerve action potential could not be measured in five of the cases; sural nerve biopsy revealed a decreased density of myelinated fibers in all cases. In particular, the large myelinated fibers were markedly decreased. These findings were common, regardless of the underlying disease, except in the case of CIDP in which there was only a slight decrease in the number of large myelinated fibers. Differential diagnosis based on the clinicopathological features was difficult. Therefore, in cases of ataxic neuropathy, systemic evaluation is necessary to rule out the possibility of carcinoma or various systemic diseases, especially in elderly patients.

Age Factors↗
PubMed1997

[A case of frontal gait apraxia caused by hypoxic encephalopathy].

We reported a rare case who had hypoxic-encephalopathy causing frontal apraxia of gait. The patient, a 34-year-old female, was admitted in July, 1994, complaining of difficulty in walking after anoxic brain damage caused by ventricular arrhythmia. She had difficulty in raising her feet, which appeared to be rooted to the floor. There was no evidence of motor paralysis, spasticity, rigidity or sensory loss, but she did show frontal lobe signs such as foot grasp reflex and Gegenhalten. Cranial MRI showed slight atrophy of the frontal lobe. On T2 weighted image, high-intensity areas were detected at the posterior internal capsule and corona radiata. Single photon emission CT (123I-IMP) demonstrated a low perfusion area which included the inferomedical part of the frontal lobe. After 8 months of hospitalization, her postural instability and unsteady gait slowly improved without treatment as frontal signs such as foot grasp reflex disappeared. We speculate that her apraxia of gait may result from grasp reflex and Gegenhalten.

Adult↗
PubMed1997

[A case of potassium-sensitive periodic paralysis with cardiac dysrhythmia].

The authors reported a case of potassium-sensitive periodic paralysis with cardiac dysrhythmia. The patient was a 21-year-old male and had periodic paralysis and asymptomatic cardiac dysrhythmia since the age of 12. His attacks worsened in frequency and intensity which brought him to our hospital at the age of 21. Physical examination on admission revealed slight dysmorphic features such as hypoplastic mandible and high-arched palate. He had slight proximal muscle atrophy with no myotonia. Electrocardiogram showed multifocal ventricular arrhythmia. The serum potassium levels during his paralytic attacks were normal or slightly decreased (3.6-4.2 mEq/l). Both potassium and glucose tolerance tests provoked paralytic attacks. Glucose tolerance test also aggravated his cardiac dysrhythmia. Acetazoramide administration improved his paralytic attack. Potassium-sensitive periodic paralysis with cardiac dysrhythmia can not be defined by the classification of periodic paralysis based on the serum potassium concentration. Provocative tests should be done to make a definite diagnosis and treatment should be done taking into consideration both paralytic attack and cardiac dysrhythmia.

Abnormalities, Multiple↗
PubMed1997

[A case of mitochondrial encephalomyopathy showing ophthalmoplegia, diabetes mellitus and hearing loss associated with the A3243G mutation of mitochondrial DNA].

We report a 47-year-old female patient showing clinical features of chronic progressive external ophthalmoplegia (CPEO) without stroke-like episodes. Large scale deletion of mitochondrial DNA (mtDNA) was not found in her biopsied muscle, whereas the A-->G transition at position 3243 (A3243G) was detected. The patient's mother had diabetes mellitus, suggesting maternal inheritance. This mutation is usually associated with MELAS, but wide clinical variety of the mutation has been recognized. Although several patients of CPEO with A3243G mutation (CPEO3243) have been found in the Western countries, only one case has been reported in detail in Japan. The CPEO3243 patients, including ours, show retinopathy less frequently, but diabetes mellitus and hearing loss more frequently than CPEO patients with deletions of mtDNA (CPEO delta). CPEO3243 is usually inherited maternally, but almost all CPEO delta is sporadic. With regard to COX activity of biopsied muscles, CPEO3243 resembles CPEO delta more than MELAS3243. This suggests that how the mutant mtDNA is distributed among cells or tissues may have more significant effect on clinical phenotype than what type of mtDNA mutation exists. The presence of such a CPEO3243 patient like ours could be an important suggestion toward further understanding of mitochondrial diseases.

DNA, Mitochondrial↗
PubMed1997

[A case of post-poliomyelitis muscular atrophy with cranial nerve signs and widespread muscular atrophy of the extremities].

Here we report a case of a 56-year-old male with post-poliomyelitis muscular atrophy (PPMA), who presented with cranial nerve signs and widespread atrophy of the extremities. He had suffered from poliomyelitis at the age of 2 years. After recovery from the acute stage, the paralysis remained in his left arm. He noticed muscle weakness of the right upper and lower extremities at the age of 45 years and the muscle atrophy progressed to his arms, hip and thigh at the age of 55 years. Neurological examination revealed muscle atrophy of the neck and disturbance of left V, VIII, IX, X and bilateral XI cranial nerves. We diagnosed this case as PPMA from his history and electromyographic and muscle biopsy findings which suggested chronic denervation. Among the 21 PPMA cases in the past in which the acute poliomyelitis had resulted in paralysis of the only one limb, ours was the only case that had muscle atrophy of all the limbs. Cranial nerve involvement is known to occur in acute poliomyelitis; therefore, there is a possibility that the involvement of the cranial nerves in our case might be a delayed progressive symptoms.

Cranial Nerves↗
PubMed1997

[Self-efficacy and related factors related in Parkinson's disease patients].

This study was designed to assess self-efficacy and the factors leading to higher self-efficacy in Parkinson's disease patients, as measured by General Self-Efficacy Scale (GSES). Questionnaires were mailed to patients with Parkinson's disease in Tokyo. This study surveyed 73 male and 70 female patients. Approximately 66.5% of the patients fell into the low self-efficacy group. Data was divided into 3 groups (high, moderate and low) and evaluated statistically. Approximately 66.5% of the patients fell into the low self-efficacy group. Patients in the high self-efficacy group exhibited the following features: Males: 1) The male patients in the high self-efficacy group tended to belong to more groups and had less trouble than any other groups in coping with their daily lives; 2) they generally had people to turn to for mental support outside their families, and for their daily life inside or outside their families; 3) they also felt confident that they had sufficient understanding of better life styles and how to exercise. Females: 1) The female patients in the high self-efficacy group tended to go out more often than any other groups and had places to go where they could practice hobbies and exercise; 2) they generally had people outside their families to turn to for mental support; 3) their subjective symptoms, such as freezing and dysarthria, tend to be less acute than in the moderate or low self-efficacy patients. 4) had les trouble than any other groups in coping with their housing accommodations; 5) they also felt confident that they understood how to exercise. In order to increase self-efficacy among Parkinson's disease patients, this study suggests that support, both social and psychological, and providing health education, are important.

Aged↗
PubMed1996

[Keratitis and corneal edema associated with levodopa use--a case report].

We report a patient who developed keratitis and corneal edema during treatment with carbidopa-levodopa. The patient was a 34-year-old woman who complained of apraxic gait after anoxic brain damage caused by ventricular arrhythmia. She had difficulty in walking. While doses of droxidopa, flecainide acetate and amantadine HCl were kept at the same levels as before several weeks, administration of carbidopa-levodopa was gradually increased from an initial dose of 100 mg per day to 300 mg per day over a period of 10 days in an attempt to relieve her apraxic gait. Ten days after initiation of treatment with carbidopa-levodopa, her postural instability and unsteady gait slightly improved. However, after 8 days of treatment with carbidopa-levodopa, she complained of blurred vision. Ophthalmologic examination showed keratitis (corneal endothelitis) and corneal edema. After stopping carbidopa-levodopa, the keratitis dramatically improved. Cessation of the drug therapy resulted in a return of vision to normal levels by the 7th day. Although there had been no previous reports of corneal lesion caused by levodopa, we suspected that keratitis and corneal edema were associated with carbidopa-levodopa use, especially in combination treatment with flecainide acetate, and amantadine HCl. The process was reversible and presumably could have been prevented by a shorter term of medication.

Adult↗
PubMed1996

[Pseudoradicular sensory impairment caused by parietal lesions: report of two cases].

Here we report two cases of pseudoradicular sensory impairment (PRSI) caused by cerebral infarctions. Case on was a 49-year-old male who presented with dysesthesia in the left ulnar nerve distribution, and case 2 was a 57-year-old male who developed dysesthesia and weakness in the left radial nerve distribution. In both cases, the symptoms began with dysesthesia, followed by disturbance of cortical sensation, and distal motor weakness of the left upper extremity. Although the temperature, superficial pain, tactile, and vibratory sensations were well preserved, position sense, and cortical sensations such as two-point discrimination, material discrimination and stereognostic sensations were severely disturbed. No abnormalities were found in nerve conduction studies or cervical magnetic resonance imaging (MRI). Findings of somatosensory evoked potential (SEP) indicated that cortical components (N20, P24, N35 and P55) were missing in the left ulnar nerve in case 1, and in the median nerve in case 2. MRI of the brain revealed cerebral infarctions in the right parietal lobe including the postcentral gyrus. From the above results sensory disturbances of these two cases are caused by infarctions of the right parietal lobe. The characteristics of sensory disturbances caused by parietal lesions in our cases are similar to the previous reports. In addition, we found that the impaired cortical and subcortical areas were larger than the predicted areas indicated by Penfield's somatosensory homunculus. From the thermography, we found that the dermal regions with sensory impairment were more or less hypothermal. This suggests that cortical and subcortical infarctions may lead to localized sympathetic dysfunctions of the skin.

Cerebral Cortex↗
PubMed1996

Sural nerve biopsy in vasculitic neuropathies: morphometric analysis of the caliber of involved vessels.

We performed histologic and morphometric analyses of the sural nerve in 13 patients with vasculitic neuropathies. The ratio of vessels with vasculitis, the caliber of involved vessels, and pathologic changes of myelinated fibers were evaluated. In patients with polyarteritis nodosa (PN), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE), marked vasculitis with inflammatory cell infiltration and occlusion were observed in epineurial arteries greater than 100 microns in diameter, and mild vasculitic changes were noted in arterioles 40 to 100 microns in diameter. In vessels less than 40 microns, mild vasculitis with perivascular cuffing was noted in patients with RA and SLE, but not in PN. In a patient with microscopic PN, mild inflammatory cell infiltration was encountered around small vessels at diameters less than 40 microns as well as those greater than 100 microns. In a patient with nonsystemic vasculitic neuropathy, vasculitic changes were identified only in vessels less than 40 microns. In patients with Churg-Strauss syndrome (CSS), there were no distinct findings of vasculitis in any biopsy material. In conclusion, morphometric analyses of the caliber of involved vessels may be useful in the differential diagnosis and classification of underlying vasculitic neuropathies.

Aged↗
PubMed1995

Superoxide dismutases of muscle in mitochondrial encephalomyopathies.

Immunohistochemical analyses were made of the superoxide dismutases (Mn-SOD and Cu/Zn-SOD) in biopsied muscles from 7 patients with mitochondrial encephalomyopathies that included mitochondrial encephalomyopathy, lactic acidosis and strokelike episodes (MELAS), and chronic progressive external ophthalmoplegia (CPEO). Mn-SOD mainly was present in the subsarcolemmal region, but it also was found in a coarsely granular, reticular, or diffuse pattern of staining within the muscle fibers. These Mn-SOD-positive fibers corresponded almost completely to the ragged-red fibers. The immunoreaction for Cu/Zn-SOD was weakly positive in some of the muscle fibers positive for Mn-SOD. In CPEO, Mn-SOD-positive fibers predominantly showed decreased cytochrome c oxidase (COX) activity. In MELAS, Mn-SOD-positive fibers tended to be stained deeply for COX although a few were COX-negative. These findings suggest that Mn-SOD-positive fibers can be used to make a differential diagnosis between CPEO and MELAS and that in mitochondrial encephalomyopathies Mn-SOD in the ragged-red fibers may protect against oxidative stress.

Adult↗
PubMed1995

Calbindin-D 28k immunoreactivity in the cerebellum of spinocerebellar degeneration.

We studied immunoreactivity for calbindin-D 28k (CaBP), an intracellular calcium-binding protein, in the cerebellum of control subjects and of patients with spinocerebellar degeneration (SCD) including sporadic olivopontocerebellar atrophy and familial cortical cerebellar atrophy. In the cerebellum, CaBP immunoreactivity was seen exclusively in the Purkinje cell in both SCD and control groups. However, the number of CaBP-immunoreactive Purkinje cells was significantly reduced in SCD. CaBP immunohistochemistry also disclosed abnormal morphological changes of Purkinje cells, which was not visualized on conventional strains or not clearly demonstrated on immunohistochemistry for neurofilaments. Moreover, reduced CaBP immunoreactivity was observed even in some remaining Purkinje cells of SCD suggesting that loss of CaBP precedes neuronal loss of Purkinje cell. We conclude that CaBP is a useful marker for Purkinje cell degeneration, and that reduced CaBP expression might have some association with the mechanism of the Purkinje cell degeneration in SCD.

Aged↗
PubMed1995

Malignant hyperthermia in a patient with Becker muscular dystrophy: dystrophin analysis and caffeine contracture study.

We present a 17-year-old boy with Becker muscular dystrophy (BMD) who developed hyperthermia and heart failure after general anesthesia. He presented clinical features of malignant hyperthermia (MH), and had masseter spasm and elevated body temperature (38.7 degrees C) with very high serum CK activity (107,000 IUl-1). Dystrophin tests confirmed a clinical diagnosis of BMD in the patient, i.e. faint and patchy immunostaining pattern of skeletal muscle, truncated dystrophin protein and a deletion of exons 3 and 4 of the dystrophin gene. To inquire into the mechanism of MH associated in the patient, we tested caffeine contracture reaction by the skinned fiber method. We found an increased sensitivity to caffeine only in type 1 muscle fibers. The rate of Ca(2+)-induced Ca2+ release (CICR) was normal, suggesting that the mechanism of "MH" observed in our patient with BMD is not the same as that of classical MH. A possible mechanism might be related to derangements of the sarcoplasmic reticulum membrane in BMD, which sensitize the membrane to caffeine or other agents.

Adolescent↗
PubMed1995

Single photon emission computed tomography using N-isopropyl-p-[123I]iodoamphetamine in spinocerebellar degeneration.

We investigated the clinical usefulness of N-isopropyl-p-[123I]iodoamphetamine single photon emission computed tomography (SPECT) for diagnosis of spinocerebellar degeneration. The uptake in the cerebellar hemispheres and vermis was decreased in sporadic cerebelloolivary atrophy (Holmes, n = 9) and sporadic olivopontocerebellar atrophy (OPCA, n = 6). The uptake in the pons was decreased in OPCA. The decrease of the uptake in the cerebellum and the pons was associated with clinical severity in OPCA. Our results show that semiquantitative SPECT analysis differentiates between the Holmes type and OPCA.

Adult↗
PubMed1995

Cortical auditory disorder caused by bilateral temporal infarctions.

We present a 55-year-old man who suddenly became afflicted with a bilateral auditory disturbance. Auditory acuity was preserved relatively well. Brainstem auditory evoked potentials (BAEPs) were normal. Middle latency auditory evoked potentials (MLAEPs) revealed the total absence of all waves. Brain computed tomography (CT) showed infarctions of the temporal lobes bilaterally, involving the superior temporal and transverse temporal gyri. The recognition of verbal and nonverbal sounds was also impaired. Brain CT, MLAEPs and auditory recognition tests were useful in diagnosing the cortical auditory disorder.

Auditory Diseases, Central↗
PubMed1995

Hypertrophic cranial pachymeningitis with spinal epidural granulomatous lesion.

A 67-year-old woman with a one-year history of tinnitus and headache had multiple cranial nerve palsies of V, VII, VIII, IX, X, XI and spastic paraparesis. She also had a secretory otitis media. Gd-DTPA-enhanced magnetic resonance imaging (MRI) revealed hypertrophy of the dura of the posterior fossa and spinal epidural mass which extended from C7 to T10. A biopsy of the epidural mass showed chronic granulomatous change. These lesions were completely cured with administration of antibiotics. We believe this case of double-lesion of hypertrophic cranial pachymeningitis and spinal epidural granulomatous lesion originated from a bacterial infection secondary to the secretory otitis media.

Aged↗