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Biomedical subjects

H Imai

Publications and source records attributed to H Imai.

At least 271 records · Page 15Linked to original sources
PubMed1995

Diagnosis and treatment of brainstem abscess using magnetic resonance imaging and microsurgical aspiration--case report.

A 6-year-old boy presented with a pontine abscess initially misdiagnosed as brainstem glioma, but he deteriorated rapidly and developed new symptoms of respiratory distress. Magnetic resonance (MR) imaging revealed a rapidly growing mass lesion in the pons. Microsurgical evacuation of the abscess via a suboccipital retromastoid approach resulted in neurological improvement and resolution of the lesion on MR images. Brainstem abscess can be successfully treated with early, accurate diagnosis based on MR imaging and appropriate microsurgical and antibiotic management.

Brain Abscess↗
PubMed1995

Selenium levels and glutathione peroxidase activities in blood in an andean high-altitude population.

Selenium (Se) levels in blood (whole blood, erythrocytes and serum) and blood glutathione peroxidase (GSH-Px) activity were investigated in people living at high altitude in Bolivia (4,000 m above sea level). These parameters were compared to those of people living at low altitude (300 m above sea level). The Se levels in whole blood of the high-altitude subjects did not differ significantly from those of the low-altitude subjects. However, the Se levels in erythrocytes were significantly lower in the high-altitude subjects than in the low-altitude subjects, whereas serum Se levels were higher in the high-altitude subjects than in the low-altitude subjects. GSH-Px activity (Unit/g Hb) was significantly lower in the high-altitude subjects than in the low-altitude subjects. The mean corpuscular Hb concentration (MCHC), an indicator of the age of erythrocytes, in the high-altitude subjects was significantly higher than in the low-altitude subjects. These results show that the GSH-Px activity in the blood of the high-altitude subjects is relatively low. This may be due to their aged erythrocytes and/or to relatively low Se intake in the high-altitude population compared with low-altitude population.

Adolescent↗
PubMed1995

[Semantic/syntactic priming effects and their processing stages].

Three priming experiments were conducted to investigate associative and syntactic information processing in the Japanese language. Unlike in English, associative relation and syntactic plausibility can be manipulated independently. Subjects were given either a lexical decision or naming task because previous studies suggest that these tasks are sensitive to different processing stages. Two prime-target SOAs. 250 ms and 700 ms, were used. The results revealed that syntactic plausibility of associated prime-target pairs was processed differently from that of unassociated ones. When prime-target pairs were unassociated, syntactic plausibility priming was found with the 700 ms SOA in the lexical decision task, but no priming was found in the naming task. This result supports the previous claim that syntactic information is processed post-lexically. In contrast, when prime-target pairs were associated, syntactic plausibility priming was found both with 250 ms and 700 ms SOAs not only in the lexical decision but in the naming task. This suggests that syntactic plausibility of associated prime-target pairs is processed at the lexical rather than post-lexical stage.

Adult↗
PubMed1995

[Endovascular treatment of cerebral vasospasm with intra-arterial papaverine infusion].

Thirty-one cases of cerebral vasospasm following subarachnoid hemorrhage were treated with intraarterial papaverine infusion. Symptomatic cases were nineteen, and asymptomatic cases were twelve. Papaverine (120 mg/saline 50 ml, 30 min) was injected superselectively to vasospastic vessels through a microcatheter. The rate of symptomatically improved cases was 63% initially, but about two thirds of those cases had recurrence within a day. The 63% of symptomatic cases showed infarction in spite of papaverine infusion. Three cases of recurrent vasospasm after intra-arterial papaverine underwent PTA and showed good dilatation of vasospastic vessels. The complications of our intra-arterial papaverine were hypotension in two cases, convulsion in one case and transient disturbed consciousness in one case. We experienced no fatal complications. Overall outcome was ADL1 (19%), ADL2 (25%), ADL3 (44%), ADL4 (0%), ADL5 (6%), and death (6%). Since the effect of intra-arterial papaverine infusion is of short duration and weak, combination of PTA and papaverine may be necessary. It is recommended to use papaverine for vasospasm in distal arteries such as M2, A1, A2, and to carry out PTA for proximal arteries such as ICA and M1.

Adult↗
PubMed1995

Streptococcal pneumoniae polysaccharide increases IgA-class antibody activity under the immunological memory of a protein antigen: two signals on experimental IgA nephropathy.

We designed the following experiment in order to clarify the factors that induce a hyper-immune state of IgA. Six-week-old Balb/c mice were immunized with bovine gammaglobulin (BGG) at 0 and 2 weeks, followed by the administration of phosphorylcholine-BGG (PC-BGG) at 3 and 5 weeks to obtain an immunological memory. At 6 weeks, we divided the mice into three groups: one was a saline group used as a control, another was a PC-BGG group used to investigate T-cell dependent antigen, and the last was a streptococcal pneumoniae polysaccharide (R36A) group used to investigate T-cell independent antigen. We compared the antibody activity in response to BGG, and glomerular immune deposition among the groups. In the control group, antibody activities did not change, and all stainings on glomerular immune deposits were negative. In the PC-BGG group, IgG-class antibody activity was significantly suppressed (p < 0.05), but IgA- and IgM-class antibodies were not affected. The intensity of glomerular deposition of IgM was level one positivity (TFS: 116.7 +/- 20.2 (mean +/- SD)). In the R36A group, polysaccharide produced significant increases (almost four times) in IgA-class and IgM-class antibody activity under the condition of immunological memory (IgA: p < 0.05, IgM: p < 0.005). The intensity of IgA was between weak and level one positivity (TFS: 60.8 +/- 6.3), but the intensity of IgM was weak positive (TFS: 36.7 +/- 10.4). This became a predominant glomerular deposition of IgA in the R36A group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

IgA nephropathy associated with hyper IgAnemia, psoriasis or pustulosis and ossification.

This is a report on two cases of IgA nephropathy associated with psoriasis vulgaris, having hyper IgAnemia (above 500 mg/dl) and ossification. Case 1 is a 47-year-old woman with a 7-year history of psoriasis vulgaris, and case 2 is a 57-year-old man with a 17-year history of this disease. IgA was 526 and 1,356 mg/dl, respectively. HLA analysis showed A2, A26 (10), Bw62 (15), Bw46, Cw3, DRw12 (5), and DRw8 in the former, and A2, A11, B13, Bw46, Cw11, DR4, and DRw8 in the latter. Renal biopsy specimens disclosed mild mesangial proliferative glomerulonephritis and moderate mesangial proliferative glomerulonephritis with predominant IgA deposition in mesangial area, respectively. A bone-scintigraphy revealed a high uptake of radioisotopes in the left shoulder, the vertebra, the sacroiliac joint, both sides of the knees and ankles, and the sterno-cost-clavicular area. An X-ray study showed ossification of the posterior longitudinal ligament (OPLL) in the former, and ankylosing spinal hyperostosis (ASH) in the latter. A review of the literature discloses three other case reports of hyper IgAnemia, IgA nephropathy, psoriasis or pustulosis, and ossification. The alertness of dermatologists, orthopedic surgeons, rheumatologists, and general practitioners will be required to attain to a more frequent diagnosis of the above combination.

Female↗
PubMed1995

[A 51-year-old man with early onset parkinsonism].

We report of 51-year-old man with early onset parkinsonism. The patient was well until 38 years of age, when he noted a difficulty in the use of his right leg; this difficulty improved after he received a medicine from his physician. He did not take medicine regularly, and he noted difficulty in standing up from a chair and in rolling over at age 40. Tremor was not a feature, but he noted slowness in his movements at age 42; at age 49, he noted diurnal fluctuation in his symptoms and at times he experienced hallucination. He was admitted to our hospital in September of 1992 for the first time when he was 50-year-old. At that time, neurologic examination revealed an alert and somewhat bradyphrenic man; Hasegawa dementia rating scale was 20/30. Cranial nerves were intact except for masked face and small voice. He showed stooped posture and small step gait cogwheel rigidity was noted in the four limbs more on the left; tremor was absent. Deep reflexes were within normal range and the sensation was intact. As he showed diurnal fluctuation in his symptoms, his medication was switched to levodopa 3,000 mg/day without a peripheral decarboxylase inhibitor. He was discharged for out patient follow up. But he did not take drugs regularly, and his neurologic condition deteriorated; he was admitted to another hospital. Neurologic examination at that time was essentially similar to that of his first admission to our hospital, except that he showed more severe rigidity and akinesia; again tremor was not detected. His cranial CT scan showed a mild ventricular dilatation without cortical or brain stem atrophy. During his hospital stay, he developed episodes of oculogyric crisis during peak dose of levodopa, and orthostatic hypotension. He developed pneumonia and expired on October 28, 1993. He was discussed in a neurological CPC, and the chief discussion arrived at the conclusion that the patient had early onset Parkinson's disease of Lewy body type. As differential diagnoses, early onset parkinsonism without Lewy body, pure form of diffuse Lewy body disease, pallidoluysian atrophy, and other conditions were considered; however, all of those possibilities were excluded. Early onset parkinsonism without Lewy body would have much earlier onset than this patient, and diffuse Lewy body disease would show more profound dementia 13 years after the onset. Pallidoluysian atrophy would be complicated with some dystonic features. Post-mortem examination showed marked discoloration and degeneration of the substantia nigra. The degeneration was most prominent in the ventrolateral tier of the substantia nigra.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain↗
PubMed1995

[Neurological involvements with transient gait disturbance in subacute phase of Kawasaki disease; a case report].

A 1-year-and-9-months old boy with gait disturbance during the 3rd week of Kawasaki disease (KD) was described. He had been previously healthy, and developed high fever and rash. The diagnosis of KD was based on 5 of 6 major criteria on the 3rd clinical day. He was initially treated with intravenous gamma-globulin 400 mg/kg/day for five days. On the 17th clinical day, the patient developed gait disturbance after most clinical signs disappeared. His gait was wide- based and unstable. Generalized hypotonia with poor traction response was also seen. Pyramidal tract signs including exaggerated patellar and Achilles tendon reflexes and positive bilateral Mendel-Bechterew reflex were presented. Cerebrospinal fluid was normal. Brain CT, MRI, and 123I-IMP SPECT images were normal without broad hemorrhage or infarction of the cerebral parenchyma. Gait disturbance recovered spontaneously within one month without any sequelae.

Central Nervous System Diseases↗
PubMed1995

[A 57-year-old woman with gait disturbance, headache, character change, convulsion, and coma].

We report a 57-year-old woman with progressive gait disturbance, headache, character change, convulsion and coma. She was well until 55 years of age, when she noted an onset of unsteady gait. At times she experienced transient weakness in her right hand, which was followed some difficulty in articulation. She was admitted to our service for the work up on April 6, 1992. Neurologic examination at that time revealed an alert Japanese lady in no acute distress. She was oriented to all spheres, however, she was somewhat bradyphrenic and had some disturbance in recent memory. Higher cerebral functions appeared intact. The visual acuity and visual fields were normal as were the optic fundi. Pupils were round and isocoric reacting promptly to light. Ocular movement was full, however, horizontal nystagmus was noted upon right lateral gaze. The sensation of the face was intact. She showed right facial paresis of the central type. Hearing was intact. She showed slurred speech and some difficulty in swallowing. The tongue was deviated to the right. Her gait was wide based and unsteady; tandem gait was difficult, however, walking on toes and on heels were performed well. No cerebellar ataxia was noted, but she showed some clumsiness in her right hand. Deep reflexes were symmetric and normally reactive; plantar response was extensor bilaterally. Sensation was intact; no meningeal sign was elicited. Routine laboratory work up was unremarkable; the CSF was under a borderline pressure (180 mmH2O) and contained 39 mg/dl of protein and 59 mg/dl of sugar. Cranial CT scan revealed diffuse low density areas involving bilateral cerebral white matter as well as the brain stem; MRI revealed high signal intensity lesions in those areas; gadolinium enhancement was negative; cortical sulci were effaced and the anterior part of the left lateral ventricle was compressed without deviation of the midline structure. The patient was treated with steroid pulse therapy without effect. She was discharged for out patient follow up, however, she developed a convulsion which was followed by loss of consciousness, and was admitted again to our service. She had never gained consciousness after this episode, and remained in the state of akinetic mutism. Follow-up CT and MRI did not show much change, although the area of high signal density lesions slightly enlarged on June 1, 1993. Her clinical course was complicated by drug induced bone marrow suppression and nephrotic syndrome. She expired on September 8, 1993 after developing sudden drop of blood pressure and bradycardia.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain Neoplasms↗
PubMed1995

[Bone mineral quantifying of methods in hyperparathyroidism].

Bone mineral densities (BMDs) in both cortical and trabecular bone decrease in primary hyperparathyroidism (PHP) and renal hyperparathyroidism (RHP). Bone mineral parameters in the second metacarpal bone were studied by digital image processing method (DIP). Lumbar BMD (L-BMD) and mid-radial BMD (R-BMD) were measured by dual energy X-ray absorptiometry (DXA). All indexes of bone mass at all measured sites in both PHP and RHP were significantly lower than normal those in controls. The decrease in appendicular BMD was more remarkable than that in LBMD. After parathyroidectomy (PTX), all indexes of bone mass with the exception of the MCI increase especially, in L-BMD. This discrepancy in dicates that PTH affects cortical bone and trabecular bone in dependently. Mild and moderate oversecretion of PTH has an anabolic effect, while a high of PTH has a catabolic effect on trabecular bone. The quantification of bone minerals is useful in follow-up studies and evaluation of the therapeutical response in hyperparathyroidism.

Absorptiometry, Photon↗
PubMed1995

[Amnestic syndrome after right temporo-occipital subcortical hemorrhage].

A case of right temporo-occipital subcortical hemorrhage with amnestic syndrome was reported. A 65-year-old woman presented with visual disturbance and headache. CT and MRI demonstrated a hemorrhagic lesion in the right occipital lobe involving parahippocampal gyrus. Neurological examination on admission revealed left homonymous hemianopsia and anterograde and retrograde amnesia. Neuropsychological examination revealed marked recent memory disturbance, but she had visual retention and verbal retention, and her value in WAIS (Wechsler Adult Intelligence Scale) was normal. After 40 days, she was discharged without improvement of amnesia. These findings suggest that the cortico-medial temporal lobe pathway was disturbed by subcortical hemorrhage, and we think there are connective fibers between visual and verbal memory systems. This is the first report of hippocampal amnesia following temporo-occipital subcortical hemorrhage.

Aged↗
PubMed1995

[A 65-year-old woman with dysarthria, dysphagia, weakness, and gait disturbance].

We report a 65-year-old woman with progressive dysarthria, dysphagia, weakness, and gait disturbance. The patient was well until 59 years of age (January of 1986) when she noted bilateral ptosis. One year later, she noted a gradual onset of difficulty in speech (articulation). Her speech slowly deteriorated and she noted weakness in chewing power and difficulty in swallowing in addition. In October 1987, she developed emotional incontinence. In January of 1988, she started to drag her left foot. She was admitted to our hospital on June 13 of 1988. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed no dementia; her higher cerebral functions appeared intact. Ptosis was present bilaterally more on the right. She showed difficulty in opening her eyes on command; no contraction of the frontal muscles was seen upon attempted eye opening. There was a moderate limitation in the vertical gaze. Forced laughing and crying were seen. Facial muscles were moderately weak without apparent atrophy. The movement of the soft palate was very weak, and swallowing disturbance was more prominent for liquid staff. The tongue appeared somewhat small, however, no fasciculation was noted. Her step was small and the posture was stooped. Retropulsion was present, however, Romberg's sign was absent. No muscle atrophy was apparent, however, diffuse mile to moderate muscle weakness was noted in all four limbs. Cerebellar sign was absent. Deep tendon reflexes were exaggerated bilaterally, and Babinski sign was present on the left side. Sensation was intact. Routine blood tests were unremarkable as was a cranial CT scan. Her ptosis did not improve after 10 mg of edrophonium injection. CSF was also normal. She was transferred to another hospital but her neurological disabilities further progressed. In 1989, she was totally unable to move her limbs; she could only move her eyes; still consciousness was clear without dementia. She developed respiratory difficulty and expired on July 25, 1992. She was discussed in a neurological CPC, and the opinions were divided into ALS and primary lateral sclerosis (PLS). The chief discussant arrived at the conclusion that the patient might have had the pyramidal form of ALS. Postmorten examination revealed marked myelin pallor in the anterior as well as lateral corticospinal tracts. Pyramidal tract degeneration was prominent starting at the level of the cerebral peduncle and was continued to be seen until the level of lumbar cord. The number of anterior horn cells showed only slight decrease in the cervical level, however, it was normal in the lumbar cord.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1995

[A 21-year-old man with distal dominant progressive muscle atrophy].

We report a 21-year-old man with distal dominant progressive muscle atrophy. The patient was apparently well until 17 years of age when he noted a decrease in exercise tolerance. One year later, he noted difficulty in arising his heels when the walked. He was admitted to our service for the work up in June 10, 1992. On admission, the patient was rather slender in the body build up; otherwise general physical examination was unremarkable. Upon neurologic examination, mental status and higher cerebral functions were normal. In the cranial nerves, the sternocleidomastoid muscles were atrophic bilaterally; other cranial nerves appeared intact. His gait was unstable and he showed steppage gait; walking on toes and heels were impossible. Distal dominant muscle atrophy was noted in both upper and lower extremities. Muscle strength in the deltoid, biceps brachii and triceps brachii was normal. In the lower extremities, both tibialis anterior and triceps surae muscles were weak (3/5). The iliopsoas and quadriceps femoris muscles were normal, however, the adductor muscles of the thigh showed marked weakness (2/5). Myotonia was absent. Deep reflexes were decreased; sensation was intact. Routine blood tests were unremarkable; CK was 96 IU/l, lactate 6.9 mg/dl, and pyruvate 0.61 mg/dl. After an ischemic forearm exercise test, blood lactate level rose to 22.5mg/dl (base line 11.2), and blood ammonia to 88.3 micrograms/dl (base line 71.2). EMG showed myogenic changes and myotonic discharges. A diagnostic biopsy was performed. The patient was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had type III glycogen storage disease. The differential diagnosis included rimmed vacuole type myopathy, Miyoshi type distal muscular dystrophy, Welander type muscular dystrophy, adult type acid-maltase deficiency, and lysosomal glycogen storage disease with normal acid maltase. However, characteristic clinical presentation of initial weakness in the triceps surae muscle associated with atrophy of the sternocleidomastoid muscle confirmed best of the clinical characteristics of type III glycogen storage disease; the only finding which did not fit with its diagnosis was elevation of the blood lactate level after the ischemic exercise test. The muscle biopsy specimen showed marked vacuole formation; approximately 20 to 30% of the vacuoles were rimmed vacuoles, however, the majority was not rimmed. PAS staining on an epon-embedded specimen revealed marked accumulation of PAS-positive materials in those vacuoles as well as in the interfascular space. The non-rimmed vacuoles were not positively stained in the acid-phosphatase staining, which exclude the diagnosis of acid maltase deficiency. No mitochondrial abnormalities were found.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

Gamma-heavy chain deposition disease showing nodular glomerulosclerosis.

We describe a 35-year-old woman who had nodular glomerulosclerosis associated with deposition of fragmented gamma (gamma 1)-heavy chains. She presented with edema of lower legs, mild proteinuria, and hematuria. Laboratory examination revealed hypocomplementemia, and a small amount of monoclonal IgG-lambda (lambda) in the blood. Renal biopsy disclosed prominent nodular expansion of the mesangium. Ultrastructurally, the nodules were composed of electron dense deposits and fibrillar structures. An immunofluorescent study showed depositions of gamma-heavy chains and C3 in the central portion of nodules and capillary walls, whereas kappa (kappa)-, lambda-light chains, and Fab fragments of the heavy chain were negative. The accumulation of collagen I, IV, V, and VI was demonstrated in the mesangium. Western blot analysis of serum protein disclosed fragmented gamma-heavy chains that did not combine with light chains. Glomerular nodular lesions, thus, can occur in heavy chain deposition disease, as in light chain deposition disease. Fragmented gamma-heavy chains may also induce hypocomplementemia by the activation of the complement pathway.

Adult↗
PubMed1995

[Progressive supranuclear palsy].

Progressive supranuclear palsy (PSP) was a distinct clinicopathological syndrome described by Steele, Richardson and Olszewski in 1964. In 1974, Narabayashi and the present author described a syndrome of levodopa unresponsive pure akinesia or freezing without rigidity or tremor affecting gait, hand writing and speech. In a series of subsequent reports in Japan, evidence has indicated that pure akinesia often represents a pre-oculomotor form of PSP. In this sense, the syndrome of pure akinesia/PSP is proposed. The pathogenesis and etiology of PSP and related conditions remain to be cleared.

Diagnosis, Differential↗