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Biomedical subjects

M Sakuta

Publications and source records attributed to M Sakuta.

At least 37 records · Page 2Linked to original sources
PubMed1994

[Gastric acid secretion and absorption of levodopa in patients with Parkinson's disease--the effect of supplement therapy to gastric acid].

Since an oral regimen of levodopa has been instituted for treatment of Parkinson's disease, its absorption and metabolism has been well demonstrated. However, its chemical characteristics of high solubility in acid solution and low solubility in water have not been well known. We paid attention to this characteristic and studied the relationship between its absorption and gastric acid secretion in 38 patients with Parkinson's disease who became refractory to therapy of levodopa. We measured the pH and amount of collected fasting gastric juice. Gastric acid secretion was decreased in 22 patients (58%). In ten of these 22 patients, 30 ml of lemon juice was prescribed in every administration of levodopa as a supplement to gastric acid for two weeks. Increases of L-dopa concentration after 60 min. and 180 min. were observed after lemon juice supplement therapy. Among the Parkinson symptoms, rigidity, akinesia, and small step gait were improved in every case except one patient who showed decrease of L-dopa concentration at 180 minutes. However, improvement of tremor was less remarkable. We consider this supplement therapy to gastric acid is one of the effective and useful methods in the management of Parkinson's disease.

Aged↗
PubMed1993

Giant somatosensory evoked magnetic field in patients with myoclonus epilepsy.

We investigated somatosensory evoked magnetic fields (SEFs) and somatosensory evoked potentials (SEPs) in patients with myoclonus epilepsy. The median nerve was stimulated at the wrist, and responses were recorded over the contralateral hemisphere. The source of the enlarged cortical component of the giant SEF was localized on the post-central sensory cortex. The P1 component of the giant cortical response was composed mainly of a tangentially oriented dipole at area 3b. This is the first magnetoencephalographic analysis of an abnormally enlarged somatosensory cortical response.

Aged↗
PubMed1993

Pure progressive autonomic failure: a clinicopathological study.

Two cases of pure progressive autonomic failure (PAF) are presented. A postmortem study of one case (case 2) showed a pathology resembling that of Parkinson's disease. Marked cell loss was noted in the substantia nigra, nucleus ceruleus, and intermediolateral column of the spinal cord, while cell loss in the sympathetic ganglion was not remarkable. This case may be an exceptionally rare case of late-onset PAF in which autonomic failure was mainly ascribed to preganglionic (and central) pathology, although autonomic function tests suggested postganglionic sympathetic disorder in both cases.

Aged↗
PubMed1993

Portal-systemic encephalopathy and hypothalamic hypothyroidism: effect of thyroid hormone on ammonia metabolism.

We describe a 53-year-old woman with portal-systemic encephalopathy and altered thyroid function. Endocrinological studies revealed low levels of free thyroid hormone with an inappropriately low level of thyroid-stimulating hormone that responded to bolus injection of thyrotropin-releasing hormone with a normal but somewhat delayed pattern. On the diagnosis of hypothalamic hypothyroidism, she was treated with levothyroxine sodium. Thyroid hormone replacement improved not only the symptoms of hypothyroidism but the hyperammonemia and consciousness disturbance, which suggested a hitherto undescribed possibility that hypothyroidism may be an exacerbation factor of hyperammonemia and portal-systemic encephalopathy.

Ammonia↗
PubMed1993

[A case of coccidioidomycosis with central nervous system involvement].

We report a 44-year-old Japanese man with chronic meningitis due to coccidoiodomycosis. He was admitted to our hospital because of pneumonia after the business trip to Phoenix, Arizona. Coccidioid immitis was cultured from periathric abscess on the sternoclavicular joint. He became asymptomatic by 5-FC administration. One year later, however, he complained of headache and fever. Coccidiodial meningitis was diagnosed by cerebrospinal fluid (CSF) examination. Both systemic and intrathecal administration of miconazole and oral itraconazole were ineffective. While meningitis was not cured for three years, normal pressure hydrocephalus (NPH) developed. CSF cell count fell into normal range after administration of fluconazole (800 mg/day) for thirteen months, but NPH continued. This is the first report of coccidiodimycosis with CNS involvement in Japan.

Adult↗
PubMed1993

[Propriospinal myoclonus--a case report].

Propriospinal myoclonus is one type of myoclonus that is proposed to originate in the spinal cord and spread up and down via propriospinal tract. There are a few reports describing the detailed electrophysiological findings of this myoclonus. In this communication, we present the results of electrophysiological analysis of a patient with propriospinal myoclonus. A 23-year-old woman suddenly noticed abdominal pain, which spontaneously faded in a few hours. Irregular involuntary flexion jerks of the trunk appeared spontaneously without pain or hiccups after this episode. It involved the bilateral axial muscles; sternocleidomastoid muscles (SCM), paravertebral muscles (PVM), abdominal muscles (ABD), and intercostal muscles (ICM), but not the limb muscles. It was worsened by the mental stress, but not by her posture or position. While she slept, the jerks were not observed. Routine laboratory examinations were all normal. Magnetic resonance imaging of the spinal cord revealed no abnormalities. The electrophysiological studies done on this patient are polymyography, back-averaging of the EEG activity preceding spontaneous jerks (jerk-locked averaging (JLA), and movement related cerebral potential (MRCP) preceding the involuntary jerks and voluntary abdominal movements. No EEG activities preceding the myoclonus were demonstrated by JLA or MRCP. No MRCP recorded preceding the myoclonus suggests that the jerk is not a self-initiated or externally triggered voluntary movement. Polymyography revealed that the jerks involved the bilateral axial muscles including SCM, PVM, ICM, and ABD, but not the limb muscles. Homologous muscles were activated synchronously. The duration of EMG bursts was variable ranging 50 to 250 ms in these muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[FDG-PET in an amnestic and hypersomnic patient with bilateral paramedian thalamic infarction].

A 67-year-old patient was admitted to our hospital owing to coma and tetraplegia. MRI showed T2 weighed high intensity areas in the pontine tegmentum, lower aspect of the right cerebellar hemisphere, left half of medulla oblongata, and bilateral paramedian thalamus. He showed marked recovery by urokinase injection becoming able to walk in a few months, but severe amnesia and hypersomnia persisted even 5 months after onset. EEG showed diffuse alpha activity with occasional delta waves in frontal leads. Intelligence was considered normal (WAIS score; verbal IQ 97, performance IQ 102, total IQ 99), through performance on Wechsler memory Scale-R (Revised Japanese edition, WMS-R) and Benton Visual Retention Test indicated impairment of both verbal and visual memory. Verbal memory was impaired to a greater degree than visual memory (Scores of WMS-R: verbal memory index 60, visual memory index 98, index of general memory 72, attention index 95, index of delayed memory 71). He was able to finish only 0 and 1 categories on two trials of the Wisconsin Card Sorting Test. FDG (18F-fluorodeoxyglucose)-PET showed diffuse areas of decreased metabolism in bilateral thalami, frontal lobes, cingulate gyri and medial temporal lobes. The bilateral thalamic lesion seemed to affect the following structures, as judged from MRI: 1) The anterior thalamic peduncle including most of the reciprocal connections between dorsomedial nucleus of thalamus (MD nucleus) and the frontal lobe, 2) The inferior thalamic peduncle which serves as the reciprocal pathway between MD nucleus and medial temporal lobe, especially the amygdala (component of Yakovlev circuit), and 3) The inferior part of mammillothalamic tract (component of Papez circuit).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[A case of fibromuscular dysplasia presenting with Wallenberg syndrome, and developing a giant aneurysm of the internal carotid artery in the cavernous sinus].

A 25-year-old man developed Wallenberg syndrome (WS). At that time his carotid angiography was normal. When he was 28 years old, he suffered from retinal artery embolism in the left eye. At the age of 30 years, he had an acute onset of abducens nerve palsy in his right eye. The carotid angiography showed a giant aneurysm at the cavernous sinus portion in the right internal carotid artery. At his age of 38, the right oculomotor, trochlear and trigeminal nerves were involved. A vertebral angiography revealed a bead-like formation, and a diagnosis of fibromuscular dysplasia (FMD) was made. An intensive angiographic examination revealed many stenotic or dilated lesions in the carotid, vertebral, coronary, renal, and hepatic arteries. A sural nerve biopsy specimen revealed that the sural vein was involved. In Japan only one case of FMD presenting with WS is known. FMD should be under consideration as an underlying disease, when WS occurred in younger patients with few risk factors. In this patient an angiography revealed no abnormality in the cavernous sinus portion of the internal carotid artery, when he suffered from WS. However, eight years later he was proved to have a giant aneurysm in the cavernous sinus portion. In conclusion, we support the hypothesis that aneurysm may originate from angiographically normal arterial wall in FMD.

Adult↗
PubMed1992

[Naming difficulties seen in a case of alexia with agraphia caused by a left postero-inferior temporal lesion].

A 71-year-old right-handed man presented writing and reading difficulties as well as naming difficulties. Neuropsychological examinations revealed mild fluent type aphasia accompanied by alexia and agraphia predominantly affecting kanji and also severe naming difficulties. Brain MRI showed cerebral subcortical hemorrhage extending from the anterior one-third of the left temporal lobe to the temporo-occipital junction involving the fusiform gyrus. The analysis of the several reported cases with severe alexia with agraphia for kanji including ours revealed a close correlation between the severity of kanji writing disturbances and that of naming difficulties. It was also shown that cases with severe naming difficulties had lesion extending anteriorly to the anterior middle temporal gyrus or medially to the parahippocampal gyrus, suggesting that the disconnection between the parahippocampal gyrus and other cortices including the temporal lobe was essential for production of naming difficulties.

Aged↗
PubMed1992

[The effect of anticholinergic drugs on 123I-IMP SPECT in Parkinson's disease].

Several reports have suggested that anticholinergics have some associations with mental deterioration in Parkinson's disease (PD). We investigated the effect of anticholinergics on regional cerebral uptake of tracer in PD patients using N-isopropyl p-[I-123] iodoamphetamine SPECT. Sixteen pairs of region of interest (ROI) were located in the cortex, a pair in the basal ganglia, thalamus, and cerebellum. The size of each ROI was about 16 mm x 16 mm. Regional cerebral uptake ratio (rCUR) was calculated by the next equation: rCUR = (total count in an ORI)/(mean of total count in the cerebellar ROIs). The comparison consisted of two parts; (1) 7 PD patients (age 59-76 (65.4 +/- 6.7 mean +/- S.D.)) who had been on chronic anticholinergic therapy underwent SPECT and Wechsler Adult Intelligence Scale (WAIS) twice, for the first time when they were on anticholinergics and second a month after discontinuation of anticholinergics. All but two patients performed significantly better on WAIS after discontinuation than when they were on anticholinergics. The improvement was about 10 points in total IQ. (2) 11 PD patients (age 52-79 (64.5 +/- 8.6 mean +/- S.D.)) on chronic anticholinergic therapy including all but two patients mentioned above (group A) and 25 PD patients (age 52-88 (66.7 +/- 9.8 mean +/- S.D.)) not receiving anticholinergics (group B) also underwent SEPCT. In the comparison (1), at all but two ROIs was the mean rCUR higher after discontinuation than when they were on anticholinergics and the difference was significant at 10 ROIs out of 32 ROIs in the cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[A case of topographical disturbance following a left medial parieto-occipital lobe infarction].

A 59-year-old man was admitted to our hospital for his sudden-onset right hemianopsia. Thirty days after the onset, neuropsychological examination revealed obvious topographical disorientation and mild optic ataxia. Magnetic resonance imaging showed abnormal intensity area at the left medial parietooccipital region and left splenium of the corpus callosum. Although single photon emission CT showed uptake decrement in the left hemisphere, almost normal uptake was observed in the right hemisphere. He could recognize landmarks, but fail to recognize the relative position of landmarks. Therefore, his topographical disorientation was considered to be due to perceptual disturbance, memory disturbance of relative position of landmarks, or both. He was right-handed with no sinistral relative, and showed dyslexia and dysgraphia early in his clinical course. The laterality index of the dichotic listening test revealed the right ear dominance. These results indicated that his left hemisphere was language dominant. His topographical disorientation could be caused by the medial parieto-occipital lesion in the dominant hemisphere.

Cerebral Infarction↗
PubMed1992

[The role of interleukin-6 in Crow-Fukase syndrome].

We measured serum interleukin-6 (IL-6) levels in 14 patients with Crow-Fukase syndrome. Five out of 14 patients with Crow-Fukase syndrome showed high serum IL-6 levels above 10 pg/ml, which was statistically significant in comparison with control subjects with other neurological diseases. Serial studies of serum IL-6 levels in two patients revealed the increase before the exacerbation of clinical symptoms of edema, and pleural or cardiac effusion, and the fall after the treatment by high dose pulsed methylprednisolone. We suggest that serum IL-6 level appears to be a useful marker to predict its exacerbation. Also we performed immunohistochemical study on cutaneous angioma from three Crow-Fukase syndrome patients using anti-IL-6 antibody. The cytoplasm of endothelial cells of cutaneous angioma from two patients was positively stained, which might imply the abnormality of endothelial cells in Crow-Fukase syndrome.

Endothelium, Vascular↗
PubMed1992

[A case of progressive hemiatrophy with type 2 muscle atrophy in muscle biopsy].

We reported a case of progressive hemiatrophy, whose skeletal muscle biopsy revealed type 2 fiber atrophy. This patient, a 40-year-old woman, noticed left leg atrophy at the age of 39. She had a history of minor trauma of the left thigh at the age of 30. On admission, physical examination revealed atrophy of various parts of her left side of body, predominantly in the left leg. There was no dermatological or neurological abnormalities except these atrophies. Hematological and biochemical examinations were normal. EEG, EMG, nerve conduction studies and autonomic function tests were normal in either side of the body. MRI study showed reduced muscle bulk as well as subcutaneous fatty tissue especially in her left leg. Skeletal muscle biopsy of her left quadriceps femoris muscle revealed type 2 fiber atrophy and type 1 fiber predominance. However, no abnormality was found in the intramuscular nerves. We considered that type 2 muscle fiber atrophy was one of the cause of atrophy of this case.

Adult↗
PubMed1992

[Gerstmann-Sträussler-Scheinker disease with heterozygous codon change at prion protein codon 129].

A 53-year-old male was admitted to our hospital for progressive dementia and gait disturbance which had started at the age of 48. Examination indicated dementia, dysarthria, dysphagia, bilateral pyramidal signs, apraxia of the limbs, and extrapyramidal signs such as fine finger tremors, and rigidity of limbs. There were no cerebellar signs or myoclonus. His mother and elder brother showed similar symptoms and died at the ages of 53 and 50, respectively. EEG was normal. CT and MRI showed mild brain atrophy, but no cerebellar atrophy. T2 weighted image indicated low intensity areas covering bilateral caudate nuclei and putamina. A heterozygous amino acid change from methionine to valine was noted at codon 129 of the prion protein of the patient as well as in one of his son. The most likely diagnosis was Gerstmann-Sträussler-Scheinker (GSS) disease without cerebellar atrophy. GSS may include a broad spectrum of brain pathology. Whether the codon change is associated with pathology without cerebellar atrophy is a problem that awaits further investigation.

Atrophy↗
PubMed1992

[A case of portal-systemic encephalopathy presenting characteristic MR images in globus pallidus, hypothalamus, corpus callosum, pontine base, and middle cerebellar peduncle].

A 53-year-old woman developed symptoms of slow speech, mild dementia, increased deep tendon reflex, ataxic gait, flapping tremor, and dystonic posture during two years. She had liver cirrhosis and hyperammonemia, which suggested a diagnosis of portal-systemic encephalopathy. MR T1-weighted images showed increased signal intensity in globus pallidus, internal capsule, substantia innominata, and a part of hypothalamus. T2-weighted images revealed abnormal findings as follows: high intense area in middle cerebellar peduncle, and low signal intensity of corpus callosum and pontine base. This is the first report about MRI abnormalities in substantia innominata, corpus callosum, and pontine base in a patient with portal-systemic encephalopathy.

Brain↗
PubMed1992

[XYY syndrome associated with motor neuropathy].

We described a case of XYY syndrome associated with motor neuropathy. The case was a 27-year-old male, who had 47-XYY chromosome karyotype. His symptoms were distal dominant muscle weakness and muscle atrophy in his lower extremities without objective sensory disturbance. He had no mental retardation or family history of neurologic diseases. The electrophysiological and pathological examinations revealed that his symptoms were due to peripheral motor neuropathy (neuronal type). His motor neuropathy may be of sporadic type. There may be some relation in the pathogenesis between XYY syndrome and motor neuropathy, although in the literature, XYY syndrome with motor neuropathy had not been reported so far.

Adult↗