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Biomedical subjects

F Udaka

Publications and source records attributed to F Udaka.

At least 73 records · Page 4Linked to original sources
PubMed1992

Accessory nerve neuroma presenting as recurrent jugular foramen syndrome.

We report a patient with spontaneous recovery and recurrence of a jugular foramen syndrome secondary to an accessory nerve neuroma. He showed sudden onset of unilateral palsy of the ninth, tenth and eleventh cranial nerves in 1982. He recovered almost fully and in 1990 the palsies recurred. MRI revealed a small mass in the right jugular foramen. The tumour was resected via suboccipital craniectomy, and diagnosed as a neuroma of the eleventh cranial nerve.

Accessory Nerve↗
PubMed1992

SPECT findings in Parkinson's disease associated with dementia.

Dementia in Parkinson's disease is thought to be attributable not only to subcortical lesions but also to cortical alterations, especially frontal lobe dysfunction. To evaluate cortical function, the regional cerebral blood flow (rCBF) was estimated of 13 demented and 13 non-demented age matched patients with Parkinson's disease compared with that of 10 age matched controls using I-123 iodoamphetamine single photon emission tomography (IMP-SPECT). The rCBF of the nondemented Parkinson's patients showed no significant differences from that of the control subjects. In the demented patients, the bilateral frontal and parietal and left temporal regional blood flow was significantly less than in the controls. Four demented patients showed isolated frontal hypoperfusion, 8 showed fronto-parietal hypoperfusion, and 1 showed isolated parietal hypoperfusion. Frontal hypoperfusion was therefore present in 12 of the 13 demented patients, and this finding agrees with the frontal lobe dysfunction hypothesis. Parietal rCBF had a significant positive correlation with cortical functions such as calculation and language ability in the MMSE scores. The parietal and temporal reduction in rCBF probably reflects the presence of Alzheimer pathology, cortical Lewy body disease, or both.

Aged↗
PubMed1992

[Autonomic dysfunction of central nervous system disorders].

Central nervous system disorders, such as cerebrovascular or spinal cord lesions often cause dysfunctions of the autonomic nervous system. In most cases of acute cerebrovascular accidents, blood pressure is transiently elevated. Some patients, especially with pontine or thalamic hemorrhage, suffer from extremely high fever. In patients with large lesions in the cerebral hemisphere or lesions in the brainstem, cardiopulmonary state may be affected. In spite of absence of acute myocardial infarction, electrocardiogram may show ST-T changes resembling acute myocardial infarction. Cheyne-Stokes respiration or sleep apnea can occur. Lesions in the medulla oblongata cause dysfunctions of automatic respiration. Patients with large cerebrovascular lesions in the unilateral hemisphere often show transient hyperhidrosis on the contralateral side. Prognosis of patients with these autonomic failures is poor. In patients with spinal shock, blood pressure and heart rate are reduced. In chronic stage, autonomic hyperreflexia, such as attacks of episodic hypertension can occur. Lesions in the high cervical cord often bring nonsymptomatic perforating gastric ulcer.

Autonomic Nervous System Diseases↗
PubMed1991

Cerebellar ataxia with glutamic aciduria.

We report a case of cystinuria and glutamic aciduria, presenting with progressive cerebellar manifestations. She had cerebellar type dysarthria and limb ataxia. Head MRI revealed cerebellar atrophy. Urinary amino acid analysis showed excessive excretion of glutamate and the dibasic amino acids (cystine, arginine, lysine, and ornithine). Cystine and glutamic acid are thought to be transported in a common membrane transport system. Reduction of glutamic acid and cystine in the cerebrospinal fluid was revealed. A relationship between cystinuria and cerebellar manifestation was discussed.

Adult↗
PubMed1991

[A case of persistent proatlantal intersegmental artery with status epilepticus].

A 48-year-old woman with status epilepticus was admitted to our hospital. On admission, she was comatose with horizontal conjugate deviation of eye balls to the left side. Convulsive seizure of Jacksonian type involved initially the left mouth angle and sequentially the left arm and leg, developing into general convulsion. Routine laboratory examinations revealed no significant abnormality. CT scan was normal but carotid angiogram showed a persistent proatlantal intersegmental artery on the left side. Convulsive seizure lasted five days, followed by left hemiparesis. She recovered completely two weeks later. The origin of her illness remained unclear but the causal relationship between neurological symptoms and the persistent primitive artery was presumed.

Arteries↗
PubMed1990

MRI demonstration of cortical laminar necrosis and delayed white matter injury in anoxic encephalopathy.

We performed serial radiological examinations on a patient with anoxic encephalopathy. In the early term after the anoxic insult, T1-weighted MRI revealed high signal intensity areas distributed laminarly in the cerebral cortex and diffusely in the putamen, which were thought to reflect the cortical necrosis and necrosis in the putamen. Single photon emission computed tomography using I-123 isopropylamphetamine showed persistent hypoperfusion in the arterial watershed zones. T2-weighted MRI performed several months after the anoxic episode revealed diffuse high-intensity lesions in the arterial water-shed zones. These delayed-onset white matter lesions continued to extend over several months.

Adult↗
PubMed1990

MR demonstration of a unilateral olivary hypertrophy caused by pontine tegmental hematoma.

Two patients with unilateral olivary hypertrophy (OH) following a pontine tegmental hematoma are presented. Both showed palatal myoclonus and one patient showed an extremity myorhythmia on the opposite side of OH. The magnetic resonance (MR) examination demonstrated an abnormal unilateral hyperintense lesion in the ventral part of medulla oblongata on T2-weighted images. The MR findings were highly suggestive of the pathological nature of the lesion, showing the value of MR.

Cerebral Hemorrhage↗
PubMed1990

A case of anorexia nervosa with acute renal failure resulting from rhabdomyolysis.

Symptoms of acute renal failure were observed in an anorexia patient who had a history of frequent vomiting. The acute renal failure might have resulted from rhabdomyolysis subsequent to a disturbance of electrolyte balance. This acute renal failure might have resulted in death if not treated. We postulate that even a mild case of anorexia nervosa should be carefully observed to prevent such possible tragedy.

Acute Kidney Injury↗
PubMed1990

Magnetic resonance imaging of medial medullary infarction.

Medial medullary infarction is characterized by ipsilateral hypoglossal nerve palsy, contralateral hemiparesis sparing the face, and contralateral disturbance of deep sensation. Although it is possible to make a clinical diagnosis in typical patients, diagnosis is difficult if hypoglossal nerve palsy is absent. We describe a patient with medial medullary infarction without hypoglossal nerve palsy. The patient suffered from left hemiplegia and homolateral disturbance of deep sensation. Magnetic resonance imaging revealed the site of the lesion to be in the medial portion of the upper medulla oblongata. The result of somatosensory evoked potential testing was compatible with disturbance of the medullary medial lemniscus. In a review of the literature, we examined the relation between clinical features and lesion location in 16 patients with medial medullary infarction and compared these to the present patient. Motor paresis was present in every patient, while disturbance of deep sensation was recorded in nine of 13 patients and hypoglossal nerve palsy in six of 14 patients. In atypical patients with medial medullary infarction (such as the present patient), magnetic resonance imaging is necessary to detect the lesion and to make a clinical diagnosis.

Aged↗
PubMed1990

[Medial medullary infarction demonstrated by MRI].

A 67-year-old woman with medial medullary infarction is reported, including clinical manifestations, MRI and angiographical findings, and results of evoked potentials. She suffered from contralateral hemiplegia and disturbance of deep sensation. Motor paresis of the tongue was absent. Magnetic resonance imaging revealed a lesion in the medial portion of the medulla oblongata. The 17 cases previously reported with medial medullary infarction are reviewed. Only 3 cases had triad of medial medullary infarction, contralateral hemiparesis, deep sensory disturbance, and ipsilateral hypoglossal paresis. Therefore, lesion detection is necessary to diagnose medial medullary infarction. Most infarctions limited to the upper third of the medulla were caused by occlusions of vertebral arteries or their branches and prognosis was good. In contrast, infarctions in the lower two thirds were caused by occlusions of anterior spinal arteries and their branches and the prognosis was poor. Thus localization of the lesion using MRI plays an important role to predict the prognosis.

Aged↗
PubMed1990

[A case of chronic progressive radiation myelopathy successfully treated with corticosteroid].

One patient who underwent radiation therapy for laryngeal cancer two years earlier developed chronic progressive radiation myelopathy and exhibited localized swelling of the cervical spinal cord at the C4 level and resultant blocking of the subarachnoid space on myelography and CT myelography. The condition responded markedly to the administration of corticosteroid except for persisting mild spasticity and sensory disturbances. On myelography and CT myelography half a year later, the cervical spinal cord showed no swelling. The corticosteroid therapy is considered to be useful for radiation myelopathy.

Aged↗
PubMed1989

Adult T-cell leukemia initially manifesting as facial diplegia.

We report an unusual case of adult T-cell leukemia (ATL) initially manifesting as facial palsy due to ATL meningitis, which was caused by lymphoid cells in the cerebrospinal fluid (CSF) with a different phenotype from those in the blood. A DNA southern blot analysis of the blood cells confirmed the diagnosis of ATL. The aberrant cells in the CSF contained nuclei with simple indentations and responded well to the initial chemotherapy, while leukemic cells in the blood showed lobulated or convoluted nuclei and were resistant to treatment. Flow cytometry performed before treatment demonstrated that the majority of the cells in the CSF were CD3+CD4+CD8-CD25+, consistent with ATL, whereas they expressed the CD45R antigen, which the blood ATL cells did not. These differences in the subphenotype, cell morphology, and responsiveness to treatment among the ATL cells in blood and CSF suggest that a single clone or subclone with heterogeneous nature was not generated, before the final development of ATL.

Adult↗
PubMed1989

[Study on the concentration of 5-hydroxyindoleacetic acid (5-HIAA) in the lumbar cerebrospinal fluid (CSF) in neurological diseases].

Experimental evidence has shown that the amount of 5-HIAA in the CSF reflects the metabolism of serotonin in the brain if this metabolite is eliminated from the brain and flows into the CSF at a constant rate. We studied the concentration of 5-HIAA in the lumbar CSF in several neurological diseases to elucidate the alteration in abnormalities of serotonin metabolism. The concentration of 5-HIAA in the CSF was measured in 94 patients with cerebral infarction, 30 with vascular dementia, 25 with dementia of the Alzheimer type, 28 with Parkinson's disease and 6 with hypoxic encephalopathy. Patients with cerebral infarction were classified into 24 with a solitary cerebral infarct and 70 with multiple cerebral infarcts. Patients with Parkinson's disease were subdivided into 12 with various psychiatric symptoms including depressive state, hallucination and/or intellectual impairment and 16 without psychiatric symptoms. Patients with hypoxic encephalopathy consisted of 5 with apallic syndrome and one patient with Lance-Adams syndrome. The concentration of 5-HIAA in solitary cerebral infarct, multiple cerebral infarcts and vascular dementia did not exhibit a significant difference from that in control cases (54.6 +/- 23.1 ng/ml). But patients with dementia of the Alzheimer type (34.5 +/- 10.9, p less than 0.001) showed a significantly lower concentration. This fact seems to reflect the pathological finding that the number of large neurons is decreased and neurofibrillary tangles are increased in the nucleus raphe dorsalis of patients with Alzheimer type dementia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

CT findings of cerebral paragonimiasis in the chronic state.

The CT findings in 5 patients with cerebral paragonimiasis in the chronic state are presented. The findings were: 1) multiple, densely calcified areas with a variety of round or nodular shapes in the brain, 2) a large low density area surrounding or connecting with the calcified areas, and 3) cortical atrophy and ventricular dilatation. The relation between the CT findings and the previously reported plain skull X-ray findings or neuropathological findings are discussed.

Adult↗