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Y Terayama

Publications and source records attributed to Y Terayama.

At least 19 recordsLinked to original sources
PubMed1998

Age-related cerebrovascular disease alters the symptomatic course of migraine.

Migraine headaches usually decrease in frequency and severity and often cease during advancing age. Occasionally, migraineurs report late-life migrainous accompaniments, i.e., auras without headache, particularly when typical migraine attacks terminate or diminish following major or minor strokes, at which time the auras may become atypical. Clinical observations such as these suggest that degenerative cerebrovascular changes accompanying aging may modify the course of migraine headaches particularly those with aura. To test this hypothesis, we quantitated age-related changes in cerebral vasodilator capacitance by measuring local cerebral blood flow utilizing xenon contrast computed tomography (CT) scanning before and after oral administration of the pharmacological cerebral vasodilator, acetazolamide (Diamox). Measurements were compared among 27 normal volunteers without headache (aged 24-94 years; mean age 61.1 +/- 17.6) and 37 carefully categorized groups of migraine patients (aged 27-83 years; mean age 59.4 +/- 12.4). The normals comprised Group A. Migraineurs were divided into two subgroups: Group B consisted of 27 migraineurs with and without aura who continued to suffer from incapacitating and frequent headaches and Group C consisted of 10 migraineurs who no longer suffered from severe and frequent headaches, two of whom still complained of atypical auras of the "late-life migrainous accompaniments" type. Cerebral vasodilator capacitance significantly declined with advancing age among normals and the two groups of migraineurs, confirming the development of age-related cerebrovascular diseases. Global CBF increases after Diamox in Group B (with persistent and severe migraine), were significantly greater compared with normals without headache, and with Group C consisting of migraineurs whose headaches had decreased, subsided, or become replaced by late-life migrainous accompaniments (Group C). Results establish that cerebrovasodilator capacitance declines with advancing age, probably due to progressive cerebral atherosclerosis, since these declines were accentuated by risk factors for stroke, particularly TIAs or documented lacunar infarcts by CT. Progressive impairments of cerebral vasodilator capacitance among migraineurs were associated with: (i) reductions in frequency and severity of migrainous cephalalgia and (ii) appearance of late-life migrainous accompaniments.

Adult↗
PubMed1998

Risk factors for cerebral degenerative changes and dementia.

It is concluded that the most important determinants for cerebral neurodegenerative changes and cognitive decline during aging are neuronal shrinkage and/or loss, which are accelerated by certain risk factors: e.g. TIAs, hypertension, heart disease, hyperlipidemia, smoking, heavy alcohol consumption, male gender, low educational status, family history of cerebrovascular disease and absence of estrogen replacement therapy among women. Some of these risk factors are remediable by therapeutic interventions, including prevention of TIAs and medications that control hypertension, heart disease, hyperlipidemia and estrogen replacement in postmenopausal women, as well as abstention from abuse of tobacco and alcohol. Cerebral neurodegenerative changes measured by neuroimaging appear to be premorbid markers for depleted neuronal and synaptic reserves which predispose to the onset of dementias of both VAD and DAT types. Normal subjects at risk for cognitive decline include those with TIAs, hypertension and heart disease since these risk factors measurably accelerate cerebral atrophy, ventricular enlargement, leukoaraiosis, and decline in cortical perfusion.

Adult↗
PubMed1998

[Clinicopathological investigation of malignant alteration in nasal and paranasal sinus papilloma using flow cytometric DNA ploidy].

Among tumors of the head and neck, nasal and paranasal sinus papilloma is a relatively rare benign tumor. However, it is different from other benign nasal and paranasal tumors, in histological morphology, and in higher probabilities of recurrence, complication with malignant tumor, and malignant alteration. In this study, we examined clinically and pathologically 30 patients with nasal and paranasal sinus papilloma who underwent operations in our department between 1975 and 1994. The tumor occurred in the opening of the maxillary sinus in 19 patients and in the nasal septum in 7 patients. Destruction of bone was observed in 12 patients. Pathological examination revealed inverted papilloma in 17 patients, exophytic papilloma in 13 patients, and atypia in 4 patients. Recurrence was observed in 9 patients, and malignant alteration was observed in 5 patients. Using paraffin sections, aneuploidy was assessed by flow cytometric DNA ploidy. Diploid in 25 cases (83.3%) and aneuploid in 5 cases (16.7%) were observed. Risk factors of malignant alteration in nasal and paranasal papilloma are considered to be 1) developmental morphology, 2) destruction of bones, 3) atypia in pathology, 4) recurrence before progression to malignancy, and 5) the presence of aneuploidy. The 5 patients in whom malignant alteration was observed each showed 4 of the 5 risk factors, suggesting that malignant alteration is most likely to occur in nasal and paranasal papilloma that show 4 or 5 risk factors. The period up to malignant alteration varies; in one patient, it was more than 10 years. Therefore, follow-up observation over a long period is required.

Adult↗
PubMed1997

Normal human aging: factors contributing to cerebral atrophy.

Factors that accelerate rates of 'normal' age-related cerebral atrophic and degenerative changes are important because they may predispose to cognitive declines. To determine characteristic patterns of normal aging, risk factors were correlated with serial neurological-neuropsychological examinations, CT measures of progressive cerebral atrophy, local tissue hypodensities, or perfusional declines. Both cross-sectional and longitudinal designs were utilized. Ninety-four cognitively and neurologically normal aging volunteers, 15 with a history of transient ischemic attacks (TIAs), were followed for mean intervals of 3.0+/-2.1 years. Results indicated that: (1) after age 60, cerebral atrophy, polio- and leuko-araiosis doubled and cerebral perfusion decreased, with marked individual variations; (2) risk factors independently accelerating cerebral atrophy and cortico-subcortical perfusional declines included TIAs, hypertension, smoking, hyperlipidemia, excessive alcohol consumption and male gender; (3) progressive leuko-araiosis correlated directly with cortical atrophy and cortical perfusional declines. We posit that: (1) cerebral atrophy and degenerative changes result from neuronal shrinkage and/or loss, which are accelerated by TIAs, hypertension, smoking, hyperlipidemia, excessive alcohol consumption and male gender; (2) accelerated cerebral atrophic and degenerative changes identified by neuroimaging should be considered as markers for depleted neuronal synaptic reserves, which predispose to cognitive declines. Interventions available for controlling some of these risk factors include control of TIAs, hypertension, and hyperlipidemia, as well as tobacco and alcohol withdrawal.

Adult↗
PubMed1997

Prognostic value of admission blood pressure in patients with intracerebral hemorrhage. Keio Cooperative Stroke Study.

BACKGROUND AND PURPOSE: Patients with acute stroke on admission to the hospital are often found to have high blood pressure. The purpose of the present study was to investigate the prognostic value of admission blood pressure in patients with acute intracerebral hemorrhage, including putaminal, thalamic, subcortical, cerebellar, and pontine hemorrhage. METHODS: A total of 1701 patients with intracerebral hemorrhage of the putamen (n = 776; mean +/- SD age, 58 +/- 14 years) thalamus (n = 538; 63 +/- 12 years), subcortex (n = 153; 61 +/- 16 years), cerebellum (n = 110; 64 +/- 11 years), and pons (n = 124; 59 +/- 13 years) were examined. The mean blood pressure on admission in patients with a fatal outcome was compared with that in patients who survived. RESULTS: The mean age in each patient group (putaminal, thalamic, subcortical, cerebellar, and pontine hemorrhage) with fatal outcome was older than that with nonfatal outcome, while ANCOVA indicated no correlation between age and blood pressure on admission or age and volume of hematoma. The mean arterial blood pressure on hospital admission was 126.9 +/- 25.8 mm Hg (+/-SD) in cases of putaminal. 127.4 +/- 22.6 mm Hg in thalamic, 116.4 +/- 20.6 mm Hg in subcortical, 123.5 +/- 23.9 mm Hg in cerebellar, and 133.0 +/- 26.0 mm Hg in pontine hemorrhage. The mean blood pressure on admission in patients with a fatal outcome among those with putaminal (136.0 +/- 36.3 mm Hg) and thalamic (133.2 +/- 22.1 mm Hg) hemorrhage was significantly higher than that in those with a nonfatal outcome (123.8 +/- 20.6 mm Hg for putaminal, 101.6 +/- 22.5 mm Hg for thalamic) (P < .01). No correlation between mean blood pressure and outcome was observed in the patients with subcortical (116.5 +/- 22.2 mm Hg for nonfatal, 114.9 +/- 22.0 mm Hg for fatal outcome), cerebellar (125.2 +/- 22.2 mm Hg, 116.9 +/- 28.8 mm Hg), and pontine (129.9 +/- 23.8 mm Hg, 136.0 +/- 27.7 mm Hg) hemorrhage. The volume of hematoma on admission in patients with fatal outcome with putaminal (58.2 +/- 24.4 mL), thalamic (27.0 +/- 13.1 mL), subcortical (32.9 +/- 14.4 mL), and cerebellar (31.4 +/- 28.6 mL) hemorrhage was greater than that in those with nonfatal outcome (20.8 +/- 11.4 mL, 7.1 +/- 4.8 mL, 18.3 +/- 10.6 mL, and 8.1 +/- 4.2 mL, respectively; P < .01), while no correlation between volume of hematoma and outcome was observed in patients with pontine hemorrhage. CONCLUSIONS: The above data suggest that an increased mean blood pressure and volume of hematoma on admission in putaminal and thalamic hemorrhage were related to increased mortality, while in patients with subcortical, cerebellar, and pontine hemorrhage, the mean blood pressure was not related to the clinical outcome.

Age Factors↗
PubMed1997

Classification, diagnosis and treatment of vascular dementia.

Vascular dementia (VAD) is considered to be the second most common cause of dementia in Europe and the US. In Asia and many developing countries, it is more common than dementia of the Alzheimer's type (DAT). VAD is the most preventable form of dementia associated with later life. The pathogenesis of VAD is multifactorial, and it represents a heterogeneous, not a homogeneous, clinical entity. Classification of VAD by pathogenesis is important for its prevention and treatment. Control of the risk factors for VAD reduces its incidence and stabilises or improves cognitive performance following stroke. Proper diagnostic evaluation of VAD requires: (i) a well defined quantitative assessment of the cognitive deficits present; (ii) assessment of risk factors for stroke; (iii) identification of cerebral vascular lesions by history, neurological examination and neuroimaging; (iv) exclusion of other causes of dementia; (v) establishment of a positive diagnosis of possible, probable or definite VAD versus DAT or mixed VAD/DAT; and (vi) identification of the temporal relationship between cognitive deficits and cerebral vascular lesions. VAD can be subdivided into 8 major types, as follows: (i) multi-infarct dementia secondary to large cerebral emboli [type 1]; (ii) strategically placed infarctions causing dementia [type 2]; (iii) multiple subcortical lacunar lesions secondary to atherosclerosis or degenerative arteriolar changes [type 3]; (iv) Binswanger's disease (arteriosclerotic subcortical leukoencephalopathy) [type 4]; (v) mixtures of types 1, 2 and 3 [type 5]; (vi) haemorrhagic lesions causing dementia [type 6]; (vii) subcortical dementia secondary to hereditary factors (type 7); and (viii) mixtures of DAT and VAD (type 8). Treatment is dictated by the pathogenetic subtype of VAD that is present.

Dementia, Vascular↗
PubMed1997

[A case of Guillain-Barré syndrome treated with plasma exchange and intravenous high-dose immune globulin].

We describe a 69-year-old female with Guillain-Barré syndrome (GBS) whose paresthesia and weakness improved after plasma exchange (PE) and intravenous high-dose immune globulin (i.v.I.G.). She felt a paresthesia in her right arm, and 7 days later she noticed right arm weakness followed by gait disturbance within 2 days. She received a series of 6 PEs, but paresthesia and weakness did not improve. Following the last PE trial of this series, she was treated by i.v.I.G. (0.4 g/kg) for 5 days. After i.v.I.G., paresthesia and weakness improved in a few days. After 2nd series of 6 PEs, she was able to walk. In this clinical course, the treatment of i.v.I.G. after PE seemed to be effective. This case raises the possibility that i.v.I.G. might be the treatment in GBS patients with insufficient effect of PE.

Aged↗
PubMed1996

Surgical results of tympanoplasty with hokudai-shaped partial and total ossicular replacement prostheses.

The surgical results of tympanoplasty using a ceramic partial ossicular replacement prosthesis (PORP) or a ceramic total ossicular replacement prosthesis (TORP) were analyzed. The present study included 25 ears in 22 patients who underwent tympanoplasty between December 1986 and September 1994 and were followed up for more than 6 months postoperatively. Because the ceramic prosthesis was extruded from 2 of the 25 ears, the surgical results in the other 23 ears were analyzed, Surgical results were assessed according to a criterion that permits comparison with data from around the world. The criterion considers a postoperative airbone gap within 20 dB as a success. According to this criterion, the success rate was 90.9% for PORP, 50.0% for TORP, and 69.6% in total. These results are comparable with those found at other centers.

Adolescent↗
PubMed1996

[A case of Paget's disease with progressive sensorineural hearing loss involved in the bilateral bony labyrinths].

Paget's disease of the bone is a chronic, progressive disease of unknown etiology characterized by abnormal bony resorption and deposition. It is a common skeletal disease in Europe and North America, while in Japan it is very rare. Paget's disease of the temporal bone has been reported to cause hearing loss frequently. We report a 50-year-old woman with Paget's disease who had progressive bilateral sensorineural hearing loss and right vestibular dysfunction. CT and 3 Dimensional CT (3D-CT) images demonstrated resorption of the entire bony labyrinth and its surroundings on both sides and that the temporal bone elsewhere remained intact. Bone scans revealed disease symmetrically in the bilateral otic capsules. Previous studies indicated that the bone changes in Paget's disease in the petrous pyramid begin in areas best supplied with marrow tissue and that the otic capsule is relatively spared until advanced changes are present in the remainder of the petrous pyramid. But, this patient mainly had foci in the bilateral otic capsules and the pattern was similar to cochlear otosclerosis. 3D-CT was useful for differentiation of Paget's disease and cochlear otosclerosis. The pattern of the affected areas indicated that this is a very rare situation even in the reports of Europe and North America, where the disease is rather common.

Diagnosis, Differential↗
PubMed1996

[Estimation of catecholamine release based on dialyzer clearance rate during hemodialysis].

To estimate catecholamine (CA) release during hemodialysis (HD), plasma-free and conjugated CAs and their dialyzer clearance rates were measured in 10 HD patients (age; 49.8 +/- 15.2 years, duration of HD; 5.8 +/- 5.0 years). Although free dopamine (f-DA) and all conjugated CAs decreased to about one half of the pre-HD levels at the end of HD, no significant change was seen in free norepinephrine (f-NE) and epinephrine (f-E) during HD. For every CA, the clearance rate was the highest in the sulfate and the lowest in the glucuronide form, and NE was the highest in every form. In the comparison between the measured CA and calculated CA using the clearance rate and the pre-HD level, the measured values of f-NE and f-E were significantly higher than the calculated values, unlike the results for f-DA and conjugated CAs. The difference in f-NE between the measured and the calculated values correlated negatively with the change in mean blood pressure (delta MBP), and delta MBP was also correlated with the ultrafiltration volume. From these data, it was suggested that f-NE was released by the decrease of MBP due to the increase of ultra-filtration volume during HD.

Adult↗
PubMed1995

Activated leukocytes, endothelial cells, and effects of pentoxifylline: observations by VEC-DIC microscopy.

Using video-enhanced contrast (VEC)-differential interference contrast (DIC) microscopy, ultrastructural observations were made of the activation of polymorphonuclear leukocytes (PMNLs), the interaction between activated PMNLs and endothelial cells (ECs), and the effects of pentoxifylline (PTX). The ECs were obtained from a commercial source as human umbilical cord vein endothelial cells (HUVECs) or were obtained from pig or rat brains. They were cultured on a coverglass with DMEM for about 1 week. The human PMNLs were obtained from the authors' venous blood. The control appearance of the PMNLs resembled an elastic ball covered with fine villi. The PMNL was activated spontaneously and became flattened on the glass surface within 10 min in the observation chamber. The activation of the PMNLs was estimated arbitrarily from the polymorphous changes in cell shape, agitation of the intracellular granules, and apparent increase in adhesiveness. Preadministered PTX prevented such PMNL activation, and the PMNLs remained round for more than 15 min. PMNL activation was accelerated by chemoattractants (PAF, fMLP, and PMA). In one case, a PMNL that had been activated by PMA tended to recover its round shape with PTX, but finally ended by swelling and bursting. When PMNLs were introduced into the EC-containing chamber, they became entrapped by the ECs and activated, with degranulation followed by release of a smoke-like material. After about 3 h, the EC with an attached PMNL shrank and fell into a state of coagulation necrosis. When PTX was introduced at the time of adhesion of the flattened PMNL, the PMNL appeared to be deactivated, becoming smaller and assuming its previous round shape, and detached from the EC. PTX prevented the spontaneous activation of PMNLs, and of deactivated PMNLs even after their adherence to the endothelium.

Animals↗
PubMed1994

CT changes associated with normal aging of the human brain.

CT was used to measure changes in cerebral gray and white matter tissue densities associated with normal aging, using a cross-sectional design, in order to provide normative data for comparisons with abnormal aging such as dementias of Alzheimer's and vascular types. Cerebral compartmental densities were measured using plain CT, and their perfusion values were recorded during stable xenon inhalation (CT-CBF), among 81 neurologically and cognitively normal volunteers of different ages. Results led to the conclusion that cortical gray matter tissue densities progressively decline (polio-araiosis) after age 60. Cortical polio-araiosis is coupled with regional hypoperfusion but not with cortical atrophy. It is speculated that the cortical hypodensity identified by CT imaging parallels declines in cortical synaptic density, as reported from autopsy studies using anti-synaptophysin staining of cerebral cortex obtained from normal people above and below age 60. The coupling of cortical hypoperfusion with polio-araiosis is believed to reflect age-related reductions of cortical metabolic demands as reported by PET. During normal aging leuko-araiosis correlates directly with cortical atrophy, suggesting that anterograde axonal degeneration resulting from cortical neuronal dearborization play a role in its causation.

Adult↗
PubMed1994

Prospective studies of cerebral perfusion and cognitive testing among elderly normal volunteers and patients with ischemic vascular dementia and Alzheimer's disease.

To compare longitudinal changes of cerebral perfusion (CBF) and cognitive status in two common forms of dementia in the elderly, 42 patients with ischemic vascular dementia (IVD), 44 patients with dementia of the Alzheimer type (DAT), and 120 elderly normal volunteers were evaluated prospectively over a mean interval of 3.35 years. Subjects were at least age sixty, (mean age 71.1). Mean bihemispheric cerebral blood flow and cognitive test scores of control subjects were significantly higher than those of both demented groups at entry and remained so. After adjustment for initial CBF, course over time was similar for all groups. Group variability was similar for CBF but not for cognition. Both IVD and DAT patients were more variable than controls but similar to each other. Throughout, DAT patients showed greater cognitive impairments than IVD patients. Cognitive impairments stabilized among IVD patients treated by control of risk factors, antiplatelet or anticoagulant therapy but declined progressively among DAT patients.

Age Factors↗
PubMed1993

Cognitive recovery correlates with white-matter restitution after head injury.

Longitudinal measurements of local cerebral perfusion (LCBF) and local partition coefficients (L lambda) using xenon-enhanced computed tomography were examined in six patients who had suffered from head injury at a mean age of 30 +/- 9.3 years. They were selected from a larger group with head injury because all were observed longitudinally to make excellent cognitive recovery some years after acute cerebral trauma. Results were compared with similar longitudinal measurements made in six age-matched neurologically normal volunteers. In the index group, cognitive test scores were reduced at the time of the first LCBP measurement but significantly improved to normal at the time of the second. The mean interval between measurements was 2.7 +/- 0.7 years. At the time of the first measurement, all six patients exhibited abnormal volumes of white matter with reduced Hounsfield numbers and LCBF and L lambda values. Abnormalities in volume of white matter and LCBF and L lambda values improved to normal at the time of the second measurement. Perfusion values for frontal cortex, putamen, and thalamus were still slightly reduced but also improved toward normal between measurements. Cognitive recovery correlated best with restoration of white matter integrity, suggesting that following head injury, cognitive impairments may be associated with temporary disconnections of corticothalamic projection systems.

Adult↗
PubMed1993

Correlations of leuko-araiosis with cerebral atrophy and perfusion in elderly normal subjects and demented patients.

CT images of leuko-araiosis in brain slices were quantified according to volumes of reduced Hounsfield units in frontal periventricular white matter in groups of elderly patients with multi-infarct dementia (MID, n = 23) and dementia of the Alzheimer type (DAT, n = 16). Volumes of leuko-araiosis, estimates of atrophic cerebral tissue, and local cerebral perfusion utilising inhalation of xenon gas as the indicator were correlated on the same CT slices. Ratios of frontal leuko-araiosis to total brain tissue volume were similar for patients with MID and DAT (mean 5.7 (SD 2.1)% v 6.5 (3.2%)), and both were significantly greater than ratios in elderly normal volunteers (3.1(1.3)%, 0 < 0.001). Cerebral atrophy (measured as the ratio of volumes of cerebrospinal fluid to total brain area) for DAT patients was 17.0 (6.7)%, which was greater than for MID patients (12.5 (5.4)%; p < 0.05) and both types of patients showed more cerebral atrophy than did age matched, elderly normal subjects. Cerebral perfusion was decreased in all regions measured in patients with MID and DAT compared with elderly normal subjects. Multi variate regression analyses correlated frontal leuko-araiosis with reductions of local cerebral blood flow in subcortical grey matter (p < 0.025) in patients with vascular dementia but not in those with DAT. These quantitative measures implicate decreased perfusion due to atherosclerosis in territories supplied by the deep penetrating cerebral arteries in the pathogenesis of leuko-araiosis in patients with vascular dementia, but suggest a different pathogenesis for leuko-araiosis in Alzheimer's disease.

Aged↗
PubMed1993

Cerebral circulation in the elderly.

A great deal of knowledge has been accumulated in recent years, concerning the aging human brain in health and disease, with the advent of newer methods of measuring cerebral blood flow (CBF) and metabolism. It is well documented that even in normal aging, the functional metabolism of the brain and its blood supply inevitably decline. This accounts for the widespread clinical observations that the young tolerate disorders of the brain better than do the elderly. It also accounts for difficulties in correctly diagnosing and treating cognitive disorders among the elderly. Neuronal and vascular reserves become progressively depleted during normal aging, so that one or more different disease processes may contribute to cognitive declines. Computed tomography (CT) densitometry, coupled with xenon-enhanced CT CBF measurements, provide a noninvasive method for separating the changes within cerebral cortex, subcortex, and white matter that occur in normal aging from those due to pathological abnormalities.

Aged↗
PubMed1992

White matter lesions in the elderly.

The advent of neuroimaging has brought medical attention to the frequency of unsuspected white matter lesions in the brains of elderly people. In 1987 Hachinski suggested the term "leuko-araiosis" to identify such white matter abnormalities detected by computed tomography and magnetic resonance imaging to emphasize that their etiology and clinical relevance require clarification. Since then, leuko-araiosis has been recognized among approximately ten percent of apparently normal, elderly people over age sixty-five. The severity and frequency of leuko-araiosis increases with advancing age, risk factors for stroke, history of strokes particularly of the lacunar type and dementia of both the vascular and Alzheimer type. Current concepts concerning the pathogenesis and neurological concomitants of leuko-araiosis are reviewed. The etiology of leuko-araiosis may be heterogeneous but is most likely ischemic in nature. However, as white matter lesions progress among the elderly they are likely to become associated with cognitive impairments and motor dyspraxias presumably resulting from cortico-subcortical disconnections, particularly involving the frontal cortex and basal ganglia and may themselves be considered a radiological "risk factor" or precursor for dementia.

Aged↗