[A case of pancreatic pseudocyst with splenic infarction].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Tanabe.
Explore the source record for details and available documents.
We encountered a 45-year-old right-handed man who had suffered a predominant right thalamic infarction and complained of memory loss. Performance on the Miyake Test (recall of ten pairs of related and unrelated words), the Rey Osterrieth Complex Figures, the Benton Test of Visual Retention and the Wechsler Memory Scale-R disclosed a severe verbal memory disturbance associated with a little, if any, visual memory disturbance. An MRI study revealed bilateral lesions limited to the thalamus involving most of the right anterior nucleus (AN), mediodorsal nucleus (MD), ventrolateral nucleus (VL), and centromedial nucleus (CM), as well as a small part of the left MD, and CM. HM-PAO-SPECT scans showed areas of decreased cerebral blood flow not only in the right thalamus but in the medial and basilar region of the right temporal lobe. It is noteworthy that our patient had a predominant right thalamic lesion and exhibited a severe verbal memory disturbance rather than visual memory disturbance. This suggests that the right hemisphere is dominant for verbal memory function in this patient.
Bilateral vocal cord abductor paralysis (VCAP) is frequently associated with multiple system atrophy (MSA) and the early clinical manifestation of VCAP is nocturnal inspiratory stridor simulating heavy snoring observed in patients with obstructive sleep apnea syndrome. We examined six MSA patients with nocturnal stridor and four disease controls including sleep apnea syndrome. Vocal cord movements were analyzed by laryngofiberscopy during both wakefulness and sleep induced by intravenous administration of diazepam. The results were as follows: First, the stenotic portion in the upper airway tract was the larynx (the vocal cords) in MSA patients with stridor, while the soft palate or the pharynx in the disease controls. Second, in the MSA patients, while awake-laryngofiberscopy showed abduction restriction suggestive of VCAP in only one of the six patients, sleep-laryngofiberscopy showed obvious paradoxical movement of the vocal cord in all the rests, where the vocal cords abducted in expiration and adducted in inspiration. In addition, there were two patterns in the inspiratory vocal cord position during sleep: one pattern where vocal glottis was still opening at the posterior one-third area and the other pattern where vocal glottis was almost completely closed through total length of the cords. Tracheostomy should be considered in the latter stage of VCAP.
We report a 23-year-old female with infantile onset chronic inflammatory demyelinating polyneuropathy. Muscle weakness was noticed when she was 1 year old, and, together with sensory disturbances, gradually progressed in an asymmetric manner. Nerve conduction studies disclosed slowing of conduction velocities, temporal dispersion, and decreased amplitude of compound muscle action potentials, the degrees of which were markedly different amongst different nerves even in the same limbs. The sural nerve biopsy showed various degrees of nerve fiber amongst different fascicles. Marked inter-nerve and intra-nerve differences of involvement and clinical improvement after steroid therapy supported the diagnosis of chronic inflammatory demyelinating polyneuropathy. It should be noted that even after a long clinical course of 23 years, her clinical symptoms remained asymmetrical and multi-focal lesions could be clearly demonstrated.
In the long course of Parkinson disease, we encounter the elevation of serum creatine kinase (CK) occasionally. Such elevation was not necessarily accompanied by severe symptoms as malignant syndrome. To delineate the basis of its situation, we selected the patients showing CK-elevation from 697 cases of Parkinson disease who had entered our hospital and their serum CK level had been measured. The cases with common cause of CK-elevation like trauma or myocardial infarction were excluded in advance. Those patients with CK-elevation were investigated with reference to age, gender, severity, duration of illness, dementia, and psychiatric symptoms retrospectively. High CK level was observed in 95 cases who were composed predominantly of advanced male patients. No obvious anticipatory cause of CK-elevation like a modification of anti-parkinson drug was recognized in 65 cases. On the other hand, CK-elevation caused by the modification of anti-parkinson drug was recognized in 10 cases. CK-elevation was observed in patients with dementia, delirium, and hallucination at higher rate. Most of these patients with CK-elevation did not show high fever and did not necessarily meet the criteria of malignant syndrome. However, 9 cases who showed marked increase of CK level over 10 times of upper limit of normal value contained some cases who had features of malignant syndrome. In Parkinson disease, especially in advanced cases dopamine may be unstable controlled in a few locations of their brain. Some situation of the disease may elicit imbalance of dopamine in patients' brain and induce CK elevation as in the similar condition in which neuroleptics are administrated.
Explore the source record for details and available documents.
Novel N-(4-oxochroman-8-yl)amide derivatives 1 were synthesized and tested for their ability to inhibit rabbit small intestinal ACAT (acyl-CoA:cholesterol acyltransferase) in vitro and to lower serum total cholesterol in cholesterol-fed rats in vivo. Among the synthesized compounds, N-(7-alkoxy-4-oxochroman-8-yl)amide derivatives showed potent ACAT inhibitory activity both in vitro and in vivo. The structure-activity relationships of these N-(4-oxochroman-8-yl)amides and related compounds are discussed on the basis of these two assays. The carbonyl group at position 4 of the 4-chromanone was essential for potent ACAT inhibitory activity. N-(Chromon-8-yl) derivatives were less potent than N-(4-oxochroman-8-yl) derivatives. An alkoxy group at position 7 of the 4-chromanone moiety was important for potent ACAT inhibitory activity. In the N-(7-alkoxy-4-oxochroman-8-yl)amide derivatives, another necessary factor to elicit the potent ACAT inhibitory activity was lipophilicity of the molecules. The highly lipophilic acid amides N-(7-methoxy-4-oxochroman-8-yl)-2,2-dimethyldodecanamide (35) and 4-[[6-(4-chlorophenoxy)hexyl]oxy]-N-(7-methoxy-4-oxochroman-8- yl)benzamide (63) showed potent activity. Introduction of a highly lipophilic alkoxy group at position 7 of the 4-chromanone moiety instead of methoxy group also resulted in potent activity. In this case, highest inhibitory activity was obtained by N-[7-(decyloxy)-4-oxochroman-8-yl]-2,2-dimethylpropanamid e (65). The most potent compound, N-(7-methoxy-4-oxochroman-8-yl)-2,2-dimethyldodecanamide (35, TEI-6522), showed significant ACAT inhibitory activity (rabbit small intestine IC50 = 13 nM, rabbit liver IC50 = 16 nM), foam cell formation inhibitory activity (rat peritoneal macrophage IC50 = 160 nM), and extremely potent serum cholesterol-lowering activity in cholesterol-fed rats (61% at a dose of 0.1 mg/kg/day po).
Twenty-three patients with aneurysmal subarachnoid haemorrhage (SAH), who showed an ST segment elevation in their electrocardiograms (ECG), were examined. There were 12 males and 11 females, with a mean age of 61 years. The clinical condition on admission was Hunt and Kosnik grade II in four, III in seven, IV in one, and V in 11 patients. Computerized tomography (CT) also revealed many cases of diffuse, thick SAH or intracerebral or intraventricular haematoma. Laboratory examinations including serum electrolyte, pH, and PaO2 revealed no abnormalities that might have influenced the ECG. Elevation in the levels of myocardial enzymes in serum was observed in two of the nine patients examined, although the elevation was only slight in one of them. Echocardiography, which was performed on several occasions on all patients, and cardiac catheterization, which was performed on eight patients, revealed a reduction in the motion of the left ventricular apex that was synchronous with ST segment elevation. This is the first report about these phenomena. No abnormalities were observed in the coronary artery. The elevated ST segment was normalized within one week in all patients, accompanied by normalization of the apical wall motion recorded on echocardiograms. In four patients, however, T wave inversion accompanied the improvement of the ST segment and was normalized within three months after the onset. These results suggest that ST segment elevation in the acute stage of SAH reflects transient cardiac dysfunction rather than myocardial injury. In some patients, however, the elevated serum levels of myocardial enzymes or T wave inversion suggested the presence of myocardial injury. Close follow-up seems to be necessary in such cases.
Linkage and haplotype analysis of eleven early-onset Alzheimer disease (AD) families was performed in relation to D21S210 and microsatellite DNA polymorphisms localized on chromosome 14q24.3. Linkage analysis of eight informative families out of eleven early-onset AD families disclosed the highest LOD score of 3.45 (theta = 0.00) at D14S77, while the locus of beta/A4 amyloid protein precursor gene was formally excluded within 10 cM from D21S210, given the evidence of recombinations in five families. Transmission disequilibrium study between the patients and controls without dementia indicated significant differences at D14S43 (p = 0.0001) and D14S71 (p = 0.02). Association study between genotypes linked or related to onset of AD and those of control also revealed a significant difference at D14S43 (p < 0.05), suggesting the existence of linkage disequilibrium. Moreover, the haplotypes at D14S43 linked with the onset of AD indicated a significant relationship with the mean age at onset. These results support that the major locus of early-onset familial AD is located on 14q24.3, and its close linkage to D14S43 and the existence of allelic heterogeneity were suggested.
A 27-year-old man with Behçet's disease presented with dyskinesia of the right hand and leg, but without paresis. MRI showed a discrete lesion in the internal segment of the left globus pallidus. SPECT (single photon emission tomography) disclosed increased perfusion in the hand and leg area of the left motor cortex and ipsilateral thalamus compared to that of the corresponding regions on the right. The dyskinesia was considered to be produced by disinhibition of the motor cortex due to loss of inhibitory inputs from the ipsilateral pallidum via the thalamus. Double transcranial magnetic stimulation revealed loss of suppression (loss of intracortical inhibition) of the left motor cortex while it showed normal suppression on the right, even though conventional techniques of magnetic stimulation failed to show any changes in excitability of the left motor cortex. We conclude that it is possible to detect changes of motor cortical excitability caused by dysfunction of some inputs from the basal ganglia by using the double cortical stimulation technique here described.
Three cases of histologically-proven Machado-Joseph disease (MJD) (clinically, types II and III) are described with special reference to the peripheral nervous system. We systematically and quantitatively analyzed the myelinated fiber densities in various nerves of three MJD patients and compared the results with the patients' clinical features and the pathological findings for the central nervous system (CNS). The results obtained were (1) motor system: The number of intermediate gammamotoneuron fibers was decreased prominently in all three MJD patients. In the type III MJD cases, the number of large alpha-motoneuron fibers also were decreased. (2) Sensory system: it generally was less involved than the motor system at the root level; but the large fibers of the distal portion were vulnerable. (3) Oculomotor system: the number of large oculomotor fibers was decreased markedly in all three cases, but there was relative preservation of parasympathetic fibers. (4) Autonomic system: the preganglionic sympathetic fibers from the intermediate lateral nucleus generally were preserved. These results suggest that in MJD the vulnerability of the peripheral nerves reflects the degree of loss of their original neuronal cells and varies according to the clinical phenotype. The characteristic peripheral neuropathy of MJD may be the result of axonal degeneration due to perikaryal neuronal damage in the central nervous system.
Vocal cord abductor paralysis (VCAP) is rare in Parkinson's disease (PD), while it is frequent in multiple system atrophy (MSA). Although VCAP is a life-threatening complication it has not yet been clarified whether there is any difference in the mechanism of VCAP between PD and MSA. Examining 3 autopsy-proven PD patients who developed severe VCAP requiring tracheostomy, we found the following differences in the mechanism of VCAP between MSA and PD: (1) clinical and laryngofiberscopic examination showed that VCAP in PD was not exacerbated during sleep, unlike in MSA; (2) On histological examination of the intrinsic laryngeal muscles, the posterior cricoarytenoid muscle demonstrated no abnormalities in PD, while the muscle showed characteristic neurogenic atrophy in MSA. There seemed to be two types of VCAP, namely the nonparalytic type observed in PD, and the paralytic type observed in MSA. Severe dysphagia requiring tube-feeding was common among PD patients who presented with VCAP. Although the relationship between VCAP and dysphagia is unknown, one should be aware of the possibility of fatal VCAP in PD patients with severe dysphagia.
We investigated the number of tyrosine hydroxylase (TH)-immunoreactive neurons in the C1 and A2 regions of the medulla, the sites of the baroreflex arc, in 7 patients with multiple system atrophy (MSA), 8 with Parkinson's disease (PD), 9 with amyotrophic lateral sclerosis (ALS), and 12 age-matched normal subjects to analyze the relationship between cardiovascular dysfunction and medullary catecholaminergic neurons. Orthostatic hypotension (OH) was marked in all the MSA patients and moderate in three PD patients. Three of the five ALS patients who had been on respirators showed lability of blood pressure; paroxysmal hypertension and nocturnal hypotension without compensatory tachycardia. All the MSA patients showed extremely marked decrease of TH-immunoreactive neurons in both the C1 and A2 regions. In the patients with Parkinson's disease, numerous TH-immunoreactive neurons contained Lewy bodies that were immunostained by antibody to TH. TH-immunoreactive neurons were decreased very markedly in the A2 regions of two patients with OH, and three patients without OH showed fairly marked decreases in the C1 or A2 region. In contrast, the number of TH-immunoreactive neurons in ALS was the same as in normal subjects. In MSA and some PD patients, orthostatic hypotension may partly be due to the involvement of the medullary catecholaminergic neurons. The lability of blood pressure in ALS probably is not related to the medullary catecholaminergic neurons.
A very rare case of traumatic basilar impression is reported. The patient, a 57-year-old man, was hit on the head vertically in the parietal region. X ray of the cervical spine and computed tomography (CT) scans showed intracranial indentation of the atlas and the odontoid process with a depressed fracture around the foramen magnum. There are no previous reports about this type of fracture.
A very rare case of wooden foreign body intrusion into the posterior cranial fossa is reported. The patient, a 16-month-old girl, fell down while holding chopsticks and was injured in the right pre-auricular region. Computed tomographic scans revealed a linear low-density area ranging from the right external auditory meatus to the fourth ventricle through the petrous portion of the temporal bone, passing near the middle cerebellar peduncle. Right temporal craniotomy was performed to abrade the petrous bone, resulting in removal of the chopstick fragment. The patient had an uneventful postoperative course and was discharged in ambulant condition, only with right hearing difficulty.
PURPOSE: Several reports have suggested a risk of injury to the middle cranial fossa and middle ear during arthroscopic procedures in the superior joint space of the temporomandibular joint (TMJ). However, there has been no anatomic study of directions and distances of the TMJ from the posterior portal in relation to the risk of mandibular fossa injury. In this study, the angles and depths at which the risk is greatest for injury to the deepest point of the mandibular fossa (DP) and to the middle ear during arthroscopy were analyzed. MATERIALS AND METHODS: Three-dimensional measurements of 96 mandibular fossae in 48 dry skulls were made. RESULTS: It was found that the distance from the lateral rim of the fossa to DP and Hugier's canal was 9.50 +/- 2.07 mm and 17.04 +/- 3.09 mm, respectively. The most dangerous angle for DP injury in the Frankfort horizontal plane (FH plane) was an inclination of the instrument base of -8 degrees dorsad and 17 and 19 degrees caudad in the frontal plane. The most dangerous angle for Hugier's canal injury was a tilting of the instrument base of 15 degrees ventrad in the FH plane and -2 degrees craniad in the frontal plane. However, these values showed a wide range. CONCLUSION: It was concluded that great care must be exercised in manipulation of instruments near the DP and Hugier's canal to avoid injury to the middle ear or penetration into the middle cranial fossa.
The presence of centromeric DNA was studied in micronuclei isolated from the blood of male ddY mice after five weekly intraperitoneal injections of mitomycin C (MMC), 1-beta-D-arabinofuranosylcytosine (Ara-C), colchicine (COL) or vinblastine sulfate (VBL). In agreement with our earlier findings, about half of the micronuclei isolated from vehicle control mice showed centromere signals as analyzed by fluorescence in situ hybridization (FISH) with a mouse major (gamma) satellite DNA probe. In an earlier experiment with mice acutely exposed to the same chemicals, the clastogens MMC and Ara-C did not reduce the proportion of micronuclei with centromere signals. In the present study, however, MMC and Ara-C decreased the proportion of micronuclei with centromeres. In contrast, the spindle poisons COL and VBL increased the proportion of micronuclei that contained centromeres.
The orthologous immunoglobulin C epsilon 1 gene (IGHE) of the common chimpanzee, pygmy chimpanzee, orangutan, white-handed gibbon, and Japanese macaque was assigned to the human chromosome 14 homologue in each species and regionally mapped by fluorescence in situ hybridization to PTR15q32 (common chimpanzee), PPA15q32 (pygmy chimpanzee), PPY15q32 (orangutan), HLA17qter (white-handed gibbon), and MFU7q29 (Japanese macaque). The gene localized to the terminal region of the chromosome in each species, and so this probe provides a new telomeric DNA marker for nonhuman primates.