[Analysis of misdiagnosed gastric cancer with special reference to the gastrocamera].
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Biomedical subjects
Publications and source records attributed to T Hayashida.
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A 58-year-old male with systemic T-cell lymphoma involving the brainstem eccentrically, showed varying abnormal auditory brainstem responses (ABRs). The initial ABR demonstrated a prolonged V wave peak latency and an I-V IPL on admission. Four months later, all waves were absent bilaterally. Neuropathological examination at autopsy revealed that most of the nuclei and tracts associated with the auditory system were destroyed by lymphoid cell infiltration. It suggested that in the early stages of this disease, lymphoid cells could have involved the lower brainstem and, subsequently, in the advanced stages invaded the inferior colliculus.
We investigated the postcaloric nystagmus that is related to positional change in 24 patients with spinocerebellar degeneration (SCD) and compared it with that in normal subjects. Six ears of 3 patients exhibited no evaluable caloric response. In 42 ears of 21 patients, the primary phase of caloric nystagmus was definitely observed. In 37 of 42 (88%) ears, postcaloric nystagmus was observed. The postcaloric nystagmus from a positional change in patients with SCD was significantly larger than that in control subjects. Furthermore, it was significantly exaggerated in patients with brainstem and cerebellar lesions in comparison with patients with pure cerebellar lesions. The degree of disturbance coming from visual suppression had only a limited correlation with the exaggerated postcaloric nystagmus. Also discussed are possible other factors affecting the exaggerated postcaloric nystagmus.
The postcaloric nystagmus (PCN) by positional change from the supine position to the upright position and other neurootological findings were studied. Twenety-one patients with a clinical diagnosis of spinocerebellar degeneration or Arnold-Chiari malformation were studied. There was a significant negative correlation between maximum slow phase eye velocity in postcaloric nystagmus by positional change (V2) and maximum slow phase eye velocity in optokinetic nystagmus pattern test (r = -0.47; n = 21). Moreover, patients with vertical gaze nystagmus (VN) had significantly larger V2 than patients without VN. However, there was no significant difference for V2 between patients with and without rebound nystagmus. Through these studies, the authors discussed probable mechanisms and responsible lesions for the exaggerated PCN by positional change.
Regional selectivity of gentamicin (GM) ototoxicity was studied in guinea pigs (GPs) using electrophysiological, morphological, autoradiographic and immunohistological observations following combined treatment with GM (150 mg/kg i.m.) and ethacrynic acid (EA) (30 mg/kg i.c. or i.v., 1.5 h after GM injection). The GPs were either continuously stimulated every 5 min with a series of 256 clicks (70 dB peSPL, 10/s) during 3 h for monitoring fast changes in VIII nerve compound action potential (CAP) after the EA injection, and thereafter kept in the animal quarters (background noise of 60 dB SPL) (group I), or similarly monitored for only 10 min after the EA injection and thereafter kept in a soundproof room (around 0 dB SPL) (group II). Whenever GM labelling was observed it was localized only in the sensory hair cells. From 3 h after EA injection, the GPs in group I presented threshold elevations in the high-frequency region, which progressed to 60-80 dB at all frequencies at and after 48 h. Parallel to the threshold pattern, GM uptake in outer hair cells (OHCs) was seen with an increasing concentration from apex toward base from 3 to 24 h, while after 48 h almost all OHCs were destroyed and inner hair cells (IHCs) were marked by GM. In group II no changes in CAP thresholds were observed until more than 24 h, although GM was detected in the hair cells from 6 h on. At this early stage, the distribution of GM lacked a clear pattern, particularly without a clear apex-base gradient, and GM deposits were found only around the basal body. However in both groups, in late stage (greater than 24 h), the base-apex gradient was more pronounced and GM was found throughout the cell body, with a marked concentration below the cuticular plate. These results suggest that GM may penetrate hair cells around the basal body and that activating the cells by sound potentiates both GM uptake and its intracellular toxicity.
AIM: To identify lesions responsible for vocal cord abductor paralysis (VCAP) in multiple system atrophy (MSA), we performed a morphometric study of the nucleus ambiguus which innervates the intrinsic laryngeal muscles. METHODS: Two autopsied cases of MSA presenting with VCAP and one control were examined. Both cases of MSA showed selective neurogenic atrophy of the posterior cricoarytenoid muscles among the intrinsic laryngeal muscles, while no abnormalities were seen in the control. From a block of the medulla oblongata, sections 10 microm thickness were cut serially without spacing and stained with cresyl violet. The ambiguus neurons were counted in all the sections to make a histogram. RESULTS: In the control case, ambiguus neurons showed densely populated areas and sparsely populated areas alternately with significant difference in the mean neuronal density between two areas. In MSA, ambiguus neurons were significantly decreased in number at all levels. It indicates that the neurogenic atrophy of the posterior cricoarytenoid muscle is derived from the neuronal loss of the nucleus ambiguus. CONCLUSION: Though it has still been controversial whether or not the ambiguus neurons are decreased in number in MSA with VCAP, we speculated possible reasons for the disagreement on the involvement of the nucleus ambiguus as follows: different mechanism of VCAP are playing role, and histometric data have been disturbed by factors such as split-cell counting error and marked variation in the distribution of the ambiguus neurons.