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Biomedical subjects

M Okusa

Publications and source records attributed to M Okusa.

5 recordsLinked to original sources
PubMed1999

Effects of discrimination difficulty on cognitive event-related brain potentials in patients with cochlear implants.

Cognitive event-related brain potentials (ERPs) recorded during a 2-tone discrimination (oddball) task were examined in 8 patients with cochlear implants. The aim of this study is to investigate the effects of discrimination difficulty formed by 4 conditions of stimulus contrast: the target stimuli were set at 2000, 1500, 1200, or 1100 Hz, and nontarget stimuli were set at 1000 Hz throughout. The averaged ERPs recorded after the target stimuli revealed N100, P200, N200, and P300 peaks, whereas those after the nontarget stimuli showed only N100 and P200 peaks. The peak latencies of the ERP components of early information processings (N100 and P200) were not significantly increased among the 4 conditions. In contrast, the latencies of late cognitive components (N2b and P300, whose peak latencies were longer than 250 msec) and reaction times were significantly increased as target discriminability decreased. In conclusion, early information processings were not delayed by the discrimination difficulty, but cognitive processings were delayed in patients with cochlear implants. Because the N2b amplitude, which is considered to be associated with controlled processings, was much larger than that previously reported from subjects with normal hearing, it is suggested that patients with cochlear implants make a considerable effort to process their poor auditory information.

Adult↗
PubMed1996

[Statistical analysis of recovery from sudden deafness among treatment groups].

This study examined 131 patients with idiopathic sudden deafness in whom the averaged of five frequency hearing levels was greater than 60dB. Since combined pharmacotherapy has been used in the treatment of idiopathic sudden deafness, it is hard to make a quantitative analysis of single-drug efficacy. We used a single-drug treatment in turn to assess the drug efficacy within 30 days after the onset. There was no significant difference among patients treated within 6 days and not less than 7 days after the onset with steroid therapy, PGE1 therapy, and defibrinogenation therapy. Similarly, there was no significant difference among patients treated within 6 days and not less than 7 days after the onset with steroid and defibrinogenation combined therapy, steroid and PGE1 combined therapy, and steroid, defibrinogenation and Lasix-Vitamin combined therapy. In case of no steroid effect, treatment with defibrinogenation, PGE1 and Lasix-Vitamin therapy could achieve hearing improvement.

Adolescent↗
PubMed1993

Hearing recovery in sudden deafness patients using a modified defibrinogenation therapy.

Ninety-eight patients with idiopathic sudden deafness were treated with a modified defibrinogenation (DF) therapy including batroxobin, low molecular dextran, vasodilators and vitamins. Hearing improvement was evaluated with two methods: categorical judgement and improvement rate (%). By categorical judgement, 60 patients (61% of the total) were classified into recovery or good improvement categories. The improvement rate was calculated for each of the 93 patients, and the average value was 64%. Modified DF therapy was effective especially for patients with severe hearing loss of 70-90 dB with flat audiogram. Although serum fibrinogen significantly decreased after batroxobin administration there was no correlation between the concentration of fibrinogen and hearing recovery. When prognostic factors were studied, the interval between the onset of hearing loss and start of treatment, initial hearing level, and the existence of vertigo all had significant correlation with the degree of hearing recovery.

Adenosine Triphosphate↗
PubMed1993

Tinnitus suppression by electrical promontory stimulation in sensorineural deaf patients.

In 62 patients, whose hearing acuity was normal or profoundly impaired, tinnitus suppression was attempted through electrical promontory stimulation (EPS) with a Promontory Stimulator (Cochlear Co.). The causes of tinnitus were idiopathic sudden deafness, ototoxicity, noise induced hearing loss, labyrinthitis, Meniere's disease, acoustic neuroma and unknown origin. Reduction of tinnitus was achieved in 46 of 68 ears (67.6%). Of these, EPS was most effective in cases of noise induced hearing loss (100.0%; 3/3), followed by those of idiopathic sudden deafness (87.5%; 14/16), Meniere's disease (83.3%; 5/6), labyrinthitis (75.0%; 6/8), ototoxicity (66.6%; 4/6) and unknown origin (76.4%; 13/17). The treatment had hardly any effect on patients with acoustic neuroma (8.3%; 1/12). Twenty patients reported residual inhibition with a duration ranging from several hours to one week. Our results suggest that tinnitus due to cochlear lesions can be suppressed by EPS. This technique may also be useful for differentiation between tinnitus resulting from cochlear lesions and from retrocochlear lesions.

Adolescent↗