情動ストレス刺激直後における脳波の経時的変化を定量的に評価した。被験者は健常成人22名で, 心身状態をCornell Medical Index (以降, CMI) を用いて評価し, 領域I を健常群, 領域II, III, IVをCMI 高値群に分類した。被験者には, 安静, 快, 不快の視聴覚動画像刺激を提示し, 180 秒間にわたって脳波を測定した。十分な休息を挟みながら, 各刺激提示を3試行, ランダムな順序で実施した。1試行180 秒間のうち, アーチファクトを除いた152 秒間について, α帯域の平均スケログラム値 (ウェーブレットスペクトル値) を求め, 3試行分の平均値について, 測定部位ごとに, 刺激間, 被験者間の比較を行った。さらに, 実験開始前の安静閉眼の無負荷状態を基準値とし, 4 秒ごとの相対平均スケログラム値を求め, 刺激後の経時的変化を回帰分析を用いて定量化した。その結果, 健常群ではCMI 高値群と比較して, 情動刺激に対する反応が大きく鋭敏であった。健常群のスケログラム値は, 安静刺激では無負荷状態と同値に近づき, 不快刺激では増加した。心身状態の違いにより, 情動ストレス負荷後の脳波の経時的変化に違いがみられた。

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上肢運動機能評価システムを用いて, 幼・小児期の視標追跡等速描円運動能力の発達を定量的に表現するモデルについて検討した。被験者は3歳から12歳の405名および対照として20歳の52名である。定量化には12パラメータ (動径成分ずれ平均/標準偏差・偏角成分ずれ平均/標準偏差・移動距離平均/標準偏差・x成分加速度パワースペクトル残差二乗和・y成分加速度パワースペクトル残差二乗和・筆圧平均/標準偏差・筆圧変化平均/標準偏差) を用いた。これらのパラメータに対して因子分析を行ったところ, 描画巧緻性, 顫動安定性, 筆圧安定性の3因子が抽出された。描画巧緻性および顫動安定性は双曲線的な発達を表し, 筆圧安定性は直線的発達を示すものの, 6～7歳を境とする2段階の発達傾向がみられた。これらの結果より, 視標追跡等速描円運動能力の発達について因子分析による3次元モデルを提案する。

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計測した腰部神経誘発磁場からその発生源である神経電気活動を再構成する実験を行った。対象は健常な成人5名 (21–32 歳; 平均 25.4) で, 脛骨神経を両足関節部内果後方で電気刺激し, 下位腰椎の背側皮膚上から神経誘発磁場を測定した。そして計測した磁場データに対して空間フィルターを適用して神経電気活動の再構成を行った。その結果, 5例全てで腰部の神経電気活動が尾側から頭側に向かって伝播する様子を再構成することにより可視化に成功した。

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To determine the relationship between skull surface brainstem auditory evoked potentials (BAEPs) and near-field potentials, short latency auditory-evoked potentials were directly recorded from the brainstem surface in humans and cats using monopolar and bipolar recording techniques. However, monopolar recordings did not sufficiently define BAEP generator sources. Detection results of phase-reversal bipolar recordings in cats demonstrated the importance of two-electrode positions, fiber directions, and impulse directions. In contrast, responses recorded from bipolar electrodes on the contralateral caudal pons demonstrated that only the component associated with time at P3 revealed a phase reversal. These results suggested that waves I, II, and III in humans corresponded to the same components in cats. In addition, wave III generated the structures in the contralateral pons, which was likely the contralateral superior olive to the stimulated ear. Further studies combining other experimental techniques are needed to determine the exact BAEP generators.

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The present study determined the generation sites of brainstem auditory evoked potentials (BAEPs) and the effects of space-occupying lesions. The subjects were assigned to six groups: midbrain tumor, pontine intramedullary tumor, IVth ventricle tumor, C-P angle tumor, clival tumor, and cervico-medullary space-occupying lesions according to location and effect of brainstem compression. In the midbrain tumor group, most pineal tumors did not have an effect on BAEPs, because they stayed in the rostral half of the midbrain. In the midbrain tumor, which primarily involved the midbrain tegmentum, including the quadrigeminal plate, only wave V on BAEPs was severely attenuated from left and right stimulation. An additional tumor in the unilateral side of the ponto-midbrain junction exhibited attenuation of wave IV to ipsilateral stimulation, and of wave V to contralateral stimulation, from the lesion side. Results of midbrain tumors suggested that the generator(s) of wave V were located in the lower midbrain, and generators and/or pathways of waves IV and V were present on the opposite side of the brainstem to the stimulated ear.
Effects on BAEPs in cases with pontine intramedullary tumors and IVth ventricle tumors the long tracts were similar, i.e., wave III was easily affected even if symptoms remained mild. In contrast, in the C-P angle tumor group, when the T/BS ratio reached 80%, the wave V or wave IV/V complex on the BAEP contralateral stimulation to the lesion side was lost. These suggested that auditory tracts generating waves IV and V were located more laterally in the lower pons than wave III.
Four kinds of tumors—IVth ventricle tumor, cerebellar tumor, C-P angle tumor, and cervico-medullary tumor—exhibited similar unilateral BAEP abnormalities, i.e., wave II was absent or severely attenuated, and the succeeding components were delayed. According to MRI and neurological findings, tumor lesions in the former two cases of the above-mentioned four cases did not affect the VIIIth nerve, but rather compressed the cochlear nucleus. Those results strongly suggested that wave II was generated by cochlear nucleus.
In summary, results from the present study showed the following: 1) wave V was generated in the caudal region of the midbrain tegmentum; 2) generators and/or pathways of waves IV and V were on opposite sides at the rostral pons level; 3) generators and/or pathways of waves IV and V were more lateral in the caudal half of the pons than wave III; and 4) wave II was generated in and around the cochlear nucleus.

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