Alzheimer’s association internal conference on prevention of dementia, june 18-21, 2005, marriot wardman hotel, washington, d
T. Musha; Brain Functions Lab., Yokohama, Japan
T. Takao; Kurashiki Heisei Hospital, Kurashiki, Japan
What is DIMENSION (Diagnosis Method of Neuronal Dysfunction)
Scalp potentials for the EEG alpha-component in a normal subject are well approximated by a potential distribution
generated by an optimal single current dipole generator (mathematical model), and its goodness-of-fit (dipolarity) D is close to 1 (Fig.1). In an AD patient the scalp potential distribution is distorted with local neuronal impairments (Fig.2), and the potential distribution becomes unstable. Let the mean and standard deviation of dipolarity be denoted as Dα and Dσ. DIMENSION Diagram
gram as shown in Fig.3, where 25 very mild AD and 33 moderately severe AD patients together with 56 age-matched normal con-trols were DIMENSION-analyzed. All the data on the diagram are distributed within a
fan-beam area. With an increase of the syn-
aptic-neuronal impairment as a result of progression of AD spatial and temporal fluc-tuations of neuronal activity increase; they
are somewhat correlated. It turns out that diagnosis of neuronal impairment can be done in terms of either Dα or Dσ.
A patient (female 82 years old) visited our hospital accompanied by her husband complaining severe memory loss. Her
MMSE score was 26 and Dα was 0.969 (normal region). Six months later her MMSE score increased to 27 but Dα de-creased to 0.961. Two months later her MMSE score was 25 but Dα went further down to 0.957 (subnormal region). Then medication (Aricept) started together with rehabilitation, and four months later her MMSE score still stayed at 25 but
Dα was recovered to 0.970 (normal region). In nine months after the medication and rehabilitation started her MMSE was still 25 but Dα was 0.955, hence the effect of the treatment was lost. As is seen in this figure both the MMSE score and the Dα value were going down after the 22nd month. From this trend we conclude the initial state of this patient was MCI because she was not normal nor demented but the neuronal activity was continuously going down.
(1) J. Hara, T. Musha and W. R. Shankle, Approximating dipoles from human EEG activity: the effect of dipole source configuration on dipolarity using single dipole mod-els, IEEE Trans. Biomed. Eng., 46, 2, 125-129, 1999; J. Hara, W. R. Shankle and T. Musha, Cortical Atrophy in Alzheimer's Disease Unmasks Electrically Silent Sulci and Lowers EEG Dipolarity, IEEE Trans. Biomed. Eng., vol.46, no.8, 905-910, 1999. (2) T.Musha, T.Asada, F.Yamashita, T.Kinoshita, H.Matsuda, M.Uno, Z.Chen and W.R.Shankle, "A new EEG method for estimating cortical neuronal impairment that is sensitive to early stage Alzheimer’s disease," Clinical Neurophysiology, 113 (2002) 1052-1058. (3) T.Musha, T.Asada, F.Yamashita, T.Kinoshita, H.Matsuda, M.Uno, Z.Chen and W.R.Shankle, "A new EEG method for estimating cortical neuronal impairment that is sensitive to early stage Alz-heimer’s disease," Clinical Neurophysiology, 113 (2002) 1052-1058.
CODICE ANTIDOPING DEL MOVIMENTO OLIMPICO Elenco delle classi di sostanze vietate e dei metodi proibiti 2003 Approvato dalla Giunta Nazionale Coni con provvedimento n. 735 del 21 novembre 2002. 1° GENNAIO 2003 I. CLASSI DI SOSTANZE VIETATE STIMOLANTI a Le sostanze vietate della classe (A.a) includono i seguenti esempi con entrambi i loro isomeri L e D: amifenazolo, amfetam
Nicotine & Tobacco Research Nicotine & Tobacco Research Advance Access published July 9, 2010 Original Investigation The use of snus for quitting smoking compared with medicinal products Karl Erik Lund, Ph.D., 1 Ann McNeill, Ph.D., 2 & Janne Scheffels, Ph.D. 1 1 Norwegian Institute for Alcohol and Drug Research, Oslo, Norway 2 UK Centre for Tobacco Control Studies