S21-4. Neuropathological hypothesis of sleep dysfunction in Schizophrenia

S21-4. Neuropathological hypothesis of sleep dysfunction in Schizophrenia

e28 Society Proceedings / Clinical Neurophysiology 124 (2013) e19–e38 S19-1. A face recognition study with morphing human face into monkey face—Emi ...

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Society Proceedings / Clinical Neurophysiology 124 (2013) e19–e38

S19-1. A face recognition study with morphing human face into monkey face—Emi Yamada, Katsuya Ogata, Tomokazu Urakawa, Shozo Tobimatsu (Kyushu University, Fukuoka, Japan) In general, N170 in response to human face is larger in amplitude than other face categories, and N170 shows larger amplitude for the inverted face than for the upright face (face inversion effect, FIE). However, it is still controversial that the differences in N170 among the face categories are due to physical variances such as contrast and spatial frequency (SF). In order to elucidate the face- and species-specificity of N170, high-density ERPs were recorded in 10 adults while viewing morphing faces between human and monkey. We used two types of stimuli with controlled SF and uncontrolled one. When viewing the controlled SF stimuli, both amplitudes and latencies of N170 were significantly modulated in proportion to the human ratio. Moreover, the larger amplitudes of FIE were observed only for faces which contained higher human ratio though the latencies were delayed in all faces. In contrast, N170 showed no differences among the stimuli using the uncontrolled SF stimuli. However, FIE showed similar trends observed under the controlled SF stimuli in both latencies and amplitudes. These findings suggest the importance of SF and human ratio on N170. Therefore, we conclude that N170 reflects species-specific face processing and that FIE is influenced by species. doi:10.1016/j.clinph.2013.02.066

S20-2. Event-related potentials in children: Evaluation of cognitive development—Tatsuo Fuchigami (Nihon University School of Medicine, Tokyo, Japan) Event-related potentials (ERPs) include P300 reflect various cognitive functions. Studies of ERPs in children, based on a task relevant oddball paradigm, reveal a decrease in the latency of P300 with increasing age. This developmental change could be related to maturation phenomena in cognitive processes. Squires et al. delineated P3a and P3b components in P300. In our study, P300 under the state of ignoring, likely corresponds to P3a (passive attention), whereas conventional P300 corresponds to P3b (active attention). These findings indicate a developmental difference between the P3a and P3b potentials. The development of fundamental cognitive function like passive attention reaches the adult level at an earlier age than the cognitive like active attention. To evaluate auditory spatial cognitive function, age correlations for ERPs in response to auditory stimuli with a Doppler effect shortened more rapidly with age than did the P300 latency for tone-pips, and the latencies for different conditions became similar towards the late teens. These findings provide evidence that auditory cognitive function, including auditory spatial cognitive function, had reached the adult level by about this age. P300 in response to different stimuli may provide more detailed information that could enable to evaluate cognitive development in children. doi:10.1016/j.clinph.2013.02.067

S21-1. Exercise and physical – Mental health—Sunao Uchida (Faculty of Sport Sciences, Waseda University, Tokorozawa, Japan) There has been a relatively new trend of exercise treatment for depression. Such studies have been done since 1970’s but number of the studies is increasing after 1990’s. Most of the studies show efficacy of exercise to improve mood in depressive patients, and

there have been no studies which reported deterioration of depressive symptoms. Many studies uses moderate to intensive aerobic exercise, more than 3 times a week for the treatment. Naturally, fitness level of exercise group improved after the session which usually last for three to four months. However, many previous studies lack precise control group and subject number was low. On the other hand, there have also been many studies which reports exercise effect to improve sleep quality. Such improvements also have curative effect for depression. Considering the factors of exercise, sleep and mood, there could be a scheme that exercise -> (improvement of mood, sleep and physical condition) -> improvement of depressive symptoms. For the future studies, we should further investigate appropriate exercise type, intensity and timing to establish therapeutic effect of exercise on depression. doi:10.1016/j.clinph.2013.02.068

S21-2. Influence of sleep deprivation on suppressed aversive event memory—Kenichi Kuriyama (National Center of Neurology and Psychiatry, Tokyo, Japan) Aversive memory consolidation is implicated in the pathology of PTSD. Sleep is crucial for memory consolidation, thus sleep deprivation immediately following an aversive event reduces fear by eliminating a sleep dependent memory consolidation process. Although acute insomnia could prevent development of PTSD, it is considered as a plausible risk factor for PTSD. We examined the effects of sleep deprivation and memory suppression on the subsequent enhancement of aversive event and fear memories in healthy humans. Subjects were exposed to aversive and nonaversive events, then their contextual recognition performances were tested later the same day and again after 2 days. Half of the subjects were instructed to quickly forget the events and the other half to remember. Moreover, half of the subjects were totally deprived of initial nocturnal sleep while the other half slept normally. Suppression of aversive memory acquisition not only immediately reduced the stress reaction to aversive events, but also impaired retention of event memory. However, it enhanced recognized fear and even enhanced fear when postevent sleep was deprived. Memory suppression, which provides a psychological model of memory repression, enhances fear and ruins the potential of acute insomnia. Our findings provide a hint as to clinical PTSD pathophysiology. doi:10.1016/j.clinph.2013.02.069

S21-4. Neuropathological hypothesis of sleep dysfunction in Schizophrenia—Nozomu Kotorii, Naohisa Uchimura (Kurume University School of Medicine, Fukuoka, Japan) The purpose of this lecture is to review the polysomnographic non-rapid eye movement sleep abnormalities in schizophrenic patients and to present evidence for possible pathophysiologic mechanisms. Deficits of delta wave sleep are commonly reported sleep architecture abnormalities in schizophrenia. In the1960’s, Feinberg described this abnormality and about twenty years later, he first proposed that a decline in synaptic density resulting from abnormal reorganization of brain structure during early adolescence might cause the decline in delta wave amplitude and the onset of schizophrenia. Recent neuropathological studies of schizophrenia revealed that the dendritic spine density was particularly reduced in layer three of the neocortex. And excessive spine pruning is now considered a potential factor underlying reduced cortical gray matter volume in schizophrenia.

Society Proceedings / Clinical Neurophysiology 124 (2013) e19–e38

Aberrant neuronal pruning is also believed to contribute to compromise the thalamocortical circuitry. Several recent studies have reported markedly reduced sleep spindle activity mediated by thalamocortical circuits in schizophrenia. Animal studies have reported sleep spindles have been linked to synaptic plasticity and memory consolidation. Thus, aberrant pruning can result in structural brain abnormalities and deficits of two distinct rhythms during sleep. Furthermore, each of these impairments appears to be associated with both cognitive deficits and symptoms of schizophrenia. doi:10.1016/j.clinph.2013.02.070

Workshop WS1-3. Attended video–audio polysomnographic study about patients with catathrenia (sleep related groaning)—Mutsumi Okura, Hisae Muraki (Sleep Medical Center, Osaka Kaisei Hospital, Osaka, Japan) Sleep related groaning (catathrenia), which is characterized by episodes of monotonous vocalization during sleep, has been integrated in the International Classification of Sleep Disorders 2nd edition as a new parasomnia. This condition should be differentiated from moaning during epileptic seizures, central sleep apnea, sleeprelated laryngospasm, snoring, and stridor. Attended video-polysomnography (PSG) with audio recording is necessary to make a diagnosis of catathrenia. As plysomnographic pattern of catathrenia closely resembles that of central sleep apnea, catathrenia can be easily scored erroneously or mistakenly recognized as central sleep apnea when polysomnogram alone is available. In catathrenia, a breath before an apnea is large inhalation, and associated activity in the snoring channel indicates a groaning noise. Since exhalation is prolonged, the patient’s breathing rate slows down during the episode. However, no oxygen desaturation occurs despite slower breathing rate. Catathrenia occurs both NREM and REM sleep depending on individuals. A few reports suggest that arousal mechanism plays an important role in triggering groaning, and some groups have proposed that catathrenia should be classified as sleep disordered breathing. Catathrenia can occur concomitantly with sleep bruxism and obstructive sleep apnea. In conclusion, detailed analysis of PSG data with video–audio recording is important to clarify the pathophysiology of catathrenia. doi:10.1016/j.clinph.2013.02.071

WS2-1. A case of slowly progressive muscular atrophy in post hematopoietic stem cell transplantation: Electrophysiological and pathological findings in musculoskeletal chronic graft-versus-host disease (cGVHD)—Kenji Sekiguchi a, Maki Kanzawa b, Ichizo Nishino c, Fumio Kanda a, Tatsushi Toda a, Nobuo Kohara d (a Department of Neurology, Kobe University, Kobe, Japan, b Department of Pathology, Kobe University, Kobe, Japan, c National center of Neurology and Psychiatry, Kobe, Japan, d Department of Neurology, Kobe General Hospital, Kobe, Japan) A 38-year-old man who received bone marrow transplantation four years ago for acute lymphocytic leukemia. He felt muscle cramps and became a bed-bound state because of progressing polyarthralgia in the following year. Marked muscle atrophies, mild weakness, joint contractures, and sclerotic skin changes were noted. Motor conduction studies revealed reduction in the amplitude

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(2.4 mV), in the conduction velocity (41 m/s), and in the duration (11 ms) of compound muscle action potentials in the right median nerve. In concentric needle electromyography, low amplitude polyphasic motor unit potentials discharged with rapid frequency without spontaneous discharges. Mean muscle fiber CV elicited by monopolar needle electrodes were slow compared with normal control. The electrodiagnosis was myopathic change which consists of cluster of atrophic fibers, discriminated from myositis and motor neuron disease. Muscle specimen from autopsy revealed marked atrophied muscle fibers less than 10 lm in diameter. There were no necrotic and inflammatory processes. In the fascia, small numbers of infiltrating CD8 positive T lymphocytes with proliferation of collagen fibers were seen, compatible with fasciitis. There were few reports about electrophysiological and pathological findings of fasciitis in cGVHD, which must be focused on the future as distinct from the myositis. doi:10.1016/j.clinph.2013.02.072

WS2-2. Tingling of the foot followed by walking difficulty in a 91-year-old woman—Katsumi Kurokawa a, Toshikazu Shirakawa a, Shoji Hemmi a, Yumiko Kutoku a, Yoshihide Sunada a, Masahiro Sonoo b (a Kawasaki Medical School, Okayama, Japan, b Teikyo University School of Medicine, Tokyo, Japan) A 91-year-old woman felt tingling sensation in her foot three weeks ago, followed by tingling in the hands. Soon after, her gait progressively had become unsteady. Neurological examination revealed weakness of bilateral hand muscles and toe extensors (3/5 in MRC scale), muscle wasting in hands, areflexia, superficial sensory loss showing glove-and-stocking type distribution, decreased vibration and proprioceptive sensation, and severe sensory ataxia. Cerebrospinal fluid showed 1.3 WBC/ll and 50 mg/dl protein. Guillain–Barré syndrome was suspected, although muscle wasting in her hands was atypical. Nerve conduction studies (NCS) demonstrated chronic motor and sensory demyelinating neuropathy with disproportionate distal slowing. The patterns of nerve conduction abnormalities were similar to atypical CIDP (distal acquired demyelinating symmetric neuropathy). She was treated by intravenous immunoglobulin (IVIg), then her gait improved soon after. A repeated NCS for four months after treatment showed the decrease of the distal latencies. However, nerve conduction velocity was still around 20 m/s for all examined nerves, suggesting a uniform demyelination. Anti-ganglioside and myelin associated glycoprotein antibodies were negative. Gene analysis demonstrated the DNA duplication in chromosome 17p11.2–p12. She was finally diagnosed as CMT1A associated with acquired demyelinating neuropathy (ataxic Guillain–Barré syndrome). doi:10.1016/j.clinph.2013.02.073

Oral session O1-E-2. Patterns of sensory electrophysiological abnormalities in Fisher syndrome—Yukari Sekiguchi, Sonoko Misawa, Kazumoto Shibuya, Sagiri Isose, Saiko Nasu, Satsuki Mitsuma, Yuta Iwai, Shigeki Oomori, Kazuo Shugimoto, Satoshi Kuwabara (Department of Neurology, Chiba University, Chiba, Japan) Fisher syndrome (FS) is characterized by triad of ataxia, areflexia, and ophthalmoplegia. To elucidate the pathophysiology of ataxia in FS, we reviewed extensively electrophysiological data of FS patients. We reviewed results of sensory nerve conduction studies, soleus Hreflex, postural body sway analysis and somatosensory-evoked