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LS3 Restless legs syndrome
S94
Luncheon Seminar LS1 Cognitive impairment in mood disorders K. Nakagome1 Division of Neuropsychiatry Department of Brain and Neuroscience Faculty of Medicine, Tottori University, Tottori, Japan 1
In the past 20 years, the critical importance of cognition has been highlighted from its relevance to functional status and outcome in schizophrenia. Accordingly, there has been a rapidly growing body of work on methods of enhancing cognition in schizophrenia as a means to facilitate improved outcome and quality of life for patients with schizophrenia. At the same time, this move has raised new questions about the specificity of cognitive impairment to schizophrenia and the degree to which similar cognitive impairment may be present in other disorders. Historically, mood disorders were considered to be episodic, which involve depressive, euthymic and, in case of bipolar disorder, manic phases, but recent findings have indicated that they frequently take more chronic and sustained course in terms of function and quality of life. Numerous patients with mood disorders experience difficulties in maintaining job performance as an acceptable level even after the mood level was improved. Previously, cognitive impairment was considered to be present specifically in the acute phase of illnesses, however, recent longitudinal reports show that impairment may be long lasting despite mood symptom reduction and recovery. Several reports also demonstrated that the cognitive impairment in mood disorders is a critical predictive factor of functional outcome, which is similar to the case in schizophrenia. Findings are still divergent in terms of the profile of cognitive impairment in mood disorders, presumably because mood disorders are essentially a heterogeneous group of illnesses and psychotic and nonpsychotic as well as monopolar and bipolar disorders are well recognized as qualitatively different subtypes. Interestingly, however, increasing number of reports suggest that the profile of cognitive impairment in psychotic mood disorders are very similar to that in schizophrenia, which support the hypothesis of a continuum between mood disorders and schizophrenia, in which psychotic symptoms may play an important role. LS2 Gene and cell therapy for neurodegenerative disorders H. Mochizuki1 1 Neurology Department, University of Kitasato, Kanagawa, Japan Even now, we cannot achieve complete recovery for neurodegenerative disorders, such as Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS). Most patients with ALS develop motor complications within a few years. Gene and cell therapies are new therapeutic strategies that provide neuroprotection and neurorestoration for neurons damaged by neurodegenerative disorders. This seminar will summarize a series of clinical trials that have been held around the world on gene and cell therapies for PD and ALS. Gene therapy for PD has started in the United States and Japan, and clinical trials with more than twenty patients have begun. To date, there have been no reports of notable adverse reactions caused by the administration of viral vectors. Therefore, the day will come when patients can select gene therapy as a treatment for PD. Unfortunately, gene therapy has not produced good results with ALS patients, but several clinical trials of cell transplantation for ALS patients have started in the United States. We also must pay attention to the ethical problems of providing gene therapy to patients with neurodegenerative disorders. As an ex vivo gene therapy, induced pluripotent stem (iPS) cells could be useful in the future for treating PD patients. At this seminar, I will describe some of the advances achieved using iPS cells for neurodegenerative disorders.
Oral Presentations: Luncheon Seminar LS3 Restless legs syndrome C. Trenkwalder1 1 Paracelsus-Elena Hospital, Center of Movement Disorders, Kassel, Germany The restless legs syndrome (RLS) is characterized by an overall prevalence of between 5 and 10% in the adult general population of Europe (Berger et al 2004, Tison et al 2005), in Asia there are lower prevalences (1.5% RLS in females (Mizuno et al 2005). The Essential Criteria (Allen et al 2003) for diagnosis of RLS are: (i) an urge to move the legs, usually accompanied or caused by uncomfortable and unpleasant sensations in the legs, which are (ii) worse during rest/inactivity, (iii) partially or totally relieved by movement and (iv) worse at night/in the evening. The diagnosis should be established using a clinical interview including the family history, comorbidities, sleep habits and psychiatric syndromes. The severity of RLS is documented by the IRLS (International restless legs syndrome severity scale). Additional laboratory analysis including ferritin and urea are necessary to detect acquired cases. A reduced brain iron storage, an altered dopamine system or spinal disinhibition phenomenons can influence RLS symptoms. The treatment of choice following controlled trials available are dopaminergic agents, non-ergotdopamine agonists being licensed for RLS in as many countries as Europe, the US, Australia and Asia. Opioids (Walters et al 1993), gabapentin and pregabalin are alternative treatments, but large trials are not yet available. Large-scale controlled trials are available for the non-ergot DA pramipexole (Winkelman et al 2006) and ropinirole (Trenkwalder et al 2004) and the rotigotine transdermal system (Trenkwalder et al 2008). Recommendations with low dosages mostly given before bedtime alleviate RLS nocturnal symptoms, improve subjective and objective QoSleep, reduce PLMS, and improve daytime symptoms including QoL. Augmentation (a worsening and earlier onset of RLS symptoms during the day after a dopaminergic treatment has been initiated) may limit the long-term use of levodopa and dopamine agonists (Allen et al 1996, Garcia-Borreguero et al 2007). LS4 Definition and treatment of depression T. Kinoshita1 1 Department of Psychiatry, Kansai Medical University, Osaka, Japan In contemporary Japan, depression is even said to be a “mental cold”, and the number of persons affected has been increasing at a rapid pace. The background of the times also seems to have had a major impact. In the “profit-first” philosophy, personnel downsizing is pressed forward, while on the other hand creating a highly transparent world, and being under pressure to cope with it, being overwhelmed by the volume of work, and becoming exhausted seem to often evolve into depression. If the disease classification were reorganized based on the size of disability-based economic loss, i.e., Disability Adjusted Life Year (DALY), it is claimed that in 2020 depression would rank as the number 2 disease. Moreover, in recent years depression is said to be increasing in young adults, however, we think that immature or unbalanced personality development plays a large role in adolescent depression. The names “immature-type depression” and “depression of dysthymic type” have been applied to it, and although it is included in depression, I think that such a state should be considered separately from depression per se. Pharmacotherapy is the main method of treating depression. Selective serotonin reuptake inhibitors (SSRIs), selective serotonin-norepinephrine reuptake inhibitors (SNRIs), and noradrenergic and specific serotonergic antidepressants (NaSSAs) are commonly used.
Luncheon Seminar LS1 Cognitive impairment in mood disorders K. Nakagome1 Division of Neuropsychiatry Department of Brain and Neuroscience Faculty of Medicine, Tottori University, Tottori, Japan 1
In the past 20 years, the critical importance of cognition has been highlighted from its relevance to functional status and outcome in schizophrenia. Accordingly, there has been a rapidly growing body of work on methods of enhancing cognition in schizophrenia as a means to facilitate improved outcome and quality of life for patients with schizophrenia. At the same time, this move has raised new questions about the specificity of cognitive impairment to schizophrenia and the degree to which similar cognitive impairment may be present in other disorders. Historically, mood disorders were considered to be episodic, which involve depressive, euthymic and, in case of bipolar disorder, manic phases, but recent findings have indicated that they frequently take more chronic and sustained course in terms of function and quality of life. Numerous patients with mood disorders experience difficulties in maintaining job performance as an acceptable level even after the mood level was improved. Previously, cognitive impairment was considered to be present specifically in the acute phase of illnesses, however, recent longitudinal reports show that impairment may be long lasting despite mood symptom reduction and recovery. Several reports also demonstrated that the cognitive impairment in mood disorders is a critical predictive factor of functional outcome, which is similar to the case in schizophrenia. Findings are still divergent in terms of the profile of cognitive impairment in mood disorders, presumably because mood disorders are essentially a heterogeneous group of illnesses and psychotic and nonpsychotic as well as monopolar and bipolar disorders are well recognized as qualitatively different subtypes. Interestingly, however, increasing number of reports suggest that the profile of cognitive impairment in psychotic mood disorders are very similar to that in schizophrenia, which support the hypothesis of a continuum between mood disorders and schizophrenia, in which psychotic symptoms may play an important role. LS2 Gene and cell therapy for neurodegenerative disorders H. Mochizuki1 1 Neurology Department, University of Kitasato, Kanagawa, Japan Even now, we cannot achieve complete recovery for neurodegenerative disorders, such as Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS). Most patients with ALS develop motor complications within a few years. Gene and cell therapies are new therapeutic strategies that provide neuroprotection and neurorestoration for neurons damaged by neurodegenerative disorders. This seminar will summarize a series of clinical trials that have been held around the world on gene and cell therapies for PD and ALS. Gene therapy for PD has started in the United States and Japan, and clinical trials with more than twenty patients have begun. To date, there have been no reports of notable adverse reactions caused by the administration of viral vectors. Therefore, the day will come when patients can select gene therapy as a treatment for PD. Unfortunately, gene therapy has not produced good results with ALS patients, but several clinical trials of cell transplantation for ALS patients have started in the United States. We also must pay attention to the ethical problems of providing gene therapy to patients with neurodegenerative disorders. As an ex vivo gene therapy, induced pluripotent stem (iPS) cells could be useful in the future for treating PD patients. At this seminar, I will describe some of the advances achieved using iPS cells for neurodegenerative disorders.
Oral Presentations: Luncheon Seminar LS3 Restless legs syndrome C. Trenkwalder1 1 Paracelsus-Elena Hospital, Center of Movement Disorders, Kassel, Germany The restless legs syndrome (RLS) is characterized by an overall prevalence of between 5 and 10% in the adult general population of Europe (Berger et al 2004, Tison et al 2005), in Asia there are lower prevalences (1.5% RLS in females (Mizuno et al 2005). The Essential Criteria (Allen et al 2003) for diagnosis of RLS are: (i) an urge to move the legs, usually accompanied or caused by uncomfortable and unpleasant sensations in the legs, which are (ii) worse during rest/inactivity, (iii) partially or totally relieved by movement and (iv) worse at night/in the evening. The diagnosis should be established using a clinical interview including the family history, comorbidities, sleep habits and psychiatric syndromes. The severity of RLS is documented by the IRLS (International restless legs syndrome severity scale). Additional laboratory analysis including ferritin and urea are necessary to detect acquired cases. A reduced brain iron storage, an altered dopamine system or spinal disinhibition phenomenons can influence RLS symptoms. The treatment of choice following controlled trials available are dopaminergic agents, non-ergotdopamine agonists being licensed for RLS in as many countries as Europe, the US, Australia and Asia. Opioids (Walters et al 1993), gabapentin and pregabalin are alternative treatments, but large trials are not yet available. Large-scale controlled trials are available for the non-ergot DA pramipexole (Winkelman et al 2006) and ropinirole (Trenkwalder et al 2004) and the rotigotine transdermal system (Trenkwalder et al 2008). Recommendations with low dosages mostly given before bedtime alleviate RLS nocturnal symptoms, improve subjective and objective QoSleep, reduce PLMS, and improve daytime symptoms including QoL. Augmentation (a worsening and earlier onset of RLS symptoms during the day after a dopaminergic treatment has been initiated) may limit the long-term use of levodopa and dopamine agonists (Allen et al 1996, Garcia-Borreguero et al 2007). LS4 Definition and treatment of depression T. Kinoshita1 1 Department of Psychiatry, Kansai Medical University, Osaka, Japan In contemporary Japan, depression is even said to be a “mental cold”, and the number of persons affected has been increasing at a rapid pace. The background of the times also seems to have had a major impact. In the “profit-first” philosophy, personnel downsizing is pressed forward, while on the other hand creating a highly transparent world, and being under pressure to cope with it, being overwhelmed by the volume of work, and becoming exhausted seem to often evolve into depression. If the disease classification were reorganized based on the size of disability-based economic loss, i.e., Disability Adjusted Life Year (DALY), it is claimed that in 2020 depression would rank as the number 2 disease. Moreover, in recent years depression is said to be increasing in young adults, however, we think that immature or unbalanced personality development plays a large role in adolescent depression. The names “immature-type depression” and “depression of dysthymic type” have been applied to it, and although it is included in depression, I think that such a state should be considered separately from depression per se. Pharmacotherapy is the main method of treating depression. Selective serotonin reuptake inhibitors (SSRIs), selective serotonin-norepinephrine reuptake inhibitors (SNRIs), and noradrenergic and specific serotonergic antidepressants (NaSSAs) are commonly used.