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3.5.3 TAI CHI AND PARKINSON'S DISEASE
Wednesday, 14 December 2011 / Parkinsonism and Related Disorders 18S2 (2012) S161–S234
3. The triad of enhanced SEP, back averaged potential and LLR may be dissociated, suggesting different pathophysiological mechanisms underpin these phenomena. Many forms of myoclonus lie on a spectrum between myoclonus and tremor. Some have clearcut evidence for being of cortical origin, whereas other forms are cortical-subcortical or purely subcortical. The role of subcortical structures in influencing electrophysiological phenomena is poorly understood, and merits further investigation. 3.3.2 MYOCLONUS: ELECTRO-CLINICAL MYOCLONUS SYNDROMES J.N. Caviness. Neurology, Mayo Clinic College of Medicine, Scottsdale, AZ, USA Myoclonus is defined as sudden, brief, shock-like, involuntary movements caused by muscular contractions or inhibitions. Numerous conditions and disease may give rise to myoclonus. Two major strategies are used to guide classification: etiological and neurophysiological classification systems. The etiological classification, proposed a few decades ago, organizes the myoclonus etiologies by major categories of clinical presentation. This classification consists of: (1) Physiologic (normal), (2) Essential (mostly monosymptomatic, stable), (3) Epileptic (part of a seizure disorder), and (4) Symptomatic (secondary to defined neurologic or medical illness). Neurophysiological classification schemes offer additional information to complement the etiological classification scheme proposed a few decades ago. Neurophysiological classification categorizes myoclonus according to its source, electrophysiology characteristics, and provides some insight about pathophysiology mechanism of myoclonus types. This session will discuss a physiological classification scheme that expands on the previous older system of Cortical, Subcortical, and Spinal. Based on up to date information, the presented physiological classification categories are: (1) Cortical, (2) Cortical-Subcortical, (3) Subcortical/Non-segmental, (4) Segmental, and (5) Peripheral. The cases for this session will be presented as electro-clinical syndromes that combine: (a) neuroanatomical source, (b) common clinical characteristics, (c) neuronal circuitry characteristics which may be appreciated through neurophysiological testing, and (d) symptomatic treatment strategy. 3.3.3 MYOCLONUS: CLINICAL PRESENTATION E. Roze. Neurology, Salpˆetri`ere Hospital, Paris, France Propriospinal myoclonus and myoclonus dystonia are both electroclinical syndromes. Myoclonus-dystonia is an inherited syndrome with mainly dominant paternal inheritance. In this genetically heterogeneous syndrome, mutation or deletion of the epsilon sarcoglycan gene is found in about 40% of families. The typical phenotype consists of very brief, subcortical, myoclonic jerks, which may be either isolated or associated with mild to moderate dystonia and generally predominate in the upper body. Onset in the first two decades is the rule. The pathogenic mechanism is likely to include dysfunction of the basal ganglia network. Pharmacological treatments are disappointing. Deep brain stimulation is an option in severe forms. Propriospinal myoclonus (PSM) is characterized by myoclonic jerks arising in muscles corresponding to a myelomere and spreading rostrally and caudally to the other myotomes. The trigger signal spreads slowly, along propriospinal pathways. PSM can be idiopathic or secondary to various disorders. Most patients had a myoclonic generator at the thoracic level, with a myoclonus duration between 200 ms and 2 s. Involvement of the abdominal wall muscles, worsening in the lying position, premonitory sensation and wake-sleep transition phase worsening are good clinical clues. Symptomatic treatment of PSM is not straightforward; clonazepam and zonisamide being most effective drug.
S163
Chinese Session 08:30–10:00 Alternative Medicine for PD Chairpersons: Guoguang Peng, China; Renmin Yang, China 3.5.1 ACUPUNCTURE AND PARKINSON’S DISEASE A. Liu. Qilu Hospital of Shandong University, Jinan, China Parkinson’s disease (PD) is a chronic neurodegenerative disorder with multiple etiological factors involved in disease pathogenesis. Currently, there are many treatment methods of Parkinson’s disease. Acupuncture, as a common complementary treatment has been widely used for Parkinson’s disease. Is acupuncture effective for PD? Which acupoints are specific to motor function? We analyzed the literature of acupuncture for the treatment of Parkinson disease from Jan 1994 to Nov 2010. We calculated the using frequency of all acupoints and found out the commonly used acupoints, less used acupoints, and their distribution. There were 66 articles recording the acupuncture treatment for the Parkinson disease with 147 acupoints involved. The commonly used 20 acupoints were GV20, LR3, LI4, GB20, chorea-trembing controlled area, ST36 etc, while the less used 61 were GB12, BL10, and CV6, with a basic rule of selecting points in the cephalic region and limbs. The licensed acupuncturist made the point prescription following the analyzing result for 40 PD patients from January 2011 to July 2011. Patients were evaluated before and after acupuncture with UPDRS; Fatigue Scale; HAMD; non-motor symptoms scale by experienced neurologist. We found patients received expected curative effect after the acupuncture especially improved nonmotor problem (sleep, fatigue, pain etc). 3.5.2 HERBAL MEDICINE D. Cai. Zhongshan Hospital, Fudan University, Shanghai, China Abstract not available. 3.5.3 TAI CHI AND PARKINSON’S DISEASE Z.-F. Wang. Chinese PLA General Hospital, Beijing, China Tai chi is one of Chinese martial arts that combines deep breathing and relaxation with slow and gentle movements, and is claimed helpful for human health. There were clinical studies on the effects of tai chi for Parkinson’s disease, but randomized clinical trials (RCTs) of the tai chi in Parkinson’s disease (PD) were scarce. There is insufficient evidence-based data to support or refute the efficacy of tai chi for PD. Further study should be focused on the improvement of body balance and the prevention of falls in PD. 3.5.4 NEUROPROTECTION FROM NUTRIENTS IN NEURAL CULTURE W. Rausch1 , R. Moldzio1 , K. Radad2 . 1 Department Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria; 2 Department of Pathology, King Khalid University, Abha, Saudi Arabia Aging and disease related degenerative processes leading to neuronal death are caused by a lack of supply of necessary nutrients to the brain and the action of free radicals. Fruits, vegetables and herbs and the vast array of contained flavones and polyphenols are considered beneficial. Particular Chinese herbs may be among usful candidates. Their chronic intake or use of particular ingredients thus should extend the life span of neurons thus delaying neurodegenerative diseases as e.g. Parkinsons’ disease (PD). Simple concepts are in contrast to a complex reality. A clinical proof that a particular nutrient will guarantee long lived and healthy neurons is hard to achieve. Cellular models measure the direct effects to individual neurons. They mimic neurodegeneration by release of free radicals by heavy metals, UV-light and serum
3. The triad of enhanced SEP, back averaged potential and LLR may be dissociated, suggesting different pathophysiological mechanisms underpin these phenomena. Many forms of myoclonus lie on a spectrum between myoclonus and tremor. Some have clearcut evidence for being of cortical origin, whereas other forms are cortical-subcortical or purely subcortical. The role of subcortical structures in influencing electrophysiological phenomena is poorly understood, and merits further investigation. 3.3.2 MYOCLONUS: ELECTRO-CLINICAL MYOCLONUS SYNDROMES J.N. Caviness. Neurology, Mayo Clinic College of Medicine, Scottsdale, AZ, USA Myoclonus is defined as sudden, brief, shock-like, involuntary movements caused by muscular contractions or inhibitions. Numerous conditions and disease may give rise to myoclonus. Two major strategies are used to guide classification: etiological and neurophysiological classification systems. The etiological classification, proposed a few decades ago, organizes the myoclonus etiologies by major categories of clinical presentation. This classification consists of: (1) Physiologic (normal), (2) Essential (mostly monosymptomatic, stable), (3) Epileptic (part of a seizure disorder), and (4) Symptomatic (secondary to defined neurologic or medical illness). Neurophysiological classification schemes offer additional information to complement the etiological classification scheme proposed a few decades ago. Neurophysiological classification categorizes myoclonus according to its source, electrophysiology characteristics, and provides some insight about pathophysiology mechanism of myoclonus types. This session will discuss a physiological classification scheme that expands on the previous older system of Cortical, Subcortical, and Spinal. Based on up to date information, the presented physiological classification categories are: (1) Cortical, (2) Cortical-Subcortical, (3) Subcortical/Non-segmental, (4) Segmental, and (5) Peripheral. The cases for this session will be presented as electro-clinical syndromes that combine: (a) neuroanatomical source, (b) common clinical characteristics, (c) neuronal circuitry characteristics which may be appreciated through neurophysiological testing, and (d) symptomatic treatment strategy. 3.3.3 MYOCLONUS: CLINICAL PRESENTATION E. Roze. Neurology, Salpˆetri`ere Hospital, Paris, France Propriospinal myoclonus and myoclonus dystonia are both electroclinical syndromes. Myoclonus-dystonia is an inherited syndrome with mainly dominant paternal inheritance. In this genetically heterogeneous syndrome, mutation or deletion of the epsilon sarcoglycan gene is found in about 40% of families. The typical phenotype consists of very brief, subcortical, myoclonic jerks, which may be either isolated or associated with mild to moderate dystonia and generally predominate in the upper body. Onset in the first two decades is the rule. The pathogenic mechanism is likely to include dysfunction of the basal ganglia network. Pharmacological treatments are disappointing. Deep brain stimulation is an option in severe forms. Propriospinal myoclonus (PSM) is characterized by myoclonic jerks arising in muscles corresponding to a myelomere and spreading rostrally and caudally to the other myotomes. The trigger signal spreads slowly, along propriospinal pathways. PSM can be idiopathic or secondary to various disorders. Most patients had a myoclonic generator at the thoracic level, with a myoclonus duration between 200 ms and 2 s. Involvement of the abdominal wall muscles, worsening in the lying position, premonitory sensation and wake-sleep transition phase worsening are good clinical clues. Symptomatic treatment of PSM is not straightforward; clonazepam and zonisamide being most effective drug.
S163
Chinese Session 08:30–10:00 Alternative Medicine for PD Chairpersons: Guoguang Peng, China; Renmin Yang, China 3.5.1 ACUPUNCTURE AND PARKINSON’S DISEASE A. Liu. Qilu Hospital of Shandong University, Jinan, China Parkinson’s disease (PD) is a chronic neurodegenerative disorder with multiple etiological factors involved in disease pathogenesis. Currently, there are many treatment methods of Parkinson’s disease. Acupuncture, as a common complementary treatment has been widely used for Parkinson’s disease. Is acupuncture effective for PD? Which acupoints are specific to motor function? We analyzed the literature of acupuncture for the treatment of Parkinson disease from Jan 1994 to Nov 2010. We calculated the using frequency of all acupoints and found out the commonly used acupoints, less used acupoints, and their distribution. There were 66 articles recording the acupuncture treatment for the Parkinson disease with 147 acupoints involved. The commonly used 20 acupoints were GV20, LR3, LI4, GB20, chorea-trembing controlled area, ST36 etc, while the less used 61 were GB12, BL10, and CV6, with a basic rule of selecting points in the cephalic region and limbs. The licensed acupuncturist made the point prescription following the analyzing result for 40 PD patients from January 2011 to July 2011. Patients were evaluated before and after acupuncture with UPDRS; Fatigue Scale; HAMD; non-motor symptoms scale by experienced neurologist. We found patients received expected curative effect after the acupuncture especially improved nonmotor problem (sleep, fatigue, pain etc). 3.5.2 HERBAL MEDICINE D. Cai. Zhongshan Hospital, Fudan University, Shanghai, China Abstract not available. 3.5.3 TAI CHI AND PARKINSON’S DISEASE Z.-F. Wang. Chinese PLA General Hospital, Beijing, China Tai chi is one of Chinese martial arts that combines deep breathing and relaxation with slow and gentle movements, and is claimed helpful for human health. There were clinical studies on the effects of tai chi for Parkinson’s disease, but randomized clinical trials (RCTs) of the tai chi in Parkinson’s disease (PD) were scarce. There is insufficient evidence-based data to support or refute the efficacy of tai chi for PD. Further study should be focused on the improvement of body balance and the prevention of falls in PD. 3.5.4 NEUROPROTECTION FROM NUTRIENTS IN NEURAL CULTURE W. Rausch1 , R. Moldzio1 , K. Radad2 . 1 Department Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria; 2 Department of Pathology, King Khalid University, Abha, Saudi Arabia Aging and disease related degenerative processes leading to neuronal death are caused by a lack of supply of necessary nutrients to the brain and the action of free radicals. Fruits, vegetables and herbs and the vast array of contained flavones and polyphenols are considered beneficial. Particular Chinese herbs may be among usful candidates. Their chronic intake or use of particular ingredients thus should extend the life span of neurons thus delaying neurodegenerative diseases as e.g. Parkinsons’ disease (PD). Simple concepts are in contrast to a complex reality. A clinical proof that a particular nutrient will guarantee long lived and healthy neurons is hard to achieve. Cellular models measure the direct effects to individual neurons. They mimic neurodegeneration by release of free radicals by heavy metals, UV-light and serum